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Circulation. 2003;108:e9045-e9046
doi: 10.1161/01.CIR.0000104140.79111.22
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(Circulation. 2003;108:e9045.)
© 2003 American Heart Association, Inc.

Cardiovascular News

Ruth SoRelle, MPH

Circulation Newswriter

New Measurement Gives Clues to Cardiovascular Risk

Low brachial artery flow-mediated dilation is a strong independent indicator of cardiovascular risk in patients with peripheral artery disease. It adds to the predictive value of the ankle brachial plexus index, the most powerful prognostic indicator in these patients, according to researchers from Italy in this issue of the journal Circulation (Circulation. 2003;108:2093–2098) .

In 131 patients followed up for an average of 23 months, 18 had a coronary event, 12 a cerebrovascular event, and 9 a peripheral event. In those patients who had an event, the brachial artery flow-mediated dilation was lower than in those who had no event, according to the researchers, who were led by Gregorio Brevetti, MD, of the Department of Clinical Medicine and Cardiovascular and Immunological Sciences at the University "Federico II" in Naples, Italy.

The author said that in addition to adding the measurement as an indicator of cardiovascular risk, the study provides "the first demonstration that measurement of brachial artery vasoreactivity can add to the standard cardiovascular risk prediction. Indeed, in our population, FMD [brachial artery flow-mediated dilation] improved the prognostic value of ABPI [ankle brachial plexus index], the most powerful marker of cardiovascular risk in PAD [peripheral artery disease]. Therefore, FMD measurement may be particularly useful to identify an endothelial dysfunction and PAD subgroup of claudicants at increased risk. We hope that our studies will prompt studies aimed at assessing whether patients with PAD with severe endothelial dysfunction could represent a target population for ACE inhibitors and statins, which have been shown to improve endothelial function, and reduce the cardiovascular risk."

New Surgical Procedure Valuable in Hypertrophic Obstructive Cardiomyopathy
A new procedure—mitral leaflet extension combined with septal myectomy—provides a new tool in the treatment of patients with hypertrophic obstructive cardiomyopathy, according to researchers from the Erasmus Medical Center in Rotterdam, the Netherlands, in this issue of the journal Circulation (Circulation. 2003:108:2088–2092).

Mitral leaflet extension involves the grafting of an autologous pericardial patch onto the center of the anterior mitral valve leaflet. In this study, 29 patients with hypertrophic obstructive cardiomyopathy who received this procedure were followed up for an average of 3.4 years. After surgery, the New York Heart Association function class improved from an average 2.8 to 1.3 in these patients. The width of the interventricular septum decreased from 23 to 17 mm, the left ventricular outflow tract gradient decreased from 100 to 17 mm Hg, the severity of mitral regurgitation graded on a scale from 9 to 4 decreased from 2.5 to 0.5, and the severity of the systolic anterior motion of the mitral valve graded from 0 to 3 decreased from 2.9 to 0.5. There were no deaths associated with the surgery.

The researchers, led by Folkert J. ten Cate, MD, of the Erasmus Medical Center, concluded, "MLE [mitral leaflet extension] in combination with myectomy is an effective and safe treatment for patients with HOCM [hypertrophic obstructive cardiomyopathy]. Long-term follow-up demonstrates sustained improvement. . . ." The technique adds to the surgical possibilities for treatment in this disease and might have special applications in some subgroups of patients.

New Cardiovascular Markers
Plasma myeloperoxidase levels measured when patients came into the emergency department with chest pain predicted the risk of myocardial infarction and major adverse cardiac events in 604 patients at the Cleveland Clinic Foundation in a report in the October 23, 2003, issue of The New England Journal of Medicine ( N Engl J Med. 2003;349:1595–1604[Abstract/Free Full Text]).

The authors noted that there are suggestions of links between myeloperoxidase and inflammation and cardiovascular disease. Myeloperoxidase is an abundant leukocyte enzyme that is higher in lesions that have broken or ruptured in patients with sudden death. In this study, it predicted risk of major adverse coronary events at 30 days and at 6 months in patients who were negative for troponin T and had no myocardial necrosis. The authors concluded, "Myeloperoxidase levels, in contrast to troponin T, creatine kinase MB isoform, and C-reactive protein levels, identified patients at risk for cardiac events in the absence of myocardial necrosis, highlighting its potential usefulness for risk stratification among patients who present with chest pain."

In a second article in the same issue of The New England Journal of Medicine, French, German, and Canadian researchers found that a low level of red-cell glutathione peroxidase 1 is an independent risk factor for cardiovascular events in patients with coronary artery disease.

In a prospective study of 635 patients with suspected coronary artery disease who were followed up for an average of 4.7 years, glutathione peroxidase 1 activity proved a strong univariate predictor of the risk of cardiovascular events. That risk is inversely associated with increasing quartiles of glutathione peroxidase 1 activity. Low levels of red-cell glutathione peroxidase 1 activity are independently associated with an increased risk of cardiovascular events, and the enzyme may have prognostic and treatment value.

In an accompanying editorial, Teri Manolio, MD, PhD, of the National Heart, Lung and Blood Institute, said that clinicians should view reports of such markers carefully. Do they add independent information about risk or prognosis? Is this factor found in a large percentage of the patient population and is it a strong predictor? Is the measure reproducible? Does this measure have a high sensitivity or specificity? Is there a laboratory test for the marker available? While both of the new markers in this issue of The New England Journal pass some of these tests, they do not pass them all. "Crossing the boundary from research to clinical application, however, requires replication in multiple settings, experimental evidence supporting a pathophysiologic role, and ideally, intervention trials demonstrating that modification improves the outcome. Until these steps are taken, specific interventions to modify novel markers should be reserved for investigative purposes. In the interim, however, these markers may be quite useful in identifying patients who may benefit from other therapies proven to reduce risk, since the risk generally increases with the number of risk factors present," she wrote.





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