Cooper, Leslie T.

Objective: To determine whether a bi-directional relationship exists between depression and HF within a single population of individuals receiving primary care services, using longitudinal electronic health records (EHRs). Methods: This retrospective cohort study utilized EHRs for adults who received primary care services within a large healthcare system in 2006. Validated EHR-based algorithms identified 10,649 people with depression (depression cohort) and 5,911 people with HF (HF cohort) between January 1, 2006 and December 31, 2018. Each person with depression or HF was matched 1:1 with an unaffected referent on age, sex, and outpatient service use. Each cohort (with their matched referents) was followed up electronically to identify newly diagnosed HF (in the depression cohort) and depression (in the HF cohort) that occurred after the index diagnosis of depression or HF, respectively. The risks of these outcomes were compared (vs. referents) using marginal Cox proportional hazard models adjusted for 16 comorbid chronic conditions. Results: 2,024 occurrences of newly diagnosed HF were observed in the depression cohort and 944 occurrences of newly diagnosed depression were observed in the HF cohort over approximately 4–6 years of follow-up. People with depression had significantly increased risk for developing newly diagnosed HF (HR 2.08, 95% CI 1.89–2.28) and people with HF had a significantly increased risk of newly diagnosed depression (HR 1.34, 95% CI 1.17–1.54) after adjusting for all 16 comorbid chronic conditions. Conclusion: These results provide evidence of a bi-directional relationship between depression and HF independently of age, sex, and multimorbidity from chronic illnesses.

Abstract Background: Frailty assessment has often been performed only at baseline in cohort studies. Little is known regarding factors associated with changes in frailty indices over follow up in patients with coronary artery disease (CAD). Methods: Between 11/2008 - 8/2012, 142 community-dwelling adults ≥65 years of age with prior history of CAD (angina or revascularization) participated in a study of frailty assessment at Mayo Clinic Health System in La Crosse, WI. A sample of participants (n=45) were included for frailty re-assessment using the Fried frailty criteria approximately 5 years after their baseline measures. Frailty classification was based on absence of deficits (non-frail), 1-2 deficits (intermediately frail), or 3 or more deficits (frail). Factors associated with a change in frailty indices were studied. Results: There were 45 patients that had a second assessment of frailty indices. At baseline, 24 patients (60%) were not frail while 16 patients (40%) had at least 1 frail feature. At follow up, 20 patients (50%) were not frail while 20 patients (50%) had a frail feature. Those improving were more often being married, had prior revascularization, and were without angina. Interval development of slower gait speed (r = 0.46; p=0.004) and decreased grip strength (r = -0.39; p = 0.01) were associated with worsening frailty. Conclusions: Older adults with CAD are not often frail by standard criteria; however, incident deficits develop during long term follow-up. Spousal support, absence of angina, and change in functional indices are less often associated with frailty features.

Treatment of giant cell myocarditis (GCM) can require bridging to orthotopic heart transplantation (OHT) or recovery with mechanical circulatory support (MCS). Since the roles of MCS and immunotherapy are not well-defined in GCM, we sought to analyze outcomes of patients with GCM who required MCS. A systematic search was performed in June 2019 to identify all studies of biopsy-proven GCM requiring MCS after 2009. We identified 27 studies with 43 patients. Patient-level data were extracted for analysis. Median patient age was 45 (interquartile range (IQR): 32–57) years. 42.1% (16/38) were female. 34.9% (15/43) presented in acute heart failure. 20.9% (9/43) presented in cardiogenic shock. Biventricular (BiVAD) MCS was required in 76.7% (33/43) of cases. Of the 62.8% (27/43) of patients who received immunotherapy, 81.5% (22/27) used steroids combined with at least one other immunosuppressant. Cyclosporine was the most common non-steroidal agent, used in 40.7% (11/27) of regimens. Immunosuppression was initiated before MCS in 59.3% (16/27) of cases, after MCS in 29.6% (8/27), and not specified in 11.1% (3/27). Immunosuppression started prior to MCS was associated with significantly better survival than MCS alone (p = 0.006); 60.5% (26/43) of patients received bridge-to-transplant MCS; 39.5% (17/43) received bridge-to-recovery MCS; 58.5% (24/41) underwent OHT a median of 104 (58–255) days from diagnosis. GCM recurrence after OHT was reported in 8.3% (2/24) of transplanted cases. BiVAD predominates in mechanically supported patients with GCM. Survival and bridge to recovery appear better in patients on immunosuppression, especially if initiated before MCS.

