Diastolic heart failure (or HFPEF-heart failure with preserved ejection fraction) is characterized by inadequate myocardial relaxation and diastolic filling ("stiff ventricle"), with heart failure signs and symptoms despite normal ejection fraction. The most common cause is long-standing hypertension.
Diastolic heart failure (or HFPEF-heart failure with preserved ejection fraction) is characterized by inadequate myocardial relaxation and diastolic filling ("stiff ventricle"), with heart failure signs and symptoms despite normal ejection fraction. The most common cause is long-standing hypertension. Current thinking regarding the underlying pathophysiology stresses poor diastolic reserve that is inadequate to meet the demands of exercise in HFPEF, in contrast with early studies which focused on the "stiff" ventricle in resting subjects. During exercise in normal subjects, rapidly relaxing ventricles "suck" blood out of the atria; in HFPEF, ventricular filling during exercise is markedly impaired, with cardiac output inadequate to meet demand. Other recent studies have revealed additional layers of complexity:
•Systolic abnormalities are part of HFPEF: despite grossly preserved systolic ejection fraction, systolic reserve is inadequate-systolic contractility doesn’t adequately increase with exercise. This research has shed new light on the functional limitations present in HFPEF patients.
•Poor vasodilator reserve function: normal subjects experience peripheral vasodilation with exercise; this afterload decrease enhances cardiac output to meet demand. Endothelial dysfunction in patients with HFPEF prevents this response.
Therapy: No therapy has demonstrated clear evidence for improved outcomes in diastolic heart failure. Aggressive use of beta blockers has fallen out of favor for most HFPEF patients because it can exacerbate chronotropic incompetence (inability to increase heart rate to meet cardiac output demands seen in HFPEF). The primary approach in the treatment of HFPEF remains aggressive treatment of controllable risk factors, and the use of cardiac rehabilitation to improve exercise tolerance through conditioning of peripheral tissue oxygen extraction. HFPEF and ischemic heart disease can present as comorbid conditions with four primary risk factors that can all be present in the same patient: hypertension, advanced age, renal insufficiency, and diabetes.
Diabetes appears to be a powerful independent risk factor for HFPEF, associated with abnormal left ventricular filling even in the absence of hypertension. Diastolic dysfunction is seen in 30% to 70% of patients with type 2 diabetes; the likely mechanisms include altered endothelial function, defective energy metabolism, and microvascular disease-diabetes is associated with left ventricular hypertrophy as an independent risk factor. Given that worldwide diabetes prevalence will increase from 135 million in 1995 to 300 million in 2025, primary care physicians can expect to treat an enormous number of new HFPEF patients in the coming years.
Regarding ischemic syndromes and HFPEF, it is paradoxically observed that:
•Chest pain can occur in the setting of HFPEF and relatively normal coronary arteries.
•Unstable angina is more prevalent in heart failure patients with preserved EF than with garden variety systolic dysfunction.
Echocardiography and other functional studies can help distinguish ischemic heart disease from symptomatology related to diastolic dysfunction, and is important because patients with HFPEF can present with chest pain unrelated to coronary artery disease. The lack of wall motion abnormalities or other functional changes indicative of ischemia can help avoid unnecessary angiography in this cohort.
Current Concepts in Diastolic Heart Failure: Highlights from "Diastolic Heart Failure, Beyond Recognizing a Preserved Ejection Fraction," a panel presentation at ACC.11, April 3, 2011. New Orleans, La.
Co-chairs: Anita Deswal, MD, Christopher O’Connor, MD
Synthesizing material from presenters: Eric Veslazquez, MD (Duke University), Barry Borlaug, MD (Mayo Clinic), Michael Fowler, MD (Stanford), and Carolyn Lam, MD (Mayo Clinic).
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