Daily Cardiology Research Analysis
Analyzed 172 papers and selected 3 impactful papers.
Summary
Analyzed 172 papers and selected 3 impactful articles.
Selected Articles
1. Echocardiographic Diastolic Function Grading in HFpEF: Testing the Updated 2025 ASE Criteria.
In invasively proven HFpEF, the 2025 ASE diastolic function algorithm frequently labeled patients as normal or Grade 1 despite elevated resting PAWP and showed poor sensitivity of its stress criteria (false-negative rate 90.5%). Discrimination versus noncardiac dyspnea was limited (AUC 0.61), indicating the algorithm should not be used in isolation to exclude HFpEF.
Impact: Challenges a newly proposed diagnostic standard with invasive reference, revealing substantial false negatives that could misclassify HFpEF. This is a practice-informing negative result likely to influence guideline interpretation and clinical workflows.
Clinical Implications: Do not rely solely on ASE 2025 diastolic grades to rule out HFpEF. Integrate pretest probability, invasive or exercise hemodynamics when appropriate, and HFpEF-specific diagnostic frameworks to avoid missed diagnoses.
Key Findings
- Among ambulatory HFpEF, 32.8% graded normal and 34.8% Grade 1 despite invasive HFpEF; over 60% of normal/Grade 1 had resting PAWP ≥15 mm Hg.
- ASE-recommended stress criteria identified only 9.5% of Grade 1 cases (false-negative rate 90.5%).
- Discrimination vs noncardiac dyspnea was modest (AUC 0.61); patients labeled normal/Grade 1 had a 5.37-fold higher risk of death/HF hospitalization vs controls.
Methodological Strengths
- Invasive hemodynamic reference standard with prospective cohort design and external validation.
- Evaluation across compensated ambulatory and decompensated/recompensated hospitalized cohorts.
Limitations
- Observational diagnostic evaluation; not randomized or interventional.
- Generalizability may vary across labs and imaging protocols; algorithm-specific assessment.
Future Directions: Develop HFpEF-specific diagnostic pathways integrating exercise hemodynamics and machine-learning phenotyping; prospectively test patient-centered outcomes when using alternative frameworks.
BACKGROUND: Echocardiographic grading of left ventricular diastolic function is recommended to guide diagnostic evaluation of heart failure with preserved ejection fraction (HFpEF). A new algorithm for diastolic function interpretation has been proposed, but it has not yet been systematically evaluated in HFpEF. OBJECTIVES: The purpose of this study was to determine the false-negative rate of the 2025 American Society of Echocardiography (ASE) algorithm among invasively confirmed ambulatory HFpEF, assess temporal changes in diastolic grades between decompensated and recompensated hospitalized HFpEF, and, secondarily, to compare diagnostic discrimination with existing HFpEF algorithms and prognostic associations. METHODS: Echocardiography was performed in 2 HFpEF cohorts: 1) ambulatory, compensated patients undergoing invasive hemodynamic exercise testing as part of a prospective cohort study, with an external validation cohort; and 2) hospitalized/decompensated patients both acutely and following recompensation. For secondary analyses, we included noncardiac dyspnea controls and compared performance with existing algorithms. RESULTS: In the ambulatory/compensated HFpEF cohort, 248 of 756 (32.8%) were graded normal, 263 of 756 (34.8%) had Grade 1 diastolic dysfunction, 219 of 756 (30.0%) had Grades 2 to 3, and 26 of 756 (3.4%) were indeterminate. Among those labeled normal or Grade 1, >60% had resting pulmonary artery wedge pressure ≥15 mm Hg at catheterization. In decompensated HFpEF, 22 of 88 (25.0%) showed normal or Grade 1, and this proportion increased to 45 of 88 (51.1%) after recompensation. In HFpEF with Grade 1 undergoing simultaneous hemodynamic exercise testing with stress imaging, only 11 of 116 (9.5%) met the ASE-recommended stress criteria, resulting in a 90.5% false-negative rate. Similar findings were observed in the external validation cohort. The 2025 ASE algorithm poorly discriminated HFpEF from noncardiac dyspnea (AUC: 0.61). Patients with HFpEF labeled as normal or Grade 1 had 5-fold higher risk for all-cause death or heart failure hospitalization compared with controls (HR: 5.37; 95% CI: 1.27-22.6). CONCLUSIONS: Among patients with invasively proven HFpEF, the 2025 ASE algorithm frequently assigns normal or low diastolic grades, and the recommended stress criteria detect only a minority of cases. Although echocardiography remains essential to guide HFpEF evaluation, current algorithms proposed have inadequate sensitivity. Diastolic function grades must be interpreted in the context of pretest probability and HFpEF-specific, evidence-based frameworks, rather than used in isolation to exclude disease.
