Search

Background: Intravenous ferric carboxymaltose has been shown to improve symptoms and quality of life in patients with chronic heart failure and iron deficiency. We aimed to evaluate the effect of ferric carboxymaltose, compared with placebo, on outcomes in patients who were stabilised after an episode of acute heart failure. Methods: AFFIRM-AHF was a multicentre, double-blind, randomised trial done at 121 sites in Europe, South America, and Singapore. Eligible patients were aged 18 years or older, were hospitalised for acute heart failure with concomitant iron deficiency (defined as ferritin

Introduction Arrhythmias and conduction disorders are common among patients with scleroderma. Their early identification is important, since scleroderma patients with arrhythmias have a higher mortality risk compared with scleroderma patients without arrhythmias. The aim of this study was to characterize the cardiovascular profiles of scleroderma patients with different types of arrhythmias and conduction disorders. Methods One hundred and ten consecutive patients with a diagnosis of systemic sclerosis according to the ACR criteria were included in the study. Patients underwent a 12-lead ECG and a 24-hour Holter ECG monitoring for arrhythmias and conduction disorders identification. Blood sample testing, echocardiography, spirometry, chest X-ray and, when considered appropriate, high resolution chest CT were also performed. A subgroup of 21 patients underwent NT-pro BNP level measurements. Patients’ clinical and para-clinical characteristics were compared according to the presence or absence of arrhythmias and conduction disorders. Results The prevalence of arrhythmia and conduction disturbances was 60.9%. Patients with such disorders were older (54.4 ± 13.3 vs. 49.7 ± 10.1 years, p=0.05), had a higher prevalence of pulmonary hypertension (p=0.008), valve disease (p < 0.001), especially mitral and tricuspid regurgitation, chamber enlargement on echocardiography (left atrial and right ventricular, p = 0.012 and 0.005, respectively) as well as higher NT-pro BNP levels: 265.5 ± 399.7 vs. 163 ± 264.3 pg/ml, p=0.04. Conclusion Arrhythmias and conduction disorders are common in patients with scleroderma. Patients with such disorders are older, have a higher prevalence of pulmonary hypertension, more severe mitral and tricuspid regurgitation, left atrial and right ventricular dilation on echocardiography.

Background & objectives: Secretory phospholipase A2 (sPLA2), a member of the phospholipase A2 superfamily of enzymes that hydrolyses phospholipids, is a potentially useful plasma biomarker for atherosclerotic cardiovascular disease. Cardiovascular diseases are the leading cause of mortality in women. The purpose of this study was to investigate the correlation between cardiovascular risk factors and the sPLA2 levels in women with metabolic syndrome as compared to women without metabolic syndrome and men with metabolic syndrome. Methods: Patients (n=100) with various cardiovascular risk factors consecutively evaluated at the Rehabilitation Hospital-Cardiology Department, Cluj-Napoca, Romania were enrolled during 2011, of whom 10 were excluded. The patients were divided in three groups: group 1 (37 women with metabolic syndrome), group 2 (27 men with metabolic syndrome), and group 3 (26 women without metabolic syndrome). Body weight, smoking habits, glycaemia, hypertension, and serum lipids fractions were analysed as cardiovascular factors. Serum sPLA2 activity was measured using the chromogenic method. Results: There were no statistically significant correlations between sPLA2 levels and the investigated risk factors, irrespective of patient groups. However, there were significant positive correlations between sPLA2 and hsCRP in all three groups (P

Cavo-tricuspid isthmus radiofrequency (RF) ablation is an efficient option in the treatment of atrial flutter. In the case of a well-tolerated, first episode of atrial flutter, it has a class II indication, level of evidence B, the current first-line therapeutic option being electrical cardioversion, pharmacological cardioversion or atrial overdrive pacing followed by long-term antiarrhythmic therapy. The purpose of this study was to evaluate, in a prospective manner, the recurrence rate of these two different therapeutic options after the treatment of a first episode of atrial flutter.Between January 2007 and May 2009, for 99 patients admitted to the hospital for a first episode of atrial flutter, cardioversion was attempted either by RF ablation (group 1-42 patients), or by electrical cardioversion, pharmacological cardioversion or atrial overdrive pacing followed by long-term Amiodarone therapy (group 21-57 patients). We compared the recurrence rate of atrial flutter in the 2 groups after a follow-up period of one year.In group 1, sinus rhythm was achieved in all patients, with bidirectional isthmic block being obtained for 37 patients (88.1%). In group 2, conversion to sinus rhythm was obtained in all cases. The recurrence rate was 6 times higher in group 2 vs group 1 (57.9% = 33 patients vs 9.5% = 4 patients) (p = 0.01).RF ablation should be considered as a therapeutic option in the treatment of the first episode of atrial flutter, due to its significant efficiency in maintaining sinus rhythm and to its low recurrence rate.

There are many controversial concerning the role of alcohol in these diseases.The aim of the study is to underline some of the risks and benefits of alcohol consumption in cardiovascular system, using Holtter ECG and measuring the levels of some blood constants. The study was conducted of 200 individuals of urban and rural areas of Iasi county (100 being alcohol consumers), during the 2006-2008.The cardiac arrhythmias are more frequent in rural alcoholic women, and the diastolic disturbances in drinkers. Prevalence of myocardial infarction is higher in urban non-alcoholic men.Even there are some benefits, the alcohol consumption still remain a risk factor for cardiovascular diseases. A clearer conclusion can be made if the daily alcohol intake is precisely evaluated, knowing that the patients' personal appreciation of alcohol dozes could be an error factor for the study.

