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Doctor, do you have any investigation to know how much the total plaque burden is in my coronary artery? I recently read in Forbes Sunday health supplement, It says ,it is better to know the thickness of the cap covering the plaque. So, you want me to teach you the molecular biology of Atherosclerosis ,right ? Korean Circ J.
Lp(a) is emerging as an important, yet under-recognized, potential risk factor for cardiovascular disease due to its ability to promote the development of plaques within artery walls, clot formation and aortic valve calcification. A focused update to the 2019 NLA scientific statement on use of lipoprotein(a) in clinical practice.
Background Although the impact of hypertension on carotid intima-media thickness (IMT) and plaques has been well established, its association with femoral IMT and plaques has not been extensively examined. Ultrasonography was applied to assess the AS, including thickened IMT (TIMT) and plaque in the carotid and femoral arteries.
MINOCA may be due to: coronary spasm, coronary microvascular dysfunction, plaque disruption, spontaneous coronary thrombosis/emboli , and coronary dissection; myocardial disorders, including myocarditis, takotsubo cardiomyopathy, and other cardiomyopathies. See "Mechanisms of acute coronary syndromes related to atherosclerosis".)
To prove there is no plaque rupture, you need to do intravascular ultrasound (IVUS). An angiogram is a "lumenogram;" most plaque is EXTRALUMINAL!! One of the most common is rupture of a non-obstructive plaque, with thrombus formation and OMI that spontaneously lyses and leaves a wide open artery. It can only be seen by IVUS.
Here’s the angiogram of the RCA : No thrombus or plaque rupture in the RCA (or any coronary artery) was found. This MI wasn’t caused by a ruptured plaque of CAD - it was a coronary artery dissection of the RCA. This MI wasn’t caused by a ruptured plaque of CAD - it was a coronary artery dissection of the RCA.
This registry will aim to provide world-wide physicians the most accurate information on coronary plaque to improve cardiovascular risk prediction and support the selection of patient-specific treatment,” said Dr. De Cecco. The ultimate goal is to positively impact cardiovascular health globally with a reduction in cardiovascular events."
Atherosclerotic cardiovascular disease (ASCVD), caused by plaque buildup in arterial walls, is one of the leading causes of disability and death worldwide.1,2 1,6 Until recently atherosclerosis has been thought of as the result of passive lipid accumulation in the vessel wall. 4 In the U.S.
Everyone starts with no plaque in the coronary arteries, but over a long enough time frame, everyone develops plaque in their coronary arteries. By age 80, almost everyone will have evidence of advanced plaque in their coronary arteries, as defined by a cardiac CT 1. Plaque accumulation happens in stages. You got it.
However, most adults will start to develop advanced plaque in their coronary arteries early in life. By age 66, more than half of all females will have evidence of advanced plaque in their coronary arteries, as seen on a CT calcium score. Coronary atherosclerosis, as evidenced by an abnormal CAC score, is a measure of advanced plaque.
Effect of intensive compared with moderate lipid-lowering therapy on progression of coronary atherosclerosis: a randomized controlled trial. Effect of very high-intensity statin therapy on regression of coronary atherosclerosis: the ASTEROID trial. 2019 Dec 26;381(26):2497-2505. 2004 Mar 3;291(9):1071-80. N Engl J Med.
A CT CAC scan can only identify if there is calcified atherosclerosis, where it is and to what extent. A CTCA provides much more anatomical detail and can identify advanced plaque often missed by CT Coronary Artery Calcium Score scans alone. A CT CAC scan of 0 indicates no significant amount of calcified atherosclerosis.
Share Let’s first state our goal when we are in the business of ‘Heart Disease Prevention’: To delay the onset of coronary artery disease (atherosclerosis/plaque) that might rupture and cause a heart attack. And the less plaque you have, the lower the risk of a heart attack. And it’s also WAY more common.
LDL is obviously a target against atherosclerosis. While the total body seems to do little in determining cholesterol levels, what is more scientifically shocking is slope of the curve between blood LDL levels and plaque burden is rarely linear. We must understand Fat, lipid and cholesterol are different entities. 000025% of total fat.
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