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ERROR: type should be string, got "https://profreg.medscape.com/px/getpracticeprofile.do?method=getProfessionalProfile&urlCache=aHR0cHM6Ly9lbWVkaWNpbmUubWVkc2NhcGUuY29tL2FydGljbGUvMTUwNjM4LW92ZXJ2aWV3\nDrugs & Diseases > Cardiology\nAuthor: Xiushui (Mike) Ren, MD; Chief Editor: Terrence X O'Brien, MD, MS, FACC more...\nSections Aortic Stenosis\nCardiac Catheterization and Coronary Arteriography\nRadionuclide Ventriculography\nExercise Stress Testing\nInvestigational Imaging Modalities\nElectrocardiography\nB-Type Natriuretic Peptide\nEmergency Department Care\nPercutaneous Balloon Valvuloplasty\nPrevention/Deterrence\nBeta-Adrenergic Receptor Blockers\nCardiac Glycoside\nLoop Diuretics\nAngiotensin-converting Enzyme (ace) Inhibitor\nOpioid Analgesics\nAortic stenosis is the obstruction of blood flow across the aortic valve (see the image below). Among symptomatic patients with medically treated moderate-to-severe aortic stenosis, mortality from the onset of symptoms is approximately 25% at 1 year and 50% at 2 years. Symptoms of aortic stenosis usually develop gradually after an asymptomatic latent period of 10-20 years.\nStenotic aortic valve (macroscopic appearance).\nThe classic triad of symptoms in patients with aortic stenosis is as follows [1] :\nChest pain: Angina pectoris in patients with aortic stenosis is typically precipitated by exertion and relieved by rest.\nHeart failure: Symptoms include paroxysmal nocturnal dyspnea, orthopnea, dyspnea on exertion, and shortness of breath.\nSyncope: This often occurs upon exertion when systemic vasodilatation in the presence of a fixed forward stroke volume causes the arterial systolic blood pressure to decline.\nSystolic hypertension can coexist with aortic stenosis. However, a systolic blood pressure higher than 200 mmHg is rare in patients with critical aortic stenosis.\nIn severe aortic stenosis, the carotid arterial pulse typically has a delayed and plateaued peak, decreased amplitude, and gradual downslope (pulsus parvus et tardus).\nOther symptoms of aortic stenosis include the following:\nPulsus alternans: Can occur in the presence of left ventricular systolic dysfunction\nHyperdynamic left ventricle: Unusual; suggests concomitant aortic regurgitation or mitral regurgitation\nSoft or normal S1\nDiminished or absent A2: The presence of a normal or accentuated A2 speaks against the existence of severe aortic stenosis\nParadoxical splitting of the S2: Resulting from late closure of the aortic valve with delayed A2\nAccentuated P2: In the presence of secondary pulmonary hypertension\nEjection click: Common in children and young adults with congenital aortic stenosis and mobile valve leaflets\nProminent S4: Resulting from forceful atrial contraction into a hypertrophied left ventricle\nSystolic murmur: The classic crescendo-decrescendo systolic murmur of aortic stenosis begins shortly after the first heart sound; the intensity increases toward mid systole and then decreases, with the murmur ending just before the second heart sound\nSee Presentation for more detail.\nThe following studies are used in the diagnosis and assessment of aortic stenosis:\nSerum electrolyte levels\nB-type natriuretic peptide: May provide incremental prognostic information for predicting symptom onset in asymptomatic patients with severe aortic stenosis [2] ; increased levels appear to be associated with aortic stenosis-related adverse events in asymptomatic severe aortic stenosis [3]\nElectrocardiography (ECG): Serial ECG can demonstrate the progression of aortic stenosis\nEchocardiography: Two-dimensional and Doppler\nCardiac catheterization: Can be used if clinical findings are inconsistent with echocardiogram results\nRadionuclide ventriculography: May provide information on left ventricular function\nExercise stress testing: Contraindicated in symptomatic patients with severe aortic stenosis\nSee Workup for more detail.\nThe only definitive treatment for aortic stenosis in adults is aortic valve replacement (surgical or percutaneous). The development of symptoms due to this condition provides a clear indication for replacement. [4, 5] Infants, children, and adolescents with a bicuspid valve may undergo balloon or surgical valvotomy.