Optimal left ventricular ejection fraction in risk stratification of patients with cardiac sarcoidosis.

AIMS: Identifying patients with cardiac sarcoidosis (CS) who are at an increased risk of sudden cardiac death (SCD) poses a clinical challenge. We sought to identify the optimal cutoff for left ventricular ejection fraction (LVEF) in predicting ventricular arrhythmia (VA) and all-cause mortality and to identify clinical and imaging risk factors in patients with known CS. METHODS AND RESULTS: This retrospective cohort included 273 patients with well-established CS. The primary endpoint was a composite of VA and all-cause mortality. A modified receiver operating curve analysis was utilized to identify the optimal cutoff for LVEF in predicting the primary composite endpoint. Cox proportional hazard regression analysis was used to identify independent risk factors of the outcomes. At median follow-up of 7.9 years, the rate of the primary endpoint was 38% (83 VAs and 32 all-cause deaths). The 5-year overall survival rate was 97%. The optimal cutoff LVEF for the primary composite endpoint was 42% in the entire cohort and in subjects without a history of VA. Younger age, history of VA, lower LVEF, and any presence of scar by cardiac magnetic resonance (CMR) imaging and/or positron emission tomography (PET) were found to be independent risk factors for the primary endpoint and for VA, whereas lower LVEF, baseline NT-proBNP, and any presence of scar were independent risk factor of all-cause mortality. CONCLUSION: Among patients with CS, a mild reduction in LVEF of 42% was identified as the optimal cutoff for predicting VA and all-cause mortality. Prior VA and scar by CMR or PET are strong risk factors for future VA and all-cause mortality.

Reference Ranges, Diagnostic and Prognostic Utility of Native T1 Mapping and Extracellular Volume for Cardiac Amyloidosis: A Meta-Analysis.

BACKGROUND: Cardiac MRI is central to the evaluation of cardiac amyloidosis (CA). Native T1 mapping and extracellular volume (ECV) are novel MR techniques with evolving utility in cardiovascular diseases, including CA. PURPOSE: To perform a meta-analysis of the diagnostic and prognostic data of native T1 mapping and ECV techniques for assessing CA. STUDY TYPE: Systematic review and meta-analysis. POPULATION: In all, 3520 patients including 1539 with CA from 22 studies retrieved following systematic search of Pubmed, Cochrane, and Embase. FIELD STRENGTH/SEQUENCE: 1.5T or 3.0T/modified Look-Locker inversion recovery (MOLLI) or shortened MOLLI (shMOLLI) sequences. ASSESSMENT: Meta-analysis was performed for all CA and for light-chain (AL) and transthyretin (ATTR) subtypes. Thresholds were calculated to classify native T1 and ECV values as not suggestive, indeterminate, or suggestive of CA. STATISTICAL ANALYSIS: Area under the receiver-operating characteristic curves (AUCs) and hazards ratios (HRs) with 95% confidence intervals (95% CI) were pooled using random-effects models and Open-Meta(Analyst) software. RESULTS: Six studies were diagnostic, 16 studies reported T1 and ECV values to determine reference range, and six were prognostic. Pooled AUCs (95% CI) for diagnosing CA were 0.92 (0.89-0.96) for native T1 mapping and 0.96 (0.93-1.00) for ECV, with similarly high detection rates for AL- and ATTR-CA. Based on the pooled values of native T1 and ECV in CA and control subjects, the thresholds that suggested the absence, indeterminate, or presence of CA were identified as <994 msec, 994-1073 msec, and >1073 msec, respectively, for native T1 at 1.5T. Pooled HRs (95% CI) for predicting all-cause mortality were 1.15 (1.08-1.22) for native T1 mapping as a continuous parameter, 1.19 (1.01-1.40) for ECV as a continuous parameter, and 4.93 (2.64-9.20) for ECV as a binary threshold. DATA CONCLUSION: Native T1 mapping and ECV had high diagnostic performance and predicted all-cause mortality in CA. LEVEL OF EVIDENCE: 1 TECHNICAL EFFICACY STAGE: 2.

Coronavirus disease and the cardiovascular system: a narrative review of the mechanisms of injury and management implications.

Coronavirus disease (COVID-19), first identified in Wuhan, China, in December 2019, is now a pandemic, having already spread to 188 countries, with more than 28,280,000 infections worldwide. Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) is the responsible infectious agent, and similar to other human coronaviruses, uses membrane-bound angiotensin-converting enzyme 2 (membrane-bound ACE2) for entry into the host cells. COVID-19 has important cardiovascular implications, especially for patients with pre-existing cardiovascular co-morbidities, potentially mediated through several mechanisms, including direct myocardial injury, worsening of those pre-existing cardiovascular co-morbidities, and adverse cardiovascular effects of potential therapies for COVID-19. The disease is causing a significant burden on health systems worldwide. Elective surgeries and procedures were postponed for a considerable period of time, and many patients with known cardiovascular disease (CVD) risk factors presented late to hospitals, for fear of contracting COVID-19, with serious adverse consequences. Significant negative impact on a population level is highlighted by prolonged isolation, decreased exercise and physical activity, and higher levels of depression and anxiety, all predisposing to elevated cardiovascular risk. This article provides a timely overview of COVID-19 and its impact on the cardiovascular system, focusing on the pathogenesis, potential adverse cardiovascular events, the potential treatment options, protection for health care providers and patients, and what the cardiovascular community could do to mitigate the impact of COVID-19.