Heart Failure After Right Ventricular Myocardial Infarction

PURPOSE OF REVIEW Heart failure (HF) after right ventricular myocardial infarction (RVMI) is common and complicates its clinical course. This review aims to provide a current overview on the characteristic features of RV failure with focus on acute management. RECENT FINDINGS While HF after RVMI is classically seen after acute proximal right coronary artery occlusion, RV dysfunction may also occur after larger infarctions in the left coronary artery. Because of its different anatomy and physiology, the RV appears to be more resistant to permanent infarction compared to the LV with greater potential for recovery of ischemic myocardium. Hypotension and elevated jugular pressure in the presence of clear lung fields are hallmark signs of RV failure and should prompt confirmation by echocardiography. Management decisions are still mainly based on small studies and extrapolation of findings from LV failure. Early revascularization improves short- and long-term outcomes. Acute management should further focus on optimization of preload and afterload, maintenance of sufficient perfusion pressures, and prompt management of arrhythmias and concomitant LV failure, if present. In case of cardiogenic shock, use of vasopressors and/or inotropes should be considered along with timely use of mechanical circulatory support (MCS) in eligible patients. HF after RVMI is still a marker of worse outcome in acute coronary syndrome. Prompt revascularization, careful medical therapy with attention to the special physiology of the RV, and selected use of MCS provide the RV the time it needs to recover from the ischemic insult

Experience with a Wearable Cardioverter-defibrillator in 436 Patients

The aim of the present study was to review the safety and efficiency of wearable cardioverter-defibrillators (WCDs) under current guideline-directed medical therapy (GDMT). We retrospectively analyzed 436 consecutive WCD patients seen in the years 2014-2020. Detected automatic arrhythmia alarm (AA) episodes were validated and classified as correct or incorrect. The positive predictive value (PPV) was calculated. GDMT was optimized in our outpatient clinic to maximal tolerated doses. During a total wear time (WT) of 23,527 days, 3,135 AAs were transmitted from 206 of 436 (47.2%) patients. Visual analysis revealed correct diagnoses of non-sustained ventricular tachycardia (VT) in 38 AAs from 6 patients (total PPV, 1.21%; PPV in VT patients, 41%); the remaining AAs were artifacts. No appropriate or inappropriate shocks and fatalities were recorded. LVEF significantly improved (P < .001) during the WT from 25% (range, 20%-30%) to 40% (range, 34%-46%). Defibrillators were implanted in 109 patients (27%). The PPV for VT of the WCD was very low. There were fewer instances of true VT than previously reported, and no shocks (appropriate or inappropriate) were delivered. The majority of patients greatly improved with GDMT, and device implantation rates were lower than previously reported. Improvements in arrhythmia detection algorithms are warranted. Based on our results, WCDs are rarely needed for lifesaving shocks under optimal GDMT. Keywords: Heart failure; sudden cardiac arrest; sudden cardiac death; ventricular tachycardia; wearable cardioverter-defibrillator

Endocrine hormone imbalance in heart failure with reduced ejection fraction: A cross-sectional study