\nA patient presenting with uncontrolled heart failure should be treated supportively with oxygen, cardiac and oximetry monitoring, intravenous access, loop diuretics, nitrates (keep in mind the potential nitrate sensitivity of patients with aortic stenosis), morphine (as needed and tolerated), and noninvasive or invasive ventilatory support (as indicated). Patients with severe heart failure due to aortic stenosis that is resistant to medical management should be considered for urgent surgery.\nPharmacologic therapy\nAgents used in the treatment of patients with aortic stenosis include the following:\nDigitalis, diuretics, and angiotensin-converting enzyme (ACE) inhibitors: Can be cautiously used in patients with pulmonary congestion\nVasodilators: May be used to treat for heart failure and for hypertension but should also be employed with extreme caution\nDigoxin, diuretics, ACE inhibitors, or angiotensin receptor blockers [5] : Recommended by the European Society of Cardiology (ESC)/European Association for Cardio-Thoracic Surgery (EACTS) guidelines for patients with heart failure symptoms who are not suitable candidates for surgery or transcatheter aortic valve implantation\nAccording to American College of Cardiology (ACC)/American Heart Association (AHA) guidelines, candidates for aortic valve replacement include the following patients [6] :\nSymptomatic patients with severe aortic stenosis\nPatients with asymptomatic, severe aortic stenosis undergoing coronary artery bypass surgery\nPatients with asymptomatic, severe aortic stenosis undergoing surgery on the aorta or other heart valves\nPatients with asymptomatic, severe aortic stenosis and left ventricular systolic dysfunction (ejection fraction < 0.50)\nPercutaneous balloon valvuloplasty is used as a palliative measure in critically ill adult patients who are not surgical candidates or as a bridge to aortic valve replacement in critically ill patients.\nSee Treatment and Medication for more detail.\nAortic stenosis is the obstruction of blood flow across the aortic valve. Aortic stenosis has several etiologies, including congenital (unicuspid or bicuspid valve), calcific (due to degenerative changes), and rheumatic. Degenerative calcific aortic stenosis is now the leading indication for aortic valve replacement. The favorable long-term outcome following aortic valve surgery and the relatively low operative risk emphasize the importance of an accurate and timely diagnosis (see Prognosis).\nA stenotic valve is shown in the image above. Symptoms of aortic stenosis usually develop gradually after an asymptomatic latent period of 10-20 years. Exertional dyspnea or fatigue is the most common initial complaint. Ultimately, most patients experience the classic triad of chest pain, heart failure, and syncope (see History).\nTwo-dimensional (2D) Doppler echocardiography is the imaging modality of choice to diagnose and estimate the severity of aortic stenosis and localize the level of obstruction (see Workup). The only definitive treatment for aortic stenosis is aortic valve replacement, either surgically or percutaneously. (see Treatment).\nGo to Pediatric Valvar Aortic Stenosis, Pediatric Subvalvar Aortic Stenosis, and Pediatric Supravalvar Aortic Stenosis for more complete information on these topics.\nWhen the aortic valve becomes stenotic, resistance to systolic ejection occurs and a systolic pressure gradient develops between the left ventricle and the aorta. This outflow obstruction leads to an increase in left ventricular (LV) systolic pressure. As a compensatory mechanism to normalize LV wall stress, LV wall thickness increases by parallel replication of sarcomeres, producing concentric hypertrophy. At this stage, the chamber is not dilated and ventricular function is preserved, although diastolic compliance is reduced.\nEventually, however, LV end-diastolic pressure (LVEDP) rises, which causes a corresponding increase in pulmonary capillary arterial pressures and a decrease in cardiac output due to diastolic dysfunction. The contractility of the myocardium may also diminish, which leads to a decrease in cardiac output due to systolic dysfunction. Ultimately, heart failure develops.\nIn most patients with aortic stenosis, LV systolic function is preserved and cardiac output is maintained for many years despite an elevated LV systolic pressure. Although cardiac output is normal at rest, it often fails to increase appropriately during exercise, which may result in exercise-induced symptoms.