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CAD in Women
Abstract & Commentary
By Jonathan Abrams, MD, Professor of Medicine, Division of Cardiology, University of New Mexico, Albuquerque. Dr. Abrams serves on the speaker's bureau for Merck, Pfizer, and Parke-Davis.
Source: Nicholls SJ, et al. rate of progression of coronary atherosclerotic plaque in women. J Am Coll Cardiol. 2007;49;1546-1551
Synposis: Women harbor less atherosclerotic plaque within their coronary arteries, despite the greater prevalence of atherogenic risk factors.
This study asks the question as to whether women have less obstructive coronary disease (CAD) than men. It remains unclear if the absolute burden of atherosclerotic plaque differs between men and women. The study combined 3 intravascular ultrasound (IVUS) trials to assess atheroma burden in women vs men; the investigators also attempted to evaluate the pattern of arterial remodeling in both genders. Finally, the study attempted to answer the question as to whether anti-atherosclerotic therapies as well as plaque progression are different between men and women. The methodology included a retrospective analysis of three serial IVUS trials, Reversal, Camelot and Activate. Men and women 30-75 years of age with angiographic CAD comprising at least one stenosis > 20%, and no stenosis > 50%, were evaluated. The IVUS technique and measurements have been described in the publications. Standard evaluations included measurements of total atheroma volume (TAV), percent atheroma volume (PAV), and assessment of the atheroma volume in the most and least diseased 10mm segments in each subject. A remodeling index was calculated, and was described as constrictive or expansive. CRP was measured. Adjustments were made for factors relating to plaque burden and progression, including age, hypertension, diabetes, etc. As compared to men, women tended to have a higher BMI and were more likely to have hypertension (SBP), diabetes, higher baseline total cholesterol, higher HDL cholesterol and lower triglycerides. Mean CRP in women was 4.8 mg/l vs 2.6 mg/l, (p < 0.001) in men.
RESULTS: At baseline women had less atheromatous plaque as well as atheroma volume. Arterial remodeling at the site of the greatest plaque extent was similar in men and women. Restrictive and expansive remodeling was equivalent for both sexes. Women had smaller coronary arteries and lumen volume. After adjustment for differences that might influence regression, there was no sex difference in total and percent atheroma volume. Thus, "Women were no more likely to undergo substantial progression… or substantial regression than men." Finally, an effort was made to evaluate the effect of risk factors on plaque progression; females were just as likely as males to undergo regression when LDL cholesterol was lowered below 80 mg/dl, SBP less than 120 mmHg, and CRP < 2mg. There was no statistical interaction between sex and changes in total atheroma volume, and no relationship between sex and changes in PAV related to HDL, SBP or CRP. The authors stated that "…despite the greater presence of risk factors, women contain less atherosclerotic plaque within their coronary arteries." In addition, women benefited to a comparable degree from intensive risk factor modification. It appears from the study that clusters of risk factors are more important than any individual one, and "despite the greater presence of established risk factors, women harbored less plaque." While the pattern of arterial remodeling at the site with the greatest degree of plaque did not differ between sexes, the authors suggest that women express plaque burden in relationship to vessel size as being smaller than in men. The authors conclude, "Women are likely to derive similar benefit from the use of medical therapies that result in intensive risk factor modification." They add that their data does not allow a determination of whether sex influences either the composition of plaque at baseline or modification following response to established therapies.
In conclusion, these data demonstrate that women harbor less atherosclerotic plaque within their coronary arteries, despite the greater prevalence of atherogenic risk factors. Nevertheless, intensive modification of risk factors has a similar favorable influence in both men and women on plaque progression.
These data provide a better window into the pathophysiology of CAD in women. A policy of aggressive risk modification is supported by these observations, and raises the bar for the treatment of women with risk factors even when the coronary artery disease is not obstructive. It would appear from these data that the coronary arteries of men and women behave in a similar fashion, including their responses to risk factors in the environment. The smaller arterial size in women may play a role in producing anginal symptoms, but the pathophysiology of CAD progression is the same as in men. Furthermore, in a recent report from the WISE study (Women's Ischemia Syndrome Evaluation), a subset of participants with normal coronary angiograms who continued to have chest pain one year after angiography had a much greater cardiovascular event rate than those without anginal symptoms. In that study, such women who had persistent chest pain at one year had twice the rate of a composite of cardiovascular events, including MI, stroke, CV death and CHF. The WISE data also support aggressive risk factor modification, as does the retrospective compilation of IVUS studies reviewed above. The recently published COURAGE trial strongly supports aggressive risk factor modification, including drug therapy as well as lifestyle changes. One can no longer conclude that chronic chest pain in women is benign. Furthermore, the IVUS analysis of coronary vessels resulted in similar findings in women as in men, with comparable responses to risk factor modification, and presumed comparable progression in the absence of vigorous control of hypertension, diabetes and dyslipidemia.