On-treatment blood pressure and cardiovascular mortality in adults with repaired coarctation of aorta.

BACKGROUND: Although, hypertension is common in adults with repaired coarctation of aorta (COA), there are no data about on-treatment blood pressure (BP), and its relationship to outcomes in this population. The purpose of this study was to determine the relationship between on-treatment BP and cardiovascular mortality in adults with repaired COA. METHODS: Retrospective study of adults with repaired COA on antihypertensive therapy (n = 461, age 39 ± 11). All BP measurements obtained within the first 3 years were averaged to determine the on-treatment BP, and the patients were stratified into BP quartiles using the cut-off points from the guidelines. RESULTS: Being in the upper systolic BP (SBP) quartiles (SBP 120-129, 130-139 and ≥140) was associated with higher risk of cardiovascular mortality (HR 1.05, 95%CI 1.01-1.07, HR 1.12, 95%CI 1.04 to 1.15 and HR 1.39, 95%CI 1.13 to 1.59), as compared to being the lowest SBP quartile. We observed a 7% increase in the risk of cardiovascular mortality for every 5 mmHg increase in SBP, and a 4% increase in risk of cardiovascular mortality for every 5 mmHg increase in DBP. CONCLUSIONS: Collectively, these data suggest that even s less severe form of hypertension SBP (120-129 mmHg) was not benign, and perhaps should be considered for antihypertensive therapy. A randomized controlled clinical trial is required to determine whether this group of patients (SBP 120 to 129 mmHg) would benefit from antihypertensive therapy, and to determine the optimal type and intensity of antihypertensive therapy in this population.

Rate-Adaptive Atrial Pacing for Heart Failure With Preserved Ejection Fraction: The RAPID-HF Randomized Clinical Trial.

Importance: Reduced heart rate during exercise is common and associated with impaired aerobic capacity in heart failure with preserved ejection fraction (HFpEF), but it remains unknown if restoring exertional heart rate through atrial pacing would be beneficial. Objective: To determine if implanting and programming a pacemaker for rate-adaptive atrial pacing would improve exercise performance in patients with HFpEF and chronotropic incompetence. Design, Setting, and Participants: Single-center, double-blind, randomized, crossover trial testing the effects of rate-adaptive atrial pacing in patients with symptomatic HFpEF and chronotropic incompetence at a tertiary referral center (Mayo Clinic) in Rochester, Minnesota. Patients were recruited between 2014 and 2022 with 16-week follow-up (last date of follow-up, May 9, 2022). Cardiac output during exercise was measured by the acetylene rebreathe technique. Interventions: A total of 32 patients were recruited; of these, 29 underwent pacemaker implantation and were randomized to atrial rate responsive pacing or no pacing first for 4 weeks, followed by a 4-week washout period and then crossover for an additional 4 weeks. Main Outcomes and Measures: The primary end point was oxygen consumption (V̇o2) at anaerobic threshold (V̇o2,AT); secondary end points were peak V̇o2, ventilatory efficiency (V̇e/V̇co2 slope), patient-reported health status by the Kansas City Cardiomyopathy Questionnaire Overall Summary Score (KCCQ-OSS), and N-terminal pro-brain natriuretic peptide (NT-proBNP) levels. Results: Of the 29 patients randomized, the mean age was 66 years (SD, 9.7) and 13 (45%) were women. In the absence of pacing, peak V̇o2 and V̇o2 at anaerobic threshold (V̇o2,AT) were both correlated with peak exercise heart rate (r = 0.46-0.51, P < .02 for both). Pacing increased heart rate during low-level and peak exercise (16/min [95% CI, 10 to 23], P < .001; 14/min [95% CI, 7 to 21], P < .001), but there was no significant change in V̇o2,AT (pacing off, 10.4 [SD, 2.9] mL/kg/min; pacing on, 10.7 [SD, 2.6] mL/kg/min; absolute difference, 0.3 [95% CI, -0.5 to 1.0] mL/kg/min; P = .46), peak V̇o2, minute ventilation (V̇e)/carbon dioxide production (V̇co2) slope, KCCQ-OSS, or NT-proBNP level. Despite the increase in heart rate, atrial pacing had no significant effect on cardiac output with exercise, owing to a decrease in stroke volume (-24 mL [95% CI, -43 to -5 mL]; P = .02). Adverse events judged to be related to the pacemaker device were observed in 6 of 29 participants (21%). Conclusions and Relevance: In patients with HFpEF and chronotropic incompetence, implantation of a pacemaker to enhance exercise heart rate did not result in an improvement in exercise capacity and was associated with increased adverse events. Trial Registration: ClinicalTrials.gov Identifier: NCT02145351.

Hemodynamic assessment in heart failure.

Hemodynamics play a central role in the pathophysiology of heart failure (HF), yet their proper assessment and optimization remains challenging. Heart failure is defined as the inability of the heart to deliver adequate perfusion (cardiac output) to the body at rest or exercise, or to require an elevation in cardiac filling pressures in order to do this. This bedrock definition is important because it relies on measurable quantities (filling pressures and output) that are readily assessed in the cardiac catheterization laboratory. Here we present three cases to illustrate how better understanding of the determinants of cardiac output and stroke volume: preload, afterload, contractility, and lusitropy, as well as the determinants of congestion (high filling pressures) may be used to guide optimization of hemodynamic status. The goal is that the readers will be able to think more critically when evaluating the hemodynamics of their patient in HF and recognize the complex interplay that determines the complex balance between cardiac ejection and filling capabilities, and how this alters symptoms and outcomes for patients with HF. KEY POINTS: Careful assessment of hemodynamics in the catheterization laboratory allows for actionable insight to a patient's volume status, cardiac function and can help prognosticate outcomes. Exercise hemodynamics in heart failure is a powerful tool to better understand the cause of symptoms and predict outcomes. Clinicians should aim to decrease biventricular filling pressures to normal values to improve morbidity and reduce risk for readmission. In patients with heart failure and reduced ejection fraction, clinicians should aim to decrease afterload as much as can be tolerated by the renal function and patient's symptoms. Low cardiac output can often be improved by optimizing preload and afterload rather than initiating inotropes, which should be reserved until needed. In advanced heart failure, the right heart function becomes a key determinant of symptoms and outcomes.