Introduction: Left ventricular remodelling is a process of change in size, shape, wall thickness and heart function, initiated by a noxious stimulus such as ischaemia. Methods of pharmacological and surgical inhibition or reversal of remodelling are being sought.
Aim: To assess the influence of coronary artery bypass grafting on echocardiographic measures of left ventricular size and shape in medium-term follow-up.
Methods: In a group of 30 patients three echocardiographic examinations were performed: before CABG operation, 3 months after and 20 months after the operation. Left ventricular area and volumes as well as indices of sphericity, thinning and expansion were calculated.
Results: After the operation, left ventricular areas measured in short axis and in apical four-chamber view increased among patients with a history of myocardial infarction. Improvement in the sphericity index occurred after the operation in patients with a history of myocardial infarction in whom the ejection fraction before the operation was less than 50%.
Conclusions: The left ventricular remodelling process progresses after coronary artery bypass grafting in patients with a history of myocardial infarction. Inhibition of remodelling may be expected in patients without myocardial infarction, with preserved left ventricular systolic function.
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Cureus
December 2024
Internal Medicine, Kempegowda Institute of Medical Sciences, Bangalore, IND.
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View Article and Find Full Text PDFFront Endocrinol (Lausanne)
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Department of Cardiovascular Medicine, Mayo Clinic, Rochester, MN, United States.
Diabetic cardiomyopathy (DMCM), defined as left ventricular dysfunction in the setting of diabetes mellitus without hypertension, coronary artery disease or valvular heart disease, is a well-recognized entity whose prevalence is certainly predicted to increase alongside the rising incidence and prevalence of diabetes mellitus. The pathophysiology of DMCM stems from hyperglycemia and insulin resistance, resulting in oxidative stress, inflammation, cardiomyocyte death, and fibrosis. These perturbations lead to left ventricular hypertrophy with associated impaired relaxation early in the course of the disease, and eventually culminating in combined systolic and diastolic heart failure.
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