Key result
Depressed baroreceptor sensitivity combined with chronic kidney disease in heart failure patients significantly increased the risk of cardiovascular mortality (HR 3.29) compared to those with preserved kidney function and preserved baroreceptor sensitivity.
Why the study?
Heart failure is the most common cardiovascular complication of CKD and foreshadows high morbidity and mortality, with baroreflex impairment likely contributing to cardiovascular mortality.
Does depressed baroreceptor sensitivity predict cardiovascular mortality in individuals with moderate to severe heart failure and CKD?
Cohort (n=247)
No
Does depressed baroreceptor sensitivity predict cardiovascular mortality in individuals with moderate to severe heart failure and CKD?
Depressed cardiac baroreceptor sensitivity is common in patients with mild to moderate CKD and heart failure, and is a significant independent predictor of cardiovascular mortality.
Key Points We found that cardiac baroreceptor sensitivity (BRS), which reflects the integrity of autonomic responses to changes in BP, was depressed in individuals with both CKD and heart failure compared with those with heart failure and preserved kidney function. Depressed BRS was associated with the risk of cardiovascular death, whereas CKD in the absence of depressed BRS was not associated with the risk of cardiovascular death. Our findings suggest that depressed BRS may be a critical contributor to the increased risk of cardiovascular death in individuals with CKD and heart failure. Background Heart failure is the most common cardiovascular complication of chronic kidney disease (CKD) and foreshadows a high morbidity and mortality rate. Baroreflex impairment likely contributes to cardiovascular mortality. We aimed to study the associations between CKD, heart failure, and baroreflex sensitivity (BRS) and their association with cardiovascular outcomes. Methods We retrospectively analyzed data from a cohort of 247 individuals with moderate to severe HF. All subjects underwent BRS measurements after intravenous phenylephrine along with electrocardiography, echocardiography, and laboratory measurements. We used logistic regression models to assess the association of CKD (estimated glomerular filtration rate <60 ml/min per 1.73 m 2 ) with BRS using iterative models. Cox proportional hazards models were used to assess associations of binary BRS and subgroups according to categorizations of CKD and BRS with cardiovascular mortality. Results Median eGFR among individuals with CKD was 52 (IQR 44–56) ml/min per 1.73 m 2 . eGFR was lower in those with depressed BRS (65 [IQR 54–76] ml/min per 1.73 m 2 ) compared with those with preserved BRS (73 [IQR 64–87] ml/min per 1.73 m 2 ; P ≤0.001). The majority of individuals with CKD had depressed BRS compared with those without CKD (60% versus 29%; P =0.05). In regression models, CKD and BRS were independently associated. Cardiovascular mortality was significantly increased in individuals with or without CKD and depressed BRS compared with those with preserved BRS and CKD. Conclusions Cardiac BRS is depressed in patients with mild to moderate CKD and HF and associated with cardiovascular mortality. Additional study to confirm its contribution to cardiovascular mortality, particularly in advanced CKD, is warranted.
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Charytan et al. (2022) conducted a cohort in Moderate to severe heart failure (n=247). Depressed baroreceptor sensitivity and chronic kidney disease vs. Preserved baroreceptor sensitivity and preserved kidney function was evaluated on Cardiovascular mortality (HR 3.29, 95% CI 1.49-7.27, p=0.03). Depressed baroreceptor sensitivity combined with chronic kidney disease in heart failure patients significantly increased the risk of cardiovascular mortality (HR 3.29) compared to those with preserved kidney function and preserved baroreceptor sensitivity.
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