The New England Journal of Medicine
e-mail icon  FREE NEJM E-TOC    HOME   |   SUBSCRIBE   |   CURRENT ISSUE   |   PAST ISSUES   |   COLLECTIONS   |    Advanced Search
Sign in | Get NEJM's E-Mail Table of Contents — Free | Subscribe
 
Original Article
PreviousPrevious
Volume 349:1027-1035 September 11, 2003 Number 11
NextNext

Coronary Microvascular Dysfunction and Prognosis in Hypertrophic Cardiomyopathy
Franco Cecchi, M.D., Iacopo Olivotto, M.D., Roberto Gistri, M.D., Roberto Lorenzoni, M.D., Giampaolo Chiriatti, M.D., and Paolo G. Camici, M.D.

 Sign up for free e-toc
 

This Article
-Full Text
- PDF
-PDA Full Text
-PowerPoint Slide Set

Commentary
-Perspective
 by Cannon, R. O.

Tools and Services
-Add to Personal Archive
-Add to Citation Manager
-Notify a Friend
-E-mail When Cited
-E-mail When Letters Appear

More Information
-PubMed Citation
ABSTRACT

Background Microvascular dysfunction, reflected by an inadequate increase in myocardial blood flow in response to dipyridamole infusion, is a recognized feature of hypertrophic cardiomyopathy. Its long-term effect on the prognosis is unknown. We prospectively evaluated a cohort of patients with hypertrophic cardiomyopathy after they had undergone quantitative assessment of myocardial blood flow by positron-emission tomography (PET).

Methods Fifty-one patients (New York Heart Association class I or II) were followed for a mean (±SD) of 8.1±2.1 years after PET. Twelve subjects with atypical chest pain served as controls. Measurement of flow was performed at base line and after the infusion of the coronary vasodilator dipyridamole, with the use of nitrogen-13–labeled ammonia. Patients were then divided into three equal groups with increasing values of myocardial blood flow.

Results The response of myocardial blood flow to dipyridamole was severely blunted in the patients, as compared with the controls (1.50±0.69 vs. 2.71±0.94 ml per minute per gram of tissue, P<0.001). Sixteen patients (31 percent) had an unfavorable outcome (death from cardiovascular causes, progression to New York Heart Association class III or IV, or sustained ventricular arrhythmias requiring the implantation of a cardioverter–defibrillator) 2.2 to 9.1 years after PET. Reduced blood flow in response to dipyridamole was strongly associated with an unfavorable outcome. Multivariate analysis showed that among patients in the lowest of the three flow groups the age-adjusted relative hazard of death from cardiovascular causes was 9.6 (P=0.02) and the relative hazard of an unfavorable outcome (a combined end point) was 20.1 (P=0.003), as compared with patients in the two other flow groups. Specifically, all four patients who died from heart failure and three of five who died suddenly were in this subgroup.

Conclusions In patients with hypertrophic cardiomyopathy, the degree of microvascular dysfunction is a strong, independent predictor of clinical deterioration and death. Severe microvascular dysfunction is often present in patients with mild or no symptoms and may precede clinical deterioration by years.


Source Information

From the Regional Referral Center for Myocardial Diseases, Azienda Ospedaliera Careggi, Florence (F.C., I.O., R.G.); the Cardiology Unit, Ospedale di Lucca, Lucca (R.L.); the Cardiology Unit, Ospedale di Pescia, Pescia (G.C.); the Consiglio Nazionale delle Ricerche Institute of Clinical Physiology, Pisa (P.G.C.) — all in Italy; and the Medical Research Centre, Hammersmith Hospital, Imperial College, London (P.G.C.).

Address reprint requests to Dr. Cecchi at Via Jacopo Nardi 30, 50132 Florence, Italy, or at franco.cecchi{at}asf.toscana.it.

Full Text of this Article


This article has been cited by other articles:



HOME  |  SUBSCRIBE  |  SEARCH  |  CURRENT ISSUE  |  PAST ISSUES  |  COLLECTIONS  |  PRIVACY  |  TERMS OF USE  |  HELP  |  beta.nejm.org

Comments and questions? Please contact us.

The New England Journal of Medicine is owned, published, and copyrighted © 2009 Massachusetts Medical Society. All rights reserved.