Influence of left ventricular mass, uremia and hypertension on vagal tachycardic reserve

Background Left ventricular (LV) hypertrophy, arterial hypertension and end-stage renal disease (ESRD) are associated with deranged cardiac parasympathetic regulation and increased cardiovascular risk. These conditions often co-exist but little is known about the relative contribution of LV mass, arterial blood pressure and ESRD to impaired cardiac vagal tone. We evaluated the vagal tachycardic reserve (VTR) in subjects with normal renal function (age 58.4 ± 6.6 years, n = 19) and in patients under chronic hemodialysis (HD) (age 62.6 ± 13.2 years, n = 30) having wide ranges of LV mass and blood pressure. Methods VTR was estimated from the tachycardic response to atropine (15 μg/kg intravenously) administered during a dipyridamole-atropine stress-echo test performed as part of the diagnostic work-up for identification of inducible myocardial ischemia. LV hypertrophy (defined as LV mass index > 125 g/m 2 in both genders) was present in 20 HD patients and in nine control patients. Only patients free of inducible myocardial ischemia were included in the study. Results The atropine-mediated tachycardia was: (i) significantly smaller in HD patients than in control patients (34.7 ± 7.6 versus 60.8 ± 10.5 beats/min, P< 0.01); (ii) independently and inversely related to LV mass (multiple regression; partial coefficients, -0.139 in HD patients and -0.382 in controls, both P < 0.01) and to mean blood pressure (-0.171 in HD patients and -0.268 in controls, both P< 0.01). Conclusions LV mass is the strongest (inverse) determinant of VTR. Blood pressure as well as the patient's renal status are also independent correlates of VTR, and the concomitance of LV hypertrophy and ESRD exacerbates the impairment of VTR.