A  string galvanometer  is a sensitive fast-responding measuring instrument that uses a single fine filament of wire suspended in a strong magnetic field to measure small currents. In use, a strong light source is used to illuminate the fine filament, and the optical system magnifies the movement of the filament allowing it to be observed or recorded by photography.
The principle of the string galvanometer remained in use for  electrocardiograms  until the advent of electronic vacuum-tube amplifiers in the 1920s. [ 1 ]


Submarine cable telegraph systems of the late 19th century used a  galvanometer  to detect pulses of electric current, which could be observed and transcribed into a message. The speed at which pulses could be detected by the galvanometer was limited by its mechanical inertia, and by the inductance of the multi-turn coil used in the instrument.  Clément Adair, a French engineer, replaced the coil with a much faster wire or "string" producing the first string galvanometer. [ 2 ]


For most telegraphic purposes it was sufficient to detect the existence of a pulse. In 1892  André Blondel  described the dynamic properties of an instrument that could measure the wave shape of an electrical impulse, an  oscillograph . [ 1 ]


Augustus Waller had discovered electrical activity from the heart and produced the first electrocardiogram in 1887. [ 3 ]  But his equipment was slow. Physiologists worked to find a better instrument. In 1901,  Willem Einthoven  described the science background and potential utility of a string galvanometer, stating "Mr. Adair has already built an instrument with a wires stretched between poles of a magnet. It was a telegraph receiver." [ 4 ]  Einthoven developed a sensitive form of string galvanomter that allowed photographic recording of the impulses associated with the heartbeat. He was a leader in applying the string galvanometer to physiology and medicine, leading to today's electrocardiography. [ 5 ]   Einthoven was awarded the 1924  Nobel prize in Physiology or Medicine  for his work. [ 6 ]


Previous to the string galvanometer, scientists were using a machine called the capillary  electrometer  to measure the heart’s electrical activity, but this device was unable to produce results of a diagnostic level. [ 7 ]   Willem Einthoven  adapted  the string galvanometer at  Leiden University  in the early 20th century, publishing the first registration of its use to record an electrocardiogram in a  Festschrift  book in 1902. The first human electrocardiogram was recorded in 1887; however, it was not until 1901 that a quantifiable result was obtained from the string galvanometer. [ 8 ]  In 1908, the physicians  Arthur MacNalty , M.D. Oxon, and  Thomas Lewis  teamed to become the first of their profession to apply electrocardiography in medical diagnosis. [ citation needed ]


Einthoven's galvanometer consisted of a silver-coated  quartz  filament of a few centimeters length (see picture on the right) and negligible mass that conducted the electrical currents from the heart. This filament was acted upon by powerful  electromagnets  positioned either side of it, which caused sideways displacement of the filament in proportion to the current carried due to the  electromagnetic field . The movement in the filament was heavily magnified and projected through a thin slot onto a moving photographic plate. [ 9 ] [ 10 ]


The filament was originally made by drawing out a filament of glass from a crucible of molten glass. To produce a sufficiently thin and long filament an  arrow  was shot across the room so that it dragged the filament from the molten glass. The filament so produced was then coated with  silver  to provide the conductive pathway for the current. [ 11 ]  By tightening or loosening the filament it is possible to very accurately regulate the sensitivity of the galvanometer. [ 9 ]


The original machine required water cooling for the powerful electromagnets, required 5 operators [ 12 ]  and weighed some 600 lb. [ 10 ]


Patients are seated with both arms and left leg in separate buckets of saline solution. These buckets act as electrodes to conduct the current from the skin's surface to the filament. The three points of electrode contact on these limbs produces what is known as  Einthoven's triangle , a principle still used in modern-day ECG recording. [ 13 ]


A  stromuhr  (literally:  German  for  stream clock ) was a medical instrument designed by  Carl Ludwig  in 1867 to measure the strength of flow in major arteries and veins [ 1 ]  by means of animal experiments. [ 2 ]


For this purpose, the arteries were cut across and the stromuhr was attached between the proximal and distal stumps. The stromuhr had to be filled with the whole blood of the test animal or with a blood substitute solution beforehand. [ 3 ]


Subcutaneous implantable cardioverter defibrillator , or  S-ICD,  is an implantable medical device for detecting and terminating   ventricular tachycardia  and  ventricular fibrillation  in patients at risk of sudden cardiac arrest. [ 1 ]  It is a type of  implantable cardioverter defibrillator  but unlike the transvenous ICD, the S-ICD lead is placed just under the skin, leaving the heart and veins untouched.


The S-ICD was developed to reduce the risk of complications associated with transvenous leads. [ 2 ]  Potential complications, such as infections in the bloodstream and the need to remove or replace the leads in the heart, are minimised or entirely eliminated with the S-ICD system.


The generator is smaller than the S-ICD generator, which may result in a less visible implanted device. This could improve the time needed to get used to the implantable device, although this is subjective. The procedure can usually be done under local anesthesia and light sedation. The transvenous ICD is capable of  pacing  for  bradycardia  and delivering  antitachycardia pacing  (ATP).   However, device-related complications were numerically more frequent in patients with transvenous ICDs, inappropriate shocks are less frequent that in those with subcutaneous ICDs. [ 3 ]


The leads go into the vein and heart and will grow into the heart wall over time. This may increase the chance of complications if the leads need to be removed or replaced, as the procedure to extract an intracardiac leads can be a challenge. Because the leads need to go into the heart they need to be relatively thin and flexible, since they have to pass through (and remain in) the heart valve(s) and need to flex with every heartbeat. This makes the leads more vulnerable to lead fracture (and therefore complications). It has been demonstrated that  device-related complications were numerically more frequent in patients with transvenous ICDs. [ 3 ]  Due to the position of the pulse generator under the collarbone, it can be more visible with clothing with low neckline.


Patients who are relatively older, who need ICD for secondary prevention, or who have concomitant bradycardia requiring pacing, or heart failure requiring  cardiac resynchronisation therapy  are more suitable for transvenous ICD implantation. An older patient with ischemic cardiomyopathy and documented symptomatic ventricular tachycardia is a typical example. [ 4 ]


The lead does not go into the heart, which means it leaves the veins and the heart completely intact. This reduces chance of complications (e.g. systemic infections). Because the lead does not go into the heart it can be thicker and more robust. This minimizes / reduces the chance of lead fracture. In the event the system needs to be explanted, the procedure is a relatively simple surgical procedure.


The pulse generator is larger than most transvenous ICD pulse generators. This could result in a longer time needed to get used to it, although this is subjective. Depending on the physique of a person, the S-ICD may be more visible with bare chest. The procedure usually requires deep sedation or general anaesthesia, as creating a larger pocket between the muscles and tunnelling the lead over the sternum, as well as performing defibrillation threshold testing, can be quite painful. The S-ICD can deliver only temporary post-shock pacing, but cannot otherwise address bradycardia and cannot deliver anti-tachycardia pacing.  Inappropriate shocks were numerically more frequent in those with subcutaneous ICDs. [ 3 ]  Defibrillation testing has traditionally been considered mandatory in patients with subcutaneous implantable cardioverter–defibrillator to confirm appropriate ventricular fibrillation detection. [ 5 ]  However, PRAETORIAN-DFT  randomised clinical trial  is aiming to demonstrate non-inferiority of omitting DFT in patients undergoing S-ICD implantation in which the S-ICD system components are optimally positioned by calculated PRAETORIAN score. [ 6 ]


Patients who are relatively younger, who need ICD for primary prevention, and who do not require pacing or cardiac resynchronisation therapy, are more suitable for S-ICD implantation. A young survivor of aborted  sudden cardiac death  is a typical example.


SynCardia Systems, LLC , headquartered in  Tucson, Arizona , was founded in 2001 and is the sole manufacturer and provider of the world's only clinically proven and commercially approved Total Artificial Heart. [ 1 ]


The SynCardia temporary  Total Artificial Heart  (TAH) has been in clinical use for more than 35 years. [ 2 ]


SynCardia was founded in 2001 by cardiothoracic surgeon  Jack G. Copeland , MD; biomedical engineer Richard G. Smith, MSEE, CCE; and interventional cardiologist Marvin J. Slepian, MD; with Steven Langford BSEE, as General Manager.  Today, SynCardia is a wholly owned subsidiary of Picard Medical and remains the sole manufacturer and provider of the world’s only commercially approved Total Artificial Heart. In clinical use for more than 35 years, the SynCardia temporary Total Artificial Heart (TAH-t) is the most widely used and extensively studied Total Artificial Heart in the world.


In 2004, the  FDA  approved the SynCardia TAH (formerly known as the "CardioWest temporary Total Artificial Heart”) as a bridge to donor  heart transplant [ 1 ]  in cardiac transplant-eligible candidates at risk of imminent death from end-stage biventricular failure. [ 3 ]


SynCardia's products include the original 70cc TAH; the newer, smaller 50cc TAH, designed to fit patients of smaller stature, including more women and adolescents; the Companion 2 (C2) Hospital Driver, which provides pneumatic power to the TAH from implant through patient recovery in the hospital; and the Freedom Portable Driver, a smaller, portable pneumatic pump for the TAH that allows stable patients who meet discharge criteria to enjoy life at home while they wait for a matching donor heart. [ 2 ]


In addition to its being used as a bridge to transplant in the U.S., Canada and Europe, the 70cc TAH has supported several patients as a  destination therapy  in adult patients who are not eligible for transplant. The longest patient supported by the SynCardia Total Artificial Heart on a person who became not eligible for transplant was over 6 years and 9 months. He lived a near normal lifestyle at home with his wife. The smaller 50cc TAH is currently approved for use as a bridge to transplant for both pediatric and adult patients. [ 2 ]


In September 2016, SynCardia was acquired by Versa Capital Management, LLC, a Philadelphia-based private equity investment firm and then was acquired by Piccard Medical in September 2021, which has provided additional financial and operational resources. [ 4 ]


A documentary about the SynCardia TAH was released in 2016. [ 5 ]  Patrick Schnegelsberg was named CEO of SynCardia. [ 6 ]


Testosterone and the cardiovascular system  are the effects that the male hormone  testosterone  has on the  cardiovascular system .


