ABIM Advanced HF key terms

A peptide released by ventricular myocytes in response to wall stretch and pressure overload. Elevated levels support the diagnosis of heart failure, track severity, and predict adverse outcomes, but rise with age, kidney disease, and atrial fibrillation.

Stroke volume divided by end-diastolic volume, expressed as a percentage. It classifies heart failure into reduced, mildly reduced, and preserved categories, guides drug and device selection, and carries prognostic value, though it correlates imperfectly with symptoms.

The heart failure phenotype with left ventricular ejection fraction of 40 percent or less. It carries the strongest evidence base for neurohormonal blockade and device therapy, and treatment that improves survival is titrated to the highest tolerated doses.

The combination of drugs proven to reduce mortality in heart failure with reduced ejection fraction: a renin-angiotensin system inhibitor or ARNI, a beta blocker, a mineralocorticoid receptor antagonist, and an SGLT2 inhibitor, each titrated toward target dose.

A fixed-dose combination of a neprilysin inhibitor and an angiotensin receptor blocker. Compared with enalapril it further reduced death and hospitalization in HFrEF and is recommended in place of an ACE inhibitor or ARB in eligible patients.

Steroid receptor blockers such as spironolactone and eplerenone that antagonize aldosterone. They reduce mortality in HFrEF, require monitoring of potassium and renal function, and are generally avoided when estimated GFR is very low.

Oral agents that block sodium-glucose cotransport in the proximal tubule. Empagliflozin and dapagliflozin reduce heart failure hospitalization and cardiovascular death across the ejection fraction spectrum, including patients without diabetes, through effects beyond glucose lowering.

Biventricular pacing that resynchronizes ventricular contraction in patients with a wide QRS complex, typically left bundle branch block. It improves symptoms and survival in selected HFrEF patients with reduced ejection fraction and prolonged QRS duration.

Incremental exercise testing with measurement of respiratory gas exchange. Peak oxygen consumption objectively quantifies functional capacity, helps distinguish cardiac from pulmonary limitation, and is used to justify transplant or mechanical support when severely reduced.

Failure of loop diuretics to relieve congestion despite escalating doses. Causes include reduced renal perfusion, distal sodium reabsorption, and gut edema limiting absorption; management uses intravenous dosing, combination diuretics, and treatment of the underlying cause.

Infiltration of the myocardium by transthyretin amyloid fibrils, either hereditary or wild-type, causing a restrictive cardiomyopathy with thick walls. Diagnosis uses bone scintigraphy with exclusion of light-chain disease; tafamidis slows progression in selected patients.

A drug that inhibits the funny current in the sinus node, slowing heart rate without reducing contractility. In HFrEF it may reduce hospitalization in patients in sinus rhythm with resting heart rate at or above 70 despite beta blockade.

Advanced, refractory heart failure with persistent severe symptoms at rest despite optimized therapy, frequent hospitalizations, and intolerance of standard drugs. It prompts evaluation for transplant, mechanical support, inotropes, or palliative care.

A seven-level scale describing patients with advanced heart failure from crash-and-burn shock to resting-limited symptoms. Lower profiles denote greater instability and urgency, and the scale guides timing of durable mechanical support.

A five-stage classification from at-risk through beginning, classic, deteriorating, and extremis. Higher stages indicate worsening hypoperfusion and escalating support; the framework standardizes communication, trial enrollment, and prognostication in shock.

A catheter-mounted microaxial pump placed across the aortic valve that pulls blood from the left ventricle into the ascending aorta. It provides temporary flow support in cardiogenic shock or high-risk percutaneous coronary intervention, with risks of hemolysis and limb ischemia.

Extracorporeal membrane oxygenation with venous drainage and arterial return, bypassing the heart and lungs. It supports refractory shock or respiratory failure but increases left ventricular afterload and can cause differential hypoxia and bleeding.

An implanted continuous-flow pump that draws blood from the left ventricle and returns it to the aorta. Used as destination therapy or bridge to transplant, it improves survival and quality of life in selected patients but brings bleeding, thrombosis, infection, and right heart failure.

A balloon-tipped catheter advanced to the pulmonary artery to measure right atrial, pulmonary artery, and wedge pressures and cardiac output. In shock it distinguishes preload, congestion, and output states that guide diuretics, vasodilators, and inotropes.

Right ventricular dysfunction that follows left ventricular assist device implantation when the unprepared right ventricle cannot handle increased venous return. It presents as low output with elevated central venous pressure and is managed with pulmonary vasodilators, inotropes, and careful volume removal.

