Daily Cardiology Research Analysis
Three high-impact cardiology studies stand out today. A network meta-analysis of 26 RCTs in STEMI with multivessel disease found complete revascularization—especially immediate—reduces MACE versus culprit-only PCI. A large prospective registry (J-PRIDE) showed that in lesions with discordant physiology, FFR guidance outperforms NHPR for outcomes after deferral decisions. A 25-year European cohort (PREVEND) quantified sex-specific lifetime risks and modifiable contributors to HFpEF and HFrEF, sha
Summary
Three high-impact cardiology studies stand out today. A network meta-analysis of 26 RCTs in STEMI with multivessel disease found complete revascularization—especially immediate—reduces MACE versus culprit-only PCI. A large prospective registry (J-PRIDE) showed that in lesions with discordant physiology, FFR guidance outperforms NHPR for outcomes after deferral decisions. A 25-year European cohort (PREVEND) quantified sex-specific lifetime risks and modifiable contributors to HFpEF and HFrEF, sharpening prevention targets.
Research Themes
- Coronary physiology and revascularization strategies in STEMI
- Risk stratification using invasive indices (FFR vs NHPR)
- Sex-specific lifetime risk and prevention of heart failure phenotypes
Selected Articles
1. Optimal Strategy for Complete Revascularization in ST-Segment Elevation Myocardial Infarction and Multivessel Disease: A Network Meta-Analysis.
Across 26 RCTs (n=15,902), complete revascularization reduced MACE compared with culprit-only PCI. Immediate CR further reduced MACE versus staged CR (RR 0.74), largely driven by MI reduction; the advantage attenuated when excluding procedural MI. Benefits were consistent whether guidance was angiographic or physiology-based.
Impact: This synthesis unifies disparate RCTs and provides practice-directing evidence favoring immediate complete revascularization in multivessel STEMI. It clarifies the magnitude and drivers of benefit and nuances related to procedural MI.
Clinical Implications: For hemodynamically stable multivessel STEMI, prioritize complete revascularization during the index procedure when feasible, with awareness that some MI reduction reflects procedural factors. Institutional protocols should enable immediate CR with careful lesion selection and operator expertise.
Key Findings
- Complete revascularization reduced MACE vs culprit-only PCI (immediate CR RR 0.48; staged CR RR 0.65).
- Immediate CR reduced MACE vs staged CR (RR 0.74), consistent with angiographic and functional guidance.
- MI reduction with immediate CR attenuated when procedural MI was excluded (RR 0.65; 95% CI 0.36–1.16).
Methodological Strengths
- Network meta-analysis of 26 RCTs with 15,902 patients; comprehensive comparison across timing and guidance strategies
- Rigorous assessment of heterogeneity and sensitivity analyses excluding procedural MI
Limitations
- Potential trial-level heterogeneity (patient selection, operator expertise, definition of MI across trials)
- Attenuation of MI benefit after excluding procedural MI complicates interpretation of mechanism
Future Directions: Head-to-head RCTs comparing immediate vs staged CR with standardized MI definitions and patient-centered outcomes; implementation studies optimizing workflow and lesion selection.
BACKGROUND: In patients with ST-segment elevation myocardial infarction (STEMI) and multivessel coronary artery disease, most but not all randomized trials have reported that complete revascularization (CR) offers advantages over culprit vessel-only revascularization. In addition, the optimal timing and assessment methods for CR remain undetermined. OBJECTIVES: The purpose of this study was to identify the optimal revascularization strategy in patients with STEMI and multivessel disease, using a network meta-analysis of randomized controlled trials. METHODS: We searched PUBMED and EMBASE for randomized trials evaluating revascularization strategies in patients with STEMI and multivessel disease through July 2024. A network meta-analysis was performed analyzing CR vs culprit vessel-only revascularization as well as the timing of CR (immediate CR vs staged CR). Outcomes were also assessed with 4 CR strategies based on whether revascularization was immediate or staged and whether it was angiographically guided or functionally guided. The primary outcome was major adverse cardiovascular events (MACE). RESULTS: A total of 26 randomized trials that enrolled 15,902 patients were included. The mean weighted duration of follow-up was 25.2 ± 15.7 months. MACE was reduced with both immediate CR and staged CR compared with culprit-vessel-only treatment (RR: 0.48; 95% CI: 0.36-0.64 and RR: 0.65; 95% CI: 0.52-0.82, respectively), whether with angiographic or functional guidance. Immediate CR was associated with reduced MACE compared with staged CR (RR: 0.74; 95% CI: 0.56-0.97), whether CR was guided angiographically or functionally (RR: 0.77; 95% CI: 0.61-0.99 and RR: 0.49; 95% CI: 0.27-0.89, respectively) caused by reductions in MI. However, when the analysis was restricted to studies that reported both all MI and nonprocedural MI, the benefit of immediate CR in reducing MI compared with staged CR was diminished after excluding procedural MI (RR: 0.44; 95% CI: 0.27-0.71 with procedural MI vs RR: 0.65; 95% CI: 0.36-1.16 without procedural MI). CONCLUSIONS: Among patients with STEMI and multivessel disease, outcomes were better with immediate or staged CR compared with culprit vessel-only treatment, whether with angiographic or functional guidance.
