Role of N-terminal pro-B-type natriuretic peptide and troponin T in predicting right ventricular recovery in myocardial infarction.

OBJECTIVES: The determinants of right ventricular (RV) recovery after successful revascularization in ST-elevation myocardial infarction (STEMI) patients are not clear. Besides, the relationship between Troponin T (TnT), N-terminal pro-B-type natriuretic peptide (NT-proBNP) and improvement in RV function is also unknown. This study hypothesizes that a lower TnT and NT-proBNP level would be associated with RV recovery. METHODS: One hundred forty-eight STEMI patients were included in our study. Echocardiography were performed before and 12-18 weeks after discharge. Patients were divided into three groups according to the changes in tricuspid annular plane systolic excursion (TAPSE) as 53 patients with ≥10% change, 41 patients with 1-9% change, and 54 patients ≤0% change. RV recovery was accepted as ≥10% TAPSE improvement and the predictors of RV recovery were investigated. RESULTS: RV recovery was detected in 35.8% of the patients. Low baseline left ventricular ejection fraction (OR: 0.91 [0.84-0.98], p=0.023), NT-proBNP (OR: 0.93 [0.89-0.98], p=0.014), TnT (OR: 0.84 [0.68-0.93], p=0.038), inferior myocardial infarction (OR: 2.66 [1.10-6.40], p=0.028), wall motion score index ratio (OR: 0.93 [0.88-0.97], p=0.002) and post-percutaneous coronary intervention TIMI flow 3 (OR: 5.84 [1.41-24.22], p=0.015) were determined as independent predictors of RV recovery. Being in the high TnT group 4.2 times, and being in the high NT-proBNP group 5.3 times could predict the failure to achieve RV recovery. Furthermore, when high TnT level was combined with high NT-proBNP level, the odds ratio of failure to achieve RV recovery was the highest (OR: 8.03 [2.59-24.89], p<0.001). CONCLUSIONS: Lower TnT and lower NT-proBNP level was associated with better improvement in RV function in STEMI patients.

Growth Differentiation Factor 15 is Related with Left Ventricular Recovery in Patients with ST-Elevation Myocardial Infarction after Successful Reperfusion by Primary Percutaneous Intervention.

BACKGROUND: The determinants of left ventricular (LV) recovery after successful revascularization in ST-elevation myocardial infarction (STEMI) patients are not clear. In addition, the relationship between growth differentiation factor15 (GDF-15) and left ventricular ejection fraction (LVEF) improvement is also unknown. This study hypothesizes that a low GDF-15 level would be associated with LVEF recovery. METHODS: One hundred and sixty-one STEMI patients were included in this study. Echocardiographic examinations were performed before and 12-18 weeks after discharge. The patients were divided into three groups according to the changes in LVEF as 62 patients with ≥ 10% change, 47 patients with 1-9% change, and 52 patients ≤ 0% change. LV recovery was defined as ≥ 10% LVEF improvement and the predictors of LV recovery were investigated. Moreover, two groups were created according to GDF-15 values, and the follow-up/baseline echocardiographic parameters were compared between these groups. RESULTS: LV recovery was detected in 38.5% of the patients. Low baseline LVEF [odds ratio (OR): 0.85, 95% confidence interval (CI) 0.82-0.94, p = 0.001], low GDF-15 (OR: 0.79, 95% CI 0.68-0.93, p = 0.004), previous angina (OR: 2.34, 95% CI 1.10-4.96, p = 0.027), and symptom-to-balloon time (OR: 0.97, 95% CI 0.95-1.00, p = 0.043) were independent predictors of LV recovery. The ratios of follow-up/baseline LV end-diastolic volume index, LV end-systolic volume index and wall motion score index were lower in the low GDF-15 group (0.96 vs. 1.04, p < 0.001; 0.96 vs. 1.10, p < 0.001; 0.89 vs. 0.96, p < 0.001). Moreover, being in the low GDF-15 group was associated with LV recovery (OR: 2.93, 95% CI 1.43-6.02, p = 0.001). CONCLUSIONS: Lower GDF-15 level was associated with better LV improvement and less adverse remodeling in STEMI patients.

Pentraxin-3 is Associated with Adverse Diastolic Remodeling in Patients with ST-Elevation Myocardial Infarction after Successful Reperfusion by Primary Percutaneous Intervention.

BACKGROUND: Determinants of adverse diastolic remodeling in ST-elevated myocardial infarction (STEMI) after successful revascularization are not well established. Besides, the relationship between Pentraxin-3 (PTX-3) and diastolic function deterioration is unknown. This study hypothesizes that PTX-3 level would be associated with diastolic remodeling. MATERIALS AND METHODS: Ninety-eight STEMI patients were included in our study. Echocardiography was performed before and 12-18 weeks after discharge. Two groups were generated according to the PTX-3 value, and the follow-up/baseline echocardiographic parameters were compared. Diastolic adverse remodeling was accepted as a persistent restrictive filling pattern or an increase in at least one grade of diastolic dysfunction. The independent predictors of diastolic adverse remodeling were investigated. RESULTS: Adverse diastolic remodeling was detected in 19.3% of patients. High left ventricular mass index (odds ratio [OR]: 1.096, confidence interval [CI] 95%: 1.023-1.174, P = 0.009), high PTX-3 (OR: 1.005, CI 95%: 1.001-1.009, P = 0.024), and failing to achieve thrombolysis in myocardial infarction flow 3 after percutaneous coronary intervention (OR: 6.196, CI 95%: 1.370-28.023, P = 0.005) were determined as independent predictors of adverse diastolic remodeling. The ratio of follow-up/baseline left atrial volume index was higher in the high PTX-3 group (1.15 vs. 1.05, P = 0.029). Moreover, being in the high PTX-3 group predicted adverse diastolic remodeling at 7.4 times. CONCLUSION: Higher PTX-3 level is associated with adverse diastolic remodeling in STEMI patients.

