Oxidative stress impairs endothelial function and may play an important role in the pathogenesis of acute cardiovascular diseases. Advanced oxidation protein products (AOPP) were proposed as one of the possible markers of oxidative injury, which originates under oxidative and carbonyl stress and increase global inflammatory activity. The present study was undertaken to compare AOPP concentrations in a control group of healthy individuals without ICHS (I), patients with stable angina pectoris (II), patients with acute coronary syndrome over 48 hours without ST elevations (III), and patients with ST elevation myocardial infarction (IV). Coronaronary angiography, risk factors and anamnestic data were analyzed. We examined 73 probands with signs of myocardial ischemia, mean age of 61.5 years (64 % males) subjected to coronarography and 21 healthy individuals. No significant difference was found between venous blood and coronary samples, or between infarction and non-infarction arteries in the group IV. AOPP concentrations in healthy individuals in the group I (82.9 ± 29.3 mmol/l) did not differ significantly from patients in group II (89.6 ± 26.7 mmol/l) and group III (112.3 ± 54.6 mmol/l). A significant difference in AOPP values was found between the groups I and IV, and between the groups II and IV (82.9 ± 29.3 mmol/l vs. 125.8 ± 101 mmol/l, p = 0.02, and 89.6 ± 26.7 mmol/l vs. 125.8 ± 101 mmol/l, p = 0.02). No correlations were found between AOPP and body mass index (BMI), nicotinism, left ventricular ejection fraction, parameters of glucose and lipid metabolism. ROC analysis revealed that AOPP concentrations of 89 mmol/l had 64 % sensitivity and 71 % specificity for revealing an acute coronary syndrome (AUC 0.65, 95 % CI 0.55-0.80). AOPP are significantly increased in patients with acute coronary syndromes with ST segment elevation, but also tend to increase in patients with non-ST elevation myocardial infarction. Our observations suggest that AOPP may be used as a marker of oxidative stress and as a prognostic factor for severe forms of cardiovascular disease. A cutoff value of 89 mmol/l can be used with 64 % sensitivity and 71 % specificity for revealing acute coronary syndrome.
Pulmonary vein ablations cause an increased systemic procoagulant state as reflected by fibrin turnover, fibrinolysis activation and endothelial perturbation. The activation of the coagulation cascade could be decreased by early heparin administration.
Normal perfusion or fixed defects predict a benign prognosis in patients after successful PTCA. The presence of stress-induced reversible defects appears to be the best predictor of future cardiac events.
These findings suggest a benign prognosis in patients with normal SPECT (regardless of the L:H ratio). Conversely, all patients with ischemia are at high risk for future cardiac events. Quantification of the Tl-201 lung uptake seems to be valuable in evaluations of disease prognosis, especially in patients with fixed defects.
Myosin light chains-1 (MLC-1) have been recently associated with the markers of heart function (NYHA, LVEF, NT-proBNP). Verification of the relationship between markers of heart function (New York Heart Association classification (NYHA), left ventricle ejection fraction determination (LVEF), N terminal prohormone of natriuretic peptide B type BNP (NT-proBNP) and concentrations of myosin light chains-1 (MLC-1) was assesed. Patients examined for dyspnea without signs of acute coronary syndrome. All patients underwent echocardiography (calculation of left ventricle ejection fraction-LVEF) and in the serum of all subjects NT-proBNP (ELEIA) and MLC-1 (ELISA) were determined. In the 38 patients (21 men, 17 women), mean age of 58 years (±12 years as 1 SD), a significant negative correlation was found between NT-proBNP and LVEF (r =-0.47; p = 0.02, Spearman). The median levels of NT pro-BNP were closely associated with NYHA classification (type II-584 ng/l, type III-2792 ng/l, type IV-6400 ng/l; p < 0.05). Individuals with clinical NYHA IV differed significantly in median MLC-1 concentrations from persons with clinical NYHA classification II and III (type II-5.7 ng/l, type III-8.9 ng/l, type IV-17 ng/l; p <0.05). A significant negative correlation between MLC-1 and LVEF (-0.35; p <0.03) and significant positive correlations between MLC-1 and NT-proBNP (-0.42; p <0.012) were found. In conclusion MLC-1 cannot be used as a diagnostic marker in differential diagnosis of dyspnea.
