Atrial Fibrillation as a Predictor of Mortality in High Risk COVID-19 Patients: A Multicentre Study of 171 Patients.

PURPOSE: Certain patient demographics and biomarkers have been suggested to predict survival in patients infected with COVID-19. However, predictors of outcome in patients who are critically ill are unclear. MATERIALS AND METHODS: We performed a multicentre analysis of 171 consecutive patients with confirmed COVID-19 who were admitted to the intensive care unit (ICU) between 1 March 2020 and 30 April 2020 and were followed until 23 May 2020. Demographic data, past medical history, laboratory values, echocardiographic and telemetry data were analysed. Patient status was classified as either alive or deceased at hospital discharge or the end of follow-up period. RESULTS: Mean patient age was 66±13 and 57% were male. Mortality rate of this ICU cohort at the end of follow-up was 46.2%. A multivariable logistic regression analysis identified the presence or history of atrial fibrillation (Odds Ratio 4.8, p=0.004) as a significant cardiovascular attribute that contributed to increased mortality. CONCLUSION: Mortality of critically ill COVID-19 patients is high. This study suggests a relationship between atrial fibrillation and increased mortality from COVID-19. Early aggressive treatment patients with high risk characteristics, such as atrial fibrillation could improve clinical outcome.

Effect of combined renal denervation and pulmonary vein isolation in atrial fibrillation recurrence in hypertensive patients: A meta-analysis.

BACKGROUND: Atrial Fibrillation (AF) is the most common cardiac arrhythmia and hypertension is the most common risk factor associated with AF. The addition of renal sympathetic nerve denervation (RSDN) to pulmonary vein isolation (PVI) in AF patients with hypertension has been reported to improve clinical outcomes. METHODS: A systematic search was performed for studies on patients with AF and hypertension that compared RSDN with PVI versus PVI-alone. Risk ratio (RR) for categorical variables and mean difference (MD) for continuous variables with 95% confidence intervals were used. RESULTS: Seven studies with a total of 734 patients were included. A total of 340 patients were in the RSDN + PVI group (46.32%) and 394 (53.67%) in the PVI group. A total of 608 patients had paroxysmal AF (83%) while 126 patients had persistent AF (17%). At 12 months follow-up, RSDN + PVI decreased the overall risk of AF recurrence in hypertensive patients with RR 0.60 [95% CI 0.50-0.72, P < .00001]. A subgroup analysis performed in patients with drug-resistant hypertension showed a similar reduction in AF recurrence with RR 0.61 [95% CI: 0.47-0.79, P = .0002). Procedure duration MD + 28.05 min [95% CI: 18.88-37.23, P < .00001] and fluoroscopy duration MD + 5.59 min [95% CI: 3.31-8.19, P < .00001] were significantly longer with the RSDN + PVI group. There was no significant difference in complications between the two groups. CONCLUSION: The addition of RSDN to PVI in patients with AF and hypertension appears safe and decreases AF recurrence. Similar results were observed in patients with drug-resistant hypertension. Larger trials are needed to confirm these results.

Right Coronary Artery-to-Right Atrial Fistula Accompanied by Multiple Right Coronary Artery Aneurysms: A Case Report.

A coronary artery aneurysm (CAA) denotes a localized dilation of the coronary artery, while a coronary artery fistula signifies an aberrant connection between a coronary artery and a cardiac chamber or adjacent vessel. Here, we present a case study of a 68-year-old female with a previously diagnosed right coronary artery-to-right atrial fistula concomitant with multiple right coronary artery aneurysms. Initially asymptomatic, the patient subsequently manifested atrial fibrillation. Management involved augmenting the patient's home regimen with metoprolol tartrate, followed by successful cardioversion and restoration of sinus rhythm. Given the stability of the fistula and the absence of symptomatic exacerbation, no further interventional measures were undertaken. The patient was discharged with an adjusted metoprolol regimen and scheduled follow-up with her cardiologist. Subsequent imaging assessments unveiled progressive fistula expansion alongside the development of concurrent CAA, inciting deliberations concerning optimal treatment modalities.

Cholesterol crystals induce mechanical trauma, inflammation, and neo-vascularization in solid cancers as in atherosclerosis.

Background and aims: Cancer and atherosclerosis share common risk factors and inflammatory pathways that promote their proliferation via vascular endothelial growth factor (VEGF). Because CCs cause mechanical injury and inflammation in atherosclerosis, we investigated their presence in solid cancers and their activation of IL-1ß, VEGF, CD44, and Ubiquityl-Histone H2B (Ub-H2B), that promote cancer growth. Methods: Tumor specimens from eleven different types of human cancers and atherosclerotic plaques were assessed for CCs, free cholesterol content and IL1-ß by microscopy, immunohistochemistry, and biochemical analysis. Breast and colon cancer cell lines were cultured with and without CCs to select for expression of VEGF, CD44, and Ub-H2B. Western blot and immunofluorescence were performed on cells to assess the effect of CCs on signaling pathways. Results: Cancers displayed higher CC content (+2.29 ± 0.74 vs +1.46 ± 0.84, p < 0.0001), distribution (5.06 ± 3.13 vs 2.86 ± 2.18, p < 0.001) and free cholesterol (3.63 ± 4.02 vs 1.52 ± 0.56 µg/mg, p < 0.01) than cancer free marginal tissues and similarly for atherosclerotic plaques and margins (+2.31 ± 0.51 vs +1.44 ± 0.79, p < 0.02; 14.0 ± 5.74 vs 8.14 ± 5.52, p < 0.03; 0.19 ± 0.14 vs 0.09 ± 0.04 µg/mg, p < 0.02) respectively. Cancers displayed significantly increased expression of IL1-ß compared to marginal tissues. CCs treated cancer cells had increased expression of VEGF, CD44, and Ub-H2B compared to control. By microscopy, CCs were found perforating cancer tumors similar to plaque rupture. Conclusions: These findings suggest that CCs can induce trauma and activate cytokines that enhance cancer growth as in atherosclerosis.

