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-Heart transplant is a treatment for selected patients with hypertrophic cardiomyopathy (HCM). However, the prevalence, clinical profile and outcome of this subgroup of HCM patients are uncertain. Therefore, we sought to determine the occurrence, clinical characteristics and prognosis of HCM patients who underwent cardiac transplantation in the United States during a 15-year period. METHODS AND
-Demographic, clinical and survival outcome of 26,706 adult (age >/=18 years) heart-only transplant recipients between January 1990 to December 2004 were acquired from the United Network of Organ Sharing (UNOS) Registry. Pre-transplant diagnoses were classified as: HCM (n=303; 1%) and non-HCM (26,403; 99%) [comprised of threepatient subgroups: 1) ischemic cardiomyopathy (n=14,308; 54%); 2) dilated cardiomyopathy (n=11,760; 44%); and 3) restrictive cardiomyopathy (n=335; 1%)]. Study follow-up began at the time of heart transplant and was 76+/-44 months among survivors. The 1-, 5-, and 10-year overall transplant survival for HCM patients was 85%, 75%, and 61%, with a trend toward greater survival compared to non-HCM transplant patients (82%, 70%, 49%; log rank test, p=0.05). However, propensity matched, covariate-adjusted Cox regression model analysis showed better survival over time (p<0.01) among the HCM patients. When HCM post-transplant survival was compared to each of the non-HCM patient subgroups, HCM patients had more favorable survival than those transplanted for ischemic cardiomyopathy (p=0.02). In contrast, HCM post-transplant survival did not differ from those patients transplanted for restrictive (p=0.08) or dilated cardiomyopathy (p=0.25).
-HCM patients comprise a small subset (1%) of the overall population of patients who undergo heart transplantation in the United States. Nonetheless, survival following transplant among HCM patients is comparable to patients transplanted for non-HCM cardiovascular diseases, with possible enhanced survival over time.
1 Hypertrophic Cardiomyopathy Center, Division of Cardiology, Tufts Medical Center, Boston, MA;
This article was published in the following journal.
Name: Circulation. Heart failure
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An autosomal dominant inherited form of HYPERTROPHIC CARDIOMYOPATHY. It results from any of more than 50 mutations involving genes encoding contractile proteins such as VENTRICULAR MYOSINS; cardiac TROPONIN T; ALPHA-TROPOMYOSIN.
A group of diseases in which the dominant feature is the involvement of the CARDIAC MUSCLE itself. Cardiomyopathies are classified according to their predominant pathophysiological features (DILATED CARDIOMYOPATHY; HYPERTROPHIC CARDIOMYOPATHY; RESTRICTIVE CARDIOMYOPATHY) or their etiological/pathological factors (CARDIOMYOPATHY, ALCOHOLIC; ENDOCARDIAL FIBROELASTOSIS).
A form of CARDIAC MUSCLE disease, characterized by left and/or right ventricular hypertrophy (HYPERTROPHY, LEFT VENTRICULAR; HYPERTROPHY, RIGHT VENTRICULAR), frequent asymmetrical involvement of the HEART SEPTUM, and normal or reduced left ventricular volume. Risk factors include HYPERTENSION; AORTIC STENOSIS; and gene MUTATION; (FAMILIAL HYPERTROPHIC CARDIOMYOPATHY).
One of the three polypeptide chains that make up the TROPONIN complex. It is a cardiac-specific protein that binds to TROPOMYOSIN. It is released from damaged or injured heart muscle cells (MYOCYTES, CARDIAC). Defects in the gene encoding troponin T result in FAMILIAL HYPERTROPHIC CARDIOMYOPATHY.
Inflammatory processes of the muscular walls of the heart (MYOCARDIUM) which result in injury to the cardiac muscle cells (MYOCYTES, CARDIAC). Manifestations range from subclinical to sudden death (DEATH, SUDDEN). Myocarditis in association with cardiac dysfunction is classified as inflammatory CARDIOMYOPATHY usually caused by INFECTION, autoimmune diseases, or responses to toxic substances. Myocarditis is also a common cause of DILATED CARDIOMYOPATHY and other cardiomyopathies.
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