doi: 10.1161/01.CIR.0000027972.86188.69
(Circulation. 2002;105:e9115.)
© 2002 American Heart Association, Inc.
Cardiovascular News
Circulation Newswriter
Statin Use Reduces Risk for Women With Cardiovascular Disease in HERS
The Heart and Estrogen/Progestin Replacement Study (HERS) shocked many in the gynecological and cardiology realm when it demonstrated that there was no cardiovascular advantage associated with the use of hormone replacement therapy in postmenopausal women with heart disease. In fact, early analysis of data from >2700 women demonstrated that there might even be a significant early risk with hormone replacement therapy.
In this week’s issue of Circulation (Circulation. 2002;105:2962–2967), researchers analyzed data from the HERS study in terms of statin use. Led by David M. Herrington, MD, MHS, of the Department of Internal Medicine/Cardiology at Wake Forest University School of Medicine in Winston-Salem, NC, the researchers found that when statin users were compared with subjects who did not take statins, those who took the cholesterol-lowering medications had lower rates of cardiovascular and venous thromboembolic events and total mortality.
In addition, although hormone replacement therapy resulted in a significant increase in early risk for primary events in those who do not use statins, there are no early risks for those who did use the statins. The researchers concluded, "Despite the potent effects of statins on risk for clinical events, differential use of statins among the two arms does not appear to explain the overall null effect of hormone replacement therapy in HERS. A suggestion that statins attenuate the early increased risk for cardiovascular events associated with HRT requires further confirmation." All in all, they conclude, there is strong evidence that women with coronary disease would benefit from statin use.
Sounding Out the Genes
Doppler tissue imaging is an increasingly sophisticated technique used in a variety of diagnostic areas. In an interesting report in this week’s issue of Circulation (Circulation. 2002;105:2992–2997), Carolyn Y. Ho, MD, from the Cardiovascular Division of the Brigham and Women’s Hospital and Harvard Medical School in Boston, Mass, along with colleagues from the University of Wisconsin, the Minneapolis Heart Institution Foundation, and the Department of Genetics at the Harvard Medical School and Howard Hughes Medical Institute, used echocardiographic studies that included Doppler tissue imaging to identify individuals with a specific genotype that predisposed them to develop first left ventricular hypertrophy, considered diagnostic of hypertrophic cardiomyopathy.
In the study, individuals who had a positive genotype for hypertrophic cardiomyopathy with ß-myosin heavy chain mutations with left ventricular hypertrophy and individuals with the same genotype but without left ventricular hypertrophy were compared with normal controls.
The left ventricular ejection fraction was significantly higher in the groups who had the disease-specific genotype. However, mean early diastolic myocardial velocities were significantly lower in both groups with the genotype positive for disease. A mean early diastolic myocardial velocity had an 86% specificity and 75% sensitivity for identifying individuals with the positive genotype, regardless of whether they had left ventricular hypertrophy or not. However, when the left ventricular ejection fraction was 
68% and the mean early diastolic myocardial velocity was <15 cm/s, the combination of tests was 100% specific and 44% sensitive in predicting the affected genotype.
The authors concluded that abnormalities of diastolic function that could be assessed by Doppler tissue imaging will precede development of left ventricular hypertrophy in the individuals with hypertrophic cardiomyopathy caused by ß-myosin heavy chain mutations. A combination of the mean early diastolic myocardial velocity and left ventricular ejection fraction identified the individuals with the affected genotype with high specificity.
"It is intriguing that the combination of relatively reduced EA (mean early diastolic myocardial) velocity and increased EF (ejection fraction) was a highly specific marker for affected genetic status in our population; a finding that could assist in the preclinical diagnosis of HCM (hypertrophic cardiomyopathy). ... Determining the strength of this association and whether this finding is specific only for ß-myosin heavy chain mutations or occurs with other genetic causes of HCM, warrants further study."
Early Statin Therapy Doesn’t Play Well
Giving statins to patients within 7 days of their having experienced an acute coronary syndrome appears to have no effect on improving outcomes, according to researchers who evaluated databases from 2 randomized trials—SYMPHYONY and 2nd SYMPHONY (Sibrafan vs Aspirin to Yield Maximum Protection from Ischemic Heart Events Post-acute Coronary Syndromes). In the June 19, 2002, issue of the Journal of the American Medical Association (JAMA. 2002;287:3087–3095), scientists led by L. Kristen Newby, MD, of Duke Clinical Research Institute in Durham, NC, concluded that although there was no relationship between statin use soon after the acute coronary syndrome and improved outcome, analysis of some subsets indicated that the value of early statin therapy could vary with cholesterol levels. Confirmation of this finding, however, would have to wait for clinical trials with a large enough enrollment to prove the point.
Representatives from the 2 studies evaluated the 90-day and 1-year outcomes in patients who had received a statin within 7 days of the acute coronary event. A total of 12 365 patients were randomized between those who received early statin therapy and those who survived >5 days after the event and never received a statin.
After statistical adjustments, there was no benefit from early statin treatment in rates of mortality, myocardial infarction, or recurrent ischemia. However, they concluded, "In the absence of evidence for harm and with demonstrated improvement in long-term compliance, initiation of statin therapy during hospitalization should be considered. However, until the observed interaction between cholesterol levels and the relationship of early treatment with outcomes can be confirmed or refuted, clinicians should use caution in starting statin therapy during the acute phase of ACS in people who do not meet current treatment guidelines."
When It Hurts but You Don’t Know Why
The troublesome ailment known as cardiac syndrome X, characterized by typical angina, an abnormal exercise test result, and normal arteries on angiogram, may result from subendocardial hypoperfusion, a condition demonstrated by British researchers led by Jonathan R. Panting, MB, MRCP, from the Royal Brompton Hospital and the National Heart and Lung Institute at Imperial College, London, during cardiovascular magnetic resonance imaging with an adenosine infusion. Twenty patients with cardiac syndrome X and 10 matched controls underwent the procedure, which is detailed in the July 20, 2002, issue of the New England Journal of Medicine (N Engl J Med. 2002;346:1948–1953).
In their discussion of the work, Dr Panting and his colleagues note that their results "show that patients with syndrome X have significantly different perfusion responses to adenosine than matched controls. ... These findings, combined with the occurrence of chest pain during stress in patients with syndrome X, support the hypothesis that subendocardial ischemia is the cause of the angina. However, whether there is an actual absolute reduction in subendocardial perfusion with stress in patients with syndrome X is unresolved, because current techniques for myocardial-perfusion cardiovascular magnetic resonance imaging in humans do not generate reliable absolute measures. This question might be resolved with further developments in quantification with perfusion cardiovascular magnetic resonance imaging, or possibly with the latest generation of high-resolution PET scanners." They advocate further research involving syndrome X patients to better understand the pathophysiology of the syndrome.
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