Journal of Cardiac Failure最新文献

Background: Sacubitril/valsartan is a key therapy for heart failure with reduced ejection fraction (HFrEF). However, concerns remain regarding its potential impact on cognitive function since neprilysin inhibition may influence amyloid-β (Aβ) metabolism. This study evaluates the effect of sacubitril/valsartan on plasma biomarkers of neurodegeneration.

Methods: Plasma neuromarkers, i.e. Aβ40, Aβ42, neurofilament light chain (NfL), and total tau (t-tau) were measured at baseline, 3 months, and 1 year after sacubitril/valsartan initiation using the single-molecule array (SIMOA) technology in a HFrEF cohort from a prospective registry with biobank. Comparisons were made for baseline vs. 3 months and baseline vs 1-year follow-up.

Results: A total of 31 HFrEF patients (median age: 61 years, 74% male, NT-proBNP: 2333 pg/ml) were included. Aβ40 increased transiently at 3 months [228.6 pg/ml (Q1-Q3: 157.8-321.1) vs. 138.8 (110.0-202.2), p < 0.001] but remained unchanged at 1 year [215.0 (106.5-290.9), p = 0.052]. Aβ42 remained stable [9.90 (6.67-12.49) and 8.43 (5.57-11.86) vs. 7.84 (6.50-11.02) pg/ml, p = 0.108 and 0.771], resulting in a reduced Aβ42/Aβ40 ratio at both follow-ups [0.039 (0.036-0.049) at 3 months, p < 0.001; 0.048 (0.041-0.060) at 1 year, p = 0.026 vs. 0.055 (0.052-0.061)]. Total tau remained unchanged [1.13 (0.91-1.90) and 1.21 (0.85-1.65) vs. 1.03 (0.82-1.53) pg/ml, p = 0.068 and 0.188], while NfL increased at 1 year [28.3 (16.5-78.6) vs. 22.6 (15.1-46.9) pg/ml, p = 0.013], with no short-term change [25.3 (15.0-51.3), p = 0.502].

Conclusion: Sacubitril/valsartan therapy in HFrEF patients leads to a transient increase in Aβ40 and a sustained reduction in the Aβ42/Aβ40 ratio. Stable t-tau and short-term stable NfL levels provide reassurance regarding the absence of immediate neuronal injury, while an NfL increase observed at 1 year may indicate ongoing heart failure progression rather than direct neurotoxicity. These findings highlight the need for cautious interpretation of the Aβ42/Aβ40 ratio in neurocognitive assessments among patients treated with ARNi. Further studies are warranted to clarify the long-term cognitive implications of sacubitril/valsartan in HFrEF.

Background: Heart failure-related cardiogenic shock (HF-CS) accounts for a growing proportion of cardiogenic shock (CS)-related admissions to contemporary cardiac intensive care units. Limited data exist comparing nonischemic (NICM) and ischemic cardiomyopathy (ICM) in this setting.

Methods and results: We sought to examine the differences in patients' characteristics, in-hospital treatments and outcomes in individuals admitted with ICM and NICM HF-CS. The study population included CS admissions within the Critical Care Cardiology Trials Network registry from 2017-2022. CS due to acute myocardial infarction or secondary causes was excluded. Admission characteristics, in-hospital treatments and outcomes were captured. The primary outcome of all-cause in-hospital mortality for ICM vs NICM was compared by using multivariable logistic regression; 2463 hospital admissions for HF-CS, including 902 (36.6%) admissions with ICM and 1561 (63.4%) admissions with NICM, were included. Patients with ICM more commonly had pre-existing comorbidities, pre-admission cardiac arrest and higher Sequential Organ Failure Assessment scores. The use of inotropes and temporary mechanical circulatory support was similar; however, the rates of mechanical ventilation and renal-replacement therapies were higher for ICM. Patients with ICM were less likely to undergo cardiac transplantation but had similar rates of durable left ventricular assist device implantation. After multivariable adjustment, patients with ICM were significantly more likely to die during the index hospitalization (OR 1.56, 95% CI 1.26-1.93; P < 0.001).

Conclusions: Among patients admitted to cardiac intensive care units with HF-CS, patients with ICM were sicker, less likely to undergo cardiac transplantation, and more likely to die when compared with patients with NICM.

Background: The epidemiology and prognostic significance of acute non-cardiac organ dysfunction across cardiogenic shock (CS) subtypes are not well-defined.

Methods: CS admissions from 2017-2022 in the Critical Care Cardiology Trials Network Registry were classified as acute myocardial infarction-related CS (AMI-CS), acute-on-chronic heart failure-related CS (AoC HF-CS), or de novo HF-CS, and categorized as having at least moderate respiratory, kidney, liver, and/or neurologic dysfunction using established criteria. Burden of organ dysfunction was defined as no organ dysfunction (NOD), single organ dysfunction (SOD), or multi (≥2) organ dysfunction (MOD). Multivariable models were used to evaluate associations of burden and type of non-cardiac organ dysfunction with in-hospital death.

