Correspondence
Secular Trends in Coronary Atherosclerosis
N Engl J Med 1997; 336:224-226January 16, 1997
- Article
To the Editor:
Enriquez-Sarano et al. (Aug. 1 issue)1 observed no change in angiographic measures of coronary atherosclerosis in 601 patients with isolated nonischemic valvular regurgitation, both mitral (n = 385) and aortic (n = 216), between 1980 and 1989. They acknowledge the limitations of the study, particularly with respect to the generalization of results to the general population.
The point of interest and perhaps concern is that both patients with aortic regurgitation and those with mitral regurgitation were included in the study. The hemodynamics of coronary blood flow in these two conditions are clearly different. In aortic regurgitation large-caliber coronary arteries are often observed and result from both neurohumoral and mechanical factors.2 According to the principle of Glagov et al., vascular enlargement occurs early in the atherosclerotic process, so that atheroma may be present but not recognizable angiographically.3 Therefore, in patients with aortic regurgitation, atherosclerosis may not be detectable angiographically until a greater plaque burden is present than in those with mitral regurgitation or no valvular lesion. In our opinion it would therefore be relevant to determine whether the prevalence of angiographically detectable coronary disease was similar in the two groups and whether the proportion remained constant over the study period. In addition, we believe that the validity of generalizing prevalence data, with respect to the presence of coronary disease in asymptomatic patients, from those with aortic regurgitation (36 percent of the study population) to the general population is dubious.
3 ReferencesPeter Ruygrok, M.B., Ch.B.
Green Lane Hospital, Auckland 3, New ZealandVictor Umans, M.D., Ph.D.
Alkmaar Medical Center, 1815 JD Alkmaar, the Netherlands1
Enriquez-Sarano M ,Klodas E ,Garratt KN ,Bailey KR ,Tajik AJ ,Holmes DR Jr . Secular trends in coronary atherosclerosis -- analysis in patients with valvular regurgitation. N Engl J Med 1996;335:316-322
Full Text | Web of Science | Medline2
Vita JA ,Treasure CB ,Ganz P ,Cox DA ,Fish RD ,Selwyn AP . Control of shear stress in the epicardial coronary arteries of humans: impairment by atherosclerosis. J Am Coll Cardiol 1989;14:1193-1199
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Glagov S ,Weisenberg E ,Zarins CK ,Stankunavicius R ,Kolettis GJ . Compensatory enlargement of human atherosclerotic coronary arteries. N Engl J Med 1987;316:1371-1375
Full Text | Web of Science | Medline
To the Editor:
As Enriquez-Sarano et al. state, previous studies of secular trends in atherosclerosis during the decline in death from coronary heart disease in the United States have been contradictory. Their rigorous examination of this issue demonstrates that no reduction in the prevalence of coronary atherosclerosis has occurred during a period in which death from coronary causes has declined dramatically.
These findings are in agreement with those of studies carried out during the period in which death from coronary heart disease was increasing. Morris analyzed autopsy records from a London hospital for the years 1907 to 1949, over a period in which death from coronary heart disease greatly increased and the prevalence of coronary atherosclerosis declined.1 A similar trend for the prevalence of severe atherosclerosis of the abdominal aorta emerged from a study of records dating from the 19th century to 1982 at St. Bartholomew's Hospital.2 The absence of concordance between trends in coronary atherosclerosis and trends in death from coronary heart disease led Morris 1 to postulate that changes in thrombotic tendency may underlie the trends in death from coronary causes. This hypothesis3 led to important work demonstrating that hemostatic function was associated with coronary heart disease.4
The absence of concordance between recent trends in coronary atherosclerosis and death from coronary heart disease could reflect the lack of a decline in the incidence of coronary heart disease as opposed to mortality. This pattern of a rapid decrease in death from coronary heart disease, with small or no decreases in incidence, has been seen in several studies in different countries. Some authors suggest that declines in death from coronary heart disease are close to expectations based on trends in risk factors.5 This possibility fails to recognize the similar nature of associations of risk factors with death from coronary heart disease and the incidence of coronary heart disease. If trends in risk factors led to large declines in death from coronary heart disease, they should also have produced large declines in the incidence of coronary heart disease, but no such declines have been seen.
