Hypertension as a Road to Treatment of Heart Failure with Preserved Ejection Fraction

Hypertension heralds the diagnosis of heart failure (HF) with preserved ejection fraction (HFpEF) in 75–85% of cases and shares many of its adverse outcomes as well as its acute and chronic symptoms. This review provides important new data about the pathophysiology and mechanisms that connect hypertension and HFpEF as well as therapy used in both conditions.

The traditional model of HFpEF pathophysiology emphasizes the role of hypertension causing increased afterload on the left ventricle (LV), leading to LV hypertrophy (LVH) and subsequent LV diastolic dysfunction. Recent work has provided valuable insights into the mechanisms underlying the transition from hypertension to HFpEF, showing that the pathophysiology extends beyond LVH and diastolic dysfunction. An evolving paradigm suggests that HFpEF is inflammatory in nature with multifactorial pathophysiology, affected by age-related changes and comorbidities. Hypertension shares many of the proinflammatory mechanisms of HFpEF. Furthermore, hypertension precedes HFpEF in the majority of cases. Because of its clinically heterogeneous nature, development of standardized therapies for HFpEF has been challenging. As there are standardized approaches to hypertension, we suggest that similar approaches be used for the treatment of HFpEF, including medical and non-medical therapies. With medical therapies, a treat-to-target blood pressure (BP) strategy could be employed, such as systolic BP < 130 mmHg. With non-medical therapies, approaches to deal with physical inactivity, obesity, and sleep apnea could be used.

Due to its heterogeneity, delineation of standardized therapies for HFpEF has been challenging. Focusing on the tremendous overlap of hypertensive heart disease with HFpEF, it is proposed that approaches currently used to guide therapies for hypertension be applied to the treatment of HFpEF.