Heart Failure with Preserved Ejection Fraction (HFpEF)
Heart Failure is a common clinical problem with a prevalence of at least 1 to 3% globally. It is estimated that we should be having 8 to 10 million people with HF in our country. HF is the common endpoint for many cardiac and noncardiac disease processes, all of which impair the structure and function to a point where the heart is unable to pump blood to meet the needs of the peripheral tissues or can only do so at the cost of increasing load further on the failing heart.
When we talk of HF in general, we usually refer to HF with low pumping efficiency of the heart as the pump which in scientific terms is called HF with low ejection fraction (HF rEF), where the LVEF is <40%. However, it is important to remember that there is an entity where all the features of HF can exist with a LVEF > 50%. This constitutes around 50% of the patients with HF. In between comes a category of patients with mildly reduced ejection fraction who have an LVEF 41% to 49% with evidence of spontaneous or provokable increased left ventricular filling pressures (LVFPs), characterized by abnormalities in echocardiography and blood markers.
The diagnosis of HFpEF can be challenging, particularly in patients with overt signs or symptoms of congestion. However, approximately 50% of patients with heart failure are classified as HFpEF and it is an entity quite distinct from HFrEF. The underlying causes differ significantly from HFrEF. Increasing age, female sex, obesity, diabetes, sleep apnoea, high blood pressure, pulmonary hypertension and chronic lung disease are the common associations. Its recognition can be difficult since a cursory echocardiography done reveals a normal contraction pattern. The symptoms do not differentiate it from HFrEF. It is not uncommon that many of these patients are being followed up by general physicians and at times by pulmonologists and continue to suffer with only drugs being given as bronchodilators, nebulizers and diuretics (water pills like furosemide or torsemide)
Obesity is a major risk factor for the development of HFpEF. Obesity is a chronic systemic inflammatory state that induces hormonal abnormalities that stress the cardiovascular system. Overweight and obese individuals demonstrate subclinical changes in the structure and function of the left ventricle, even in the presence of a normal ejection fraction. Increased adiposity is associated with a stiff heart . Central obesity is associated with age-related increases in ventricular end-systolic elastance in women but not in men; obesity and female sex are significant risk factors for the development of HFpEF. Abnormalities in skeletal muscle and vascular endothelium significantly contribute to this decreased reserve. Exercise tolerance and capacity are decreased in patients with HFpEF, as demonstrated by more severe dyspnoea and fatigue.
The diagnosis is dependent on a high index of suspicion in patients where symptoms of HF are present in face of a normal LVEF. Echocardiographic evaluation needs a detailed examination of the relaxing pattern of the heart called the diastolic function. Essentially it is a stiff heart. In addition, a blood marker NT pro BNP available also as a point of care blood test clinches the diagnosis. This blood test convincingly differentiates shortness of breath of because of lung disease from a cardiac cause.
Evolution of 3 Pillars for managing HFpEF
Till very recently the management was only treating the underlying associations like hypertension, diabetes if present and symptomatic relief of congestion by giving diuretics. However, a breakthrough came as recently as 2022 when a study called DELIVER first time showed that a drug belonging to the group called SGLT2 inhibitors (Dapagliflozin followed by Empagliflozin) which excrete sugar from flood through urine along with many other important effects reduced the combined risk of worsening heart failure and cardio vascular death in this group of patients. This was the first pillar.
The 2nd important pillar which evolved was a drug from the group of GLP1 analogues (Semaglutide and now another agent Tirzapatide) brought in for treating diabetes but with an important property of weight reduction. Two recent trials have shown that these agents in obese persons with HFpEF when given either of these agents improves the quality of life, exercise tolerance and hospitalizations for worsening heart failure.
Recently Finerenone a drug which was being used in diabetic chronic kidney disease with albuminuria has been shown to be useful for the treatment of HFpEF. The FINEARTS trial has demonstrated it significantly reduced the composite of total worsening heart failure events and death from cardiovascular causes, making it the third pillar.
Thus, a variety of HF which was defying drug treatment has become amenable to drug therapy. It can like HFrEF have agents which not only improve the quality of life but reduce heart failure admissions and hopefully improve survival also. All the three can be given together for an added benefit under supervision.
Author is Founder Director Gauri Kaul Foundation
