Submission
| Title: | Central Apnea Severity is Related to Changes in Natriuretic Peptide Levels During Decongestive Treatment of Acute Decompensated Heart Failure. |
| Presenter: | Nicholas Harrison |
| Institution: | Indiana University School of Medicine |
| Authors: | Shalini Manchanda, Department of Medicine, Division of Sleep Medicine, IUSM; Henry Ludwig, Department of Emergency Medicine, IUSM; Peter Pang, Department of Emergency Medicine, IUSM; Ankit Desai, Department of Medicine, Division of Cardiology, IUSM; |
Abstract
| Background/Significance/Rationale: | Cheyne-Stokes Central Apnea (CS-CA), is common in heart failure (HF) and associated with morbidity and mortality. The pathophysiology of CA-CS is unknown. We tested whether brain natriuretic peptide (BNP), a biomarker secreted specifically by myocardial cells under stress from congestion, was associated with severity of CS-CA during acute HF (AHF) decongestive treatment. |
| Methods: | We analyzed 85 consecutive hospital days from 30 prospectively-enrolled patients with cardiologist-adjudicated AHF and echocardiographic evidence of elevated cardiac pressures at admission. Daily data collected included biomarkers (BNP, troponin, electrolytes, renal/hepatic function), vitals, treatments, physical exam, pulmonary edema quantification by lung ultrasound, demographics, medical history, and continuous central-apnea monitoring. Central apnea index (CAI), scored by a blinded Board-Certified sleep medicine physician, was compared to BNP and other covariates through time by linear mixed modeling. |
| Results/Findings: | The final model explained 95% of variance in CAI between treatment days and patients (i.e. adjusted R2 = 0.953). BNP steadily declined in response to decongestive treatment through hospitalization. Each 10% daily change in BNP was associated with a concordant 4.7% change in CAI (p<0.01), after adjusting for covariates. Other significant (p<0.05) daily predictors of CAI were diuretic dosing, tachycardia, serum albumin, anion gap, high-flow oxygen, and history of central sleep apnea. |
| Conclusions/Discussion: | For the first time in humans we show that CS-CA is directly associated with treatment-responsive changes in myocardial cellular stress after adjusting for biomarkers and measures of alternative proposed pathophysiologic mechanisms (e.g. metabolic alkalosis, pulmonary edema severity and pulmonary gas exchange, renal dysfunction, et al.). |
| Translational/Human Health Impact: | While efforts to develop treatment strategies for CS-CA in HF have largely focused on ventilatory support and/or acid base status as potential physiologic targets, our results point to the importance of relieving underlying myocardial |
