Tomasz Chamiec

Effect of Supplemental Oral l-Arginine on Exercise Capacity in Patients With Stable Angina Pectoris

A randomized, double-blind, placebo-controlled study in patients with clinical symptoms of stable angina pectoris and healed myocardial infarction (n = 22) has shown that oral supplementation with L-arginine (6 g/day for 3 days) increases exercise capacity (tested on a Marquette case 12 treadmill according to the modified Bruce protocol). Results suggest that the inefficient L-arginine/nitric oxide system contributes to limitation of myocardial perfusion and/or peripheral vasodilation during maximum exercise in patients with stable angina pectoris.

Effects of oral L-arginine supplementation on exercise-induced QT dispersion and exercise tolerance in stable angina pectoris.

We assessed the effects of L-arginine (an endogenous precursor of nitric oxide) on the magnitude of exercise-induced QT dispersion in patients with coronary artery disease. The study had a randomized double-blind cross-over design. Twenty-five patients with stable coronary artery disease underwent two separate exercise tests: after oral administration of L-arginine (6 g/24 h for 3 days) or placebo. Indications for cessation of exercise included: pulse limit, exhaustion, chest pain, ST segment depression >2 mm. We found that arginine significantly increased exercise duration from 604+/-146 to 647+/-159 s (P<0.03). However, it had no effect on the sum of exercise-induced ST segment depressions (1.9+/-2.3 and 2.4+/-3.3 on and off arginine, respectively, NS). Exercise shortened QT interval to a similar extent in patients treated with placebo or arginine. QT dispersion changed during exercise from 55+/-21 to 60+/-19 ms (NS) and from 60+/-21 to 53+/-17 ms (NS), respectively. We conclude that, in patients with coronary artery disease, oral supplementation of L-arginine does not affect exercise-induced changes in QT interval duration, QT dispersion or the magnitude of ST segment depression. However, it significantly increases exercise tolerance, most likely due to improved peripheral vasomotion. These results may be of clinical and therapeutic importance.

Effects of antioxidant vitamins C and E on signal-averaged electrocardiogram in acute myocardial infarction

Experimental studies indicate that oxygen-free radicals contribute to ischemic myocardial damage and affect electric properties of cellular membranes. We hypothesize that an association exists between an oxygen-free radical-induced component of myocardial ischemic injury and altered electric function that underlies the genesis of ventricular late potentials in the course of myocardial infarction. If so, antioxidant vitamins C and E may prevent alterations in the signal-averaged electrocardiogram (SAECG). To test this hypothesis, we investigated the effect of supplementation with vitamins C and E on the indices of the SAECG in patients with acute myocardial infarction (AMI). Sixty-one patients with AMI were randomized to receive conventional treatment and vitamins C and E, each 600 mg/day, orally for 14 days (supplemented group, n = 33) or conventional treatment only (control group, n = 28). SAECG was recorded on days 1 or 2 and between days 9 and 13 (mean 10). Serum ascorbic acid, tocopherol, plasma lipid peroxides, and oxygen-free radical production by isolated leukocytes were measured on days 1 or 2 and between days 12 and 14. In the control group, SAECG showed an increase in mean QRS and low-amplitude ( < 40 microV) signal durations, from 99 +/- 10 to 111 +/- 13 ms (p < 0.001) and from 31 +/- 8 to 38 +/- 10 ms (p < 0.001), respectively, and a decrease in the root-mean-square voltage of the last 40 ms of the QRS complex, from 36 +/- 25 to 21 +/- 11 microV (p < 0.002). In vitamin-supplemented patients, all these indices remained unchanged. Oxygen-free radical production by isolated leukocytes was decreased compared with that in controls (p < 0.02). Supplementation was confirmed by elevation of serum ascorbic acid and tocopherol. Results support the hypothesis that in patients with AMI, oxygen-free radical-induced cellular damage contributes to alterations in electric function of the heart as seen on the SAECG.

Increase of R-wave in pre-discharge ergometric test after myocardial infarction indicates advanced left ventricular injury, latent serious arrhythmias and worse prognosis

Changes in R-wave amplitude during exercise tests performed soon after myocardial infarction (15-31 days, mean 22) were analyzed in 78 men in relation to left ventricular injury (determined by 2-D echocardiography), ventricular arrhythmias (24-h Holter monitoring) and survival after myocardial infarction. It has been found that in patients with mild left ventricular injury (n = 51, Heger index < or = 3) the sum of the R-wave amplitude in 15 precordial leads recorded immediately after exercise decreased by 3.7 +/- 10% in comparison with resting values. In the patients with major left ventricular injury (n = 26, Heger Index > 3) the sum of R-wave amplitude after exercise increased by 12.9 +/- 17.5% (P < 0.001). Positive linear correlation (r = 0.35, P < 0.01) was observed between the level of left ventricular wall motion disturbances and R-wave amplitude changes. In patients with normal or slightly disturbed cardiac rhythm (n = 42, Lown scale 0-2) the sum of the R-wave amplitude after exercise decreased by 5 +/- 18% as compared to resting values, whereas in the patients with complex arrhythmias (n = 23, Lown scale 3-5) the sum of R-wave amplitude increased amounting to 9.9 +/- 17% (P < 0.001). Out of 17 patients who died during 5-year follow up, 16 displayed an increase or no change of the sum of R-wave amplitude. The same kind of relations between R-wave amplitude changes and left ventricular injury or cardiac arrhythmias were noted in patients with anterior and inferior myocardial infarction.(ABSTRACT TRUNCATED AT 250 WORDS)