Daily Cardiology Research Analysis
Analyzed 183 papers and selected 3 impactful papers.
Summary
Analyzed 183 papers and selected 3 impactful articles.
Selected Articles
1. The Natural History of Massive Left Ventricular Hypertrophy in Pediatric Hypertrophic Cardiomyopathy: A Multiregistry Analysis.
Across two major pediatric HCM registries (n=587), massive LVH clustered in early-childhood, sarcomere-positive disease, with higher adverse-event risk. Notably, nearly one-quarter of those with massive LVH demonstrated significant regression in maximal wall thickness over time, refining risk trajectories in pediatric HCM.
Impact: Defines the natural history of a high-risk pediatric HCM phenotype while identifying a nontrivial rate of regression, informing surveillance and timing of interventions.
Clinical Implications: Children with massive LVH warrant intensified surveillance and early risk stratification (e.g., for ICD candidacy), but recognition of potential wall thickness regression argues for dynamic reassessment rather than fixed risk labeling.
Key Findings
- Among 587 pediatric HCM patients, 186 had massive LVH and were diagnosed at a younger age.
- Massive LVH was linked to higher adverse-event risk compared with non-massive LVH.
- Nearly one-quarter of children with massive LVH experienced significant regression in maximal wall thickness.
Methodological Strengths
- Multiregistry design leveraging SHaRe and IPHCC with harmonized phenotyping
- Clinically meaningful definition of massive LVH and longitudinal assessment
Limitations
- Observational registry design limits causal inference
- Abstract truncation precludes detailed reporting of event rates and statistical metrics
Future Directions: Prospective, genotype-informed risk models integrating dynamic wall thickness changes could refine ICD and therapy decisions in pediatric HCM.
BACKGROUND: Massive left ventricular hypertrophy (LVH) is a risk factor for sudden cardiac death in children with hypertrophic cardiomyopathy (HCM), but little is understood about its natural history. METHODS: Patients with pediatric-onset HCM identified from 2 registries (SHaRe [Sarcomeric Human Cardiomyopathy Registry] and IPHCC [International Paediatric Hypertrophic Cardiomyopathy Consortium]) with or without massive LVH were compared. Massive LVH was defined as absolute maximal left ventricular wall thickness (MLVWT) ≥30 mm or MLVWT RESULTS: We identified 587 patients (54 female [30%]). In 186 children with massive LVH, age at diagnosis was younger (median, 9.2 years [interquartile range, 2.1-13.1 years]) versus 13.6 years (9.7-15.5 years; CONCLUSIONS: In pediatric HCM, massive LVH disproportionately affects those diagnosed in early childhood with sarcomeric disease, with increased risk for adverse events. Significant MLVWT regression is seen in nearly a quarter of patients.
2. Redefining Right Ventricular Function: Incremental Prognostic Utility of Effective RVEF on CMR in Functional Tricuspid Regurgitation-A Multicenter Validation Study.
In 769 patients across derivation and validation cohorts with at least moderate functional TR, CMR-derived effective RVEF (≤25%) independently predicted all-cause mortality and improved risk prediction beyond conventional RVEF and clinical markers. eRVEF tracked with more advanced biventricular remodeling and greater fibrosis burden.
Impact: Establishes a physiologically grounded, imaging-based RV performance metric that outperforms standard RVEF in TR, with external validation and incremental prognostic value.
Clinical Implications: eRVEF can refine risk stratification in functional TR and may inform timing and candidacy for transcatheter tricuspid interventions and advanced therapies.
Key Findings
- An eRVEF threshold ≤25% identified higher mortality risk (derivation cohort HR 1.72; external validation HR 2.66–2.86).
- eRVEF added significant prognostic information beyond conventional RVEF (model chi-square improved; P=0.011).
- Lower eRVEF associated with worse biventricular remodeling, higher TR burden, and greater LGE.
Methodological Strengths
- CMR-based quantification with physiologic definition of forward RV output
- External validation across two independent cohorts and robust multivariable adjustment
Limitations
- Observational design with potential referral and selection biases
- Applicability primarily to functional TR; generalizability to other etiologies requires study
Future Directions: Prospective interventional studies should test whether eRVEF-guided management improves outcomes and validate thresholds across scanners and centers.