Adiponectin is decreased and leptin increased in overweight subjects. In turn, exercise has controversial effect upon adiponectin and leptin plasmatic levels.To study the effect of acute exercise upon plasmatic levels of adiponectin and leptin in normal and overweight subjects.We studied 79 subjects, 42 males and 37 females, aged 56 +/- 9 years, divided into two groups. Group I consisted of 19 patients with body mass index (BMI)25 kg/(m)2 and group II consisted of 60 overweight subjects (BMI25 kg/(m)2). All subjects were submitted to a maximal symptom limited exercise stress testing on cycloergometer, upon classical protocols (mean effort 103 +/- 27 Ws). Venous blood samples were obtained before exercise (sample I) and at 30 minutes after the effort was stopped (sample II); adiponectin and leptin levels were determined, using ELISA method.At rest adiponectin is significantly decreased and leptin increased in overweight subjects. In turn, during exercise the values of the two adipokines were not significantly different from those registered at rest in both groups, even if the adiponectin remained at a low level and leptin decreased at the limit of significance in overweight subjects. Considering men and women, the data are similar for men but, after exercise, overweight women registered a significant reduction of the leptin values. Also at rest adiponectin levels are more increased in overweight women (p = 0.01). This suggests that overweight women can be protected in comparison with men and exercise could add a supplementary benefice.Acute exercise has little effect upon adiponectin and leptin levels, but rest adiponectin is increased and leptin significantly decreased during exercise in overweight women and could be beneficial to this category of subjects.

The best evaluation of the severity and prognosis of heart failure patients is obtained by the maximal exercise stress testing, but for the very large number of HF patients and for evaluation of their daily effort capacity submaximal stress testing, mainly 6 minutes walking test are used. The limit of 6mWT is that during it the patients are not motivated to walk and also, the periphery, so important for heart failure patients, is not equally involved.To compare a new fixed walking test-400m walking test with 6MWT and maximal exercise testing.There were investigated 20 patients with dilated cardiomyopathy (DCM). The patients were included in the study after the relief of the congestive syndrome. Each patient was submitted in three consecutive days to a maximal symptom-limited exercise stress test on cycloergometer, a six minutes walking test, a 400 meters walking test. The last one consisted of walking on a corridor 40 meters long, at a speed chosen by the patient himself. The results were expressed in seconds representing the necessary time to cover the established 400 meters of distance.During cycloergometer exercise stress test the calculated mean peak VO2 was 15.2 +/- 1.4 mlO2/kg/min (4.32 METs). The mean distance walked during 6MWT was 350 +/- 34m and the mean time needed to walk 400m (400mWT) was 300 +/- 27 seconds. The correlation between peak VO2 and distance walked during 6MWT was -0.40, a similar but negative value (r = -0.42) being registered between peak VO2 and time registered during 400mWT. Only weak correlation was registered between LVEF and all the three tests. In turn the correlation between distance registered during 6MWT and time registered during 400mWT was excellent: r = -0.60.400mWT is a useful tool for the evaluation of submaximal effort capacity of CHF patients. Its value to evaluate exercise capacity is similar with that of the 6 MWT, but 400mWT can assure a better evaluation of peripheral involvement.

It is very well known that in clinical practice, according to the published guidelines, the heart failure patients are undertreated. There are striking differences in applying the guidelines in various countries and, up to the present, there are no consistent data for Romania.There were studied 459 heart failure patients admitted in the Cardiology Department of a general hospital in Cluj-Napoca, Romania. They were evaluated from the point of view of the drugs used during hospitalization and recommended to be taken after discharge.The patients, 393 males and 66 females, aged 61+9 years (lower in comparison with other countries) were included in NYHA III and IV class, except 3%, in NYHA II class. The ischemic etiology was registered in 56% of the patients. Drug treatment was as follows: diuretics--86.98%, ACEI--77.77%, beta blockers--55.95, ARB's--7%, digoxin--51.63%, aldosterone antagonists--49%, nitrates--61.28%, statins--24%, antithrombotic therapy--60% (antiplatelet--45.75%, anticoagulants--28.5%), antiarrythmics--27.91% (mainly amiodarone). In comparison with other European countries, the use of RAAS antagonists is similar, there are more beta blockers and nitrates used, but there is less use of antithrombotic therapy (especially anticoagulation) and of statins.Even though Romania still belongs to the group of developing countries, the drug treatment of heart failure patients does not much differ from the treatment applied in developed countries.

Brain natriuretic peptide (BNP) is a sensitive and specific marker of left ventricular (LV) function. The acute effect of beta blockers upon plasma BNP levels in CHF patients has been less studied but it is important because of the initial possible depressing effect upon LV function.To investigate the acute effect of oral Metoprolol upon plasma proBNP levels in CHF patients.There were included 56 patients with congestive heart failure, 38 with ischemic heart disease and 18 with idiopathic dilated cardiomyopathy, 40 males and 16 females, aged between 25 and 65 years, who were compared with 19 healthy individuals, 12 males and 7 females, of the same age. All patients were free of beta blockers treatment. Plasma Nt-proBNP was determined in fasting state using ELISA method (NV250 fmol/mL). After this, every patient received 50 mg Metoprolol succinate and at three hours (considered as peak plasmatic concentration) venous blood samples were again obtained and Nt-proBNP determined.NT-pro BNP was increased (1400 +/- 130 fmol/mL) in heart failure patients and normal (187 +/- 17.2 fmol/mL) in healthy controls. After Metoprolol the plasmatic level of NT-proBNP was not significantly different in both healthy controls (162 +/- 13.3 fmol/mL) and heart failure patients (1419 +/- 133 fmol/ml) in comparison with baseline values. After Metoprolol NT-proBNP decreased (from 1266 +/- 121 to 1120 +/- 107, p0.05) in III NYHA class patients and increased (from 1457 +/- 142 to 1530 +/- 150, p0.05) in IV NYHA class patients. It remained unchanged in patients with LVEF30% (1384 +/- 140 vs 1389 +/- 129 fmol/mL) and increased (from 1480 +/- 134 to 1690 +/- 161 fmol/mL, p0.05) in patients with LVEF30%; it was not significantly modified in patients with atrial fibrillation in comparison with those in sinus rhythm (1348 +/- 132 vs 1516 +/- 168 fmol/mL).Beta blockers do not have a severe depressant effect on left ventricular performance in all patients with systolic heart failure. A LVEF30% suggests, but the lack of modification of NT-proBNP levels after administration of 50 mg Metoprolol confirm, that the beta blocking treatment can be initiated with higher doses than those recommended until now.

