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By taking blood samples from volunteers at regular intervals and analyzing their lipoproteins, Dr. Gofman is now convinced that he has enough experience to forecast whether a given individual will suffer from atherosclerosis. (Other researchers are not sure that he is right. Three laboratories—at Harvard, the University of Pittsburgh and the Cleveland Clinic—have been running experiments to prove or disprove the Gofman thesis.) Still to be explored is the possibility that a more fundamental mechanism is involved: a defect in body chemistry—the way in which an individual metabolizes either fats or proteins.
The Question of Filtration. Then there is a little-known aspect of human circulation on which Dr. Page and others have been working. It may go far to solve the riddle of how atherosclerosis begins. In addition to the direct blood flow down the bore of the arteries to its destination in the capillaries, parts of it also perfuse through the arterial walls. Thus they reach many of the body's tissues and supply them with nourishing chemicals.
The "filtration concept" of atherosclerosis is that as the blood fraction passes into the artery walls it may break down some of the less stable combinations containing cholesterol. These are most likely to be the beta-lipoproteins, containing the big, flabby cholesterol molecules. If something removes the protein coating, which makes it possible for the combination to circulate in the blood as though in solution, then the insoluble fatty cholesterol molecule is left in the artery wall. If this happens often enough, the artery wall will thicken, roughen and begin to break down.
The Old & the Young. When a coronary branch has been narrowed sufficiently to slow the blood to a virtual standstill, a thrombus (clot) will form and block the flow altogether. However, only a minority of heart attacks are fatal, and many are not even detected during the victim's lifetime. Why the difference between a dramatic thrombosis as in the case of President Eisenhower and the individual who sleeps through his heart attack? The answer lies in the gradualness of the process that narrows the coronary artery concerned. If it constricts slowly for months, the heart brings into play its self-repair system and develops collateral circulation, i.e., nearby branches enlarge to carry more blood to neighboring parts of the heart muscle. Thus when the final shutdown comes, its original blood flow has already been diverted. In cases like the President's, the collateral circulation has to develop after the attack.
Equally striking is the contrast between the resiliency of many older men after a heart attack and the way in which younger men may succumb. A noted example last week was Cinemactor John Hodiak, 41, who seemed in excellent health—he had just passed an insurance examination—but had a quickly fatal attack while shaving. There are undoubtedly many cases in which a younger man will be killed simply because his disease is new while an older man with slowly developing disease will already have compensated, through collateral circulation, for a shutdown in an artery of the same size.