Association between excess catecholamine synthesis and polymorphic premature ventricular contraction.

BACKGROUND: The reasons for the etiology of premature ventricular contractions (PVCs) are not specifically known. Many patients are resistant to medical treatment, and a factor that would predict response to medical treatment cannot be identified. This study aims to investigate if a high catecholamine level results in polymorphic PVC. METHODS: This study was obtained by prospective data registry analysis. A total of 100 patients, 50 from the PVC group, and 50 from the control group have been evaluated. The participants who were included in the patient group had a polymorphic PVC of 5% or more in their 24-h Holter evaluations. Metanephrine showing the level of adrenaline and normetanephrine, showing the level of noradrenaline levels have been measured from these urine samples. RESULT: There was no difference between the two groups in terms of biochemical and essential characteristics. Normetanephrine level has been significantly higher in the PVC group compared to the control group (323.9 ± 208.9 µg to 129.25 ± 67.88 µg; p < 0.001). Similarly, metanephrine level has also been higher in the PVC group (124.75 ± 82.43 µg to 52.615 ± 36,54 µg; p < 0.001). A positive and moderate correlation has been identified between the number and ratio of PVC and the metanephrine and normetanephrine levels. CONCLUSION: In this study, we found that the catecholamine levels were higher in the polymorphic PVC group than in the healthy volunteers. Also, an increase in the number and rate of PVC has been observed as the catecholamine levels increased. CLINICAL TRIAL REGISTRATION: Urine Levels of Metanephrine and Normetanephrine in Patients With Frequent PVC; ClinicalTrials.gov number NCT03447002.

Is electrophysiological study a novel predictor for permanent pacemaker implantation after transcatheter aortic valve implantation?

Background/aim: Despite advancements in valve technology and increased clinical experience, complications related to conduction defects after transcatheter aortic valve implantation (TAVR) have not improved as rapidly as expected. In this study, we aimed to predict the development of complete atrioventricular (AV) block and bundle branch block during and after the TAVR procedure and to investigate any changes in the cardiac conduction system before and after the procedure using electrophysiological study. Materials and methods: A total of 30 patients who were scheduled for TAVR at our cardiovascular council were planned to be included in the study. TAVR was performed on patients at Erciyes University Medical Faculty Hospital as a single center between May 2019 and August 2020 Diagnostic electrophysiological study was performed before the TAVR procedure and after its completion. Changes in the cardiac conduction system during the preprocedure, intra-procedure, and postprocedure periods were recorded. Results: Significant increases in baseline cycle length, atrial-His (AH) interval, his-ventricular (HV) interval and atrioventricular (AV) distance were observed before and after the TAVR procedure (p = 0.039, p < 0.001, p = 0.018, p < 0.001, respectively). During the TAVR procedure, the preprocedural HV interval was longer in patients who developed AV block and bundle branch block compared to those who did not and this difference was statistically significant (p = 0.024). ROC curve analysis revealed that a TAVR preprocedure HV value >59.5 ms had 86% specificity and 75% sensitivity in detecting AV block and bundle branch block (AUC = 0.83, 95% CI: 0.664-0.996, p = 0.013). The preprocedure HV distance was 98 ± 10.55ms in the group with permanent pacemaker implantation and the mean value in the group without permanent pacemaker implantation was 66.27 ± 15.55 ms, showing a borderline significant difference (p = 0.049). Conclusion: The prolongation of HV interval in patients with AV block and bundle branch block suggests that the block predominantly occurs at the infra-hisian level. Patients with longer preprocedural HV intervals should be closely monitored for the need for permanent pacemaker implantation after the TAVR procedure.

Effects of Smoking on Very-Long Term Mortality after First ST Elevation Myocardial Infarction. / Efeitos do Ato de Fumar na Mortalidade de Longo Prazo após Infarto do Miocárdio por Elevação de ST.

BACKGROUND: The smoking paradox has been a matter of debate for acute myocardial infarction patients for more than two decades. Although there is huge evidence claiming that is no real paradox, publications supporting better outcomes in post-MI smokers are still being released. OBJECTIVE: To explore the effect of smoking on very long-term mortality after ST Elevation myocardial infarction (STEMI). METHODS: This study included STEMI patients who were diagnosed between the years of 2004-2006 at three tertiary centers. Patients were categorized according to tobacco exposure (Group 1: non-smokers; Group 2: <20 package*years users, Group 3: 20-40 package*years users, Group 4: >40 package*years users). A Cox regression model was used to estimate the relative risks for very long-term mortality. P value <0.05 was considered as statistically significant. RESULTS: There were 313 patients (201 smokers, 112 non-smokers) who were followed-up for a median period of 174 months. Smokers were younger (54±9 vs. 62±11, p: <0.001), and the presence of cardiometabolic risk factors were more prevalent in non-smokers. A univariate analysis of the impact of the smoking habit on mortality revealed a better survival curve in Group 2 than in Group 1. However, after adjustment for confounders, it was observed that smokers had a significantly increased risk of death. The relative risk became higher with increased exposure (Group 2 vs. Group 1; HR: 1.141; 95% CI: 0.599 to 2.171, Group 3 vs Group 1; HR: 2.130; 95% CI: 1.236 to 3.670, Group 4 vs Group 1; HR: 2.602; 95% CI: 1.461 to 4.634). CONCLUSION: Smoking gradually increases the risk of all-cause mortality after STEMI.

