This is an early acute myocardial infarction. Note the prominent pink contraction bands.In this condition, there may be previous myocardial infarction, but the disease results from severe coronary atherosclerosis involving all major branches. The result is an inadequate vascular supply which leads to myocyte loss. The myocyte loss coupled with fibrosis in the form of interstitial collagen deposition results in decreased compliance, which along with the accompanying cardiac dilation, results in overload of remaining myocytes. This keeps the process going, with compensation by continuing myocyte hypertrophy. There may even be compensation through hyperplasia as well as hypertrophy, which can explain the enormous size (2 to 3 times normal size) of the resulting heart. Eventually, the heart can no longer compensate, and cardiac failure ensues with arrhythmias and/or ischemic events. There is slow, progressive heart failure with or without a history of a previous MI or anginal pain. Ischmic cardiomyopathy is responsible for as much as 40% of the mortality in IHD. (Anversa et al, 1995)


Here are two views of very early ischemic changes, with beginning loss of cross-striations within myocardial fibers, but the cardiac fiber nuclei are still present and there is not yet an inflammatory infiltrate. This represents an evolving infarction less than 12 hours old.In this condition, there may be previous myocardial infarction, but the disease results from severe coronary atherosclerosis involving all major branches. The result is an inadequate vascular supply which leads to myocyte loss. The myocyte loss coupled with fibrosis in the form of interstitial collagen deposition results in decreased compliance, which along with the accompanying cardiac dilation, results in overload of remaining myocytes. This keeps the process going, with compensation by continuing myocyte hypertrophy. There may even be compensation through hyperplasia as well as hypertrophy, which can explain the enormous size (2 to 3 times normal size) of the resulting heart. Eventually, the heart can no longer compensate, and cardiac failure ensues with arrhythmias and/or ischemic events. There is slow, progressive heart failure with or without a history of a previous MI or anginal pain. Ischmic cardiomyopathy is responsible for as much as 40% of the mortality in IHD. (Anversa et al, 1995)


This is normal myocardium. There are cross striations and central nuclei. Pale pink intercalated disks are also present.In this condition, there may be previous myocardial infarction, but the disease results from severe coronary atherosclerosis involving all major branches. The result is an inadequate vascular supply which leads to myocyte loss. The myocyte loss coupled with fibrosis in the form of interstitial collagen deposition results in decreased compliance, which along with the accompanying cardiac dilation, results in overload of remaining myocytes. This keeps the process going, with compensation by continuing myocyte hypertrophy. There may even be compensation through hyperplasia as well as hypertrophy, which can explain the enormous size (2 to 3 times normal size) of the resulting heart. Eventually, the heart can no longer compensate, and cardiac failure ensues with arrhythmias and/or ischemic events. There is slow, progressive heart failure with or without a history of a previous MI or anginal pain. Ischmic cardiomyopathy is responsible for as much as 40% of the mortality in IHD. (Anversa et al, 1995)


The atheromatous plaque around this thrombus in a coronary artery has many cholesterol clefts and foam cells as well as fibrin and hemorrhage.Ischemic heart disease is caused by an imbalance between the myocardial blood flow and the metabolic demand of the myocardium. Reduction in coronary blood flow is mosst often related to progressive atherosclerosis with increasing occlusion of coronary arteries. Blood flow can be further decreased by superimposed events such as vasospasm, thrombosis, or circulatory changes leading to hypoperfusion. (Bergmark et al, 2022). Coronary artery perfusion depends upon the pressure differential between the ostia (aortic diastolic pressure) and coronary sinus (right atrial pressure). Coronary blood flow is reduced during systole because of Venturi effects at the coronary orifices and compression of intramuscular arteries during ventricular contraction. Factors reducing coronary blood flow include: Decreased aortic diastolic pressure, Increased intraventricular pressure and myocardial contraction. Coronary artery stenosis, which can be further subdivided into the following etiologies: Fixed coronary stenosis, Acute plaque change (rupture, hemorrhage), Coronary artery thrombosis, Vasoconstriction, Aortic valve stenosis and regurgitation. Increased right atrial pressure 40 micron collateral vessels are present in all hearts with pressure gradients permitting flow, despite occlusion of major vessels. In general, the cross-sectional area of the coronary artery lumen must be reduced by more than 75% to significantly affect perfusion. Coronary atherosclerosis is diffuse (involving more than one major arterial branch) but is often segmental, and typically involves the proximal 2 cm of arteries (epicardial). (Anversa et al, 1995). Percutaneous coronary intervention (PCI) following coronary angiography can aid in re-establishing myocardial perfusion. "Thrombolytic therapy" with agents such as streptokinase or tissue plasminogen activators (TPA) such as alteplase is often used following onset of symptoms and to try and lyse a recently formed thrombus. Such therapy with lysis of the thrombus can re-establish blood flow in a majority of cases. This helps to prevent significant myocardial injury, if early in the course of events, and can at least help to reduce further damage. Anti-platelet therapy can also be used. (Kumar and Cannon, Part II, 2009) (Bergmark et al, 2022)


This severely narrowed coronary artery has the remaining lumen filled by thrombus.Ischemic heart disease is caused by an imbalance between the myocardial blood flow and the metabolic demand of the myocardium. Reduction in coronary blood flow is mosst often related to progressive atherosclerosis with increasing occlusion of coronary arteries. Blood flow can be further decreased by superimposed events such as vasospasm, thrombosis, or circulatory changes leading to hypoperfusion. (Bergmark et al, 2022). Coronary artery perfusion depends upon the pressure differential between the ostia (aortic diastolic pressure) and coronary sinus (right atrial pressure). Coronary blood flow is reduced during systole because of Venturi effects at the coronary orifices and compression of intramuscular arteries during ventricular contraction. Factors reducing coronary blood flow include: Decreased aortic diastolic pressure, Increased intraventricular pressure and myocardial contraction. Coronary artery stenosis, which can be further subdivided into the following etiologies: Fixed coronary stenosis, Acute plaque change (rupture, hemorrhage), Coronary artery thrombosis, Vasoconstriction, Aortic valve stenosis and regurgitation. Increased right atrial pressure 40 micron collateral vessels are present in all hearts with pressure gradients permitting flow, despite occlusion of major vessels. In general, the cross-sectional area of the coronary artery lumen must be reduced by more than 75% to significantly affect perfusion. Coronary atherosclerosis is diffuse (involving more than one major arterial branch) but is often segmental, and typically involves the proximal 2 cm of arteries (epicardial). (Anversa et al, 1995). Percutaneous coronary intervention (PCI) following coronary angiography can aid in re-establishing myocardial perfusion. "Thrombolytic therapy" with agents such as streptokinase or tissue plasminogen activators (TPA) such as alteplase is often used following onset of symptoms and to try and lyse a recently formed thrombus. Such therapy with lysis of the thrombus can re-establish blood flow in a majority of cases. This helps to prevent significant myocardial injury, if early in the course of events, and can at least help to reduce further damage. Anti-platelet therapy can also be used. (Kumar and Cannon, Part II, 2009) (Bergmark et al, 2022)


This is thrombosis in a coronary artery. Such a thrombus severely narrows or occludes the lumen and can produce a sudden ischemic event. "Sudden death" as well as infarction can occur.Ischemic heart disease is caused by an imbalance between the myocardial blood flow and the metabolic demand of the myocardium. Reduction in coronary blood flow is mosst often related to progressive atherosclerosis with increasing occlusion of coronary arteries. Blood flow can be further decreased by superimposed events such as vasospasm, thrombosis, or circulatory changes leading to hypoperfusion. (Bergmark et al, 2022). Coronary artery perfusion depends upon the pressure differential between the ostia (aortic diastolic pressure) and coronary sinus (right atrial pressure). Coronary blood flow is reduced during systole because of Venturi effects at the coronary orifices and compression of intramuscular arteries during ventricular contraction. Factors reducing coronary blood flow include: Decreased aortic diastolic pressure, Increased intraventricular pressure and myocardial contraction. Coronary artery stenosis, which can be further subdivided into the following etiologies: Fixed coronary stenosis, Acute plaque change (rupture, hemorrhage), Coronary artery thrombosis, Vasoconstriction, Aortic valve stenosis and regurgitation. Increased right atrial pressure 40 micron collateral vessels are present in all hearts with pressure gradients permitting flow, despite occlusion of major vessels. In general, the cross-sectional area of the coronary artery lumen must be reduced by more than 75% to significantly affect perfusion. Coronary atherosclerosis is diffuse (involving more than one major arterial branch) but is often segmental, and typically involves the proximal 2 cm of arteries (epicardial). (Anversa et al, 1995). Percutaneous coronary intervention (PCI) following coronary angiography can aid in re-establishing myocardial perfusion. "Thrombolytic therapy" with agents such as streptokinase or tissue plasminogen activators (TPA) such as alteplase is often used following onset of symptoms and to try and lyse a recently formed thrombus. Such therapy with lysis of the thrombus can re-establish blood flow in a majority of cases. This helps to prevent significant myocardial injury, if early in the course of events, and can at least help to reduce further damage. Anti-platelet therapy can also be used. (Kumar and Cannon, Part II, 2009) (Bergmark et al, 2022)


This is thrombosis in the anterior interventricular (left anterior descending) coronary artery opened longitudinally here over the surface of the heart. This is another complication of atherosclerosis. The purpose of thrombolytic therapy (as with streptokinase or with tissue plasminogen activator, or TPA) is to dissolve recently formed thrombi and re-establish circulation before irreversible myocardial damage has been done, or at least to prevent additional myocardial injury.Ischemic heart disease is caused by an imbalance between the myocardial blood flow and the metabolic demand of the myocardium. Reduction in coronary blood flow is mosst often related to progressive atherosclerosis with increasing occlusion of coronary arteries. Blood flow can be further decreased by superimposed events such as vasospasm, thrombosis, or circulatory changes leading to hypoperfusion. (Bergmark et al, 2022). Coronary artery perfusion depends upon the pressure differential between the ostia (aortic diastolic pressure) and coronary sinus (right atrial pressure). Coronary blood flow is reduced during systole because of Venturi effects at the coronary orifices and compression of intramuscular arteries during ventricular contraction. Factors reducing coronary blood flow include: Decreased aortic diastolic pressure, Increased intraventricular pressure and myocardial contraction. Coronary artery stenosis, which can be further subdivided into the following etiologies: Fixed coronary stenosis, Acute plaque change (rupture, hemorrhage), Coronary artery thrombosis, Vasoconstriction, Aortic valve stenosis and regurgitation. Increased right atrial pressure 40 micron collateral vessels are present in all hearts with pressure gradients permitting flow, despite occlusion of major vessels. In general, the cross-sectional area of the coronary artery lumen must be reduced by more than 75% to significantly affect perfusion. Coronary atherosclerosis is diffuse (involving more than one major arterial branch) but is often segmental, and typically involves the proximal 2 cm of arteries (epicardial). (Anversa et al, 1995). Percutaneous coronary intervention (PCI) following coronary angiography can aid in re-establishing myocardial perfusion. "Thrombolytic therapy" with agents such as streptokinase or tissue plasminogen activators (TPA) such as alteplase is often used following onset of symptoms and to try and lyse a recently formed thrombus. Such therapy with lysis of the thrombus can re-establish blood flow in a majority of cases. This helps to prevent significant myocardial injury, if early in the course of events, and can at least help to reduce further damage. Anti-platelet therapy can also be used. (Kumar and Cannon, Part II, 2009) (Bergmark et al, 2022)