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.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 aged55 years with cardiovascular disease (68.1% of them with IHD). The study was carried out using general practitioner's files.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 (p0.05), ACEI in 69.1% and 79.8 % (p0.05), beta blockers in 69.1% and 74.3 % (p0.05) and statins in 48.9% and 48.6% (p0.05). 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 p0.05, PCI 5.3% in women and 13.8% in men p0.05.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.

Several studies showed that elevated plasma levels of lipoprotein(a) [Lp(a)] represent a predictor for cardiovascular risk. Based on already existing literature data, we aim to study the relationship between Lp(a), lipids and other cardiovascular risk factors in individuals with or without coronary heart disease.We performed a cross-sectional transversal study on 208 patients (100 men and 108 women) aged between 37-75, with or without old myocardial infarction. In all the patients were evaluated the cardiovascular risk factors, the plasma level of the lipid fractions and Lp(a). The relationship between Lp(a) and the lipid and non-lipid risk factors were evaluated by the logistic regression method.The myocardial infarction group had higher values of plasma levels of Lp(a) (0.37 +/- 0.28 vs. 0.29 +/- 0.23 g/L, p0.05), and LDL-C (125.66 +/- 41.21 vs. 113.44 +/- 46.64 mg/dL, p0.05), than the group without coronary heart disease, as well as higher values of plasmatic TC/HDL-C ratio (4.31 +/- 1.55 vs. 4.08 +/- 1.29, p0.05), with significantly decreased plasmatic levels of HDL-C (45.88 +/- 12.04 vs. 53.22 +/- 23.12 mg/dL, p0.05). The association between the high Lp(a) plasma levels and the severity of coronary vessels number involved was significant. Multivariate analysis performed with adjustments for cardiovascular risk factors showed that the Lp(a), LDL-C and CT/HDL-C ratio levels are significant and independent predictive markers of coronary heart disease.The results show that the high Lp(a) plasma levels represent an independent cardiovascular risk factor, with superior risk prediction than the conventional lipid fractions. Our results confirm the Lp(a) as a marker for cardiovascular risk assessment in clinical practice.

Cardiac peptides are increased at rest in heart failure patients representing a useful diagnostic tool for this condition. Recently it has been demonstrated that cardiac peptides increase also during myocardial ischemia. Cardiac peptides increase during exercise in heart failure patients, but it has not been established yet if the increase is the same in ischemic and nonischemic patients.There were studied 50 heart failure patients, 32 ischemic and 18 nonischemic, 35 males and 15 females aged 61.8 +/- 11.61 after the relief of congestive syndrome, which was submitted to a symptom-limited exercise stress test on a cycloergometer. Blood samples were obtained at rest and at a peak effort and the plasmatic values of NT-proBNP (NV250 fmoles/mL) and of NT-proANP (NV1950 fmoles/mL) were determined using the ELISA method.At rest, both NT-proBNP and NT-proANP were more increased in nonischemic (1104.33 +/- 730; 3275.55 +/- 3424) than in ischemic patients (685.68 +/- 452.01, 2265.0 +/- 2552.32) with significant differences only for NT-proBNP (p=0.016). During exercise NT-proBNP increase from 836.40 +/- 596.34 to 1403.92 +/- 2126.21 and NT-proANP from 2628.80 +/- 2903.41 to 3701.30 +/- 3237.76, the final values being again more increased in nonischemic patients (NT-proBNP-2945.44 +/- 3257.89; NT-proANP-3174 +/- 2905); for NT-proBNP p0.05. The results suggest that the stretching effect during exercise is more increased at the ventricular level in comparison with the atrial level (67% increase for NT-proBNP and only 40% for NT-proANP). Surprisingly, myocardial ischemia does not increase additionally cardiac peptides either at rest or during exercise. Our data suggest that the intracardiac pressure is more important than ischemia in determining the increase of cardiac peptides in heart failure patients because the left ventricular ejection fraction was lower in nonischemic patients (40.03 +/- 5.5 vs 38.11 +/- 4.07).Cardiac peptides are increased, both at rest and during exercise, in nonischemic heart failure patients in comparison with ischemic ones, probably in relationship with the lower left ventricular systolic function.