2. Prediabetes, Subclinical Myocardial Injury or Stress, and Heart Failure Risk for Adults With Hypertension.
In hypertensive adults, prediabetes combined with elevated hs-cTnI or NT-proBNP substantially increased incident HF risk (HR 4.20 and 5.20, respectively) compared with normoglycemia and no myocardial injury/stress. Longitudinal 25% increases in these biomarkers alongside prediabetes further identified the highest-risk subgroup.
Impact: Demonstrates additive risk from metabolic dysregulation and subclinical cardiac injury/stress, supporting integrated biomarker and glycemic profiling for HF prevention in a large, well-characterized cohort.
Clinical Implications: In hypertensive patients—especially those with prediabetes—consider combined use of hs-cTnI and NT-proBNP for HF risk stratification and to target preventive strategies (BP optimization, weight loss, SGLT2 inhibitors where appropriate).
Key Findings
- Prediabetes plus elevated hs-cTnI was associated with a 4.20-fold higher HF risk versus normoglycemia without myocardial injury.
- Prediabetes plus elevated NT-proBNP conferred a 5.20-fold higher HF risk.
- A ≥25% 12-month rise in hs-cTnI or NT-proBNP with prediabetes identified the highest risk subgroup (hs-cTnI HR 3.05; NT-proBNP HR 2.39).
Methodological Strengths
- Large, adjudicated outcomes from SPRINT with both baseline and longitudinal biomarker assessments.
- Multivariable Cox models with joint-category analyses capturing additive risk.
Limitations
- Post hoc analysis; residual confounding and limited HF event counts may affect precision.
- Generalizability beyond SPRINT’s inclusion criteria may be limited.
Future Directions: Test biomarker-guided prevention strategies (e.g., SGLT2i initiation) in prediabetic hypertensives with elevated hs-cTnI/NT-proBNP; evaluate cost-effectiveness and implementation pathways.