BACKGROUND AND AIMS Sustained neurohormonal activation plays a central role in the progression of heart failure (HF). Other endocrine axes may also be affected. It was the aim of this study to examine the endocrine profile (thyroid, parathyroid, glucocorticoid, and sex hormones) in a contemporary sample of patients with HF and reduced ejection fraction (EF) on established disease-modifying therapy. METHODS This study prospectively measured morning fasting hormones in 52 ambulatory and stable HF patients with EF < 50% on disease-modifying therapy (mean age 63 ± 11 years, 29% female, mean LVEF 32 ± 9.6%) and compared them to 54 patients at elevated risk for HF (61 ± 12 years, 28% female) and 62 healthy controls (HC; 61 ± 13 years, 27% female). Main comparisons were performed using one-way analysis of variance. Associations with biomarkers were studied with linear regression. RESULTS HF patients showed a reduced free triiodothyronine (fT3)/free thyroxine (fT4) ratio compared to HC (0.30 ± 0.06 vs. 0.33 ± 0.05, p = 0.046). Parathyroid hormone (PTH) and cortisol were increased in HF compared to both HC (median [IQR] 59 [50-84] vs. 46 [37-52] ng/L, p < 0.001 and 497 ± 150 vs. 436 ± 108 nmol/L, p = 0.03, respectively) and patients at risk (both p < 0.001). Total testosterone was reduced in male HF compared to HC (14.4 ± 6.6 vs. 18.6 ± 5.3 nmol/L; p = 0.01). No differences in TSH, estradiol, progesterone, and prolactin were found. Lower fT3 levels were found in HF with EF < 40% versus EF 40%-49% (4.6 ± 0.3 vs. 5.2 ± 0.7 pmol/L, p = 0.009). In HF patients, fT3 was an independent predictor of NT-proBNP and high-sensitivity troponin T in multiple regression analysis. PTH was positively associated with NT-proBNP. CONCLUSION There is evidence of endocrine hormonal imbalance in HF with reduced EF beyond principal neurohormones and despite the use of disease-modifying therapy

Impaired retinal micro-vascular function in patients with atrial fibrillation

BACKGROUND Cardiovascular (CV) risk factors and CV diseases, in particular heart failure, are strongly associated with impaired microvascular retinal endothelial function. Whether atrial fibrillation (AF) contributes to vascular dysfunction is not clear. Therefore, the aim of this study was to investigate the impact of AF on retinal microvascular function. METHODS In this study, vascular function was measured non-invasively with flicker-light induced vasodilatation of retinal arterioles (FIDart%). Patients with a history of AF and risk factors for heart failure (HF) or heart failure (n = 69; age 67.9 ± 9.2 years, 71% male, 35% HFrEF, 56% paroxysmal, 25% persistent, 19% permanent AF), as well as age, sex and ejection fraction matched patients with absent history of AF (n = 66; age 63.4 ± 10.6 years, 67% male, 47% HFrEF) were included. Patients with AF were further divided into those with paroxysmal AF (in sinus rhythm - AF$_{SR}$: n = 38, age 71.4 ± 9.2, 73% male), and those with AF at the time of the study visit. RESULTS Retinal microvascular function was impaired in patients with AF compared to patients without AF (FIDart% 1.1% [0.3-2.8] vs. 2.7% [1.3-5.1], p < 0.001). Patients currently in AF have poorer retinal microvascular function (FIDart% 0.8% [0.1-1.9) compared to patients with a history of AF but currently in SR at the time of retinal function measurement (1.5% [0.6-4.9] p = 0.017). In patients with AF, impaired retinal vascular function was independently associated with larger left atrial volume (mean 49.8 ± 18.4), even after correction for confounding factors in different models (SCR = -0. 251 to -0.256, p = 0.035-0.01). CONCLUSIONS AF in patients with heart failure is associated with impaired vascular function, even if currently in sinus rhythm. The association of retinal microvascular dysfunction with left atrial volume, a surrogate for elevated cardiac filling pressures, may further highlight the important interplay between the vasculature and elevated filling pressures in the development of AF

Bone morphogenic protein-4 availability in the cardiac microenvironment controls inflammation and fibrosis in autoimmune myocarditis

Myocarditis is an inflammatory heart disease that leads to loss of cardiomyocytes and frequently precipitates fibrotic remodeling of the myocardium, culminating in heart failure. However, the molecular mechanisms underlying immune cell control and maintenance of tissue integrity in the inflamed cardiac microenvironment remain elusive. In this study, we found that bone morphogenic protein-4 (BMP4) gradients maintain cardiac tissue homeostasis by single-cell transcriptomics analyses of inflamed murine and human myocardial tissues. Cardiac BMP pathway dysregulation was reflected by reduced BMP4 serum concentration in patients with myocarditis. Restoration of BMP signaling by antibody-mediated neutralization of the BMP inhibitors gremlin-1 and gremlin-2 ameliorated T cell-induced myocardial inflammation in mice. Moreover, progression to inflammatory cardiomyopathy was blocked through the reduction of fibrotic remodeling and preservation of cardiomyocyte integrity. These results unveil the BMP4–gremlin axis as a druggable pathway for the treatment of myocardial inflammation, limiting the severe sequelae of cardiac fibrosis and heart failure