The predominant androgen in men, testosterone, has shown to substantially decline throughout the  aging process . [ 1 ] [ 2 ]  The decline in both serum and total testosterone with age have been linked to several disease states in men. [ 1 ] [ 3 ] [ 4 ]  In particular,  cardiac failure  and  ischemic heart disease  have been linked to this natural biochemical decline in testosterone. [ 5 ] [ 6 ] [ 7 ]  Previously, the higher cardiovascular risk in men has been attributed in part to the negative effects of systemic testosterone, however, more recent research has highlighted the protective nature of testosterone against cardiovascular disease. [ 5 ]  The magnitude and mechanism of action by which low testosterone in men is influential in the pathogenesis of cardiovascular risk and the potential benefits of testosterone therapy has yet to be fully determined. [ 1 ]


Low testosterone is associated with an increased risk for  coronary artery disease  through the promotion of a pro-atherosclerotic environment. [ 5 ] [ 8 ] [ 9 ]  Some research has identified testosterone as a  vasodilator  and an  endothelium -repairing hormone within many regions in the body, including the coronary arteries. [ 10 ] [ 11 ]  Recent research depicts testosterone as important in decreasing the production of inflammatory cytokines such as  tumor necrosis factor alpha ,  interleukin-1beta  and  interleukin-6 , which are influential in atherosclerotic profiles. [ 10 ] [ 12 ]  Although it is believed that the reduction in inflammatory cytokines is related to a decreased atherosclerotic profile, the full explanation of this mechanism requires further research. [ 12 ] [ 13 ]


Testosterone has also shown to be effective as an anti-atherosclerotic through preventing aortic  cholesterol  deposition in both rabbits fed high cholesterol diets and mice with low-density lipoprotein gene knockout. [ 10 ] [ 14 ]  Fatty deposition within the aorta associated with low endogenous testosterone has been determined to be independent of the androgen receptor. [ 10 ]  Although the mechanism has yet to be fully determined, aromatase activity and the activation of estrogen receptor alpha is partially responsible for the atherosclerotic profile characteristic of low testosterone. [ 10 ]


Decreased systemic testosterone in men has also been reported in men with heart failure, whereby the severity of the disease is proportional to the reduction in systemic testosterone levels. [ 5 ]  Although a direct mechanism of action is not fully understood, some research attribute low testosterone to advancing side effects of heart failure, such as decreased exercise ability, decreased muscle mass, fatigue/ dyspnea  and  cachexia . [ 5 ]


Physiological testosterone is crucial for normal functionality in men. Long-term administration of physiological testosterone in mouse models has shown to be atheroprotective by increasing the HDL portion of cholesterol (the anti-atherosclerotic cholesterol). [ 10 ] [ 15 ]  The beneficial action of testosterone in elevating the HDL fraction can be attributed to its conversion via aromatase activity in adipose tissue into 17-beta estradiol and its subsequent activation of estrogen alpha-receptors; thus, more testosterone leads to greater conversion into estrogen and thus a healthier lipid profile. [ 10 ]  This understanding has been determined in several studies, although results of these studies are contradictory. [ 10 ] [ 16 ] [ 17 ]


Testosterone replacement therapy  in men diagnosed with pre-existing heart disease has been related to an increased risk of myocardial infarction. [ 18 ]  Furthermore, recent research has linked testosterone replacement therapy to an increase in deaths and other cardiovascular occurrences in men whom document a history of coronary artery disease. [ 19 ]  Further research is required to determine the full extent to which testosterone replacement therapy in aging men plays a role in the risk and/or advantage of cardiovascular occurrences. [ 20 ]


However, when given to men with  hypogonadism  in the short- and medium-term, testosterone replacement therapy does not increase the risk of cardiovascular events (including strokes and heart attacks and other heart diseases). The long-term safety of the therapy for this condition is not known yet. [ 21 ] [ 22 ]


The  third heart sound  or  S 3  is a rare extra  heart sound  that occurs soon after the normal two "lub-dub" heart sounds (S 1  and S 2 ). S 3  is associated with  heart failure .


It occurs at the beginning of the middle third of  diastole , approximately 0.12 to 0.18 seconds after S 2 . [ 1 ]  This produces a rhythm classically compared to the cadence of the word " Kentucky " with the final syllable (" -CKY [ 2 ] ") [ 3 ]  representing S 3 . One may also use the phrase "Slosh’-ing- IN " to help with the cadence (Slosh S 1 , -ing S 2 , -in S 3 ), as well as the pathology of the S 3  sound, [ 4 ]  or any other number of local variants.


S 3  may be normal in people under 40 years of age and some trained athletes but should disappear before middle age.  Re-emergence of this sound late in life is abnormal [ 5 ]  and may indicate serious problems such as  heart failure .  The sound of S 3  is lower in pitch than the normal sounds, usually faint, and best heard with the  bell  of the  stethoscope . [ citation needed ]


It has also been termed a  ventricular gallop  or a  protodiastolic gallop  because of its place in early diastole. It is a type of  gallop rhythm  by virtue of having an extra sound; the other gallop rhythm is called  S 4 . The two are quite different, but they may sometimes occur together forming a  quadruple gallop . If the  heart rate  is also very fast ( tachycardia ), it can become difficult to distinguish between S 3  and S 4  thus producing a single sound called a  summation gallop . S 3  is a dull, low-pitched sound best heard with the bell placed over the cardiac apex with the patient lying in the left lateral decubitus position. This heart sound when present in a child or young adult implies the presence of a supple ventricle that can undergo rapid filling. Conversely, when heard in a middle-aged or older adult, an S 3  is often a sign of disease, indicating increased ventricular filling due to congestive  heart failure  or severe mitral or tricuspid regurgitation. [ 6 ]


S 3  is thought to be caused by the undulation of blood back and forth between the walls of the ventricles initiated by the inflow of blood from the atria. The reason the third heart sound does not occur until the middle third of diastole is probably that, during the early part of diastole, the ventricles are not filled sufficiently to create enough tension for reverberation. It may also be a result of tensing of the  chordae tendineae  during rapid filling and expansion of the  ventricle . [ citation needed ]  Recent research suggests that  mitral valve  annulus diameter is one of the more important factors in producing the S3 sound. [ 7 ]


It is associated with  heart failure , [ 8 ]  caused by conditions which have:


S3 can also be due to tricuspid regurgitation, and could indicate hypertensive heart disease. [ citation needed ]


In conditions affecting the  pericardium  or diseases that primarily affect the heart muscle ( restrictive cardiomyopathies ) a similar sound can be heard, but is usually more high-pitched and is called a 'pericardial knock'.The S3 can also be confused with a widely split S2, or a mitral opening snap, but these sounds are typically of much higher pitch and occur closer to the onset of S2. [ citation needed ]


The condition itself does not need to be treated, but rather the underlying cause requires correction. Depending on the  etiology  the gallop rhythm may resolve spontaneously. [ citation needed ]


U.S. National STEMI Receiving Centers  are medical centers that specialize in receiving ST segment elevation  myocardial infarction  (STEMI) cases. These myocardial infarctions, or heart attacks, are due to fully blocked  coronary arteries . [ 1 ]


Since 2006, the  American College of Cardiology  and the  American Heart Association  have worked to implement a national designation of "STEMI Receiving Center" across the U.S., much like the certifications of trauma centers. [ 1 ]


STEMI patients account for over 400,000 of all Americans with MI. [ 2 ] [ 3 ]


The Utstein Style  is a set of guidelines for uniform reporting of  cardiac arrest . The Utstein Style was first proposed for  emergency medical services  in 1991.  The name derives from a 1990 conference of the  European Society of Cardiology , the European Academy
of Anesthesiology, the European Society for Intensive Care Medicine, and related national societies, held at the  Utstein Abbey  on the island of  Mosterøy, Norway .


Examples of cardiac arrest registries based on the Utstein Style include the  Cardiac Arrest Registry to Enhance Survival ,  Resuscitation Outcomes Consortium ,  Save Hearts in Arizona Registry and Education , and the  National Registry of CardioPulmonary Resuscitation .


VA conduction , also named  Ventriculoatrial conduction  and sometimes referred to as  Retrograde conduction , is the conduction backward phenomena in the  heart , where the conduction comes from the  ventricles  or from the  AV node  into and through the  atria . [ 1 ]


Retrograde VA conduction results in many different  symptoms , primarily those symptoms result from the delayed, nonphysiologic timing of  atrial  contraction in relation to  ventricular   contraction . [ 2 ]


A  vagal maneuver  is an action used to stimulate the parasympathetic nervous system by activating the  vagus nerve . The vagus nerve is the longest nerve of the  autonomic nervous system  and helps regulate many critical aspects of human physiology, including heart rate, blood pressure, sweating, and digestion through the release of  acetylcholine . Common maneuvers that activate the vagus nerve include the  Valsalva maneuver  and  carotid sinus massage , which can serve diagnostic or therapeutic functions.


There are both diagnostic and therapeutic indications for the use of vagal maneuvers in clinical practice.


Diagnostic:


Therapeutic:


While many physical maneuvers can elicit autonomic responses, only some are appropriate for use in a clinical setting. The vagal maneuvers most often used for diagnostic or therapeutic purposes are those that can be reliably performed at bedside or in an office setting with minimal risk. A list of vagal maneuvers are listed below: [ 12 ] [ 4 ]


Other less clinically useful physical maneuvers that elicit a similar autonomic response through stimulation of the vagus nerve include:


Vagal maneuvers serve to stimulate the  vagus nerve  ( cranial nerve X ) through various mechanisms. The longest nerve in the body, the vagus nerve serves both motor and sensory functions through afferent and efferent signaling to and from the brain. The vagus nerve releases the neurotransmitter acetylcholine, [ 13 ]  and is a main mediator for the parasympathetic nervous system.


The vagus nerve exits the skull through the  jugular foramen , moving down through the  carotid sheath  and dividing many times to influence multiple organ systems and directly innervating the pharynx, larynx, esophagus, heart, lung, and GI tract. Due to this wide nerve distribution, many physiologic process may be influenced through its stimulation, including heart rate and blood pressure. [ 14 ]


Stimulation of the vagus nerve through vagal maneuvers is thought to effect afferent fibers that carry sensory information from its distribution throughout the body to the  nucleus tractus solitarii  (NTS) in the dorsal medullary complex, where it is then relayed to other areas of the brain. This stimulation can also be done more directly through a therapy called  Vagus Nerve Stimulation (VNS) , which utilizes an implanted neuro-stimulator device and is approved clinically for controlling seizures in epilepsy patients and drug resistant depression. [ 15 ]


Vagal maneuvers make use of the vagus nerve's afferent and efferent bifunctional role, triggering reflexes (like the  baroreceptor reflex ,  chemoreceptor reflex ) and utilizing those afferent nerve fibers to increase nerve activity. This results in increased parasympathetic signaling through its efferent distribution and is mediated by the chemical messenger acetylcholine. [ 4 ]


A  ventricular assist device  ( VAD ) is an  electromechanical  device that provides support for cardiac pump function, which is used either to partially or to completely replace the function of a failing  heart . VADs can be used in patients with acute (sudden onset) or chronic (long standing)  heart failure , which can occur due to  coronary artery disease ,  atrial fibrillation ,  valvular disease , and other conditions. [ 1 ] [ 2 ]


VADs may be used to manage a variety of cardiac diseases and can be categorized based on which ventricle the device is assisting, and whether the VAD will be temporary or permanent.