IMPORTANCE: It is unclear whether and the extent to which subclinical myocardial injury or stress coexisting with prediabetes is associated with the risk of heart failure (HF). OBJECTIVE: To evaluate the joint associations of prediabetes and subclinical myocardial injury or stress with incident HF risk. DESIGN, SETTING, AND PARTICIPANTS: This post hoc prospective cohort study analyzed data from the Systolic Blood Pressure Intervention Trial (SPRINT). Two analytic samples were used: (1) adults with hypertension without diabetes or prior HF for the baseline biomarkers analysis and (2) participants with biomarker measurements at both baseline and 12 months for the longitudinal biomarkers' change. Prediabetes was defined as a fasting plasma glucose level of 100 to 125 mg/dL. Subclinical myocardial injury was defined as a high-sensitivity cardiac troponin I (hs-cTnI) level of 6 ng/L or higher in men and 4 ng/L or higher in women and subclinical myocardial stress defined as an N-terminal pro-B-type natriuretic peptide (NT-proBNP) level of 125 pg/mL or higher. A 25% or greater increase in any biomarker concentration from baseline to 12 months defined longitudinal change. Data were analyzed between January 1 and May 31, 2025. MAIN OUTCOMES AND MEASURES: The primary outcome was adjudicated incident HF. Cox proportional hazards models were used to estimate hazard ratios (HRs) for HF across joint categories of prediabetes and biomarker elevation. RESULTS: Of 8234 participants (mean [SD] age, 68 [9] years; 37.1% women), 3271 (39.7%) had prediabetes, 2942 (35.7%) had subclinical myocardial injury, and 3593 (43.6%) had subclinical myocardial stress. Over a median follow-up of 3.2 years (IQR, 2.8-3.8 years), 122 participants developed HF. Compared with normoglycemia and no myocardial injury, those with both prediabetes and injury had the highest HF risk (HR, 4.20; 95% CI, 2.31-7.63); similar findings were observed for myocardial stress (HR, 5.20; 95% CI, 2.52-10.70). In the longitudinal analysis (median follow-up, 2.3 years [IQR, 1.9-2-8 years]), 7449 participants with both prediabetes and a 25% or greater increase in hs-cTnI or NT-proBNP level had the highest risk of HF (for hs-cTnI: HR, 3.05; 95% CI, 1.58-5.88; for NT-proBNP: HR, 2.39; 95% CI, 1.28-4.46). CONCLUSIONS AND RELEVANCE: These findings suggest that among adults with hypertension, prediabetes in combination with subclinical myocardial injury or stress is associated with a significantly elevated risk for HF. These findings support the integration of glycemic status and cardiac biomarkers profiling to improve HF risk stratification and guide prevention.
3. Volumetric non-invasive cardiac mapping for accessible global arrhythmia characterization.
This study introduces an imageless, volumetric ECG imaging framework that reconstructs 3D cardiac activation using Green’s function-based inverse source modeling. It reduced arrhythmia origin localization error by 59.3% versus surface-only approaches and produced activation patterns consistent with clinical diagnoses in four challenging patient cases.
Impact: Addresses a fundamental limitation of ECGI by enabling intramyocardial mapping, potentially decreasing reliance on invasive electrophysiology for localization. The methodological advance could reshape pre-procedural planning for ablation and device therapy.
Clinical Implications: Non-invasive 3D activation mapping could improve arrhythmia localization, guide ablation targets, and refine candidate selection and optimization for cardiac resynchronization therapy (CRT). If validated in larger cohorts, it may reduce procedural times and complications.
Key Findings
- Volumetric ECGI reconstructed 3D intramyocardial activation from body-surface potentials using a Green’s function inverse source formulation.
- Compared to surface-only ECGI, geodesic error in arrhythmia origin localization was reduced by 59.3% in simulations.
- In four patient cases (PVC from RVOT, LBBB, VT, WPW), recovered activation patterns aligned with clinical diagnoses.
- Demonstrated feasibility on a public myocardial infarction dataset and on synthetic premature ventricular beats.
Methodological Strengths
- Novel volumetric inverse solution enabling intramyocardial mapping without imaging.
- Cross-validation in simulations plus clinically diverse patient cases.
Limitations
- Small clinical sample (n=4) limits generalizability and outcome correlation.
- No head-to-head comparison with invasive electroanatomic mapping as a reference standard.
Future Directions: Prospective multicenter studies comparing volumetric ECGI against invasive mapping with procedural outcomes; robustness analyses to noise/modeling assumptions; integration with imaging for hybrid anatomical-functional guidance.
BACKGROUND: Cardiac arrhythmias are a major cause of morbidity and mortality increasing the risk of stroke, heart failure, and sudden cardiac death. Imageless electrocardiographic Imaging has emerged as an accessible non-invasive alternative for cardiac electrical mapping from body surface potentials. However, conventional electrocardiographic imaging is restricted to epicardial reconstructions, reducing its reliability in accurately identifying arrhythmias arising from deeper myocardial structures. We aim to overc