Hypertension as an Independent Risk Factor for In-Patient Mortality in Hospitalized COVID-19 Patients: A Multicenter Study.

Despite the lack of direct evidence that hypertension increases the likelihood of new infections, hypertension is known to be the most common comorbid condition in COVID-19 patients and also a major risk factor for severe COVID-19 infection. The literature review suggests that data is heterogeneous in terms of the association of hypertension with mortality. Hence, it remains a topic of interest whether hypertension is associated with COVID-19 disease severity and mortality. Herein, we perform a multicenter retrospective analysis to study hypertension as an independent risk for in-hospital mortality in hospitalized COVID-19 patients. This multicenter retrospective analysis included 515 COVID-19 patients hospitalized from March 1, 2020 to May 31, 2020. Patients were divided into two groups: hypertensive and normotensive. Demographic characteristics and laboratory data were collected, and in-hospital mortality was calculated in both groups. The overall mortality of the study population was 25.3% (130 of 514 patients) with 96 (73.8%) being hypertensive and 34 (26.2%) being normotensive (p-value of 0.01, statistically non-significant association). The mortality rate among the hypertensive was higher as compared to non-hypertensive; however, hypertensive patients were more likely to be old and have underlying comorbidities including obesity, diabetes mellitus, coronary artery disease, congestive heart failure, stroke, chronic kidney disease (CKD), chronic obstructive pulmonary disease (COPD), and cancer. Therefore, multivariable logistic regression failed to show any significant association between hypertension and COVID-19 mortality. To our knowledge, few studies have shown an association between hypertension and COVID-19 mortality after adjusting confounding variables. Our study provides further evidence that hypertension is not an independent risk factor for in-hospital mortality when adjusted for other comorbidities in hospitalized COVID-19 patients.

Heart Failure Patients and Implications of Obesity: A Single-Center Retrospective Study.

Background and objective The prevalence of heart failure (HF) is on the rise; currently, it affects around five million people in the United States (US) and the prevalence is expected to rise from 2.42% in 2012 to 2.97% in 2030. HF is a leading cause of hospitalizations and readmissions, accounting for a major economic burden to the US healthcare system. Obesity is a widely accepted risk factor of HF; however, data regarding its independent association with HF mortality and morbidity is heterogeneous. Globally, more than two-thirds of deaths attributable to high body mass index (BMI) are due to cardiovascular diseases (CVD). This study aimed to investigate the potential role of obesity (BMI >30 Kg/m2) in HF patients in terms of 30-day readmissions, in-hospital mortality, and the use of noninvasive positive pressure ventilation (NIPPV). Methods In this single-center, retrospective study, all adult (age: >18 years) patients who were hospitalized with a primary diagnosis of HF at the Abington Jefferson Hospital from January 2015 to January 2018 were included. Demographic characteristics were collected manually from electronic medical records. Outcomes were 30-day readmission due to HF, all-cause in-hospital mortality, and requirement for NIPPV. Multivariable logistic regression analysis was conducted to investigate the association of obesity with HF outcomes. Results A total of 1,000 patients were initially studied, of these 800 patients were included in the final analysis based on the inclusion criteria. Obese patients showed higher odds for 30-day readmissions and the use of NIPPV compared to non-obese patients. There was no significant difference in in-hospital mortality in obese vs. non-obese patients. Conclusions Based on our findings, BMI >30 Kg/m2 is an independent risk factor for HF readmissions. Additionally, our results highlight the importance of guidelines-directed medical therapy (GDMT) for HF exacerbation, a low threshold for use of NIPPV in obese patients, promotion of lifestyle modifications including weight loss, and early follow-up after discharge to prevent HF readmissions in the obese population.

The Heart Failure Clinic: Improving 30-Day All-Cause Hospital Readmissions.