There is a fibrin cap at the right with disruption in this atheromatous plaque in a coronary artery. Note the many "foam" cells (pale because of lipid) and cholesterol clefts.Ischemic heart disease is caused by an imbalance between the myocardial blood flow and the metabolic demand of the myocardium. Reduction in coronary blood flow is mosst often related to progressive atherosclerosis with increasing occlusion of coronary arteries. Blood flow can be further decreased by superimposed events such as vasospasm, thrombosis, or circulatory changes leading to hypoperfusion. (Bergmark et al, 2022). Coronary artery perfusion depends upon the pressure differential between the ostia (aortic diastolic pressure) and coronary sinus (right atrial pressure). Coronary blood flow is reduced during systole because of Venturi effects at the coronary orifices and compression of intramuscular arteries during ventricular contraction. Factors reducing coronary blood flow include: Decreased aortic diastolic pressure, Increased intraventricular pressure and myocardial contraction. Coronary artery stenosis, which can be further subdivided into the following etiologies: Fixed coronary stenosis, Acute plaque change (rupture, hemorrhage), Coronary artery thrombosis, Vasoconstriction, Aortic valve stenosis and regurgitation. Increased right atrial pressure 40 micron collateral vessels are present in all hearts with pressure gradients permitting flow, despite occlusion of major vessels. In general, the cross-sectional area of the coronary artery lumen must be reduced by more than 75% to significantly affect perfusion. Coronary atherosclerosis is diffuse (involving more than one major arterial branch) but is often segmental, and typically involves the proximal 2 cm of arteries (epicardial). (Anversa et al, 1995). Percutaneous coronary intervention (PCI) following coronary angiography can aid in re-establishing myocardial perfusion. "Thrombolytic therapy" with agents such as streptokinase or tissue plasminogen activators (TPA) such as alteplase is often used following onset of symptoms and to try and lyse a recently formed thrombus. Such therapy with lysis of the thrombus can re-establish blood flow in a majority of cases. This helps to prevent significant myocardial injury, if early in the course of events, and can at least help to reduce further damage. Anti-platelet therapy can also be used. (Kumar and Cannon, Part II, 2009) (Bergmark et al, 2022)


There is hemorrhage into a coronary artery plaque, one complication of atherosclerosis, seen here grossly.Ischemic heart disease is caused by an imbalance between the myocardial blood flow and the metabolic demand of the myocardium. Reduction in coronary blood flow is mosst often related to progressive atherosclerosis with increasing occlusion of coronary arteries. Blood flow can be further decreased by superimposed events such as vasospasm, thrombosis, or circulatory changes leading to hypoperfusion. (Bergmark et al, 2022). Coronary artery perfusion depends upon the pressure differential between the ostia (aortic diastolic pressure) and coronary sinus (right atrial pressure). Coronary blood flow is reduced during systole because of Venturi effects at the coronary orifices and compression of intramuscular arteries during ventricular contraction. Factors reducing coronary blood flow include: Decreased aortic diastolic pressure, Increased intraventricular pressure and myocardial contraction. Coronary artery stenosis, which can be further subdivided into the following etiologies: Fixed coronary stenosis, Acute plaque change (rupture, hemorrhage), Coronary artery thrombosis, Vasoconstriction, Aortic valve stenosis and regurgitation. Increased right atrial pressure 40 micron collateral vessels are present in all hearts with pressure gradients permitting flow, despite occlusion of major vessels. In general, the cross-sectional area of the coronary artery lumen must be reduced by more than 75% to significantly affect perfusion. Coronary atherosclerosis is diffuse (involving more than one major arterial branch) but is often segmental, and typically involves the proximal 2 cm of arteries (epicardial). (Anversa et al, 1995). Percutaneous coronary intervention (PCI) following coronary angiography can aid in re-establishing myocardial perfusion. "Thrombolytic therapy" with agents such as streptokinase or tissue plasminogen activators (TPA) such as alteplase is often used following onset of symptoms and to try and lyse a recently formed thrombus. Such therapy with lysis of the thrombus can re-establish blood flow in a majority of cases. This helps to prevent significant myocardial injury, if early in the course of events, and can at least help to reduce further damage. Anti-platelet therapy can also be used. (Kumar and Cannon, Part II, 2009) (Bergmark et al, 2022)


This cross section of coronary artery demonstrates nearly complete lumenal occlusion. If this occurs slowly, there is time for collateral circulation to develop.Ischemic heart disease is caused by an imbalance between the myocardial blood flow and the metabolic demand of the myocardium. Reduction in coronary blood flow is mosst often related to progressive atherosclerosis with increasing occlusion of coronary arteries. Blood flow can be further decreased by superimposed events such as vasospasm, thrombosis, or circulatory changes leading to hypoperfusion. (Bergmark et al, 2022). Coronary artery perfusion depends upon the pressure differential between the ostia (aortic diastolic pressure) and coronary sinus (right atrial pressure). Coronary blood flow is reduced during systole because of Venturi effects at the coronary orifices and compression of intramuscular arteries during ventricular contraction. Factors reducing coronary blood flow include: Decreased aortic diastolic pressure, Increased intraventricular pressure and myocardial contraction. Coronary artery stenosis, which can be further subdivided into the following etiologies: Fixed coronary stenosis, Acute plaque change (rupture, hemorrhage), Coronary artery thrombosis, Vasoconstriction, Aortic valve stenosis and regurgitation. Increased right atrial pressure 40 micron collateral vessels are present in all hearts with pressure gradients permitting flow, despite occlusion of major vessels. In general, the cross-sectional area of the coronary artery lumen must be reduced by more than 75% to significantly affect perfusion. Coronary atherosclerosis is diffuse (involving more than one major arterial branch) but is often segmental, and typically involves the proximal 2 cm of arteries (epicardial). (Anversa et al, 1995). Percutaneous coronary intervention (PCI) following coronary angiography can aid in re-establishing myocardial perfusion. "Thrombolytic therapy" with agents such as streptokinase or tissue plasminogen activators (TPA) such as alteplase is often used following onset of symptoms and to try and lyse a recently formed thrombus. Such therapy with lysis of the thrombus can re-establish blood flow in a majority of cases. This helps to prevent significant myocardial injury, if early in the course of events, and can at least help to reduce further damage. Anti-platelet therapy can also be used. (Kumar and Cannon, Part II, 2009) (Bergmark et al, 2022)


This cross section of coronary artery demonstrates >75% narrowing, which would be associated with angina.Ischemic heart disease is caused by an imbalance between the myocardial blood flow and the metabolic demand of the myocardium. Reduction in coronary blood flow is mosst often related to progressive atherosclerosis with increasing occlusion of coronary arteries. Blood flow can be further decreased by superimposed events such as vasospasm, thrombosis, or circulatory changes leading to hypoperfusion. (Bergmark et al, 2022). Coronary artery perfusion depends upon the pressure differential between the ostia (aortic diastolic pressure) and coronary sinus (right atrial pressure). Coronary blood flow is reduced during systole because of Venturi effects at the coronary orifices and compression of intramuscular arteries during ventricular contraction. Factors reducing coronary blood flow include: Decreased aortic diastolic pressure, Increased intraventricular pressure and myocardial contraction. Coronary artery stenosis, which can be further subdivided into the following etiologies: Fixed coronary stenosis, Acute plaque change (rupture, hemorrhage), Coronary artery thrombosis, Vasoconstriction, Aortic valve stenosis and regurgitation. Increased right atrial pressure 40 micron collateral vessels are present in all hearts with pressure gradients permitting flow, despite occlusion of major vessels. In general, the cross-sectional area of the coronary artery lumen must be reduced by more than 75% to significantly affect perfusion. Coronary atherosclerosis is diffuse (involving more than one major arterial branch) but is often segmental, and typically involves the proximal 2 cm of arteries (epicardial). (Anversa et al, 1995). Percutaneous coronary intervention (PCI) following coronary angiography can aid in re-establishing myocardial perfusion. "Thrombolytic therapy" with agents such as streptokinase or tissue plasminogen activators (TPA) such as alteplase is often used following onset of symptoms and to try and lyse a recently formed thrombus. Such therapy with lysis of the thrombus can re-establish blood flow in a majority of cases. This helps to prevent significant myocardial injury, if early in the course of events, and can at least help to reduce further damage. Anti-platelet therapy can also be used. (Kumar and Cannon, Part II, 2009) (Bergmark et al, 2022)


This cross section of coronary artery demonstrates occlusive atherosclerosis complicated by calcification (the blue material in this section).Ischemic heart disease is caused by an imbalance between the myocardial blood flow and the metabolic demand of the myocardium. Reduction in coronary blood flow is mosst often related to progressive atherosclerosis with increasing occlusion of coronary arteries. Blood flow can be further decreased by superimposed events such as vasospasm, thrombosis, or circulatory changes leading to hypoperfusion. (Bergmark et al, 2022). Coronary artery perfusion depends upon the pressure differential between the ostia (aortic diastolic pressure) and coronary sinus (right atrial pressure). Coronary blood flow is reduced during systole because of Venturi effects at the coronary orifices and compression of intramuscular arteries during ventricular contraction. Factors reducing coronary blood flow include: Decreased aortic diastolic pressure, Increased intraventricular pressure and myocardial contraction. Coronary artery stenosis, which can be further subdivided into the following etiologies: Fixed coronary stenosis, Acute plaque change (rupture, hemorrhage), Coronary artery thrombosis, Vasoconstriction, Aortic valve stenosis and regurgitation. Increased right atrial pressure 40 micron collateral vessels are present in all hearts with pressure gradients permitting flow, despite occlusion of major vessels. In general, the cross-sectional area of the coronary artery lumen must be reduced by more than 75% to significantly affect perfusion. Coronary atherosclerosis is diffuse (involving more than one major arterial branch) but is often segmental, and typically involves the proximal 2 cm of arteries (epicardial). (Anversa et al, 1995). Percutaneous coronary intervention (PCI) following coronary angiography can aid in re-establishing myocardial perfusion. "Thrombolytic therapy" with agents such as streptokinase or tissue plasminogen activators (TPA) such as alteplase is often used following onset of symptoms and to try and lyse a recently formed thrombus. Such therapy with lysis of the thrombus can re-establish blood flow in a majority of cases. This helps to prevent significant myocardial injury, if early in the course of events, and can at least help to reduce further damage. Anti-platelet therapy can also be used. (Kumar and Cannon, Part II, 2009) (Bergmark et al, 2022)


