Yuxi Liu

Background: Improving health status is a fundamental goal after myocardial infarction (MI). Whether health status differs between type 1 and type 2 MI is unknown. Methods: In this prospective study, 150 patients hospitalized with type 1 (n=75) and type 2 MI (n=75) were enrolled. Health status was assessed at baseline, 1, and 4 months using the EuroQol 5‐Dimension 5‐Level visual analogue scale, 7‐item Seattle Angina Questionnaire, Patient‐Reported Outcomes Measurement Information System Physical Function, Patient‐Reported Outcomes Measurement Information System Fatigue, FRAIL Scale, and Patient Health Questionnaire‐9. Results: A total of 149 baseline, 92 one‐month, and 92 four‐month assessments were analyzed. Patients with type 2 MI were older, were more frequently women, and had more comorbidities. Baseline health status was similar between type 2 and type 1 MI (EuroQol 5‐Dimension 5‐Level visual analog scale, 66.20±22.17 versus 69.36±20.67; P =0.37). At 1 and 4 months, the EuroQol 5‐Dimension 5‐Level visual analog scale was lower for type 2 MI, and adjusted analyses demonstrated less improvement (difference, − 4.8 points; P =0.04). Patients with type 2 MI had lower physical function and greater frailty throughout follow‐up. Baseline fatigue and depression were similar but modestly worse for type 2 MI at follow‐up. Baseline 7‐item Seattle Angina Questionnaire scores were higher for type 2 MI but were similar between groups at follow‐up. Conclusions: Although baseline overall health status was similar, patients with type 2 MI experienced smaller improvements in health status and reported a greater burden of frailty and impaired physical function over 4 months. These findings highlight the need to address health status domains beyond angina after type 2 MI.

Background: Transthyretin amyloid cardiomyopathy (ATTR‐CM) carries high risk for all‐cause mortality (ACM), cardiovascular mortality (CVM), and cardiovascular hospitalization (CVH). NT‐proBNP (N‐terminal pro‐B‐type natriuretic peptide) and serum TTR (sTTR) are prognostic biomarkers in transthyretin amyloid cardiomyopathy, but their combined value for integrated risk stratification remains unknown. We evaluated the relationship between baseline NT‐proBNP and sTTR and their prognostic value in ATTRIBUTE‐CM (Efficacy and Safety of Acoramidis in Transthyretin Amyloid Cardiomyopathy). Methods: ATTRIBUTE‐CM was a phase 3, randomized, double‐blind, placebo‐controlled trial. Among 632 participants randomized to acoramidis or placebo, baseline NT‐proBNP and sTTR concentrations were evaluated post hoc for associations with baseline characteristics, Kansas City Cardiomyopathy Questionnaire overall scores, 6‐minute walk distance, National Amyloidosis Center stage, Geriatric Nutritional Risk Index score, and subsequent time to ACM/first CVH and CVM/first CVH through Month 30. Results: Higher baseline NT‐proBNP and lower sTTR were associated with greater disease severity and were inversely correlated. Using multivariable linear regression, sTTR remained inversely correlated with NT‐proBNP. Using multivariable Cox analyses, baseline NT‐proBNP and sTTR were each independently associated with ACM/first CVH and CVM/first CVH. Higher baseline NT‐proBNP combined with lower sTTR conferred higher risk and shorter time to event. Acoramidis reduced risk of ACM/first CVH and CVM/first CVH regardless of baseline NT‐proBNP/sTTR, National Amyloidosis Center stage, or Geriatric Nutritional Risk Index. Conclusions: Baseline NT‐proBNP and sTTR were additively prognostic for ACM/first CVH and CVM/first CVH in patients with transthyretin amyloid cardiomyopathy. Their joint measurement may be useful for enhanced staging, risk stratification, and prognostication in transthyretin amyloid cardiomyopathy. Acoramidis demonstrated consistent clinical efficacy regardless of baseline NT‐proBNP/sTTR status. Registration: URL: https://clinicaltrials.gov/study/NCT03860935 ; Unique Identifier: NCT03860935. Registered: February 2019.

