Effect of calcium antagonists on exercise tests.

The aim of this study was to investigate the anti-ischemic and antianginal activity and the duration of the new dihydropyridine calcium blocker nisoldipine (NIS) in patients with stable angina pectoris. The research was carried out on 16 patients, all male, 41-68 (mean of 58) years of age, with stable angina pectoris and fixed ischemic threshold (variations < 15%). After a 10-day washout period, patients were randomized to treatment with either 10 mg of nisoldipine or placebo (PL), twice daily for 21 days, according to a double-blind, crossover design. Patients underwent maximal symptom-limited exercise testing at 10 W/min on a bicycle ergometer, twice during the washout period, and once at the end of each treatment period, 3 and 12 h after oral administration of the drugs. In comparison with placebo, nisoldipine increased the ischemic threshold (N, 704 +/- 45 s; PL, 548 +/- 35 s; p < 0.01) and anginal threshold (N, 766 +/- 44 s; PL, 699 +/- 42 s; p < 0.01) for at least 12 h, and the ST-segment depression significantly decreased at maximal work (PL, 2.4 +/- 0.1 mm; N, 1.8 +/- 0.2 mm; p < 0.01) and at maximal common work (PL, 2.4 +/- 0.1 mm; N, 1.15 +/- 0.2 mm; p < 0.01). Similar to placebo the rate-pressure product was not significantly changed at higher submaximal effort after N, but it was significantly increased at the level of ischemic threshold, suggesting an increase in coronary blood flow to ischemic zones. Nisoldipine possesses anti-ischemic and antianginal activity lasting at least 12 h. This activity seems to be due to an increase in coronary blood flow to ischemic zones.

[Does a genetic predisposition for infarction expansion exist? Evaluation of genetic polymorphisms of the renin-angiotensin system]. / Esiste una predisposizione genetica per l'espansione infartuale? Valutazione dei polimorfismi genetici del sistema renina-angiotensina.

Aim of this study is to carry out a genetic analysis of polymorphisms of the renin-angiotensin system in a genetically homogeneous population, in patients with and without myocardial infarction (AMI) expansion and to evaluate the influence of non genetic, mechanical factors. The study was conducted on 299 patients with first AMI. Ecocardiography studies were performed on all patients on day 1 and 3 from the onset of AMI and before discharge. Eighty-four patients were excluded because of inadequate quality of echocardiograms and 215 (163 males, 52 females) were admitted. Of these, 157 had no evidence of AMI expansion (EXP-) while 58 had expansion (EXP+). DNA was extracted by standard methods from blood samples. Age and gender had no influence on AMI expansion. Anterior infarction (p < 0.000001) and Q-wave infarction (p < 0.00002) were found more frequently in EXP+. Peak of creatine phosphokinase was higher in EXP+ than in EXP- (p < 0.00001). The percent of patients treated with thrombolysis or with hypertension and/or left ventricular hypertrophy was not significantly different in the two groups. AGT MT235 polymorphism of angiotensinogen gene, I/D polymorphism of ACE gene and AT1 A1166C of AT1 receptor of angiotensin II were not significantly different in two groups. Stratified analysis showed that in patients with anterior AMI (n = 87), with a higher risk of AMI expansion, there is a significant difference (p < 0.02) in ACE genotype between EXP- and EXP+. Odds ratio assuming the dominant effect of I allele (II+ ID < DD) was 3.35 (confidence interval 1.41-7.56) with increased risk of expansion. More extension studies are need to verify if these results can contribute to early identification of patients at higher risk and to optimize therapeutic approach.