STEMI and heart failure in the elderly: role of adverse remodeling

Abstract

The elderly population (age > or = 65 years) has been increasing worldwide. In North America and Europe, both heart failure (HF) and ST-segment elevation MI (STEMI) are more prevalent in the elderly. Morbidity, hospitalizations and costs associated with HF are higher in the elderly. Despite improved therapies, the bulk of cardiovascular deaths occur in the elderly. Survivors of acute STEMI develop progressive ventricular remodeling that leads to HF. There are several reasons for the increased HF burden in the elderly. First, there is a lack of clinical trial data exclusively in elderly patients for specific therapy of adverse remodeling post-STEMI and HF with low ejection fraction (HF/low-EF) or HF with preserved ejection fraction (HF/PEF). Second, there is the lack of data on the impact of aging on remodeling during healing post-STEMI and HF. Third, HF therapy in the elderly is more challenging because of aging-specific biological changes and associated comorbidities and polypharmacy. More research on aging and post-STEMI remodeling and clinical trials on post-STEMI remodeling and HF in the elderly are needed, especially in the "older-elderly" population segment aged > or =75 years.

Role of ACE2 in diastolic and systolic heart failure

“…The expression of ACE2 shows a dramatic decrease with aging independent of gender [41]. The age-associated loss of ACE2 function may lead to further activation of the renin-angiotensin system resulting in greater adverse remodeling and worsened clinical outcomes in elderly patients [42,43].…”

Prevention of heart failure in the elderly: when, where and how to begin?

“…Unless appropriate preventive strategies and measures are implemented urgently, the prevalence, related complications and total burden of HF in the elderly men and women will very likely expand and tax future healthcare systems even more. Several authors have commented on the economic burden due to mortality, morbidity, hospitalization, emergency department visits in the growing adult and elderly populations with HF [5][6][7][8][9][10][11][12][13][14]. Prevention of HF in the present and future elderly populations should therefore be a healthcare priority.…”

“…The aging continuum, cardiovascular risk exposure and the march to heart failure Expanding knowledge of the biology of aging [8][9][10][11] and aging-related changes in cardiovascular (CV) structure and function [15][16][17][18] suggest that the aging heart may itself be a substrate for CV disease including HF. In the last 3 decades, a constellation of typical aging-related physiological and pathophysiological changes typical in the CV system (Table 1) and pathobiological changes ( Table 2) as well as an aging phenotype (Table 3) have been recognized [8,10]. Several lines of evidence strongly suggest that aging is a continuous biological process during which progressive changes in CV structure, physiology and biochemistry occur and negatively impact cardiac function and contribute to HF [8,10].…”

“…In the last 3 decades, a constellation of typical aging-related physiological and pathophysiological changes typical in the CV system (Table 1) and pathobiological changes ( Table 2) as well as an aging phenotype (Table 3) have been recognized [8,10]. Several lines of evidence strongly suggest that aging is a continuous biological process during which progressive changes in CV structure, physiology and biochemistry occur and negatively impact cardiac function and contribute to HF [8,10]. Taken together, these characteristic changes can provide the rational basis for identifying targets for interventions during the aging process with the goal of preventing the march to HF.…”

The continuing saga of aging and heart failure

“…It drew attention to the arbitrary chronological definition of the elderly and the importance of the changing demographics with respect to the growing population of elderly people with major aging-related cardiovascular (CV) diseases that lead to HF, such as hypertension and myocardial infarction [1]. In that issue, a group of clinicianscientists discussed pertinent aspects of epidemiology and management of elderly patients with STEMI and HF [2,3]. Other expert clinician-scientists addressed, in the context of aging and HF, the role of inflammatory implications and fibrogenic pathways [4], autophagy [5], sarcoplasmic reticulum calcium signaling [6], stem cells [7], adiponectin [8], resveratrol and longevity [9], telomeres [10], osteopontin [11] and beta-adrenergic signaling [12].…”