Ventricular Assistance


First, VADs can be categorized based on whether they are designed to assist the right  ventricle  (RVAD) or the left ventricle (LVAD) or to both ventricles (BiVAD). The type of VAD implanted depends on the type of underlying  heart disease  (e.g. patients with right ventricular failure from  pulmonary arterial hypertension  may require an RVAD, versus those with left ventricular failure from a  myocardial infarction  may require an LVAD). The LVAD is the most common device applied to a defective heart (it is sufficient in most cases; the right side of the heart is then often able to make use of the heavily increased blood flow), but when the pulmonary arterial resistance is high, then an (additional) right ventricular assist device (RVAD) might be necessary to resolve the problem of cardiac circulation. If both an LVAD and an RVAD are needed a BiVAD is normally used, rather than a separate LVAD and RVAD. [ citation needed ]


Duration


VADs can further be divided by the duration of their use (i.e. temporary versus permanent). Some VADs are for short-term use, [ 3 ]  typically for patients recovering from  myocardial infarction  (heart attack) and for patients recovering from  cardiac surgery ; some are for long-term use (months to years to perpetuity), typically for patients with advanced  heart failure [ citation needed ]


Temporary use of VADs may vary in scale (e.g. days to months) depending on a patient's condition. Certain types of VADS may be used in patients with signs of acute (sudden onset) heart failure or cardiogenic shock as a result of an infarction, valvular disease, among other causes. [ 4 ]  In patients with acute signs of heart failure, small  percutaneous  (introduced to the heart through the skin into a blood vessel rather than through an incision) VADs such as the  Impella  5.5, Impella RP, and others can be introduced to either the left or right ventricle (depending on the patient-specific needs) using a wire and that is introduced through the arteries or veins of the neck, axilla, or groin. [ 5 ]


Long-term use of VADs may also vary in its scale (i.e. months to permanently). VADs that are intended for long term use are also termed "durable" VADS, due to their design to function for longer periods of time compared to short term VADs (e.g. Impella, etc.). The long-term VADs can be used in a variety of scenarios. First, VADs may be used as  bridge to transplantation  (BTT) – keeping the patient alive, and in reasonably good condition, and able to await heart transplant outside of the hospital. Other "bridges" include bridge to candidacy (used when a patient has a  contraindication  to heart transplantation but is expected to improve with the VADs support) , bridge to decision (used to support a patient while their candidacy status is decided), and bridge to recovery (used until a patient’s native heart function improves after which the device would be removed). [ 6 ]  In some instances, VADs are also used as  destination therapy  (DT) which indicates that the VAD will remain implanted indefinitely. VADs as destination therapy are used in circumstances where patients are not candidates for transplantation and will thus rely on the VAD for the remainder of their life. [ 7 ] [ 8 ]


Other Cardiac Support Devices


Some devices are designed to support the heart and its various components/function but are not considered VADs, below are some common examples.


Pacemakers  and Internal Cardiac Defibrillators (ICDs) –  the function of a VAD differs from that of an  artificial cardiac pacemaker  in that a VAD pumps  blood , whereas a pacemaker delivers electrical impulses to the heart muscle.


Total Artificial Heart –  VADs are distinct from  artificial hearts , which are designed to assume cardiac function, and generally require the removal of the patient's heart. [ 9 ]


Extracorporeal Membrane Oxygenation (ECMO) – is a form of mechanical circulatory support typically used in critically ill patients in cardiogenic shock that is established by introducing cannula into the arteries and or veins of the neck, axilla or groin. Generally, a venous cannula pulls deoxygenated blood from the patient's veins into an oxygenating device at the patient's bedside, after which a motor powered pump moves the oxygenated blood is back to the body (either into a vein or the arterial system, typically the aorta). There are different ECMO configurations (venoarterial ECMO, venovenous ECMO, etc.) the end goal remains the same; to oxygenate blood and return it to the body. [ 10 ]  In this sense, the ECMO circuit bypasses one or both ventricles and is therefore not in contact with the patient's native ventricle and is generally not considered a type of VAD.


The  pumps  used in VADs can be divided into two main categories – pulsatile pumps, [ 11 ]  which mimic the natural pulsing action of the heart, and continuous-flow pumps. [ 12 ]  Pulsatile VADs use  positive displacement pumps . [ 13 ] [ 14 ] [ 15 ]  In some pulsatile pumps (that use compressed air as an energy source [ 16 ] ), the volume occupied by blood varies during the pumping cycle. If the pump is contained inside the body then a vent tube to the outside air is required.


Continuous-flow VADs are smaller and have proven to be more durable than pulsatile VADs. [ 17 ]  They normally use either a  centrifugal pump  or an  axial flow pump . Both types have a central rotor containing permanent magnets. Controlled electric currents running through coils contained in the pump housing apply forces to the magnets, which in turn cause the rotors to spin. In the centrifugal pumps, the rotors are shaped to accelerate the blood circumferentially and thereby cause it to move toward the outer rim of the pump, whereas in the axial flow pumps the rotors are more or less cylindrical with blades that are helical, causing the blood to be accelerated in the direction of the rotor's axis. [ 18 ]


An important issue with continuous flow pumps is the method used to suspend the rotor. Early versions used solid bearings; however, newer pumps, some of which are approved for use in the EU, use either  magnetic levitation  ("maglev") [ 19 ] [ 20 ] [ 21 ]  or  hydrodynamic suspension .


The first left ventricular assist device (LVAD) system was created by  Domingo Liotta  at Baylor College of Medicine in Houston in 1962. The first LVAD was implanted in 1963 by Liotta and E. Stanley Crawford. The first successful implantation of an LVAD was completed in 1966 by Liotta along with Dr.  Michael E. DeBakey . The patient was a 37-year-old woman, and a paracorporeal (external) circuit was able to provide mechanical support for 10 days after the surgery. [ 23 ]  The first successful long-term implantation of an LVAD was conducted in 1988 by Dr.  William F. Bernhard  of  Boston Children's Hospital  Medical Center and Thermedics, Inc. of Woburn, MA, under a  National Institutes of Health  (NIH) research contract which developed HeartMate, an electronically controlled assist device. This was funded by a three-year $6.2 million contract to Thermedics and Children's Hospital, Boston, MA, from the  National Heart, Lung, and Blood Institute , a program of the NIH. [ 24 ]  The early VADs emulated the heart by using a "pulsatile" action where blood is alternately sucked into the pump from the left ventricle then forced out into the aorta. Devices of this kind include the HeartMate IP LVAS, which was approved for use in the US by the  Food and Drug Administration  (FDA) in October 1994. These devices began to gain acceptance in the late 1990s as heart surgeons including  Eric Rose ,  O. H. Frazier  and  Mehmet Oz  began popularizing the concept that patients could live outside the hospital. Media coverage of outpatients with VADs underscored these arguments. [ 25 ]


More recent work has concentrated on continuous-flow pumps, which can be roughly categorized as either centrifugal pumps or  axial flow   impeller  driven pumps. These pumps have the advantage of greater simplicity resulting in smaller size and greater reliability. These devices are referred to as second-generation VADs. A side effect is that the user will not have a  pulse , [ 26 ]
or that the pulse intensity will be seriously reduced. [ 27 ]


A very different approach in the early stages of development was the use of an inflatable cuff around the aorta. Inflating the cuff contracts the aorta and deflating the cuff allows the aorta to expand – in effect the aorta becomes a second left ventricle. A proposed refinement is to use the patient's skeletal muscle, driven by a  pacemaker , to power this device – which would make it truly self-contained. However, a similar operation ( cardiomyoplasty ) was tried in the 1990s with disappointing results. [ citation needed ]


At one time  Peter Houghton  was the longest surviving recipient of a VAD for permanent use. He received an experimental Jarvik 2000 LVAD in June 2000. Since then, he completed a 91-mile charity walk, published two books, lectured widely, hiked in the Swiss Alps and the American West, flew in an ultra-light aircraft, and traveled extensively around the world. He died of  acute kidney injury  in 2007 at the age of 69. [ 28 ] [ 29 ]   Since then, patient Lidia Pluhar has exceeded Houghton's longevity on a VAD, having received a HeartMate II in March 2011 at age 75, and currently continues to use the device.  In August 2007 the International Consortium of Circulatory Assist Clinicians (ICCAC) was founded by Anthony "Tony" Martin, a nurse practitioner (NP) and clinical manager of the mechanical circulatory support (MCS) program at Newark Beth Israel Medical Center, Newark, N.J. The ICCAC was developed as a 501c3 organization, dedicated to the development of best practices and education related to the care of individuals requiring MCS as a bridge to heart transplantation or as destination therapy in those individuals who don't meet the criteria for heart transplantation. [ 30 ]


The majority of VADs on the market today are somewhat bulky. The smallest device approved by the FDA, the HeartMate II, weighs about 1 pound (0.45 kg) and measures 3 inches (7.6 cm). This has proven particularly important for women and children, for whom alternatives would have been too large. [ 45 ]  As of 2017, HeartMate III has been approved by the FDA. It is smaller than its predecessor HeartMate II and uses a full maglev impeller instead of the cup-and-ball bearing system found in HeartMate II. [ 46 ]


The HeartWare HVAD works similarly to the VentrAssist—albeit much smaller and not requiring an abdominal pocket to be implanted into. The device has obtained CE Mark in Europe, and FDA approval in the U.S.  The HeartWare HVAD could be implanted through limited access without  sternotomy , however in 2021 Medtronic discontinued the device. [ 47 ] [ 44 ]


In a small number of cases left ventricular assist devices, combined with drug therapy, have enabled the heart to recover sufficiently for the device to be able to be removed ( explanted ). [ 7 ] [ 8 ]  Several surgical approaches, including interventional decommissioning, off-pump explantation using a custom-made plug and complete LVAD removal through redo sternotomy, have been described with a 5-year survival of up to 80%. [ 48 ]


A series of studies involving the use of the HeartMate II LVAD have proven useful in establishing the viability and risks of using LVADs for bridge-to-transplantation and destination therapy.