The angiotensin converting enzyme (ACE) I/D polymorphism influences the plasmatic ACE levels, the highest being registered in the DD form. Similarly, the DD genotype is frequently associated with a CC homozygote genotype of the AT1 receptors. The polymorphism was studied mainly in hypertensive patients.To investigate the genetic polymorphism of renin angiotensin aldosterone system (RAAS) in patients with heart failure as a possible factor in determining the degree of the RAAS activation.The study included 36 NYHA III and IV class heart failure patients, 20 males and 16 females, aged 71.03 +/- 9.52 years. The distribution of ACE gene insertion, deletion (I/D) and AT1 receptors Al166C gene polymorphism were determined. Analyses of ACE and AT1 receptors genotypes were performed by polymerase chain reaction (PCR).The distribution of genetic ACE polymorphism was: D/D-47.22% (17 p); I/D-22.22% (8 p); I/I-30.55% (11 p). The identified AT1 receptors genotypes were as follows: AA-50% (18 p); AC-41.66% (15 p), CC-8.33% (3p). The two types of genetic polymorphism were associated in both the 20 hypertensive patients: DD+AA-35% (7 p); DD+AC -25% (5 p); DD+CC-10% (2 p) and the 16 patients without hypertension: DD+AA-6.25% (lp); DD + AC-18.75% (3p). LEVF was40% in 10 patients, 40% of them presenting pathogenetic polymorphism (DD+AC or DD+CC.Heart failure patients frequently present combinations of genetic polymorphism of RAAS probably involved in the development of neurohormonal pathogenic mechanism of the disease. This combination may be independent by the association with hypertension, and also in relationship with low ejection fraction.

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.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 (nv3 pg/ml) and serum lipid fractions were determined in each patient and the prevalence of anemia (Htor = 41% in men; Htor = 38% in women) was established. Left ventricular ejection fraction (LVEF) was determined by using 2D echo.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); p0.05. 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 LVEF40% (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.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.

To investigate if apoB, apoA-I and apoB/apoA-I ratios are independent risk factors for coronary heart disease and to determine their value in relationship with serum lipid fractions in evaluating the risk of coronary events.We carried out a comparative observational study on 289 subjects divided into two groups: 144 subjects with old myocardial infarction, and 145 subjects without coronary heart disease, but with cardiovascular risk factors. None of the subjects received lipid-lowering drugs in the previous 3 months.The mean values of lipid fractions were lower in subjects with myocardial infarction than in subjects without coronary heart disease: total cholesterol (186.06 +/- 48.11 vs. 206.93 +/- 42.28 mg/dl, p = 0.0001), LDL-cholesterol (118.57 +/- 42.95 vs. 129.53 +/- 39.75 mg/dl, p = 0.023), HDL-cholesterol (43.64 +/- 12.32 vs. 50.48 +/- 21.09 mg/dl, p = 0.0008) and triglycerides (145.38 +/- 62.74 vs. 167.56 +/- 82.11 mg/dl, p = 0.01). The plasmatic levels of apoB were higher in subjects with myocardial infarction (1.12 +/- 0.57 vs. 0.86 +/- 0.27 g/l, p = 0.0001), but the apoA-I was lower (1.31 +/- 0.47 vs. 1.40 +/- 0.39 g/l, p = 0.101). The multivariate analysis indicated that plasmatic concentrations of apoB over 1.7 g/l are closely correlated with myocardial infarction (OR 3.96; 95% CI 2.87-5.02, p = 0.001) independent of other covariables such as age, smoking, diabetes, hypertension, lipid CT/HDL-C and the LDL-C/HDL-C ratio. The protective effect of apolipoprotein A1 against cardiovascular events after the adjustment for other cardiovascular risk factors (OR 0.72; 95% CI 0.57-0.83, p = 0.004) was also independent in multivariate analysis.These results highlight the significance of apoA-I and apoB in the evaluation of the cardiovascular risk. From this point of view, their predictive value is superior to that of serum lipid fractions. The data suggest that the determination of apoA-I and apoB is useful enough to be introduced in current clinical practice.

Both heart variability (HRV) and heart rate recovery (HRR) after exercise are considered to reflect the sympathetic-vagal balance and low values of them have negative prognostic significance, especially in ischemic patients. The main goal of the research was to establish if there is a correlation between HRR and HRV in ischemic patients and if interchangeability between them is possible. There were studied 63 patients with ischemic heart disease: old myocardial infarction, stable angina. unstable angina and silent ischemia. All patients performed exercise stress testing, the heart rate recovery being calculated as the difference between peak heart rate and the rate determined at one minute after the exercise was stopped. The "time-domain" HRV parameters SDANN, SDNN, RMSSD were automatically calculated during a 24 hours Holter ECG monitoring. The mean values were HRR: 39.24 +/- 17.47 beats/min (abnormal in 6% of the patients); HRV: SDNN-112.75 +/- 37.87 msec, SDANN-103.02 +/- 33.25 msec, RMSSD-50.21 +/- 48.15 msec (low HRV in 68.3% of the patients). There was no significant correlation between HRR and HRV's parameters (p0.05). There was no significant difference between HRR's mean in subjects with normal or abnormal values of HRV parameters (p0.05). Thus, in our study, the HRV values cannot be predicted by the determination of HRR, HRV parameters being more sensible than HRR to reveal increased sympathetic drive.

With the development of modern civilization and with continuous changing of job characteristics, occupational stress becomes increasingly important. Physicians are an exposed category and they are prone to develop stress-related disease and risk behaviors.We conduct a study among 118 physicians. The Romanian version of Job Content Questionnaire was mailed to all the subjects. We investigate the main scales of JCQ: decision latitude (DL), psychological job demands (PJD) and social support (SoS), along with the prevalence of risk behaviors, depression and sleeping problems.The final response rate was 112 (94.9%). The differences between women and men are significant for psychological demands (36.55 versus 32.9, P0.01), decision latitude (73.83 versus 67.05) and skill discretion (36.47 versus 34.6). Age positively correlated with SD (r = 0.40), DA (r = 0.40) and PJD (r = 0.29) in women and negatively with CoS (r = -0.39) in men. PJD negatively correlated with SS (r = -0.5) and CoS (r = -0.28) in women and with CoS (r = -0.54) in men. Smoking (32% women and 56% men) and sedentary behavior (over 60% women and men) positively correlated with PJD and negatively with social support in both men and women.The issue of professional stress is very important in modern medicine. Age and gender can be determinants of job strain, but also of job characteristics. Many studies have shown positive relations between job strain, and some harmful habits such as tobacco smoking and sedentary lifestyle; we have to outline again the importance of organizational factors in managing both stress and satisfaction at workplace.

