Clinical InvestigationCongestive Heart FailureMatrix metalloproteinases and tissue remodeling in hypertrophic cardiomyopathy
Section snippets
Patients and methods
We included 67 HCM patients from two referral hospitals in Spain (Hospital Universitario Virgen de la Arrixaca from Murcia and Hospital General Universitario from Alicante) [44 men (67.5%)] 49±14 years of age. The criteria for diagnosis of HCM was the presence of a left ventricular wall thickness of at least 15 mm without any other cause that could lead to ventricular hypertrophy, and in the case of first-degree relatives of affected individuals, proposed familial criteria were used.21 A
Results
Clinical data of patients are resumed in Table I. Forty-five patients (67%) showed impaired functional class (New York Heart Association ≥II), and only 2 patients presented systolic dysfunction. About half of the patients (48%) had gadolinium enhancement assessed by CMR. Fifty patients (75%) showed any risk factors for sudden death (median, 2 [interquartile range 0-3]).
Discussion
It has been described that collagen turnover is enhanced in HCM, maintaining collagen I synthesis over degradation.12 So, the carboxyl-terminal propeptide of procollagen type I, a serum marker of collagen synthesis, is increased in patients with HCM, with decreased concentration of MMP-1 and raised concentration of its inhibitor, TIMP-1.14 Interestingly, an important increase in collagen content has been shown in young patients with HCM who died suddenly.22 These features are associated with
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