The heart failure specialists of tomorrow: a network for young cardiovascular scientists and clinicians

The "Heart failure specialists of Tomorrow" (HoT) group gathers young researchers, physicians, basic scientists, nurses and many other professions under the auspices of the Heart Failure Association of the European Society of Cardiology. After its foundation in 2014, it has quickly grown to a large group of currently 925 members. Membership in this growing community offers many advantages during, before, and after the 'Heart Failure and World Congress on Acute Heart Failure'. These include: eligibility to receive travel grants, participation in moderated poster sessions and young researcher and clinical case sessions, the HoT walk, the career cafe, access to the networking opportunities, and interaction with a large and cohesive international community that constantly seeks multinational collaborations.Peer reviewe

Endothelial dysfunction in COVID-19: Current findings and therapeutic implications

Coronavirus disease 2019 (COVID-19) increases the risk of several non-pulmonary complications such as acute myocardial injury, renal failure or thromboembolic events. A possible unifying explanation for these phenomena may be the presence of profound endothelial dysfunction and injury. This review provides an overview on the association of endothelial dysfunction with COVID-19 and its therapeutic implications. Endothelial dysfunction is a common feature of the key comorbidities that increase risk for severe COVID-19 such as hypertension, obesity, diabetes mellitus, coronary artery disease or heart failure. Preliminary studies indicate that vascular endothelial cells can be infected by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), and evidence of widespread endothelial injury and inflammation is found in advanced cases of COVID-19. Prior evidence has established the crucial role of endothelial cells in maintaining and regulating vascular homeostasis and blood coagulation. Aggravation of endothelial dysfunction in COVID-19 may therefore impair organ perfusion and cause a procoagulatory state resulting in both macro- and microvascular thrombotic events. Angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs) and statins are known to improve endothelial dysfunction. Data from smaller observational studies and other viral infections suggests a possible beneficial effect in COVID-19. Other treatments that are currently under investigation for COVID-19 may also act by improving endothelial dysfunction in patients. Focusing therapies on preventing and improving endothelial dysfunction could improve outcomes in COVID-19. Several clinical trials are currently underway to explore this concept

Endothelial dysfunction in cardiovascular disease and Flammer syndrome-similarities and differences

The endothelium has increasingly been recognized as a smart barrier and a key regulator of blood flow in micro- and macrovascular beds. Endothelial dysfunction marks a stage of atherosclerosis and is an important prognostic marker for cardiovascular disease. Yet, some people who tend to be slim and physically active and with rather low blood pressure show a propensity to respond to certain stimuli such as emotional stress with endothelial-mediated vascular dysregulation (Flammer syndrome). This leads to characteristic vascular symptoms such as cold hands but also a risk for vascular-mediated diseases such as normal-tension glaucoma. It is the aim of this review to delineate the differences between Flammer syndrome and its "counterpart" endothelial dysfunction in the context of cardiovascular diseases

The heart failure specialists of tomorrow: a network for young cardiovascular scientists and clinicians

The "Heart failure specialists of Tomorrow" (HoT) group gathers young researchers, physicians, basic scientists, nurses and many other professions under the auspices of the Heart Failure Association of the European Society of Cardiology. After its foundation in 2014, it has quickly grown to a large group of currently 925 members. Membership in this growing community offers many advantages during, before, and after the 'Heart Failure and World Congress on Acute Heart Failure'. These include: eligibility to receive travel grants, participation in moderated poster sessions and young researcher and clinical case sessions, the HoT walk, the career café, access to the networking opportunities, and interaction with a large and cohesive international community that constantly seeks multinational collaborations