Abstract

Smoking exposure is always associated with aging, especially in old age. Aged-related changes in an old-aged smoker, but otherwise normal heart mimic those changes associated with cardiac diseases, including myocardial infarction and alterations to cardiac valves and coronary arteries. Human cardiac aging generates a complex phenotype. Experimental evidence in animal models has indicated smoking exposure attenuation cardioprotective with age such as left ventricular hypertrophy and heart failure, yet information regarding myocardial dysfunction in old age is limited. Cardiac aging is a human physiologic change which has the slowly progressive functional declines and structural changes with age from physiologic to pathologic transfer. Normal aging in old man must be in the absence of major cardiovascular risks such as high blood pressure. Smoking may stimuli first induce a phase of cardiac hypertrophy, especially in left ventricular individual. Aging affects cardiovascular function in the same manner as smoking exposure. However, aging also shows relative adaptive responsiveness to eliminate damaged and exhausted cells from birth to senescence. Inflammation response is the major role in the adaptive pathological aging from physiological responsiveness. Therefore, remodeling of the aging cardiac typically involves a large net loss of active cardiac myocytes, reactive cardiac of the remaining cells, and increased accumulation of connective tissue.

Keywords: Smoking exposure; Cardiac diseases; Cardiac aging; Physiologic to pathologic transfer; Cardiac hypertrophy; Inflammation response