\nDiastolic dysfunction may occur as a consequence of impaired LV relaxation and/or decreased LV compliance, as a result of increased afterload, LV hypertrophy, or myocardial ischemia. LV hypertrophy often regresses following relief of valvular obstruction. However, some individuals develop extensive myocardial fibrosis, which may not resolve despite regression of hypertrophy.\nIn patients with severe aortic stenosis, atrial contraction plays a particularly important role in diastolic filling of the LV. Thus, development of atrial fibrillation in aortic stenosis often leads to heart failure due to an inability to maintain cardiac output.\nIncreased LV mass, increased LV systolic pressure, and prolongation of the systolic ejection phase all elevate the myocardial oxygen requirement, especially in the subendocardial region. Although coronary blood flow may be normal when corrected for LV mass, coronary flow reserve is often reduced.\nMyocardial perfusion is thus compromised by the relative decline in myocardial capillary density and by a reduced diastolic transmyocardial (coronary) perfusion gradient due to elevated LV diastolic pressure. Therefore, the subendocardium is susceptible to underperfusion, which results in myocardial ischemia.\nAngina results from a concomitant increased oxygen requirement by the hypertrophic myocardium and diminished oxygen delivery secondary to diminished coronary flow reserve, decreased diastolic perfusion pressure, and relative subendocardial myocardial ischemia.\nThere may exist a causal association between LDL-C-related genetic variants and aortic valve disease. In a community-based study consisting of 6942 subjects with data on aortic valve calcium and more than 28,000 subjects with aortic stenosis (follow-up, >16 y), Smith et al found that genetic predisposition toward elevations in low-density lipoprotein cholesterol (LDL-C) (as indicated by genetic risk scores [GRSs])—but not elevated high-density lipoprotein cholesterol (HDL-C) or triglycerides GRSs—were associated with the presence of aortic valve calcium and the incidence of aortic stenosis. [7] Whether early intervention aimed at reducing LDL-C levels may help to prevent aortic valve disease is unknown.\nMost cases of aortic stenosis are due to the obstruction at the valvular level. Common causes are summarized in Table 1.\nTable 1. Common Causes of Aortic Stenosis Among Patients Requiring Surgery (Open Table in a new window)\nAge < 70 years (n=324)\nAge >70 years (n=322)\nBicuspid AV (50%)\nPostinflammatory (25%)\nDegenerative (18%)\nUnicommissural (3%)\nHypoplastic (2%)\nIndeterminate (2%)\nBicuspid (27%)\nValvular aortic stenosis can be either congenital or acquired.\nCongenital valvular aortic stenosis\nCongenitally unicuspid, bicuspid, tricuspid, or even quadricuspid valves may cause aortic stenosis. In neonates and infants younger than 1 year, a unicuspid valve can produce severe obstruction and is the most common anomaly in infants with fatal valvular aortic stenosis. In patients younger than 15 years, unicuspid valves are most frequent in cases of symptomatic aortic stenosis.\nIn adults who develop symptoms from congenital aortic stenosis, the problem is usually a bicuspid valve. Bicuspid valves do not cause significant narrowing of the aortic orifice during childhood. The altered architecture of the bicuspid aortic valve induces turbulent flow with continuous trauma to the leaflets, ultimately resulting in fibrosis, increased rigidity and calcification of the leaflets, and narrowing of the aortic orifice in adulthood.\nA cohort study by Tzemos et al of 642 ambulatory adults with bicuspid aortic valves found that during the mean follow-up duration of 9 years, survival rates were not lower than for the general population. However, young adults with bicuspid aortic valve had a high likelihood of eventually requiring aortic valve intervention. [8]\nCongenitally malformed tricuspid aortic valves with unequally sized cusps and commissural fusion (“functionally bicuspid” valves) can also cause turbulent flow leading to fibrosis and, ultimately, to calcification and stenosis. Clinical manifestations of congenital aortic stenosis in adults usually appear after the fourth decade of life.