Evolution of a Geriatric Syndrome: Pathophysiology and Treatment of Heart Failure With Preserved Ejection Fraction

Bharathi Upadhya, MD; Barbara Pisani, MD; Dalane W. Kitzman, MD

Disclosures

J Am Geriatr Soc. 2017;65(11):2431-2440. 

In This Article

Noncardiac Comorbidities

Noncardiac comorbidities are common in older adults with HFpEF and are related to the high rate of non-HF admissions and deaths.[47] Individuals with HFpEF have a high prevalence of obesity and diabetes mellitus. About three-quarters of normotensive individuals with well-controlled diabetes mellitus without CAD have evidence of LV diastolic dysfunction on echocardiographic tissue Doppler imaging.[54] Approximately 85% of older HFpEF adults are overweight or obese, a rate twice that in the general population, and the HFpEF epidemic has largely paralleled the obesity epidemic.[55] Excess adipose tissue can produce impairments relevant to HFpEF through two general categories of mechanisms: local or mechanical and systemic or metabolic. Examples of local or mechanical mechanisms are enhanced pericardial restraint,[56] low oxygen diffusion from capillaries to working skeletal muscle cells,[57] accelerated coronary atherosclerosis associated with epicardial adipose, and accelerated renal dysfunction associated with perirenal fat. Excess adipose tissue can also produce adverse systemic or metabolic effects, including promoting inflammation, hypertension, insulin resistance, and dyslipidemia and impairing cardiac, arterial, skeletal muscle, and physical function,[58–60] all of which are common in individuals with HFpEF and contribute to its pathophysiology.[61]

Up to one-third of individuals with HFpEF may have COPD,[47,62] which exacerbates symptoms and increases mortality.[1,47,62] Moreover, individuals with HFpEF are more likely than those with HFrEF to have a COPD diagnosis.[63] Even in the absence of a formal COPD diagnosis, individuals with HFpEF have multiple pulmonary abnormalities that contribute to their symptoms and poor outcomes.[64] Sleep-disordered breathing, pre- and postcapillary pulmonary hypertension, and restrictive lung disease are highly prevalent in individuals with obesity and hypertension and may contribute to clinical HF and dyspnea.[65] Obstructive sleep apnea is common in individuals with HFpEF, with a prevalence of 69% to 81%, and is independently associated with a worse prognosis, even when HF therapy is optimal.[66] In addition, the pulmonary vasculature responds to hypoxia with vasoconstriction, leading to increases in RV and LV afterload, which can lead to chronic pulmonary remodeling.[67] Furthermore, RV dysfunction is common in individuals with HFpEF and is predictive of clinical outcome.[39] Anemia is more prevalent in individuals with HFpEF than in those with HFrEF and is associated with greater risk of HF hospitalization and overall mortality.[68] HFpEF and chronic kidney disease commonly coexist and have shared pathogenic mechanisms, such as neurohumoral activation, inflammation, and oxidative stress.[69]

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