BACKGROUND: Objective indices of functional capacity in patients with diabetic cardiomyopathy and stage B heart failure (HF) have not been comprehensively defined. We sought to characterize the cardiopulmonary exercise characteristics of individuals with diabetic cardiomyopathy at high risk for overt HF. METHODS: The relationships from cardiopulmonary exercise testing with clinical and laboratory characteristics of participants with diabetic cardiomyopathy were evaluated using baseline data from the ARISE-HF trial (Aldose Reductase Inhibition for Stabilization of Exercise Capacity in Heart Failure). Cluster phenogroups with different comorbidities and their corresponding functional capacity profiles were identified. RESULTS: Among study participants (n=689), the median (Q1, Q3) peak oxygen uptake and ventilatory efficiency (slope of the ratio of minute ventilation/carbon dioxide production) were 15.7 (interquartile range, 13.0–18.0) mL/kg per minute and 31.2 (interquartile range, 27.2–34.1), respectively. Lower peak oxygen uptake was associated with older age, female sex, higher body mass index, higher N-terminal pro-B-type natriuretic peptide, and an increasing burden of noncardiac comorbid conditions but was not associated with cardiac troponin T or echocardiogram-derived strain, left atrial volume index, E/e′, or right ventricular systolic pressure. Elevated left ventricular mass index was the only echocardiographic abnormality associated with lower peak oxygen uptake. Multivariable analysis revealed that female sex, higher body mass index, and no history of dyslipidemia were independently associated with lower baseline peak oxygen uptake. Cluster analysis revealed 3 clusters with profiles of different cardiovascular/exercise parameters and health status profiles. CONCLUSIONS: Baseline cardiopulmonary exercise testing data from the ARISE-HF trial highlight predominant associations of extracardiac clinical and demographic variables with significant impairment in exercise capacity despite strict fulfillment of diagnostic criteria for stage B HF. REGISTRATION: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT04083339.

Background: Higher lipoprotein(a) and oxidized phospholipid concentrations are associated with increased risk for coronary artery disease and valvular heart disease. The role of lipoprotein(a) or oxidized phospholipid as a risk factor for incident heart failure (HF) or its complications remains uncertain. Methods and Results: A total of 1251 individuals referred for coronary angiography in the Catheter Sampled Blood Archive in Cardiovascular Diseases (CASABLANCA) study were stratified on the basis of universal definition of HF stage; those in stage A/B (N=714) were followed up for an average 3.7 years for incident stage C/D HF or the composite of HF/cardiovascular death. During follow‐up, 105 (14.7%) study participants in stage A/B progressed to symptomatic HF and 57 (8.0%) had cardiovascular death. In models adjusted for multiple HF risk factors, including severe coronary artery disease and aortic stenosis, individuals with lipoprotein(a) ≥150 nmol/L were at higher risk for progression to symptomatic HF (hazard ratio [HR], 1.90 [95% CI, 1.15–3.13]; P =0.01) or the composite of HF/cardiovascular death (HR, 1.71 [95% CI, 1.10–2.67]; P =0.02). These results remained significant after further adjustment of the model to include prior myocardial infarction (HF: HR, 1.89, P= 0.01; HF/cardiovascular death: HR, 1.68, P =0.02). Elevated oxidized phospholipid concentrations were similarly associated with risk, particularly when added to higher lipoprotein(a). In Kaplan‐Meier analyses, individuals with stage A/B HF and elevated lipoprotein(a) had shorter time to progression to stage C/D HF or HF/cardiovascular death (both log‐rank P <0.001). Conclusions: Among individuals with stage A or B HF, higher lipoprotein(a) and oxidized phospholipid concentrations are independent risk factors for progression to symptomatic HF or cardiovascular death. Registration: URL: https://wwwclinicaltrials.gov ; Unique identifier: NCT00842868.

The patient carries a de-novo heterozygous missense mutation (c.3686 A>T p.Asp1229Val) in the SCN2A gene. This mutation was evaluated as a pathogenic mutation based on the standards and guidelines of ACMG (American College of Medical Genetics and Genomics) and clinical research publications...