Results: Among 3,904 CS admissions, 29.4% had AMI-CS, 50.9% had AoC HF-CS, and 19.7% had de novo HF-CS. AMI-CS and de novo HF-CS had greater prevalence of MOD (35.0% and 33.9%, respectively) compared with AoC HF-CS (23.1%; p<0.01). In-hospital mortality was higher with greater burden of organ dysfunction in the overall CS cohort (SOD vs. NOD: adjusted odds ratio [aOR] for in-hospital death 2.5, 95% confidence interval [CI] 2.0-3.2; MOD vs. NOD: aOR 6.5, 95% CI 5.1-8.2) and across each CS subtype. Kidney dysfunction was the most prognostically important form of organ dysfunction in the overall cohort (aOR 4.1, 95% CI 3.4-5.0) and for each CS subtype.

Conclusion: Admissions for AoC HF-CS had a lower burden of acute non-cardiac organ dysfunction compared with admissions for de novo HF-CS and AMI-CS. However, acute non-cardiac organ dysfunction burden was similarly adversely prognostic across all CS subtypes.

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Background: Donor-recipient size matching is a key factor in donor selection in heart transplantation (HT). One approach uses predicted heart mass (PHM), derived from the Multi-ethnic Study of Atherosclerosis (MESA). We sought to examine whether predicted left ventricular mass (PLVM) derived from the Dallas Heart Study (DHS) is associated with post-transplant outcomes.

Methods: The study cohort included participants without pre-existing cardiac disease in DHS who had a cardiac MRI (n=1,746). A PLVM model was derived by linear regression. The DHS PLVM and MESA PHM were tested for correlation. The associations of DHS PLVM and MESA PHM with 1-year mortality post-HT were assessed in the United Network for Organ Sharing Registry in three eras (Era 1: 1/1/2011-12/31/2014, Era 2: 1/1/2015-10/17/2018, and Era 3 10/18/2018 - 12/31/2021). A pre-specified threshold for low donor-to-recipient mass ratio (< 0.86) was used in Kaplan Meier survival estimation and univariate and multivariable Cox proportional hazard models.

Results: The DHS cohort had a median age of 43 (IQR 36-52) years, 49% male, 40% Black, and 18% Hispanic ethnicity. DHS PLVM was highly correlated with MESA PHM: r = 0.96, p <0.001. In Era 1, a low donor-to-recipient mass ratio by DHS PLVM was associated with increased 1-year mortality (log-rank p<0.001) as was MESA PHM (log rank p = 0.002). However, in Eras 2 and 3, a low donor-to-recipient mass ratio by either DHS PLVM or MESA PHM was not associated with increased 1-year mortality.

Conclusion: PLVM was highly correlated with PHM. A low donor-to-recipient mass ratio, whether assessed by PLVM or PHM, was associated with 1-year mortality post-HT in a historical era but not in the current era under the new allocation system. These findings suggest that other factors may be contributing to donor selection and mortality risk in the modern era.

Background: Heart failure (HF) with mildly reduced or preserved ejection fraction (HFpEF) accounts for over half of cases of HF, with obesity playing a key role. Residual risk remains high despite available therapies. Glucagon-like peptide-1 receptor agonists (GLP-1RAs) have shown potential cardiometabolic benefits, but their role in HFpEF remains unclear.

Methods: A systematic review and meta-analysis of randomized controlled trials evaluating GLP-1RAs in HFpEF were conducted. Studies evaluating GLP-1RA in combination with glucose-dependent insulinotropic polypeptide (GIP) were also included. The analyzed outcomes included cardiovascular (CV) death, worsening HF events and their composite. Hazard ratios (HRs) with 95% confidence intervals (CIs) were pooled by using a random-effects model.

Results: Six randomized controlled trials involving 8788 patients were included. GLP-1RAs significantly reduced the composite outcome of CV death or worsening HF events (HR: 0.68 [0.51-0.89]; P = 0.006, I² = 47%) as well as worsening HF events alone (HR: 0.56 [0.38-0.82]; P = 0.003, I² = 51%). No significant reduction was observed for CV death alone (HR: 0.86 [0.67-1.12]; P = 0.27, I² = 0%).

Conclusion: GLP-1RAs reduce worsening HF events and the composite of CV death or worsening HF in HFpEF, particularly in patients with obesity or diabetes. These findings support their role as a promising therapy requiring further HFpEF-focused trials.

Background: Cardiogenic shock (CS) can be complicated by severe valvular heart disease (VHD). We analyzed cardiac intensive care unit (CICU) admissions according to VHD status.

Methods and results: The Critical Care Cardiology Trials Network is a multicenter network of tertiary CICUs. Centers contributed data from consecutive admissions during 2-month annual snapshots from 2017-2023. CS admissions were classified as having CS attributed to VHD, CS with noncausative VHD or CS without severe VHD. Demographics and therapies were compared. Unadjusted and adjusted odds ratios for in-hospital mortality were calculated. We analyzed 5242 admissions with CS (4.1% attributed to VHD, 18.8% with noncausative VHD, 77.1% without severe VHD). Mitral regurgitation (32.1%) and aortic stenosis (27.9%) were the most common pathologies in CS attributed to VHD. Admissions with CS attributed to VHD more commonly had LVEF ≥ 40% on admission (present in 62.8%, 22.6% and 15.1%, respectively; P < 0.001). Valve intervention was performed in 32.1% of those with CS attributed to VHD. Unadjusted in-hospital mortality in admissions with CS attributed to VHD was 40.0%, compared to 33.4% and 30.3% in the other groups.

Conclusions: VHD is the underlying cause of CS in a minority of CICU admissions but is associated with high in-hospital mortality rates.