FUNDAMENTO: O paradoxo do fumante tem sido motivo de debate para pacientes com infarto agudo do miocárdio (IM) há mais de duas décadas. Embora haja muitas evidências demonstrando que não existe tal paradoxo, publicações defendendo desfechos melhores em fumantes pós-IM ainda são lançadas. OBJETIVO: Explorar o efeito do fumo na mortalidade de longo prazo após infarto do miocárdio por elevação de ST (STEMI). MÉTODOS: Este estudo incluiu pacientes com STEMI que foram diagnosticados entre 2004 e 2006 em três centros terciários. Os pacientes foram categorizados de acordo com a exposição ao tabaco (Grupo 1: não-fumantes; Grupo 2: <20 pacotes*anos; Grupo 3: 2-040 pacotes*anos; Grupo 4: >40 pacotes*anos). Um modelo de regressão de Cox foi utilizado para estimar os riscos relativos para mortalidade de longo prazo. O valor de p <0,05 foi considerado como estatisticamente significativo. RESULTADOS: Trezentos e treze pacientes (201 fumantes e 112 não-fumantes) foram acompanhados por um período médio de 174 meses. Os fumantes eram mais novos (54±9 vs. 62±11, p: <0,001), e a presença de fatores de risco cardiometabólicos foi mais prevalente entre os não-fumantes. Uma análise univariada do impacto do hábito de fumar na mortalidade revelou uma curva de sobrevivência melhor no Grupo 2 do que no Grupo 1. Porém, após ajustes para fatores de confusão, observou-se que os fumantes tinham um risco de morte significativamente maior. O risco relativo tornou-se maior de acordo com a maior exposição (Grupo 2 vs. Grupo 1: RR: 1,141; IC95%: 0,599 a 2.171; Grupo 3 vs. Grupo 1: RR: 2,130; IC95%: 1,236 a 3,670; Grupo 4 vs. Grupo 1: RR: 2,602; IC95%: 1,461 a 4,634). CONCLUSÃO: O hábito de fumar gradualmente aumenta o risco de mortalidade por todas as causas após STEMI.

Efeitos do Ato de Fumar na Mortalidade de Longo Prazo após Infarto do Miocárdio por Elevação de ST / Effects of Smoking on Very-Long Term Mortality after First ST Elevation Myocardial Infarction

Resumo Fundamento O paradoxo do fumante tem sido motivo de debate para pacientes com infarto agudo do miocárdio (IM) há mais de duas décadas. Embora haja muitas evidências demonstrando que não existe tal paradoxo, publicações defendendo desfechos melhores em fumantes pós-IM ainda são lançadas. Objetivo Explorar o efeito do fumo na mortalidade de longo prazo após infarto do miocárdio por elevação de ST (STEMI). Métodos Este estudo incluiu pacientes com STEMI que foram diagnosticados entre 2004 e 2006 em três centros terciários. Os pacientes foram categorizados de acordo com a exposição ao tabaco (Grupo 1: não-fumantes; Grupo 2: <20 pacotes*anos; Grupo 3: 2-040 pacotes*anos; Grupo 4: >40 pacotes*anos). Um modelo de regressão de Cox foi utilizado para estimar os riscos relativos para mortalidade de longo prazo. O valor de p <0,05 foi considerado como estatisticamente significativo. Resultados Trezentos e treze pacientes (201 fumantes e 112 não-fumantes) foram acompanhados por um período médio de 174 meses. Os fumantes eram mais novos (54±9 vs. 62±11, p: <0,001), e a presença de fatores de risco cardiometabólicos foi mais prevalente entre os não-fumantes. Uma análise univariada do impacto do hábito de fumar na mortalidade revelou uma curva de sobrevivência melhor no Grupo 2 do que no Grupo 1. Porém, após ajustes para fatores de confusão, observou-se que os fumantes tinham um risco de morte significativamente maior. O risco relativo tornou-se maior de acordo com a maior exposição (Grupo 2 vs. Grupo 1: RR: 1,141; IC95%: 0,599 a 2.171; Grupo 3 vs. Grupo 1: RR: 2,130; IC95%: 1,236 a 3,670; Grupo 4 vs. Grupo 1: RR: 2,602; IC95%: 1,461 a 4,634). Conclusão O hábito de fumar gradualmente aumenta o risco de mortalidade por todas as causas após STEMI.

