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Official Journal of the Italian Society of Angiology and Vascular Pathology
Indexed/Abstracted in: EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 0,752
Online ISSN 1827-1618
Migliore T. 1, Parrella L. S. 1, Caputi A. 1, Silvestri N. 1, Romano R. 1, Pace L. 2, Imbriaco M. 2, Losi M. A. 1, Betocchi S. 1
1 Departments of Clinical Medicine and Cardiovascular and Immunological Sciences Federico II University, Naples, Italy
2 Biomorphological and Functional Sciences Federico II University, Naples, Italy
Aim. The aim of this study was to evaluate the effect of insulin-like growth factor 1 (IGF1) and transforming growth factor b-1 (TGFb-1) on collagen turnover, left ventricular (LV) hypertrophy and on passive diastolic function of the LV in hypertrophic cardiomyopathy (HCM).
Methods. This study group comprised 34 patients with non-dilated HCM. Procollagen I amino-terminal propeptide (PINP) and collagen I carboxy-terminal telopeptide (ICTP) were measured by radioimmunoassay. Matrix metalloproteinase 9 (MMP 9), IGF1 and TGF‚-1 were determined by enzyme-linked immunosorbent assay. The difference in duration between transmitral forward (A) and pulmonary venous retrograde (Ar) waves, was considered as an estimate of passive diastolic function; the ratio between the peak flow velocity at rapid filling at the mitral level (E) and E’ measured by tissue Doppler was considered an estimate of active diastolic function. LV mass was measured and normalized to body surface area (LVMi) by cardiac magnetic resonance imaging.
Results. LVMi correlates to E/E’ (r=0.597, P=0.019 ) and is inversely related to A-Ar (r=0.453, P=0.015). TGFb-1 is directly related to active MMP 9 (r=0.439, P=0.012 ). IGF1 is directly related to PICP-ICTP (r=0.347, P=0.501), that expresses the balance between collagen I synthesis and its degradation.
Conclusion. The study demonstrated that in HCM, LVMi influences active and passive diastolic dysfunction and that IGF1 stimulates collagen synthesis and TGFb-1 is related to LV hypertrophy.