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Atherosclerosis and stroke.

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Atherosclerosis and Stroke
William C. Taylor, MD,” and William M. Landau, MDT
In their review of atherosclerosis in relation to stroke, Yatsu
and Fisher say, “The role of reduction in blood cholesterol
levels. . . cannot be minimized” 111. W e believe that the data
support the opposite conclusion.
Major studies demonstrate the failure of blood cholesterol
levels to predict the risk of stroke. In the Framingham Study
no significant relation between blood cholesterol level and
risk of stroke has generally been seen, although an inverse
relation between cholesterol and risk of stroke was found in
some groups [2, 31. Although a recent report about men
screened for the Multiple Risk Factor Intervention Trial
found an increase in the rate of death from nonhemorrhagic
stroke in middle-aged American men with elevated blood
cholesterol levels, this finding was counterbalanced by an
inverse relation between the blood cholesterol level and the
risk of hemorrhagic stroke [4}.Similarly, prospective studies
of Japanese and Japanese-American men also found an inverse relation between cholesterol and intracerebral hemorrhage; these studies failed to show any significant association
between cholesterol levels and risk of cerebral infarction
15, 61.
Intervention trials designed to observe the effect of lowering cholesterol on the development of coronary heart disease
among middle-aged men have shown no reduction in the
rate at which stroke occurred; if anything, a few more strokes
seemed to occur in the men treated with cholesterollowering regimens {7-91.
The suggestion that lowering blood cholesterol levels will
reduce the rate at which strokes occur is not supported by
the available evidence.
“Dioision of General Medicine and Primavy Care
Beth Israel Hospital
Harvard Medical School
Boston, M A
+Departmentof Nearology
Washington University School of Medicine
St LouiJ. MO
Yatsu FM, Fisher M. Atherosclerosis: current concepts on
pathogenesis and interventional therapies. Ann Neurol 1989;
Gordon T, Kannel WB, Castelli WP, Dawber TR. Lipoproteins,
cardiovascular disease, and death: The Framingham Study. Arch
Intern Med 1981;141:1128-1131
Cupples LA, VAgostino RB. Some risk factors related to the
annual incidence of cardiovascular disease and death using pooled
repeated biennial measurements: Framingham Heart Study, 30year followup. In: Kannei WB, Woif PA, Garrison, eds. The
Framingham Study: an epidemiological investigation of cardiovascular disease: Section 34. Washington DC: U.S. Department of
Health and Human Services, 1987 (NIH Publication no. 872703)
Is0 H, Jacobs DR Jr, Wentworth D, et al. Serum cholesterol
levels and six-year mortahty from stroke in 350,977 men
screened for the Multiple Risk Factor Intervention Trial. N Engl
J Med 1989;320:904-910
5. Tanaka H, Ueda Y, Hayashi M, et al. Risk factors for cerebral
hemorrhage and cerebral infarction in a Japanese rural community. Stroke 1980;11:14-21
6. Kagan A, Popper JS, Rhoads GG. Factors related to stroke incidence in Hawaii Japanese men. The Honolulu Heart Study.
Stroke 1980;11:14-2 1
7 . Oliver MF, Heady JA, Morris JN, Cooper J. A cooperative trial
in the primary prevention of ischaemic heart disease using
clofibrate. Report from the Committee of Principal Investigators.
Br Heart J 1978;40:1069-1118
8. Lipid Research Clinics Program. Lipid Research Clinics Coronary
Primary Prevention Trial. I. Reduction in incidence of coronary
heart disease. JAMA 1984;251:351-364
9. Frick MH, Elo 0,Haapa K, et al. Helsinlu Heart Study: Primaryprevention trial with gemfibrozil in middle-aged men with dyslipidemia. N Engl J Met1 1987;317:1237-1245
Frank M. Yatsu, MD,* Kasturi Ranganna, PhD,”
Rita Alam, PhD,* Juergen Kraus,“
Thomas DeGraba, MD,* and Marc Fisher, MDf
Debate over reducing serum cholesterol to prevent coronary
heart disease (CHD) rages in the scientific literature and lay
press {l-33. Despite polarization of opinions, a developing
conventional wisdom favors cholesterol reduction. Momentum for this view was enhanced by the Lipid Research
Primary Prevention Trial in the United
States, the Helsinki Heart Study from Finland, the Consensus Report on Cholesterol from the National Institutes of
Health, and the National Cholesterol Education Program
14-71, In our review on atherothrombotic brain infarction
(ABI), we reasoned that arguments for cholesterol lowering
can be extended to ABI as another clinical expression of
the same pathological processes as C H D 181. In their rebuttal, Landau and Taylor recapitulate arguments used against
cholesterol-lowering for C H D and also point out absence of
similar prospective studies for ABIs. Since the latter investigations remain to unfold, we take issue with the seemingly
nihilistic position that attacks the exercise of reasoned clinical
judgment. Just as the heuristic views on economics by the
Nobel Prize winner Herbert Simon served to explain decision-making from incomplete data, clinical judgments must
be similarly fashioned.
The uncertainty does, however, serve to emphasize the
need for more extensive investigations into ABI pathophysiology to identify more precisely stroke-prone individuals.
An example is our finding of an elevated low density lipoprotein (LDL) to high density lipoprotein (HDL) ratio in “malignant” carotid stenoses [9]. To explore these clues we are
undertaking the following: cloning the HDL receptor,
amplification of which should lead to effective HDL manipulation; analyzing in vivo HDL and LDL metabolism (synthesis and fractional catabolic rates) and the likely tole of teceptors in regulating activity [101; and investigating gene
polymorphism for apoprotein A1 (apo AI), the major protein of HDL, particularly with restriction enzymes PstI and
SacI, for usefulness in identifying individuals at risk for ABI.
These molecular biological thrusts into ABIs are exciting for
their promise, but current needs for ABI-risk intervention
demand practical guidelines. At present, this approach requires that we get to the heart of the matter, both literally
108 Copyright 0 1990 by the American Neurological Association
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