The case for exercise

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IPII~RS

have been observed between isolated heart preparations and clinical studies. In the isolated heart, an inotropic stimulation increases the slope of the end-systolic pressure-dimension relation, with negligible change in volume intercept, 3 whereas in humarls a significant change in intercept is found. 4 Because of these differences, the influence of the parietal pericardium and of the right ventricle on LV stress-volume relation during ejection might be worth investigating.

H. Pouleur, MD M. F. Rousseau, MD C. van Eyll, MSEE Brussels, Belgium

1. Colan SD, Borow KM, Gamble WJ, Sanders SP. Effects of enhanced aflerload (methoxamlna) and contractile state (dobutamine) on the left ventrlcular late-systolic wall stress-dimension relation. Am J Cardlol 1983; 52:1304-1309. 2. Pouleur H, Roe~eau MF, van Eyll C, Van Mechekm H, Bras~mr I.A, Chadlar ~ Assessmentof left venfrlcular contractility from late systolic stress-volume relations. Circulation 1982;65:1204-1212. 3. Suga H, Sagawa K, Shouku JUt. Load independence of the instantaneouspressure-volumeratio of the canine left ventricle and effects of epinephrine and heart rate on the ratio. Circ Res 1973;32:314-322. 4. Borow KM, Neumann A, Wynne J. Sensitivity of endsystolic pressure-dimension and pressure-volame relations to the inotropic state in humans. Circulation 1982;65:988-997.

R E P L Y : W e appreciate the additional comments by Pouleur, Rousseau and van Eyll concerning our study. W e are in agreement with their observations and do not feelthat we have anything further to add. Steven D. Colan, MD Boston, Massachusetts THE CASE FOR EXERCISE

I read with interest "The Case for Exercise" by Dr. George Sheehan in the January 1984 issue of the Journal. I believe that he is somewhat evading the issue of discussing data regarding exercise in medical practice today. Though not as scientifically well studied as we would like, there are certainly definite published data to support that exercise is beneficial in both primary and secondary management of coronary artery disease. "Evidence in American and European studies and in epidemiologic surveys is convincing. It is time for us to be more scientific about the role of exercise in the practice of medicine today rather than candidly saying that it "improves the quality and quantity of life," causes "renewed self-esteem" and lowers "negative emotions." Exercise capacity in medical practice is determined by a physician-supervised exercise test and administered by means of prescriptive exercise programs. Exercise is a science and widely used both in basic and clinical research particularly in the specialty of cardiovascular medicine. We therefore need to treat exercise with the scientific respect it deserves. Gerald F. Fletcher, MD Atlanta, Georgia

REPLY: I agree with Fletcher that exercise should be treated with scientific respect. What I propose is that we take the fully re-

searched and proved physiologic effects of exercise and use them in practice. That is the "quantity" I write of--increased physical work capacity and improved maximal oxygen uptake. I too dislike the word "quality." It is much too soft, but psychological studies do show favorable changes in specific qualities needed for the good life--vigor, coping, creativity and self-esteem. I believe we should not be mired down in this unending debate over the effect of exercise on pathology. Fletcher feels the evidence is there, and many equally knowledgable observers think not. As a result, practitioners are immobilized and still awaiting direction. What I claimed for exercise can be proved--things that are "as scientifically well-studied as we would like." Both Fletcher and I are in the same camp. We both want patients to exercise, but our tactics are different. My years in the field have convinced me that the best case for exercise is the one for fitness. This whole exercise phenomenon arose, not from health care specialists, but the people themselves; for those reasons I recommend the quantity and quality of life they receive from the hours spent in motion. George Sheehan, MD Red Bank, New Jersey

