A fatal complication after repair of post-infarction ventricular septal rupture: heparin-induced thrombocytopenia with thrombosis: case report

interior, theater, 196

Thrombin activatable fibrinolysis inhibitor: Its role in slow coronary flow

The slow coronary flow (SCF) phenomenon is characterized by slow progression of angiographic contrast medium in the coronary arteries in the absence of stenosis in the epicardial vessels. The pathophysiological mechanisms of SCF phenomenon remain uncertain. Several hypotheses, however, have been suggested for SCF phenomenon, including an early form of atherosclerosis, small vessel dysfunction, dilatation of coronary vessels, imbalance between vasoconstrictor and vasodilatory factors, platelet function disorder, and inflammation. Atherosclerosis and inflammation are the most accepted mechanisms for the pathogenesis of SCF. Thrombin activatable fibrinolysis inhibitor (TAFI) was described as a new inhibitor of fibrinolysis recently and plays an important role in coagulation and fibrinolysis. In previous studies, the role of TAFI was associated with inflammation and evolution of atherosclerosis in coronary artery disease. There are no data available about TAFI levels in patients with SCF phenomenon investigated by angiography. Our goal was to evaluate TAFI antigen (Ag) levels in patients with SCF and to determine the association of the TAFI Ag level with traditional cardiovascular risk factors in our study. The study group constituted 41 patients with angiographically confirmed SCF and 46 patients with normal coronary flow as the control group. The TAFI Ag levels of each patient were determined. Between the control and study group, a statistical difference in the levels of TAFI Ag (p < 0.05) was observed. The TAFI Ag level was significantly higher in the SCF group than the control group (132.21 +/- 21.14 versus 122.15 +/- 21.59). We have demonstrated that TAFI might be a risk factor for the development of SCF independently of conventional cardiovascular risk factors. In addition, TAFI Ag levels were positively correlated with C-reactive protein (CRP) known as an acute phase reactant. Our findings support the reports of previous studies that increased TAFI levels may be associated with inflammation. Further large studies are required to evaluate the importance of TAFI antigen levels in relation to the development of SCF

The Factors Affecting Stent Restenosis and Target Lesion Revascularization

[Abstract Not Available

Predictors of chronic total occlusion in a non-culprit artery in patients undergoing coronary angiography for acute coronary syndrome: mean platelet volume and serum uric acid

Congress of the European-Society-of-Cardiology (ESC) -- AUG 29-SEP 02, 2015 -- London, ENGLAND[Abstract Not Available]European Soc Cardio

Angiographic Evalutation of Stents and Grafts in Long Term Period in Patients Undergoing Coronary By Pass Surgery with Patent Stented

[Abstract Not Available

High Levels of Serum Uric Acid Impair Development of Coronary Collaterals in Patients With Acute Coronary Syndrome

We evaluated the association of serum uric acid (SUA) level and development of coronary collateral vessels (CCVs) in patients with acute coronary syndrome (ACS). Patients (n = 224) with ACS were included in the study. Coronary collateral vessels were graded according to the Rentrop scoring system. Rentrop grade 0 was accepted as absence of CCV (group 1; n = 117) and Rentrop grade ≥1 was accepted as presence of CCV (group 2; n = 107). Rentrop 0-1 (poor CCV) were determined in 167 patients and Rentrop 2-3 (good CCV) were determined in 57 patients. Both presence of CCV ( P &lt; .001) and development of good CCV ( P = .003) were significantly associated with low levels of SUA. We suggest that high levels of SUA affect the CCV development negatively in nondiabetic and nonhypertensive patients with ACS. </jats:p

The relationship between lipoprotein(a) and coronary artery disease, as well as its variable nature following myocardial infarction

Purpose: The present study aimed to investigate the relationship between the severity of coronary artery disease (CAD) and level of Lipoprotein (LP)(a). Methods: The study included 52 CAD patients and a control group consisting of 38 individuals. The patients were classified into three groups based on the clinical form of CAD (stable angina pectoris, SAP, unstable angina pectoris,UAP, and myocardial infarction,MI), and were further divided into three groups based on CAD severity (1-, 2- and 3-vessel). Serum Lp(a) levels were monitored 4, 8, and 24 h, 10 and 30 days following acute MI in 18 patients. Results: Based on regression analysis, Lp(a) was not correlated with other lipoproteins or with risk factors of CAD, such as body mass index, smoking, family history, diabetes, age, gender, and hypertension (r = 0.08-0.22). 72% of the patients in the CAD group and 24% of the control group had an Lp(a) level > 30 mg dL–1 (P = 0.004), and Lp(a) levels were higher in 3-vessel patients than in 2-vessel and 1-vessel CAD patients (86% vs. 68%, P = 0.02 and 86% vs. 62%, P=0.01, respectively). Serum Lp(a) levels were higher in the UAP and MI groups than in the SAP group (48 ± 44.7 mg dL–1, 49 ± 36.1 mg dL–1 and 31.2 ± 22.3 mg dL–1 , respectively,P=0.02). Lp(a) levels increased after acute MI, and reached peak levels 10 days post-MI (41% increase, P=0.001) and remained considerably elevated (18%) 30 days post-MI (P=0.01). Conclusion: Serum Lp(a) was higher in the UAP and MI patients in comparison with the SAP patients, and was higher in 3-vessel CAD in comparison with 1- and 2-vessel CAD patients