Selective Cardiac Neuroadrenergic Abnormalities in Hypertensive Patients with Left Ventricular Hypertrophy

Background sed sympathetic drive to the heart might contribute to the development and progression of myocardial damage in hypertensive patients (HTs). This study assessed the possible presence of abnormalities in myocardial uptake of 123I-metaiodobenzylguanidine (MIBG), a marker of sympathetic activity, in HTs with left ventricular hypertrophy (LVH). s HTs with LVH and 10 matched normotensive controls underwent clinical and laboratory examination, as well as LVH determination by echocardiography. The presence of myocardial ischemia was ruled out by exercise stress testing. Global and regional myocardial uptake of 123I-MIBG was determined in both groups using planar and single proton emission tomography scintigraphy. In addition, thallium-201 (Tl-201) myocardial scintigraphy was performed in HTs. The heart/mediastinum (H/M) ratio on planar 123I-MIBG images at different time points was compared between HTs and controls. Moreover, regional cardiac uptake of 123I-MIBG was compared between groups and, within the HTs group, with regional Tl-201 uptake. s study times, the H/M ratio was lower in HTs than in controls (all p <0.05). A significant reduction in 123I-MIBG uptake in the mid-inferolateral and mid-inferior segments was observed in HTs compared to controls. Also, a significant reduction in 123I-MIBG uptake compared to Tl-210 uptake was observed in non-septal segments of HTs. sions c abnormalities in global and regional uptake of 123I-MIBG, as well as impaired 123I-MIBG compared to Tl-201 uptake, are present in HTs with LVH. Given the effect of sympathetic nervous system on the heart, these abnormalities might play a role in hypertension-related cardiac damage.