Journal of Cardiac Failure最新文献

Background: Heart transplantation from hepatitis C-positive donors is on the rise, yet there exists divergence in approaches to managing recipients of these organs. Practices range from prophylactic treatment of recipients prior to transplantation to delayed treatment following the detection of viremia, with no established consensus on the optimal approach.

Methods: An online survey was conducted among the heart transplant centers in the United States and Canada from January 2023-February 2024. The survey gathered comprehensive information from the institutions regarding direct antiviral (DAA) therapies used, timing and duration of DAA, frequency of viral load testing, adverse effects, virological response, and immunosuppressive therapy modifications. The treatment pathways were categorized based on the timing of treatment initiation into prophylactic, preemptive or reactive approaches. Analysis was restricted to adult transplant programs in the U.S. that had an HCV transplant protocol and performed at least 1 HCV NAT-positive transplant. The Scientific Registry of Transplant Recipients database was queried for total heart transplants using hepatitis C virus nucleic acid testing (HCV NAT)-positive donors.

Results: Of 122 heart transplant programs, 35 (28.7%) institutions responded; 689 heart transplants (49.1%) using HCV NAT-positive donors were captured across institutions. Among 30 U.S. institutions performing adult heart transplantation with HCV NAT-positive donor hearts, 5 (16.7%) used prophylactic, 9 (30%) preemptive and 16 (53.3%) reactive treatment pathways. Most employed pan-genotype DAA therapies for a median of 12 weeks. Significant heterogeneity existed in treatment and monitoring protocols.

Conclusion: Practice patterns for management of HCV NAT-positive donor hearts vary significantly. Establishing registries and randomized control trials for these patients is crucial for guiding future practices.

Background: The interstitial fluid compartment is disproportionally expanded in heart failure (HF). Enhancing sweat rate removes fluids and sodium directly from the interstitial compartment.

Objectives: To study the feasibility and efficacy of direct interstitial decongestion in hospitalized HF patients.

Methods: We used a device designed to enhance fluid and salt expulsion via the eccrine sweat glands. Patients were treated for 1 to 6 days in the hospital. Following discharge, home therapy continued for 30 to 60 days (1-4 treatments/week). The primary efficacy endpoint for the in-hospital phase was a fluid loss of ≥500 mL per ≥4 hours per treatment. Secondary performance endpoints included changes in congestion score and N-terminal pro b-type natriuretic peptide (NT-proBNP) levels, evaluated for each phase separately.

Results: We studied 15 patients, 12 completing both the hospital and home phases. During the in-hospital phase, median weight change due to device therapy was 2.4 kg (interquartile range [IQR] 2.20-3.77), and the primary endpoint was met in 86% of treatment sessions. During the home treatment, median weight loss was 3.1 kg (IQR 0.6 to 7.4 Kg). Congestion score declined from 6 (IQR 6-7) to 1 (IQR 1-1.5) at the end of home therapy (P = 0.002). Median NT-proBNP levels decreased from 7732 (IQR 4694-9746) to 4984 pg/mL (IQR 3559-8950, P = 0.01) during the hospital phase and to 3596 ng/mL (IQR 1640-5742, P = 0.02) at the end of home therapy.

Conclusion: Fluid removal via the skin is an effective strategy for enhancing decongestion in hospitalized patients with acute decompensated heart failure. Following hospital discharge, device therapy was associated with additional improvement in decongestion.

Background: The HEART-FID trial (Randomized Placebo-Controlled Trial of Ferric Carboxymaltose [FCM] as Treatment for Heart Failure with Iron Deficiency) is the largest trial to test intravenous iron (ferric carboxymaltose [FCM]) vs placebo in patients with heart failure and iron deficiency. The results showed a modest but nonstatistically significant reduction in important clinical outcomes, including all-cause mortality.

Objectives: We sought to understand the factors associated with all-cause mortality.

Methods: Data concerning patients enrolled in the HEART-FID trial were used to determine factors associated with all-cause mortality via multivariable models. The models included key clinical characteristics, including treatment interactions identified in the primary analysis (age by sex and country of enrollment). All-cause mortality at 12 months and over the full duration of follow-up (median 23.1 months) was evaluated by using Cox proportional hazard regression.

Results: A total of 3065 patients had 737 all-cause mortality events over the duration of the trial, with 289 events occurring in the first 12 months. Fewer patients randomized to FCM died by 12 months compared with the placebo group (131 receiving FCM vs 158 receiving placebo; hazard ratio 0.82 [95% confidence interval: 0.65-1.04]). Patients who died were more likely to be older and to have diabetes, atrial fibrillation, lower ejection fractions and estimated glomerular filtration rates and higher N-Terminal pro B-type natriuretic peptide (NT-proBNP) levels. The 3 multivariable factors most strongly associated with all-cause mortality at 12 months were NT-proBNP level, country of enrollment and 6-minute walk test distance. Similar results were seen for predicting all-cause mortality over the entire follow-up; the addition of an age × sex × FCM interaction yielded statistically significant results, with greater association of benefit from FCM found in older women than in other subgroups of patients.

Conclusion: FCM, compared with placebo, was associated with a potentially clinically meaningful (but not statistically significant) reduction in all-cause mortality, with key predictors of mortality being natriuretic peptide level, country of enrollment and 6-minute walk test distance.

Heart failure (HF) is associated with poor prognosis, especially when it progresses to cardiogenic shock (CS), where survival rates substantially decline. A key area of interest is the role of blood lactate as a biomarker in these conditions. Lactate is produced under normal physiological conditions but increases with impaired tissue perfusion, a hallmark of HF and CS. Elevated lactate levels result from increased production, reduced clearance or both and are often associated with worse outcomes. Traditionally considered a byproduct of anaerobic metabolism, lactate is now recognized as an important energy substrate, particularly in myocardial tissue during periods of metabolic stress. Recent studies suggest that dynamic lactate monitoring, including lactate clearance (LC), may provide critical insights into patients' prognoses and responses to therapy. Serial measurements of lactate have been shown to predict survival in critically ill patients, including those with HF and CS. In CS, elevated lactate levels correlate with increased mortality risk, and LC is emerging as an important parameter in treatment protocols. Despite growing evidence of lactate's clinical relevance, research is needed to establish standardized thresholds and optimal monitoring timelines. Understanding the complexities of lactate metabolism and its role in HF and CS could lead to improved risk stratification and more personalized treatment approaches.

The author describes her personal experience with a cardiac diagnosis to demonstrate how wellness disparities are often rooted in historical constructions of "ideal" physical presentation that are both racialized and gendered. Her experiential analysis contends that failure to contextualize patients and divorce them from these historically problematic constructions is used to justify their profound disability and death.