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Recent studies have proved close relations between cardiovascular and endocrinic systems. This relation has been observed in acromegaly, the disease connected with unrestrained secretion of growth hormone. The aim of the study was to assess Holter monitoring and echocardiography of acromegalic patients. The study group consisted of 28 acromegalic patients, including 15 patients with hypertension, was considered. As control groups we examined 20 patients with essential hypertension and 20 normotensive healthy subjects: All subjects underwent twenty-four hour Holter recordings, complete M-mode, two-dimentional and spectral Doppler echocardiography. Ventricular premature complexes occurred in 65% of acromegalic patients. Frequency and severity of ectopic beats were significantly increased compared to control groups. Left ventricular ejection fraction was considered to be normal, although significant decreased compared to healthy subjects. Left ventricular mass was above normal value in acromegalic patients--no significant difference was found between hypertensive and normotensive acromegalics. Doppler examination has shown the abnormalities of left and right ventricular filling in 89% of acromegalics. We have observed the correlations between left and right ventricular filling indices and the duration of the disease, and left ventricular mass. Left ventricular hypertrophy frequently occurs in acromegalic patients and this is not simply secondary to systemic hypertension. The prevalence of ventricular arrhythmias in acromegalic patients seems to be associated with left ventricular hypertrophy. Doppler examination suggests impaired left and right diastolic filling in patients with acromegaly.

Myocardial perfusion scintigraphy is a non-invasive method helpful for evaluating the coronary heart disease. Its use may be particularly indicated in cases of inconclusive ECG (i.e. in left bundle branch block, LBBB). On the other hand there are observations indicating the decreased accumulation of the radiotracer in the septal segments of myocardium in patients with left bundle branch block (LBBB). This phenomenon previously described for the thallium-201, recently was also reported in the MIBI 99mTc studies. Purpose of the present study were: (1) to check the frequency of the diminished uptake of the radiotracer (MIBI 99mTc) in the LBBB patients, and (2) to test its interference with the evaluation of the coronary heart disease.Our observation material included 42 patients in mean age 49 +/- 7 yr (26 women) divided into 3 groups: Group I--12 patients without intraventricular conduction disorders and with normal coronarography (the reference group), Group II--15 patients with LBBB and no signs of coronary artery disease in angiography and Group III--15 patients with LBBB and coronary artery disease confirmed by angiography. All patients underwent stress-rest perfusion scintigraphy according to a 2-days protocol. Submaximal bicycle exercise test was performed using the Bruce protocol. A single-head SPECT scintillation camera (DIACAM-Siemens) was used to acquire 64 views over 180 degrees. Acquisition was started 60-90 minutes after injection of MIBI 99mTc (800 MBq). After generating tomographic images their reorientation towards the left ventricle axes and creating the bull's eye polar maps were carried out with the aid of manufacturer's programs.The mean decrease of the radiotracer accumulation in the septal segment was similar in both groups of patients with LBBB (32.7 +/- 9.5 vs 28.5 +/- 8.6 in stress and 27.6 +/- 9.5 vs 27.5 +/- 7.9 in rest in groups II and III, respectively). It was, however, significantly less pronounced in the reference (I) group (the mean decrease being 17.7 +/- 4.7 or 16.9 +/- 5.5 in stress and rest studies, respectively). Distribution of MIBI 99mTc in the myocardium was more homogeneous in the reference group (the maximal differences of the radiotracer accumulation never exceeded 45%) than in the LBBB groups. In the group II defects of the maximal depth over 46% were observed in 9 patients (60%), and in the group C in 12 patients (80%). In 6 patients of the latter group maximal depth of decets exceeded 56% (value never found in group II).The diminished uptake of MIBI 99mTc in the septal segment of the left ventricle is a common phenomenon. In some cases it may interfere with the evaluation of the perfusion scintigraphic studies. The more pronounced defects, however, may be significant for the coronary artery disease.

The aim of this study was to estimate the results of tilt table testing in two groups of healthy adolescents--swimmers and control. Cardio-vascular reactions on tilting were determined by the measurements of heart rate (HR), systolic (SBP) and diastolic blood pressure (DBP). The study was carried out in accordance with the Polish Cardiac Society procedure. The positive tilt table testing results were observed in most young swimmers and in about thirty per cent of controls. The differences in the cardiovascular reactions were observed, too. The clinical interpretation and usefulness of these results must be established by future investigations.

Obesity is known to be a risk factor of cardiac death, that is associated first of all with cardiac arrhythmias. Increased QT dispersion (QTd) and ventricular late potentials (LP) are measurable indices of ventricular arrhythmias risk. The aim of this study is to asses QTd and LP in women with obesity. 62 obese women (mean BMI 36.7 kg/m2) and 15 apparently healthy subjects (mean BMI 24.5 kg/m2) were included in our study. QTd and correlated QT interval dispersion (QTdc) were calculated from 12-lead ECG. LVM were assessed from echocardiograms. LP were obtained by signal averaging of surface electrocardiograms.QTd, QTdc, LVM were significantly higher in patients. We found LP in six cases and higher QTdc in this subgroup. According to our research, increased QTd in obese women seems to be associated with left ventricular hypertrophy and increased QTd is significantly higher in subjects with LP.