\nAcquired valvular aortic stenosis\nThe main causes of acquired aortic stenosis include degenerative calcification and, less commonly, rheumatic heart disease.\nDegenerative calcific aortic stenosis (also called senile calcific aortic stenosis) involves progressive calcification of the leaflet bodies, resulting in limitation of the normal cusp opening during systole. This represents a consequence of long-standing hemodynamic stress on the valve and is currently the most frequent cause of aortic stenosis requiring aortic valve replacement. The calcification may also involve the mitral annulus or extend into the conduction system, resulting in atrioventricular or intraventricular conduction defects.\nRisk factors for degenerative calcific aortic stenosis include advanced age, hypertension, hypercholesterolemia, diabetes mellitus, and smoking. The available data suggest that the development and progression of the disease are due to an active disease process at the cellular and molecular level that shows many similarities with atherosclerosis, ranging from endothelial dysfunction to, ultimately, calcification. [9]\nIn rheumatic aortic stenosis, the underlying process includes progressive fibrosis of the valve leaflets with varying degrees of commissural fusion, often with retraction of the leaflet edges and, in certain cases, calcification. As a consequence, the rheumatic valve often is regurgitant and stenotic. Coexistent mitral valve disease is common.\nOther, infrequent causes of aortic stenosis include obstructive vegetations, homozygous type II hypercholesterolemia, Paget disease, Fabry disease, ochronosis, and irradiation.\nIt is worthwhile to note that although differentiation between tricuspid and bicuspid aortic stenosis is frequently made, it is often difficult to determine the number of aortic valve leaflets. A study comparing operatively excised aortic valve structure evaluation by cardiac surgeons versus pathologists found that valve structure determination was frequently incongruous. [10]\nSevere aortic stenosis is rare in infancy, occurring in 0.33% of live births, and is due to a unicuspid or bicuspid valve. Most patients with a congenitally bicuspid aortic valve who develop symptoms do not do so until middle age or later. Patients with rheumatic aortic stenosis typically present with symptoms after the sixth decade of life.\nAortic sclerosis (aortic valve calcification without obstruction to blood flow, considered a precursor of calcific degenerative calcific aortic stenosis) increases in incidence with age and is present in 29% of individuals older than 65 years and in 37% of individuals older than 75 years. In elderly persons, the prevalence of aortic stenosis is between 2% and 9%.\nDegenerative calcific aortic stenosis usually manifests in individuals older than 75 years and occurs most frequently in males. [4]\nPatients with severe aortic stenosis may be asymptomatic for many years despite the presence of severe LV outflow tract obstruction (LVOTO). LVOTOs have been associated with “high heritability.” One study suggests that 20% of patients with isolated LVOTO had an affected first-degree relative with undetected bicuspid aortic valves. [11]\nAsymptomatic patients, even with critical aortic stenosis, have an excellent prognosis for survival, with an expected death rate of less than 1% per year; only 4% of sudden cardiac deaths in severe aortic stenosis occur in asymptomatic patients. A new proposed aortic stenosis grading classification that integrates valve area and flow-gradient patterns has been found to allow for better characterization of the clinical outcome among patients with asymptomatic severe aortic stenosis. [12]\nIn general, the presence of low-gradient \"severe stenosis\" (defined as aortic valve area < 1.0 cm2 and mean gradient 40 mmHg), representing up to 40% of all patients with aortic stenosis, is considered to be associated with a poor prognosis. [13] However, the prospective Simvastatin and Ezetimibe in Aortic Stenosis (SEAS) study found that such patients have an outcome similar to that of patients with moderate stenosis. [14] A more recent study found that symptomatic paradoxical low-gradient severe aortic stenosis is associated with a poorer prognosis even after adjustment for flow status and aortic stenosis severity. [15] Moreover, the investigators indicated there may be a possible link to heart failure with preserved ejection fraction in some symptomatic patients. [15]\nAmong symptomatic patients with medically treated, moderate-to-severe aortic stenosis, mortality rates from the onset of symptoms are approximately 25% at 1 year and 50% at 2 years. More than 50% of deaths are sudden. In patients in whom the aortic valve obstruction remains unrelieved, the onset of symptoms predicts a poor outcome with medical therapy; the approximate time interval from the onset of symptoms to death is 1.5-2 years for heart failure, 3 years for syncope, and 5 years for angina.