This week’s JACC offers an excellent paper by Kitzman and co-workers on what is now called “Heart Failure with Preserved Ejection Fraction,” or HFPEF, (or huff-puff…).
The article reports on the cardiopulmonary physiology of 48 patients with “pure” huff-puff (no amyloid or hypertrophic cardiomyopathy) compared to 25 healthy controls. All were subjected to measurement of VO2 max and echocardiography, and the echo-derived cardiac output estimate was validated (to a reasonable extent) by radionuclide angiography.
The findings were surprising but confirm some earlier studies: Huff-puff does not seem to be due to an inability to expand diastolic volume (although end-diastolic volume at rest is decreased in Huff-puff compared to controls). Key pathophysiologic components seem to be 1) inability to increase heart rate with exercise (chronotropic incompetence); 2) inability to reduce end-systolic volume at peak exercise (yielding a relatively lower stroke volume, likely due to decreased contractility); 3) some peripheral phenomenon that interferes with oxygen extraction (calculated A-v O2 difference was reduced at peak exercise in huff-puff patients).
The accompanying editorial also offers a helpful review on the subject and on the evolution of the nomenclature.
A key unanswered question/speculation regards the role of calcium-channel blockers in this condition and to a lesser extent, beta-blockers. Both are currently “class IIb” therapies for huff-puff.