By Bodh I. Jugdutt
This publication synthesizes the foremost examine advances in molecular, biochemical and translational elements of getting older and middle failure during the last 4 many years and addresses destiny instructions in administration and drug discovery. It offers scientific concerns and molecular mechanisms on the topic of middle failure, together with the altering demographics within the getting older inhabitants with middle failure; high blood pressure and prevention of diastolic middle failure within the getting older inhabitants; polypharmacy and antagonistic drug reactions within the getting older inhabitants with center failure; adjustments within the middle that accompany advancing age from people to molecules; aging-associated adjustments in myocardial irritation and fibrosis and aging-related adjustments in mitochondrial functionality and implications for middle failure remedy. The ebook succinctly summarizes the massive quantity of knowledge on those key themes and highlights novel pathways that must be explored. that includes contributions from prime clinician-scientists, Aging and middle Failure: Mechanisms and Management is an authoritative source at the significant medical matters in center failure treatment within the aged for cardiologists, gerontologists and internists.
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Extra info for Aging and Heart Failure: Mechanisms and Management
4 Heart failure and changes in cardiovascular biology and pathobiology with aging • • • • • • • • • • • • • • Vascular remodeling – ↑ Ventricular-arterial stiffening and altered coupling – ↑ Systolic blood pressure and pulse pressure Ventricular remodeling and ↑ mass/volume ratio – ↑ Extracellular matrix (fibrillar collagen) and ↑ fibrosis – ↑ Advanced glycation end products (AGES) – ↑ Collagen cross-linking – Diastolic dysfunction and impaired relaxation – ↓ Cardiac reserve Atrial remodeling and atrial fibrillation – Cellular and subcellular remodeling – Altered responses to stress – Altered responses to injury and impaired healing CV remodeling due to lifelong exposure to CV risk factors – ↑ Interaction with CV risk factors – ↑ Risk of coronary heart disease and sequelae – ↑ Risk of peripheral artery disease and sequelae – ↑ Risk of cerebrovascular disease and sequelae – ↑ Risk of comorbidities and sequelae – ↑ Cardiorenal interactions and sequelae – ↑ CV events • • • • • • • • • • • ↓ Leukocyte and tissue telomere length Altered gene regulation Altered cellular and subcellular functions Altered mitochondrial population and function ↓ Myocyte number, ↑ myocyte size Altered contractile pathways, ↓ myocardial contractility Isomyosin shift ↓ Excitation–contraction coupling ↑ Fibrosis-related genes, ↑ fibrosis and collagen matrix ↑ Myocardial stiffness, ↑ vascular remodeling and stiffness ↑ End-systolic stiffness (chamber elastance) ↓ Diastolic compliance Altered immune responses, altered repair responses Altered responses to injury, impaired healing Remodeling of beta-adrenergic system Altered neurohumoral pathways ↑ Angiotensins and endothelins, ↑ angiotensin II Altered stress response pathways ↑ Oxygen-free radicals, ↑ oxidative stress and damage Altered cardiac and arterial responses to stress Altered metabolism and metabolic reserve ↑, increase; ↓, decrease; CV cardiovascular ↑, increase; ↓, decrease hypothesized that aging is associated with global remodeling that involves changes in CV structure as well as cellular, subcellular, biochemical, molecular, physiological, and pathophysiological pathways and responses [19–21].
Taken together, these characteristic changes can provide the rational basis for identifying targets for specific interventions during the aging process with the goal of preventing the march to HF. I. Jugdutt 18 Telomeres, Telomere Length and Telomerase Activity, and Implications for Prevention Aging-Related Telomere Shortening in Cardiovascular Disease from Population Studies Evidence since the 1990s suggest that telomeres serve as a mitotic clock  and mean telomere length may serve as a marker of biological aging at the cellular level  that is heritable .
21 A leading pioneer of preventive cardiology, the late Dr. William B. Kannel, who led the Framingham Heart Study (FHS) from 1966 to 1979 , was among those who are credited with coining the term “coronary risk factors” . Kannel played a major role in identifying correctable predisposing CV risk factors . In a longitudinal study of 186 men and women aged between 30 and 59 years, Kannel and associates confirmed the association of three risk factors (hypertension, hypercholesterolemia, and electrocardiographic evidence of left ventricular hypertrophy) with increased risk of CHD over a 6-year period .
Aging and Heart Failure: Mechanisms and Management by Bodh I. Jugdutt