Renin Genetic Polymorphism in Heart Failure Patients.

BACKGROUND: Genetic polymorphism of renin-angiotensin-aldosterone system affects the pathogenesis of hypertension (HTN), ischemic heart disease (IHD) and heart failure (HF). The purpose of our study is to analyze A/G renin genetic polymorphism in heart failure patients. METHODS: We investigated renin polymorphism in 83 subjects hospitalized in the Cardiology Department of the Rehabilitation Hospital Cluj-Napoca, using the PCR amplification method. 43 patients were diagnosed with heart failure [NYHA III-IV class], and 40 subjects without cardiovascular disease (control group). The NT-proBNP and the presence of cardiovascular risk factors were assessed. RESULTS: Heart failure etiology was IHD in 60.46% of patients. The average value of NT-pro BNP was 2991.24 ± 2034.6 pg/ml. As it was expected, HF patients presented low lipid levels: total cholesterol = 162.36 ± 38.28 mg/dl, LDL-Cholesterol = 104.88 ± 27.60 mg/dl, triglycerides= 109.12 ± 55.84 mg/dl, HDL-Co = 35.68 ± 9.55 mg/dl. A/G renin genetic polymorphism [with pathogenic potential] in heart failure patients was of 60.46% (homozygote 4.65% and heterozygote 55.81%). Conversely, pathogenic mutations were found only in 38.46% of hypertensive patients, but also in 55.88% and 22.22% patients with obesity/overweight and diabetes. The heterozygote form was found in only 37.5% of control subjects. CONCLUSION: This study showed no involvement of A/G renin polymorphisms in the pathogenesis of HF.

Drug secondary prevention in postmenopausal women with ischemic heart disease.

UNLABELLED: It is known that, in comparison with men, women with cardiovascular disease are undertreated, including drug treatment. This aspect was less studied with respect to drugs used for secondary prevention. METHODS: In an urban Romanian community there was studied a representative sample of 150 postmenopausal women with cardiovascular disease (62.7% of them with ischemic heart disease-IHD). We considered the secondary prevention by drugs. The results were compared with those registered in a similar sample of 160 men aged >55 years with cardiovascular disease (68.1% of them with IHD). The study was carried out using general practitioner's files. RESULTS: According to the literature, there were considered as preventive drugs: antiplatelet agents, statins, beta blockers and ACEI. Aspirin was used in 56.4% of the women and 72.5% of the men (p<0.05), ACEI in 69.1% and 79.8 % (p>0.05), beta blockers in 69.1% and 74.3 % (p>0.05) and statins in 48.9% and 48.6% (p>0.05). The results show that antiplatelet drugs are underused in ischemic patients, but especially in women. The maximum use of preventive drugs in women was registered after acute myocardial infarction (beta blockers 85.7%, statins 50%, aspirin 60.7%, ACEI 75%). In turn, the myocardial revascularization by CABG and PCI is low in both groups, but much less in women than in men: CABG 1.1% in women, 4.6% in men p>0.05, PCI 5.3% in women and 13.8% in men p<0.05. CONCLUSION: In postmenopausal women with ischemic heart disease the secondary prevention by drugs is similar with that applied in men, except aspirin and ACEI, which are underused.

Correlation between sTNFR-I and other negative prognostic factors in patients with chronic heart failure.

UNLABELLED: Tumor necrosis factor (TNF-alpha) and plasma levels of soluble tumor necrosis factor receptor I (sTNFR-I) are increased in patients with heart failure as an expression of chronic inflammation, representing a negative prognostic factor. Anemia and low serum lipid fraction are also negative prognostic factors, whose relationship with sTNFR-I has been less studied. METHODS: The study investigated 54 patients with heart failure, 40 ischemic and 14 nonischemic, 35 males and 19 females, aged 65 +/- 10 years. Plasma sTNFR-I values (nv < 3 pg/ml) and serum lipid fractions were determined in each patient and the prevalence of anemia (Ht < or = 41% in men; Ht < or = 38% in women) was established. Left ventricular ejection fraction (LVEF) was determined by using 2D echo. RESULTS: sTNFR-I was increased in patients with heart failure--222.79 +/- 97.08 pg/ml. Anemia was found in 40.74% of the patients, sTNFR-I being significantly increased in patients with anemia (242.82 +/- 49.12 pg/ml) compared to patients without anemia (194.9 +/- 117.3); p < 0.05. TChol (152.63 +/- 55.4 vs 177.81 +/- 38.52 mg%), LDLChol (101.47 +/- 42.4 vs 113.59 +/- 28.3 mg%) and TG (96.22 +/- 59.12 vs 132.09 +/- 96.55 mg%) were insignificantly lower in patients with anemia. Patients with anemia and low LVEF did not present higher sTNFR-I values (236.548 +/- 47.2) compared to patients with LVEF > 40% (245.75 +/- 52.1). A weak negative correlation r = -0.31 was noted between sTNFR-I and Ht in anemic patients and also between sTNFR-I and TChol (r = -0.31), LDLchol (r = -0.28), TG(r = -0.22). No correlation could be established between TChol, LDLchol, TG and Ht. CONCLUSION: In patients with heart failure, increased sTNFR-I as an expression of chronic inflammation is correlated with both anemia and low serum lipid fractions even if the exact nature of the relationship has yet to be established. There is no direct correlation between anemia and low serum lipid fractions.

The acute effect of ACEI and ARB's upon endothelin in heart failure patients.

PURPOSE OF THE STUDY: to compare the acute effect of ACEI and ARB's upon the plasmatic endothelin level in heart failure patients. METHODS: There were studied 30 patients with congestive heart failure, III-IV functional NYHA class, that were not under ACEI or ARB's treatment. In all the patients the endothelinl-21 plasmatic level was determined. After this, 20 patients, representing group I, received a single dose of 1 mg trandolapril, and 10 patients, representing group II, received a single dose of 40 mg telmisartan. After 24 hours, the plasmatic endothelin 1-21 level was determined again. RESULTS: The mean endothelial plasmatic level was similar in both groups (group I: 0.358+/-0.04 fmol/ml; group II: 0.345+/-0.038). After 24 hours, the endothelin level decreased to 0.295+/-0.03 fmol/ml for group I (p<0.05) and to 0.287+/-0.029 fmol/ml for group II (p<0.05), suggesting that both ACEI and ARB's are equally efficient in decreasing endothelin. The initial endothelinl-21 level was inversely correlated with LVEF (r = -0.989), and the degree of the decrease of endothelinl-21 after both ACEI and ARB's is directly correlated with the initial endothelinl-21 level (r =0.64). CONCLUSION: The acute administration of ACEI and ARB's in heart failure patients decreases the endothelin level, both categories of drugs having the same effects.