Evidence for the role of chronic inflammation in atherogenesis has been well documented. Selectins mediate the first step in leukocyte adhesion and may contribute to the pathogenesis of stable and unstable angina.The study group consisted of 59 patients (pts) with coronary artery disease (CAD) documented coronarographically: 27 pts with stable exertional angina (group A), 32 pts with unstable angina (group B). 20 healthy persons were the control group (group C). Serum levels of E-selectin and P-selectin were measured by ELISA method both before and after the treadmill ECG stress test (ST) in groups A and C. In group B the measurements were carried out at 6, 24, and 48 hours following an episode of chest pain.There were no differences between the baseline serum levels of selectins as determined in groups A and C. In patients with stable angina, the post-ST concentrations of E-selectin were significantly higher (68.8 +/- 29 ng/ml) in comparison to both baseline (38.7 +/- 15 ng/ml), and group C-values (pre-ST: 35.1 +/- 16; post-ST: 49.9 +/- 15 ng/ml). In unstable patients, serum P-selectin levels were higher when compared to those found in groups A and C (group A: 142.3 +/- 24; group B: 190.1 +/- 99; group K: 136.4 +/- 33 ng/ml). No differences between selectins concentrations were observed at fixed times after an episode of chest pain.Soluble selectins levels in pts with stable angina are comparable to those of healthy persons. Significant increase of E-selectin concentration as induced by ST may reflect endothelial response to exercise. Patients with unstable angina had elevated levels of P-selectin, which seems to be associated with enhanced platelet and leukocyte activation. The serum levels of selectins may indirectly reflect clinical condition of pts with CAD.

The risk of sudden cardiac death is higher in patients with obesity, particularly in the upper body obesity. The most common cause of cardiac events are serious ventricular arrhythmias. Delayed cardiac repolarization leading to the prolongation of the QT interval is a well characterised precursor of arrhythmias. The QT interval dispersion reflects inhomogeneity of repolarization. The aim of this study was to assess QT interval dispersion (QTd) in obese women and to establish the relationship between obesity and QTd. 62 patients with obesity (group 1) and 15 apparently healthy women (group 2) were included in our study. Obese subjects were distinguished in accordance to the waist to hip ratio (WHR) into three subgroups: 1a--obese women with upper body obesity; 1b--obese women with WHR: 0.75-0.85; 1c--obese women with lower body obesity. A standard 12-lead ECG was performed in each subjects and QTd, QTdc (QT correlated interval dispersion), QTdR (QTd ratio) were calculated. The left ventricular mass (LVM) and left ventricular mass index (LVMI) were obtained from echocardiograms. We found QTd, QTdc, QTdR and LVM, LVMI to be significantly higher in obese women as well as positive correlation between BMI and both LVM, LVMI. QTdR was significantly higher in subgroup 1a compared with subgroup 1c.1) QT interval dispersion was increased in obese women compared with healthy subjects, 2) supposedly increased QTd was associated with the type of obesity.

TNF-alpha as a pleiotropic, proinflammatory cytokine seems to play a role in the pathogenesis of atherosclerosis and coronary artery disease (CAD). TNF-alpha is binding to two cell surface receptors and its serum activity is modified by soluble forms of these receptors: sTNF-R I and sTNF-R II. The aim of this study was to assess serum concentrations of TNF-alpha, sTNF-R I and sTNF-R II in patients (pts) with CAD. We examined serum concentrations of TNF-alpha, sTNF-R I and sTNF-R II by ELISA in: 45 pts with stable exertional angina (group I); 32 pts with unstable angina (group II) within 6, 24, and 48 h after the chest pain; and 23 pts before and 6, 24, and 48 h after PTCA (group III). The control group (group C) consisted of 20 healthy subjects. We evaluated: clinical state of patients and results of some diagnostic examinations (lipids, ECG, echocardiography, coronary angiography). Mean serum concentrations of TNF-alpha were significantly higher in pts ith CAD (group I: 18.25 +/- 5.5 pg/ml; group II: 17.24 +/- 4.0 pg/ml; group III: 18.70 +/- 0.6 pg/ml; p0.001) than in healthy pts (8.31 +/- 1.4 pg/ml). In turn mean serum concentrations of sTNF-R I were significantly higher both in group I (1399.6 +/- 536.3 pg/ml; p0.05) and III (1544.0 +/- 391.4 pg/ml; p0.01) than in control group (1093.9 +/- 456.9 pg/ml). There were not differences in mean serum concentrations of sTNF-R II. We found no differences between mean serum concentrations of TNF-alpha, sTNF-R I and sTNF-R II either after the chest pain (group II); or before and after PTCA (group III). In group I mean TNF-alpha correlated with serum triglycerides and HDL-cholesterol (r = 0.412 and r = -0.424; p0.01); sTNF-R I correlated with LDL-cholesterol (r = -0.309; p0.05); and sTNF-R II correlated with total cholesterol and LDL-cholesterol (r = 0.311 and r = 0.316; p0.05). The serum concentrations of TNF-alpha are increased in patients with CAD, but this does not reflect the clinical state of patients. In pts with stable angina these increased levels of TNF-alpha may be accompanied with higher concentrations of sTNF-R I--it seems to be the compensatory mechanism in long-term atherosclerosis. Lipid disturbances may influence the cytokines metabolism in pts with CAD.