Abstract Background The smoking paradox has been a matter of debate for acute myocardial infarction patients for more than two decades. Although there is huge evidence claiming that is no real paradox, publications supporting better outcomes in post-MI smokers are still being released. Objective To explore the effect of smoking on very long-term mortality after ST Elevation myocardial infarction (STEMI). Methods This study included STEMI patients who were diagnosed between the years of 2004-2006 at three tertiary centers. Patients were categorized according to tobacco exposure (Group 1: non-smokers; Group 2: <20 package*years users, Group 3: 20-40 package*years users, Group 4: >40 package*years users). A Cox regression model was used to estimate the relative risks for very long-term mortality. P value <0.05 was considered as statistically significant. Results There were 313 patients (201 smokers, 112 non-smokers) who were followed-up for a median period of 174 months. Smokers were younger (54±9 vs. 62±11, p: <0.001), and the presence of cardiometabolic risk factors were more prevalent in non-smokers. A univariate analysis of the impact of the smoking habit on mortality revealed a better survival curve in Group 2 than in Group 1. However, after adjustment for confounders, it was observed that smokers had a significantly increased risk of death. The relative risk became higher with increased exposure (Group 2 vs. Group 1; HR: 1.141; 95% CI: 0.599 to 2.171, Group 3 vs Group 1; HR: 2.130; 95% CI: 1.236 to 3.670, Group 4 vs Group 1; HR: 2.602; 95% CI: 1.461 to 4.634). Conclusion Smoking gradually increases the risk of all-cause mortality after STEMI.

Evaluation of the relationship between pseudo-hypertension and the parameters of subclinical atherosclerosis.

BACKGROUND: Methods using for determining the subclinical atherosclerosis have gained growing interest in the recent years. However, the effects of pseudo-hypertension on the parameters of subclinical atherosclerosis are uncertain. We aimed to evaluate the relationship between pseudo-hypertension and subclinical atherosclerosis in individuals diagnosed with pseudo-hypertension. METHODS: A total of 122 patients who underwent radial elective coronary angiography were included in the present study. These patients were divided into two groups based on the difference between invasive and noninvasive blood pressure (BP) measurements: pseudo-hypertension group who had a difference ≥15 mmHg in SBP or ≥10 mmHg in DBP levels between invasive and noninvasive measurements (n = 28), and the other group who did not have any difference as described on these levels (n = 94). In order to evaluate the subclinical atherosclerosis; flow-mediated dilatation (FMD), carotid intima-media thickness (IMT), pulse wave velocity (PWV), and augmentation index were recorded in all patients. Two groups were compared with respect to these parameters. RESULTS: The median age of the pseudo-hypertension group was 76 years, while the median age of the other group was 63.5 years (P < 0.0001). The incidence of concomitant hypertension was higher in the pseudo-hypertension group as compared to the other group (P < 0.001). There was a significant difference in augmentation index, cardiac output, PWV, FMD, and IMT values between two groups (P = 0.016, P = 0.023, P <0.001, P < 0.001, P < 0.001, respectively). CONCLUSIONS: The present results demonstrated that there was a strong correlation between pseudo-hypertension and the parameters of subclinical atherosclerosis; augmentation index, PWV, FMD, and carotids IMT.

An investigation of the relationship between arterial aortic stiffness and coronary slow flow that was detected during coronary angiography.

AIM: Increased intimal thickness in coronary arteries, extensive calcification, and atheromatous plaque that does not cause luminal irregularities in a significant portion of the patients with coronary slow flow (CSF). Arterial stiffness is an indicator for atherosclerosis. We aimed to investigate the relation between coronary slow flow phenomenon (CSFP) and arterial stiffness. METHOD: Total of 73 patients were included in the study, and a control group was formed with 64 individuals. Aortic stiffness index ß (ASIß) and pulse wave velocity (PWV) were used as the determinant of arterial stiffness in all analyses. RESULT: Pulse wave velocity values were significantly higher in the coronary slow flow group than the control group (P < .001). PWV, aortic stiffness index ß (ASIß) values were found to be significantly higher in the CSF group. ASIß value was 3.4 ± 1.0 in CSF patients and 2.2 ± 0.6 in the control group (P < .001). Receiver operating characteristic curve (ROC) analysis showed that PWV predicted coronary slow flow with 97% sensitivity and 90% specificity for 7.15 cutoff value. And aortic stiffness index was found to predict coronary slow flow with 83% sensitivity and 75% specificity for 2.63 cutoff value. CONCLUSION: Our findings prove that coronary slow flow phenomenon should be considered a subgroup of coronary artery diseases and that increased PWV is an indicator of CSFP.