The Harefield Recovery Protocol Study (HARPS) is a clinical trial to evaluate whether advanced heart failure patients requiring VAD support can recover sufficient myocardial function to allow device removal (known as explantation). HARPS combines an LVAD (the HeartMate XVE) with conventional oral heart failure medications, followed by the novel β2 agonist  clenbuterol . This opens the possibility that some advanced heart failure patients may forgo heart transplantation. [ 57 ]


The REMATCH (Randomized Evaluation of Mechanical Assistance for the Treatment of Congestive Heart Failure) clinical trial began in May 1998 and ran through July 2001 in 20 cardiac transplant centers around the USA. The trial was designed to compare long-term implantation of left ventricular assist devices with optimal medical management for patients with end-stage heart failure who require, but do not qualify to receive cardiac transplantation. As a result of the clinical outcomes, the device received FDA approval for both indications, in 2001 and 2003, respectively. [ 58 ]


According to a retrospective cohort study comparing patients treated with a left ventricular assist device versus inotrope therapy while awaiting heart transplantation, the group treated with LVAD had improved clinical and metabolic function at the time of transplant with better blood pressure, sodium, blood urea nitrogen, and creatinine. After transplant, 57.7% of the inotrope group had  kidney failure  versus 16.6% in the LVAD group; 31.6% of the inotrope group had right heart failure versus 5.6% in the LVAD group; and event-free survival was 15.8% in the inotrope group versus 55.6% in the LVAD group. [ 59 ]


There are a number of potential risks associated with VADs. The most common of these are bleeding events, stroke, pump thrombosis, and infections. [ 60 ]


Bleeding


Because the VADs generally result in blood flowing over a non-biologic surface (e.g. metal, synthetic polymers, etc.) this can result in formation of blood clots, also referred to as  thrombosis . Due to these  clotting  abnormalities,  anticoagulation  medications are used to decrease the risk of thrombosis. One device, the HeartMate XVE, is designed with a biologic surface derived from  fibrin  and does not require long term anticoagulation (except aspirin); unfortunately, this biologic surface may also predispose the patient to infection through selective reduction of certain types of leukocytes, however this device was phased out of use starting in 2009 in favor of newer devices. [ 61 ] [ 62 ]


Due to the use of anticoagulation, bleeding is the most common postoperative early complication after implantation or explantation of VADs, necessitating reoperation in up to 60% of recipients. [ 63 ] [ 64 ]  Most commonly bleeding occurs in the gastrointestinal tract resulting in dark or bright red stools, [ 65 ]  however if trauma to the head occurs, intracranial bleeding may also occur. [ 66 ]  Bleeding events may require massive blood transfusions and incur certain risks including infection, pulmonary insufficiency, increased costs, right heart failure, allosensitization, and viral transmission, which can prove fatal or preclude transplantation. [ 64 ]  When bleeding occurs, it impacts the one year Kaplan-Meier mortality. [ 63 ]  In addition to complexity of the patient population and the complexity of these procedures contributing to bleeding, the devices themselves may contribute to the severe coagulopathy that can ensue when these devices are implanted. [ 67 ]


Ischemic Stroke and Pump Thrombosis


In patients with VADs, ischemic strokes and pump thrombosis occur when there is inadequate anticoagulation to counter act the blood's tendency to form blood clots when exposed to the foreign materials in a VAD. Stroke risk varies based on the type of VAD in place and other risk factors. [ 60 ]  Both atrial fibriliation and high blood pressure may increase risk of stroke and high blood pressure can increase a patient's risk of stroke in the setting of VAD use. [ 68 ]  However, it is difficult to measure blood pressure in LVAD patients using standard blood pressure monitoring and the current practice is to measure by  Doppler ultrasonography  in  outpatients  and invasive  arterial blood pressure  monitoring in  inpatients . [ 69 ]


Infections


Infections in VAD patients occur because the artificial surfaces of the devices serve as a surface for bacterial and or fungal growth. [ 70 ]  Most infections are classified as driveline infections, which are infections that occur where the device's power cord enters the skin (usually in the upper abdomen) [ 70 ]


VAD-related infection can be caused by a large number of different organisms: [ 71 ] [ 70 ]


Other immune system related problems include  immunosuppression . Some of the  polyurethane  components used in the devices cause the deletion of a subset of  immune cells  when blood comes in contact with them. This predisposes the patient to  fungal  and some  viral  infections necessitating appropriate  prophylactic therapy . [ 72 ]


Considering the multitude of risks and lifestyle modifications associated with ventricular assist device implants, [ 73 ]  it is important for prospective patients to be informed prior to decision making. [ 74 ]  In addition to physician consult, various Internet-based patient directed resources are available to assist in patient education. [ 75 ] [ 76 ]


This is a partial list and may never be complete
 Referenced additions are welcome


A  ventricular outflow tract  is a portion of either the  left ventricle   or  right ventricle  of the  heart  through which  blood  passes in order to enter the  great arteries . [ 1 ]


The right ventricular outflow tract ( RVOT ) is an  infundibular  extension of the ventricular cavity that connects to the  pulmonary artery . The left ventricular outflow tract ( LVOT ), which connects to the  aorta , is nearly indistinguishable from the rest of the ventricle. The outflow tract is derived from the secondary heart field, during cardiogenesis. [ 2 ]


Both the left and right outflow tract have their own term. The right outflow tract is called "conus arteriosus" from the outside, and infundibulum from the inside. In the left ventricle the outflow tract is the "aortic vestibule". They both possess smooth walls, and are derived from the embryonic bulbus cordis [ 3 ]


In both left and right ventricle there are specific structures separating the inflow and outflow of blood. In the right ventricle, the inflow and outflow is separated by the supraventricular crest. In the left ventricle, the anterior cusp of the mitral valve is responsible for separating the flow of blood. [ 4 ]


A form of  ventricular tachycardia  originating from this anatomical structure is called RVOT tachycardia. [ 5 ]


The RVOT is pathophysiologically affected in  Brugada syndrome . [ 6 ]


Wave intensity analysis [ 1 ]  provides a method to calculate the properties of arterial waves that give rise to  arterial blood pressure , based on measurements of pressure, P, and velocity, U, waveforms ( Figure 1 ). Wave intensity analysis is applicable to the evaluation of circulatory physiology and quantifying the pathophysiology of disorders such as coronary artery disease.
The method is based on discrete, successive wave fronts (wavelets) and is carried out in the time domain. These wavelets travel forward and backwards in the arteries with amplitudes

 Δ
 P

 {\textstyle \Delta P}

  and

 Δ
 U

 {\textstyle \Delta U}

 . The wave intensity,

 Δ
 I

 {\textstyle \Delta I}

 , of a particular wavelet is defined as

 Δ
 I
 =
 Δ
 P
 Δ
 U

 {\displaystyle \Delta I=\Delta P\Delta U}

 It is related to  sound intensity  in acoustics and describes the power per unit area carried by the wavelet. From the theory discussed below, there is a relationship between the pressure amplitude and the velocity amplitude of a wavelet

 Δ

 P

 ±

 =

 1
 2

 (
 Δ

 P

 ±

 ±
 ρ
 c
 Δ

 U

 ±

 )

 {\displaystyle \Delta P_{\pm }={\frac {1}{2}}(\Delta P_{\pm }\pm \rho c\Delta U_{\pm })}

 where ρ is the density of blood and c is the wave speed of the wavelet. From these equations, generally known as the  water hammer  equations, it follows that the wave intensity for forward wavelets

 Δ

 I

 +

 >
 0

 {\textstyle \Delta I_{+}>0}

  and for backward wavelets

 Δ

 I

 −

 <
 0

 {\textstyle \Delta I_{-}<0}

 . The ability to determine the direction of a wavelet from its sign is the basis of the practical utility of wave intensity analysis.


The pressure amplitude of a wavelet can be positive (compression) or negative (decompression) and the velocity amplitude can be positive (acceleration) or negative (deceleration). The measured changes

 Δ
 P

 {\displaystyle \Delta P}

  and

 Δ
 U

 {\displaystyle \Delta U}

  are the sums of the amplitudes of the forward and backward wavelets arriving at the measurement site at the time of the measurement and so the wave intensity

 Δ
 I

 {\displaystyle \Delta I}

  is sometimes called net wave intensity. The

 Δ
 I

 {\displaystyle \Delta I}

  in the Figure 2 shows the normal pattern in the aorta and illustrates four important features:


Departures from this pattern of wave intensity is usually indicative of pathology.


The additivity of the forward and backward wavelets coinciding at the site of measurement at a particular time can be combined algebraically with the water-hammer equations  to calculate the magnitudes of the two wavelets [ 2 ]

 Δ

 P

 ±

 =

 1
 2

 (
 Δ

 P

 ±

 ±
 ρ
 c
 Δ

 U

 ±

 )

 {\displaystyle \Delta P_{\pm }={\frac {1}{2}}(\Delta P_{\pm }\pm \rho c\Delta U_{\pm })}

 This method assumes that the wave speed is constant. In general, the wave speed is a function of the pressure. A more complex method of separation involving integrals along the characteristics is available. [ 3 ]  The forward and backward waveforms follow from summing the magnitudes of the sequential wavelets

 P

 ±

 =
 Σ
 Δ

 P

 ±

 {\displaystyle P_{\pm }=\Sigma \Delta P_{\pm }}

 The pressure shown in Figure 1 is separated into its forward and backward components in Figure 3. This separation is carried out in the time domain and can be applied to irregular, non-periodic data. For periodic heart beats this separation coincides closely with the separation obtained using Fourier analysis methods. [ 4 ]


Wave intensity analysis is based on the 1-D equations for the conservation of mass and momentum of the blood in the elastic arteries (first published by   Euler  in 1775) and a relationship between the cross-sectional area of the artery and the pressure within it (generally called a 'tube law'). The resultant equations are hyperbolic in form and can be solved using the  method of characteristics . The method is based on the identification of 'characteristic' directions along which the partial differential equations reduce to ordinary differential equations. For the arteries these characteristic directions were (

 x
 ±
 c
 t

 {\textstyle x\pm ct}

 ) where

 c

 {\displaystyle c}

  is the wave speed

 c
 =

 1

 ρ

 D

 {\displaystyle c={\frac {1}{\sqrt {\rho {\mathcal {D}}}}}}

 where

 D

 =

 1
 A

 d
 A

 d
 P

 {\displaystyle {\mathcal {D}}={\frac {1}{A}}{\frac {dA}{dP}}}

  is the distensibility of the artery wall. These characteristic directions describe the path of the wavelets in

 (
 x
 ,
 t
 )

 {\displaystyle (x,t)}

 . The derivation of an equation for the local wave speed is a significant advantage of the method of characteristics.


A method for estimating local wave speed from clinically measurable data is important in wave intensity analysis. The most common approach is referred to as the 'P-U loop' method. During the initial compression wave at the start of systole when the forward wave is dominant the local wave speed is estimated from the slope of the P-U loop

 c
 ≈

 1
 ρ

 |

 d
 P

 d
 U

 |

 i
 n
 i
 t
 i
 a
 l

 s
 y
 s
 t
 o
 l
 e

 {\displaystyle c\approx {\frac {1}{\rho }}\left|{\frac {dP}{dU}}\right|_{initial\;systole}}

 In cases where there is no period during the cardiac cycle when it is obvious that forward waves dominate another method, generally called the 'sum of squares' method [ 5 ]  is applicable:

 c
 ≈

 1
 ρ

 Σ
 Δ

 P

 2

 Σ
 Δ

 U

 2

 {\displaystyle c\approx {\frac {1}{\rho }}{\sqrt {\frac {\Sigma \Delta P^{2}}{\Sigma \Delta U^{2}}}}}

 Here the sums are taken over a complete cardiac period. This estimation has been used extensively in the wave intensity analysis of measurements in the coronary arteries. [ 6 ]  It should be remembered that both of these estimates are approximations and should be used with caution.


Wave intensity analysis was developed at an era when intra-arterial pressure and velocity waveforms were measured most commonly in the clinic. Other methods of clinical measurements have emerged (e.g. ultrasound and magnetic resonance imaging) and wave intensity analysis has been recast in terms of the parameters that are measured. No systematic notation has been developed to distinguish the different variants. This is a possible source of confusion.


Although wave intensity has some clinical applications, its main influence has been on the basic understanding of arterial  hemodynamics . The first publication pointed out that the deceleration of blood in the aorta during late systole is mainly due to forward deceleration waves rather than backward reflections from the periphery. [ 9 ]  Backward wavelets are present as indicated by the negative wave intensity during mid-systole but most of the deceleration is caused by forward decompression waves generated when the contraction of the ventricle can not keep up with the flow of blood established by the initial contraction wave.


