AHA Scientific Statement on Right Heart Failure
- Konstam MA, Kiernan MS, Bernstein D, et al., on behalf of the American Heart Association Council on Clinical Cardiology; Council on Cardiovascular Disease in the Young; and Council on Cardiovascular Surgery and Anesthesia.
- Evaluation and Management of Right-Sided Heart Failure: A Scientific Statement From the American Heart Association. Circulation 2018;Apr 19:[Epub ahead of print].
The following are summary points from the American Heart Association (AHA) Scientific Statement on the evaluation and management of right-sided heart failure (HF):
- Afterload is a primary determinant of normal right ventricular (RV) function, and RV ejection fraction (RVEF) is inversely proportional to pulmonary artery pressure. Accordingly, RV systolic function is highly sensitive to changes in afterload, with minor increases in afterload causing large decreases in stroke volume. Acute right heart failure (RHF) can occur because of abruptly increased RV afterload (pulmonary embolus, hypoxia, acidemia) or decreased RV contractility (RV ischemia, myocarditis, postcardiotomy shock). Each condition represents a unique hemodynamic challenge for the RV. Chronic RHF most commonly results from gradual increases in RV afterload caused by pulmonary hypertension (PH) most frequently from left heart failure, although chronic volume overload from right-sided lesions such as tricuspid regurgitation can also lead to its development.
- RV function is equally important in patients with HF with preserved EF (HFpEF). In this population, however, it is difficult to distinguish primary RV pathology from that resulting from secondary PH, given the afterload dependency of RV function.
- Although patients with inferior myocardial infarction (MI) have, in general, a better prognosis than those with anterior MI, the presence of RV involvement increases the risk of death, shock, and arrhythmia.
- Postoperative acute RHF is associated with increased mortality, prolonged length of stay, and increased resource use.
- After cardiac transplantation, diagnosis of primary graft dysfunction of the RV alone requires both right atrial pressure >15 mm Hg, pulmonary capillary wedge pressure <15 mm Hg, and cardiac index <2.0 L x min−1 x m−2, and transpulmonary gradient <15 mm Hg and pulmonary artery systolic pressure <50 mm Hg, or the need for an RV assist device.
- In patients undergoing isolated left ventricular assist device (LVAD) implantation, ≥20% experience acute RHF, which is a leading cause of premature morbidity and mortality. Patients with a history of chemotherapy-associated cardiomyopathy appear to be at higher risk than those with other forms of nonischemic or ischemic disease. Late RHF in the LVAD recipients, after initial hospital discharge, occurs in approximately 10% of patients, and is similarly associated with reduced survival and lower health-related quality of life and functional capacity. The complex physiology of RHF complicates accurate prediction of postoperative events, and risk prediction scores are unable to incorporate intraoperative parameters or events that can precipitate acute RHF. Such events include volume loading from transfusions and short-term increases in pulmonary vascular resistance secondary to hypoxia, acidemia, or increases in airway pressure from mechanical ventilation. Furthermore, prediction models cannot model RV-LVAD interactions and the direct impact of LVAD hemodynamics on RV function, including volume loading of the right-sided circulation and geometric changes in the contractile pattern of the interventricular septum that affect RV stroke volume. Other limitations of risk scores include the heterogeneity of populations studied and the variability in definitions of RHF use.
- The prevalence of acute RHF in the setting of acute pulmonary embolism (PE) ranges from 25% to 60%. Predictors of RV dysfunction include >50% of the pulmonary artery tree occluded by thrombus. Patients with evidence of RV dysfunction have a 2.4- to 3.5-fold increase in mortality compared with those without RV dysfunction. Given the poor prognosis, guidelines on the management of acute PE recommend early detection of RV dysfunction to guide risk stratification and therapeutic decision making.
- The prevalence of arrhythmogenic RV cardiomyopathy (ARVC) is estimated to be 1 in 2,000-5,000, and ARVC affects men more frequently than women. A familial component is identified in >50% of patients. ARVC is associated with sudden cardiac death, and indications for implantable cardioverter-defibrillator therapy in ARVC are available.
- Many patients with congenital heart disease (particularly atrial septal defect, Ebstein’s anomaly, transposition of great arteries, single ventricle) have significant RV involvement because of right-sided valvular lesions, intracardiac shunting, or the presence of a systemic RV.
- Clinical RHF may manifest as acute RHF, chronic RHF, cardiorenal syndrome, cardiohepatic syndrome, or gastrointestinal (GI) manifestations (poor GI absorption and malnutrition).
- Evaluation includes chest x-ray, electrocardiogram, cardiac imaging (echocardiography, cardiac magnetic resonance imaging, multi-detector computed tomography, radionuclide imaging), right heart catheterization/hemodynamic evaluation, risk prediction models, and biomarkers.
- Management of acute RHF includes management of fluid volume (diuretics, renal replacement therapy) and vasoactive therapies (5-phosphodiesterase inhibitors, inotropes, vasopressors).
- Management of chronic RHF includes discussing the pros and cons of diuretics, angiotensin-converting enzyme inhibitors, hydralazine, beta-blockers, digoxin, and pulmonary vasoactive medications including 5-phosphodiesterase inhibitors. The role of palliative medicine has been discussed.
- Utilization of mechanical circulatory support includes discussion on extracorporeal membrane oxygenation, and temporary and permanent devices to support the right heart. Other surgical procedures discussed include tricuspid and pulmonary valve surgery and cardiac surgery.
Clinical Topics: Arrhythmias and Clinical EP, Cardiac Surgery, Cardio-Oncology, Congenital Heart Disease and Pediatric Cardiology, Geriatric Cardiology, Heart Failure and Cardiomyopathies, Invasive Cardiovascular Angiography and Intervention, Noninvasive Imaging, Pulmonary Hypertension and Venous Thromboembolism, Vascular Medicine, Implantable Devices, SCD/Ventricular Arrhythmias, Atrial Fibrillation/Supraventricular Arrhythmias, Cardiac Surgery and Arrhythmias, Cardiac Surgery and CHD and Pediatrics, Cardiac Surgery and Heart Failure, Congenital Heart Disease, CHD and Pediatrics and Arrhythmias, CHD and Pediatrics and Imaging, CHD and Pediatrics and Interventions, CHD and Pediatrics and Prevention, Acute Heart Failure, Chronic Heart Failure, Heart Failure and Cardiac Biomarkers, Heart Transplant, Mechanical Circulatory Support, Pulmonary Hypertension, Interventions and Imaging, Interventions and Structural Heart Disease, Interventions and Vascular Medicine
Keywords: Adrenergic beta-Antagonists, Angiotensin-Converting Enzyme Inhibitors, Arrhythmias, Cardiac, Biological Markers, Blood Pressure, Cardiac Catheterization, Cardiac Surgical Procedures, Cardio-Renal Syndrome, Cardiotoxicity, Death, Sudden, Cardiac, Diagnostic Imaging, Defibrillators, Implantable, Diuretics, Extracorporeal Membrane Oxygenation, Geriatrics, Heart Defects, Congenital, Heart Failure, Heart Transplantation, Heart-Assist Devices, Hypertension, Pulmonary, Myocardial Infarction, Myocarditis, Phosphodiesterase 5 Inhibitors, Pulmonary Embolism, Renal Replacement Therapy, Stroke Volume, Thrombosis, Tricuspid Valve Insufficiency, Ventricular Function, Right
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