The research considers the hypothesis that stressful professions, such as engine driver, influence the morbidity and mortality through cardiovascular diseases and favour some harmful habits with an impact upon cardiovascular morbidity.There were selected for study 496 engine drivers, males, and a control group of 305 males. They were questioned about: name, address, family history, pathological personal history, alcohol intake, smoking, diet habits, physical activity, sleeping hours and stress perception. There were measured: height, weight, blood pressure. There were determined: fasting plasma glucose, cholesterol, triglycerides, HDL-cholesterol and LDL-cholesterol.Hypertension was registered in 23.5% of the engine drivers and in only 9.5% the control group (P0.05). Dyslipidemia was noted in 57.4% of the engine drivers and 52.45% of the control group. Prevalence of smoking and overweight was higher in the control group. Unhealthy dietary patterns and physical inactivity were present in both groups, the circadian rhythms were altered only for engine drivers and questionnaires for stress perception showed higher irritability in the control group.The prevalence of some risk factors is higher for engine drivers, but for the others it is not. Also it seems that professional stress favours some harmful habits such as tobacco smoking, but the control group smokes more and they are inactive individuals with a great amount of irritability. The results do not totally sustain the idea we started from, that engine driver is a stressful profession; it seems that the effort/reward imbalance is more important than job-demand itself.

Several studies suggested the role of the genes of the rennin-angiotensin system in the pathogenesis of essential arterial hypertension.We investigated 100 consecutive hypertensive patients (42 males and 58 females; mean +/- SD age, 55.14 +/- 9.49 years) for M235T and T174M polymorphisms. Seventy six normotensive patients (28 males and 48 females; mean +/- SD age, 54.94 +/- 9.56 years) formed the control group.M235T and T174M polymorphisms were analyzed using PCR-RFLP methods.The carrier frequency of M235T polymorphism in the AGT gene was 73% in hypertensive patients and 34.21% in normotensive patients (OR 5.2, 95%CI [2.72-9.93], p0.01, chi2 test). The carrier frequency of T174M polymorphism in the AGT gene was 42% in hypertensive patients and 11.84% in normotensive patients (OR 5.39, 95%CI [2.41-12.01], p0.01, chi2 test).Essential arterial hypertension is associated with polymorphisms in the AGT gene, M235T and T174M.

It is not well known what should be the benefits of a prolonged physical rehabilitation program after an acute myocardial infarction.Our study is an open, randomized comparison of a long-term versus a standard rehabilitation program. Sixty-seven patients with acute myocardial infarction were included in an outpatient physical rehabilitation program of 6-8 weeks. Of these, 22 randomly selected patients continued the program until the 36th month (Group A). Twenty-five of the others were rechecked after 36 months, and represented the controls (Group B). For both groups, at the end of this period, a cycloergometer exercise test evaluated the exercise capacity of subjects and an echocardiogram was performed to determine left ventricular systolic and diastolic function.The maximal exercise capacity increased from 147 +/- 13.8 W to 178 +/- 16.4 W in Group A (p0.01), but it decreased from 144 +/- 13.2 to 132 +/- 12.8 W in group B. Functional aerobic impairment decreased from 29 +/- 2.7% to 22 +/- 2.1% in Group A, but it increased from 26 +/- 2.5% to 37 +/- 3.8% in Group B. The ejection fraction and diastolic function parameters were not significantly modified during the 36 months, for both groups.Long-term physical rehabilitation is useful in patients after an acute myocardial infarction to increase effort capacity, but left ventricular performance is not significantly changed.

Ischemic preconditioning is generally a short duration phenomenon, but during acute myocardial infarction a better inhospital outcome of patients with previous angina suggests that the effect of ischemic preconditioning could be longer than it was considered until now. It was also demonstrated that during successive exercise stress testings (ET) ST depression became lesser as a consequence of ischemic preconditioning. We investigated the possible occurrence of ischemic preconditioning during rehabilitation of ischemic patients. There were studied 43p with old myocardial infarction or stable effort angina, 29 men and 14 women, aged 33-68 years, divided in two groups: group I (19p) was included in a cardiac rehabilitation programme (15-20 sessions) and group II (24p) was not. All the patients were submitted to two ET at a month interval, for group I before and after cardiac rehabilitation programme. The peak-effort level was significantly greater for group I (80.26 +/- 7.2w vs 93.42 +/- 8.3w p0.05) but not for group II (65.5 +/- 5.8w vs 72.91 +/- 6.5w p0.05) during the two ET. The double product (21.573 +/- 3122 vs 24.168 +/- 3423 for group I and 23.551 +/- 3100 vs 21.000 +/- 2752 for group II) was not significantly different (p0.05) during the two ET. The same unsignificant modification was noted for maximal ST depression for group II (1.458 +/- 0.32 vs 1.166 +/- 0.21 mm p0.05) but not for group I patients in which maximal ST depression during the second ET was significantly less than during the first ET (1.52 +/- 0.23 vs 0.736 +/- 0.12 mm p0.05). Because cardiac rehabilitation does not influence the ischemic threshold and because the lesser maximal ST depression during the second ET was noted at the same, or even greater, double product (MVO2), we consider that it can be attributed to ischemic preconditioning.

