Purpose: To describe the mechanics and possible clinical importance of left ventricular (LV) rotation, exemplify techniques to quantify LV rotation and illustrate the temporal relationship of cardiac pressures, electrocardiogram and LV rotation.
Materials And Methods: Review of the literature combined with selected examples of echocardiographic measurements.
Results: Rotation of the left ventricle around its longitudinal axis is an important but thus far neglected aspect of the cardiac cycle. LV rotation during systole maximizes intracavitary pressures, increases stroke volume, and minimizes myocardial oxygen demand. Shearing and restoring forces accumulated during systolic twisting are released during early diastole and result in diastolic LV untwisting or recoil promoting early LV filling. LV twist and untwist are disturbed in a number of cardiac diseases and can be influenced by several therapeutic interventions by altering preload, afterload, contractility, heart rate, and/or sympathetic tone.
Conclusions: The concept of LV twisting and untwisting closely linking LV systolic and diastolic function may carry potential diagnostic and therapeutic importance for the management of critically ill patients. Future clinical studies need to address the feasibility of assessing LV twist and untwist as well as the relevance of its therapeutic modulation in critically ill patients.
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http://dx.doi.org/10.1007/s00134-010-2053-8 | DOI Listing |
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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