The novel coronavirus (SARS-CoV-2) is primarily a respiratory pathogen and its clinical manifestations are dominated by respiratory symptoms, the most severe of which is acute respiratory distress syndrome (ARDS). However, COVID-19 is increasingly recognized to cause an overwhelming inflammatory response and cytokine storm leading to end organ damage. End organ damage to heart is one of the most severe complications of COVID-19 that increases the risk of death. We proposed a two-fold mechanism responsible for causing acute coronary events in patients with COVID-19 infection: Cytokine storm leading to rapid onset formation of new coronary plaques along with destabilization of pre-existing plaques and direct myocardial injury secondary to acute systemic viral infection. A well-coordinated immune response is the first line innate immunity against a viral infection. However, an uncoordinated response and hypersecretion of cytokines and chemokines lead to immune related damage to the human body. Human Coronavirus (HCoV) infection causes infiltration of inflammatory cells that cause excessive production of cytokines, proteases, coagulation factors, oxygen radicals and vasoactive molecules causing endothelial damage, disruption of fibrous cap and initiation of formation of thrombus. Systemic viral infections also cause vasoconstriction leading to narrowing of vascular lumen and stimulation of platelet activation via shear stress. The resultant cytokine storm causes secretion of hypercoagulable tissue factor without consequential increase in counter-regulatory pathways such as AT-III, activated protein C and plasminogen activator type 1. Lastly, influx of CD4+ T-cells in cardiac vasculature results in an increased production of cytokines that stimulate smooth muscle cells to migrate into the intima and generate collagen and other fibrous products leading to advancement of fatty streaks to advanced atherosclerotic lesions. Direct myocardial damage and cytokine storm leading to destabilization of pre-existing plaques and accelerated formation of new plaques are the two instigating mechanisms for acute coronary syndromes in COVID-19.

Introduction Erdheim–Chester disease is a rare, multisystem hematologic disease. Cardiovascular involvement is seen in patients with Erdheim–Chester disease and can lead to increased morbidity and mortality. In this series, we report various cardiovascular manifestations of patients with Erdheim–Chester disease. Methods This study includes patients with Erdheim–Chester disease who were referred to our institution from 12/3/2009 through 12/13/2017. All patients had biopsy‐proven Erdheim–Chester disease. Clinical data, multimodality imaging, and cardiac tests were reviewed. Results Cardiovascular findings in 24 patients with Erdheim–Chester disease were included in the study. We reviewed available transthoracic echocardiograms, whole body PET/CT scans, and CMR studies. Most patients were male and mean age at the time of diagnosis was 58 years. Pericardial involvement (13%), myocardial infiltration (25%), endocardial involvement (4%), valvular disease (17%), aortic/vascular disease (17%), conduction system infiltration (8%), and coronary artery disease (25%) were present. At a median follow‐up of 5.5 years, mortality was 17%. Conclusions Erdheim–Chester disease can involve various cardiovascular structures and is frequently diagnosed on an imaging modality. Some patients had asymptomatic involvement, but others presented with ischemic heart disease, heart failure, valvular disease, and conduction system abnormalities. Early recognition of cardiovascular involvement of Erdheim–Chester disease is needed because of high morbidity and mortality.

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Background Recurrence of atrial fibrillation (AF) after catheter ablation (CA) remains common and studies have shown about 5%–9% annual recurrence rate after CA. We sought to assess the echocardiogram derived left atrial appendage (LAA) emptying velocity as a predictor of AF recurrence after CA. Objective To determine if LAA emptying is a marker of recurrence of AF post‐CA Methods A total of 303 consecutive patients who underwent CA for AF between 2014 and 2020 were included. Baseline clinical characteristics and echocardiographic data of the patients were obtained by chart review. LAA emptying velocities were obtained from transesophageal echocardiogram (TEE). LA voltage was obtained during the mapping for CA. Chi‐square test and nominal logistic regression were used for statistical analysis. An receiver operator characteristic curve was used to determine LAA velocity cut‐off. Results Mean patient age was 61.7 ± 10.5; 32% were female. Mean LAA emptying velocity was 47.5 ± 20.2. A total of 103 (40%) patients had recurrence after CA. In the multivariable model, after adjusting for potential confounders, LAA emptying velocity of ≥52.3 was associated with decreased AF recurrence postablation (odds ratio [OR]: 0.55; 95% confidence interval  [CI]: 0.31–0.97; p = .03*). There were 190 (73%) patients in normal sinus rhythm during TEE and CA, and sensitivity analysis of these patients showed that LAA velocity ≥52.3 remained associated with decreased AF recurrence (OR: 0.35; 95% CI: 0.15–0.82; p = .01*). Conclusion LAA emptying velocity measured during preprocedural TEE can serve as a predictor of AF recurrence in patients undergoing CA.

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