Daily Cardiology Research Analysis
Three impactful cardiology studies advance risk stratification and clinical decision-making. LGE features on CMR robustly stratify ventricular arrhythmic risk in biopsy-proven sarcoidosis. Donor–recipient height oversizing in DCD heart transplantation predicts higher mortality, and OCT shows cumulative traditional risk factors align with more vulnerable culprit plaque phenotypes in ACS.
Summary
Three impactful cardiology studies advance risk stratification and clinical decision-making. LGE features on CMR robustly stratify ventricular arrhythmic risk in biopsy-proven sarcoidosis. Donor–recipient height oversizing in DCD heart transplantation predicts higher mortality, and OCT shows cumulative traditional risk factors align with more vulnerable culprit plaque phenotypes in ACS.
Research Themes
- Imaging-based risk stratification in cardiomyopathy and ACS
- Transplant donor–recipient matching and outcomes in DCD heart transplantation
- Linking cumulative traditional risk factors to plaque vulnerability by OCT
Selected Articles
1. Extent and Features of Late Gadolinium Enhancement Stratify Arrhythmic Risk in Patients With Biopsy-Proven Sarcoidosis.
In 324 biopsy-proven sarcoidosis patients followed for 4.6 years, LGE extent, right ventricular septal/free wall involvement, and multifocal LGE independently predicted ventricular arrhythmias/device therapy, but not HF/HTx or all-cause mortality. The authors propose a CMR-based algorithm that stratifies arrhythmic risk into four tiers.
Impact: This study converts CMR LGE from a descriptive marker into a practical risk stratifier for malignant ventricular arrhythmias in cardiac sarcoidosis, offering clear imaging features that inform device therapy decisions.
Clinical Implications: CMR LGE location (RV septum/free wall) and multifocality can guide arrhythmic risk discussions and ICD consideration beyond LGE presence alone, improving individualized management in cardiac sarcoidosis.
Key Findings
- LGE extent independently predicted ventricular arrhythmia/device therapy (per SD HR 1.03; P=0.047).
- RV septal (HR 5.43) and RV free-wall LGE (HR 4.30) markedly increased arrhythmic risk.
- Multifocal LGE strongly predicted arrhythmic events (HR 4.62); LGE was not predictive of HF/HTx or all-cause mortality.
Methodological Strengths
- Biopsy-proven sarcoidosis cohort with systematic CMR LGE phenotyping
- Meaningful clinical endpoints with multi-year follow-up and multivariable analyses
Limitations
- Observational design with potential referral/selection bias
- External validation of the proposed algorithm was not reported
Future Directions: Prospective, multi-center validation of the LGE-based algorithm and integration with PET, T1/T2 mapping, and electrophysiologic markers to refine ICD decision pathways.
2. Plaque Vulnerability and Cardiovascular Risk Factor Burden in Acute Coronary Syndrome: An Optical Coherence Tomography Analysis.
Across 2,187 ACS plaques, a higher number of traditional risk factors aligned with more vulnerable culprit plaque features (lipid-rich core, TCFA, macrophages, microvessels, cholesterol crystals), increasing rupture and decreasing erosion prevalence. In nonculprit plaques, macrophages and cholesterol crystals—and cumulative vulnerable features—also rose with risk factor burden.
Impact: This OCT study mechanistically links cumulative traditional risk factors with culprit plaque vulnerability patterns in ACS, reinforcing rigorous multi-risk-factor control and informing targeted anti-thrombotic and anti-inflammatory strategies.
Clinical Implications: Patients with multiple risk factors may harbor more rupture-prone culprit plaques; aggressive, multifaceted risk-factor modification and vigilant secondary prevention are warranted, potentially informing intensity of lipid-lowering and anti-inflammatory therapies.
Key Findings
- Among 1,581 culprit plaques, lipid-rich core, TCFA, macrophages, microvessels, and cholesterol crystals increased with number of risk factors.
- Plaque rupture prevalence rose with risk factors, while erosion decreased.
- In nonculprit plaques, macrophages, cholesterol crystals, and cumulative vulnerable features increased with risk factor burden.
Methodological Strengths
- Large-scale OCT phenotyping across culprit and nonculprit lesions
- Systematic stratification by cumulative risk factor burden with trend analyses
Limitations
- Observational, cross-sectional association without outcome linkage
- Potential confounding from unmeasured factors and selection bias
Future Directions: Prospective studies to test whether intensified multi-risk-factor control reduces OCT-defined vulnerability and to link plaque phenotypes with clinical outcomes.
3. Outcomes of Donor-Recipient Size Mismatch in Donation After Circulatory Death Heart Transplantation.
In 1,631 DCD heart transplants, donor–recipient height oversizing >5% independently increased in-hospital and mid-term mortality, whereas weight and predicted heart mass mismatch did not. This suggests height-specific matching may be more critical for DCD graft selection.
Impact: Provides large-scale, DCD-specific evidence that height oversizing—not weight or PHM—drives mortality risk, directly informing donor selection policies in a rapidly expanding transplant modality.
Clinical Implications: Avoid donor–recipient height oversizing (>5%) when allocating DCD hearts; transplant programs may adapt matching algorithms and consent counseling to reflect increased risk with height mismatch.
Key Findings
- Height oversizing >5% increased in-hospital mortality (OR 2.106; p=0.014).
- Height oversizing also increased longer-term mortality (HR 1.737; p=0.005).
- Weight and predicted heart mass mismatches were not independently associated with mortality.
Methodological Strengths
- Large, contemporary national registry with multivariable adjustment
- DCD-specific analysis isolating height, weight, and predicted heart mass
Limitations
- Retrospective observational design with residual confounding
- Median follow-up ~12 months limits long-term inference
Future Directions: Prospective validation and mechanistic studies on why height oversizing affects DCD graft performance; refine allocation algorithms and explore mitigation via ex vivo perfusion strategies.