Although uncommon, the incidence of ventricular arrhythmia is high in certain subsets of patients after coronary artery bypass grafting. Arterial baroreflex dysfunction has been linked to increased risk of ventricular arrhythmia and sudden cardiac death. The aim of the current study was to explore arterial baroreflex function during the early recovery phase and up to five months after surgery. Electrocardiogram and beat-to-beat blood pressures were registered in patients (n=92) undergoing coronary artery bypass grafting five weeks and five months after surgery. Healthy subjects (n=31) were examined for comparison. The arterial baroreflex sensitivity and the baroreflex effectiveness index were calculated. The baroreflex sensitivity and the baroreflex effectiveness index were reduced by 36% and 64%, respectively (P<0.01 for both) in patients five weeks after coronary artery bypass grafting compared to healthy subjects (HS). Values increased during follow-up but the baroreflex effectiveness index remained reduced by 55% in patients compared to HS five months after cardiac surgery (P<0.01). Arterial baroreflex dysfunction prevails both early and long-term after coronary artery bypass grafting. Reduced modulation of cardiac parasympathetic nervous activity could contribute to the increased risk of ventricular arrhythmia observed during the early recovery phase after cardiac surgery.
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http://dx.doi.org/10.1510/icvts.2008.198747 | DOI Listing |
PM R
January 2025
Department of Physical Medicine and Rehabilitation, Mayo Clinic, Rochester, Minnesota, USA.
Background: Individuals with spinal cord injury (SCI) commonly have autonomic dysreflexia (AD) with increased sympathetic activity. After SCI, individuals have decreased baroreflex sensitivity and increased vascular responsiveness.
Objective: To evaluate the relationship between baroreflex and blood vessel sensitivity with AD symptoms.
Acta Physiol (Oxf)
February 2025
Department of Physiology, Graduate School of Health and Sports Science, Juntendo University, Chiba, Japan.
Aim: Chronic stress elevates blood pressure, whereas regular exercise exerts antistress and antihypertensive effects. However, the mechanisms of stress-induced hypertension and preventive effects through exercise remain unknown. Thus, we investigated the molecular basis involved in autonomic blood pressure regulation within the amygdala.
View Article and Find Full Text PDFFront Neurol
December 2024
Center for Data Science, Nell Hodgson Woodruff School of Nursing, Emory University, Atlanta, GA, United States.
Background: Traumatic brain injury (TBI) disrupts normal brain tissue and functions, leading to high mortality and disability. Severe TBI (sTBI) causes prolonged cognitive, functional, and multi-organ dysfunction. Dysfunction of the autonomic nervous system (ANS) after sTBI can induce abnormalities in multiple organ systems, contributing to cardiovascular dysregulation and increased mortality.
View Article and Find Full Text PDFAm J Physiol Heart Circ Physiol
January 2025
Department of Pharmacology, Physiology and Neurobiology, University of Cincinnati College of Medicine, Cincinnati, OH.
Lower body negative pressure (LBNP) has been used for decades in humans to model arterial baroreceptor unloading and represents a powerful tool for evaluating cardiovascular responses to orthostatic challenge. However, LBNP studies in animals have been limited to conditions of anesthesia or sedation, where cardiovascular reflexes are altered. Given the consequent uncertainties, the usefulness of LBNP studies in these preclinical models has been severely hampered.
View Article and Find Full Text PDFJ Physiol
December 2024
Daniel Baugh Institute for Functional Genomics and Computational Biology, Department of Pathology and Genomic Medicine, Thomas Jefferson University, Philadelphia, PA, USA.
Loss of cardiac physiological function following myocardial infarction (MI) is accompanied by neural adaptations in the baroreflex that are compensatory in the short term, but then become associated with long-term disease progression. One marker of these adaptations is decreased baroreflex sensitivity, a strong predictor of post-MI mortality. The relative contributions of cardiac remodelling and neural adaptation in the sensory, central brainstem and peripheral ganglionic loci to baroreflex sensitivity changes remain underexplored.
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