34
SIR,-According to Professor Kaplan (May 26, p. 1140) the "flaws" in my paper (April 21, p. 861) are "so many and so serious as to negate its entire validity". By publishing it, he maintains, The Lancet has given countenance to a concept that could threaten the "effective treatment of hypertension". What do his six charges amount to? (1) He starts by saying that 80 mm Hg diastolic pressure in the U.K. is equivalent to about 70 in the U.S. and that I should have pointed out this difference. But surely most readers of The Lancet know of the American preference for the fifth phase and can make the necessary adjustments for themselves. Incidentally, it is the intra-arterial diastolic pressure that presents at levels some 7-10 mm Hg lower than that at which the fourth phase is recognised at the moment of auscultatory muffling;’ after exclusion of the break-away sounds the stethoscopic gap between the two phases seldom reaches 5 mm Hg. Below 90 mm Hg in the U.K. becomes roughly the same as below 85 mm Hg in the U.S.A., and 100-109 becomes 95-104. Thus the relative risk of infarction that I found after pressure reduction into the lower of these two pressure ranges remains more than five-fold greater than after reduction into the higher range whichever Korotkoff sound is taken as the common standard for measurement. (2) Kaplan next criticises the selection, matching, and control of patients and asks for the criteria for inclusion or exclusion from the study. In my paper I devoted twenty-eight lines to this point. Watching of controls for risk factors was done by a secretary in a way designed to ensure that she could not know the corresponding final diastolic pressures. (3) He asks how patients who "dropped out" came to be "included in a paper purporting to show damage from therapy" apparently having failed to notice that among the 13 patients who ultimately became non-attenders, all identified and included, 6 were dead, 5 of them having had a myocardial infarction. (4) "Much of the final data", Kaplan claims, depend upon "expected" pressure values. The relative-risk comparisons in all the 169 patients, and in the 102 patients with stable control, were derived solely from observed final diastolic pressure recordings. "Expected" changes were considered separately. (5) Kaplan dismisses, without explanation, some well-known studies that have raised doubts about the general assumption that hypertension is a potent cause of coronary atheroma. (6) He accuses me of neglecting data, including the Frammaterial. Yet I specifically refer to the rising parallel between hypertension and the clinical manifestations of coronary heart-disease that is shown in the Framingham studies. What I dispute is that this should be taken as proof that sustained high blood-pressure plays an important role in coronary atherogenesis. The inference is ill-founded. Rising pressure tends to precipitate angina and myocardial infarction in patients with pre-existing coronary atheroma whatever its origins. I emphasised the fact that, despite modest induced pressure falls in many of my patients, cardiovascular complications apart from infarction "did not exceed the incidence expected during treatment". Kaplan says nothing of this, yet he sees my paper as a threat to the "effective, sensible therapy of hypertension". I agree with Professor Boyd (June 2, p. 1197) that a pressure fall to 80 mm Hg probably does not often precipitate infarction. But the clinical reduction of blood-pressure, fo many diverse reasons, is an imprecise and unpredictable exer cise. My findings suggest that, even when aimed at levels wel above 80 mm Hg, treatment may still occasionally overshoo the mark to a degree that threatens critical myocardial isch2e mia, perhaps with infarction and sudden death. The polic should be one of reduction, not to "normality" but into a
"optimum" ual,
range, calculated as far as possible for the individlikely to be considerably higher than "nor-
level that is
mal".
ingham
1. Kirkendall WM, Burton AC, Epstein FH, Freis ED. Recommendations for human blood pressure determination by sphygmomanometers Circulation
1967; 36: 980-988.
