The Lethal Abscess

By far the most common form of heart attack is an occlusion (shutdown) caused by a thrombosis (clot formation) in one of the coronary arteries, which supply blood to the heart's own muscular walls. Physicians have long known that the dangerous clots usually form where a coronary artery is narrowed by a scaly deposit, or "plaque," of chalky, fatty material. But for all its importance, a nagging question has remained unanswered: How does the fatal clot really form?

This week, in the American Journal of Pathology, two San Francisco doctors offer an unexpected reply: the clot forms as the result of a reaction between arterial blood and material from a diseased part of the artery's walls. Along with the scaly deposit, it makes a plug that blocks blood flow.

Three-Ply Wall. Since it is impossible to observe such a process in living man, the investigators had to reconstruct their evidence from the dead. Cardiologist Meyer Friedman and Dutch-born Physiologist G. J. Van den Bovenkamp of the Harold Brunn Institute at Mount Zion Medical Center persuaded pathologists in hospitals near San Francisco to send them the occluded segment of coronary artery from each heart-attack victim on whom they had performed an autopsy. The two researchers sliced the coronary specimens crosswise, and after examining countless paper-thin specimens under the microscope, worked out the sequence of a typical coronary occlusion.

The process begins, they report, with the laying down of the familiar chalky and fatty material, largely cholesterol, inside the artery (see diagram). Then, by processes not yet understood, an "abscess" forms either within the artery's innermost layer (intima) or between the intima and the middle layer (media) of the three-ply artery wall. But this is no ordinary abscess, filled with pus. It is a special, possibly unique type, containing the debris of broken-down cells from the blood and the artery walls, a fatty paste, crystals of cholesterol, and calcium.

The abscesses, the doctors found, varied greatly in size, but as they grew their diseased walls became thinner and weaker. In 39 of the 40 cases studied, the abscess eventually burst. Its contents spilled into the blood flowing through the artery, and some blood flowed back into the abscess cavity.

Sudden Death. In at least 26 cases, the abscess burst outward, into the artery, and in ten the blood burst into the abscess. Either way, the result was the same. Blood mixed with material from inside the abscess to produce a clot that filled the artery cavity too tightly to be pushed along, thus blocking the arterial flow.* That part of the heart muscle beyond the plug, deprived of nourishing blood and oxygen, lost its elastic muscularity, disrupted the heart's delicate electrical-conduction system, and eventually stopped working. In some cases the victims of these occlusions were dead even before their blood-starved heart muscle had time to do any damage. Eleven succumbed instantly or within a few minutes; ten others died within a week.

*In other forms of blood-vessel disease, clots form elsewhere in the body (especially in the legs) and are carried along in the blood flow until they are stopped at a narrow place. This process is called thromboembolism.

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