Antithrombotic treatment patterns and stroke prevention in patients with atrial fibrillation in TURKEY: inferences from GARFIELD-AF registry.

The corner stone of atrial fibrillation therapy includes the prevention of stroke with less adverse effects. The Global Anticoagulant Registry in the FIELD-Atrial Fibrillation (GARFIELD-AF) study provided data to compare treatment strategies in Turkey with other populations and every-day practice of stroke prevention management with complications. METHODS: GARFIELD-AF is a large-scale registry that enrolled 52,014 patients in five sequential cohorts at >1,000 centers in 35 countries.This study initiated to track the evolution of global anticoagulation practice, and to study the impact of NOAC therapy in AF. 756 patients from 17 enrolling sites in Turkey were in cohort 4 and 5.Treatment strategies at diagnosis initiated by CHA2DS2-VASc score, baseline characteristics of patients, treatment according to stroke and bleeding risk profiles, INR values were analyzed in cohorts.Also event rates during the first year follow up were evaluated. RESULTS: AF patients in Turkey were mostly seen in young women.Stroke risk according to the CHADS2 score and CHA2DS2-VASc score compared with world data. The mean of risk score values including HAS-BLED score were lower in Turkey than world data.The percentage of patients receiving FXa inhibitor with or without an antiplatelet usage was more than the other drug groups. All-cause mortality was higher in Turkey. Different form world data when HAS-BLED score was above 3, the therapy was mostly changed to antiplatelet drugs in Turkey. CONCLUSION: The data of GARFIELD-AF provide data from Turkey about therapeutic strategies, best practices also deficiencies in available treatment options, patient care and clinical outcomes of patients with AF.

Evaluation of the diagnostic and prognostic use of gated myocardial perfusion single-photon emission computed tomography in patients with acute chest pain: comparison with the SYNTAX score.

OBJECTIVE: The aim of this study was to evaluate the diagnostic and prognostic efficacy of gated single-photon emission computed tomography (GSPECT) in patients with acute chest pain and to compare quantitative GSPECT parameters and the coronary angiographic SYNTAX score. MATERIALS AND METHODS: A total of 168 patients who presented with clinical symptoms of acute chest pain were enrolled in the study. Study participants were divided into two groups according to the risk of acute coronary syndrome (ACS): low-intermediate and high risk. All participants underwent rest or stress-GSPECT (R/S-GSPECT). Coronary angiography was performed in all high-risk patients and the SYNTAX score was determined. All patients were followed for 24 ± 3 months and monitored for the occurrence of major adverse coronary events (MACE). RESULTS: Among patients with low-intermediate ACS risk, R-GSPECT and S-GSPECT were associated with 100 and 86% sensitivity, 99 and 98% specificity, 100 and 98% negative predictive value, 80 and 86% positive predictive value, and 98 and 97% accuracy, respectively. At follow-up, MACE occurred in 16 patients. Among high-risk patients, GSPECT quantitative parameters were the most significant predictors of MACE in Cox regression analysis. CONCLUSION: R/S-GSPECT, a noninvasive diagnostic method, is associated with an excellent safety profile and exceptional diagnostic and prognostic accuracy in cases of ACS.

Does Serum Bilirubin level on admission predict TIMI flow grade and in-hospital MACE in patients with STEMI undergoing primary PCI.

We evaluated the association of total bilirubin with post-percutaneous coronary intervention (PCI) coronary blood flow and in-hospital major adverse cardiac events (MACEs) in patients with ST-segment elevation myocardial infarction (STEMI) undergoing primary PCI. A total of 536 consecutive patients with STEMI (male 79%, mean age = 59.9 ± 12.6 years) admitted within 6 hours from symptom onset were enrolled. Patients were divided into 2 groups based on the thrombolysis in myocardial infarction (MI) flow grade. In-stent thrombosis, nonfatal MI, and in-hospital mortality were significantly higher in no-reflow group (P = .007, P = .002, and P < .001, respectively). On multivariate regression, the total bilirubin levels remained independent predictors of no-reflow (odds ratio [OR] 1.586, 95% confidence interval [CI] 1.02-2.47; P = .042) and in-hospital MACE (OR 1.399, 95% CI 1.053-1.857; P = .020). Serum bilirubin levels were independently associated with no-reflow and in-hospital MACE in patients with STEMI undergoing primary PCI.

