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Cytochrome P450 17A1 (CYP17A1) catalyses the formation and metabolism of steroid hormones. They are involved in blood pressure (BP) regulation and in the pathogenesis of left ventricular hypertrophy. Therefore, altered function of CYP17A1 due to genetic variants may influence BP and left ventricular mass. Notably, genome wide association studies supported the role of this enzyme in BP control. Against this background, we investigated associations between single nucleotide polymorphisms (SNPs) in or nearby the CYP17A1 gene with BP and left ventricular mass in patients with arterial hypertension and associated cardiovascular organ damage treated according to guidelines. Patients (n = 1007, mean age 58.0 +/- 9.8 years, 83% men) with arterial hypertension and cardiac left ventricular ejection fraction (LVEF) 40% were enrolled in the study. Cardiac parameters of left ventricular mass, geometry and function were determined by echocardiography. The cohort comprised patients with coronary heart disease (n = 823; 81.7%) and myocardial infarction (n = 545; 54.1%) with a mean LVEF of 59.9% +/- 9.3%. The mean left ventricular mass index (LVMI) was 52.1 +/- 21.2 g/m(2.7) and 485 (48.2%) patients had left ventricular hypertrophy. There was no significant association of any investigated SNP (rs619824, rs743572, rs1004467, rs11191548, rs17115100) with mean 24 h systolic or diastolic BP. However, carriers of the rs11191548 C allele demonstrated a 7% increase in LVMI (95% CI: 1%-12%, p = 0.017) compared to non-carriers. The CYP17A1 polymorphism rs11191548 demonstrated a significant association with LVMI in patients with arterial hypertension and preserved LVEF. Thus, CYP17A1 may contribute to cardiac hypertrophy in this clinical condition.
There is evidence of substantial benefit of cardiac rehabilitation (CR) for patients with low exercise capacity at admission. Nevertheless, some patients are not able to perform an initial exercise stress test (EST). We aimed to describe this group using data of 1094 consecutive patients after a cardiac event (71 +/- 7 years, 78% men) enrolled in nine centres for inpatient CR. We analysed sociodemographic and clinical variables (e.g. cardiovascular risk factors, comorbidities, complications at admission), amount of therapy (e.g. exercise training, nursing care) and the results of the initial and the final 6-min walking test (6MWT) with respect to the application of an EST. Fifteen per cent of patients did not undergo an EST (non-EST group). In multivariable analysis, the probability of obtaining an EST was higher for men [odds ratio (OR) 1.89, P=0.01], a 6MWT (per 10 m, OR 1.07, P<0.01) and lower for patients with diabetes mellitus (OR 0.48, P<0.01), NYHA-class III/IV (OR 0.27, P<0.01), osteoarthritis (OR 0.39, P<0.01) and a longer hospital stay (per 5 days, OR 0.87, P=0.02). The non-EST group received fewer therapy units of exercise training, but more units of nursing care and physiotherapy than the EST group. However, there were no significant differences between both groups in the increase of the 6MWT during CR (123 vs. 108 m, P=0.122). The present study confirms the feasibility of an EST at the start of CR as an indicator of disease severity. Nevertheless, patients without EST benefit from CR even if exercising less. Thus, there is a justified need for individualized, comprehensive and interdisciplinary CR.