We studied the relationship between Chlamydia pneumoniae antibodies, C-reactive protein (CRP) and interleukine 8 (IL-8) in 87 patients with ischemic heart disease: 29 patients with acute myocardial infarction, 18 patients with unstable angina pectoris and 40 patients with stable effort angina. We determined in all patients IgG and IgA antibodies to Chlamydia pneumoniae, CRP and IL-8. Species specific antibodies to Chlamydia pneumoniae (IgG and IgA) were detected by indirect ELISA technique (Savyon Diagnostics Ltd, Israel). Interleukine-8 measured by a commercially available ELISA kit (CLB, Amsterdam, The Netherlands). CRP was determined by radial immunodiffusion (Mancini). The IgG antibodies were present in 25 patients (29%), the greatest percentage being noted in patients with unstable angina pectoris (50%). The IgA antibodies were present, as a sign of chronic Chlamydia pneumoniae infection, in 56% of the patients with IgG antibodies. CRP was positive in 52% of the 25 patients with positive IgG antibodies, but in only 34% of the 62 patients without IgG antibodies (p0.01). IL-8 was positive in 12% of the patients with IgG antibodies, and in 21% of the patients without IgG antibodies but the difference is not significant (p0.05). It is concluded that there is a relationship between the presence of the Chlamydia pneumoniae infection and inflammatory reaction in patients with ischemic heart disease, but the neutrophils are not implied in this process.

The statins have a moderate lowering effect upon triglycerides, one hypothesis suggesting an inhibitory effect upon liver VLDL synthesis. Because VLDL synthesis is related to other hepatic protein synthesis we studied the effect of Simvastatin upon serum cholinesterase activity and factor VII activity, which are also synthetized at hepatic level.39 patients with ischaemic heart disease, proved by coronarography and moderate hypercholesterolaemia received for two months 20 mg Simvastatin (Zocor). The value of total Co, LDLCo, HDLCo, triglycerides, serum cholinesterase activity and factor VII activity were determined before and after treatment, by standard methods.Triglycerides were, together with total Co, significantly lowered during the two months treatment with Simvastatin, but the values of serum cholinesterase and factor VII activity were not significantly modified. This suggests that moderate doses of Simvastatin do not depress liver protein synthesis.Simvastatin does not lower the triglycerides level through depression of liver protein syntesis, other mechanisms being probably involved.

Animal studies show that nitric oxide is involved in delayed ischaemic preconditioning.To determine whether plasma nitrates/nitrites (NOx-, as measure of nitric oxide) are modified by two consecutive effort tests and whether these changes translate into clinical improvement.There were studied 22 patients with ischemic heart disease, who performed two effort tests at 24-hour interval. Plasma NOx- level was determined and compared before and after both stress tests. Peak effort, double product at peak effort and maximal ST segment depression were considered clinical end-points and were compared between the two tests.Plasma NOx- increased slightly after the first exercise test compared to pre-test value (17.05 +/- 1.6 vs. 15.38 +/- 1.4 micromol/ml). In turn, after the second test a significant rise of NOx- level (23.65 +/- 2.2 vs. 15.10 +/- 1.3 micromol/ml, p0.03) was noticed. The pre-test value was practically identical between the two tests. Peak effort and double product at peak effort remained unchanged between the two tests. Although the ischaemic stress was the same, ST depression was significantly lower (p0.01) at the second test (0.85 +/- 0.06 vs. 1.73 +/- 0.16 mm).Our study shows an increase of plasma NOx- level after the second of two consecutive exercise stress tests at 24 hour interval, along with a decrease of electrocardiographic consequences of approximately the same ischemic stress. These findings are consistent with experimental data in animals, which point to nitric oxide as both trigger and effector of ischaemic preconditioning.

It was suggested recently that ischemic preconditioning can occur in clinical practice. We investigated this hypothesis in 26 patients with old myocardial infarction (MI) or stable angina pectoris, subjected to two successive exercise testings at 1 hour interval. The ST depression was significantly lesser during the second exercise testing (1.83 +/- 0.12 mm, vs 1.02 +/- 0.14 mm p0.01) at the same double product (DP) (24.877 +/- 1206 vs 24.711 +/- 1152 p0.05) and peak effort (76.92 +/- 6.63 w vs 75.96 +/- 6.27 w p0.05). The improvement was attributed to ischemic preconditioning.

Recent studies suggested an improving of left ventricular (LV) systolic function during exercise training in patients with old myocardial infarction. Twenty patients with old myocardial infarction (3-6 weeks) were included in an exercise training programme (mainly cycloergometer) for 2 to 8 weeks. Before and after the exercise training programme, the effort capacity and LV systolic function were determined through exercise testing on cycloergometer and echocardiography. The peak effort raised from 4.39 to 5.27 METs (p0.05) and the difference DAF-DAM was reduced from 25% to 12% (p0.05). The double product (DP) at peak effort raised nonsignificantly (4.91%, p0.05), but at submaximal effort levels DP decreased significantly on each effort step (12.16%, p0.05). In turn, LV systolic function calculated parameters were practically the same before and after the exercise training programme. (EDD 54.3 vs 5.3 mm, ESD 39.3 vs 38 mm, EDV 160 vs 169 ml, ESV 60.6 vs 54.8 ml, EF 54.1% vs 57.8%, SF 27.6% vs 31.2%). It is concluded that exercise training raised the effort capacity in patients with old myocardial infarction, mainly through peripheral mechanisms, LV systolic function being unchanged. It is also important that exercise training have not any detrimental effect upon LV systolic function and consequently exercise training programmes can be applied and can be useful also in patients with old myocardial infarction and impaired LV systolic function.