Evaluation of beta-blockers on left ventricular dyssynchrony and reverse remodeling in idiopathic dilated cardiomyopathy: A randomized trial of carvedilol and metoprolol.

BACKGROUND: The effect of b-blockage on cardiac dyssynchrony in idiopathic dilated cardio-myopathy (IDC) is unknown. This study evaluated the impact of carvedilol and metoprolol succinate on left ventricular (LV) dyssynchrony and reverse remodeling in IDC. METHODS: In this small, prospective, double-blind study, we randomly assigned 81 IDC patients to receive carvedilol or metoprolol succinate. Echocardiographic measurements (dyssynchrony, LV volumes and ejection fraction [EF]) and N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels were obtained at baseline and at first and sixth month of therapy. RESULTS: A total of 74 (91%) patients completed all investigations at sixth month (38 and 36 taking carvedilol and metoprolol succinate, respectively). In the carvedilol group, reduction in LV end diastolic volume (D LVEDV at 6 months, 50 ± 15 mL to 40 ± 17 mL, p = 0.03) and increase in LVEF (D LVEF, 7 ± 2% to 5 ± 3%, p = 0.02) was higher compared to the metoprolol group. Also improvement in inter-ventricular dyssynchrony achieved with carvedilol was higher than metoprolol (D interventricular delay at 6 months, 11 ± 8 ms to 6 ± 7 ms, p = 0.03). However, improvement in intraventricular dyssynchrony was similar in the two groups (D intraventricular delay, 9 ± 7 ms to 9 ± 6 ms, p = 0.91). Improvements in LV mechanical dyssynchrony and reverse remodeling achieved with both drugs were accompanied by reduction in NT-proBNP levels in both carvedilol and metoprolol groups (1614 ± 685 pg/mL to 654 ± ± 488 pg/mL and 1686 ± 730 pg/mL to 583 ± 396 pg/mL, respectively, p < 0.001 for both). CONCLUSIONS: Although reduction in LVEDV and increase in LVEF was higher with carvedilol, improvement in intraventricular dyssynchrony was similar in carvedilol and metoprolol groups.

Serum gamma-glutamyltransferase and the burden of atherosclerosis in patients with acute coronary syndrome.

OBJECTIVES: We evaluated the relationship between serum gamma-glutamyltransferase (GGT) levels and the burden of atherosclerosis in patients with acute coronary syndrome (ACS). STUDY DESIGN: This study involved 180 patients (139 male, 41 female; mean age 63±11 years) with the diagnosis of ACS (non-ST elevation myocardial infarction and unstable angina) who underwent coronary angiography on the first day after hospital admission. The burden of atherosclerosis was assessed by the number of involved vessels, and the Gensini and Syntax scores. Serum GGT levels were measured by enzymatic caloric test. RESULTS: Patients with high Syntax scores (>=33) were more frequently diabetic, hypertensive, and had higher GGT and creatinine levels compared to the patients with low Syntax scores (<=23). Similarly, patients with >=3 diseased vessels were more frequently diabetic, hypertensive, and smokers. In addition, these patients were older and had higher serum glucose, urea and GGT levels. Correlation analysis revealed that the level of GGT was significantly associated with Gensini and Syntax scores, number of diseased vessels, and the number of critical lesions (r=0.378 p<0.001, r=0.301 p<0.001, r=0.159 p=0.036, r=0.355 p<0.001, respectively). Multivariate linear regression analysis demonstrated that increased GGT level was an independent risk factor for high Gensini and Syntax scores (p=0.029 and p=0.035, respectively), together with age (p=0.001 and p=0.002, respectively) and serum glucose levels (p=0.017 and p=0.012, respectively). CONCLUSION: Serum GGT levels on admission are associated with increased burden of atherosclerosis in patients with ACS. This may account for the cardiovascular outcomes associated with increased GGT levels.

Tenascin-C as predictor of left ventricular remodeling and mortality in patients with dilated cardiomyopathy.

