To assess the complex interplay between morning surge (MS), the autonomic reflex response at the cardiovascular level, and target organ damage (arterial stiffening, left ventricle hypertrophy).
Fifty-nine consecutive elder patients (>65 years old) underwent a 24-h ambulatory blood pressure monitoring. Pulse wave velocity (PWV) was measured as an indicator of arterial stiffness. Autonomic status was assessed by scoring five conventional tests [handgrip, orthostatic pressor response, Valsalva maneuver, heart rate variation during deep breathing (‘I:E’), and immediate heart rate response to standing (‘30 : 15’)].
(a) MS was correlated to left ventricle mass (P<0.005), the orthostatic pressor response (P<0.02), and blood pressure variability (BPVar) (P<0.0001) (n=59). (b) PWV explained 61.4% of MS variation for MS values 40 mmHg or less (84% of patients) (P<0.03, n=49) and 38% of MS variation in nondippers (P<0.04, n=25). (c) There were sex-related differences. PWV was associated with the orthostatic pressor response (P<0.02), ‘I:E’ values (P<0.04) and the ‘30 : 15’ test (P<0.04) in men (n=14). In women (n=41), the ‘I:E’ values were associated with MS and BPVar (P<0.003).
MS was closely related to PWV (arterial stiffening) and BPVar in a small urban sample of cardiovascular patients. MS was also associated with dysautonomia (orthostatic blood pressure/heart rate response to challenges), mostly with impaired parasympathetic modulation. MS and high BPVar cause left ventricular hypertrophy, whereas arterial stiffness alters baroreceptor sensitivity, which in turn affects BPVar, perpetuating a vicious cycle. These findings, although obtained in a small number of participants, provide relevant information not yet available in the local databases.
Institute of Cardiological Research (ININCA), University of Buenos Aires, National Research Council (UBA-CONICET), Buenos Aires, Argentina
This paper is dedicated to the memory of Daniel Grana, persistent worker, unselfish friend, and excellent researcher, who died suddenly at age 55, leaving us mired in deep shock and sadness.
This paper was partially presented at the Congress of the European Society of Cardiology. Stockholm, Sweden, 28 August–1 September 2010.
Correspondence to Jose Milei, MD, PhD, Institute of Cardiological Research (ININCA), University of Buenos Aires, National Research Council (UBA-CONICET), Marcelo T de Alvear 2270 (C1122AAJ), Buenos Aires, Argentina Tel/fax: +54 114 508 3888; e-mail: firstname.lastname@example.org
Received October 14, 2011
Accepted February 27, 2012