Serum cardiac markers in patients with acute myocardial infarction: oxidative stress, C-reactive protein and N-terminal probrain natriuretic Peptide.

The aim of this study was to investigate the predictive value of an oxidative stress, C-reactive protein (CRP) and N-terminal probrain natriuretic peptide (NT-proBNP) biomarkers in acute myocardial infarction (AMI). The study population contained 100 patients with AMI and 40 healthy subjects. Malondialdehyde (MDA) was measured as thiobarbituric acid reactive substances. Total antioxidant status (TAC) was assayed with colorimetric method. CRP and NT-proBNP was quantitated by immunoassay. MDA, CRP and NT-proBNP levels were found significantly high in patients with AMI as compared to healthy controls (p<0.01). Patients were divided into six groups based on the presence of disease history before AMI. In patients with non-disease before AMI. MDA, CRP and NT-proBNP levels were lowest among the patient groups. MDA levels in patients with hyperlipidemia/ diabetes/renal disease were higher than the other groups. TAC levels in patients with hypertension were lower than as compared to healthy controls (p<0.05). CRP levels in hypertension + hyperlipidemia patients and NT-proBNP levels in cardiovascular + hypertension patients were found high as compared to other patient groups. It is concluded that serum levels of MDA, CRP and NT-proBNP were significantly increased in patients with AMI and these markers were strongly predictive in AMI.

A pericardial hydatid cyst masquerading as acute inferolateral myocardial infarction--a case report.

A case of pericardial hydatid cyst adjacent to the inferoposterial wall of the left ventricle is reported. Significant ST segment elevations in leads D2, D3, aVF, V5, and V6 on surface electrocardiography and sudden onset of severe chest pain mimicked acute inferolateral myocardial infarction. However, cardiac catheterization and coronary angiography showed normal coronary arteries and normal left ventricular cavity. The ST segment elevation in the inferolateral leads disappeared a few days after surgical resection of the cyst. Cardiac hydatid cyst should be considered in the differential diagnosis of patients with angina-like chest pain in endemic areas.

Increased levels of soluble adhesion molecules E-selectin and P-selectin in patients with cardiac syndrome X.

The role of endothelial dysfunction and platelet activation in patients with cardiac syndrome X is controversial. The aim of this study was to investigate the plasma levels of circulating E- and P-selectin molecules in patients with syndrome X. The study included 21 patients with cardiac syndrome X (11 men and 10 women, mean age = 56 +/- 5 years) and 20 patients with significant coronary artery disease who had stable angina pectoris (11 men and 9 women, mean age = 60 +/- 8 years). Twenty-two age- and sex-matched subjects (12 men and 10 women, mean age = 58 +/- 8 years) undergoing diagnosis of atypical chest pain in whom coronary arteries were found normal and exercise test had no signs of ischemia served as the control group. Syndrome X was defined as presence of typical chest pain on exertion or at rest with positive exercise test and angiographically normal epicardial coronary arteries with no evidence of coronary spasm after intracoronary infusion of ergonovine maleate. The mean plasma concentrations of P-selectin were significantly elevated both in patients with coronary artery disease and syndrome X as compared with control subjects (49.15 +/-7.47 and 42.80 +/- 8.93 vs 22.63 +/-6.47 ng/mL, p < 0.001). Similarly, both patients with coronary artery disease and syndrome X had higher plasma concentrations of E-selectin than the control group (78.85 +/- 16.69 and 68.38 +/- 15.30 vs 36.43 +/- 4.72 ng/mL, p < 0.001). In conclusion, patients with syndrome X had increased plasma concentrations of soluble adhesion molecules, E-selectin and P-selectin, reflecting an ongoing chronic inflammation involved with endothelial dysfunction and enhanced platelet activation/damage in this setting.

Increased blood coagulation and platelet activation in patients with infective endocarditis and embolic events.