Interaction between bacteria and cholesterol crystals: Implications for endocarditis and atherosclerosis.

BACKGROUND: The interaction between pathogenic bacteria and cholesterol crystals (CCs) has not been investigated. However, CCs are found extensively in atherosclerotic plaques and sclerotic cardiac valves. Interactions between pathogenic bacteria and CCs could provide insights into destabilization of atherosclerotic plaques and bacterial adhesion to cardiac valves. METHODS: Staphylococcus aureus and Pseudomonas aeruginosa were used to assess in vitro bacterial adhesion to CCs and proliferation in the presence of CCs compared to plastic microspheres and glass shards as controls. Ex vivo studies evaluated bacterial adhesion to atherosclerotic rabbit arteries compared to normal arteries and human atherosclerotic carotid plaques compared to normal carotid arteries. Scanning electron microscopy (SEM) was used to visualize bacterial adhesion to CCs and confocal microscopy was used to detect cholesterol binding to bacteria grown in the presence or absence of CCs. RESULTS: In vitro, S. aureus and P. aeruginosa displayed significantly greater adhesion, 36% (p<0.0001) and 89% (p<0.0001), respectively, and growth upon exposure to CCs compared to microspheres or glass shards. Rabbit and human atherosclerotic arteries contained significantly greater bacterial burdens compared to controls (4× (p<0.0004); 3× (p<0.019), respectively. SEM demonstrated that bacteria adhered and appeared to degrade CCs. Consistent with this, confocal microscopy indicated increased cholesterol bound to the bacterial cells. CONCLUSIONS: This study is the first to demonstrate an interaction between bacteria and CCs showing that bacteria dissolve and bind to CCs. This interaction helps to elucidate adhesion of bacteria to sclerotic valves and atherosclerotic plaques that may contribute to endocarditis and plaque destabilization.

Meta-Analysis of Valve-in-Valve Transcatheter Aortic Valve Implantation Versus Redo-surgical Aortic Valve Replacement in Failed Bioprosthetic Aortic Valve.

This meta-analysis was conducted to compare clinical outcomes of valve-in-valve transcatheter aortic valve implantation (ViV-TAVI) versus redo-surgical aortic valve replacement (Redo-SAVR) in failed bioprosthetic aortic valves. We conducted a comprehensive review of previous publications of all relevant studies through August 2020. Twelve observational studies were included with a total of 8,430 patients, and a median-weighted follow-up period of 1.74 years. A pooled analysis of the data showed no significant difference in all-cause mortality (OR 1.15; 95% CI 0.93 to 1.43; p = 0.21), cardiovascular mortality, myocardial infarction, permanent pacemaker implantation, and the rate of moderate to severe paravalvular leakage between ViV-TAVI and Redo-SAVR groups. The rate of major bleeding (OR 0.36; 95% CI 0.16 to 0.83, p = 0.02), procedural mortality (OR 0.41; 95% CI 0.18 to 0.96, p = 0.04), 30-day mortality (OR 0.58; 95% CI 0.45 to 0.74, p <0.0001), and the rate of stroke (OR 0.65; 95% CI 0.52 to 0.81, p = 0.0001) were significantly lower in the ViV- TAVI arm when compared with Redo-SAVR arm. The mean transvalvular pressure gradient was significantly higher post-implantation in the ViV-TAVI group when compared with the Redo-SAVR arm (Mean difference 3.92; 95% CI 1.97 to 5.88, p < 0.0001). In conclusion, compared with Redo-SAVR, ViV-TAVI is associated with a similar risk of all-cause mortality, cardiovascular mortality, myocardial infarction, permanent pacemaker implantation, and the rate of moderate to severe paravalvular leakage. However, the rate of major bleeding, stroke, procedural mortality and 30-day mortality were significantly lower in the ViV-TAVI group when compared with Redo-SAVR.

Meta-analysis Examining the Usefulness of Angiotensin Receptor blockers for the Prevention of Aortic Root Dilation in Patients With the Marfan Syndrome.

The Marfan syndrome (MFS) patients are highly predisposed to thoracic aortic aneurysm and/or dissection, with virtually every patient having evidence of aortic disease at some point during their lifetime. We conducted a meta-analysis to investigate the efficacy of angiotensin receptor blockers (ARBs) in slowing down the progression of aortic dilatation in MFS patients. PUBMED, EMBASE, and COCHRANE databases were searched for relevant articles published from inception to February 1, 2020. We included randomized clinical trials evaluating the effect of ARBs on aortic root size in patients with MFS with a follow-up period of at least 2.5 years. Seven studies were included with a total of 1,510 patients. Our analysis demonstrated a significantly smaller change in aortic root and ascending aorta dilation in the ARBs treated group when compared with placebo (mean difference 0.68; 95% confidence interval [CI] -1.31 to -0.04; p = 0.04, I2 = 94%, and mean difference -0.13, 95% CI -0.17 to -0.09; p < 0.00001, I2 = 0%, respectively). ARBs as an add-on therapy to beta-blockers resulted in a significantly smaller change in aortic root dilation when compared with the arm without ARBs (mean difference -2.06, 95% CI -2.54 to -1.58; p < 0.00001, I2 = 91%). However, there was no statistically significant difference in the number of clinical events (aortic complications/surgery) observed in the ARBs arm when compared with placebo (Risk ratio of 1.01, 95% CI 0.74 to 1.38; p = 0.94, I2 = 0%). In conclusion, ARBs therapy is associated with a slower progression of aortic root dilation when compared with placebo and as an addition to beta-blocker therapy.