Context: Myocarditis is a known cause of death in athletes. As we consider clearance of athletes to participate in sports during the COVID-19 pandemic, we offer a brief review of the myocardial effects of SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) through the lens of what is known about myocarditis and exercise. All athletes should be queried about any recent illness suspicious for COVID-19 prior to sports participation. Evidence Acquisition: The PubMed database was evaluated through 2020, with the following keywords: myocarditis, COVID-19, SARS-CoV-2, cardiac, and athletes. Selected articles identified through the primary search, along with position statements from around the world, and the relevant references from those articles, were reviewed for pertinent clinical information regarding the identification, evaluation, risk stratification, and management of myocarditis in patients, including athletes, with and without SARS-CoV-2. Study Design: Systematic review. Level of Evidence: Level 3. Results: Since myocarditis can present with a variety of symptoms, and can be asymptomatic, the sports medicine physician needs to have a heightened awareness of athletes who may have had COVID-19 and be at risk for myocarditis and should have a low threshold to obtain further cardiovascular testing. Symptomatic athletes with SARS-CoV-2 may require cardiac evaluation including an electrocardiogram and possibly an echocardiogram. Athletes with cardiomyopathy may benefit from cardiac magnetic resonance imaging in the recovery phase and, rarely, endocardial biopsy. Conclusion: Myocarditis is a known cause of sudden cardiac death in athletes. The currently reported rates of cardiac involvement of COVID-19 makes myocarditis a risk, and physicians who clear athletes for participation in sport as well as sideline personnel should be versed with the diagnosis, management, and clearance of athletes with suspected myocarditis. Given the potentially increased risk of arrhythmias, sideline personnel should practice their emergency action plans and be comfortable using an automated external defibrillator.

Myocarditis is an inflammatory disease of the heart that may occur because of infections, immune system activation, or exposure to drugs. The diagnosis of myocarditis has changed due to the introduction of cardiac magnetic resonance imaging. We present an expert consensus document aimed to summarize the common terminology related to myocarditis meanwhile highlighting some areas of controversies and uncertainties and the unmet clinical needs. In fact, controversies persist regarding mechanisms that determine the transition from the initial trigger to myocardial inflammation and from acute myocardial damage to chronic ventricular dysfunction. It is still uncertain which viruses (besides enteroviruses) cause direct tissue damage, act as triggers for immune-mediated damage, or both. Regarding terminology, myocarditis can be characterized according to etiology, phase, and severity of the disease, predominant symptoms, and pathological findings. Clinically, acute myocarditis (AM) implies a short time elapsed from the onset of symptoms and diagnosis (generally <1 month). In contrast, chronic inflammatory cardiomyopathy indicates myocardial inflammation with established dilated cardiomyopathy or hypokinetic nondilated phenotype, which in the advanced stages evolves into fibrosis without detectable inflammation. Suggested diagnostic and treatment recommendations for AM and chronic inflammatory cardiomyopathy are mainly based on expert opinion given the lack of well-designed contemporary clinical studies in the field. We will provide a shared and practical approach to patient diagnosis and management, underlying differences between the European and US scientific statements on this topic. We explain the role of histology that defines subtypes of myocarditis and its prognostic and therapeutic implications.

To our knowledge, natural history has not been reported for cardiac sarcoidosis (CS) diagnosed by pathologic evaluation of the apical core at left ventricular assist device (LVAD) implantation or cardiac transplantation. We retrospectively identified 232 consecutive patients meeting CS criteria. Of these patients, 54 were diagnosed by pathologic confirmation of CS, 10 after evaluation of the apical core (LVAD implant) or explanted heart (transplant). We compared clinical characteristics at initial evaluation and outcomes for these 10 patients with those of 10 patients with known CS before LVAD implant/transplant. In the study group, five patients (50%) had confirmed extracardiac sarcoidosis before LVAD implant/transplant; five had not been diagnosed with sarcoidosis. Mean (standard deviation) left ventricular ejection fraction at initial evaluation was 23% (16%), and left ventricular end-diastolic dimension was 61 (10) mm. Four patients died during follow-up; however, no survival difference was found for the 10 patients diagnosed incidentally and the group with a previous diagnosis or institutional LVAD/transplant cohorts. Patients diagnosed with CS on pathological examination of the apical core/explanted heart may have severe dilated cardiomyopathy as the initial presentation. Outcomes for patients with CS after advanced heart failure therapies may be comparable with those of non-CS patients.

Background Recent investigations suggest that inflammation and autoimmunity might have a role in the pathophysiology of atrial fibrillation (AF). Given that abnormal ventriculovascular coupling often coexists with AF, we hypothesize that autoimmune vasculitis plays a significant role in the pathogenetic mechanism of AF. Methods and Results A standardized retrospective population‐based case–control study was conducted to evaluate the association between autoimmune vasculitis and AF, and all‐cause mortality. The study included 8459 patients with a new diagnosis of AF and 8459 age‐, sex‐, and registration calendar year–matched controls in Olmsted County, Minnesota, between January 1, 1980 and December 31, 2010. The association of each clinical characteristic, diagnosis, and treatment was assessed using conditional logistic regression to account for the matched case–control study design. Cox proportional hazards regression models and Kaplan‐Meier curves were used to detect independent predictors of mortality and examine cumulative survival. Of a total of 16 918 patients (mean age 72.3+14.4 years; 48.7% women), 320 (1.9%) were diagnosed with autoimmune vasculitis before the index date during the 30‐year period. Among the cases, the prevalence of any autoimmune vasculitis was 2.3%, whereas the frequency of autoimmune vasculitis in controls was 1.5% ( P <0.001). After adjusting for potential confounders, the odds of autoimmune vasculitis in AF cases was 1.5 times higher than in controls (odds ratio, 1.47; 95% CI, 1.04–2.01; P =0.03). Patients with AF and autoimmune vasculitis had worse 5‐year survival than those without autoimmune vasculitis or AF (44.7% versus 77.2%; log‐rank P <0.001). Conclusions Autoimmune vasculitis is significantly associated with AF and independently confers worse survival. These observations may represent one mechanism linking autoimmunity and inflammation to the pathogenesis and prognosis of AF.