Journal of the American College of Cardiology © 2010 by the American College of Cardiology Foundation Published by Elsevier Inc.
Vol. 55, No. 1, 2010 ISSN 0735-1097/10/$36.00
CORRESPONDENCE
Letters to the Editor
Delayed Hyperenhancement Magnetic Resonance Imaging for Sudden Cardiac Death Risk Stratification in Hypertrophic Cardiomyopathy We have read with great interest the consensus guidelines introduced by Goldberger et al. (1) concerning the evaluation of noninvasive risk stratification techniques for identification of patients at risk for sudden cardiac death (SCD). Concerning hypertrophic cardiomyopathy (HCM), the authors conclusively support that the use of electrocardiography, signal-averaged electrocardiography, treadmill exercise test, and 2-dimensional echocardiography, along with obtaining a detailed personal and familial history, can successfully assess risk for SCD, even though no randomized trials exist using these parameters (1). SCD among HCM patients is mainly connected to the occurrence of ventricular tachycardia/ventricular fibrillation (VT/VF) (2). Many studies suggest that the extent of myocardial disarrayfibrosis, predisposing to re-entry phenomena as part of a general arrhythmogenic tendency, constitutes the main stimulus for VT/VF incidence (3,4). Delayed hyperenhancement magnetic resonance imaging (MRI) accurately detects myocardial fibrosis degree, and a statistically powerful correlation between fibrosis extent and incidence of VT/VF in HCM seems to have been established by previous studies (5,6). However, the role of delayed hyperenhancement MRI as well as its diagnostic and prognostic utility in assessment of SCD risk are not discussed in this consensus document. Obviously, more cohort studies are needed to establish an etiological relationship between scar size and the possibility of sudden death. Notwithstanding, delayed hyperenhancement MRI along with the aforementioned “screening” practices could offer a more precise estimation of risk for SCD in HCM patients. Georgios K. Efthimiadis *Efstathios D. Pagourelias *Cardiomyopathies Laboratory First Cardiology Department Medical School Aristotle University of Thessaloniki AHEPA Hospital Stilp. Kyriakidi 1 Thessaloniki 54636 Greece E-mail:
[email protected] doi:10.1016/j.jacc.2008.09.068
REFERENCES
1. Goldberger JJ, Cain ME, Hohnloser SH, et al. American Heart Association/American College of Cardiology Foundation/Heart Rhythm Society scientific statement on noninvasive risk stratification techniques for identifying patients at risk for sudden cardiac death: a scientific statement from the American Heart Association Council on Clinical Cardiology Committee on Electrocardiography and Arrhythmias and Council on Epidemiology and Prevention. J Am Coll Cardiol 2008;52:1179 –99. 2. Maron BJ, Shen WK, Link MS, et al. Efficacy of implantable cardioverter- defibrillators for the prevention of sudden death in patients with hypertrophic cardiomyopathy. N Engl J Med 2000;342: 365–73. 3. Varnava AM, Elliott PM, Mahon N, Davies MJ, McKenna WJ. Relation between myocyte disarray and outcome in hypertrophic cardiomyopathy. Am J Cardiol 2001;88:275–9. 4. Choudhury L, Mahrholdt H, Wagner A, et al. Myocardial scarring in asymptomatic or mildly symptomatic patients with hypertrophic cardiomyopathy. J Am Coll Cardiol 2002;40:2156 – 64. 5. Kwon DH, Setser RM, Popovic ZB, et al. Association of myocardial fibrosis, electrocardiography and ventricular tachyarrhythmia in hypertrophic cardiomyopathy: a delayed contrast enhanced MRI study. Int J Cardiovasc Imaging 2008;24:617–25. 6. Adabag AS, Maron BJ, Appelbaum E, et al. Occurrence and frequency of arrhythmias in hypertrophic cardiomyopathy in relation to delayed enhancement on cardiovascular magnetic resonance. J Am Coll Cardiol 2008;51:1369 –74.
On Call at the Wisconsin Heart Hospital I had just gotten home from rounds. While opening the Sunday newspaper, the phone rang. Dr. Clyde said, “Linda Bonobo was very lethargic and wouldn’t get up for breakfast. Her breathing is labored and her edema is worse. We’re taking her to the hospital now.” Linda is a 51-year-old insulin-dependent diabetic, mother of 12, who presented a month ago with edema, ascites, lethargy, anorexia, and shortness of breath. Echocardiography showed anteroapical dyskinesis of the left ventricle, and ejection fraction 35%. She was treated with furosemide, lisinopril, metoprolol, and aspirin. Her appetite and level of physical activity improved. Her abdomen seemed less protuberant. Linda has no prior history of heart disease. She has had insulindependent diabetes for 5 years. Her urine has recently been negative for glucose. Her low-density lipoprotein was 72 mg/dl, and her high-density lipoprotein was 142 mg/dl. No family history is available: Linda was born in the wild in the jungles of the Democratic Republic of Congo. Heart disease is a frequent cause of death in bonobos living in captivity. Being eaten by humans as “bush meat” is often the cause of death in wild bonobos. Bonobos are an endangered species. I parked in the Heart Hospital lot and walked across the street to the Milwaukee Zoo. The Animal Health Center is just inside the