Various studies have looked at the magnitudes of the forward and backward peaks of wave intensity in various pathologies. [ 7 ]  In the 1990s, Aloka introduced clinical ultrasound scanners that measured the instantaneous wave intensity directly from simultaneous measurements of diameter (by B-mode) and blood velocity (by Doppler). Recent studies suggest that wave intensity calculated from catheter measurements in the pulmonary artery can be used to differentiate between  pulmonary arterial hypertension  and  chronic thromboembolic pulmonary hypertension . [ 10 ]


Wave intensity analysis is frequently used in the study of coronary artery hemodynamics where impedance analysis is seldom, if ever, used. [ 11 ]  It played an important role in the development of the  Instantaneous Wave-free Ratio  as a measure of the functional effect of  stenoses  in the coronary arteries. This method informs an interventional cardiologist if stenting is required by measuring the ratio of downstream and upstream pressures during a period in mid-diastole when the net wave intensity is minimal. Large scale clinical trials have shown that this index is "at least as good as" the Functional Flow Resistance Index which requires the injection of a potent  vasodilator .


A  wearable cardioverter defibrillator  ( WCD ) is a non-invasive, external device for patients at risk of  sudden cardiac arrest  (SCA). [ 1 ]  It allows physicians time to assess their patient's arrhythmic risk and see if their ejection fraction improves before determining the next steps in patient care. It is a leased device. A summary of the device, its technology and indications was published in 2017 and reviewed by the EHRA Scientific Documents Committee. [ 2 ]


A wearable cardioverter defibrillator (WCD) is an external device with a built-in  defibrillator . The WCD is worn directly on the body by patients who are at transient risk for  sudden cardiac death  (SCD) for short-term risk mitigation and it does not require surgery for use. A WCD is also a temporary therapeutic option in case an  implantable cardioverter defibrillator  (ICD) cannot be implanted immediately. The WCD enables patients to continue their normal life without constantly worrying about their risk for SCD.


The WCD is a non-invasive medical device. It consists of a fabric garment, electrodes located in the fabric garment for sensing and delivering an electrical shock, and a battery-powered device that monitors the patient and connects to the electrodes and defibrillation pads. The WCD is worn under the clothing during the entire day. The WCD should only be removed when taking a shower or bath. The electrodes lie directly on the skin. The monitoring device constantly records heart rate and rhythm. [ 3 ]  If life-threatening  cardiac arrhythmias , such as  ventricular tachycardia  (VT) or  ventricular fibrillation  (VF) are detected, the defibrillator delivers one or more treatment shock(s) in order to restore a normal heart rhythm. Since the time between a cardiac arrest and defibrillation is directly linked to survival, [ 4 ] [ 5 ]  a treatment shock must be delivered within a few minutes after an event to be effective. With every passing minute without treatment, the chances of patient survival is reduced by 7-10%. [ 6 ] [ 7 ]  From detecting a life-threatening cardiac arrhythmia to automatically delivering a treatment shock, the WCD usually needs less than a minute. The first treatment shock success rate for resuscitating patients from SCD is 98%. [ 8 ]  Intervention from bystanders or emergency personnel is not required for the WCD to work.


The use of the WCD is recommended for the prevention of SCD in the 2006 international joint guidelines from the American College of Cardiology, American Heart Association, and European Society of Cardiology (ACC/AHA/ESC), [ 9 ]  European Society of Cardiology (ESC) guidelines from 2015 [ 10 ]  and 2021, [ 11 ]  and American Heart Association, American College of Cardiology, Heart Rhythm Society (AHA/ACC/HRS) guidelines from 2017. [ 12 ] [ 13 ]  The International Society for Heart and Lung Transplantation (ISHLT) recommends wearable external defibrillators as a bridge therapy for patients waiting for a heart transplant in their Guidelines for the Care of Cardiac Transplant Candidates. [ 14 ]  In the United Kingdom (UK) the WCD LifeVest® from ZOLL is available for temporary use on a monthly rental basis since 2017. [ 15 ]


The WCD is a temporary therapeutic option for patients waiting for an ICD, patients with an ICD that had to be removed (e.g., due to infection), or patients who can't have an ICD but are at transient risk for SCD. [ 16 ]   The WCD allows physicians time to assess their patient's cardiac arrhythmic risk, make appropriate treatment plans and monitor cardiac output before or after an invasive cardiac procedure (such as bypass surgery, stent placement or heart transplant) or in patients at high risk for SCD after myocardial infarction (MI). [ 17 ]


Usual wearing time of a WCD is about 3 months but depends on the patient's needs and the prescription of the treating physician.


The use of cardiac defibrillation started in 1947 - first in an open chest and ten years later through a closed chest with high energy levels. In 1972, cardiac defibrillation with intracardiac electrodes delivering much less energy of as low as 30 joules was established, following the development of portable units delivering high energy levels of up to 1000 volt. At Johns Hopkins University, doctors Mirowski, Mower and colleagues started developing implantable cardioverter defibrillators (ICD), and were able to implant an ICD in the first human by 1980. Over the years, the ICD was further improved and is now a standard outpatient procedure. [ 19 ] [ 20 ]  There are limiting factors for direct prophylactic implantation of an ICD. For example, a diagnosed high risk for SCD may be temporary, which would oppose an implantation intended for lifetime use. Per current guidelines (e.g., the ESC guidelines from 2015 and 2021) a patient has to wait at least 40 to 90 days after the cardiac event (e.g., myocardial infarction or newly diagnosed heart failure with reduced left ventricular function) before the decision to implant an ICD should be made. [ 21 ]  An external, wearable cardioverter-defibrillator with defibrillation features similar to an ICD could be a solution to be used as “bridge” to protect these patients from SCD.


In 1986, M. Stephen Heilman and Larry Bowling founded LIFECOR and started the development of the first wearable cardioverter defibrillator (WCD). It was named LifeVest®. This WCD was extensively tested for three years in multi-centre and multinational clinical trials (WEARIT and BIROAD) in the United States and Europe. The results were used to improve the WCD and were also the basis for FDA approval in 2001 for use of the WCD for adult patients who are at high risk for SCD, who are not suitable candidates for an ICD or who refuse to have one. [ 22 ] [ 23 ]  14 years later (2015), FDA approval was received for the use of the WCD in children, who are at high risk for SCD and are not candidates for an ICD or do not receive one due to lack of parental consent. [ 24 ]  In 2000, prior to the FDA approvals, the WCD had already received the European CE-certification. [ 25 ]


In 1986,  M. Stephen Heilman  and Larry Bowling founded Lifecor and along with a team of former Intec employees who developed the first  implantable cardioverter defibrillator  (ICD) began development of the WCD. The WCD was extensively tested for three years in 17 major medical centers across the United States and Europe. The clinical data collected from those trials [ 26 ]  allowed Lifecor to obtain FDA approval for use of the WCD in the United States. [ citation needed ]


In 2001, the FDA approved the LifeVest wearable cardioverter defibrillator (model 2000). [ 27 ] [ 28 ] [ 29 ]  The Lifecor business was acquired by ZOLL Medical Corporation in 2006 and Asahi Kasei in 2012. As of 2015, the LifeVest was available in the United States, Europe, Japan, Australia, Israel and Singapore. [ 30 ]


The WCD LifeVest is marketed in the United Kingdom, United States, Europe, Japan, and several other countries worldwide. According to ZOLL, the LifeVest has been prescribed to more than 200,000 patients worldwide. In July 2021, the FDA approved a second WCD product for the market developed by Kestra Medical Technologies, Inc. This new device has an alternative fabric and garment style specifically for women. [ 31 ]


The WCD is covered by most health plans in the United States, including commercial, state, and federal plans as Durable Medical Equipment (DME) for those patients at high risk of cardiac arrest, including: [ citation needed ]


The WCD uses dry, non-adhesive ECG electrodes to continuously monitor the patient's heart rhythm. Three defibrillation electrodes are placed in the fabric garment, one on the chest (approximately at the level of the apex of the heart) and two on the back (between the shoulder blades). The ECG electrodes are placed inside the fabric garment on the chest providing two independent ECG leads. Prior to delivering a therapeutic shock, the dry defibrillator electrodes automatically deploy conductive gel to protect the skin from possible injury from the treatment. The WCD can deliver up to five consecutive shocks per sequence. Life-saving therapy typically occurs within a minute of the onset of an arrhythmia. The patient is warned when a treatment sequence has been started, e.g. by siren alarms and spoken information. Through interaction with the WCD, an unjustified shock delivery can be prevented by the patient as long as she/he is conscious. If the patient fails to respond, e.g., because the patient has lost consciousness due to an arrhythmia, gel is automatically ejected from under the defibrillation electrodes. If the arrhythmia resolves on its own, no treatment shock is delivered. Action from bystanders is not required, but they are warned by voice information not to touch the patient during defibrillation and to call emergency services. [ 32 ]


In the electrode belt, four dry, non-adhesive ECG electrodes continuously monitor the patient's heart rhythm. Three defibrillation electrodes are placed in the vest, one on the chest (approximately at the level of the apex of the heart) and two on the back (between the shoulder blades). The ECG electrodes are placed at inside of the vest on the chest providing two independent ECG leads. Prior to delivering a therapeutic shock, the dry defibrillator electrodes automatically deploy conductive gel to protect the skin from possible injury from the treatment. The WCD can deliver up to five consecutive shocks per sequence. Life-saving therapy typically occurs within a minute of the onset of an arrhythmia.The patient is warned when a treating sequence has been started e.g. by siren alarms and spoken information. By pressing two response buttons on the monitor simultaneously, an unjustified shock delivery can be prevented by the patient as long as she/he is conscious. If the patient fails to respond, e.g., because the patient has lost consciousness due to an arrhythmia, gel is automatically ejected from under the defibrillation electrodes. If the arrhythmia resolves on its own, no treatment shock is delivered. Action from bystanders is not required, but they are warned by voice information not to touch the patient during defibrillation and to call the emergency doctor.


The patient receives two rechargeable batteries for the WCD. One will be used to operate the monitoring device, the other is charged for daily replacement. Conspicuous ECG sequences or treatments are automatically transmitted to a secure server. The treating physician can view and analyze them via password-protected access. Before a WCD is handed to a patient, the WCD is fitted to the patient for accurate ECG signal detection and the patient receives detailed training to ensure correct handling of the WCD. [ 3 ]


The efficacy and effectiveness of the WCD has been tested in clinical trials and several international post-marketing studies. If the WCD is worn correctly and ECG signal detection is optimal, the success rate of the first shock is approximately 98%. [ 33 ]  Hence, the WCD is as effective as an ICD in treating VT and VF. [ 34 ]  Long term follow-up studies showed that approximately 90% of all patients treated with the WCD are still alive one year after the heart failure incident. [ 35 ]
Since the WCD is a non-invasive garment, no injuries or scars remain after use and shock delivery. For effective protection, the WCD should be worn 24 hours a day and should only be removed for personal hygiene.