This cross section of coronary artery demonstrates the extent of the intimal plaque at the right above the internal elastic lamina.Ischemic heart disease is caused by an imbalance between the myocardial blood flow and the metabolic demand of the myocardium. Reduction in coronary blood flow is mosst often related to progressive atherosclerosis with increasing occlusion of coronary arteries. Blood flow can be further decreased by superimposed events such as vasospasm, thrombosis, or circulatory changes leading to hypoperfusion. (Bergmark et al, 2022). Coronary artery perfusion depends upon the pressure differential between the ostia (aortic diastolic pressure) and coronary sinus (right atrial pressure). Coronary blood flow is reduced during systole because of Venturi effects at the coronary orifices and compression of intramuscular arteries during ventricular contraction. Factors reducing coronary blood flow include: Decreased aortic diastolic pressure, Increased intraventricular pressure and myocardial contraction. Coronary artery stenosis, which can be further subdivided into the following etiologies: Fixed coronary stenosis, Acute plaque change (rupture, hemorrhage), Coronary artery thrombosis, Vasoconstriction, Aortic valve stenosis and regurgitation. Increased right atrial pressure 40 micron collateral vessels are present in all hearts with pressure gradients permitting flow, despite occlusion of major vessels. In general, the cross-sectional area of the coronary artery lumen must be reduced by more than 75% to significantly affect perfusion. Coronary atherosclerosis is diffuse (involving more than one major arterial branch) but is often segmental, and typically involves the proximal 2 cm of arteries (epicardial). (Anversa et al, 1995). Percutaneous coronary intervention (PCI) following coronary angiography can aid in re-establishing myocardial perfusion. "Thrombolytic therapy" with agents such as streptokinase or tissue plasminogen activators (TPA) such as alteplase is often used following onset of symptoms and to try and lyse a recently formed thrombus. Such therapy with lysis of the thrombus can re-establish blood flow in a majority of cases. This helps to prevent significant myocardial injury, if early in the course of events, and can at least help to reduce further damage. Anti-platelet therapy can also be used. (Kumar and Cannon, Part II, 2009) (Bergmark et al, 2022)


This composite picture demonstrates cross sections of coronary artery with  atherosclerosis. At the left the lumen is about 50% occluded. At the right, there has been thrombosis with organization and recanalization to leave three small remaining lumens.Ischemic heart disease is caused by an imbalance between the myocardial blood flow and the metabolic demand of the myocardium. Reduction in coronary blood flow is mosst often related to progressive atherosclerosis with increasing occlusion of coronary arteries. Blood flow can be further decreased by superimposed events such as vasospasm, thrombosis, or circulatory changes leading to hypoperfusion. (Bergmark et al, 2022). Coronary artery perfusion depends upon the pressure differential between the ostia (aortic diastolic pressure) and coronary sinus (right atrial pressure). Coronary blood flow is reduced during systole because of Venturi effects at the coronary orifices and compression of intramuscular arteries during ventricular contraction. Factors reducing coronary blood flow include: Decreased aortic diastolic pressure, Increased intraventricular pressure and myocardial contraction. Coronary artery stenosis, which can be further subdivided into the following etiologies: Fixed coronary stenosis, Acute plaque change (rupture, hemorrhage), Coronary artery thrombosis, Vasoconstriction, Aortic valve stenosis and regurgitation. Increased right atrial pressure 40 micron collateral vessels are present in all hearts with pressure gradients permitting flow, despite occlusion of major vessels. In general, the cross-sectional area of the coronary artery lumen must be reduced by more than 75% to significantly affect perfusion. Coronary atherosclerosis is diffuse (involving more than one major arterial branch) but is often segmental, and typically involves the proximal 2 cm of arteries (epicardial). (Anversa et al, 1995). Percutaneous coronary intervention (PCI) following coronary angiography can aid in re-establishing myocardial perfusion. "Thrombolytic therapy" with agents such as streptokinase or tissue plasminogen activators (TPA) such as alteplase is often used following onset of symptoms and to try and lyse a recently formed thrombus. Such therapy with lysis of the thrombus can re-establish blood flow in a majority of cases. This helps to prevent significant myocardial injury, if early in the course of events, and can at least help to reduce further damage. Anti-platelet therapy can also be used. (Kumar and Cannon, Part II, 2009) (Bergmark et al, 2022)


This coronary artery opened longitudinally demonstrates severe atherosclerosis.Ischemic heart disease is caused by an imbalance between the myocardial blood flow and the metabolic demand of the myocardium. Reduction in coronary blood flow is mosst often related to progressive atherosclerosis with increasing occlusion of coronary arteries. Blood flow can be further decreased by superimposed events such as vasospasm, thrombosis, or circulatory changes leading to hypoperfusion. (Bergmark et al, 2022). Coronary artery perfusion depends upon the pressure differential between the ostia (aortic diastolic pressure) and coronary sinus (right atrial pressure). Coronary blood flow is reduced during systole because of Venturi effects at the coronary orifices and compression of intramuscular arteries during ventricular contraction. Factors reducing coronary blood flow include: Decreased aortic diastolic pressure, Increased intraventricular pressure and myocardial contraction. Coronary artery stenosis, which can be further subdivided into the following etiologies: Fixed coronary stenosis, Acute plaque change (rupture, hemorrhage), Coronary artery thrombosis, Vasoconstriction, Aortic valve stenosis and regurgitation. Increased right atrial pressure 40 micron collateral vessels are present in all hearts with pressure gradients permitting flow, despite occlusion of major vessels. In general, the cross-sectional area of the coronary artery lumen must be reduced by more than 75% to significantly affect perfusion. Coronary atherosclerosis is diffuse (involving more than one major arterial branch) but is often segmental, and typically involves the proximal 2 cm of arteries (epicardial). (Anversa et al, 1995). Percutaneous coronary intervention (PCI) following coronary angiography can aid in re-establishing myocardial perfusion. "Thrombolytic therapy" with agents such as streptokinase or tissue plasminogen activators (TPA) such as alteplase is often used following onset of symptoms and to try and lyse a recently formed thrombus. Such therapy with lysis of the thrombus can re-establish blood flow in a majority of cases. This helps to prevent significant myocardial injury, if early in the course of events, and can at least help to reduce further damage. Anti-platelet therapy can also be used. (Kumar and Cannon, Part II, 2009) (Bergmark et al, 2022)


This coronary artery demonstrates yellowish atherosclerotic plaques grossly.Ischemic heart disease is caused by an imbalance between the myocardial blood flow and the metabolic demand of the myocardium. Reduction in coronary blood flow is mosst often related to progressive atherosclerosis with increasing occlusion of coronary arteries. Blood flow can be further decreased by superimposed events such as vasospasm, thrombosis, or circulatory changes leading to hypoperfusion. (Bergmark et al, 2022). Coronary artery perfusion depends upon the pressure differential between the ostia (aortic diastolic pressure) and coronary sinus (right atrial pressure). Coronary blood flow is reduced during systole because of Venturi effects at the coronary orifices and compression of intramuscular arteries during ventricular contraction. Factors reducing coronary blood flow include: Decreased aortic diastolic pressure, Increased intraventricular pressure and myocardial contraction. Coronary artery stenosis, which can be further subdivided into the following etiologies: Fixed coronary stenosis, Acute plaque change (rupture, hemorrhage), Coronary artery thrombosis, Vasoconstriction, Aortic valve stenosis and regurgitation. Increased right atrial pressure 40 micron collateral vessels are present in all hearts with pressure gradients permitting flow, despite occlusion of major vessels. In general, the cross-sectional area of the coronary artery lumen must be reduced by more than 75% to significantly affect perfusion. Coronary atherosclerosis is diffuse (involving more than one major arterial branch) but is often segmental, and typically involves the proximal 2 cm of arteries (epicardial). (Anversa et al, 1995). Percutaneous coronary intervention (PCI) following coronary angiography can aid in re-establishing myocardial perfusion. "Thrombolytic therapy" with agents such as streptokinase or tissue plasminogen activators (TPA) such as alteplase is often used following onset of symptoms and to try and lyse a recently formed thrombus. Such therapy with lysis of the thrombus can re-establish blood flow in a majority of cases. This helps to prevent significant myocardial injury, if early in the course of events, and can at least help to reduce further damage. Anti-platelet therapy can also be used. (Kumar and Cannon, Part II, 2009) (Bergmark et al, 2022)


These serial sections of a coronary artery demonstrate grossly the appearance of lumenal narrowing with atherosclerosis.Ischemic heart disease is caused by an imbalance between the myocardial blood flow and the metabolic demand of the myocardium. Reduction in coronary blood flow is mosst often related to progressive atherosclerosis with increasing occlusion of coronary arteries. Blood flow can be further decreased by superimposed events such as vasospasm, thrombosis, or circulatory changes leading to hypoperfusion. (Bergmark et al, 2022). Coronary artery perfusion depends upon the pressure differential between the ostia (aortic diastolic pressure) and coronary sinus (right atrial pressure). Coronary blood flow is reduced during systole because of Venturi effects at the coronary orifices and compression of intramuscular arteries during ventricular contraction. Factors reducing coronary blood flow include: Decreased aortic diastolic pressure, Increased intraventricular pressure and myocardial contraction. Coronary artery stenosis, which can be further subdivided into the following etiologies: Fixed coronary stenosis, Acute plaque change (rupture, hemorrhage), Coronary artery thrombosis, Vasoconstriction, Aortic valve stenosis and regurgitation. Increased right atrial pressure 40 micron collateral vessels are present in all hearts with pressure gradients permitting flow, despite occlusion of major vessels. In general, the cross-sectional area of the coronary artery lumen must be reduced by more than 75% to significantly affect perfusion. Coronary atherosclerosis is diffuse (involving more than one major arterial branch) but is often segmental, and typically involves the proximal 2 cm of arteries (epicardial). (Anversa et al, 1995). Percutaneous coronary intervention (PCI) following coronary angiography can aid in re-establishing myocardial perfusion. "Thrombolytic therapy" with agents such as streptokinase or tissue plasminogen activators (TPA) such as alteplase is often used following onset of symptoms and to try and lyse a recently formed thrombus. Such therapy with lysis of the thrombus can re-establish blood flow in a majority of cases. This helps to prevent significant myocardial injury, if early in the course of events, and can at least help to reduce further damage. Anti-platelet therapy can also be used. (Kumar and Cannon, Part II, 2009) (Bergmark et al, 2022)


This is a normal coronary artery with a nice, big, unobstructed lumen for supplying plenty of blood to the myocardium.Ischemic heart disease is caused by an imbalance between the myocardial blood flow and the metabolic demand of the myocardium. Reduction in coronary blood flow is mosst often related to progressive atherosclerosis with increasing occlusion of coronary arteries. Blood flow can be further decreased by superimposed events such as vasospasm, thrombosis, or circulatory changes leading to hypoperfusion. (Bergmark et al, 2022). Coronary artery perfusion depends upon the pressure differential between the ostia (aortic diastolic pressure) and coronary sinus (right atrial pressure). Coronary blood flow is reduced during systole because of Venturi effects at the coronary orifices and compression of intramuscular arteries during ventricular contraction. Factors reducing coronary blood flow include: Decreased aortic diastolic pressure, Increased intraventricular pressure and myocardial contraction. Coronary artery stenosis, which can be further subdivided into the following etiologies: Fixed coronary stenosis, Acute plaque change (rupture, hemorrhage), Coronary artery thrombosis, Vasoconstriction, Aortic valve stenosis and regurgitation. Increased right atrial pressure 40 micron collateral vessels are present in all hearts with pressure gradients permitting flow, despite occlusion of major vessels. In general, the cross-sectional area of the coronary artery lumen must be reduced by more than 75% to significantly affect perfusion. Coronary atherosclerosis is diffuse (involving more than one major arterial branch) but is often segmental, and typically involves the proximal 2 cm of arteries (epicardial). (Anversa et al, 1995). Percutaneous coronary intervention (PCI) following coronary angiography can aid in re-establishing myocardial perfusion. "Thrombolytic therapy" with agents such as streptokinase or tissue plasminogen activators (TPA) such as alteplase is often used following onset of symptoms and to try and lyse a recently formed thrombus. Such therapy with lysis of the thrombus can re-establish blood flow in a majority of cases. This helps to prevent significant myocardial injury, if early in the course of events, and can at least help to reduce further damage. Anti-platelet therapy can also be used. (Kumar and Cannon, Part II, 2009) (Bergmark et al, 2022)