The differentiation between chronic pulmonary thromboembolic hypertension (CTEPH) and pulmonary arterial hypertension (PAH) remains a clinical challenge. The aim of our study was to evaluate the usefulness of both echocardiographically and invasively derived pulmonary artery pulsatility indexes in the etiologic differentiation of patients with CTEPH and PAH. We retrospectively analyzed the results of echocardiographic and invasive hemodynamic examinations in 125 patients with either CTEPH (n = 62) or PAH (n = 63). Invasive data were obtained in 52 patients with CTEPH and 43 PAH patients. Using echocardiography, pulmonary artery systolic (PASP), diastolic (PADP) and mean (PAMP) pressures were estimated from velocities of tricuspid regurgitation and pulmonary regurgitation, respectively. Pulse pressure (PP) was calculated as the difference between PASP and PADP. To obtain pulmonary artery pulsatility indexes, we normalized PP by PASP (PP/PASP), by PAMP (PP/PAMP) and by PADP (PP/PADP). Pulsatility indexes assessed by echocardiography did not differ between CTEPH and PAH patients except for PP/PAMP [PP/PAMP (1.82 ± 0.33 vs. 1.40 ± 0.3, p < 0.001)]. Invasively derived pulsatility indexes were significantly higher in subjects with CTEPH (0.60 ± 0.08 vs. 0.53 ± 0.09 for PP/PASP; 0.98 ± 0.21 vs. 0.81 ± 0.21 for PP/PAMP; 1.58 ± 0.52 vs. 1.21 ± 0.41 for PP/PADP; all p < 0.001). The areas under the receiver-operating characteristic curves analysis showed that no cutoff value allowed discriminating between CTEPH and PAH by using echocardiographically or invasively derived pulsatility indices. Invasively derived pulmonary artery pulsatility indexes as well as echocardiographically determined PP/PAMP indexes are higher in CTEPH compared to PAH. However, due to the important overlap no optimal threshold values of these parameters can be given to allow satisfactory discrimination of the two diseases in clinical practice.
A case study of a patient suffering from severe chronic congestive heart failure resulting from ischemic cardiomyopathy in whom a biventricular (BiV) pacing system was implanted is reported. After a 1-year follow-up, left ventricular (LV) ejection fraction improved dramatically from an initial 15% to 60%, left ventricular end-diastolic diameter decreased, as did left atrial dimension. Tissue Doppler data and acute hemodynamic measurements taken during the biventricular pacemaker implantation procedure are presented. The case represents an exceptional example of left ventricular reverse remodeling with practically normalized left ventricular function after 1 year of synchronized pacing.
Endothelial dysfunction (ED) is generally considered to be the initial step in the progression to atherosclerosis but there is still much uncertainty about the role of the microvascular form of angina in patients with a normal coronary angiogram with regard to ED. The authors investigated the extent of endothelial perturbation and thereby whether the microvascular form of angina precedens macroscopic atherosclerosis by means of non-invasive ultrasound measurement of the intima-media thickening (IMT) in common carotid artery and flow mediated dilatation (FMD) in the brachial artery. 28 patients with stable angina with positive exercise test and ST segment depression (22 females, 6 males, average age 54 years) were compared with a control group consisting of 28 patients with no clinical signs of coronary artery disease (18 females, 10 males, average age 53 years). No significant difference in FMD% (7.3 vs. 10.8, p = 0.07) was found between the groups, though specific measurements (average dilatation of the brachial artery induced by ischemic insult, peak blood flow and peak hyperemic flow) differed considerably. Also IMT did not vary significantly between the groups (0.74 vs. 0.65, p = 0.08). In patients with IMT > 0.8 mm (6 patients in each group) a significant decrease of FMD was found as compared with patients with normal IMT (p < 0.05). It was concluded that in patients with increased IMT an inverse relationship between FMD and IMT exists both in patients with microvascular angina and in the healthy control subjects whereas in the group of patients with normal IMT no ED was demonstrated. This supports the hypothesis that the microvascular form of angina is the early stage of coronary artery atherosclerosis and this escapes angiographic recognition.
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