{'fraction_non_alphanumeric': 0.03440278314650174, 'fraction_numerical': 0.030923850019327407, 'mean_word_length': 4.675438596491228, 'pattern_counts': {'":': 0, '<': 1, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Influence of risk factors on nitric oxide metabolites at the initial stage of juvenile acute myocardial infarction.

Few data are accessible about the nitric oxide (NO) stable end-products (nitrite/NO2 − and nitrate/NO3 − :N O x) in acute coronary syndromes. An increase in inducible NO synthase (iNOS) was found during experimental myocardial infarction [13] and this increase persisted for 2 weeks. In experimental models of acute myocardial infarction (AMI) other authors [2] observed a NOx increase, a correlation between NOx level and iNOS activity and an inhibitory action carried out by S-methylisothiourea, that is an iNOS inhibitor [5]. The NOx level was also measured in a small group of patients with myocardial infarction in whom the peak of NOx elevation occurred 2 and 3 days after the onset of symptoms, suggesting that the NOx increase was dependent on the macrophagical iNOS activation induced by cytokines [1]. Similar results were recently observed in large groups of patients with AMI [6,11]. Now we report the evaluation of the plasma NOx in a group of young patients with recent AMI, subdivided according to the number of main cardiovascular risk factors (RF). We enrolled 105 subjects (97 men and 8 women) aged <46 years; the mean age was 39.6 ± 5.5 years (range 19–45 years). The time interval between AMI onset and the NOx determination was 13 ± 7 days. Regarding the main risk factors, 83% were cigarette smokers or ex-smokers and 49% had family history of coronary artery disease; hypercholesterolemia was present in 51%, essential hypertension in 24% and diabetes mellitus in 12%. According to the number of cardiovascular RF we subdivided AMI subjects into three groups: 33 subjects had 0–1 RF, 35 had 2 RF and 37 had 3–5 RF. On fasting venous blood the NOx level was evaluated by a micromethod which measures the concentration of both NO metabolites (nitrite plus nitrate). At first nitrate was converted into nitrite by a nitrate reductase, then nitrite was measured by spectrophotometry after addition of the Griess reagent. The data were expressed as means ± SD. The statistical difference between normal controls and the subgroups of AMI subjects was examined using the one-way ANOVA model while the Bonferroni posttest was used to compare each pair of subgroups. The obtained results showed that in each subgroup of AMI subjects the mean value of NOx was increased in comparison with normal controls, in whom the NOx level was 24.38 ± 15.67 µM. The mean values of NOx were in fact respectively 57.11±24.75 µM in the subgroup with 0–1 RF, 63.76±31.93 µM