You Say “Tomato,” I Say “Tomahto”: What Is Heart Failure With Preserved Systolic Function?

What is the rationale for using the term “heart failure with preserved ejection fraction” instead of diastolic heart failure?

The author has had a lazy habit of dividing heart failure into 2 simple categories—systolic and diastolic. In so doing, he is admittedly behind the times. A recent “Top Paper” was a marvelous educational addition to the depth and breadth of heart failure.¹ More so, it focused on heart failure with preserved ejection fraction (HFpEF), or what has been more commonly referred to as “diastolic dysfunction” (as opposed to “systolic failure”: heart failure with reduced ejection fraction, or HFrEF). The paper summarizes important “clinical bottom lines,” and some of those follow.

1. Why call it HFpEF?

The American College of Cardiology and the American Heart Association (ACC/AHA) prefer the term HFpEF to replace diastolic dysfunction and diastolic heart failure. HFpEF is more than a simple diastolic filling problem. Patients can also experience impairment in systolic function, chronotropic incompetence, pulmonary hypertension, and a host of other problems. HFpEF is a multifaceted pathology common in high-risk patients.

2. Who is at risk for developing HFpEF?

Persons with HFpEF are older and have hypertension and atrial fibrillation. Women are afflicted more than men by a ratio of 2:1. Other contributors include obesity, diabetes, and insulin resistance. These are all risk factors that frequent primary care practice.

3. How can we protect our patients against HFpEF?

Blood pressure must be controlled to target! Diuretics, specifically chlorthalidone, reduce the risk of HFpEF more than amlodipine, lisinopril, or doxazosin. Hypertension is a significant risk factor.

4. How does one diagnose HFpEF?

According to the ACC/AHA guidelines, “the single most useful diagnostic test in the evaluation of HF” is the echocardiogram.² Other tests (ECG, N-terminal pro-B-type natriuretic peptide [NT-proBNP], etc.) are discussed as well.

5. How should HFpEF be treated when symptomatic heart failure occurs?

First, reduce preload—the ventricle is “stiff.” Nitrates (“ntg”) starting at 10 mcg/min with lower dose furosemide than is used for HFrEF alleviate symptoms of dyspnea and pulmonary edema. There is a caveat, however. Persons with HFpEF may respond to “ntg” with greater drops in blood pressure than persons with HFrEF. One can also combine thiazides, such as chlorthalidone, with spironolactone to treat volume overload. Bottom line: after heart failure is mitigated, control the blood pressure with whatever it takes! Angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers can be used, but data for mortality reductions are not robust as they are with HFrEF. If atrial fibrillation is a complication, it will greatly compromise diastolic filling. Slow the ventricular rate or offer rhythm control when appropriate. If rate control is chosen, anticoagulation is required.

RELEVANCE TO PRIMARY CARE

Like all the previous “In the Clinics,” this one has tremendous value for primary care practice. The contents contain approaches to decrease the frequency of HFpEF, namely all blood pressures treated to target. Acute HFpEF complicated by dyspnea and/or pulmonary edema with hospitalization responds to a different regimen than HFrEF. The recommendations are primary care staples for use in a typical population with multiple cardiovascular risk factors.