a
Department of Medicine, Victoria Hospital, Blackpool FY3 8NR
I. MCD. G. STEWART
HIGH-DENSITY LIPOPROTEIN MAY NOT BE ANTIATHEROGENIC AFTER ALL
SIR,-Since the re-establishment of the inverse correlation between plasma high-density lipoprotein (HDL) concentrations and coronary heart-disease (CHD)’ an enormous effort has been made to clarify the protecting mechanism as well as the basis for the regulation of plasma-HDL levels. The evidence for an inverse relation between plasma-HDL-cholesterol (HDL-chol) and coronary atherosclerosis and its clinical complications has recently been reviewed. The protecting effect of HDL from CHD has been reported to be independent of the levels of other plasma lipoproteins.z-5 However, in the Tromse
study
and in the
Cooperative Lipoprotein Phenotyping study
HDL-cholesterol, cholesterol in d
SIR,-According to Professor Kaplan (May 26, p. 1140) the "flaws" in my paper (April 21, p. 861) are "so many and so serious as to negate its entire validity". By publishing it, he maintains, The Lancet has given countenance to a concept that could threaten the "effective treatment of hypertension". What do his six charges amount to? (1) He starts by saying that 80 mm Hg diastolic pressure in the U.K. is equivalent to about 70 in the U.S. and that I should have pointed out this difference. But surely most readers of The Lancet know of the American preference for the fifth phase and can make the necessary adjustments for themselves. Incidentally, it is the intra-arterial diastolic pressure that presents at levels some 7-10 mm Hg lower than that at which the fourth phase is recognised at the moment of auscultatory muffling;’ after exclusion of the break-away sounds the stethoscopic gap between the two phases seldom reaches 5 mm Hg. Below 90 mm Hg in the U.K. becomes roughly the same as below 85 mm Hg in the U.S.A., and 100-109 becomes 95-104. Thus the relative risk of infarction that I found after pressure reduction into the lower of these two pressure ranges remains more than five-fold greater than after reduction into the higher range whichever Korotkoff sound is taken as the common standard for measurement. (2) Kaplan next criticises the selection, matching, and control of patients and asks for the criteria for inclusion or exclusion from the study. In my paper I devoted twenty-eight lines to this point. Watching of controls for risk factors was done by a secretary in a way designed to ensure that she could not know the corresponding final diastolic pressures. (3) He asks how patients who "dropped out" came to be "included in a paper purporting to show damage from therapy" apparently having failed to notice that among the 13 patients who ultimately became non-attenders, all identified and included, 6 were dead, 5 of them having had a myocardial infarction. (4) "Much of the final data", Kaplan claims, depend upon "expected" pressure values. The relative-risk comparisons in all the 169 patients, and in the 102 patients with stable control, were derived solely from observed final diastolic pressure recordings. "Expected" changes were considered separately. (5) Kaplan dismisses, without explanation, some well-known studies that have raised doubts about the general assumption that hypertension is a potent cause of coronary atheroma. (6) He accuses me of neglecting data, including the Frammaterial. Yet I specifically refer to the rising parallel between hypertension and the clinical manifestations of coronary heart-disease that is shown in the Framingham studies. What I dispute is that this should be taken as proof that sustained high blood-pressure plays an important role in coronary atherogenesis. The inference is ill-founded. Rising pressure tends to precipitate angina and myocardial infarction in patients with pre-existing coronary atheroma whatever its origins. I emphasised the fact that, despite modest induced pressure falls in many of my patients, cardiovascular complications apart from infarction "did not exceed the incidence expected during treatment". Kaplan says nothing of this, yet he sees my paper as a threat to the "effective, sensible therapy of hypertension". I agree with Professor Boyd (June 2, p. 1197) that a pressure fall to 80 mm Hg probably does not often precipitate infarction. But the clinical reduction of blood-pressure, fo many diverse reasons, is an imprecise and unpredictable exer cise. My findings suggest that, even when aimed at levels wel above 80 mm Hg, treatment may still occasionally overshoo the mark to a degree that threatens critical myocardial isch2e mia, perhaps with infarction and sudden death. The polic should be one of reduction, not to "normality" but into a
"optimum" ual,
range, calculated as far as possible for the individlikely to be considerably higher than "nor-
level that is
mal".
ingham
1. Kirkendall WM, Burton AC, Epstein FH, Freis ED. Recommendations for human blood pressure determination by sphygmomanometers Circulation
1967; 36: 980-988.
a
Department of Medicine, Victoria Hospital, Blackpool FY3 8NR
I. MCD. G. STEWART
HIGH-DENSITY LIPOPROTEIN MAY NOT BE ANTIATHEROGENIC AFTER ALL
SIR,-Since the re-establishment of the inverse correlation between plasma high-density lipoprotein (HDL) concentrations and coronary heart-disease (CHD)’ an enormous effort has been made to clarify the protecting mechanism as well as the basis for the regulation of plasma-HDL levels. The evidence for an inverse relation between plasma-HDL-cholesterol (HDL-chol) and coronary atherosclerosis and its clinical complications has recently been reviewed. The protecting effect of HDL from CHD has been reported to be independent of the levels of other plasma lipoproteins.z-5 However, in the Tromse
study
and in the
Cooperative Lipoprotein Phenotyping study
HDL-cholesterol, cholesterol in d
