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

Author(s):  
Mustafa Umut Somuncu ◽  
Fatih Pasa Tatar ◽  
Belma Kalayci ◽  
Ahmet Avci ◽  
Naile Eris Gudul ◽  
...  

Abstract 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.

2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
E Nakou ◽  
R Fisher ◽  
C Tountas ◽  
E Corcoran ◽  
A Dhariwal ◽  
...  

Abstract Introduction For some individuals infection with SARS-CoV-2 leading to COVID-19 can result in a life-threatening multi-system disease. Multiple potential pathophysiological mechanisms for the development of cardiovascular complications have been postulated [1]. Early reports suggested that more than a third of hospitalised patients undergoing TTE had evidence of LV impairment [2]. Purpose To ascertain the incidence of ventricular impairment among critically ill adults with COVID-19 admitted to the intensive care unit (ICU). Methods Retrospective analysis of transthoracic echocardiograms (TTE) performed on patients admitted to ICU with COVID-19 between 10th March and 10th May 2020. Archived studies were reviewed by accredited professionals. Studies were performed according to a modified British Society of Echocardiography (BSE) Level 1 protocol [3], with the addition of right ventricle (RV) focused apical 4 chamber, as well as apical 2 and 3 chamber views, and without ECG synchronisation as per infection control protocols. In the majority of patients the left ventricular ejection fraction (LVEF) was estimated from biplane Simpson's method. The RV function was assessed using the TAPSE in most patients. In the remaining patients the LV or RV function was visually assessed. Results Of 179 patients admitted to ICU, 85 (47.5%) had at least one TTE of diagnostic quality. Studies were performed a median of 7 days after ICU admission (IQR 3–17 days). Baseline and clinical characteristics and key echocardiographic measurements are summarised in table 1. The majority of patients were undergoing mechanical ventilation at the time of the scan (94.1%). One hundred and fifty-nine patients (89%) had elevated Troponin T (≥14ng/L) on the day of the study. LV systolic impairment (LVSD) was present in 5 patients (6.0%). This was known to be chronic in 3 patients (1 with coronary artery disease, 1 with chemotherapy induced cardiomyopathy and 1 with dilated cardiomyopathy of unknown aetiology), whilst pre-morbid cardiac function was unknown in the other 2 patients. No patient had severe LVSD (LVEF ≤35%). RV systolic dysfunction (RVSD) was found in 25 patients (31.3%). Amongst patients receiving mechanical ventilation there was no significant difference in Positive End Expiratory Pressure (PEEP) between patients with and without RVSD (9.4cmH2O vs. 9.8cmH2O, p=0.64), however there was a non-significant trend towards lower PaO2/FiO2 (P/F ratio) amongst patients with RVSD (18.9kPa vs 25.7kPa, p=0.07). Conclusions In contrast to other studies which have reported high frequency of LV impairment amongst hospitalised patients with COVID-19 [3], de novo LVSD was rarely found in this study, occurring in just 2 patients (2.4%), and being severe in neither. RV dilatation and systolic impairment were commonly found. A trend towards lower P/F ratios in patients with RVSD suggests severity of lung injury may be a factor in developing RV impairment. FUNDunding Acknowledgement Type of funding sources: None.


2021 ◽  
Vol 41 (2) ◽  
Author(s):  
Ana C.A. Casarotti ◽  
Daniela Teixeira ◽  
Ieda M. Longo-Maugeri ◽  
Mayari E. Ishimura ◽  
Maria E.R. Coste ◽  
...  

Abstract Despite early reperfusion, patients with ST segment elevation myocardial infarction (STEMI) may present large myocardial necrosis and significant impairment of ventricular function. The present study aimed to evaluate the role of subtypes of B lymphocytes and related cytokines in the infarcted mass and left ventricular ejection fraction obtained by cardiac magnetic resonance imaging performed after 30 days of STEMI. This prospective study included 120 subjects with STEMI submitted to pharmacoinvasive strategy. Blood samples were collected in subjects in the first (D1) and 30th (D30) days post STEMI. The amount of CD11b+ B1 lymphocytes (cells/ml) at D1 were related to the infarcted mass (rho = 0.43; P=0.033), measured by cardiac MRI at D30. These B1 cells were associated with CD4+ T lymphocytes at D1 and D30, while B2 classic lymphocytes at day 30 were related to left ventricular ejection fraction (LVEF). Higher titers of circulating IL-4 and IL-10 were observed at D30 versus D1 (P=0.013 and P&lt;0.001, respectively). Titers of IL-6 at D1 were associated with infarcted mass (rho = 0.41, P&lt;0.001) and inversely related to LVEF (rho = −0.38, P&lt;0.001). After multiple linear regression analysis, high-sensitivity troponin T and IL-6 collected at day 1 were independent predictors of infarcted mass and, at day 30, only HDL-C. Regarding LVEF, high-sensitivity troponin T and high-sensitivity C-reactive protein were independent predictors at day 1, and B2 classic lymphocytes, at day 30. In subjects with STEMI, despite early reperfusion, the amount of infarcted mass and ventricular performance were related to inflammatory responses triggered by circulating B lymphocytes.