BACKGROUND: Several cardiac biomarkers, especially brain natriuretic peptide (BNP) and N-terminal (NT)-proBNP, have been used as predictors of prognosis and negative remodeling in DCM. In the present study, we aimed to evaluate the prognostic value of tenascin-C in dilated cardiomyopathy (DCM) and whether it can be used to determine reverse remodeling in patients with DCM. METHODS: Sixty-six patients with DCM were followed up for 12 months after initiation of medical treatment including carvedilol, ramipril (candesartan if ramipril was not tolerated), spironolactone, and furosemide. Tenascin-C and NT-proBNP measurements and transthoracic echocardiography were performed at baseline and at 12 months. RESULTS: At 12 months, a significant improvement in New York Heart Association class (2.57 ± 0.6 vs. 1.87 ± 0.5; P < 0.0001), left ventricular end-diastolic volume (217 ± 47 vs 203 ± 48; P < 0.0001), left ventricular ejection fraction (29.1 ± 5.5 vs 30.9 ± 3.8; P < 0.0001), NT-proBNP (2019 ± 558 vs 1462 ± 805; P < 0.0001), and tenascin-C (76 ± 19 vs 48 ± 28; P < 0.0001) values were observed, compared with baseline. Importantly, decrease in tenascin-C values were correlated with increase in left ventricular ejection fraction. Tenascin-C (odds ratio [OR], 1.896; <95% confidence interval [CI], 1.543-2.670; P = 0.02), diabetes mellitus (OR, 2.456; G95% CI, 1.987-3.234; P = 0.01) and hypertension (OR: 2.106, <95% CI, 1.876-2.897; P = 0.03) were independent predictors of mortality in patients with DCM. CONCLUSION: Reverse ventricular remodeling obtained with carvedilol, ramipril/candesartan, and spironolacton is associated with decreases in left ventricular end-diastolic volume, left ventricular end-systolic volume, tenascin-C levels, and NT-proBNP levels. Consequently, tenascin-C may be used to evaluate reverse remodeling in patients with DCM.

An investigation of tenascin-C levels in rheumatic mitral stenosis and their response to percutaneous mitral balloon valvuloplasty.

OBJECTIVE: The purpose of this study was to evaluate the tenascin-C levels in severe rheumatic mitral stenosis before and after percutaneous mitral balloon valvuloplasty (PMBV). SUBJECTS AND METHODS: Forty patients with severe mitral stenosis requiring PMBV and 20 age-matched healthy subjects were included in the study. The mitral valve areas, mitral gradients and systolic pulmonary artery pressure (sPAP) were measured by echocardiography. The sPAP values and mitral gradients were also measured by catheterization before and after PMBV. The blood tenascin-C levels were measured before PMBV and 1 month after the procedure. RESULTS: The echocardiographic mean mitral gradients had a significant decrease after PMBV (11.7 ± 2.8 vs. 5.6 ± 1.7 mm Hg; p < 0.001) and also those of catheterization (13.9 ± 4.4 vs. 4.0 ± 2.4 mm Hg; p < 0.001). Mitral valve areas increased significantly after PMBV (from 1.1 ± 0.1 to 1.8 ± 0.2 cm(2), p < 0.001). Tenascin-C levels decreased significantly in patients after PMBV (from 15.0 ± 3.8 to 10.9 ± 3.1 ng/ml; p < 0.001). Tenascin-C levels were higher in patients with mitral stenosis before PMBV than in healthy subjects (15.0 ± 3.8 and 9.4 ± 2.9 ng/ml; p < 0.001, respectively). There were no significant differences between patients with mitral stenosis after PMBV and healthy subjects (10.9 ± 3.1 and 9.4 ± 2.9 ng/ml; p = 0.09, respectively). There was a significant positive correlation between tenascin-C levels and sPAP (r = 0.508, p < 0.001). In multivariant analysis, tenascin-C predicted mitral stenosis (p = 0.004, OR: 2.31). CONCLUSIONS: Tenascin-C was an independent predictor for rheumatic mitral stenosis.

Improved arterial stiffness in mitral stenosis after successful percutaneous balloon valvuloplasty.

BACKGROUND: Rheumatic mitral stenosis (MS) is still a common disease in developing countries with high morbidity and mortality rates. The purpose of the study was to evaluate arterial stiffness in severe MS before and after percutaneous mitral balloon valvuloplasty (PMBV). METHODS: Thirty patients with MS in sinus rhythm requiring PMBV and 20 age-gender matched healthy volunteers. The analyze of pulse wave velocities (PWV) were performed using of the carotid artery at the femoral by PWV technique on patients at baseline and a week after PMBV. RESULTS: The values of PWV were significantly decreased after successful PMBW in MS patients. Mitral mean gradients and systolic pulmonary artery pressures (sPAP) both on echocardiography and catheterization also had a significant decrease after PMBW. The mitral valve areas were significantly increased after PMBW. There was a highly significant negative correlation between mitral valve areas and PWV values. A highly significant positive correlation was seen between mitral mean gradient on catheterization and PWV (r = 0.830, p 〈 0.001). There was also a significant correlation between sPAP on catheterization and PWV values (r = 0.639, p 〈 0.001). Echocardiographic mitral mean gradients and PWV were highly positive correlated with each other (r = 0.841, p 〈 0.001). The sPAP on echocardiography had also a highly positive correlation with PWV (r = 0.681, p 〈 0.001). CONCLUSIONS: Mitral stenosis is a cause of impaired arterial stiffness and after the enlargened mitral valve area arterial stiffness improved in patients with MS.