Automated external defibrillators (AED) are portable electronic devices designed to analyze the heart rhythm and inform the operator whether defibrillation is required. They are intended for people of the general population with an unknown risk for heart failure and are usually available in public places and first responder ambulances. AEDs are designed for use by laypersons and provide simple audio and visual instructions for the operator to follow. Electrode pads, placed by an operator on the chest of the patient, are for monitoring and defibrillation. [ 36 ]  In contrast to the ICD and WCD, an AED needs the immediate activity of a bystander in order to prevent the SCD.


WCDs are intended for patients with a known transient risk for SCD and meant for temporary use as described above.The WCD is the ideal therapeutic option to prevent SCD in patients until it is clear that a patient's heart issues are indeed permanent and long-term protection with an ICD must be applied.[36]


Implantable cardioverter-defibrillators (ICD) are electronic devices implanted in the chest with a lead to the right ventricle of the heart. They are intended for patients with permanent risk for SCD. An ICD is, like a WCD, designed to detect and terminate cardiac arrhythmias by emergency defibrillation. [ 37 ]  An extensive invasive surgery is necessary for implantation of the ICD, which is associated with a number of risks and morbidity. Therefore, the decision for an ICD should be carefully taken. [ 38 ]  The WCD is the ideal therapeutic option to prevent SCD in patients until it is clear that a patient's heart issues are indeed permanent and long-term protection with an ICD must be applied. [ 39 ]


The WCD allows patients at high risk for SCD who are discharged from the hospital to return to most of the normal daily activities without constantly worrying about their heart issues and possible fatal outcomes. A retrospective study investigating quality of life in patients who had been fitted with a WCD found that the majority did not feel any impairment in terms of mobility (68%), self-care (83%), daily routine (75%), pain (64%) and mental health (57%). [ 40 ]  Another prospective study evaluating depression and anxiety in patients eligible for WCD found a trend for better improvement of depression scores in patients who actually received the WCD. [ 41 ]


Currently a study on the use of the WCD started in the UK.


In case of questions concerning which activities are possible, the manufacturer recommends consulting with the treating physician. The manufacturer also advises to avoid activities in loud and/or high vibration environments due to the possibility of missing an alert from WCD.


The WCD is generally recommended as temporary therapy for all patients who are at risk of SCD and can be prescribed in the UK as a monthly rental device.


According to the international guidelines of ACC/AHA/ESC in 2006, the ESC in 2015 and 2021 as well as AHA/ACC/HRS in 2017  [ 42 ] [ 43 ] [ 44 ] [ 45 ]  patients that may benefit from a WCD include:


Patients with reduced left ventricular pump systolic function (LVEF) of ≤ 35%


Newly diagnosed Ischemic Heart Failure Patient with Reduced Ejection Fraction (HFrEF)


Patients with ventricular fibrillation (VF) or sustained ventricular tachycardia (VT)


Patients on the waiting list for a heart transplantation


Bridging the waiting time for patients


Newly diagnosed non-ischemic heart failure patient with reduced ejection fraction, including dilated cardiomyopathies (DCM) and New York Heart Association (NYHA) stage II-III heart failure patients


Patients in a risk phase of pregnancy cardiomyopathy (peripartum CM/PPCM)


The ISHLT has listed the WCD as a class I recommendation in its Guidelines for the Care of Cardiac Transplant Candidates since 2006. [ 46 ]  This means that patients waiting for a heart transplantation who are discharged from hospital should receive a wearable defibrillator to bridge the waiting time until receiving the transplant. The WCD is one of the procedures or treatments for which there is evidence and general agreement that it is beneficial, useful and effective in the given condition. [ 47 ]


WCD has also been used in the specific circumstance where patients have an ICD but require temporary explantation for radiotherapy in the location of the ICD generator. [ 48 ]


After European CE-certification and FDA approval of WCD (LifeVest), a number of retrospective and prospective registries verified the efficacy and safety of the WCD. Data from more than 30,000 patients who have used the WCD are published for an expansive variety of indications. In the following only an excerpt is presented.


Meta-analyses


A meta-analysis of 11 comparable studies with approximately 20,000 non-overlapping patients in different indications was published by Nguyen et al. [ 49 ]  They found an overall mortality rate of 1.4%, a VT/VF rate of 2.6% and a VT/VF-related mortality rate of only 0.2% across all patients. 1.7% of the patients (9.1 patients/100 patient years) had received an appropriate treatment, which was successful in 96%. The inappropriate shock rate was <1.0%.


A systematic cross-indication review and meta-analysis of studies reporting treatment rates of WCD was conducted by Masri et al. in 2019. [ 50 ]  They analysed 28 studies and over 30,000 patients. Over a period of 3 months, 5 per 100 patients received appropriate WCD treatment shocks, and only 2 per 100 patients received inappropriate treatment shocks. Analyses of selection or publication bias (e.g., Egger-test) revealed, that there were no differences between independent and manufacturer-sponsored studies, and no differences between prospective and retrospective studies. According to the authors, the rate of patients, who were appropriately treated with the WCD over 3 months of follow-up, was substantial and much higher in observational studies compared to the RCT included in the analysis. The mortality rate was very low at 0.7 per 100 patients over 3 months.


Randomized controlled trial data


[ 51 ] [ 52 ]


The first and to this date only randomized controlled trial (RCT) on WCD use with post-MI patients is the VEST Trial, which was first published by Olgin et al. in 2018. [ 53 ]  In total 2,302 patients were included in the intention-to-treat (ITT) analysis. The primary outcome of the VEST-study, arrhythmic mortality, was 1.6% in the WCD group vs. 2.4% in the control group. The difference was not significant despite a 33% relative risk reduction (RRR). The secondary outcome of the VEST-study, all-cause mortality, was 3.1% in the WCD group and 4.9% in the control group. The difference was significant with a 36% reduction in mortality (RRR). Notably, in this study the average daily wearing time was only 14 to 18 hours/day, hence much lower than supposed according to observational studies. An additional as-treated analysis (ATT) provided as supplemented appendix to the original publication, revealed statistical significance in all mortality endpoints, thus positive results for the use of the WCD. In a per protocol analysis (PPA) published in 2020, [ 54 ]  the reduction in arrhythmic mortality was 62% and in all-cause mortality 75%, both significant results, which is comparable to the results shown in the ATT analysis.


These results indicated that the WCD is highly effective in reducing mortality rates in patients with a high risk for SCD. Essential factors in successful WCD therapy in everyday clinical practice are high wearing compliance and the use of the monitoring system provided by the manufacturer (ZPM Network).


Health technology assessments (HTA)


Aidelsburger and colleagues published the results of an HTA in 2020. [ 55 ]  The authors analysed data from 49 studies and concluded the WCD is a safe and effective intervention in cases of sudden cardiac arrest during the time needed for determination of long-term risk management strategies, that the WCD is reliable in detecting VT/VF events and shows a high rate of appropriate shocks which lead to a high rate of successful VT/VF terminations.
Cortesi and colleagues published the results from another HTA in 2021. [ 56 ]  They focused on cost-efficacy comparing the WCD to “standard of care” in patients at risk for SCD after MI or ICD explantation. The authors found that the WCD is a cost-effective treatment option in patients after MI using the data from the VEST study. In patients after ICD explantation the WCD provided even a cost saving of €1,782 compared to 3 weeks hospitalization in a low intensity hospital (standard of care) using data from the Italian NHS. The authors concluded that for the Italian NHS the WCD use contributes to a more effective utilization of resources and to the improvement of patient care in clinical practice. [ 57 ]


Currently an HTA is planned to be conducted in the UK.


The  West of Scotland Coronary Prevention Study  (also known as  WOSCOPS ) was a landmark [ 1 ]   randomized controlled trial , published in 1995, that investigated the effects of  pravastatin , a  cholesterol-lowering drug , on  primary prevention  of  coronary heart disease  (CHD) in men with  hypercholesterolemia . Conducted in the early 1990s, this study provided critical evidence on the benefits of statins in reducing cardiovascular events in individuals without a history of CHD. It concluded that statin treatment reduced CHD events by 31% after nearly five years of treatment. [ 2 ]


Cardiovascular disease, particularly CHD, is a leading cause of death globally. High  low-density lipoprotein  (LDL) cholesterol levels are a well-established risk factor for developing CHD. While previous studies [ 3 ] [ 4 ] [ 5 ]  had demonstrated the benefits of lipid-lowering agents in patients with existing CHD, the WOSCOPS was one of the first large-scale trials to evaluate the efficacy of statins for primary prevention in individuals without a prior history of cardiovascular events. [ 2 ]


WOSCOPS was a multicenter, randomized, double-blind, placebo-controlled trial conducted in Scotland. The study enrolled 6,595 men aged 45 to 64 years (average 55 years) with elevated total cholesterol levels (average 272 mg/dl) and LDL cholesterol levels (average 192 mg/dL) and no previous history of myocardial infarction. The enrollment period was from February 1989 through September 1991. Participants were randomly assigned to receive either pravastatin (40 mg daily) or a placebo. The primary endpoint was the incidence of nonfatal myocardial infarction and death from CHD. Secondary endpoints included all-cause mortality, coronary revascularization procedures, and stroke. The patients were followed an average of 4.9 years after enrollment. Patient medical records and the national death registry were used to determine clinical results. [ 2 ] [ 6 ]


The results of the WOSCOPS, published in 1995, [ 2 ]  demonstrated several significant benefits of pravastatin therapy for the primary prevention of CHD:


The findings of the WOSCOPS had substantial implications for the prevention of CHD. This trial added to the evidence that the incidence of CHD can be reduced with statin therapy. [ 7 ]  Long-term follow-up demonstrated a sustained reduction in death and coronary events. [ 8 ]


The WOSCOPS was a pivotal trial that contributed to the broader acceptance and use of statins in the primary prevention of cardiovascular disease. Its findings have been corroborated by subsequent studies and meta-analyses, reinforcing the role of statins in reducing the risk of CHD in various populations. [ 9 ]


Windkessel effect  (German: Windkesseleffekt) is a term used in  medicine  to account for the shape of the  arterial blood pressure  waveform in terms of the interaction between the  stroke volume  and the  compliance  of the aorta and large  elastic arteries  (Windkessel vessels) and the  resistance  of the smaller arteries and  arterioles .  Windkessel when loosely translated from  German  to English means 'air chamber', [ 1 ] [ 2 ]  but is generally taken to imply an  elastic reservoir . [ 3 ]  The walls of large elastic arteries (e.g.  aorta ,  common carotid ,  subclavian , and  pulmonary arteries  and their larger branches) contain elastic fibers, formed of  elastin .  These arteries distend when the  blood pressure  rises during  systole  and recoil when the blood pressure falls during  diastole .  Since the rate of blood entering these elastic arteries exceeds that leaving them via the  peripheral resistance , there is a net storage of blood in the aorta and large arteries during systole, which discharges during diastole. The compliance (or  distensibility ) of the aorta and large elastic arteries is therefore analogous to a  capacitor  (employing the  hydraulic analogy ); to put it another way, these arteries collectively act as a  hydraulic accumulator .