Isometric effort increases the severity of mitral regurgitation (MR) by augmenting the afterload and the regurgitant fraction. The worsening of MR may be different in various patients and can explain the differences in effort capacity of patients with identical rest mitral regurgitation. We studied 25 patients with MR of various etiologies, submitted to handgrip (maximal voluntary contraction), the severity of MR being evaluated by the determination of regurgitant area (colour Doppler). There was a 42% increase of the regurgitant area from 3.26 to 4.66 cm2 (p0.05). The increase was greater for ischemic MR (59%) than for MR in dilated cardiomyopathy (26%), the last value not being explained by a lower EF because rest EF was similar in patients with and without an increase of MR severity during maximal voluntary contraction. The individual analysis of the results showed an increase of the MR severity in 1/2 of the patients, in whom the left atrial dimension was greater, though the effort capacity was the same in the two subsets of patients. It is concluded that colour Doppler is a simple and valuable method for studying the influence of isometric exercise upon MR severity, this being increased in 1/2 of the patients, with a positive correlation with ischemic etiology of the disease, left atrial dimension, but not with the patients' effort capacity.

Early cardiac involvement has been reported in type I diabetes mellitus. This study was undertaken to evaluate the relationship of systolic blood pressure (SBP), erythrocyte magnesium (MgE) and left ventricular diastolic function (LVDF). Forty-four patients with insulin-dependand diabetes (IDD) aged 26 to 31 years, without apparent cardiac complications 8.5 +/- 6 years after the onset of disease were studied. They were compared with 20 healthy subjects of the same age who comprised the control group. Left ventricular diastolic function was evaluated by isotopic technetium 9m ventriculography with a Gamma-Picker scintilation chamber, by determining maximum left ventricular filling velocities (I, VFmax). The MgF was measured by EDTA titrimetry. Patients were divided into two subgroups depending on the SBP: Group A (20 patients) with a mean SBP of 136 +/- 4.2 mmHf and Group B (24 patients) with a mean SBP of 118 +/- 4.4 mmHg; the control group had a mean SBP of 110 +/- 4.4 mmHg. The following results were obtained. [table: see text] The authors conclude that even small increases of SBP may, with a decrease in Mg, be a risk factor for early cardiac complications in IDD in young adults.

The efficacy of amiodarone for atrial fibrillation (AF) prophylaxis is well established, but the large doses used until recently may be harmful during long-term therapy, especially because of the pulmonary fibrosis it generates. Recently, similar good results have been reported in using low-dose amiodarone. We studied the prophylactic effect of long-term therapy of low-dose amiodarone (200 mg/day) in 26 patients with AF of various etiologies. During a period of six months to four years, 46% of patients were free of any arrhythmic attack. The paroxysmal attacks of AF continued in 35% of patients, but with a lower frequency. In 19% of patients AF became chronic during amiodarone therapy. The best results were registered in patients over sixty, with stable sinus rhythm in 75% of cases, probably in relation to the ischemic etiology of AF and the anti-ischemic associated effect of amiodarone. The stability of sinus rhythm was greater (50% vs 38%, p0.05) when the treatment with amiodarone was started within the first six months from the first AF attack. Our results supported the use of low-dose amiodarone as a first-line drug for the long-term prophylaxis of AF, mainly in older patients.

Doppler echography is now the most accurate noninvasive method for studying valvular prostheses, but the values considered to prove a normal function are still controversial. We studied by echo Doppler 95 valvular mechanical (M) and biological (B) prostheses, in mitral (Mi) and aortic (Ao) position in patients without clinical signs of prosthetic dysfunction. The data obtained for Ao prostheses (maximal transprosthetic gradient (MxG): M-20.47 mmHg, B-7.95 mmHg; mean transprosthetic gradient (MG): M-7.98 mmHg, B-3.9 mmHg) are in agreement or even better than literature data. For Mi prostheses the prosthetic area (PA) and pressure half time (PHT) values are in normal limits but the MG (M-5.087 mmHg, B-5.9 mmHg) is slightly superior to the data reported in the literature. Proving the value of echo Doppler for the study of valvular prostheses our results suggest to adopt larger limits of normality for mitral prostheses. They also sustain the necessity of a first Doppler examination before the patient is discharged from the hospital after valvular replacement.

The usefulness of physical rehabilitation in patients with valvular heart disease is now well established. But, mainly in mitral stenosis, the isometric exercises are under question, because of the risk of sudden rise in capillary pulmonary pressure. In order to clarify this aspect we have studied the effect of isometric exercise upon Doppler data in mitral stenosis.in 25 patients with mitral stenosis the Doppler indices of severity-mitral valve area (MVA), pressure half time (PHT), maximal velocity (MxV), mean pressure gradient (MPG)-were determined before and after 3-4 minutes of handgrip performed with a dynamometer at 30% of the maximal voluntary contraction (MVC). There are no significant differences of Doppler parameters before and during handgrip: MVA (1.56 +/- 0.30/1.49 +/- 0.53 cm2), PHT (171 +/- 72/150 +/- 58 ms) MPG (7.07 +/- 2.61/7.21 +/- 1.8 mmHg), MxV (2.186 +/- 0.79/2.276 +/- 0.73 m/s). The results suggest that mild isometric exercise does not alter hemodynamic parameters in mitral stenosis. Consequently isometric exercise can be included in physical programmes of rehabilitation for this category of patients.

