Background: Left ventricular (LV) diastolic dysfunction (DD) is a hallmark of heart failure with preserved ejection fraction (HFpEF). Right ventricular (RV) function is a strong and independent prognostic factor in this population, but its correlation with LV DD has not yet been explored. 3D echocardiography allows for accessible, accurate, reproducible analyses of RV function. Our study aims to assess the association between LV diastolic function and RV function (measured via automated 3D echocardiography software) Hypothesis: The RV enlarges and its systolic function decreases, in a graded fashion, with increasing degrees of LV DD Methods: We conducted a prospective, single-center, cross-sectional cohort study in patients with clinically indicated echocardiography and 3D RV assessment. We excluded patients with non-WHO group 2 pulmonary hypertension, non-sinus rhythm during echocardiogram, and those with a LVEF <40%. We conducted an interim analysis of the first 187 patients. Patients were stratified according to DD grading, and different RV parameters were compared using ANOVA Results: 187 patients underwent interim analysis, 65% were women. Mean age 60±17 years, 64% African-American, 16% Hispanic, 12% Caucasian. Mean BMI 29±6 kg/m 2 . Mean LVEF and LV GLS were 57±10% and -17.7±3.6, respectively. A graded worsening in RV systolic function and morphology were noted in patients with DD. Patients with grade II/ III DD had worse RV EDV (146±42 mL), RV FAC (32±9%), TAPSE (19±5 mm), and RVEF (40±9%), than patients without DD (RV EDV 114±36 mL, p=0.0011; RV FAC 39±7.4%, p<0.001; TAPSE 21±5 mm, p<0.001; and RVEF 47±8%, p<0.001), and grade I DD Conclusion: Our results suggest that there is a graded worsening in the RV function and morphology as LV diastolic function worsens in patients with preserved EF. This denotes the importance of widespread, accurate, and reproducible RV assessment during standard echocardiography
Arrhythmias or conduction system disease are not the most common manifestation of COVID-19 infection in patients requiring hospital admission. Torsade de pointes typically occurs in bursts of self-limiting episodes with symptoms of dizziness and syncope. However, it may occasionally progress to ventricular fibrillation and sudden death. In this article, we report a case of COVID-19 patient who developed polymorphic ventricular tachycardia with torsade de pointes morphology with normal QTc interval in the setting of fever. An 81-year-old woman was admitted with symptoms of COVID-19. She was treated with hydroxychloroquine, azithromycin, and doxycycline at an outside facility and finished the treatment 5 days prior to admission to our facility. Her course was complicated by atrial fibrillation with rapid ventricular response requiring cardioversion. Later, she developed two episodes of polymorphic ventricular tachycardia with TdP morphology with normal QTc. There was a correlation with fever triggering the ventricular tachycardia. We advocated aggressive fever control given the QTc was normal and stable. Following fever control, the patient remained stable and had no abnormal rhythm. COVID-19 patients are prone to different arrhythmias including life-threatening ventricular arrhythmias with normal left ventricular systolic function and normal QTc, and they should be monitored for fever and electrolyte abnormality during their hospital stay.
Atrial fibrillation (AF) is the most common arrhythmia in the United States and the most common cause of embolic cerebrovascular events, with the majority of these thrombi originating in the left atrial appendage. The left atrial appendage (LAA) has separate developmental, ultrastructural, and physiological characteristics from the left atrium. Although LAA anatomy is highly variable, it can be categorized into 4 types: cactus, cauliflower, chicken wing, and windsock. The cauliflower type is associated with higher stroke risk in patients with nonvalvular AF. Although the cornerstone of therapy to prevent embolic strokes from AF has been anticoagulation with thrombin inhibitors, a large group of patients are unable to tolerate anticoagulation due to bleeding. This has led to the development and advancement of multiple surgical and percutaneous LAA closure devices to prevent embolic cerebrovascular accidents without the need for anticoagulation. In this article, we discuss the outcomes of major studies that utilized surgical LAA occlusion and its effectiveness. Furthermore, we summarize nonsurgical methods of LAA closure and future directions regarding LAA closure.
