Cardiac Magnetic Resonance Imaging as a Risk Stratification Tool in COVID-19 Myocarditis.

The aim of this retrospective study was to identify myocardial injury after COVID-19 inflammation and explore whether myocardial damage could be a possible cause of the persistent symptoms following COVID-19 infection in previously healthy individuals. This study included 139 patients who were enrolled between January and June 2021, with a mean age of 46.7 ± 15.2 years, of whom 68 were men and 71 were women without known cardiac or pulmonary diseases. All patients underwent clinical work-up, laboratory analysis, cardiac ultrasound, and CMR on a 1.5 T scanner using a recommended protocol for morphological and functional assessment before and after contrast media application with multi-parametric sequences. In 39% of patients, late gadolinium enhancement (LGE) was found as a sign of myocarditis. Fibrinogen was statistically significantly higher in patients with LGE than in those without LGE (4.3 ± 0.23 vs. 3.2 ± 0.14 g/L, p < 0.05, respectively), as well as D-dimer (1.8 ± 0.3 vs. 0.8 ± 0.1 mg/L FEU). Also, troponin was statistically significantly higher in patients with myocardial LGE (13.1 ± 0.4 ng/L) compared to those with normal myocardium (4.9 ± 0.3 ng/L, p < 0.001). We demonstrated chest pain, fatigue, and elevated troponin to be independent predictors for LGE. Septal LGE was shown to be a predictor for arrhythmias. The use of CMR is a potential risk stratification tool in evaluating outcomes following COVID-19 myocarditis.

Prognostic Implications of the Timing of ST-Elevation Myocardial Infarction Development in Relation to COVID-19 Infection.

Background: Patients with ST-segment elevation myocardial infarction (STEMI) and COVID-19 infection have a worse clinical course and prognosis. The prognostic significance of the timing of STEMI in relation to COVID-19 infection was not investigated. Objectives: To assess whether the time of STEMI development in relation to COVID-19 infection (concurrent or following the infection) influenced the short-term prognosis. Methods: This was an observational study of consecutive COVID-19 patients with STEMI admitted to the COVID-hospital Batajnica (February 2021-March 2022). The patients were divided into the "STEMI first" group: patients with STEMI and a positive polymerase chain reaction test for COVID-19, and the "COVID-19 first" group: patients who developed STEMI during COVID-19 treatment. All patients underwent coronary angiography. The primary endpoint was in-hospital all-cause mortality. Results: The study included 87 patients with STEMI and COVID-19 (Mage, 66.7 years, 66% male). The "STEMI first" group comprised 54 (62.1%) patients, and the "COVID-19 first" group included 33 (37.9%) patients. Both groups shared a comparatively high burden of comorbidities, similar angiographic and procedural characteristics, and high percentages of performed percutaneous coronary interventions with stent implantation (90.7% vs. 87.9%). In-hospital mortality was significantly higher in the "COVID-19 first" group compared to the "STEMI first" group (51.5% vs. 27.8%). Following adjustment, the "COVID-19 first" group had a hazard ratio of 3.22 (95% confidence interval, 1.18-8.75, p = .022) for in-hospital all-cause death, compared with the "STEMI first" group (reference). Conclusion: Clinical presentation with COVID-19 infection, followed by STEMI ("COVID-19 first"), was associated with greater short-term mortality compared to patients presenting with STEMI and testing positive for COVID-19 ("STEMI first").

Predictors and prognostic implications of hospital-acquired pneumonia in patients admitted for acute heart failure.

Introduction: Data on predictors and prognosis of hospital acquired pneumonia (HAP) in patients admitted for acute heart failure (AHF) to intensive care units (ICU) are scarce. Better knowledge of these factors may inform management strategies. This study aimed to assess the incidence and predictors of HAP and its impact on management and outcomes in patients hospitalised for AHF in the ICU. Methods: this was a retrospective single-centre observational study. Patient-level and outcome data were collected from an anonymized registry-based dataset. Primary outcome was in-hospital all-cause mortality and secondary outcomes included length of stay (LOS), requirement for inotropic/ventilatory support, and prescription patterns of heart failure (HF) drug classes at discharge. Results: Of 638 patients with AHF (mean age, 71.6 ± 12.7 years, 61.9% male), HAP occurred in 137 (21.5%). In multivariable analysis, HAP was predicted by de novo AHF, higher NT proB-type natriuretic peptide levels, pleural effusion on chest x-ray, mitral regurgitation, and a history of stroke, diabetes, and chronic kidney disease. Patients with HAP had a longer LOS, and a greater likelihood of requiring inotropes (adjusted odds ratio, OR, 2.31, 95% confidence interval, CI, 2.16-2.81; p < 0.001) or ventilatory support (adjusted OR 2.11, 95%CI, 1.76-2.79, p < 0.001). After adjusting for age, sex and clinical covariates, all-cause in-hospital mortality was significantly higher in patients with HAP (hazard ratio, 2.10; 95%CI, 1.71-2.84; p < 0.001). Patients recovering from HAP were less likely to receive HF medications at discharge. Discussion: HAP is frequent in AHF patients in the ICU setting and more prevalent in individuals with de novo AHF, mitral regurgitation, higher burden of comorbidities, and more severe congestion. HAP confers a greater risk of complications and in-hospital mortality, and a lower likelihood of receiving evidence-based HF medications at discharge.

Incidence, risk assessment and prevention of sudden cardiac death in cardiomyopathies.

Cardiomyopathies are a significant contributor to cardiovascular morbidity and mortality, mainly due to the development of heart failure and increased risk of sudden cardiac death (SCD). Despite improvement in survival with contemporary treatment, SCD remains an important cause of mortality in cardiomyopathies. It occurs at a rate ranging between 0.15% and 0.7% per year (depending on the cardiomyopathy), which significantly surpasses SCD incidence in the age- and sex-matched general population. The risk of SCD is affected by multiple factors including the aetiology, genetic basis, age, sex, physical exertion, the extent of myocardial disease severity, conduction system abnormalities, and electrical instability, as measured by various metrics. Over the past decades, the knowledge on the mechanisms and risk factors for SCD has substantially improved, allowing for a better-informed risk stratification. However, unresolved issues still challenge the guidance of SCD prevention in patients with cardiomyopathies. In this review, we aim to provide an in-depth discussion of the contemporary concepts pertinent to understanding the burden, risk assessment and prevention of SCD in cardiomyopathies (dilated, non-dilated left ventricular, hypertrophic, arrhythmogenic right ventricular, and restrictive). The review first focuses on SCD incidence in cardiomyopathies and then summarizes established and emerging risk factors for life-threatening arrhythmias/SCD. Finally, it discusses validated approaches to the risk assessment and evidence-based measures for SCD prevention in cardiomyopathies, pointing to the gaps in evidence and areas of uncertainties that merit future clarification.