The coronavirus disease 2019 (COVID-19) caused by the severe acute respiratory syndrome coronavirus-2 has affected the health of people across the globe. Cardiovascular diseases (CVDs) have a significant relationship with COVID-19, both as a risk factor and prognostic indicator, and as a complication of the disease itself. In addition to predisposing to CVD complications, the ongoing pandemic has severely affected the delivery of timely and appropriate care for cardiovascular conditions resulting in increased mortality. The etiology behind the cardiac injury associated with severe acute respiratory syndrome coronavirus-2 is likely varied, including coronary artery disease, microvascular thrombosis, myocarditis, and stress cardiomyopathy. Further large-scale investigations are needed to better determine the underlying mechanism of myocardial infarction and other cardiac injury in COVID-19 patients and to determine the incidence of each type of cardiac injury in this patient population. Telemedicine and remote monitoring technologies can play an important role in optimizing outcomes in patients with established CVD. In this article, we summarize the various impacts that COVID-19 has on the cardiovascular system, including myocardial infarction, myocarditis, stress cardiomyopathy, thrombosis, and stroke.

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Background Inflammatory bowel disease (IBD) is associated with an increased acute coronary syndrome (ACS) risk. Data are limited regarding the epidemiology and outcomes of ACS in patients with IBD. Methods A retrospective cohort analysis of patients with IBD admitted for ACS in the U.S. Healthcare Cost and Utilization Project National Inpatient Sample for 2005 to 2015 was conducted. We analyzed trends in IBD-ACS admissions and mortality, differences in risk profiles, management strategies, and in-hospital mortality between IBD-ACS and non-IBD ACS and between ulcerative colitis (UC) and Crohn disease (CD). Results We studied 6,872,415 non-IBD ACS and 24,220 IBD-ACS hospitalizations (53% with CD). During the study period, the number of hospitalizations for IBD-ACS increased, particularly those related to CD. Compared with non-IBD ACS, patients with IBD-ACS had a lower prevalence of cardiovascular risk factors and similar rates of coronary angiography and revascularization. The in-hospital mortality rate was lower with IBD-ACS (3.9%) compared with non-IBD ACS (5.3%; odds ratio, 0.81; 95% confidence interval, 0.69-0.96; P = 0.011) and was stable between 2005 and 2015. Risk factors, ACS management strategies, and mortality were similar between CD and UC. Coagulopathy, weight loss, and gastrointestinal bleeding were more frequent in IBD-ACS and were strong independent predictors of mortality. Conclusions Hospitalizations for ACS in patients with IBD increased in recent years but death rates were stable. The ACS-related risk profiles and mortality were modestly favorable with IBD-ACS than with non-IBD ACS and were similar between CD and UC. Complications more frequently associated with IBD were strongly associated with mortality. These findings indicate that aggressive management of IBD and ACS comorbidities is required to improve outcomes.

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ObjectiveWe evaluated the sex differences in 6-month heart failure (HF) hospitalisation risk in acute myocardial infarction (AMI) survivors.MethodsFor this retrospective cohort analysis, adult survivors of an AMI between January and June 2014 were identified from the US Nationwide Readmissions Database. The primary outcome was a HF hospitalisation within 6 months. Secondary outcomes were fatal HF hospitalisation and the composite of index in-hospital HF or 6-month HF hospitalisation.ResultsOf 237 549 AMI survivors, females (37.9%) were older (70±14 years vs 65±13 years; p<0.001), had a higher prevalence of cardiac comorbidities and a lower revascularisation rate compared with males. The primary outcome occurred in 12 934 patients (5.4%), at a 49% higher rate in females (6.8% vs 4.6% in males, p<0.001), which was attenuated to a 19% higher risk after multivariable adjustment. Findings were consistent across subgroups of age, AMI type and major risk factors. In the propensity-matched time-to-event analysis, female sex was associated with a 13% higher risk for 6-month HF readmission (6.4% vs 5.8% in males; HR 1.13, 95% CI 1.05 to 1.21, p<0.001), and the increased risk was evident early on after the AMI. Fatal HF rate was similar between groups (4.7% vs 4.6%, p=0.936), but females had a higher rate of the composite HF outcome (36.2% vs 27.5%, p<0.001).ConclusionIn a large all-comers AMI survivors’ cohort, females had a higher HF hospitalisation risk that persisted after adjustment for baseline risk differences. This was consistent across several clinically relevant subgroups and was evident early on after the AMI.

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3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors are ubiquitously prescribed for cardiovascular disease (CVD) prevention and treatment. However, the use of statins has been linked to the development of new-onset diabetes mellitus (NODM), which could possibly increase future CVD risk. This phenomenon necessitates a clear discussion of the possible etiologies of this relationship and its broader clinical consequences. We discuss the reported incidence of NODM in statin users through a rigorous review of data from metaanalyses of randomized control trials examining this association. We also highlight the various possible mechanisms responsible for the development of statin-induced diabetes mellitus. Finally, we examine the clinical implications of this effect on future CVD risk and identify specific patient factors that can be used for risk-stratification strategies. Data from 14 randomized control trials metaanalyses suggest a 9-33% higher risk of NODM with statin use. Several cellular, molecular, and genetic mechanisms, as well as lifestyle habits, have been identified as potential underlying factors responsible for this elevated risk. The principle mode of the diabetogenic action of statins is still unclear, though it is likely the result of a complex interplay of pancreatic and extrapancreatic effects. It is understood that patient populations with a greater predisposition to diabetes mellitus, and those with thicker epicardial adiposity are more at risk for the development of statininduced NODM. Despite these observations, robust data from a variety of investigations suggest that the CVD preventative benefits of statin treatment significantly outweigh the risks associated with the development of NODM. Nevertheless, further study must better identify the causative mechanisms involved in this process, its natural history, and the unique factors that will help clinicians risk stratify and appropriately monitor patients on statin therapy.