Key result
Type 2 diabetes mellitus significantly exacerbated left ventricular concentric hypertrophy in patients with postinfarction cardiosclerosis and arterial hypertension, increasing relative posterior wall thickness by 30.0%.
Why the study?
The study evaluated myocardial structural and functional changes in patients with postinfarction cardiosclerosis, hypertension, and type 2 diabetes according to LV systolic function and heart failure functional class.
Observational (n=158)
Answers are grounded in this paper and cite their sources.
Type 2 diabetes mellitus exacerbates left ventricular concentric hypertrophy and remodeling in patients with postinfarction cardiosclerosis and arterial hypertension.
The article evaluates the structural and functional changes of the myocardium in patients with postinfarction cardiosclerosis, hypertension and type 2 diabetes depending on the systolic function of the left ventricle and the functional class of chronic heart failure. A study of 68 patients with postinfarction cardiosclerosis, hypertension and type 2 diabetes mellitus was performed. The comparison group included 60 patients with postinfarction cardiosclerosis, the control group -30 almost healthy individuals. Type 2 diabetes mellitus is a potentiator of left ventricular myocardial remodeling in patients with systolic dysfunction caused by postinfarction cardiosclerosis. Comorbidity of postinfarction cardiosclerosis, arterial hypertension and type 2 diabetes mellitus leads to the progression of postinfarction remodeling.
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Kravchun et al. (2021) conducted an observational in Postinfarction cardiosclerosis, arterial hypertension, and type 2 diabetes mellitus (n=158). Type 2 diabetes mellitus vs. Postinfarction cardiosclerosis and arterial hypertension without type 2 diabetes was evaluated on Left ventricular relative posterior wall thickness (LVRPWT) (30.0% increase, p=<0.05). Type 2 diabetes mellitus significantly exacerbated left ventricular concentric hypertrophy in patients with postinfarction cardiosclerosis and arterial hypertension, increasing relative posterior wall thickness by 30.0%.
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