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Apoptosis in myocytes in end-stage heart failure

Article Abstract:

Heart failure may be a result of myocyte apoptosis, the biologically regulated programmed cell death of muscle cells. Researchers found evidence of apoptosis in five of seven hearts taken from patients with severe heart failure who were receiving a heart transplant. In contrast, locally apoptotic tissue was identified from four patients with recent heart attacks only near the damaged region. The hearts of four car accident victims contained few apoptotic cells. The prevention of cell death may become a future therapeutic angle for the treatment of heart disease and heart failure.

Research, Causes of, Medical examination, Cell death, Muscle cells, Heart failure, Heart muscle, Myocardium

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Coronary risk factors and plaque morphology in men with coronary disease who died suddenly

Article Abstract:

Smoking and elevated cholesterol increase the risk of sudden death in men with coronary artery disease but they do so by different mechanisms. Researchers examined the atherosclerotic plaques in the coronary arteries of 113 men who had died suddenly. Some men had evidence of blood clots in the arteries whereas others had ruptured plaques. Smokers were more likely to have blood clots and elevated cholesterol was associated with the rupture of a plaque. Smoking may cause blood clots because it increases platelet aggregation, a process involved in blood clotting.

Risk factors, Smoking, Sudden death, Hypercholesterolemia

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Intraplaque hemorrhage and progression of coronary atheroma

Article Abstract:

Bleeding inside a coronary artery plaque may make the plaque become bigger and more unstable, according to an autopsy study of 24 patients who died suddenly from heart disease. Plaques are deposits of cholesterol and other substances that block coronary arteries, causing coronary artery disease. Plaques that become unstable can rupture, causing a heart attack.

Development and progression, Hemorrhage, Atherosclerotic plaque

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