Club 35 Poster session 1: Wednesday 3 December 2014, 09:00-16:00 * Location: Poster area

Left ventricle hypertrophy (LVH) is strongly associated with stroke and myocardial infarction in hypertensive patients. Hypertensive heart characterized by cardiomyocytes hypertrophy, fibroblasts proliferation, enlargement of interstitial collagen volume and their ratio disorders which result in dangerous complications. Renin-angiotensin-aldosterone system (RAAS) and insulin-like growth factor 1 (IGF-1) play significant role in development of myocardial fibrosis and LV remodelling in hypertensive patients. The purpose of the study is to evaluate relations between activity of RAAS and interstitial fibrosis markers and left ventricle geometry models in hypertensive patients. Were examined 286 patients (both men and women) with Hypertension 2-3 grade and stable ischemic heart disease 2-3 functional class complicated by chronic heart failure I-III NYHA functional class. The mean age of patients 53 (3.7) years. Patients with arrhythmias, diabetes mellitus were excluded from the study. In all patients was performed EchoCG (ASE/EAE recommendations 2005) and were evaluated plasma levels of aldosteron, angiotensin 2, angiotensin-converting enzyme (ACE), tissue inhibitor of metalloproteinases-1 (TIMP-1), IGF-1. HF NYHA functional class was determined by using the 6MWT. Statistical significance was defined at the level of methods for p<0,05. Results of the study are shown in Table 1. Thus, the results of the study show that interstitial myocardium fibrosis and activity of RAAS were significantly higher in patients with concentric hypertrophy and eccentric hypertrophy. <tbl id="CHAPTERsub90337TB1" loc="display"><caption> LV remodelling, RAAS and fibrosis </caption><tblbdy top-stubs="3"><r><c ra="m" cspan="1" rspan="3">Parameters</c><c ca="c" cspan="4" rspan="1"><bottom-border>LV geometry model</c></r><r><c ra="t" cspan="1" rspan="1">Normal geometry</c><c ra="t" cspan="1" rspan="1">Concentric remodelling</c><c ra="t" cspan="1" rspan="1">Eccentric hypertrophy</c><c ra="t" cspan="1" rspan="1">Concentric hypertrophy</c></r><r><c ra="t" cspan="1" rspan="1">n=148</c><c ra="t" cspan="1" rspan="1">n=36</c><c ra="t" cspan="1" rspan="1">n=50</c><c ra="t" cspan="1" rspan="1">n=52</c></r><r><c cspan="1" rspan="1">Angiothensin 2, pg/ml</c><c cspan="1" rspan="1">37.8 (11.6)</c><c cspan="1" rspan="1">39.0 (16.4)</c><c cspan="1" rspan="1">47.4 (13.4)</c><c cspan="1" rspan="1">57.7 (10.5)*†</c></r><r><c cspan="1" rspan="1">ACE, u/l</c><c cspan="1" rspan="1">45.8 (16.7)</c><c cspan="1" rspan="1">38.9 (17.1)</c><c cspan="1" rspan="1">62.5 (35.3)*</c><c cspan="1" rspan="1">73.8 (25.9)*</c></r><r><c cspan="1" rspan="1">Aldosterone, pg/ml</c><c cspan="1" rspan="1">121.5 (27.5)</c><c cspan="1" rspan="1">95.8 (43.4)</c><c cspan="1" rspan="1">144.5 (38.3)*</c><c cspan="1" rspan="1">143.2 (38.9)*</c></r><r><c cspan="1" rspan="1">TIMP-1, ng/ml</c><c cspan="1" rspan="1">276.9 (80.3)</c><c cspan="1" rspan="1">249.8 (83.2)</c><c cspan="1" rspan="1">359.9 (119.5)*‡</c><c cspan="1" rspan="1">403.1 (128.5)*‡</c></r><r><c cspan="1" rspan="1">IGF-1, ng/ml</c><c cspan="1" rspan="1">162.6 (23.6)†</c><c cspan="1" rspan="1">158.3 (18.9)†</c><c cspan="1" rspan="1">139.9 (19.7)</c><c cspan="1" rspan="1">155.5 (24.5)†</c></r><r><c cspan="1" rspan="1">Interstitial collagen volume fraction, %</c><c cspan="1" rspan="1">3.03 (0.78)</c><c cspan="1" rspan="1">3.66 (0.96)*</c><c cspan="1" rspan="1">4.47 (0.98)*‡</c><c cspan="1" rspan="1">5.34 (0.97)*†‡</c></r></tblbdy><tblfn id="TN1"> *- p<0.05 in comparison with patients with normal geometry; † - p<0.05 in comparison with patients with eccentric hypertrophy; ‡ - p<0.05 in comparison with patients with concentric remodelling. Results are shown in M (SD). </tblfn></tbl>