The  lipid hypothesis  (also known as the  cholesterol  hypothesis ) is a  medical theory  postulating a link between  blood cholesterol  levels and the occurrence of  cardiovascular disease . A summary from 1976 described it as: "measures used to lower the plasma lipids in patients with  hyperlipidemia  will lead to reductions in new events of  coronary heart disease ". [ 1 ]  It states, more concisely, that "decreasing blood cholesterol [...] significantly reduces coronary heart disease". [ 2 ]


As of 2023, there is international clinical acceptance of the lipid hypothesis. [ 3 ] [ 4 ] [ 5 ] [ 6 ]


In 1856, the German  pathologist   Rudolf Virchow  first described  lipid  accumulation in arterial walls. [ 7 ]  However, the initial connection between  arteriosclerosis  and dietary cholesterol would not be established until the research of Russian pathologist  Nikolay Anichkov , prior to  World War I . [ 8 ]  In 1913, a study by Anichkov showed that rabbits fed on  cholesterol  developed lesions in their arteries similar to  atherosclerosis , suggesting a role for cholesterol in  atherogenesis . [ 9 ]


Dutch physician  Cornelis de Langen  noted the correlation between nutritional cholesterol intake and incidence of  gallstones  in   Javanese  people in 1916. [ 10 ] [ 11 ]  de Langen showed that the traditional Javanese diet, poor in cholesterol and other lipids, was associated with a low level of blood cholesterol and low incidence of  cardiovascular disease  (CVD), while the prevalence of CVD in Europeans living in Java on a Western diet was higher. [ 10 ]  Since de Langen published his results only in Dutch, his work remained unknown to most of the international scientific community until the 1940s and 1950s. [ 10 ]  By 1951, it was accepted that, although the causes of  atheroma  were still unknown, fat deposition was a major feature of the disease process. "The so-called fatty flecks or streaks of arteries are the early lesions of atherosclerosis and... may develop into the more advanced lesions of the disease." [ 12 ]


With the emergence of CVD as a major cause of death in the Western world in the middle of the 20th century, the lipid hypothesis received greater attention. In the 1940s, a University of Minnesota researcher,  Ancel Keys , postulated that the apparent epidemic of  heart attacks  in middle-aged American men was related to their mode of life and possibly modifiable physical characteristics. He first explored this idea in a group of Minnesota business and professional men that he recruited into a prospective study in 1947, the first of many cohort studies eventually mounted internationally. The first major report appeared in 1963 and the men were followed through until 1981. [ 13 ]  After fifteen years follow-up, the study confirmed the results of larger studies that reported earlier on the predictive value for heart attack of several risk factors: blood pressure, blood cholesterol level, and cigarette smoking. [ 13 ]


Keys presented his diet-lipid-heart disease hypothesis at a 1955 expert meeting of the  World Health Organization  in Geneva. [ 14 ]  In response to criticism at the conference, Keys recruited collaborating researchers in seven countries to mount the first cross-cultural comparison, the years-long  Seven Countries Study , which is still under observation today. This was to compare the heart attack risk in populations of men engaged in traditional occupations and being from cultures with different diets, especially in the proportion of fat calories of different composition. [ 15 ]  There was also criticism before the study began: Yerushalmy and Hilleboe pointed out that Keys had selected for the study the countries that would give him the results he wanted, while leaving out data from sixteen countries that would not; they also pointed out that Keys was studying a "tenuous association" rather than any possible proof of  causality . [ 16 ]  Keys then joined the nutrition committee of the  American Heart Association  (AHA), successfully promulgated his idea, and in 1961, the AHA became the first group anywhere in the world to advise cutting back on saturated fat (and dietary cholesterol) to prevent heart disease. [ 17 ]  This historic recommendation was reported on the cover of  Time Magazine  in that same year. [ 18 ]


The Seven Countries Study was formally started in fall 1958 in  Yugoslavia . In total, 12,763 males, 40–59 years of age, were enrolled in seven countries, in four regions of the world (United States, Northern Europe, Southern Europe, Japan). One cohort is in the United States, two cohorts in Finland, one in the Netherlands, three in Italy, five in Yugoslavia (two in Croatia, and three in Serbia), two in Greece, and two in Japan. The entry examinations were performed between 1958 and 1964 with an average participation rate of 90%, lowest in the US, with 75%, and highest in one of the Japanese cohorts, with 100%. [ 19 ]


Keys' book  Eat Well and Stay Well   [ 20 ]  popularized the idea that reducing the amount of  saturated fat  in the diet would reduce cholesterol levels and the risks of serious diseases due to atheroma. [ 21 ]  Keys was followed during the rest of the 20th century by an accumulation of work that repeatedly demonstrated associations between cholesterol levels (and other modifiable risk factors including smoking and exercise) and risks of heart disease. These led to the acceptance of the lipid hypothesis as orthodoxy by much of the medical community. [ 22 ]  By the end of the 1980s, there were widespread academic statements that the lipid hypothesis was proven beyond reasonable doubt, [ 23 ] [ 24 ] [ 25 ]  or, as one article stated,  "universally recognized as a law."   [ 26 ] [ 27 ] [ 28 ] [ 29 ] [ 30 ]


The medical consensus supports the lipid hypothesis as evidence from separate  meta-analyses ,  prospective  epidemiologic studies and  randomized clinical trials  have demonstrated that elevated levels of  LDL  blood cholesterol are a significant risk factor for cardiovascular disease. [ 3 ]


The  National Lipid Association  have stated that by 2012, a wealth of evidence including numerous clinical trials examined by the Cholesterol Treatment Trialists' Collaboration has confirmed the lipid hypothesis. [ 31 ]  Too much LDL (called "bad cholesterol") can lead to fatty deposits building up in the arteries, which increases the risk of cardiovascular disease. A 2017 consensus statement from the  European Atherosclerosis Society  concluded that "consistent evidence from numerous and multiple different types of clinical and genetic studies unequivocally establishes that LDL causes ASCVD." [ 3 ]  The consensus statement noted:


Most publications that question the causal effect of LDL on the development of ASCVD tend to cite evidence from individual studies or a small group of highly selected studies, often without a quantitative synthesis of the presented evidence. Therefore, to avoid this type of selection bias, we have based our conclusions on the totality of evidence from separate meta-analyses of genetic studies, prospective epidemiologic studies, Mendelian randomization studies, and randomized clinical trials. This evidence base includes over 200 studies involving over 2 million participants with over 20 million person-years of follow-up and more than 150 000 cardiovascular events. Together these studies provide remarkably consistent and unequivocal evidence that LDL causes ASCVD. [ 3 ]


A review from the  Journal of the American College of Cardiology  in 2018 concluded:


The causal effect of LDL and other apo B–containing lipoproteins on the risk of cardiovascular disease is determined by both the magnitude and the cumulative duration of exposure to these lipoproteins. The goal of maintaining optimal lipid levels throughout life is to keep the concentration of circulating LDL and other apo B–containing lipoproteins low to minimize the number of particles that become retained in the arterial wall and thereby minimize the rate of progression of atherosclerotic plaques. [ 32 ]


The 2021  Canadian Cardiovascular Society  Guidelines say "We recommend that for any patient with triglycerides > 1.5 mmol/L, non- HDL-C  or  ApoB  be used instead of LDL-C as the preferred lipid parameter for screening (Strong Recommendation, High-Quality Evidence)". [ 33 ]


The  European Society of Cardiology  have noted:


For almost a century, evidence has been overwhelming that lipids and diet are related and have a negative impact on CVD. It is also clear that lipids, and especially LDL, play a crucial role in atherosclerosis. However, groups of “non-believers” decelerated developments and clinical progress, sometimes for decades. [ 34 ]


In 2023, the  World Heart Federation  published a report which stated that high levels of low-density lipoprotein (LDL) cholesterol are a major risk factor for cardiovascular diseases and that elevated LDL cholesterol contributed to 3.8 million deaths in 2021. [ 6 ]


The  National Lipid Association  (NLA) is an American non-profit multidisciplinary medical society that aims to enhance the practice of lipid management in  clinical medicine . The NLA focuses on the prevention of  cardiovascular disease  and other lipid-related disorders. [ 1 ]


The National Lipid Association was formed in 1997 and has over 2,000 members. [ 2 ] [ 3 ]  It provides medical education for healthcare professionals and physicians to advance knowledge and certification in clinical  lipidology . [ 2 ]  Joseph Saseen is the current president of NLA. [ 4 ] [ 5 ]  In 2014, the NLA proposed a working definition of  statin  intolerance and made general recommendations for health professionals. [ 6 ] [ 7 ]


The NLA have stated that by 2012, a wealth of evidence including numerous clinical trials examined by the Cholesterol Treatment Trialists' Collaboration has confirmed the  lipid hypothesis . [ 8 ]


The NLA publishes the  Journal of Clinical Lipidology . [ 9 ]


In 2019, the NLA's Nutrition and Lifestyle Task Force published a scientific statement based on a comprehensive review of recent clinical evidence on the effects of low and very- low-carbohydrate diets  on the management of body weight and other cardiometabolic risk factors. [ 10 ] [ 11 ]  The statement concluded that low and very-low-carbohydrate die are not superior to other dietary approaches for weight loss and are difficult to maintain in the long term. [ 10 ] [ 11 ]


In 2021, the NLA published a scientific statement on lipid measurements in the management of cardiovascular diseases. [ 12 ]


In 2022, the NLA published a scientific statement on statin intolerance, updating the definition which now classifies statin intolerance as either partial or complete. [ 13 ]  The 2022 statement recommends different strategies to help patients stay on statin medications, and alternative medications to those who cannot tolerate statins. [ 1 ] [ 14 ]


The  Seven Countries Study  is an  epidemiological   longitudinal study  directed by  Ancel Keys  at what is today the  University of Minnesota  Laboratory of Physiological Hygiene & Exercise Science (LPHES). Begun in 1956 with a yearly grant of US$200,000 from the  U.S. Public Health Service , the study was first published in 1978 and then followed up on its subjects every five years thereafter.


As the world's first multicountry epidemiological study, it systematically examined the relationships between lifestyle, diet,  coronary heart disease  and  stroke  in different populations from different regions of the world. It directed attention to the causes of coronary heart disease and stroke, but also showed that an individual’s risk can be changed.


