Cholesterol Crystals Suggest Looming Heart Attack
By HospiMedica International staff writers Posted on 28 Aug 2017 |
Image: Cholesterol crystals arising from within the artery wall, causing tearing and damage (Photo courtesy of MSU).
Cholesterol crystals that pierce the arterial plaque and intima trigger local and systemic inflammation that can lead to a myocardial infarction (MI), according to a new study.
Researchers at Michigan State University (MSU; East Lansing, USA) conducted a study involving 240 emergency room patients who died of MI in order to examine the role of cholesterol in the crystallized state on atherosclerosis and plaque rupture, and its contribution to acute MI and stroke. To visualize the cholesterol crystals, the researchers processed the tissue without ethanol. They found that cholesterol expands when crystallizing from the liquid to the solid state, which is the presumed cause of plaque rupture by the sharp-tipped crystals growing out of the plaque’s necrotic core.
The researchers found that in patients who died of MI, culprit coronary lesions had extensive cholesterol crystals perforating the fibrous cap and intima, while atherosclerotic patients who died of other causes did not have such perforating crystals. They also found that cholesterol crystals traveling downstream from the plaque rupture site can scrape the endothelium and promote vasospasm, and that cholesterol crystals lodging into the muscle can trigger an inflammation with necrosis, independent of circulatory compromise or ischemia. The study was published on May 1, 2017, in Cardiovascular Innovations and Applications.
“In previous studies, we showed that when cholesterol goes from a liquid to a solid, or crystal state, it expands in volume like ice and water. This expansion inside the wall of the artery can tear it and block blood flow causing a heart attack or stroke,” said senior author George Abela, MD, chief cardiologist at MSU. “Since cholesterol crystals form very early in the process of heart disease, with great potential to aggravate atherosclerosis, we can target new therapies by reducing cholesterol crystal deposits early on or use an inhibitor to block the inflammatory biomarker.”
Cholesterol is a modified steroid in the form of a lipid molecule, biosynthesized by all animal cells, and is an essential structural component comprising up to 30% of all cell membranes. Cholesterol also serves as a precursor for the biosynthesis of steroid hormones, bile acid, and vitamin D.
Related Links:
Michigan State University
Researchers at Michigan State University (MSU; East Lansing, USA) conducted a study involving 240 emergency room patients who died of MI in order to examine the role of cholesterol in the crystallized state on atherosclerosis and plaque rupture, and its contribution to acute MI and stroke. To visualize the cholesterol crystals, the researchers processed the tissue without ethanol. They found that cholesterol expands when crystallizing from the liquid to the solid state, which is the presumed cause of plaque rupture by the sharp-tipped crystals growing out of the plaque’s necrotic core.
The researchers found that in patients who died of MI, culprit coronary lesions had extensive cholesterol crystals perforating the fibrous cap and intima, while atherosclerotic patients who died of other causes did not have such perforating crystals. They also found that cholesterol crystals traveling downstream from the plaque rupture site can scrape the endothelium and promote vasospasm, and that cholesterol crystals lodging into the muscle can trigger an inflammation with necrosis, independent of circulatory compromise or ischemia. The study was published on May 1, 2017, in Cardiovascular Innovations and Applications.
“In previous studies, we showed that when cholesterol goes from a liquid to a solid, or crystal state, it expands in volume like ice and water. This expansion inside the wall of the artery can tear it and block blood flow causing a heart attack or stroke,” said senior author George Abela, MD, chief cardiologist at MSU. “Since cholesterol crystals form very early in the process of heart disease, with great potential to aggravate atherosclerosis, we can target new therapies by reducing cholesterol crystal deposits early on or use an inhibitor to block the inflammatory biomarker.”
Cholesterol is a modified steroid in the form of a lipid molecule, biosynthesized by all animal cells, and is an essential structural component comprising up to 30% of all cell membranes. Cholesterol also serves as a precursor for the biosynthesis of steroid hormones, bile acid, and vitamin D.
Related Links:
Michigan State University
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