Heart failure-related recurrent hospitalizations are widely recognized as a source of burden to both patients and the health system. Hospital discharges represent a transition of care and can often become a catalyst for readmission. One strategy in reducing this burden is the implementation of dedicated heart failure clinics. We conducted a retrospective review of all patients discharged from an inner city safety-net public hospital with a discharge diagnosis of heart failure. Patients followed in the Heart Clinic (HC) were compared to those with standard follow-up. All included cases were followed for 30 days after discharge to determine whether an all-cause readmission occurred. There were 258 patient discharges with an overall sicker population in the HC cohort. The HC group had a better event-free survival with a 67.1% reduction in readmission (log rank *p < .05). In concluding, a dedicated heart failure clinic reduced 30-day readmissions for patients who were discharged after having an acute exacerbation of heart failure.

Stress-induced cardiomyopathy.

A woman in her early 70s presented with chest pain, dyspnoea and diaphoresis 30 min after her husband expired in our hospital. Cardiac markers were elevated and there were acute changes in ECG suggestive for acute coronary syndrome. Echocardiogram showed apical akinesis, basal segment hyperkinesis with an ejection fraction of 30%. Cardiac catheterisation was performed showing non-obstructive coronary arteries, leading to the diagnosis of stress-induced cardiomyopathy. The patient improved with medical management. Repeat echocardiogram 2 months later showed resolution of heart failure with an ejection fraction of 65-70%.

Mortality and atrial fibrillation: is there a causal relationship?

Almost all studies show that atrial fibrillation (AF) is associated with increased mortality. What is less certain is whether this association is a straightforward cause-and-effect relationship, or if AF is merely a marker of severity of cardiovascular disease(s) or the aging process. AF can lead to the worsening of left ventricular filling, contribute to loss of atrioventricular synchrony, affect cardiac remodeling, and even cause a tachycardia-induced cardiomyopathy. AF could be a marker for underlying atherosclerotic disease that itself determines mortality, or the increased oxygen consumption associated with an increasing ventricular rate may lead to ischemia secondary to increased myocardial consumption and precipitate acute coronary syndromes. Although it is generally accepted that the stasis of atrial blood in AF promotes clot formation, studies have shown increases in specific coagulation factors-all of which have the ability to increase morbidity and/or mortality through their elevations. Another possibility is that AF is not the cause of the hypercoagulable state, but is instead a marker of such a state.

Is there a need to continue anticoagulation following "successful" atrial fibrillation ablation?

Atrial fibrillation (AF) is the most common clinically significant arrhythmia worldwide, and its incidence is increasing. There has been increasing interest in ablation therapy to treat atrial fibrillation. One reason some patients undergo AF ablation might be to obviate the need for warfarin therapy, although current guidelines do not support this rationale. The current review shows that it is difficult to define a true "cure" postablation, as many of these patients will go on to experience future paroxysms of AF (either symptomatic or silent). The mechanism underlying embolism in patients with AF is not completely understood, and no long-term evidence exists that "successfully ablated" patients return to a baseline risk of stroke comparable to an AF-naive population. The authors recommend continued long-term anticoagulation post-AF ablation in patients satisfying CHADS criteria for elevated stroke risk.

New heparin dosing regimen for diabetics undergoing percutaneous coronary intervention.

It has been previously demonstrated that diabetics are less sensitive to heparin compared to non-diabetics. We hypothesized that an initial heparin dose of 80 IU per kilogram administered to diabetics rather than 70 IU per kilogram might yield a more optimal initial ACT of 300 to 350 seconds when glycoprotein IIb/IIIa receptor antagonists are not used. We prospectively studied 130 elective PCI patients without diabetes treated with 70 IU per kilogram of unfractionated heparin and 81 elective PCI patients with diabetes treated with 80 IU per kilogram, and compared the initially achieved ACT. The mean heparin dose given per kg was greater (by intention) in diabetics versus non-diabetics. Despite that, there was no significant difference in the initially achieved ACT in diabetics and non-diabetics.