Writing in 1975, project officer Henry Blackburn identified two "strikingly polar attitudes", characterising them as persisting "academic" and "pragmatic" views with "much talk from each and little listening between." [ 1 ]


In the 1940s, a University of Minnesota researcher,  Ancel Keys , postulated that the apparent epidemic of heart attacks in middle-aged American men was related to their mode of life and possibly modifiable physical characteristics. He first explored this idea in a group of Minnesota business and professional men (executives aged 45 to 55) that he recruited into a prospective study in 1947, the first of many  cohort studies  eventually mounted internationally. The U.S. Public Health Service agreed to fund the study (and then set up and proceeded to fund the  Framingham Heart Study  on a larger scale). The Minnesota men were followed through 1981 and the first major report appeared in 1963 after the fifteen-year follow-up study. [ 2 ] [ 3 ]


The study contributed much to survey methods and confirmed larger studies that reported earlier on the predictive value for heart attack of several characteristics, the now-traditional risk factors of  blood pressure  and blood  cholesterol  level and cigarette  smoking . Keys traveled widely with his wife Margaret who tested people's serum cholesterol. They sent their samples back to Minnesota for analysis. In 1952, Keys's hypothesis that coronary heart disease could be related to diet was first published in  Voeding  in The Netherlands. [ 4 ]  His work in post-wartime  Naples  led him to seek organization and funding for studies of different populations, as did his subsequent work in  Uganda ;  Cape Town , South Africa;  Sardinia ;  Bologna ; and  Ilomantsi , Finland; and with Japanese men living in  Hawaii  and in  Japan . He decided to concentrate on men living in  villages , rather than those in cities where the population moved around frequently. [ 3 ]


In the mid-1950s, with improved methods and design, Keys recruited collaborating researchers in seven countries to mount the first cross-cultural comparison of heart attack risk in populations of men engaged in traditional occupations in cultures contrasting in diet, especially in the proportion of fat calories of different composition, the Seven Countries Study still under observation today.


The Seven Countries Study was formally started in fall 1958 in  Yugoslavia . In total, 12,763 males, 40–59 years of age, were enrolled as 16 cohorts, in seven countries, in four regions of the world (United States, Northern Europe, Southern Europe, Japan). One cohort is in the United States, two cohorts in Finland, one in the Netherlands, three in Italy, five in Yugoslavia (two in  Croatia , and three in  Serbia ), two in Greece, and two in Japan. The entry examinations were performed between 1958 and 1964 with an average participation rate of 90%, lowest in the US, with 75% and highest in one of the Japanese cohorts, with 100%. [ 5 ]  The study has continued for more than 50 years.


The Seven Countries Study suggested that the risk and rates of  heart attack and stroke  (CVR), both at the population level and at the individual level,  correlated  directly and independently to the level of total serum cholesterol, in seven sampled out countries. It demonstrated that the correlation between blood cholesterol level and coronary heart disease (CHD) risk from 5 to 40 years follow-up is found consistently across different specially selected cultures in these seven countries. Cholesterol and obesity correlated with increased mortality from cancer. [ 6 ] [ 7 ] [ 8 ]  The Seven Countries Study suggested that elevated blood pressure ( hypertension ) was correlated with risk of coronary heart disease and stroke. It showed that the  mortality rate  after a coronary heart disease event or stroke was associated with the level of hypertension. In several cohorts of the study, stroke deaths exceeded deaths from coronary heart disease. [ 9 ] [ 10 ]  It hinted that differences in overall mortality between the different regions of the seven countries are largely associated with variation in cardiovascular mortality. [ 11 ]  Coronary deaths in the United States and Northern Europe greatly exceeded those in Southern Europe, even when controlled for age, cholesterol, blood pressure, smoking, physical activity, and weight.


The Seven Countries Study was investigated further in regard to an eating pattern loosely characterized as the  Mediterranean Diet . [ 12 ] [ 13 ] [ 14 ] [ 11 ] [ 15 ]  What exactly is meant by "Mediterranean Diet" today, was detailed by  Antonia Trichopoulou  (wife of  Dimitrios Trichopoulos ), [ 16 ]  and Anna Ferro-Luzzi. [ 17 ]  The diet was publicized and popularized by Greg Drescher of the Oldways Preservation and Exchange Trust and by  Walter Willett  of the  Harvard School of Public Health . [ 18 ] [ 19 ] [ 20 ] [ 21 ] [ 22 ]


The Seven Countries Study also showed that the slowly changing habits of a population in the Mediterranean region, from a healthy, active lifestyle and diet, to a less active lifestyle and a diet influenced by the  Western pattern diet , significantly correlated with increased risk of heart disease. [ 23 ] [ 24 ]  Meanwhile, it has been confirmed by other researchers that there is an inverse association between adherence to the  Mediterranean Diet  and the incidence of fatal and non- fatal heart disease in initially healthy middle-aged adults in the Mediterranean region. [ 25 ]


The Seven Countries Study, along with other studies, e.g., the  Framingham Heart Study  and the  Nurses' Health Study , showed the importance of  overweight ,  obesity  and regular  exercise  as health issues. [ 26 ] [ 27 ] [ 28 ] [ 29 ]  It showed a correlation between good cardiovascular health and dementia in the general population. It also showed that cardiovascular risk factors in mid life are significantly associated with increased risk of dementia death later in life. [ 30 ]  It indicated that cigarette smoking is a highly significant predictor of the development of coronary heart disease, leading to excess rates of  angina pectoris ,  myocardial infarction  (MI) and coronary death, along with other studies about smoking, e.g., the Framingham Heart Study and the  British Doctors Study . [ 31 ] [ 32 ] [ 33 ] [ 34 ]


Initial results from the Seven Countries Study in North Karelia (Finland) prompted public pressure for the authorities to act to reduce historically high levels of chronic disease in the region. The results influenced a subsequent public health program, the  North Karelia Project , which ran from 1972 until 1997, and which had among its aims a reduction in levels of peoples' saturated fat intake. [ 35 ]


Charles Antzelevitch  is an American cardiovascular research scientist in the fields of cardiac electrophysiology and cardiac arrhythmia syndromes. [ 1 ]


Antzelevitch graduated from  Queens College, City University of New York  with a BA in biology. He earned a  PhD  in  pharmacology  from  State University of New York Upstate Medical University  in 1978. [ 1 ]  From 1977 to 1980, he held a postdoctoral fellowship in the department of experimental cardiology at the Masonic Medical Research Laboratory (MMRL) in  Utica , New York. [ 2 ]


After his fellowship, he joined the staff of the  MMRL as a research scientist. In 1984, he was named executive director and director of research at the MMRL and was appointed the Gordon K. Moe Scholar, an endowed chair in experimental cardiology, in 1987. [ 2 ]


Antzelevitch was a member of the faculty at  State University of New York Upstate Medical University  in  Syracuse ,  New York , from 1980 until 2015. In 1980, he received an appointment as assistant professor in the department of pharmacology there. In 1983, he was promoted to associate professor and then in 1986, to research professor. He became professor of pharmacology in 1995. [ 2 ] [ 3 ]  In 2015, Antzelevitch moved to the Lankenau Institute for Medical Research (LIMR), where he was appointed professor and executive director of cardiovascular research and director of research at the Lankenau Heart Institute. In 2020, he was designated as distinguished professor emeritus at LIMR. [ 4 ] [ 1 ]


Antzelevitch was president of the  International Cardiac Electrophysiology Society  from 1996 to 1998 [ 5 ]  and has served as secretary/treasurer since 1998. [ 6 ]  He serves as Associate Editor of  Heart Rhythm  journal as well as on the editorial board of several other peer-reviewed medical publications, including  Journal of Electrocardiology [ 7 ]  and  Journal of the American College of Cardiology . [ 8 ]  He received the Distinguished Scientist Award from the North American Society of Pacing and Electrophysiology (NASPE), currently the  Heart Rhythm Society  (HRS 2002), [ 9 ]  Excellence in Cardiovascular Science Award from the NE Affiliate of the  American Heart Association  (AHA 2003), [ 10 ]  Carl J. Wiggers Award from the  American Physiological Society  (2007), [ 11 ] [ 12 ]  Distinguished Scientist Award from the  American College of Cardiology  (ACC 2011), [ 9 ] [ 13 ]  Distinguished Service Award from the Cardiac Electrophysiology Society (2015), [ 14 ]  the Douglas P. Zipes Lecture Award from the  Heart Rhythm Society  (2016) [ 10 ]  and the Lifetime Achievement Award from the  American College of Cardiology  (ACC 2020). [ 15 ]


Deepak L. Bhatt  is a US  interventional cardiologist , researcher, and educator. He is known for novel clinical trials in cardiovascular prevention, intervention, and heart failure. As of 2024, he is the director of  Mount Sinai Fuster Heart Hospital  in  New York City  and the Dr.  Valentin Fuster  Professor of  Cardiovascular Medicine  at the  Icahn School of Medicine at Mount Sinai  Health System. [ 1 ] [ 2 ]  Prior, he served as the executive director of Interventional Cardiovascular programs at  Brigham and Women’s Hospital  Heart and Vascular Center and a professor of medicine at  Harvard Medical School . [ 3 ] [ 4 ]  He was given the  American College of Cardiology 's Distinguished Mentor Award in 2018, and in 2019, the  American Heart Association  presented him with its Distinguished Scientist award. [ 5 ]  As of 2024,  Google Scholar  reports that he has been cited 294,036  times, has an  h-index  of 201, and an  i10-index  of 1,261.


Bhatt graduated  Boston Latin School , earned his science degree as a  National Merit Scholar  from  MIT , an MD from  Cornell  and an MPH from  Harvard . [ 6 ]  He received his Executive MBA from the  University of Oxford  in 2024. [ 7 ]


He trained in internal medicine and cardiology at the  University of Pennsylvania  and  Cleveland Clinic , completing fellowships in interventional cardiology and cerebral and peripheral vascular intervention. He served as chief interventional fellow at Cleveland Clinic [ 8 ]  where he worked as an interventional cardiologist, associate professor of medicine, director of the interventional cardiology fellowship, associate director of the cardiovascular medicine fellowship, and associate director of the cardiovascular coordinating center. [ 9 ]


Later, he became the Chief of Cardiology at the  VA Boston Healthcare System  and, subsequently, the Interventional Cardiovascular Programs executive director at Brigham and Women’s Hospital. Additionally, he was a Senior Investigator in the  TIMI  Study Group and Editor-in-Chief of the Harvard Heart Letter. [ 8 ]  In 2012, he was appointed a professor of medicine at  Harvard Medical School . [ 10 ]


As of 2024, Bhatt serves on the Board of Directors and Science and Technology Committee of  Bristol Myers Squibb . [ 11 ]  He is on the cardiovascular advisory board for  McKinsey  and is a consultant to Broadview Ventures. He had previously served on the Board of Directors of the Boston VA Research Institute and as a Trustee of the  American College of Cardiology . [ 7 ]   He serves on the Board of Directors of the American Heart Association New York City chapter. [ 12 ]


Bhatt focuses on several areas of cardiology, including interventional cardiology, heart attacks, stroke, prevention, and heart failure, as well as related areas such as high cholesterol, diabetes, and obesity. [ 13 ]  AD Scientific Index ranks him as one of the top 3% of scientists worldwide in his field. [ 14 ]


Recent trials as of 2024 include:


Brigham and Women’s Hospital chose Bhatt in 2014 as the Eugene Braunwald Scholar and in 2016 presented him with the Research Mentor Award, and in 2017 he was awarded the Eugene Braunwald Teaching Award for Excellence in the Teaching of Clinical Cardiology. [ 6 ]  He was given the American College of Cardiology’s Distinguished Mentor Award in 2018, [ 20 ]  and in 2019, the American Heart Association’s Distinguished Scientist Award. [ 5 ] [ 21 ]  He received  NLA ’s Honorary Lifetime Membership Award in 2021, and the Society for Cardiovascular Angiography and Interventions’ Master Designation in 2022. [ 2 ]  Also in 2022, Research.com recognized him with its Best Scientists award. [ 13 ]  He was listed by the  Web of Science Group  as a Highly Cited Researcher from 2014 to 2024. [ 12 ] [ 22 ]


Bhatt is the Editor of the first and second editions of  Cardiovascular Intervention: A Companion to Braunwald’s Heart Disease [ 23 ]  and of  Opie's Cardiovascular Drugs: A Companion to Braunwald's Heart Disease . [ 24 ]  He is one of the co-editors of  Braunwald’s Heart Disease . [ 25 ]   Elsevier  credits him with a total of 11 titles as an author, chapter contributor, and editor. [ 26 ]


Bhatt was Senior Associate Editor for News and Clinical Trials for  ACC .org, member of the Healio | Cardiology Today Editorial Board, [ 27 ]  and Editor-in-Chief of the  Journal of Invasive Cardiology,  which also lists him as: [ 28 ]


As of 2024,  Google Scholar  reports that he has been cited 294,036 times, has an h-index of 201  and an i10-index of 1,261. [ 32 ]


Bhatt has authored or co-authored over 2,000 publications [ 33 ]  and has been listed by the Web of Science Group as a highly cited researcher from 2014 to 2024. [ 34 ] [ 35 ] [ 36 ] [ 22 ]


Bhatt's most cited, peer-reviewed articles include:


Javed Butler  is an  American   cardiologist  and  academic , recognized for his contributions to  cardiovascular medicine , particularly in  heart failure  research. He serves as the Maxwell A. and Gayle H. Clampitt Endowed Chair, president, and chief research executive at Baylor Scott & White Research Institute, and senior vice president at  Baylor Scott & White Health  in  Dallas, Texas . He is a fellow of  Heart Failure Society of America ,  European Society of Cardiology ,  American College of Cardiology , and  American Heart Association . [ 1 ] [ 2 ] [ 3 ] [ 4 ]


Born in  Karachi ,  Pakistan , Butler completed his higher secondary education at  Adamjee Science College  and received his  MBBS  from  Aga Khan University  in 1990. He moved to the  United States  for further medical training, earning a  MPH  from the  Harvard T.H. Chan School of Public Health  in 1998 and a  MBA  from  Emory University 's  Goizueta Business School  in 2015. [ 5 ]


Butler completed his residency in  primary care   internal medicine  at  Yale University , where he also served as Chief Resident. His specialization in cardiovascular disease was further developed through fellowships in Cardiovascular Disease and Heart Failure & Transplantation at  Vanderbilt University . He pursued additional specialization in  cardiac imaging  at  Massachusetts General Hospital ,  Harvard University . [ 6 ] [ 7 ]


Butler began as an instructor of medicine at  Yale University  (1994–1995) and later served as assistant professor at  Vanderbilt University  (1999–2006), where he was medical director of both the  Heart Transplant  and  heart-lung transplant  programs. In 2007, he joined  Emory University  as a full professor of medicine and director of the Heart Failure Research Program. [ 8 ]


At  Stony Brook University , Butler served as Director of Cardiovascular Medicine and co-director of the Heart Institute (2014–2017), where he held the Charles A. Gargano Chair in Cardiology. [ 9 ]  From 2018 to 2022, he chaired the Department of Medicine at the  University of Mississippi Medical Center , where he was also a professor of Physiology and Biophysics and held the Patrick H. Lehan Chair in Cardiovascular Research. [ 10 ] [ 11 ]


Butler has combined clinical work with research, education, and leadership, directing heart failure and transplant programs at Vanderbilt and Tennessee Valley Healthcare systems. He served as Deputy Chief Science Officer for the  American Heart Association  (AHA) from 2009 to 2016. [ 12 ]


He has chaired committees for the Heart Failure Society of America and the  American College of Cardiology , and represented the U.S. on the  European Society of Cardiology  Heart Failure Guidelines panel. Butler is a  Fellow  of the AHA, ACC, HFSA, and ESC. [ 13 ] [ 14 ]


Butler chairs the U.S. Food and Drug Administration's Cardio-Renal Advisory Committee, co-chairs the NIH-funded HeartShare study on heart failure progression, and serves as principal investigator for several international cardiovascular trials. He is ranked as one of the top cardiovascular experts globally. [ 15 ] [ 16 ]


Butler is a heart failure expert, with research spanning prevention to advanced therapies, including  cardiac transplantation  and  ventricular assist devices . He has led or participated in over 100 clinical trials, developed the Atlanta Cardiomyopathy Consortium, and helped establish the NIH-funded Heart Failure Network at Emory University. [ 17 ] [ 18 ]


Butler is an associate editor for the  European Heart Journal , section editor for the  Journal of the American College of Cardiology: Heart Failure , guest editor for the  European Journal of Heart Failure , and serves on the editorial board of  Circulation . He has also peer-reviewed for journals, including the  New England Journal of Medicine ,  Journal of the American Medical Association  (JAMA), and  Lancet . [ 19 ]


Arthur DeBoer , (July 2, 1917-July 31, 2007), was an American  cardiologist  specializing in  cardiac surgery  at  Northwestern University 's  Feinberg School of Medicine . DeBoer was one of the pioneer cardiac surgeons in  Chicago  and was on staff at Wesley Memorial Hospital (later called  Northwestern University Hospital ).  DeBoer was the hospital's first chief of cardiothoracic surgery, and performed the first  open heart operation  at Wesley Memorial Hospital in 1958. [ citation needed ]  He served as Chair of Northwestern's Department of Cardiovascular Surgery until 1975.  [ 1 ]  He was also a pioneer in research on  congenital heart defects .


He was born to John and Lucy DeBoer in  Gallatin County, Montana , and was a graduate of Montana Normal School (now  University of Montana Western ) earning his B.E. Degree in 1938.  He earned a B.S. Degree from  University of Montana  while teaching school. He graduated from  Northwestern University Medical School  in 1946 and after serving his internship at Wesley Hospital he served in the U.S. Army Medical Corps in Asia. [ 1 ]


This biographical article related to a physician in the United States is a  stub . You can help Wikipedia by  expanding it .


Ying Ge  is a Chinese-American chemist who is a Professor of Cell and Regenerative Biology at the  University of Wisconsin–Madison . Her research considers the molecular mechanisms that underpin cardiac disease. She has previously served on the board of directors of the  American Society for Mass Spectrometry . In 2020 Ge was named on the Analytical Scientist Power List.


Ge was born in  China . She attended  Peking University  for her undergraduate studies, where she studied chemistry. [ 1 ]  After graduating in 1997 Ge moved to the  United States , where she joined  Cornell University  as a doctoral student. [ 1 ]  Here she started to work on mass spectrometry, using  electron-capture dissociation  to study proteins. [ 2 ]  She worked under the supervision of  Tadhg Begley  and  Fred McLafferty . After completing her doctorate, Ge worked as a research scientist at  Wyeth . [ citation needed ]


Ge joined the  University of Wisconsin–Madison  as an assistant scientist, where she oversaw the  mass spectrometry  programme. She became an Associate Professor in 2015, and full Professor in 2019. [ 3 ]


Ge develops high-resolution mass spectrometry  proteomics  to better understand cardiac disease.  To image the very large proteins of human heart tissue, Ge combines  fourier-transform ion cyclotron resonance  (FT–ICR) mass spectrometry with  electron-capture dissociation . [ 4 ]  She has worked to create a top-down disease proteomic platform that allows for the separation, detection and characterisation of the biomarkers of heart damage.


Nanoproteomics, a technique developed by Ge and co-workers, makes use of nanoparticles and high resolution mass spectrometry to capture and characterise cardiac  troponins , including  troponin I . [ 5 ] [ 6 ]  Being able to test for and characterise troponin I would help with the early detection and diagnosis of heart disease. [ 7 ]  The peptide-functionalised superparamagnetic nanoparticles are combined with top-down mass spectrometry to identify the molecular fingerprints of troponins. [ 7 ]  Rather than just detecting cardiac troponins, which is possible using  ELISA -based antibody testing, this higher level of characterisation will allow Ge to identify various forms of modified troponins, allowing a  personalised  understanding of cardiac disease. [ 7 ]


Ge served on the board of the Top-Down Proteomics Consortium, [ 8 ]  on the editorial board of the Journal of Muscle Research and Cell Motility, [ 9 ]  as treasurer for the  American Society for Mass Spectrometry  (2016-2018). [ 10 ]


Ying Ge  publications indexed by  Google Scholar .


Renata Gomes  is a  cardiovascular  specialist who focusses her work on the use of  molecular biology , imaging and  nanotechnology  applications for  regeneration  purposes. [ 1 ] [ 2 ]  She is a Professor of Veteran's Health and Biomedical Research and the Chief Scientific Officer of veteran health charity BRAVO VICTOR. [ 3 ]


Renata Gomes (born in 1985) was born in  Barcelos ,  Portugal . At a young age she was dissecting birds that had been shot by hunters in her village. In her choice of career, she was also influenced by an uncle who was a forensic doctor at the Institute of Legal Medicine at the  University of Minho  in the northern Portuguese town of  Braga . Her academic training was in the United Kingdom, where she received a Forensic Medicine and Forensic Sciences Degree from the  University of Bradford , before doing post-graduate research and training in  Cardiovascular  Biochemistry and Medicine at  University College London  and an international PhD on Cardiovascular Regeneration and  Nanotechnology  with  University of Coimbra  in Portugal, the  University of Oxford  and the  University of Eastern Finland  (Kupio). Her work with the Universities of Coimbra, Oxford and Kupio on a  nanoparticle  that can contribute to cardiovascular  regeneration  placed her first in the 2011 Science-Image Competition organised by the  British Heart Foundation . [ 1 ] [ 4 ] [ 5 ] [ 6 ] [ 7 ]


Among the people with whom she has worked was the  Nobel Prize  winner, Professor  Oliver Smithies . In Bradford, she worked over the holidays with Professor  Karin Schallreuter  on plastic surgery. While working with Professor Lino Ferreira at the  Centre for Neuroscience and Cell Biology  at Coimbra University, they had an idea to combine  stem cell  technology with nanotechnology. The research took place between 2008 and 2012. After the results were published, Gomes was nominated for and won the  Science, Engineering and Technology for Britain 2012  award, given annually by the British Parliament. In 2013 her home town of Barcelos awarded her the title of Professional of the Year. [ 2 ] [ 6 ] [ 7 ]