Effects of serum uric acid levels on coronary collateral circulation in patients with non-ST elevation acute coronary syndrome.

OBJECTIVES: The strong relationship between high level of serum uric acid (UA) and cardiovascular disease has been shown in many studies. In this study, we investigated whether serum UA levels affect coronary collateral circulation (CCC) in patients with non-ST elevation acute coronary syndrome. METHODS: The study population included 175 patients with non-ST elevation acute coronary syndrome. On the first day of admission to the hospital, blood samples were taken and UA levels were analyzed for all patients. Coronary angiography was performed on patients within 24-72 h. Rentrop collateral classification was performed. Patients were divided into two groups on the basis of UA levels: group I consisted of 102 patients (90 male, 12 female) with normal UA levels and group II consisted of 73 patients (59 male, 14 female) with elevated UA levels. RESULTS: Group 2 had a significantly higher rate of poorly developed CCC and a lower rate of well-developed CCC compared with group 1 (P=0.003 and 0.001, respectively). Patients with poor CCC had significantly higher serum UA levels compared with patients with well-developed CCC (6.5±1.1 vs. 5.5±1.7 mg/dl, P=0.028). Linear regression analyses showed that poor CCC development was significantly associated with serum UA levels (coefficient=0.22, P=0.005). CONCLUSION: Serum UA level on admission is associated with poor CCC development and may be a useful biomarker for stratification of risk in patients with non-ST elevation acute coronary syndrome.

The importance of cardiac biomarkers on remodelling after myocardial infarction.

BACKGROUND: The purpose of this study is to evaluate the importance of tenascin-C ( TNC), N-terminal pro brain natriuretic peptide (NT-proBNP) and C-reactive protein (CRP) on LV remodelling after myocardial infarction (MI). METHODS: Fifty-seven stable patients with subacute anterior MI who had total or subtotal occlusion in the infarct-related left anterior desending artery in coronary angiography were enrolled the study. 18 of patients who had total occlusion received only medical theraphy, 19 of patients who had total occlusion received successful PCI+ medical theraphy and 20 of patients who had subtotal occlusion received successful PCI+ medical theraphy. Left ventricular volumes and ejection fractions (EF) were measured with echocardiography. Serum TNC, NT-proBNP and CRP levels were measured at admission and a month after treatment. RESULTS: There was significant increase in LV end-diastolic volume (LVEDV) and LV end-systolic volume (LVESV) baseline to follow-up in total-PCI group. Baseline to follow-up; a borderline significant increase was observed in LVEDV in the total-medical group. No significant difference was seen in LV volumes and EF in the subtotal-PCI group. NT-proBNP, TNC and CRP levels were decreased in all groups. The decrease in NT-proBNP and CRP values were significant in the total-medical and subtotal-PCI group but in the total-PCI group they were not significant. The decrease of TNC was significant in all groups but the lowest decrease was seen in the total-PCI group. CONCLUSION: TNC, NT-proBNP and CRP reflect LV remodelling in accordance with echocardiography after MI. KEYWORDS: Tenascin-C; NT-pro BNP; CRP; Remodelling; Myocardial infarction.

Relationship between platelet indices and spontaneous echo contrast in patients with mitral stenosis.

AIMS: To determine the association of platelet indices with spontaneous echo contrast (SEC) in patients with mitral stenosis. METHODS AND RESULTS: A total of 232 consecutive patients with mitral stenosis who undergoing mitral balloon valvuloplasty were enrolled to the study. Patients were divided into two groups according to the formation of SEC in the left atrium. Group 1: mitral stenosis complicated with SEC; Group 2: mitral stenosis without SEC. Transthoracic echocardiography and transoesophageal echocardiography were performed for each patient. Complete blood counting parameters were measured and all routine biochemical tests were performed. There were 133 patients (mean age 42 ± 11 and 74% female) in the SEC(-) group and 99 patients (mean age 45 ± 10 and 64% female) in the SEC(+) group. Plateletcrit (0.25 ± 0.06 vs. 0.27 ± 0.07, P = 0.043) and mean platelet volume (MPV) levels (9.4 ± 1.1 vs. 10.4 ± 1.2, P < 0.001) were significantly higher in the SEC(+) group. When we divided the SEC(+) patients into four subgroups according to previously reported criteria, MPV levels increased to correlate with the degree of SEC (P < 0.001). At multivariate analysis, MPV levels [odds ratio (OR) 2.365, 95% confidence interval (CI) 1.720-3.251; P < 0.001] and PCT levels (OR 2.699, 95% CI 1.584-4.598; P= 0.033) are independent risk factors of SEC in patients with mitral stenosis. CONCLUSION: In patients with mitral stenosis, cheaply and easily measurable platelet indices including MPV and PCT levels are associated with the presence of SEC and are independent risk factors of SEC.