U S E F U L N E S S OF EXERCISE

Every age has itsgreat myths--emotionally appealing ideas,sustained in the public mind without supporting evidence. T w o of ours currently are (1) that coronary heart disease is caused by "stress" (typically defined as the daily occupation of the person afflicted), and (2) that exercise is both preventive and therapeutic. Exercise prevention (or deceleration) of coronary atherosclerosis is based, so far at least, on equal parts wishful thinking and anecdotal "evidence" that would embarrass a 1950s Anacin commercial. Worse, our current enthusiasm for postinfarction rehabilitation has convinced much of the public that exercise is uniformly beneficial in this setting--a concept equally devoid of experimental justification, an~! carrying the potential for real harm to some patients. Sheehan ("The Case for Exercise") deserves our thanks for a clear-headed restatement of the benefits of exercise, refreshingly free of myth entanglement. He lucidly describes the real value of conditioning to persons, sick or well, who possess both the coronary anatomy and the self-discipline to safely pursue physical fitness. A copy of his article should be required reading for patients who have been deluded by the current hysteria into thinking that they are depriving themselves of life, liberty and the pursuit of happiness by not exercising systematically. We should keep in mind that exercise, like virtue, is pretty much its own reward--and a sizeable one at that. We do not have to kid ourselves or our patients that it will make us live longer, in order to justify it. Even if it did, we might remember Shaw's aphorism: "Do not try to live forever--you will not succeed." John V. Russo, MD Washington, DC

T R E N D S IN C O R O N A R Y H E A R T DISE A S E Roberts, 1 in a recent editorial, pointed out the

numerous benefits that may result from regular exercise in the form of running. He also provided a portrait of Sheehan, whose philosophy and practical advice on exercise have been of interest and assistance for many years. Although in full agreement with Roberts' viewpoint, I wish to correct him on 1 matter. He stated, "The death rate from coronary heart disease is decreasing in the U.S., and the U.S. is the only country in the Western world where this is so." In fact, similar trends have been observed in New Zealand and Australia, 2-4 which are generally classified as Western countries. It is important to note this, for only by long-term monitoring on an international basis as proposed by the World Health Organization s will a full understanding of these trends emerge. D. Norman Sharpe, MD Auckland, New Zealand 1. Roberts WR. An agent with lipid-lowering, antihypartenslve, positive laotroplc, negative chronotroplc, vasodilating, diuretic, anorexlgenic, weight.reducing, cathartic, hypoglycamlc, tranquilizing, hypnotic and antldepressive qualities. Am J Cardlol 1984;53:261262. 2. Beaglehole R, Hay DR, Foster FH, Sharpe DN. Trends In coronary heart disease mortality and associated risk factors in New Zealand. NZ Med J 1981;93:371-375. 3. Beaglahole R, Bonita R, Jacksofl R, Stewart A, Sharpe DN, Fraser GE. Trends in coronary heart disease event rates in New Zealand. Am J Epidemlol. In press. 4. Plna Z, Uemara K. Trends of mortality from ischeemlc heart disease and other cardlavascular diseases in 27 countries, 1968-77. World Health Stat Q 1982;35: 11-45. 6. World Hea]~ Organization. Proposal for multinational monitoring o! ~rendsand detarmlnants in cardiovascular disease and protocol (MONICA Project). Geneva 1983. WHO Document WHO/MNC/82.1 Rev 1.

M Y O C A R D I A L UPTAKE OF TECHNETIUM-99m P Y R O P H O S P H A T E IN SYSTEMIC AMYLO I D O S I S

In response to Leinonen's report (Am J Cardial 1984;53:380-381), certain points must be emphasized about technetium-99m pyrephosphate scanning in amyloid cardiomyapathy. First, the positivity of the scan will be related to the mass of amyloid in the myocardial tissues and its calcium content. The echocardiographic findings of granularity of myocardium reflects the presence of amyloid but does not reflect its magnitude. It would have been better if they had supplied echocardiographic evidence quantitating the extent of replacement. Second, it is unconvincing that the demonstration of amyloid material in a distant organ (i.e., rectum or kidney) will reflect the degree of involvement of the heart. To confirm heavy amyloid deposition, myocardial biopsy should have been performed. Third, they failed to comment on why AA protein does not bind to technetium-99m pyrophosphate. As biopsy material was available, it would have been interesting to look at the calcium content of the AA protein. Theoretically, it would be much lower than ASc and AL amyloid proteins, which bind avidly to technetium-99m pyrephosphate. Because of this, it is not reason-