\nAlthough the obstruction tends to progress more rapidly in degenerative calcific aortic valve disease than in congenital or rheumatic disease, predicting the rate of progression in individual patients is not possible. Catheterization and echocardiographic studies suggest that, on average, the valve area declines 0.1 to 0.3 cm2 per year; the systolic pressure gradient across the valve can increase by as much as 10-15 mmHg per year. Obstruction progresses more rapidly in elderly patients with coronary artery disease and chronic renal insufficiency.\nEpicardial adipose tissue (EAT) volume appears to be associated with adverse outcomes in patients with severe aortic stenosis undergoing transcatheter aortic valve replacement (TAVR). A retrospective study of 503 such patients found EAT volume was independently associated with all-cause 1-, 2-, and 3-year mortality and the early safety endpoint at 30 days. [16]\nPossible complications of aortic stenosis include the following:\nConduction defects\nCalcific embolization\nTintinalli JE, Kelen GD, Stapczynski JS, eds. Valvular emergencies. 6th ed. Emergency Medicine: A Comprehensive Study Guide. New York: McGraw-Hill; 2004. 54.\nBergler-Klein J. Natriuretic peptides in the management of aortic stenosis. Curr Cardiol Rep. 2009 Mar. 11(2):85-93. [Medline].\nNakatsuma K, Taniguchi T, Morimoto T, for the CURRENT AS Registry Investigators. B-type natriuretic peptide in patients with asymptomatic severe aortic stenosis. Heart. 2018 Dec 7. [Medline].\nTownsend CM, et al. Sabiston Textbook of Surgery. 18th ed. Saunders; 2008:1841-1844.\n[Guideline] Vahanian A, Alfieri O, Andreotti F, et al. Guidelines on the management of valvular heart disease (version 2012): The Joint Task Force on the Management of Valvular Heart Disease of the European Society of Cardiology (ESC) and the European Association for Cardio-Thoracic Surgery (EACTS). Eur Heart J. 2012 Oct. 33(19):2451-96. [Medline]. [Full Text].\n[Guideline] Nishimura RA, Otto CM, Bonow RO, Carabello BA, Erwin JP 3rd, Guyton RA, et al. 2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2014 Jun 10. 129 (23):2440-92. [Medline]. [Full Text].\nSmith JG, Luk K, Schulz CA, et al. Association of low-density lipoprotein cholesterol-related genetic variants with aortic valve calcium and incident aortic stenosis. JAMA. 2014 Nov 5. 312(17):1764-71. [Medline].\nTzemos N, Therrien J, Yip J, Thanassoulis G, Tremblay S, Jamorski MT, et al. Outcomes in adults with bicuspid aortic valves. JAMA. 2008 Sep 17. 300(11):1317-25. [Medline].\nHughes BR, Chahoud G, Mehta JL. Aortic stenosis: is it simply a degenerative process or an active atherosclerotic process?. Clin Cardiol. 2005 Mar. 28(3):111-4. [Medline].\nRoberts WC, Vowels TJ, Ko JM. Comparison of interpretations of valve structure between cardiac surgeon and cardiac pathologist among adults having isolated aortic valve replacement for aortic valve stenosis (+/- aortic regurgitation). Am J Cardiol. 2009 Apr 15. 103(8):1139-45. [Medline].\nKerstjens-Frederikse WS, Du Marchie Sarvaas GJ, et al. Left ventricular outflow tract obstruction: should cardiac screening be offered to first-degree relatives?. 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Epicardial adipose tissue volume is associated with adverse outcomes after transcatheter aortic valve replacement. Int J Cardiol. 2019 Jul 1. 286:29-35. [Medline].\nEinarsen E, Cramariuc D, Lonnebakken MT, et al. Comparison of frequency of ischemic cardiovascular events in patients with aortic stenosis with versus without asymmetric septal hypertrophy (from the SEAS trial). Am J Cardiol. 2017 Apr 1. 119 (7):1082-7. [Medline].\nRodrigues Tda R, Sternick EB, Moreira Mda C. Epilepsy or syncope? An analysis of 55 consecutive patients with loss of consciousness, convulsions, falls, and no EEG abnormalities. Pacing Clin Electrophysiol. 