Crystallised cholesterol role in heart attacks

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US emergency room analysis found that 89% of heart attack patients has an excessive amount of cholesterol arteries obstructing the coronary arteries.

The Michigan State University study on 240 emergency room patients shows just how much of a role a person’s cholesterol plays, when in a crystallised state, during a heart attack. George Abela, lead author and chief cardiologist at MSU, analysed the material that was obstructing the coronary arteries of patients who had suffered a heart attack and found that 89% of them had an excessive amount of these crystallised structures, referred to as cholesterol crystals.

These crystals are released from plaque that can build up in the heart and is often made up of fat, calcium and other substances as well. When this material hardens over time in the arteries, it’s known as atherosclerosis.

“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,” Abela said. “This expansion inside the wall of the artery can tear it and block blood flow causing a heart attack or stroke.”

After heart attack patients entered the emergency room, Abela and his team suctioned out this plaque. They were able to see that clusters of large crystals had formed and were able to break through the plaque and walls of the arteries and then released into the heart. This caused damage by blocking blood flow. “We now know to what great extent these crystals are contributing to a heart attack,” Abela said.

This latest research also reconfirms what Abela discovered in an earlier study that cholesterol crystals activated the production of inflammation molecules, known as Interleukin-1 beta, which aggravate, or inflame, coronary arteries. “Now that we’ve shown how extensive cholesterol crystals are irritating and blocking off these arteries, treatments that dissolve these crystals may be used to reduce heart damage,” Abela said.

Some of these treatments can include the use of statin drugs – often used to lower one’s cholesterol – aspirin and solvents such as alcohol that can be injected in low doses into a vein during a heart attack. Using these options could allow doctors to improve patient outcomes and save more lives.

A recent clinical trial using an already US Food and Drug Administration-approved antibody, known as canakinumab, has also shown to block the Interleukin-1 beta inflammation molecule and reduce the chances of a cardiac event.

“Saving heart muscle is the most important aspect of treating a heart attack,” Abela said. “So, if we are able to provide patients with better, more targeted treatments, then this could help open up and calm down the aggravated artery and protect the heart muscle from injury.”

Abela also added that by simply controlling one’s cholesterol by eating a healthy diet, exercising and taking statin medications as needed, could be the best way to prevent these crystals from forming.

Abstract
Cholesterol crystals (CCs) have been associated with plaque rupture via mechanical injury and inflammation. This study evaluated the presence of CCs during acute myocardial infarction (AMI) and associated myocardial injury, inflammation, and arterial blood flow before and after percutaneous coronary intervention (PCI). Patients presenting with AMI (n=286) had aspiration of culprit coronary artery obstruction. Aspirates were evaluated for crystal content, size, composition and morphology by scanning electron microscopy, crystallography and infrared spectroscopy. These were correlated with inflammatory biomarkers, cardiac enzymes, % coronary stenosis, and Thrombolysis in Myocardial Infarction (TIMI) blush and flow grades. Crystals were detected in 254 patients (89%) and confirmed to be cholesterol by spectroscopy. Of 286 patients 240 (84%) had CCs compacted into clusters that were large enough to be measured and analyzed. Moderate to extensive CC content was present in 172 cases (60%). Totally occluded arteries had significantly larger CC clusters than partially occluded arteries (p<0.05). Patients with CC cluster area >12,000 µm2 had significantly elevated IL-1β levels (p<0.01), were less likely to have TIMI blush grade of 3 (p<0.01) and more likely to have TIMI flow grade of 1 (p<0.01). Patients with recurrent AMI had smaller CC cluster area (p<0.04), lower troponin (p<0.02) and interleukin-1 beta (IL-1β) levels (p<0.04). Women had smaller CC clusters (p<0.04). Macrophages in the aspirates were found to be attached to CCs. Coronary artery aspirates had extensive deposits of CCs during AMI. In conclusion, presence of large CC clusters was associated with increased inflammation (IL-1β), increased arterial narrowing and diminished reflow following PCI.

Authors
George S Abela, Jagadeesh K Kalavakunta, Abed Janoudi, Dale Leffler, Gaurav Dhar, Negar Salehi, Joel Cohn, Ibrahim Shah, Milind Karve, Pavan Kotaru, Vishal Gupta, Shukri David, Keerthy Narisetty, Michael Rich, Abigail Vanderberg, Dorothy R.Pathak, Fadi Shamoun

Michigan State University material
American Journal of Cardiology abstract


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