Does My Patient With Multiple Comorbidities Have Heart Failure With Preserved Ejection Fraction, and Does It Matter?

Dmitry Abramov, MD

Disclosures

J Am Board Fam Med. 2019;32(3):424-427. 

In This Article

Refocus on Patient Management

Instead of focusing on the diagnosis of HFpEF, (ie, attempting to determine whether dyspnea is cardiac in origin or whether echocardiographic abnormalities are relevant to the clinical presentation), perhaps a better approach would be to return to the diagnosis and management of key cardiac and extracardiac comorbidities[3] that are common in elderly patients with limitations to functional capacity. It should be acceptable to diagnose and manage conditions associated with fluid retention, such as anemia, obesity, diabetes, kidney disease, or atrial fibrillation without invoking the heart failure diagnosis. Each of these comorbidities is a significant stand-alone diagnosis, associated with its own symptoms (often dyspnea), diagnostic criteria, and evidence-based treatments.[3] Whether these comorbidities contribute to fluid retention through: their association with diastolic abnormalities, other ventricular myocardial abnormalities, their own unique pathophysiologies, or a combination of these remains unclear. Diuretics are the mainstay treatment of symptoms of volume overload regardless of etiology, and can be used to control symptoms regardless of whether the patient is diagnosed with HFpEF, is suspected as having HFpEF, or is presumed to have volume overload from a noncardiac etiology. Among patients with HFpEF, the diuretic spironolactone is primarily effective at lower ejection fractions (<50%), and the benefits among patients with higher ejection fractions are less certain.[16]

While the search for underlying pathophysiology continues, there is increasing evidence that comorbidities are the most prominent contributors to symptoms among patients labeled as having HFpEF. If symptomatic comorbidities require another name or label, perhaps a better one is "comorbidity associated heart failure" or even "comorbidity associated diuretic dependence." Employing terminology to more closely correlate with etiology based on subpopulations of HFpEF patients may simplify the diagnosis of a widely encountered clinical syndrome and help guide management in a way not currently possible with HFpEF.

May the diagnosis of HFpEF become more clinically relevant if ongoing trials of novel therapies, including sacubitril valsartan, empagliflozin, and others demonstrate improvement in clinical outcomes? The answer to that question has yet to be determined, as these medications may yield similar benefit in high risk primary prevention populations without the necessity of a HFpEF diagnosis. While diagnosing specific diseases that have previously fallen under the HFpEF umbrella such as Amyloid or Fabry's cardiomyopathy are increasingly critical as treatments become available, the benefit of diagnosing comorbidity associated HFpEF remains unclear. In addition, while diagnosing HFpEF may carry prognostic implications, the associated adverse prognosis may result more from a particularly advanced comorbidity burden rather than primary cardiac pathology or heart failure itself.

In conclusion, diagnosing HFpEF in the community may not be easy or even clinically relevant, and the answer to the question of, "does my patient with multiple comorbidities have HFpEF?" may be less important than using available treatments to improve the quality of life of symptomatic patients.

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