The data concerning the relation between mitral valve area (MVA), estimated invasively or by 2 D-echo and effort capacity in mitral stenosis (MS) are still controversial. Consequently we have studied the same relation, using the Doppler indices.19 patients with MS were submitted to a Doppler examination--MVA, pressure half time (PHT), mean pressure gradient (MPG)--and to a symptoms limited exercise testing on cycloergometer--effort intensity (Watts, METs) functional aerobic impairment (FAI), myocardial aerobic impairment (MAI). The "r" correlation index between these parameters was calculated. The results show no significant correlation between Doppler estimated severity of mitral stenosis and the effort capacity of the patients, even if a weak negative correlation ("r" = - 0.32) is noted between effort intensity and MPG and a weak positive correlation ("r" = + 0.41) between FAI and PHT. The conclusion is that effort capacity of patients with mitral stenosis cannot predict the severity of the disease which is to be established through other methods.

Exercise testing (ET) and adenosine testing (AT) coupled with ECG were applied in 25 patients with old myocardial infarction. ET was positive in 8 (32%) and AT in 10 (40%) patients, the sensitivity of the latter being slightly superior to the former but inferior to the sensitivity reported in the literature for AT-echocardiography. One should also notice the positivity of AT-ECG in 6 (24%) patients, with negative or inconclusive ET, and the double product (DP) at ischemic threshold which was twice as low for AT-ECG as for ET-ECG, proving that AT induced ischemia by decreasing O2 myocardial input. It is concluded that AT-ECG is useful in myocardial ischemia detection in association with ET or in patients who cannot perform ET for different reasons.

A number of 21 patients with congestive heart failure (CHF) of various etiologies were studied. All patients were subjected to a classical exercise testing (ET) on cycloergometer. The ET was repeated 24 hrs later, 6 hrs after the administration of 2 mg Perindopril (Coversyl). No statistically significant differences in duration and intensity of ET before and after Perindopril were noted for the whole group. But in 9 patients (42.8%) at least one effort level was gained. In these patients the peak double product (DP) was similar before and after Perindopril, but at submaximal effort DP was, at each level, lesser after Perindopril, suggesting a mechanism of afterload reduction in the improvement of effort capacity.

The possibility of a depressed chronotropic response to exercise in old people as an early signs of sinus node disfunction, was studied in 118 subjects over 60 years (group A) and 25 subjects under 60 years (group B), subjected to a maximal, symptom limited, exercise test (ET) using a cycloergometer. There were no significant statistical differences between the two groups as regards the heart rate (HR) at rest, increase of HR at each effort level, and mean chronotropic impairment (Chl). The mean values were the same when the subjects over 65 years were considered separately (group C). But, when the chronotropic response to ET was studied individually, it was depressed (HR increment less than 15 beats/min at each level) in 22.3% of subjects in group A and only in 4% in group B. The depression was important (increment less than 10/min) in 15% of the subjects in group A and in none of those in group B. The results suggested that about 1/4 of the old people have depressed chronotropic response to exercise attributed by us to a subclinical sinus node disfunction.

Arm exercise test (AET) is described as an alternative to the classical leg exercise test (LET). The value of these two types of exercise was studied in a group of 32 patients aged 34 to 65 years. The patients performed LET for several reasons and, after 24 hrs, AET under the same conditions. The effort level reached under LET was always greater than that achieved under AET and the calculated functional aerobic impairment (FAI) was 50% greater during AET thus supporting the idea that AET cannot be used instead of LET in determining the functional capacity (NYHA) of cardiac patients. However, AET remains useful for the determination of the occupational working capacity in certain occupational categories. The double product (DP) (or index tension time (ITT) calculated after AET represented 85% of the calculated value after LET. The results proved that MVO2 is similar for both LET and AET, but in the latter at lower levels of exercise (VO2). The LET-DP was greater than the AET-DP in 66.5% of our cases, thus suggesting that AET should be reserved for situations in which LET cannot be performed. This is also supported by the presence of ST depression during AET in only 66% of the 18 subjects with ST depression during LET and in five of the six patients without ST depression, DP-AET was lower than DP-LET.

When compared to values obtained in 40 normalweight normolipemic healthy control subjects, serum uric acid levels were found to be significantly increased in 68 subjects with type II-b and especially in 68 subjects with type IV hyperlipoproteinemia. A much lesser increase of uricemia occurred in 22 patients with type II-a. A significant positive correlation between uricemia and serum triglyceride level could be demonstrated but no such correlation was found with serum cholesterol. Overweight and hypertensive hyperlipemic subjects were presenting higher levels of serum uric acid than normalweight normotensive ones. On the other hand, clinical atherosclerosis and diabetes mellitus had no additive effects upon uricemia in hyperlipoproteinemic patients. It is suggested that hyperinsulinism and accelerated turnover of lipoproteins, often encountered in obese and hypertriglyceridemic subjects, might lead to an enhanced synthesis of purines and subsequently increased production of uric acid.

Both gamma-glutamyltransferase (gammaGT) and pseudocholinesterase (PCE) were found to be increased in hypertriglyceridemic subjects. High values of gammaGT were noted in alcoholic subjects and especially in those with either increased serum triglyceride or alanine aminotransferase higher than 16 mU/ml, while PCE was not significantly changed in alcoholic subjects. Although both enzymes were strongly correlated with the logarithm of serum triglyceride and the prebeta electrophoretic fraction, there were striking differences concerning their behavior in various hypertriglyceridemic subjects. PCE activity was high even in moderate hypertriglyceridemias but its correlation with serum triglyceride had a tendency to flatten with increasing concentration of triglyceride. However, increase of gammaGT was rather characteristic for gross hypetriglyceridemia. Short-term, triglyceride-lowering therapy was accompanied by a tendency to normalization of gammaGT, while PCE values were not influenced. An attempt was made to interpret these changes of serum-enzyme activity in hypertriglyceridemia in connection with mechanisms of lipoprotein synthesis and with the pathogeny of hyperlipemic conditions.