The Windkessel effect helps in  damping  the fluctuation in  blood pressure  ( pulse pressure ) over the  cardiac cycle  and assists in the maintenance of organ  perfusion  during diastole when cardiac ejection ceases. The idea of the Windkessel was alluded to by  Giovanni Borelli , although  Stephen Hales  articulated the concept more clearly and drew the analogy with an air chamber used in  fire engines  in the 18th century. [ 4 ]   Otto Frank , an influential German physiologist, developed the concept and provided a firm mathematical foundation. [ 2 ]  Frank's model is sometimes called a two-element Windkessel to distinguish it from more recent and more elaborate Windkessel models (e.g. three- or four-element and non-linear Windkessel models). [ 5 ] [ 6 ]


Windkessel physiology remains a relevant yet dated description of important clinical interest. The historic mathematical definition of systole and diastole in the model are obviously not novel but are here elementally staged to four degrees. Reaching five would be original work. [ citation needed ]


It is assumed that the ratio of pressure to volume is constant and that outflow from the Windkessel is proportional to the fluid pressure. Volumetric inflow must equal the sum of the volume stored in the capacitive element and volumetric outflow through the resistive element. This relationship is described by a  differential equation : [ citation needed ]


I
 (
 t
 )
 =

 P
 (
 t
 )

 R

 +
 C

 d
 P
 (
 t
 )

 d
 t

 {\displaystyle I(t)={P(t) \over R}+C{dP(t) \over dt}}


I(t)  is volumetric inflow due to the pump (heart) and is measured in volume per unit time, while  P(t)  is the pressure with respect to time measured in force per unit area,  C  is the ratio of volume to pressure for the Windkessel, and  R  is the resistance relating outflow to fluid pressure. This model is identical to the relationship between current,  I(t) , and  electrical potential ,  P(t) , in an electrical circuit equivalent of the two-element Windkessel model. [ citation needed ]


In the blood circulation, the passive elements in the circuit are assumed to represent elements in the  cardiovascular system . The resistor,  R , represents the total peripheral resistance and the capacitor,  C , represents total arterial compliance. [ 7 ]


During  diastole  there is no blood inflow since the aortic (or pulmonary valve) is closed, so the Windkessel can be solved for  P(t)  since  I(t) = 0:


P
 (
 t
 )
 =
 P
 (

 t

 d

 )

 e

 −
 (
 t
 −

 t

 d

 )

 (
 R
 C
 )

 {\displaystyle P(t)=P(t_{d})e^{-(t-t_{d}) \over (RC)}}


where  t d  is the time of the start of  diastole  and  P(t d )  is the blood pressure at the start of diastole. This model is only a rough approximation of the arterial circulation; more realistic models incorporate more elements, provide more realistic estimates of the blood pressure waveform and are discussed below.


The three-element Windkessel improves on the two-element model by incorporating another resistive element to simulate resistance to blood flow due to the characteristic resistance of the aorta (or pulmonary artery). The  differential equation  for the 3-element model is: [ citation needed ]


(
 1
 +

 R

 1

 R

 2

 )
 I
 (
 t
 )
 +
 C

 R

 1

 d
 I
 (
 t
 )

 d
 t

 =

 P
 (
 t
 )

 R

 2

 +
 C

 d
 P
 (
 t
 )

 d
 t

 {\displaystyle (1+{R_{1} \over R_{2}})I(t)+CR_{1}{dI(t) \over dt}={P(t) \over R_{2}}+C{dP(t) \over dt}}


where  R 1  is the characteristic resistance (this is assumed to be equivalent to the characteristic impedance), [ 7 ]  while  R 2  represents the peripheral resistance. This model is widely used as an acceptable model of the circulation. [ 5 ]  For example it has been employed to evaluate blood pressure and flow in the aorta of a chick embryo  [ 8 ]  and the pulmonary artery in a pig [ 8 ]  as well as providing the basis for construction of physical models of the circulation providing realistic loads for experimental studies of isolated hearts. [ 9 ]


The three-element model overestimates the compliance and underestimates the characteristic impedance of the circulation. [ 7 ]   The four-element model includes an  inductor ,  L , which has units of mass per length, (

 M

 l

 4

 {\displaystyle {M \over l^{4}}}

 ), into the proximal component of the circuit to account for the  inertia  of blood flow. This  is neglected in the two- and three- element models. The relevant  equation is:


(
 1
 +

 R

 1

 R

 2

 )
 I
 (
 t
 )
 +
 (

 R

 1

 C
 +

 L

 R

 2

 )

 d
 I
 (
 t
 )

 d
 t

 +
 L
 C

 d

 2

 I
 (
 t
 )

 d

 t

 2

 =

 P
 (
 t
 )

 R

 2

 +
 C

 d
 P
 (
 t
 )

 d
 t

 {\displaystyle (1+{R_{1} \over R_{2}})I(t)+(R_{1}C+{L \over R_{2}}){dI(t) \over dt}+LC{d^{2}I(t) \over dt^{2}}={P(t) \over R_{2}}+C{dP(t) \over dt}}


These models relate blood flow to blood pressure through parameters of  R, C ( and, in the case of the four-element model,  L) . These equations can be easily solved (e.g. by employing MATLAB and its supplement SIMULINK) to either find the values of pressure given flow and  R, C, L  parameters, or find values of  R, C, L  given flow and pressure. An example for the two-element model is shown below, where  I(t)  is depicted as an input signal during systole and diastole. Systole is represented by the  sin  function, while flow during diastole is zero.  s  represents the duration of the cardiac cycle, while  Ts  represents the duration of systole, and  Td  represents the duration of diastole (e.g. in seconds). [ citation needed ]


I
 (
 t
 )
 =

 I

 o

 sin

 [

 (
 π
 ∗

 t
 s

 )

 T
 s

 ]

  for

 t
 s

 ≤
 T
 s

 {\displaystyle I(t)=I_{o}\sin[{(\pi *{t \over s}) \over Ts}]{\text{ for }}{t \over s}\leq Ts}


I
 (
 t
 )
 =
 0

  for

 T
 s
 <
 (
 T
 d
 +
 T
 s
 )

 {\displaystyle I(t)=0{\text{ for }}Ts<(Td+Ts)}


The 'Windkessel effect' becomes diminished with age as the elastic arteries become less compliant, termed  hardening of the arteries  or  arteriosclerosis , probably secondary to fragmentation and loss of elastin. [ 10 ]  The reduction in the Windkessel effect results in increased  pulse pressure  for a given  stroke volume .  The increased pulse pressure results in elevated systolic pressure ( hypertension ) which increases the risk of  myocardial infarction ,  stroke ,  heart failure  and a variety of other cardiovascular diseases. [ 11 ]


Although the Windkessel is a simple and convenient concept, it has been largely superseded by more modern approaches that interpret arterial pressure and flow waveforms in terms of wave propagation and reflection. [ 12 ]  Recent attempts to integrate wave propagation and Windkessel approaches through a reservoir concept, [ 13 ]  have been criticized [ 14 ] [ 15 ]  and a recent consensus document highlighted the wave-like nature of the reservoir. [ 16 ]


Wireless ambulatory electrocardiography (ECG)  is a type of ambulatory  electrocardiography  with recording devices that use wireless technology, such as Bluetooth and smartphones, for at-home  cardiac monitoring  (monitoring of heart rhythms). These devices are generally recommended to people who have been previously diagnosed with  arrhythmias  and want to have them monitored, or for those who have suspected arrhythmias and need to be monitored over an extended period of time in order to be diagnosed. [ 1 ]


Wireless ambulatory ECGs work in a way similar to a regular ECG by measuring the electrical potential of the heart through the skin.  The data is saved on an application on a smartphone, and then uploaded to a computer through Bluetooth or  cloud technologies .  The information can also be sent through these technologies or through email to a doctor or cardiac technician. [ 2 ]


Wireless ambulatory ECGs are able to provide voice alarm messages when cardiac abnormalities occur, such as  bradycardia , and can record this information and provide a screen prompt for the patient to view the data.  The devices can also store mass amounts of ECG data on the phone, replay the ECG readings at a high speed, and have a low-voltage alarm function to not waste the battery life.  These characteristics of the devices are seen as benefits in comparison to current ambulatory ECG monitoring equipment such as the  Holter monitor . [ 3 ]


1. CardioSecur ACTIVE is a smartphone based 15-lead mobile ECG for patients. While conventional ECG systems use ten electrodes to depict twelve standard leads, CardioSecur requires only four electrodes. CardioSecur's four-electrode technology has been clinically validated and is an alternative to ten electrode systems. [ 4 ]
It provides an instant and personalized evaluation of ECG recordings and offers patients an immediate recommendation to act according to the applicable guidelines of professional cardiological associations. CardioSecur ACTIVE allows cardiovascular patients to gain more certainty about their cardiac activity. Additionally, it enables physicians to diagnose heart diseases faster as treating physicians can access their patients' ECG recordings through a secure database to which the recordings are automatically uploaded. Furthermore, the ECGs can be easily shared via  iMessage , email,  AirDrop  or  AirPrint . [ 5 ]


2.  Alivecor  heart monitors are currently available in the United States, the UK, and Ireland.  The device is a small handheld single-channel ECG recording device that immediately sends information to a smartphone. Recordings can then be sent to a cardiac technician or a certified cardiologist for a small cost. [ 6 ]   AliveCor obtains ECG traces through sensing plates, which can also be purchased through AliveCor. [ 7 ]   The plates are placed on fingers or the chest and the scan takes 30 seconds to complete. [ 8 ]   One of the benefits of AliveCor is the ability to record notes of how the patient was feeling prior to taking the ECG so that the physician has a clear picture of what the patterns indicate. [ 9 ]   Studies on the algorithm used in the technology have indicated that the device provides sufficiently accurate data to be able to diagnose atrial fibrillations. [ 10 ]   The accuracy has been found to be similar to Lead 1 data of a regular 12-lead ECG. [ 11 ]


3. iHealth created a wireless ECG monitor that is placed on the chest under clothing, and the data are sent to mobile phones and is readily available for healthcare professionals. [ 12 ]   The device is small and lightweight, making it easy to participate in daily activities.  It uses Bluetooth technology to send the information to cell phones, but it can also be connected to a computer via USB cable. [ 13 ]


4.  Qardio  created a wearable ECG monitor that wirelessly sends data to the smartphone for the user and health practitioners. The device can be worn every day to track heart health in real life. [ 14 ]


5.  Beurer  produces a single-channel ECG monitor without dedicated electrodes that transmits data via Bluetooth to a smartphone. It is very small and easy to carry around, but is not designed to continuously measure data. The device returns a preliminary analysis of the ECG recording, and detailed data can be later on shown to a physician. [ 15 ]


6. Lithuanian company  ZIVE , created a single-channel ECG monitor (3 channel optional), that transmits data to  iOS or Android phone. Live ECG and full ECG analysis options are available. Device is Class II CE EU certified.  [ 16 ]


