Date of Award
Open Access Honors Thesis
Background - Aldosterone is a pertinent hormone in naturally elevating blood pressure within the body by increasing fluid retention in the body via electrolyte reabsorption in the kidneys. Consequently, aldosterone can have an indirect effect on the incidence of LVH considering the hormone can reinforce high blood pressure. However, recent studies have suggested that aldosterone and the renin-angiotensin-aldosterone-system (RAAS) may have a direct role in leading to an increase in left ventricular mass. Patients with hyperaldosteronism, otherwise elevated circulating aldosterone, have shown high frequencies of LVH regardless of the presence of hypertension. Furthermore, cardiomyocytes have been seen to contain mineralocorticoid receptors that bind to aldosterone and can be affected by different RAAS inactivating medications. Overall, current research suggests there may be a regression between LVH and aldosterone.
Methods and Results – A retrospective model comparing plasma aldosterone levels and left ventricular hypertrophy measurements in a hypertensive cohort of African Americans from the AdDReaCH trial. Follow-up over the course of a year allowed for multivariate analysis to determine whether elevated levels of plasma aldosterone induced changes in left ventricular mass and diastolic function independent of blood pressure and other variables. Left ventricular hypertrophy was assessed through various left ventricular measurements from contrast-aided MRI examinations. Though average LVMI was greater in patients with greater aldosterone-renin ratios, multivariate analysis suggested that plasma aldosterone-renin ratio does not have a significant, independent relationship to the incidence and severity of LVH. Results call for further research on the topic, as the current study confounds results from prior studies.
Rahman, Tahsin M.; Levy, Phillip; and Brody, Aaron M., "The Relationship Between Aldosterone and Left Ventricular Hypertrophy in Hypertensive Patients" (2016). Honors College Theses. 31.