2010 Jul. 33(7):804-13. [Medline].\nTopol EJ, Califf RM, et al, eds. Aortic valve disease. Textbook of Cardiovascular Medicine. Section Two. 3rd ed. Philadelphia, Pa: Lippincott Williams & Wilkins; 2007:. Chap 23.\nAl-Najafi S, Sanchez F, Lerakis S. 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Circulation. 2011 Jan 25. 123(3):299-308. [Medline].\nWood S. Expanded FDA indication for Sapien valve. Medscape Medical News. September 24, 2013. [Full Text].\nZahn R, Gerckens U, EGrube E et al. Transcatheter aortic valve implantation: first results from a multi-centre real-world registry. Eur Heart Jl. 2011. 32:198–204.\nZajarias A, Cribier AG. Outcomes and safety of percutaneous aortic valve replacement. J Am Coll Cardiol. 2009 May 19. 53(20):1829-36. [Medline].\n[Guideline] Svensson LG, Adams DH, Bonow RO, et al. Aortic valve and ascending aorta guidelines for management and quality measures. Ann Thorac Surg. 2013 Jun. 95 (6 Suppl):S1-66. [Medline]. [Full Text].\nFrank RD, Lanzmich R, Haager PK, Budde U. Severe aortic valve stenosis. Clin Appl Thromb Hemost. 2017 Apr. 23 (3):229-34. [Medline].\nAbdelghani M, Mankerious N, Allali A, et al. Bioprosthetic valve performance after transcatheter aortic valve replacement With Self-Expanding versus balloon-expandable valves in large versus small aortic valve annuli: Insights from the CHOICE Trial and the CHOICE-Extend Registry. JACC Cardiovasc Interv. 2018 Dec 24. 11 (24):2507-18. [Medline].\nTable 1. Common Causes of Aortic Stenosis Among Patients Requiring Surgery\nTable 2. Criteria for Determining Severity of Aortic Stenosis\nTable 3. Indications for Aortic Valve Replacement in Aortic Stenosis\nTable 4. Guideline Recommendations for Aortic Stenosis Intervention\nMean gradient (mmHg)\nAortic valve area (cm2)\n(or < 0.5 cm2/m2 body surface area)\n< 0.5\nSymptomatic severe high-gradient AS (Stage D1)\nAsymptomatic severe AS (Stage C2) with and LVEF < 50%\nSevere AS (Stage C or D) undergoing other cardiac surgery\nAsymptomatic, very severe AS (Stage C1, aortic velocity ≥5.0 m/s) and low surgical risk\nAsymptomatic, severe AS (Stage C1) and decreased expercise tolerance or an exercise fall in blood pressure IIa\nSymptomatic severe low flow/low gradient AS with reduced LVEF (Stage D2) with a low-dose dobutamine stress study with aortic velocity ≥4.0 m/s with a value are ≤1.0 cm2 at any dobutamine dose IIa\nSymptomatic severe low flow/low gradient AS (Stage D3) who are normotensive and have an LVEF ≥50% if clinical, hemodynamic and anatomic data support valve obstruction as the most likely cause of symptoms IIa\nModerate AS (Stage B) who are undergoing other cardiac surgery IIa\nAsymptomatic severe AS (Stage C1) with rapid disease progression and low surgical risk IIb\nIntervention Selection\nAHA/ACC (2014) [6]\nESC/EACTS (2012) [5]\nSTS(2013) [53]\nSurgical AVR in patients with low or intermediate surgical risk\nTranscatheter aortic valve replacement (TAVR) for patients who have a prohibitive surgical risk and a predicted post-TAVR survival >12 mo\nTAVR for patients who have high surgical risk\nClass IIa-Reasonable\nTAVR is not recommended in patients in whom existing comorbidities would preclude the expected benefit from correction of AS\nBalloon aortic valvuloplasty (BAV) as a bridge to surgical AVR or TAVR in severely symptomatic patients\nClass IIb-Consider\nBAV as bridge to AVR in hemodynamically unstable patients with severe AS where immediate AVR is not feasible\nBAV in severely symptomatic patients where AVR is not an option for symptom relief\nBAV as a palliative measure when surgery is contraindicated because of severe comorbidities\nXiushui (Mike) Ren, MD Cardiologist, The Permanente Medical Group; Associate Director of Research, Cardiovascular Diseases Fellowship, California Pacific Medical Center\nXiushui (Mike) Ren, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American Society of Echocardiography\nTerrence X O'Brien, MD, MS, FACC Professor of Medicine/Cardiology, Director, Clinical Cardiovascular Research, Medical University of South Carolina College of Medicine; Director, Echocardiography Laboratory, Veterans Affairs Medical Center of Charleston\nTerrence X O'Brien, MD, MS, FACC is a member of the following medical societies: American College of Cardiology, American