The Novel Coronavirus Disease 2019 (COVID-19) pandemic has transformed individual lives and societal framework on a global scale, and in no other sector is this more evident than healthcare. Herein, we aim to describe the impact of the current COVID-19 pandemic and its associated restrictions on heart failure (HF) admissions. In this retrospective cohort study, we obtained administrative data for patients with a primary discharge diagnosis of HF (identified by ICD-10 code) with discharge dates ranging from January 2019 to November 2020. The study is comprised of 2 distinct sub-cohorts: HF admissions during the COVID-19 pandemic (case) period from March 2020 to October 2020 and corresponding control period during the previous year (March 2019 to December 2019). Primary outcome analysis involved comparison of total and daily HF admissions and secondary outcomes included hospital Length of Stay (LOS) and 30-day readmissions. The number of total HF admissions and average daily admissions were significantly lower in 2020 compared to 2019 (774 vs. 864; p < 0.001 and 3.17 vs. 3.53 days; p < 0.001), respectively. Average length of stay was significantly higher between March and October 2020 relative to the same months in 2019 (6.05 vs. 5.25 days; p < 0.001). Thirty-day readmission rates were also significantly higher in March-October 2020 compared to the same months in 2019 (20.6% vs. 19.1%; p < 0.001). During the pandemic, both readmission rates and length of stay for HF-related admissions were significantly impacted. The COVID-19 pandemic significantly impacted HF-related admissions as well as associated LOS and 30-day readmissions. High-risk patients should be identified carefully, and timely and appropriate treatment should be provided.
Chronic infection has long been postulated as a stimulus for atherogenesis. Pseudomonas aeruginosa infection has been associated with increased atherosclerosis in rats, and these bacteria produce a quorum-sensing molecule 3-oxo-dodecynoyl-homoserine lactone (3OC12-HSL) that is critical for colonization and virulence. Paraoxonase 2 (PON2) hydrolyzes 3OC12-HSL and also protects against the effects of oxidized phospholipids thought to contribute to atherosclerosis. We now report the response of human aortic endothelial cells (HAECs) to 3OC12-HSL and oxidized 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphocholine (Ox-PAPC) in relation to PON2 expression.Using expression profiling and network modeling, we identified the unfolded protein response (UPR), cell cycle genes, and the mitogen-activated protein kinase signaling pathway to be heavily involved in the HAEC response to 3OC12-HSL. The network also showed striking similarities to a network created based on HAEC response to Ox-PAPC, a major component of minimally modified low-density lipoprotein. HAECs in which PON2 was silenced by small interfering RNA showed increased proinflammatory response and UPR when treated with 3OC12-HSL or Ox-PAPC.3OC12-HSL and Ox-PAPC influence similar inflammatory and UPR pathways. Quorum sensing molecules, such as 3OC12-HSL, contribute to the proatherogenic effects of chronic infection. The antiatherogenic effects of PON2 include destruction of quorum sensing molecules.
Brugada syndrome (BRS) is a channelopathy with three characteristic electrocardiogram patterns and an increased risk of sudden cardiac death (SCD), in the absence of gross structural heart disease. Fever is shown to precipitate ventricular arrhythmias in patients with BRS. Here, we report a rare case of Brugada pattern in a patient with Coronavirus Disease 2019 (COVID-19) without fever. A baseline ECG should be considered for patients with COVID-19, even in the absence of fever. COVID-19 by itself may be a factor that can induce Brugada pattern ECGs.
Extra-pulmonary manifestations of severe acute respiratory syndrome coronavirus 2 [SARS-CoV-2] infection such as cardiovascular complications have been reported and previous case reports have documented evidence of myocardial damage. Currently, very few case reports of the arrhythmias associated with Coronavirus Disease 2019 [COVID-19] exist. In this case series, we demonstrate two cases of critically ill COVID-19 patients with cardiac rhythm abnormalities that might be a direct or indirect consequence of this infection. Each of the patients experienced a variety of cardiac rhythm abnormalities. None of the patients had any record of cardiac rhythm abnormalities prior to admission. The unique point of these cases is the multiple dysrhythmias in the same patients that have not been reported previously. We demonstrated that critically ill COVID-19 patients develop different arrhythmias ranging from sinus tachycardia, bradycardia, atrial fibrillation, supraventricular tachycardia, and non-sustained ventricular tachycardia. Non-sustained monomorphic ventricular tachycardia was the most common arrhythmia in the two cases despite normalization of electrolyte imbalances and avoidance of QTc prolonging agents.
