Abstract
The most typical physiopathologic abnormality in hypertrophie cardiomyopathy (HC) is diastolic dysfunction, characterized by abnormal stiffness of the left ventricle during diastole, with resultant impaired ventricular filling. This abnormality in diastolic relaxation results in elevation of left ventricular end-diastolic pressure. Impaired early diastolic filling as well as abnormal distensibility leads to a compensatory increase in the contribution of atrial systole to left ventricular filling. 1 Atrial natriuretic peptide (ANP) is a cardiac polypeptide exerting potent diuretic, natriuretic and vasodilatory activities, and is produced and secreted predominantly by the atria in response to volume or pressure overload. 2,3 The mechanism of ANP release has been attributed to increases in either atrial pressures or atrial distension. 4,5 Plasma ANP levels are increased in patients with congestive heart failure and correlate well with left ventricular end-diastolic pressure and atrial pressure in patients with this disease. 6,7 Experimental data provide evidence of ventricular activation of the ANP gene in ventricular overload. A recent report 8 indicated that ventricular ANP expression occurs as a response to disease-specific changes such as myocardial fiber disarray, hypertrophy of myocytes and fibrosis in HC. 8 Plasma ANP levels have not yet been investigated and related to the clinical status in HC. The purpose of this study was to verify whether an increase in plasma ANP levels in patients with HC exists and to establish a possible correlation between ANP levels and clinical anatomic status of patients with HC.
Published Version
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