Predicting long-term cardiovascular outcomes in myocardial infarction survivors using multiple biomarkers.

Aim: Although there are short- and long-term prognostic studies in patients with myocardial infarction (MI), the data that can be used to predict the clinical outcome following discharge is limited. Materials & methods: We analyzed creatinine kinase-MB and troponin related to myonecrosis, suppression of tumorigenicity 2 and NT-pro B-type natriuretic peptide related to myocardial stress, C-reactive protein and procalcitonin related to inflammation in 259 MI patients. Results: Being in the high group for myocardial stress (odds ratio [OR]: 3.45, 95% CI: 1.398-8.547, p = 0.004) and inflammation markers (OR: 4.30, 95% CI: 1.690-10.899, p = 0.001) predicted major cardiovascular adverse events while myonecrosis markers could not (OR: 1.70, 95% CI: 0.671-4.306, p = 0.263). Conclusion: Using multimarker risk stratification composed of inflammation and myocardial stress biomarkers improves the prediction of major cardiovascular adverse events in MI survivors.

Time delays in each step from symptom onset to treatment in acute myocardial infarction: Results from a nation-wide TURKMI registry.

OBJECTIVE: In this study, we aimed to analyze the TURKMI registry to identify the factors associated with delays from symptom onset to treatment that would be the focus of improvement efforts in patients with acute myocardial infarction (AMI) in Turkey. METHODS: The TURKMI study is a nation-wide registry that was conducted in 50 centers capable of 24/7 primary percutaneous coronary intervention (PCI). All consecutive patients (n=1930) with AMI admitted to coronary care units within 48 hours of symptom onset were prospectively enrolled during a predefined 2-week period between November 1, 2018, and November 16, 2018. All the patients were examined in detail with regard to the time elapsed at each step from symptom onset to initiation of treatment, including door-to-balloon time (D2B) and total ischemic time (TIT). RESULTS: After excluding patients who suffered an AMI within the hospital (2.6%), the analysis was conducted for 1879 patients. Most of the patients (49.5%) arrived by self-transport, 11.8% by emergency medical service (EMS) ambulance, and 38.6% were transferred from another EMS without PCI capability. The median time delay from symptom-onset to EMS call was 52.5 (15-180) min and from EMS call to EMS arrival 15 (10-20) min. In ST-segment elevation myocardial infarction (STEMI), the median D2B time was 36.5 (25-63) min, and median TIT was 195 (115-330) min. TIT was significantly prolonged from 151 (90-285) min to 250 (165-372) min in patients transferred from non-PCI centers. The major significant factors associated with time delay were patient-related delay and the mode of hospital arrival, both in STEMI and non-STEMI. CONCLUSION: The baseline evaluation of the TURKMI study revealed that an important proportion of patients presenting with AMI within 48 hours of symptom onset reach the PCI treatment center later than the time proposed in the guidelines, and the use of EMS for admission to hospital is extremely low in Turkey. Patient-related factors and the mode of hospital admission were the major factors associated with the time delay to treatment.

The relationship between a combination of vitamin D deficiency and hyperuricemia and the severity of coronary artery disease in myocardial infarction patients.

OBJECTIVE: Vitamin D deficiency has been shown to be associated with coronary artery disease (CAD). In addition, there are studies suggesting that hyperuricemia is an independent risk factor for atherosclerosis, whereas the relationship between the combination of these 2 parameters and severity of CAD remains unclear. The aim of this study was to investigate the association between the combination of vitamin D deficiency and hyperuricemia and the extent of CAD. METHODS: A total of 502 patients who had experienced myocardial infarction (MI) were included in this cross-sectional study. The 25-hydroxyvitamin D (25OHD) and serum uric acid (SUA) levels were measured in blood samples taken at the time of admission. A 2x2 factorial design was used to create groups according to the presence of hyperuricemia (>7 mg/dL) and vitamin D deficiency (<20 ng/mL). All of the patients underwent coronary angiography and the severity of CAD was determined using the Gensini score, SYNTAX score, and the number of diseased vessels. RESULTS: Both vitamin D deficiency and hyperuricemia were present in 83 patients (16.5%). Patients with hyperuricemia/vitamin D deficiency had more multivessel disease (24.1% vs 8.5%), and a higher SYNTAX score and Gensini score compared with the control group (13.9±8.0 vs. 9.5±6.3, 54.8±24.0 vs. 40.5±19.9, respectively). Age, male sex, presence of diabetes mellitus, family history of CAD, and levels of SUA and 25OHD were independent predictors of the severity of CAD. Moreover, the hyperuricemia/vitamin D deficiency group had 4 times greater odds of severe CAD than the control group. CONCLUSION: The combination of hyperuricemia and vitamin D deficiency appears to be an independent predictor of severe CAD in MI patients.