Formation of clot within a left ventricular assist device, causing hemolysis, power spikes, and reduced flow with heart failure or shock. Management ranges from antithrombotic intensification to pump exchange, depending on severity and patient stability.

Continuous intravenous milrinone or dobutamine given outside the hospital as palliation or bridge therapy for refractory stage D heart failure. It can improve symptoms and enable discharge but carries risks of arrhythmia, line infection, and increased mortality.

Rules that rank transplant candidates by medical urgency, blood type compatibility, donor size, and geographic distance. Understanding them explains how mechanical support status and waiting time affect the chance and timing of an acceptable donor offer.

A measure of the breadth of a candidate's circulating HLA antibodies, estimating the percentage of donors to whom the patient would react. High values complicate matching and predict antibody-mediated rejection, prompting virtual crossmatching and desensitization strategies.

Catheter sampling of right ventricular septal tissue, the traditional surveillance tool for acute cellular rejection after transplant. Scheduled biopsies are most intensive early after surgery and are interpreted using standardized grading, though noninvasive donor-derived cell-free DNA testing is increasingly used.

A T-lymphocyte-mediated immune response against the graft, graded by ISHLT criteria on biopsy from mild perivascular infiltrates to severe injury with hemodynamic compromise. Treatment escalates from corticosteroid pulses to antithymocyte globulin depending on grade and symptoms.

Graft injury caused by donor-specific antibodies binding capillary endothelium, with complement activation and microvascular inflammation. Diagnosis combines biopsy findings, C4d staining, and circulating antibodies; treatment includes plasmapheresis, intravenous immunoglobulin, and rituximab.

Diffuse concentric intimal thickening of coronary arteries driven by chronic immune injury, a leading cause of late graft loss. It is often silent because the graft is denervated; surveillance uses angiography and intravascular ultrasound, and treatment options are limited.

Severe ventricular failure of the newly transplanted heart in the first 24 hours, unrelated to rejection or surgical complications. It requires high-dose inotropes or mechanical support and is a major cause of early death.

A calcineurin inhibitor that blocks T-cell activation and forms the backbone of maintenance immunosuppression after heart transplant. It has a narrow therapeutic window; low levels risk rejection while high levels cause nephrotoxicity, tremor, and hyperglycemia.

A precapillary pulmonary vascular disease with mean pulmonary artery pressure above 20 mmHg, normal wedge pressure, and elevated pulmonary vascular resistance, caused by remodeling of small arteries. Causes include idiopathic disease, connective tissue disease, and congenital heart disease.

A five-group scheme organizing pulmonary hypertension by mechanism: arterial, left heart disease, lung disease or hypoxia, chronic thromboembolic disease, and multifactorial mechanisms. Group assignment determines the diagnostic pathway and whether pulmonary vasodilators are appropriate.

Pulmonary vascular resistance, calculated as the transpulmonary gradient divided by cardiac output. Above roughly 3 Wood units it marks a precapillary component; in transplant candidates marked elevation predicts right heart failure in the donor organ.

Pulmonary hypertension in left heart disease in which a reactive pulmonary vasculature raises pulmonary vascular resistance in addition to elevated wedge pressure. It identifies patients with worse prognosis and higher risk of right ventricular failure after transplant or left ventricular assist device.

Invasive measurement of pressures and flows in the right atrium, right ventricle, pulmonary artery, and wedge position. It confirms pulmonary hypertension, distinguishes precapillary from postcapillary physiology, tests vasoreactivity, and guides therapy in advanced heart failure.

Inhaled nitric oxide or another short-acting agent given during right heart catheterization in idiopathic or heritable pulmonary arterial hypertension. A positive response, meaning a fall in mean pressure without a drop in output, identifies candidates for high-dose calcium channel blockers.

Chronic thromboembolic pulmonary hypertension, group 4 disease in which organized thrombi obstruct pulmonary arteries after pulmonary embolism. Pulmonary endarterectomy is potentially curative; inoperable or residual disease is treated with riociguat or balloon pulmonary angioplasty.

Sildenafil and tadalafil enhance nitric oxide-mediated vasodilation by blocking cyclic GMP breakdown. They are used in pulmonary arterial hypertension and selected patients with heart failure and pulmonary vascular disease, but are avoided with nitrates.

The match between right ventricular contractility and the pulmonary arterial load it faces. A low ratio of tricuspid annular plane systolic excursion to pulmonary artery systolic pressure indicates uncoupling and predicts adverse outcomes in heart failure and pulmonary hypertension.