2021 ◽  

Objectives: To evaluate the severity of acute myocardial infarction (AMI) complicated with cardiogenic shock (CS), by comparison with inferior and right ventricular AMI, which is also considered a severe form of myocardial infarction. Methods: In an observational study, from 774 patients with STEMI hospitalized in our Cardiology Institute, over one year and a half, only 120 patients met the inclusion and exclusion criteria (60 patients with CS and 60 patients with right ventricular AMI). Data collected included age, sex, vital signs, oxygen saturation, respiratory rate, left ventricular ejection fraction, right ventricular dysfunction, complications during hospitalization and coronarography results. Results: Patients with CS had a more severe systolic dysfunction (median ejection fraction 22.72 ± 12.30% vs. 41.93 ± 10.50%, P < 0.0001). Single-vessel disease was the most common in both groups, left anterior descending artery being the culprit artery in most patients with cardiogenic shock, 25% of them having residual lesions with a severity >75%. Using a multivariate analysis, we observed that for patients with CS, delayed coronary angiography evaluation, as well as the presence of severe triple-vessel disease, were associated with a higher risk of death. In-hospital mortality (53.33% vs. 8.33%, P < 0.0001) and ventricular arrhythmia were significantly higher in patients with CS (48.3% vs. 11.3%, P < 0.0001). Conclusions: Our study suggests that patients with AMI and CS can be considered the most severe form of myocardial infarction and should, therefore, benefit of prompt and appropriate treatment, to improve the outcome.


2018 ◽  
Vol 2018 ◽  
pp. 1-8
Author(s):  
Elena Teringova ◽  
Martin Kozel ◽  
Jiri Knot ◽  
Viktor Kocka ◽  
Klara Benesova ◽  
...  

Background. Apoptosis plays an important role in the myocardial injury after acute myocardial infarction and in the subsequent development of heart failure. Aim. To clarify serum kinetics of apoptotic markers TRAIL and sFas and their relation to left ventricular ejection fraction (LVEF) in patients with ST-elevation myocardial infarction (STEMI) treated with primary percutaneous coronary intervention (pPCI). Methods. In 101 patients with STEMI treated with pPCI, levels of TRAIL and sFas were measured in series of serum samples obtained during hospitalization and one month after STEMI. LVEF was assessed at admission and at one month. Major adverse cardiovascular events (MACE, i.e., death, re-MI, and hospitalization for heart failure and stroke) were analysed during a two-year followup. Results. Serum level of TRAIL significantly decreased one day after pPCI (50.5pg/mL) compared to admission (56.7pg/mL), subsequently increased on day 2 after pPCI (58.8pg/mL), and reached its highest level at one month (70.3pg/mL). TRAIL levels on days 1 and 2 showed a significant inverse correlation with troponin and a significant positive correlation with LVEF at baseline. Moreover, TRAIL correlated significantly with LVEF one month after STEMI (day 1: r=0.402, p<0.001; day 2: r=0.542, p<0.001). On the contrary, sFas level was significantly lowest at admission (5073pg/mL), increased one day after pPCI (6370pg/mL), and decreased on day 2 (5548pg/mL). Significantly highest sFas level was marked at one month (7024pg/mL). sFas failed to correlate with LVEF at baseline or at one month. Both TRAIL and sFas showed no ability to predict improvement of LVEF one month after STEMI or a 2-year MACE (represented by 3.29%). Conclusion. In STEMI treated with pPCI, TRAIL reaches its lowest serum concentration after reperfusion. Low TRAIL level is associated with worse LVEF in the acute phase of STEMI as well as one month after STEMI. Higher TRAIL level appears to be beneficial and thus TRAIL seems to represent a protective mediator of post-AMI injury.


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