BACKGROUND: Inflammation-induced procoagulant changes and alterations in platelet activity appear to play an important role in thromboembolic complications of infective endocarditis (IE). HYPOTHESIS: The aim of this study was to investigate systemic coagulation activity, fibrinolytic capacity, and platelet activation in patients with IE with and without embolic events by measuring the plasma levels of prothrombin fragment 1+2 (PF1+2), thrombin-antithrombin III complex (TAT), plasminogen activator inhibitor-1 (PAI-1), beta-thromboglobulin (beta-TG), and platelet factor 4 (PF4), respectively. METHODS: The study included 76 consecutive patients (female = 55, male = 21, mean age 26 years, range 8-64 years) with definite IE according to the Duke criteria; of these, 13 (17.1%) had embolic events. RESULTS: Plasma concentrations of PF1+2 (3.2 +/- 1.3 vs. 1.7 +/- 0.7 and 1.4 +/- 0.7 nmol/l, p < 0.001, respectively) and TAT (7.3 +/- 1.5 vs. 2.9 +/- 1.2 and 2.2 +/- 1.1 ng/ml, p < 0.001, respectively) were elevated in patients with embolic events compared with patients without embolic events and control subjects. Similarly, patients with embolic events had increased plasma levels of beta-TG (63.3 +/- 10.9 vs. 33.1 +/- 11.6 and 19.1 +/- 10.6 ng/ml, p < 0.001, respectively) and PF4 (106.0 +/- 28.7 vs. 50.3 +/- 16.7 and 43.0 +/- 15.8 ng/ml, p < 0.001, respectively) compared with those without embolic events and the control group. Embolic patients also had higher PAI-1 levels than nonembolic patients and healthy subjects (14.4 +/- 6.4 vs. 8.6 +/- 5.9 and 5.4 +/- 4.3 ng/ml, p = 0.002, respectively). CONCLUSION: Patients with IE and with subsequent thromboembolism have increased systemic coagulation activation, enhanced platelet activity/damage, and impaired fibrinolysis. The resulting imbalance produces a sustained hypercoagulable state, which contributes to the increased risk of thromboembolic events in this particular group.

Effect of infective endocarditis on blood coagulation and platelet activation and comparison of patients with to those without embolic events.

Inflammation-induced procoagulant changes and alterations in platelet activity appear to play an important role in thromboembolic complications of infective endocarditis (IE). The aim of this study was to investigate systemic coagulation activity, fibrinolytic capacity, and platelet activation in IE patients with and without embolic events by measuring the plasma levels of prothrombin fragment 1 + 2, thrombin-antithrombin III complex, plasminogen activator inhibitor-1, beta-thromboglobulin, and platelet factor 4. The study included 76 consecutive patients with definite IE according to the Duke criteria. Among them, 13 (17.1%) had major embolic events. Plasma concentrations of prothrombin fragment 1 + 2 (3.2 +/- 1.3 vs 1.7 +/- 0.7 and 1.4 +/- 0.7 nmol/L, p <0.001, respectively) and thrombin-antithrombin (7.3 +/- 1.5 vs 2.9 +/- 1.2 and 2.2 +/- 1.1 ng/ml, p <0.001, respectively) were elevated in patients with embolic events compared with both patients without embolic events and control subjects. Similarly, patients with embolic events had increased plasma levels of beta-thromboglobulin (63.3 +/- 10.9 vs 33.1 +/- 11.6 and 19.1 +/- 10.6 ng/ml, p <0.001, respectively) and platelet factor 4 (106.0 +/- 28.7 vs 50.3 +/- 16.7 and 43.0 +/- 15.8 ng/ml, p <0.001, respectively) compared with those without embolic events and the control group. Embolic patients also had higher plasminogen activator inhibitor-1 levels than both nonembolic patients and healthy subjects (14.4 +/- 6.4 vs 8.6 +/- 5.9 and 5.4 +/- 4.3 ng/ml, p = 0.002, respectively). In conclusion, IE patients with subsequent thromboembolism have increased systemic coagulation activation, enhanced platelet activity/damage, and impaired fibrinolysis. The resulting imbalance produces a sustained hypercoagulable state that may contribute to the increased risk of thromboembolic events in this particular group.

Aortic valve calcification: its significance and limitation as a marker for coronary artery disease.

Aortic valve calcification (AVC) is correlated with atherosclerotic risk factors; however, its significance remains largely unknown. The aim of this study was to investigate whether AVC detected by transthoracic echocardiography can be a useful marker for the identification of significant coronary artery disease (CAD), particularly in elderly patients. The study included 432 consecutive patients with suspected CAD who were admitted for the first time for coronary angiography. Two-dimensional transthoracic echocardiography and selective coronary angiography were performed in all patients. Aortic valve calcification was defined as bright dense echoes of > 1 mm on one or more cusps and decreased mobility of the involved cusp. Aortic valve calcification was detected in 64 of the 337 patients with significant CAD, but only in 9 of 95 cases with normal or mildly stenotic coronary arteries (19% vs 9%, p < 0.001). The severity of coronary artery disease (defined as the number of obstructed vessels) was not related to the presence of AVC (p > 0.05). Stepwise multiple logistic regression analysis of the study patients revealed only age (p=0.003, odds ratio= 1.56) and AVC (p<0.001, odds ratio = 2.03) as independent predictors of CAD. When the study population was divided into two groups as those below (n = 338) and above (n = 94) 75 years old, AVC failed to be a predictor of CAD in those >75 years old (p > 0.05, odds ratio = 0.8) while it remained the most significant predictor of CAD (p<0.001, odds ratio=2.19 in patients aged <75 years. In conclusion, detection of AVC by transthoracic echocardiography may be a useful noninvasive marker for identification of significant CAD in patients younger than 75 years old. Its clinical usefulness is limited in elderly patients.