Left ventricular strain and strain rate echocardiography analysis in patients with total and subtotal occlusion in the infarct-related left anterior descending artery.

BACKGROUND: Numerous studies show that percutaneous coronary intervention has no clinical benefit in patients with total occlusion. Both regional and global left ventricle (LV) functions may be evaluated in detail by strain (S) and strain rate (SR) echocardiography. The purpose of this study is to evaluate whether S and SR echocardiography may be used to determine the total occlusion. METHOD: Sixty stable patients who have total or subtotal occlusion in the infarct-related left anterior descending artery were enrolled (Total occlusion group: 35 and subtotal occlusion group: 25 patients). In all patients, LV longitudinal S and SR data were obtained from total 14 segments. RESULTS: S values of middle and apical segments of LV were significantly lower in the total occlusion groups. In SR analysis, middle and apical values of all walls were significantly different between the groups. The total SR of the middle and apical segments was significantly lower in the total occlusion group (respectively, total SR in middle segments: -3.4 ± 0.8% vs. -4.6 ± 1.0%, P < 0.00001 and total SR in apical segments: -1.7 ± 0.5% vs. -2.8 ± 0.6%, P = 0.001). The total SR values of four walls were also significantly lower in the total occlusion group (-10.3 ± 2.0% vs. -13 ± 3.1%, P < 0.0001). For predicting total occlusion, the highest sensitivity levels (84%) were obtained in SR of middle-anterior segment. SR of middle-septum and middle-lateral segments has the highest specificity levels (86%). CONCLUSION: Total occlusion in stable patients with acute coronary syndrome has an unfavorable effect on the LV regional and global functions. Patients with total occlusion may be identified by S and SR echocardiography.

Copeptin level and copeptin response to percutaneous balloon mitral valvuloplasty in mitral stenosis.

We aimed to investigate copeptin levels in mitral stenosis (MS) patients and the behavior of copeptin after hemodynamic improvement achieved by percutaneous balloon mitral valvuloplasty (PBMV). The study involved 29 consecutive symptomatic patients with moderate to severe rheumatic MS who underwent PBMV. Twenty-eight age- and gender-matched healthy volunteers composed the control group. Blood samples for copeptin were obtained immediately before and 24 h after PBMV, centrifuged, then stored at -70°C until assayed. The copeptin level of the patient group was statistically different from that of the control group (61.8 ± 34.4 and 36.8 ± 15.2 pg/ml, respectively; p = 0.001). PBMV resulted in a significant increase in mitral valve area and a significant decrease in transmitral gradient as well as systolic pulmonary artery pressure. While hemodynamic relief was obtained, we detected a statistically significant decline in copeptin levels 24 h after PBMV compared to the baseline levels (from 61.8 ± 34.4 to 44.1 ± 18.2 pg/ml; p = 0.004).

Short-Term Left Ventricular Remodeling After Revascularization in Subacute Total and Subtotal Occlusion With the Infarct-Related Left Anterior Descending Artery.

BACKGROUND: Large randomized studies revealed that percutaneous coronary intervention has no clinical benefit in patients with total occlusion. The purpose of this study is to evaluate left ventricular remodelling after PCI for total and subtotal infarct-related left anterior desending artery in stable patients who have not received trombolytic theraphy. METHODS: Sixty stable patients with subacute anterior myocardial infarction who have total or subtotal occlusion in the infarct-related left anterior descending artery were enrolled the study (20 patient in the total-medical group, 20 patient in the total-PCI group and 20 patient in the subtotal-PCI group). All patients' left ventricular diameters, volumes and ejection fractions measured at admission and after a month. RESULTS: The necrotic segment number in scintigraphy were similar in three groups. In the total-PCI group, there were significant increases in left ventricular diastolic diameter, left ventricular end-diastolic volume and left ventricular end-systolic volume at first month. A borderline significant increase was observed in LVEDV in the total-medical group at first month. No significant difference was seen in all echocardiographic parameters in the subtotal-PCI group at a month after discharge. The percentage of increase in LVEDV was significantly higher and the percentage of increase in LVESV was borderline significantly higher in the total-PCI group than the other groups. CONCLUSIONS: In stable patients, PCI for total occlusion in the subacute phase of anterior MI causes an increase in LV remodeling. Nevertheless PCI for subtotal occlusion in the subacute phase of anterior MI may prevent LV remodeling.