Part of her time is devoted to community and humanitarian causes. She has worked with the  Small Scientists Network , based in her home town of Barcelos, which is aimed at promoting scientific curiosity among young people. Although having been treated for cancer, Gomes ran the  London Marathon  to raise money for the British Heart Foundation. While on a visit to Israel she contributed to a vaccination campaign among  Bedouins . In Israel she met  Henrique Cymerman , an Israeli journalist of Portuguese descent, with whom she decided to set up a Task Force called  Knowledge for the Benefit of Mankind , to bring together religious leaders of various faiths and other influential thinkers and young people, to find realistic solutions in favour of peace. [ 2 ] [ 7 ]


Based in London, she then worked as Head of Research and Innovation for the charity Blind Veterans UK (formerly St Dunstan's), seeking to find regenerative-medicine solutions to benefit blind veterans. In 2020 she became its Chief Scientific Officer, before the Directorate became BRAVO VICTOR. [ 2 ] [ 7 ] [ 8 ]


Roberta Anne Gottlieb  is an American  oncologist , academic, and researcher. She is a Professor, and Vice-Chair of Translational Medicine in the Department of  Biomedical Sciences  at  Cedars-Sinai Medical Center , and a Professor of Medicine at the  University of California, Los Angeles . [ 1 ]


Gottlieb published over 150 papers and has 6 patents awarded. [ 2 ]  Her research primarily focuses on the molecular basis of myocardial ischemia/ reperfusion injury  and on developing ways to mitigate damage. She has given over 200 invited talks both at scientific conferences, professional organizations and for the general public. [ 3 ]


Gottlieb is a Fellow of the  International Society for Heart Research  (FISHR), [ 4 ]  and the  American Heart Association  (FAHA), and was the Founder and CEO of Radical Therapeutix, from 2005 till 2014, and Co-Founder and Scientific Advisory Board Co-Chair, TissueNetix, from 2011 till 2018.


Gottlieb received her B.A. degree from the  Johns Hopkins University  in 1980, and her M.D. degree from  The Johns Hopkins University School of Medicine  in 1984. She completed her Residency in Pediatrics at the  University of Texas Health Science Center  in 1987, and her Fellowship in  Pediatric Hematology & Oncology  at the  University of Texas M.D. Anderson Cancer Center  in 1990. Following this, she became a Postdoctoral Fellow in Michael Karin’s lab at the  University of California San Diego School of Medicine  until 1992, and at  The Scripps Research Institute  in the lab of Bernard Babior until 1995. [ 5 ]


Gottlieb began her career as a Research Biochemist in the Department of Veterans Affairs Medical Center, San Diego in 1994. During this appointment, she also held concurrent appointments at Scripps Research Institute as an Assistant Member in the Department of Molecular and Experimental Medicine in 1995, and as an Associate Member from 1997 till 1998. In 1997, she was appointed as an Adjunct Assistant Professor in the Department of Medicine University of California San Diego School of Medicine, and from 1999 to 2006, she served at Scripps Research Institute as an Associate Professor in the Department of Molecular and Experimental Medicine. Gottlieb was appointed as the Director of San Diego State University BioScience Center from 2007 till 2013. Since 2013, she has been serving as a Research Scientist IV, and a Professor of Cardiology and Biomedical Sciences at Cedars-Sinai Medical Center, and as a Professor of Medicine at the University of California Los Angeles. [ 1 ]  At Cedars-Sinai Medical Center, she serves as the Director of Metabolism and Mitochondrial Research Core, as Curriculum Director for CSMC Clinical Scholars Program, and as Vice-Chair of Translational Medicine in the Department of Biomedical Sciences. Gottlieb retired from full-time research in March, 2022, but remains involved in several ongoing collaborations. [ 6 ]


Gottlieb leads ongoing research focused on  autophagy , [ 7 ]  mitophagy and biogenesis, with particular attention to the molecular basis of myocardial ischemia/reperfusion injury and in developing ways to mitigate damage. Her current projects are focused on the development of small-molecular cardioprotective agents for the treatment of reperfusion injury,  mitochondria  and stem cells in anthracycline-induced heart failure, rescue and role of complex I in myocardial ischemic injury, and microbial basis of cardiovascular disease. [ 8 ]


In 1994, Gottlieb described the occurrence of programmed cell death (apoptosis) in the ischemic and reperfused heart, and highlighted that programmed cell death taking place during reperfusion is a regulated process that might be blocked to salvage myocardium. [ 9 ]  Her subsequent work has explored the role of proteases and mitochondrial dysfunction in ischemia/reperfusion injury, [ 10 ]  and most recently, the importance of autophagy in mitigating reperfusion injury. [ 11 ]  She has developed tools and techniques in her lab for studying autophagy in cells and in ex vivo and in vivo models. [ 12 ]


Gottlieb was the first to suggest that autophagy served a protective role in the setting of myocardial stress. These concepts, tools, and approaches have extended beyond the cardiac field and have led to novel findings in the fields of infectious disease, diabetes, and neurology. [ 13 ]  Current efforts in her lab are focused on autophagic clearance of mitochondria and mitochondrial biogenesis as essential elements of cardioprotection; efficient removal of damaged mitochondria is important for limiting inflammation mediated by damage associated molecular pattern receptors. [ 14 ] [ 15 ]  In another study, she examined the effect of impaired autophagy on cardioprotection, [ 16 ]  and the Program Project Grant was focused on the impacts of age and obesity. [ 17 ]  Her current work is focused on mitophagy and mitochondrial biogenesis as linked processes that are tightly controlled in the heart. In 2018, she with the collaboration of Jennifer Van Eyk, developed polysome profiling and azidohomoalanine labeling to interrogate the newly-synthesized proteome. [ 18 ]  They also developed advanced proteomic methods to interrogate mitochondria (Mitoplex) [ 19 ]  and to image mitochondrial turnover (MitoTimer). [ 20 ]  In 2017, her research identified a new potential way to help cardiac muscle recover from procedures, and revealed that cardiomyocytes can be damaged by the process of stopping and starting the heart during surgeries that use cardiopulmonary bypass machines to take over the heart's functions. [ 21 ]


Gottlieb has been at the leading edge of research on mitochondria in cardiac homeostasis, which led her into the study of autophagy and mitophagy including being the first to demonstrate the critical role of  Parkin  in clearing damaged mitochondria during ischemic stress. [ 22 ]  Her work, in collaboration with cardiac surgeon Robert M. Mentzer, Jr., has extended to human studies, further validating the importance of Parkin in the human heart. [ 23 ]


Gottlieb has worked to determine the role of autophagy and mitophagy in pancreatitis. She initially studied cerulein-induced pancreatitis and now has expanded the focus to pancreatitis induced by ethanol and cigarette smoke. This work is done in collaboration with Honit Piplani and Stephen Pandol. In 2019, she highlighted how simvastatin induces autophagic flux to restore cerulein-impaired phagosome-lysosome fusion in acute pancreatitis, and also discussed the role of simvastatin in enhancing autophagic flux to prevent pancreatic cell injury and pancreatitis. [ 24 ]  She also contributed to a SEER-Medicare analysis focusing on the association of statin use after cancer diagnosis with survival in pancreatic cancer patients, and found out that statin treatment after cancer diagnosis is associated with enhanced survival in patients with low-grade, resectable PDAC. [ 25 ]


Mukesh K. Jain  is an American  physician-scientist  specializing in  cardiovascular medicine . [ 1 ]  Since March 2022 he has served as Dean of Biological Sciences at  Brown University  and Dean of Medicine at the  Warren Alpert Medical School . [ 2 ]  Jain previously served as Chief Scientific Officer at  University Hospitals Health System  and Vice-Dean for Medical Sciences at  Case Western Reserve University . [ 3 ]


Jain was born in the 1960s. [ 1 ]  He received a bachelor of science in biochemistry from the  University of Buffalo  in 1987. He earned his M.D. from the University of Buffalo's  Jacobs School of Medicine and Biomedical Sciences  in 1991. Jain completed his residency in internal medicine at  Beth Israel Deaconess Medical Center  in  Boston, Massachusetts . [ 4 ]


He subsequently completed fellowships at the  Harvard T.H. Chan School of Public Health  and at  Brigham and Women's Hospital / Harvard Medical School . [ 3 ]


Jain worked at Harvard from 1998 to 2006, serving as an Instructor of Medicine, Assistant Professor, and later Director of the Cardiovascular Transcriptional Biology Program at Brigham and Women's Hospital. Jain joined Case Western in 2006 as the founding Director of the Case Cardiovascular Research Institute, Professor of Medicine, and Ellery Sedgwick Jr. Chair and Distinguished Scientist. He was appointed Vice Dean for Medical Sciences at the university in 2016. [ 5 ]  In August 2021 he was appointed Distinguished University Professor. [ 6 ]


In October 2021, Jain was appointed Dean of Medicine and Biological Sciences at Brown University. He began as dean in March 2022, succeeding  Jack A. Elias . [ 2 ]


Jain is a vocal supporter of physician-scientists and advocate for increasing their ubiquity in the field. [ 7 ] [ 1 ]  In a 2020 article in  The Washington Post  Jain, Paul J. Utz, and Vivian G. Cheung wrote "we need a well-trained group of readied physician-scientists who can be deployed at any time to meet our nation’s medical needs, whether a  coronavirus pandemic  or other health emergencies." [ 8 ]


Marlys Laverne Koschinsky  (born 1959)  OOnt   FCAHS  is a Canadian cardiovascular researcher. As of 2015 [update] , she is the executive director at the  University of Western Ontario 's  Robarts Research Institute . Koschinsky formally served as Dean of the Faculty of Science at the  University of Windsor .


Koschinsky was born in 1959. [ 1 ]  She graduated with her  Bachelor of Science  degree in 1982 from the  University of Winnipeg  and was subsequently awarded the Chancellor's gold medal for highest standing in the 4-year science program. Following this, Koschinsky completed her PhD in biochemistry at the  University of British Columbia . In 1988, Koschinsky began her postdoctoral research in the Cardiovascular Research Group at  Genentech  in San Francisco. [ 2 ]


Following her post-doctoral work, Koschinsky became the first female research professor at  Queen's University at Kingston  in biochemistry. [ 3 ]  During the 1996–97 academic year, she was the co-recipient of the Mihran and Mary Rasmajian Award for excellence in research. [ 4 ]  Throughout her tenure at Queen's, Koschinsky accepted a 5-year scholarship from the  Heart and Stroke Foundation of Canada  and a 10-year Career Investigator award from the Heart and Stroke Foundation of Ontario. [ 2 ]  Prior to leaving Queen's, Koschinsky served as director of the Cardiac, Circulatory & Respiratory Research Program and Head of the Department of Physiology. [ 5 ]  She eventually left to become the Dean of the Faculty of Science at the  University of Windsor . [ 6 ]


During her tenure at the University of Windsor, Koschinsky became involved in outside organizations around the city including serving as vice-chair of the board of directors for WEtech Alliance and Chair of the Windsor-Essex Mission Committee. She was also a member of the steering committee for the South West Academic Health Network. Koschinsky remained as Dean of the Faculty of Science until 2015 when she accepted the position of executive director at the  University of Western Ontario 's Robarts Research Institute. [ 5 ]  As a result of her research into cardiovascular disease and the study of related risk factors, she was named a 2020 Fellow of the  Canadian Academy of Health Sciences . [ 7 ]  The following year, Koschinsky was named a Member of the  Order of Ontario . [ 8 ]


Koschinsky is married to Michael Boffa. [ 9 ]


Bruce B. Lerman  is a  cardiologist . He is the Hilda Altschul Master Professor of Medicine at  Weill Cornell Medical College , and was chief of the Division of Cardiology and director of the Cardiac Electrophysiology Laboratory at  Weill Cornell Medicine  and the  New York Presbyterian Hospital .


