Relentlessly progressive


Heart disease is the biggest killer. Cardiovascular disease means heart attacks, strokes and sudden death. We refer to these as "events." CV disease is responsible for 30% of deaths globally (1) and 33% of deaths in America every year (2). Of first events, at least 30% are sudden death (3).. Recurrent events are fatal 40-50% of the time (2,4).

Every hour 17 Americans younger than 65 die from CV disease (2).

How artery disease develops:

As time goes on (moving from left to right in the illustration below), artery disease slowly and steadily gets worse. Artery disease is caused by risk factors, which stir up the disease until the inflammation ("plaque") becomes vulnerable and dangerous. This soft gooey cholesterol-rich plaque is dangerous because it has a thin cap, which makes it vulnerable to rupture. Once the plaque ruptures, what happens next is similar to what happens when you get a laceration (because the lining on the inside of the arteries, which normally protects the blood from the tissues, is now lacerated). When the blood "sees" the tissues, those blood mechanisms for clotting kick into high gear! A thrombus (or clot) forms, which floats downstream, causing a stroke or mini-stroke. Or it stays and grows into a myocardial infarction


Why are heart attacks so unpredictable?

People who have chest pain when they exercise need a stress test to diagnose obstructive blockage (see above, far right) which needs a surgical procedure like by-pass or stent. But that's not where most heart attacks strike.

Most heart attacks shut off the blood flow suddenly and without warning. When vulnerable plaque ruptures, and a thrombus forms, the entire artery can be blocked off within moments (see Myocardial Infarction above). You would think that most heart attacks occur where plaque causes severe obstruction. Not true. Less than 20% of heart attacks do. Over 80% of heart attacks occur in "vulnerable" plaque where the blood flow was fine just moments before the heart attack (4,5). Almost everyone knows someone who has dropped dead from this disease.

Soft vulnerable plaque causing no obstruction to blood flow is so much more common than obstructive plaque needing a stent. Yet a stress test is designed to show only the obstructive blockages. That's why this disease has been so unpredictable. Until now.

Early detection:

We can determine who is at risk and how much risk they carry by testing arteries and genes. We call it screening: looking for evidence of early disease in people who have no symptoms. Such screening has been controversial in the cardiology community. Why? Patrick Forbes, the Director of Documentary Films at the BBC, explores that question in his riveting film, The Widowmaker

Executive physical examinations often give a false sense of security to high-risk patients, as do risk calculators and stress tests

cholesterol can be normal:

Half of heart attack victims have a normal cholesterol (6).


  1. World Health Organization
  2. National Vital Statistics Reports, 61:4 May 8, 2013 Data is available at the National Center for Health Statistics website:
  3. Roger VL, et al. Heart disease and stroke statistics-2012 update: a report from the American Heart Association. Circulation. 2012;125(1):e2-220.
  4. Little WC, Constantinescu M, Applegate RJ, Kutcher MA, Burrows MT, Kahl FR, Santamore WP. Can coronary angiography predict the site of a subsequent myocardial infarction in patients with mild-to-moderate coronary artery disease? Circulation. 1988;78:1157-1166
  5. Symptoms are treated with procedures like stents and bypass surgery when the degree of stenosis or obstruction is 70% or more. Yet 86% of heart attacks are caused by plaque lesions which are < 70% obstructed, and 68% of heart attacks are caused by lesions which cause a stenosis < 50%. E. Falk, PK Shah, V Fuster, Coronary Plaque Disruption, Circulation 1995;92:657
  6. Sachdeva et al. Lipid levels in patients hospitalized with coronary artery disease: an analysis of 136,905 hospitalizations in Get With The Guidelines. Am Heart Journal. 2009;157(1):111-117.e2.