Myocardial remodeling in hypertension

Abstract

Left ventricular (LV) hypertrophy and remodeling are frequently seen in hypertensive subjects and result from a complex interaction of several hemodynamic and non-hemodynamic variables. Although increased blood pressure is considered the major determinant of LV structural alterations, ethnicity, gender, environmental factors, such as salt intake, obesity and diabetes mellitus, as well as neurohumoral and genetic factors might influence LV mass and geometry. The conventional concept of hypertensive LV remodeling has been that hypertension leads to concentric hypertrophy, as an adaptive response to normalize wall stress, which is then followed by chamber dilation and heart failure. However, several lines of evidence have challenged this dogma. Concentric hypertrophy is not the most frequent geometric pattern and is less usually seen than eccentric hypertrophy in hypertensive subjects. In addition, data from recent studies suggested that transition from LV concentric hypertrophy to dilation and systolic dysfunction is not a common finding, especially in the absence of coronary heart disease. LV hypertrophy is also consistently associated with increased cardiovascular morbidity and mortality, raising doubts whether this phenotype is an adaptive response. Experimental evidence exists that a blunting of load-induced cardiomyocyte hypertrophy does not necessarily result in LV dysfunction or failure. Furthermore, the hypertrophic myocardium shows fibrosis, alterations in the coronary circulation and cardiomyocyte apoptosis, which may result in heart failure, myocardial ischemia and arrhythmias. Overall, this body of evidence suggests that LV hypertrophy is a complex phenotype that predicts adverse cardiovascular outcomes and may not be necessarily considered as an adaptive response to systemic hypertension.

Aerobic exercise training promotes physiological cardiac remodeling involving a set of microRNAs

“…These two different stimuli induce distinct morphological adaptations to the heart; in particular, to the LV. The LV remodeling by pressure overload is characterized by concentric hypertrophy, whereas LV remodeling by volume overload induces eccentric hypertrophy (70). At the cellular level, concentric hypertrophy is characterized by parallel addition of new sarcomeres and lateral growth of individual cardiomyocytes.…”

“…Cardiac hypertrophy is an adaptive response of the heart to increased cardiac workload and involves a variety of mechanical, hemodynamic, and hormonal factors (70). Although any increase in heart mass is broadly defined as a hypertrophic response, there are two very different forms of ventricular hypertrophy, one physiological and another pathological (5).…”

Mitochondrial coupling factor 6 upregulation in hypertension-induced cardiac hypertrophy

“…LV hypertrophy is frequently seen in hypertensive subjects and has been considered an adaptive response to hemodynamic overload imposed by systemic hypertension [14]. Increased blood pressure is considered the major determinant of LV structural alterations [15].…”

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