Cardiovascular disease is the main cause of death globally, accounting for over 17 million deaths each year. As the incidence of cardiovascular disease rises markedly with age, the overall risk of cardiovascular disease is expected to increase dramatically with the aging of the population such that by 2030 it could account for over 23 million deaths per year. It is therefore vitally important to understand how the heart remodels in response to normal aging for at least two reasons: i) to understand why the aged heart is increasingly susceptible to disease; and ii) since it may be possible to modify treatment of disease in older adults if the underlying substrate upon which the disease first develops is fully understood. It is well known that age modulates cardiac function at the level of the individual cardiomyocyte. Generally, in males, aging reduces cell shortening, which is associated with a decrease in the amplitude of the systolic Ca(2+) transient. This may arise due to a decrease in peak L-type Ca(2+) current. Sarcoplasmic reticulum (SR) Ca(2+) load appears to be maintained during normal aging but evidence suggests that SR function is disrupted, such that the rate of sarco/endoplasmic reticulum Ca(2+)-ATPase (SERCA)-media...Continue Reading
Expression of sarcoplasmic reticulum Ca(2+)-ATPase and calsequestrin genes in rat heart during ontogenic development and aging
Age-dependent differences in energetic status, electrical and mechanical performance of rat myocardium
An assessment of phospholipid methylation in sarcolemma and sarcoplasmic reticulum of the aging myocardium
A longitudinal study of estrous cyclicity in aging C57BL/6J mice: I. Cycle frequency, length and vaginal cytology
Altered profiles of estradiol and progesterone associated with prolonged estrous cycles and persistent vaginal cornification in aging C57BL/6J mice
Age-associated changes in plasma testosterone levels in male mice and their relation to social dominance or subordinance
Effects of chronic angiotensin I-converting enzyme inhibition on the relations between ventricular action potential changes and myocardial hypertrophy in aging rats
Ionic basis of action potential prolongation of hypertrophied cardiac myocytes isolated from hypertensive rats of different ages
Electrophysiological basis for the enhanced cardiac arrhythmogenic effect of isoprenaline in aged spontaneously hypertensive rats
Age-related alterations in the phosphorylation of sarcoplasmic reticulum and myofibrillar proteins and diminished contractile response to isoproterenol in intact rat ventricle
The role of aging on the control of contractile force by Na(+)-Ca2+ exchange in rat papillary muscle
The effects of changes to action potential duration on the calcium content of the sarcoplasmic reticulum in isolated guinea-pig ventricular myocytes
Effects of sustained low-flow ischemia on myocardial function and calcium-regulating proteins in adult and senescent rat hearts
Restoration of diastolic function in senescent rat hearts through adenoviral gene transfer of sarcoplasmic reticulum Ca(2+)-ATPase
Frequency-encoding Thr17 phospholamban phosphorylation is independent of Ser16 phosphorylation in cardiac myocytes
Impaired cell shortening and relengthening with increased pacing frequency are intrinsic to the senescent mouse cardiomyocyte
Coordinated control of cell Ca(2+) loading and triggered release from the sarcoplasmic reticulum underlies the rapid inotropic response to increased L-type Ca(2+) current
Action potential prolongation in cardiac myocytes of old rats is an adaptation to sustain youthful intracellular Ca2+ regulation
Regulation of cardiac excitation-contraction coupling by action potential repolarization: role of the transient outward potassium current (I(to))
Arterial and cardiac aging: major shareholders in cardiovascular disease enterprises: Part II: the aging heart in health: links to heart disease
Transgenic CaMKIIdeltaC overexpression uniquely alters cardiac myocyte Ca2+ handling: reduced SR Ca2+ load and activated SR Ca2+ release
Heart failure after myocardial infarction: prevalence of preserved left ventricular systolic function in the community
Force-frequency relationship in intact mammalian ventricular myocardium: physiological and pathophysiological relevance
Mechanisms underlying enhanced cardiac excitation contraction coupling observed in the senescent sheep myocardium
Effect of age on left ventricular systolic function in humans: a study of systolic isovolumic acceleration rate
Aging induces cardiac diastolic dysfunction, oxidative stress, accumulation of advanced glycation endproducts and protein modification
Age-dependent changes in myocardial matrix metalloproteinase/tissue inhibitor of metalloproteinase profiles and fibroblast function
CaMKII tethers to L-type Ca2+ channels, establishing a local and dedicated integrator of Ca2+ signals for facilitation
Akt2 ablation prolongs life span and improves myocardial contractile function with adaptive cardiac remodeling: role of Sirt1-mediated autophagy regulation
Epitope Mapping of SERCA2a Identifies an Antigenic Determinant That Induces Mainly Atrial Myocarditis in A/J Mice
TRPV4 increases cardiomyocyte calcium cycling and contractility yet contributes to damage in the aged heart following hypoosmotic stress
Echocardiographic Strain Analysis for the Early Detection of Left Ventricular Systolic/Diastolic Dysfunction and Dyssynchrony in a Mouse Model of Physiological Aging
Age-related changes in cardiac electrophysiology and calcium handling in response to sympathetic nerve stimulation
Long-term testosterone deficiency modifies myofilament and calcium-handling proteins and promotes diastolic dysfunction in the aging mouse heart
Identification of common cardiometabolic alterations and deregulated pathways in mouse and pig models of aging.
Transient receptor potential vanilloid-4 contributes to stretch-induced hypercontractility and time-dependent dysfunction in the aged heart.
Sex-Specific Prognostic Implications in Dilated Cardiomyopathy After Left Ventricular Reverse Remodeling
Treatment with a DC-SIGN ligand reduces macrophage polarization and diastolic dysfunction in the aging female but not male mouse hearts.
Transgenic overexpression of GTP cyclohydrolase 1 in cardiomyocytes ameliorates post-infarction cardiac remodeling
Evaluation of left and right ventricular systolic and diastolic electromechanical synchrony in older people: a population-based observational study
The Light and Shadow of Senescence and Inflammation in Cardiovascular Pathology and Regenerative Medicine
The Role of 17β-Estradiol and Estrogen Receptors in Regulation of Ca2+ Channels and Mitochondrial Function in Cardiomyocytes
NOX Inhibition Improves β-Adrenergic Stimulated Contractility and Intracellular Calcium Handling in the Aged Rat Heart
Age, Sex and Overall Health, Measured As Frailty, Modify Myofilament Proteins in Hearts From Naturally Aging Mice.
Extracellular matrix roles in cardiorenal fibrosis: Potential therapeutic targets for CVD and CKD in the elderly
Reduced cardiac response to the adrenergic system is a key limiting factor for physical capacity in old age.
Remodeling of t-system and proteins underlying excitation-contraction coupling in aging versus failing human heart.
Arrhythmogenesis in the aged heart following ischaemia-reperfusion: Role of Transient Receptor Potential Vanilloid 4.
Ageing Causes Ultrastructural Modification to Calcium Release Units and Mitochondria in Cardiomyocytes.
Cardiovascular Disease Pathophysiology
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Arrhythmias are abnormalities in heart rhythms, which can be either too fast or too slow. They can result from abnormalities of the initiation of an impulse or impulse conduction or a combination of both. Here is the latest research on arrhythmias.
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