Key result
Chronic hemodialysis is linked to ~43% lower atropine-mediated tachycardia compared to normal renal function.
Why the study?
The relative contribution of left ventricular mass, arterial blood pressure, and end-stage renal disease to impaired cardiac vagal tone was unclear.
Observational (n=49)
Absolute Event Rate: 34.7% vs 60.8%
p-value: p=< 0.01
LV mass and BP independently impair VTR in ESRD; leaves open whether regression improves outcomes.
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 microg/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/m2 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.
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Mircoli et al. (2003) conducted an observational in End-stage renal disease (n=49). End-stage renal disease on chronic hemodialysis vs. Normal renal function was evaluated on Atropine-mediated tachycardia (p=< 0.01). Patients on chronic hemodialysis had significantly lower atropine-mediated tachycardia compared to controls with normal renal function (34.7 vs 60.8 beats/min, P < 0.01).
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