World Hypertension Day  ( WHD ) is a day designated and initiated by  The World Hypertension League  (WHL), which is itself an umbrella to organizations of 85 national hypertension societies and leagues. The day was initiated to increase the awareness of  hypertension . This was especially important because of the lack of appropriate knowledge among hypertensive patients. [ 1 ]   The WHL launched its first WHD on May 14, 2005. Since 2006, the WHL has been dedicating May 17 of every year as WHD. [ 2 ]


In 2005, as the inaugural effort, the theme was simply "Awareness of  high blood pressure ". [ 3 ]  The 2006 theme was "Treat to goal", with a focus on keeping blood pressure under control. [ 1 ]  The recommended blood pressures are less than 140/90 mmHg for the general population and for the hypertensive population without any other complications, and less than 130/80 mmHg for those with  diabetes mellitus  or  chronic kidney disease . These are the cut-off values recommended by international and Canadian guidelines. [ 4 ] [ 5 ]  The 2007 WHD theme was " Healthy diet , healthy  blood pressure ". Through such specific themes, the WHL intends to raise awareness not only of hypertension, but also of factors contributing to an increase in the incidence of hypertension and on ways to prevent it. [ 1 ]  In an effort to empower the public, the theme for 2008 was "Measure your blood pressure…at home". Recent reports confirm the ease, accuracy and safety of blood pressure measurements using home monitors. [ 6 ] [ 7 ] [ 8 ]


For the five-year period 2013-2018, the theme of WHD was "Know Your Numbers" with the goal of increasing high blood pressure awareness in all populations around the world. [ 9 ]


Cardiac electrophysiology  is a branch of  cardiology  and  basic science  focusing on the electrical activities of the  heart . The term is usually used in clinical context, to describe studies of such phenomena by invasive (intracardiac) catheter recording of spontaneous activity as well as of cardiac responses to  programmed electrical stimulation  -  clinical cardiac electrophysiology . However, cardiac electrophysiology also encompasses  basic research  and  translational research  components. Specialists studying cardiac electrophysiology, either clinically or solely through research, are known as cardiac electrophysiologists.


Electrophysiological (EP) studies are performed to assess complex  arrhythmias , elucidate symptoms, evaluate abnormal  electrocardiograms , assess risk of developing arrhythmias in the future, and design treatment.  These procedures include therapeutic methods (typically  radiofrequency ablation , or  cryoablation ) in addition to diagnostic and prognostic procedures.  Other therapeutic modalities used in this field include  antiarrhythmic drug  therapy and implantation of  pacemakers ,  implantable cardioverter-defibrillators  and  cardiac resynchronisation therapy  devices.   [ 1 ] [ 2 ]


The cardiac electrophysiology (EP) study typically measures the response of myocardium to programmed electrical stimulation (PES) on specific pharmacological regimens in order to assess the likelihood that the regimen will successfully prevent potentially fatal sustained  ventricular tachycardia (VT)  or  ventricular fibrillation VF  (VF) in the future. Sometimes a  series  of EP study drug trials must be conducted to enable the cardiologist to select the one regimen for long-term treatment that best prevents or slows the development of VT or VF following PES. Such studies may also be conducted in the presence of a newly implanted or newly replaced cardiac pacemaker or ICD. [ 1 ]


A specialist in cardiac electrophysiology is known as an electrophysiologist, or "heart electrician" in layman' terms. Cardiac electrophysiology is a subspecialty of  cardiology  in most countries and usually requires two or more years of EP  fellowship  training after a general cardiology residency. In early 2011, the  Centers for Medicare and Medicaid Services  promoted cardiac electrophysiology to its own specialty category in the United States. Cardiac electrophysiologists are trained to perform interventional cardiac electrophysiology studies and cardiac rhythm management device implantations. [ 1 ]


Cardiac electrophysiologists specialize in a sub-area of  electrophysiology , which in turn is a sub-area of  physiology . This specialization usually requires education at the doctoral (PhD, DSc, or MD/DO) level to become a  principal investigator  for research projects. The area of research is often multi-disciplinary involving chemistry, bioelectrics, biology, and biomedical engineering. The flagship tools used by cardiac electrophysiologists overlap with the toolbox of the neuroscientist including  patch clamp  and  optical mapping . [ 3 ]


Mapping specialists (EP techs, EP physiologists) are typically educated up to the Bachelor's or Master's level and are employed by either a cardiac electrophysiology company or department. Often international certification such as Certified Electrophysiology Specialist (CEPS) by the International Board of Heart Rhythm Examiners (IBHRE) or EHRA Certified Electrophysiology Specialist (ECES) or equivalent is required.


Cardiac electrophysiology is a relatively young subdiscipline of cardiology and internal medicine. It was developed during the mid-1970s by  Hein J. J. Wellens , professor of medicine at the  University of Maastricht  in the  Netherlands  and attending cardiologist at the Academic Hospital in  Maastricht . In 1980 the first microprocessor based stimulator was developed there.


The author of the definitive textbook in the field is by the late  Mark E. Josephson , former Robinette Professor of Medicine and chief of cardiology at the  University of Pennsylvania School of Medicine  in  Philadelphia, Pennsylvania , professor of medicine at  Harvard Medical School , and attending cardiologist at  Beth Israel Deaconess Medical Center  in  Boston, Massachusetts . [ 4 ]  The most recent published edition of  Clinical Cardiac Electrophysiology: Techniques and Interpretations  is the 6th edition in 2020. [ 5 ]


The  Heart Rhythm Society , founded in 1979, promotes education and advocacy for cardiac arrhythmia professionals (including cardiac electrophysiologists) and patients. European Heart Rhythm Association, a part of  European Society of Cardiology , is active in Europe. [ 6 ]


Founded in 1985 as NASPExAM, the International Board of Heart Rhythm Examiners (IBHRE) offers knowledge based board exams for physicians and allied health professionals working in the field of cardiac electrophysiology and cardiac rhythm device management. [ 7 ]  European Heart Rhythm Association (EHRA) provides knowledge and practical competency based certification to physicians and allied health professionals [ 8 ]  as well as accreditation of cardiac electrophysiology training centres [ 9 ]  in Europe and neighbouring countries.


Electroanatomic mapping uses electric and magnetic fields to create three dimensional models of heart structures using specialized catheters.


Afterdepolarizations  are abnormal  depolarizations  of  cardiac myocytes  that interrupt phase 2, phase 3, or phase 4 of the  cardiac action potential  in the  electrical conduction system of the heart . Afterdepolarizations may lead to  cardiac arrhythmias . Afterdepolarization is commonly a consequence of  myocardial infarction ,  cardiac hypertrophy , or  heart failure . [ 1 ]  It may also result from congenital mutations associated with  calcium channels  and sequestration. [ 2 ]


Early afterdepolarizations (EADs) occur with abnormal depolarization during phase 2 or phase 3, and are caused by an increase in the frequency of abortive  action potentials  before normal repolarization is completed. [ 1 ]  EADs most commonly originate in mid- myocardial  cells and  Purkinje fibers , but can develop in other cardiac cells that carry an action potential. Phase 2 may be interrupted due to augmented opening of calcium channels, while phase 3 interruptions are due to the opening of  sodium channels . Early afterdepolarizations can result in  torsades de pointes ,  tachycardia , and other  arrhythmias . [ 3 ]  EADs can be triggered by  hypokalemia  and drugs that prolong the  QT interval , including class Ia and III  antiarrhythmic agents , as well as  catecholamines . [ 1 ]


Afterhyperpolarizations can also occur in cortical pyramidal neurons. There, they typically follow an action potential and are mediated by voltage gated sodium or chloride channels. This phenomenon requires potassium channels to close quickly to limit repolarization. It is responsible for the difference between regular spiking and intrinsically bursting pyramidal neurons. [ 4 ]


Delayed afterdepolarizations (DADs) begin during phase 4, after repolarization is completed but before another action potential would normally occur via the normal conduction systems of the heart. They are due to elevated cytosolic  calcium  concentrations, classically seen with  digoxin  toxicity. [ 5 ] [ 6 ]  The overload of the sarcoplasmic reticulum may cause spontaneous Ca 2+  release after repolarization, causing the released Ca 2+  to exit the cell through the 3Na + /Ca 2+ -exchanger. This results in a net depolarizing current. The classical feature is Bidirectional  ventricular tachycardia . Also seen in  catecholaminergic polymorphic ventricular tachycardia  (CPVT). Delayed afterdepolarization is also seen in myocardial infarction. Purkinje fibers which survive myocardial infarction remain partially depolarized due to its high concentration of cations. [ 7 ]  Partially depolarized tissue fires rapidly resulting in delayed after depolarization. [ 1 ]


Antiarrhythmic agents , also known as  cardiac dysrhythmia medications , are a class of  drugs  that are used to suppress abnormally fast rhythms ( tachycardias ), such as  atrial fibrillation ,  supraventricular tachycardia  and  ventricular tachycardia .


Many attempts have been made to classify antiarrhythmic agents. Many of the antiarrhythmic agents have multiple modes of action, which makes any classification imprecise.


The cardiac myocyte has two general types of action potentials: conduction system and working myocardium. The action potential is divided into 5 phases and shown in the diagram. The sharp rise in voltage ("0") corresponds to the influx of sodium ions, whereas the two decays ("1" and "3", respectively) correspond to the sodium-channel inactivation and the repolarizing efflux of potassium ions. The characteristic plateau ("2") results from the opening of voltage-sensitive  calcium channels . Each phase utilizes different channels and it is useful to compare these phases to the most common classification system — Vaughan Williams — described below.


The  Vaughan Williams classification [ 1 ]  was introduced in 1970 by  Miles Vaughan Williams . [ 2 ]


Vaughan Williams was a pharmacology tutor at  Hertford College , Oxford. One of his students,  Bramah N. Singh , [ 3 ]  contributed to the development of the classification system. The system is therefore sometimes known as the  Singh-Vaughan Williams classification .


The five main classes in the Vaughan Williams classification of antiarrhythmic agents are:


With regard to management of atrial fibrillation, classes I and III are used in rhythm control as medical cardioversion agents, while classes II and IV are used as rate-control agents.


Class Ia drugs prolong the action potential and has an intermediate effect on the 0 phase of depolarization.


Class Ib drugs shorten the action potential of myocardial cell and has a weak effect on the initiation of phase 0 of depolarization


Class Ic drugs do not affect action potential duration and have the strongest effect on the initiation phase 0 of depolarization


Sotalol  is also a  beta blocker [ 5 ]
 Amiodarone  has mostly Class III activity, but also I, II, & IV activity [ 6 ]


The class I antiarrhythmic agents  interfere with the sodium channel .
Class I agents are grouped by what effect they have on the Na +  channel, and what effect they have on cardiac  action potentials .


Class I agents are called membrane-stabilizing agents, "stabilizing" referring to the decrease of excitogenicity of the plasma membrane which is brought about by these agents. (Also noteworthy is that a few class II agents like propranolol also have a  membrane stabilizing effect .)