NON-DIPPING HEART RATE AND CARDIOVASCULAR RISK IN CKD PATIENTS WITH HYPERTENSION: A CRECKID INVESTIGATION

Abstract

Elevated heart rate, particularly during nighttime, has emerged as a critical factor in assessing cardiovascular risk for both individuals with pre-existing cardiovascular disease and apparently healthy individuals. This phenomenon is closely linked to increased myocardial oxygen demand, reduced diastolic filling time, and compromised coronary perfusion, ultimately disrupting the delicate balance of myocardial oxygen demand and supply. Additionally, elevated heart rate is associated with abnormal vascular shear, pulsatile stress, endothelial dysfunction, vascular stiffness, and oxidative stress. The circadian variation in heart rate, which is influenced by the sympatho-vagal balance, further underscores its significance. Notably, the absence of a substantial dip in the morning heart rate, termed "non-dipping" heart rate (less than 10% reduction), has been linked to adverse cardiovascular outcomes. The etiology of non-dipping heart rate is multifaceted, with factors such as sustained sympathetic overactivation, disruption of the endogenous circadian clock in the brain and sinoatrial node, and the presence of excessive circulating neurohormonal factors like glucocorticoids and catecholamines playing significant roles.

Cardiovascular disease (CVD) is a prevalent complication in individuals with chronic kidney disease (CKD) and is a major contributor to mortality. CKD poses a substantial public health challenge, with a prevalence ranging from 3% to 18% in the general population. The increased global burden and mortality associated with CKD are primarily attributed to the heightened risk of progressing to end-stage renal disease (ESRD) and the accompanying cardiovascular complications.