Apoptosis kinetics at reperfusion period in patients with acute ST-Segment Elevation Myocardial Infarction undergoing primary percutaneous coronary intervention and treated with thrombolytic therapy.

OBJECTIVE: To evaluate the kinetics of cardiomyocyte apoptosis in patients undergoing primary percutaneous coronary intervention and thrombolytic therapy in order to elucidate the dark side of reperfusion injury. METHODS: The prospective descriptive study was conducted at Istanbul University Cardiology Institute, Istanbul, Turkey, between June 2010 and December 2012. It comprised patients with persistent ST-segment elevation myocardial infarction who were divided into two groups. Patients in group 1 were treated with percutaneous coronary intervention, while those in group 2 received thrombolytic therapy. Cell death detection enzyme-linked immunosorbent assay kit was used for the analysis of cardiomyocyte apoptosis. Venous blood samples were collected to determine the apoptotic activity from the patients at the beginning of thrombolysis in myocardial infarction grade 3 of reperfusion in infarct-related artery according to thrombolysis in myocardial infarction classification, and after reperfusion provided at 6, 12, 24 and 72 hours. Creatine kinase, peak creatine kinase myocardial band and troponin levels were determined on admission and during 24hours of ST-segment elevation myocardial infarction . SPSS 15 was used for statistical analysis. RESULTS: There were 92 patients in the study; 48(51.6%) in group 1 and 44(48.4%) in group 2.There was no significant correlation between peak apoptotic activity levels at 72 hours of reperfusion and peak creatine kinase myocardial band (r=0.05;p=0.66) or the troponin (r=0.10;p=0.38) levels at 24 hours of ST-segment elevation myocardial infarction. Apoptotic activity levels increased at 72 hours compared to the baseline both for group 1 (p<0.001) and group 2(p<0.001). CONCLUSIONS: Reperfusion injury was not primarily related to apoptosis and it was a slowly progressive benign event in patients with ST-segment elevation myocardial infarction-acute coronary syndrome. Also, the negative impact of percutaneous coronary intervention was not available on reperfusion injury.

Long-term prognosis of mild functional tricuspid regurgitation after mitral valve replacement.

OBJECTIVE: Functional tricuspid regurgitation (FTR) is the most common type of tricuspid insufficiency and occurs approximately in 30% of patients with mitral valve disease. The major etiologic factor in the triggering of right ventricular dilation and thus causing functional tricuspid regurgitation, is pulmonary artery hypertension secondary to mitral valve disease. We aimed to analyze long-term outcomes of patients with mild tricuspid regurgitation at the time of mitral valve replacement. METHODS: Sixty-six patients with mild tricuspid insufficiency who underwent mitral valve replacement were included in this observational retrospective study. Mean follow-up time was 8.3 ± 0.7 years. Patients whose tricuspid regurgitation remained unchanged or decreased following operation were enrolled to group 1 (n=32), patients whose tricuspid regurgitation increased were included to group 2 (n=34) and data were compared statistically with t-test, Mann-Whitney U, Chi-square and Fisher Exact test. Multiple regression analysis was performed to determine independent risk factors for FTR progression. REESULTS:Preoperatively female gender (p=0.02), body surface area (p=0.04), left atrium diameter (p=0.01), functional capacity (p=0.03), right ventricle diameter (p=0.04), and left ventricle mass index (p=0.04) were found to be statistically significant between groups. In the follow-up; functional capacity, grade of tricuspid insufficiency, pulmonary artery pressure, vena contracta width (p<0.001), TAPSE (tricuspid annular plane systolic excursion index) (p=0.04), annulus diameter (p=0.02), right ventricle diameter (p=0.01), left ventricle mass index (p=0.05), and ejection fraction (p=0.02) were found to be statistically different between groups. In multiple logistic regression analysis; preoperative LA diameter (OR=5.05; 95% CI:1.49-17.12; p=0.009) and female gender (OR=10.93; 95% CI:1.77-67.31; p=0.01) were found as independent risk factors for FTR progression. CONCLUSION: This study revealed that mild FTR might advance to moderate to severe grade in more than half of the patients in the follow-up. Thus, surgical approach to even mild FTR should be individualized based on patient's risk assessment.

A Coronary Septic Embolism in Double Prosthetic Valve Endocarditis Presenting as Acute Anteroseptal ST-Segment-Elevation Myocardial Infarction.

Acute myocardial infarction caused by septic embolism is usually fatal. A 40-year-old male patient who presented within 30 minutes of severe chest pain was admitted to the emergency department. An electrocardiogram showed a maximum 6 mm of acute ST elevations at V1-V4 derivations. His body temperature was as high as 38.5ºC. Blood cultures were taken three times before parenteral ampicillin/ sulbactam treatment was administered. Later, coagulase negative staphylococci (Methicillin Sensitive Staphylococcus epidermidis) were identified from his blood cultures. Coronary angiographic examination was performed. Lobulated contours of a septic embolus was shown in the mid region of left anterior descending artery as an outcome. Trans-esophageal echocardiography showed; mobile multiple vegetations on the prosthetic mitral and aorta valves. After six weeks of antibiotherapy, he was completely healed and discharged from hospital.Six months later, he was rehospitalized and died because of complications of recurrent infective endocarditis.

QT dispersion in patients with rheumatic mitral stenosis and its relation with echocardiographic findings and serum NT-proBNP levels.

OBJECTIVES: We evaluated the value of QT interval dispersion in patients with rheumatic mitral stenosis (MS) in association with echocardiographic parameters and serum N-terminal pro brain natriuretic peptide (NT-proBNP) levels. STUDY DESIGN: The study consisted of 46 patients (39 women, 7 men; mean age 46.9±9.7 years) with moderate-to-severe rheumatic MS. All patients underwent echocardiographic examination. Blood samples for NT-proBNP were collected immediately after ECG recording. QT interval and QRS complex were measured manually on standard 12-lead surface ECGs. Electrocardiographic and echocardiographic findings and serum NT-proBNP levels were compared with those of a control group consisting of 30 healthy subjects (26 women, 4 men; mean age 46.1±7.3 years). RESULTS: Compared to controls, serum NT-proBNP levels were significantly higher in MS patients (284.6±206.5 vs. 70.2±9.3 pg/ml, p<0.001). The mean QT interval, QTc interval, and QT dispersion were significantly prolonged in MS patients compared to controls (378±25 vs. 349±21, 420±22 vs. 401±19, and 61±21 vs. 38±15 msec, respectively; p<0.005). QT and QTc dispersions were negatively correlated with mitral valve area (QT: r=-0.311, p=0.03; QTc: r=-0.327, p=0.02), and positively correlated with serum NT-proBNP level (QT: r=0.583, p<0.001; QTc: r=0.637, p<0.001). QTc dispersion was also an independent predictor of serum NT-proBNP level in regression analysis (ß=0.330, p=0.03). CONCLUSION: Our results indicate that QT dispersion is related to the echocardiographic degree of rheumatic mitral valve disease and serum NT-proBNP levels in rheumatic MS. Being a noninvasive, easy, and inexpensive method, QT dispersion may be used as a complementary tool to the clinical and echocardiographic evaluation of patients with rheumatic MS.