The prevalence of HFPEF increases with age, and the incidence doubles every decade after the age of 65 years. HFPEF is the leading cause of hospitalization in this age group [7]. Almost one in ten of those aged ≥ 80 years has this condition [8]. The 5-year survival of patients with HFPEF is almost similar to those with HFREF (heart failure with reduced ejection fraction) and is approximately 50% [9]. Patients with HFPEF are more likely to be elderly women, hypertensive, and diabetic and have atrial fibrillation. More than a fourth (30%) of the patients with HFPEF die of non-cardiovascular causes, while sudden cardiac death accounts for another fourth [10]. As age advances, the prevalence of comorbidities like sleep apnea, chronic kidney disease, and COPD increases as do the prevalence of cardiovascular diseases and risk factors. All these contribute significantly to the development of HFPEF in this age group.

In addition, HF is one of the commonest comorbidity in hospitalized elderly patients, with poor outcomes and prolonged hospital stay.

The process of aging affects the myocardium, vasculature, and results in the activation of the neurohumoral system. Consequent to the increase in collagen and decrease in elastin, the vessels become stiffer, which is compounded by calcification. This increases the afterload and has effects on cardiomyocytes with hypertrophy, fibrosis, and alterations in calcium intake in sarcoplasmic reticulum, resulting in decreased diastolic reserve. The rate of early diastolic filling of the left ventricle decreases in the elderly [11]. The mitochondria in the cardiac myocytes of the elderly have decreased capacity to generate ATP adequately during stress, thereby limiting the peak myocardial performance. The vasodilatory reserve of the vasculature is affected by reduction in the synthesis of endothelial nitric oxide and atherosclerotic changes. Neurohumoral blunting manifests as chronotropic incompetence, decreased heart rate variability, and decreased augmentation of cardiac output in response to exercise. Comorbidities like hypertension, diabetes, renal dysfunction, and obesity result in exacerbation of stiffening of ventricles and arteries. All these result in marked decline in cardiovascular reserve, and elderly are often unable to maintain a normal cardiac output in response to physiological stress like exercise or pathological processes like anemia, infection, myocardial ischemia, etc. (Table 17.2).

Decreased left ventricular compliance affects the LV filling, characterized by disproportionate increase in LV diastolic pressure in response to rise in LV volume. This causes left atrial hypertension and results in pulmonary venous congestion, pulmonary hypertension, and, subsequently, systemic venous congestion. Impaired LV filling also manifests as lower forward cardiac output, even when the ejection fraction is not affected significantly. Ventricular relaxation abnormalities cause left atrial hypertrophy predisposing to atrial fibrillation, which in turn contributes to loss of forward cardiac output. In patients with advanced diastolic dysfunction, atrial systole contributes to 25–30% of stroke volume, and when they develop atrial fibrillation, the loss of this “booster pump effect” renders them more symptomatic.