Man clutching his chest during a heart attack 400 x 276

The Wake Forest University School of Medicine is my alma mater and earlier in the week, I came upon our quarterly alumni magazine. I was at first struck by the wonderful cover photo and then chagrined as it began to dawn on me what the picture meant. You can see this warm, engaging man relating to the students at a Wake Forest basketball game and the love these young people felt for him is plainly seen in their happy expressions. The photo speaks volumes about head basketball coach Skip Prosser. It is a painfully tragic scene because the coach came in after a jog this summer and died suddenly at the age of 56. The great game was the life he lived.

Athletic Director Ron Wellman said “Prosser’s life wasn’t about championships—although he won the ACC regular-season championship in 2003—but about relationships and friends.  Skip tried to know everyone. Once you met him, you considered him a friend and he considered you a friend. On campus, he seemed to be everywhere. When he said hi, that made your day.” Somehow, looking at this haunting picture, that is believable. Events like this weigh heavily on my heart because most of them could be avoided.


Sudden death

Medical science has advanced to the point that the number of sudden deaths related to heart attack could be dramatically reduced. Leading cardiologists like Peter Libby, Erling Falk, and Steven Nissen have helped us to understand that a heart attack does not come from a fixed blockage. Myocardial infarction and cardiac sudden death almost always are the result of a ruptured vulnerable plaque. A 1995 article by Erling Falk documents that only 14% of heart attacks occur at a point in the artery where the obstruction exceeds 70%. Seventy percent of myocardial infarctions occur where the fixed obstruction is 50% or less. Since a 50% blockage seldom produces symptoms, for 70% of patients, the heart attack is the first symptom. Unfortunately, for many patients the first symptom is fatal.

In fact, the new science of arterial disease goes back nearly twenty years. The Falk article summarized findings from 4 previous studies. The summation of the data from those studies helped us understand that chronic obstruction is not the cause of a heart attack, most heart attacks occur when a newer, less obstructive plaque ruptures. The unstable plaque contains LDL cholesterol or “bad” cholesterol. That LDL cholesterol is oxidized—chemically changed—in the wall of the artery and then it is recognized as foreign by the body. The human body deals with foreign material by attacking it with white cells or pus cells. The unstable plaque is a microabscess or a tiny boil in the wall of the artery. When that boil ruptures, a toxic, inflamed gruel with the consistency of toothpaste comes in contact with the blood in the artery and sets off the clotting process. If the clot partially blocks the artery, unstable angina or an acute coronary syndrome is the result. If it totally blocks the artery, myocardial infarction is the result. The blocked artery causes death of the heart muscle downstream.

Only a few heart attacks occur as the result of severe chronic obstruction of the artery because the more obstructive plaques are much more stable. They have been present longer. The body reacts to those lesions by producing a thick cap over the cholesterol plaque and the inflammation produced by the white cells (pus) causes scar tissue formation. The inflamed cholesterol is bound up and rupture is more difficult.

This scientific understanding ties the new critical facts of arterial disease together. It explains the fact that the anticoagulant aspirin cuts the risk of heart attack by a third. It helps us understand why the clot dissolver TPA (tissue plasmin activator) aborts the heart attack process. It helps us understand why statins have power beyond cholesterol lowering in that they dramatically reduce inflammation and quickly stabilize plaque to prevent rupture. Other medications like ACE inhibitors for blood pressure and metformin for diabetes have beneficial effects on the metabolism of the arterial wall to improve arterial function and diminish plaque instability.

The highest risk patients—type 2 diabetics—have an 80% lifetime risk of heart attack or stroke. Treating pressure, glucose, and cholesterol to aggressive goals lowers the risk by roughly half for each risk factor. Dr. Steven Nissen and others have shown that aggressive lowering of the LDL cholesterol with statin therapy stabilizes the plaque and actually reverses the buildup of LDL cholesterol and pus in the wall of the artery. So, we really have a very solid understanding of how arterial disease works and the ability to produce a tremendous reduction in the risk of heart attack with medical treatment.

It is somehow ironic that one of the first two articles of the four cited in the Falk study came from Wake Forest. Dr. WC Little and his team wrote in Circulation in 1988:

Acute myocardial infarction is usually produced by the sudden total occlusion of a coronary artery by thrombus (clot), usually occurring at the site of an atherosclerotic lesion. Our study indicates that the lesion that will be the site of the thrombotic occlusion frequently is not severe when evaluated by coronary angiography weeks to years before the infarct in patients with mild-to-moderate coronary artery disease; thus, coronary angiography was not able to accurately predict the time or location of the subsequent myocardial infarction.  (my italics) In the majority (66%) of patients in this study, the myocardial infarction occurred because of the occlusion of a coronary artery that did not contain an obstructive (more than 50% diameter narrowing stenosis) on a previously performed coronary angiogram. A high-grade stenosis (more than 79% diameter narrowing) was initially present in the infarct-related artery in only one patient. Furthermore, the myocardial infarction did not occur because of occlusion of the previously patent artery with the most severe stenosis in two-thirds of the patients.”

Dr. Little and his colleagues went on to conclude:

“Because it was difficult to predict the site of the subsequent occlusion in our patients from the initial coronary angiogram, coronary bypass surgery, or angioplasty appropriately directed only at the angiographically significant lesions initially present in almost all our patients would not have been effective in preventing the majority of myocardial infarctions. This does not indicate that arteries that do not have obstructive lesions should be bypassed or dilated. Instead, effective therapy to prevent myocardial infarction may need to be directed at the entire coronary tree, not just at obstructive lesions. Such therapy to prevent myocardial infarctions might rationally include avoiding smoking, reducing serum cholesterol, administering agents that alter platelet function…

In 1988, Dr. Little was saying (New England Journal-2007) nearly 20 years ago that bypass surgery and angioplasty could not be expected to prevent heart attacks in stable patients. He predicted the results of the COURAGE trial 20 years ahead of time. That landmark trial compared optimal medical therapy with optimal medical therapy plus appropriate stenting in patients with angina, most of whom had two- and three-vessel coronary disease. There was no difference in heart attack or sudden cardiac death in the two groups after 5 years of therapy. In other words, the stent added nothing but pain relief. Additionally, in the COURAGE trial, 70% of the patients were pain-free at 5 years on medical therapy alone.

The new science of vascular disease tells us that we are doing too many catheterizations, bypasses, and stents. We are doing a miserably inadequate job of identifying high-risk patients like Skip Prosser and providing optimal management for all risk factors. We have known or should have known that for almost 20 years. Let us call it what it is—a failure of leadership. How many good men like Skip Prosser have to go down before we get this right?


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