5 ReferencesGeorge Davey Smith, M.D.
University of Bristol, Bristol BS8 2PR, United Kingdom1
Morris JN . Recent history of coronary disease. Lancet 1951;1:1-7, 69
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Finlayson R . Ischaemic heart disease, aortic aneurysms, and atherosclerosis in the City of London, 1868-1982. Med Hist Suppl 1985;5:151-168
Medline3
Meade TW ,Chakrabarti R . Arterial-disease research: observation or intervention? Lancet 1972;2:913-916
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Meade TW ,Mellows S ,Brozovic M , et al. Haemostatic function and ischaemic heart disease: principal results of the Northwick Park Heart Study. Lancet 1986;2:533-537
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Vartiainen E ,Puska P ,Pekkanen J ,Tuomilehto J ,Jousilahti P . Changes in risk factors explain changes in mortality from ischaemic heart disease in Finland. BMJ 1994;309:23-27
CrossRef | Web of Science | Medline
To the Editor:
In their study of 601 patients who underwent surgery for isolated, nonischemic valvular regurgitation, Enriquez-Sarano et al. found no significant change over time in the prevalence of coronary atherosclerosis from 1980 to 1989. We were pleased to see that this type of in vivo “screening” technique confirms our previous results found1 with the postmortem screening technique of “epidemiologic autopsy.” We used the presence or absence of coronary atherosclerosis at autopsy to estimate the true and false positive proportions of previous clinical diagnoses, and the true and false negative proportions when the disease was not clinically diagnosed. When we used these proportions to adjust the customary official rates of death from coronary heart disease, the corrected results showed much smaller downward trends for 1965, 1975, and 1985. As Enriquez-Sarano et al. point out, autopsy studies have often been regarded as too biased to allow a study of secular trends. When applied with scientific principles, however, epidemiologic autopsy can yield respectable, useful results. Both premortem and postmortem screening studies can contribute helpful research to demonstrate the true incidence of coronary atherosclerosis.
1 ReferencesBernard Burnand, M.D.
University of Lausanne, CH-1005 Lausanne, SwitzerlandAlvan R. Feinstein, M.D.
Yale University, New Haven, CT 06520-80251
Burnand B ,Feinstein AR . The role of diagnostic inconsistency in changing rates of occurrence for coronary heart disease. J Clin Epidemiol 1992;45:929-940
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Author/Editor Response
Dr. Enriquez-Sarano replies:
To the Editor: Ruygrok and Umans comment on the enlargement of the coronary arteries observed in aortic regurgitation and the potential bias that such enlargement could produce with regard to the assessment of coronary atherosclerosis. The size of the coronary arteries is increased in mitral regurgitation1 and aortic valve disease2 in relation to the increased left ventricular mass and tends to regress postoperatively. Obstructive coronary atherosclerosis is the complex result of the size of the coronary arteries, the potential compensatory enlargement associated with atherosclerosis, and the plaque volume. Because the true atherosclerotic-plaque volume is not yet measurable, it is not possible to elaborate on differences in plaque burden between aortic and mitral regurgitation.
We did not observe differences in coronary atherosclerosis between the patients with aortic and those with mitral regurgitation. The patients with aortic regurgitation as a group were younger than the patients with mitral regurgitation (59 vs. 66 years). Nevertheless, after adjustment for age, sex, and risk factors, there was no difference between groups in obstructive coronary atherosclerosis with respect to any of the three end points that we examined. Furthermore, no secular trend was observed for coronary atherosclerosis in aortic or mitral regurgitation. Therefore, there was no significant difference with regard to obstructive coronary atherosclerosis, as measured by coronary angiography, between the two groups. Consequently, our data do not suggest that the information obtained in the patients with aortic regurgitation should be treated differently from that obtained in patients with mitral regurgitation.
Davey Smith comments on the trends in atherosclerosis at a time when death from coronary disease was increasing. No data can be obtained using our methodology regarding that issue, but we agree that the absence of parallelism between death from coronary causes and the incidence of coronary atherosclerosis underlines the importance of triggering factors that may lead to acute complications even in patients with moderately obstructive atherosclerotic lesions.3 The mechanism by which a decrease in the risk factors may have participated in the decrease in death from coronary causes may not be related to a decrease in coronary atherosclerosis 4 and has not been well defined. Further analysis of the mechanisms that led to a decline in death from coronary disease are essential in order to design the most efficient intervention policies.
Burnand and Feinstein comment on the role of autopsy in epidemiologic research. We agree that the analysis of secular trends using death certificates or clinical diagnosis may not be sufficient and that more anatomical studies using autopsy or other methods are critically needed.
We hope that our study will generate much-needed research on secular trends in atherosclerosis and the mechanisms of the decrease in death from cardiovascular causes.
4 ReferencesMaurice Enriquez-Sarano, M.D.
Mayo Clinic, Rochester, MN 559051
Vassalli G ,Hess OM ,Krogmann ON , et al. Coronary artery size in mitral regurgitation and its regression after mitral valve surgery. Am Heart J 1993;126:1091-1098
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Villari B ,Hess OM ,Meier C , et al. Regression of coronary artery dimensions after successful aortic valve replacement. Circulation 1992;85:972-978
Web of Science | Medline3
Kereiakes DJ ,Topol EJ ,George BS , et al. Myocardial infarction with minimal coronary atherosclerosis in the era of thrombolytic reperfusion. J Am Coll Cardiol 1991;17:304-312
CrossRef | Web of Science | Medline4
Levine GN ,Keaney JF Jr ,Vita JA . Cholesterol reduction in cardiovascular disease -- clinical benefits and possible mechanisms. N Engl J Med 1995;332:512-521
Full Text | Web of Science | Medline
- Citing Articles (1)
Citing Articles
1
Shah Ebrahim. (1998) Editorial: There are no shortcuts to finding out what works - population laboratories are essential tools. Tropical Medicine and International Health 3:4, 256-257
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