Lerman received a BA at  Clark University  in 1972, an MD medical degree from  Loyola University  -  Stritch School of Medicine  in 1977, was an  intern  and  medical resident  in  internal medicine  at  Northwestern University , and completed a  fellowship  in  cardiovascular disease  at the  Johns Hopkins School of Medicine . [ 1 ] [ 2 ] [ 3 ]   He trained in  cardiac electrophysiology  at the  Perelman School of Medicine at the University of Pennsylvania . [ 2 ]


Lerman is a  cardiologist  in New York City, with specialties in adult  congenital heart disease  and  cardiac electrophysiology . [ 1 ]


Lerman is the Hilda Altschul Master Professor of Medicine at  Weill Cornell Medical College , and chief of the Division of Cardiology and director of the Cardiac  Electrophysiology Laboratory at  Weill Cornell Medicine  and the  New York Presbyterian Hospital . [ 2 ] [ 3 ] [ 4 ] [ 5 ] [ 6 ] [ 7 ]


He has focused in his research on clarifying the  electrophysiologic  mechanisms of the  nucleoside   adenosine , current-based  defibrillation , and determining the role of mechanoelectrical feedback as a stimulus for causing malignant  ventricular arrhythmias . [ 2 ]   He has been issued 4  patents . [ 2 ]  Lerman has focused in his clinical work on the diagnosis and treatment by  ablation  of complicated atrial and ventricular  arrhythmias , and treating life-threatening arrhythmias with implantable devices. [ 2 ]


Lerman received the Established Investigator Award from the  American Heart Association , and had received a number of grants from the  National Institutes of Health . [ 2 ]   He is on the editorial boards of a number of medical and scientific journals, including  Circulation  and   Heart Rhythm . [ 2 ]


Lerman has written or co-written over 200 medical articles, 60 book chapters, and two books. [ 8 ] [ 2 ]


Among his publications are: [ 9 ]


Merry L. Lindsey  is an American cardiac physiologist. In 2022 she was named the Dean of the School of Graduate Studies at Meharry Medical College. In 2019 she was named the Stokes-Shackleford Professor and Chair of the  University of Nebraska Medical Center  Department of Cellular and Integrative Physiology and the director of the Center for Heart and Vascular Research. In 2021, Lindsey was appointed  editor-in-chief  of the  American Journal of Physiology. Heart and Circulatory Physiology.


Lindsey was born Stuart, Florida in 1970 [ 1 ] [ 2 ]  and raised in  South Florida , [ 3 ]  where she attended South Fork High School. [ 4 ]  Following high school, Lindsey earned her undergraduate degree in biology from  Boston University  and her PhD in cardiovascular sciences from  Baylor College of Medicine . [ 3 ]


Upon completing her PhD, Lindsey worked at the  Medical University of South Carolina  as an  assistant professor  before joining the faculty at the  University of Texas Health Science Center . In 2019, she left the Mississippi Center for Heart Research to accept an appointment as the Stokes-Shackleford Professor and Chair of the Department of Cellular and Integrative Physiology at the  University of Nebraska Medical Center . [ 3 ]  Upon joining the department, Lindsey also became the founding director of the Center for Heart and Vascular Research. [ 5 ]  She joined  Meharry Medical College  as the dean of the School of Graduate Studies and Research. [ 6 ]


In 2021, Lindsey was appointed  editor-in-chief  of the  American Journal of Physiology. Heart and Circulatory Physiology , a journal published by the  American Physiological Society . [ 7 ]  She received the Vincenzo Panagia Distinguished Lecture Award from the Institute of Cardiovascular Sciences at St-Boniface Hospital Research in 2021, [ 8 ]  and the Distinguished Investigator Award from the British Society for Cardiovascular Research in 2022. [ 9 ]


Joseph Randall Moorman  (born April 4, 1953) is an American physician-scientist. He is bicentennial Professor of Advanced Medical Analytics at the  University of Virginia School of Medicine .


Moorman is the younger son of Ruth, classicist and professor at the University of Southern Mississippi, and  Charles W. Moorman III , medievalist and dean at the University of Southern Mississippi. His brother is former Norfolk Southern and Amtrak CEO  Charles Moorman . [ 1 ]


Moorman grew up in Hattiesburg, Mississippi. He received his undergraduate degree from the  University of Mississippi  and his M.D. from  University of Mississippi School of Medicine . In 1978, Moorman began his medical internship at  Duke University Medical Center , [ 2 ]   where he served as Chief Resident from 1982-1983 and Cardiology Fellow from 1983-1985. He then finished his post-doctoral research training in membrane biophysics and molecular electrophysiology at  Baylor University . [ 3 ]


From 1985-1990, Moorman was Assistant Professor of Medicine at the  University of Texas Medical Branch  and worked in the laboratory of Arthur M. Brown at  Baylor College of Medicine . [ 4 ]


In 1990, he joined the faculty of the University of Virginia School of Medicine. [ 5 ]


From 2014 to 2019, he was Editor-in-Chief of  Physiological Measurement.   [ 4 ]


From 2014 to 2021, he was Chief Medical Officer of AMP3D (Advanced Medical Predictive Devices, Diagnostics, and Displays) [ 6 ]  before the company's acquisition by Nihon Kohden. [ 7 ]


In 2014, he and DE Lake were named Edlich-Henderson  Innovators of the Year by the University of Virginia Licensing and Ventures Group.  [ 8 ]


In 2017, he was keynote speaker for the  Association for the Advancement of Medical Instrumentation  Annual Conference. [ 9 ]


While at Baylor College of Medicine, Moorman studied the biophysical properties of cloned ion channel proteins expressed in heterologous systems. [ 10 ] [ 11 ]


At the University of Virginia, Moorman and coworkers discovered a unique channel activity for the molecule phospholemman (PLM, also  FXYD1 ). [ 12 ] [ 13 ]


In 2000, Moorman and JS Richman introduced  sample entropy  as a measure of complexity in dynamical systems. [ 14 ]  This method has been successfully used to test for non-linear dynamics and temporal predictability in many systems. [ 15 ] [ 16 ] [ 17 ]  In 2011, he and DE Lake developed the  coefficient of sample entropy for use in detecting atrial fibrillation. [ 18 ]


In 2001, he and MP Griffin demonstrated unique changes in heart rate characteristics (HRC) prior to the diagnosis of sepsis in premature infants. [ 19 ]  They and their coworkers devised the HRC Index, the relative risk of illness in the next 24 hours, and showed 22% relative reduction in death rates in one of the largest randomized trials in neonatology. This work was the first effective use of Big Data and Machine Learning to save lives, [ 20 ] [ 21 ] [ 22 ]  and was recognized as one of the top 12 scientific discoveries in the past 50 years at the University of Virginia. [ 23 ] [ 24 ] [ 25 ]


[ 26 ]   Moorman and coworkers went on to develop and validate multiple Machine Learning models for early detection of illness throughout the hospital.  [ 27 ]  Advanced Medical Predictive Devices, Diagnostics and Devices (AMP3D), [ 28 ] [ 29 ]  a Charlottesville, VA, small business, licensed the intellectual property from the University of Virginia Licensing and Ventures Group, developed and implemented the Continuous Monitoring of Event Trajectories (CoMET)  [ 30 ]  display, and was acquired in 2021 by Nihon Kohden Digital Health Solutions in Irvine, CA, a subsidiary of Nihon Kohden Corporation, Japan-based maker of medical devices.


According to ResearchGate, Moorman has written and co-written 229 peer-reviewed publications.


Kiran Musunuru  is an American cardiologist who is a Professor of Medicine at the  University of Pennsylvania Perelman School of Medicine . [ 1 ]  He researches the genetics and genomics of cardiovascular and metabolic diseases. Musunuru is a leading expert in the field of  gene-editing .


Musunuru is the son of Rao and Prameela Musunuru; he was born in  New York City  and grew up in  Florida . [ 2 ]  His father is a renowned cardiologist who moved to the US from India in 1976. [ 2 ]


Musunuru obtained a degree in Biochemical Sciences from  Harvard College  in 1997. [ 1 ]  He later obtained a PhD in Biomedical Sciences from  Rockefeller University  in 2003, and an MD from  Weill-Cornell Medical College  in 2004. [ 1 ]  Musunuru also graduated with a Masters of Public Health (MPH) in Epidemiology from the  Johns Hopkins Bloomberg School of Public Health  in 2009, and an ML in Law from the  University of Pennsylvania Law School  in 2019. [ 1 ]


Musunuru was interested in heart disease early in his medical career, first training in Internal Medicine at  Brigham and Women's Hospital  and then in Cardiovascular Medicine at  Johns Hopkins Hospital . [ 3 ] [ 4 ]  He also undertook postdoctoral work at the  Massachusetts General Hospital , as well as the  Broad Institute . [ 3 ]


Musunuru's researches the genetics and genomics of cardiovascular and metabolic diseases, and is a leading expert in genome-editing techniques, particularly  CRISPR-Cas9 . His lab was the first to develop an efficient technique to genetically modify human pluripotent stem cells, and differentiate them to model disease. [ 5 ]  He discovered two novel genes involved in  coronary artery disease : SORT1 and ANGPTL3. [ 5 ]  His research aims to find genetic variants which affect the course of disease and could be used to develop protective therapies. [ 3 ]  Musunuru ultimately hopes to create a one-shot "vaccination" against heart attacks, which would introduce a complementary, loss-of-function mutation in a gene such as ANGPTL3 to lower the risk of developing cardiovascular disease in at-risk populations. [ 2 ] [ 6 ]


Musunuru has pioneered the use of genome-editing tools as therapies for heart disease. For example, some people with a variant of the PCSK9 gene have lower levels of low-density lipoprotein (LDL) cholesterol levels, and therefore have a reduced risk of heart attack. [ 4 ]  Research from Musunuru's laboratory has shown that the levels of the PCSK9 gene expression could be altered in the liver of mice using CRISPR-Cas9 gene editing technology, drastically reducing the mice's cholesterol levels. [ 4 ] [ 7 ]  Musunuru has also led research into prenatal gene editing of PCSK9 or HPD using both CRISPR-Cas9 and base editor 3 (BE3), offering a proof-of-concept for a potential new therapeutic approach for congenital genetic disorders. [ 8 ] [ 9 ]  Musunuru cofounded  Verve Therapeutics  to develop gene editing techniques for treat cholesterol altering congenital genetic disorders.


In 2019, Musunuru was among a team of researchers at the University of Pennsylvania to develop a stem cell-based test for the effect of genetic variants on heart muscle cells. [ 10 ] [ 11 ]  They used the test to determine that a 65-year-old woman's specific variant of TNNT2, a gene which has been associated with cardiomyopathy, was not pathogenic. [ 10 ]