BACKGROUND: Right ventricular ejection fraction (RVEF) is a known predictor of adverse outcomes; however, its prognostic value diminishes in tricuspid regurgitation (TR). OBJECTIVES: This study aims to assess whether effective right ventricular ejection fraction (eRVEF) offers a more physiologic assessment of RV function and improves risk stratification in patients with TR. METHODS: The derivation cohort comprised 453 consecutive patients with at least moderate functional TR (regurgitant fraction ≥30% or volume ≥30 mL) on cardiac magnetic resonance (CMR). eRVEF was calculated as the ratio of forward volume to RV end-diastolic volume. The eRVEF threshold (≤25%) was derived based on all-cause mortality data. Clinical data were collected from standardized questionnaires at the time of CMR and supplemented with electronic health records; the primary outcome was all-cause mortality. External validation was performed in 2 independent cohorts, totaling 316 patients using identical inclusion criteria. RESULTS: In the derivation cohort, impaired eRVEF was associated with more advanced biventricular remodeling, worse biventricular function, and greater burden of late gadolinium enhancement (P < 0.05 for all), which was paralleled by higher TR volume and fraction (both P < 0.05). Over a median follow-up period of 2.7 years (Q1-Q3: 0.6-6.6 years), 20% of the patients died; mortality was higher in patients with impaired versus preserved eRVEF (28% vs 12%; HR: 1.72 [95% CI: 1.16-2.54]; P = 0.007). After adjusting for known TR risk markers including age, RV size, TR severity, conventional RVEF, and clinical markers of right-sided congestion, eRVEF remained independently predictive of mortality (HR: 0.49 [95% CI: 0.24-0.97]; P = 0.042). Adding eRVEF to a model inclusive of RVEF improved mortality prediction (chi-square from 30.6 to 37.0; P = 0.011) whereas adding RVEF to eRVEF did not (chi-square from 35.4 to 37.0; P = 0.199). External validation confirmed the prognostic significance of eRVEF ≤25% in both cohorts (HR: 2.66-2.86; both P < 0.05). CONCLUSIONS: eRVEF independently predicts mortality in TR and provides incremental prognostic value over conventional prognostic markers.
3. Lipoprotein(a), High-Sensitivity C-Reactive Protein, and Incident ASCVD Risk in Individuals Without Standard Modifiable Risk Factors.
In 50,450 SMuRF-less UK Biobank participants followed for 15 years, elevated hsCRP and Lp(a) independently predicted ASCVD events, with the highest risk among those with concurrent elevations. Results were consistent using both cohort-specific and clinical thresholds and showed no interaction.
Impact: This large-scale prospective analysis clarifies that combined Lp(a) and hsCRP testing meaningfully refines risk in adults deemed low risk by conventional metrics, informing primary prevention strategies.
Clinical Implications: Consider combined Lp(a) and hsCRP measurement in SMuRF-less adults to uncover residual ASCVD risk and guide preventive strategies (lifestyle, imaging, and potential targeted therapies).
Key Findings
- Elevated hsCRP (≥75th percentile) was associated with higher ASCVD risk (sHR 1.35; 95% CI 1.16-1.57).
- Elevated Lp(a) (≥75th percentile) modestly increased ASCVD risk (sHR 1.24; 95% CI 1.06-1.45).
- Concurrent elevation of hsCRP and Lp(a) conferred the highest risk (sHR 1.64; 95% CI 1.28-2.09) with similar results using clinical thresholds (sHR 1.74; 95% CI 1.17-2.59).
Methodological Strengths
- Large prospective cohort (n=50,450) with 15-year follow-up and adjudicated ASCVD outcomes.
- Appropriate competing-risk modeling (Fine-Gray) and assessment across cohort-specific and clinical thresholds.
Limitations
- Observational design with potential residual confounding and healthy volunteer bias of UK Biobank.
- Low absolute event rate (2.2%) may limit subgroup precision and generalizability to non-European ancestries.
Future Directions: Evaluate whether combined biomarker-guided strategies improve outcomes and calibrate risk thresholds across ancestries; test the incremental value for initiating imaging or targeted therapies.
BACKGROUND: The prognostic value of jointly assessing lipoprotein(a) [Lp(a)] and high-sensitivity C-reactive protein (hsCRP) in primary prevention among individuals without standard modifiable risk factors (SMuRFs) remains unclear. METHODS: We analyzed 50,450 UK Biobank participants free of cardiovascular disease at baseline who were SMuRF-less, defined as absence of current smoking, obesity, hypertension, dyslipidemia, and diabetes. Elevated Lp(a) and hsCRP were defined using cohort-specific 75th percentile cutoffs and established clinical thresholds. Incident atherosclerotic cardiovascular disease (ASCVD), defined as nonfatal myocardial infarction, nonfatal ischemic stroke, or cardiovascular death, was ascertained. Associations were evaluated using Fine-Gray competing-risk regression models to estimate subdistribution hazard ratios (sHRs) with 95% confidence intervals (CI), accounting for competing non-cardiovascular death. RESULTS: Over 15 years of follow-up, 1,104 (2.2%) incident ASCVD events occurred. Using cohort-specific cutoffs, elevated hsCRP was associated with higher ASCVD risk (sHR 1.35, 95% CI 1.16-1.57), while elevated Lp(a) showed a more modest association (sHR 1.24, 95% CI 1.06-1.45). In joint analyses, isolated elevations of hsCRP or Lp(a) were each associated with increased risk, with the highest risk observed among individuals with concurrent elevations (sHR 1.64, 95% CI 1.28-2.09), without evidence of interaction. Similar patterns were observed using clinical cutoffs (Lp(a) ≥125 nmol/L; hsCRP ≥2.0 mg/L), with concurrent elevation conferring the greatest risk (sHR 1.74, 95% CI 1.17-2.59). CONCLUSIONS: In SMuRF-less individuals, Lp(a) and hsCRP independently predict ASCVD risk. These findings suggest that combined assessment of Lp(a) and hsCRP may provide complementary information for risk characterization among SMuRF-less adults in primary prevention.