Journal of Cardiac Failure最新文献

Background: Despite improvements in hemocompatibility-related adverse events (HRAEs) with the HeartMate 3 left ventricular assist device (LVAD), hemodynamic-related events (HDREs), such as right ventricular failure (RVF) and aortic insufficiency, still result in considerable morbidity and mortality. We investigated a comprehensive, upfront RV protection strategy combining hemodynamic, ventilatory and pharmaceutical optimization to mitigate the risk of RVF.

Methods/results: Participants were prospectively randomized in a 1:1 fashion to either the RV-protection strategy or usual care for post-operative LVAD management. The RV-protection strategy targeted RV afterload (inhaled NO ≥ 48 hrs, PCWP < 18), RV preload (CVP 8-14), RV perfusion (MAP 70-90, Hgb > 8), RV contractility (IV inotropes), rate/rhythm control (HR >100, normal sinus), ventilatory management (SpO2 >95, PaCO² < 50, plateau pressure < 30, PEEP ≤ 5), and RV geometry (echo-guided septal position). The primary outcome was survival free from any HDREs or HRAEs at 24 weeks. Secondary outcomes included severe RVF, according to INTERMACS and ARC definitions. Twenty participants were randomized: 10 to the RV-protection strategy and 10 to usual care. The median age was 60 years (IQR 54-69), 50% were Black, and 50% had ischemia. At 24 weeks, the RV-protection strategy showed significantly greater survival rates free from HDREs or HRAEs compared to usual care (80% vs 40%; P = 0.04). Event-free survival for HRAEs resulted in similar findings. No HDREs occurred with the RV protection strategy vs 3 (30%) with usual care (P = 0.067). Similarly, severe RVF according to INTERMACS or ARC did not occur in the RV protection strategy vs 3 (30%) in the usual-care cohort (P = 0.20).

Conclusions: Participants receiving a novel, comprehensive, upfront RV protection strategy post-LVAD implantation had significantly greater survival rates free from HDREs or HRAEs at 24 weeks.

During the past century, the characteristics of patients with heart failure (HF) and acute HF (AHF) have shifted from patients with severe pump failure due to rheumatic, hypertensive and ischemic heart disease to older and more obese patients with multiple severe comorbidities. The pathophysiology of AHF has shifted, in parallel, from that of advanced, end-stage pump failure caused by severe left ventricular dysfunction to age, obesity and comorbidity-related cardiovascular dysfunction combined with neurohormonal and inflammatory dysregulation or "inflammaging." With the advent of neurohormonal blockers leading to improved outcomes of patients with chronic HF, the focus of AHF therapy has also changed from care directed at early symptom improvement to therapies directed toward longer-term improvements in quality of life and outcomes. Studies conducted in the past 5 years suggest that the beneficial effects seen with the 4 pillars of guideline-directed medical therapy for HF, mostly comprising neurohormonal blockade, can be extended to AHF when these therapies are initiated and rapidly uptitrated during admission and after discharge. A recent pilot study, CORTAHF (Effect of Short-Term Prednisone Therapy on CRP Change in Emergency Department Patients With Acute Heart Failure and Elevated Inflammatory Markers), has suggested that these benefits can be extended by treating patients with AHF and markers of inflammatory activation with anti-inflammatory therapies. Future studies should further examine whether combined anti-inflammatory therapy and neurohormonal blockade can lead to the reversal of disrupted underlying pathophysiology and remission in patients with AHF.

Introduction: Ambulatory hemodynamic monitoring (AHM) of heart failure (HF) using pulmonary artery pressure (PAP) is marked by frequent changes in HF medications. We are beginning to learn how medication titrations during AHM affect mean PAP (mPAP) measured in the seated position, which reflects most waking hours.

Method: We analyzed the 12-month data from the PROACTIVE-HF trial of the Cordella Cordella, Endotronix Inc, Naperville, Illinois, United States) PAP sensor system. Seated mPAP was examined in the 14-days before and after isolated changes in medications; only those medications with ≥10 titrations were analyzed. Dependent sample Wilcoxon-signed rank test was used to compare changes in mPAP with titrations.

Results: We analyzed 456 subjects (age: 64 years, females: 40%, Black: 18%, HF with reduced ejection fraction: 46%). Loop diuretics (LD) were up-titrated 176 times in 133 patients and down-titrated 113 times in 96 patients. Before LD up-titration, mPAP increased by 1.6 ± 1.0 mm Hg; afterwards, it decreased by 2.3 ± 1.0 mm Hg (P < 0.001), with most reduction occurring within 1 week. Down-titration of LD was followed by an increase of 1.8 ± 1.3 mm Hg (P = 0.004) over the next several days. Similar trends were observed across categories of ejection fraction (≤40% and >40%). Angiotensin receptor neprilysin inhibitor (ARNI) up-titration decreased mPAP by 1.8 ± 1.9 mm Hg (P = 0.042), whereas down-titration increased mPAP by 1.5 ± 1.4 (P = 0.094). Mineralocorticoid receptor antagonist (MRA) up-titration tended to decrease mPAP (1.6 ± 2.5 mm Hg, P = 0.286,) whereas down-titration was followed by a significant increase in mPAP of 3.2 ± 1.6 mm Hg (P = 0.001).

Conclusion: The AHM platform using seated mPAP data provided valuable insights into its short-term responses to isolated changes in HF medications. The seated mPAP changed expectedly in response to the titration of LD, whereas the degree of response varied for ARNI and MRA. Ongoing investigation will further characterize the timing and variability of responses to inform algorithms for ambulatory management of PAP.