Heart Association, American Society of Echocardiography, Heart Failure Society of America, South Carolina Medical Association\nJerry Balentine, DO Professor of Emergency Medicine, New York College of Osteopathic Medicine; Executive Vice President, Chief Medical Officer, Attending Physician in Department of Emergency Medicine, St Barnabas Hospital\nJerry Balentine, DO is a member of the following medical societies: American College of Emergency Physicians, American College of Osteopathic Emergency Physicians, American College of Physician Executives, American Osteopathic Association, and New York Academy of Medicine\nEdward Bessman, MD, MBA Chairman and Clinical Director, Department of Emergency Medicine, John Hopkins Bayview Medical Center; Assistant Professor, Department of Emergency Medicine, Johns Hopkins University School of Medicine\nEdward Bessman, MD, MBA is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine\nDavid FM Brown, MD Associate Professor, Division of Emergency Medicine, Harvard Medical School; Vice Chair, Department of Emergency Medicine, Massachusetts General Hospital\nDavid FM Brown, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine\nSteven J Compton, MD, FACC, FACP, FHRS Director of Cardiac Electrophysiology, Alaska Heart Institute, Providence and Alaska Regional Hospitals\nSteven J Compton, MD, FACC, FACP, FHRS is a member of the following medical societies: Alaska State Medical Association, American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, and Heart Rhythm Society\nDaniel P Lombardi, DO Clinical Assistant Professor, New York College of Osteopathic Medicine; Attending Physician, Associate Department Director and Program Director, Department of Emergency Medicine, St Barnabas Hospital\nDaniel P Lombardi, DO is a member of the following medical societies: American College of Emergency Physicians, American College of Osteopathic Emergency Physicians, and American Osteopathic Association\nJohn A McPherson, MD, FACC, FAHA, FSCAI Associate Professor of Medicine, Division of Cardiovascular Medicine, Director of Cardiovascular Intensive Care Unit, Vanderbilt Heart and Vascular Institute\nJohn A McPherson, MD, FACC, FAHA, FSCAI is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American Heart Association, Society for Cardiac Angiography and Interventions, Society of Critical Care Medicine, and Tennessee Medical Association\nDisclosure: Abbott Vascular Corp. Consulting fee Consulting\nBekir H Melek, MD, FACC Assistant Professor of Clinical Medicine, Department of Medicine, Section of Cardiology, Tulane University School of Medicine\nGary Setnik, MD Chair, Department of Emergency Medicine, Mount Auburn Hospital; Assistant Professor, Division of Emergency Medicine, Harvard Medical School\nGary Setnik, MD is a member of the following medical societies: American College of Emergency Physicians, National Association of EMS Physicians, and Society for Academic Emergency Medicine\nDisclosure: SironaHealth Salary Management position; South Middlesex EMS Consortium Salary Management position; ProceduresConsult.com Royalty Other\nJames V Talano, MD, MM, FACC Director of Cardiovascular Medicine, SWICFT Institute\nencoded search term (Aortic Stenosis) and Aortic Stenosis\nFetal Surgery for Congenital Heart Disease\nCardiovascular Disease and Pregnancy\nDermatologic Manifestations of Cardiac Disease\nHigh Altitude Pulmonary Hypertension\nHigh-Altitude Cardiopulmonary Diseases\nPediatric Congenital Atrioventricular Block\nPostnatal Down Syndrome Imaging\nNew System Reclassifies Cardiomyopathy in Children\nNeonatal Surgeries for Complex Congenital Heart Disease Rise, Remain High After Fukushima\nNew HRS Consensus on Arrhythmogenic Cardiomyopathy\nGrowth Disorders: 10 Cases of a Developing Problem\nAccording to Cardiologists\nHow Much Physical Activity Offsets the Bad From Prolonged Sitting?\nICH Risk Increased With Low-Dose Aspirin in Primary Prevention\nPhilip Morris v Uruguay: A Story That Deserves Retelling\nVirginia Cardiologist Murdered While on Vacation in Belize\nGlucosamine Supplements Linked to Lower CVD Event Risks\nDiseases & Conditions Fetal Surgery for Congenital Heart Disease\nAdult Congenital Heart Disease in the 21st Century\nDiseases & Conditions Cardiovascular Disease and Pregnancy\nDoes Screening Newborns for Congenital Heart Disease Save Lives?"