2. Prevalence and Clinical Outcomes of Discordant Lesions Between Fractional Flow Reserve and Nonhyperemic Pressure Ratios in Clinical Practice: The J-PRIDE Registry.
In 4304 lesions, FFR–NHPR discordance occurred in 20%. Deferred discordant lesions had higher 1-year target vessel failure than concordant negative lesions. Notably, only FFR+/NHPR− lesions derived benefit from revascularization versus medical therapy, supporting FFR-guided decisions when indices disagree.
Impact: Provides high-quality prospective real-world evidence resolving a common clinical dilemma in physiology-guided PCI, with actionable guidance favoring FFR when indices disagree.
Clinical Implications: When FFR and NHPR disagree, consider revascularization for FFR-positive/NHPR-negative lesions and be cautious deferring such lesions. Concordant negative lesions remain safe to defer.
Key Findings
- FFR–NHPR discordance was present in 20% of lesions (FFR+/NHPR− 11.2%; FFR−/NHPR+ 8.8%).
- Deferred discordant lesions had higher 1-year target vessel failure vs concordant negative (7.9% and 5.5% vs 1.7%).
- Only FFR+/NHPR− lesions showed benefit from revascularization over medical therapy.
Methodological Strengths
- Prospective multicenter registry across 20 centers with lesion-level analysis
- Adjusted hazard modeling and clear physiological thresholds (FFR 0.80; NHPR 0.89)
Limitations
- Observational design with potential residual confounding and selection bias in deferral decisions
- Generalizability may vary by NHPR type and center practices
Future Directions: Randomized trials in discordant lesions testing FFR- vs NHPR-guided strategies; standardized protocols across NHPR modalities.
BACKGROUND: Limited large-scale, real-world data exist on the prevalence and clinical impact of discordance between fractional flow reserve (FFR) and nonhyperemic pressure ratios (NHPRs). METHODS: The J-PRIDE registry (Clinical Outcomes of Japanese Patients With Coronary Artery Disease Assessed by Resting Indices and Fractional Flow Reserve: A Prospective Multicenter Registry) prospectively enrolled 4304 lesions in 3200 patients from 20 Japanese centers. The lesions were classified into FFR+/NHPR-, FFR-/NHPR+, FFR+/NHPR+, or FFR-/NHPR groups according to cutoff values of 0.89 for NHPRs and 0.80 for FFR. The primary study end point was the cumulative 1-year incidence of target vessel failure (a composite of cardiac death, target vessel-related myocardial infarction, and clinically driven target vessel revascularization) on a lesion basis. RESULTS: An NHPR cutoff value of 0.89, determined using online software, predicted an FFR of 0.80 across various NHPR types. Discordance between FFR and NHPRs was observed in 20% of lesions (FFR+/NHPR-, 11.2%; FFR-/NHPRs+, 8.8%). Revascularization was deferred in 42.9% and 88.4% of the FFR+/NHPR- and FFR-/NHPR+ groups, respectively. In deferred vessels, the FFR+/NHPR- and FFR-/NHPR+ groups showed a higher 1-year incidence of target vessel failure compared with the FFR-/NHPR- group (7.9% versus 5.5% versus 1.7%; for FFR+/NHPR-, adjusted hazard ratio [aHR], 4.89 [95% CI, 2.68-8.91]; CONCLUSIONS: Discordance between FFR and NHPRs was noted in 20% of lesions, and discordant deferred lesions resulted in worse outcomes than concordant negative lesions. Although the outcomes after deferring revascularization were comparable between the FFR+/NHPR- and FFR-/NHPR+ lesions, only FFR+/NHPR- lesions showed a benefit from revascularization compared with medical treatment, suggesting that an FFR-guided strategy is superior to an NHPR-guided strategy in discordant lesions. REGISTRATION: URL: https://www.umin.ac.jp; Unique identifier: UMIN000038403.
3. Sex-specific risk factors for new-onset heart failure: the PREVEND study at 25 years.
Over 25 years in 8,558 adults, lifetime HF risk was similar overall, but men had higher HFrEF risk and women higher HFpEF risk. Eight modifiable factors (e.g., hypertension, hypercholesterolemia, obesity, AF, CKD, MI, diabetes, smoking) explained a larger share of incident HF in women, emphasizing sex-tailored prevention.
Impact: Defines sex-specific lifetime risks and the population-level impact of modifiable risk factors for HF phenotypes in a large European cohort, informing prevention strategies and policy.
Clinical Implications: Aggressively manage hypertension and lipids to prevent HFrEF in both sexes; prioritize obesity control to prevent HFpEF, particularly in women. Sex-specific risk attribution supports tailored screening and prevention programs.
Key Findings
- Lifetime HF risk: men 24.5% vs women 23.3%; HFrEF higher in men (18.1% vs 11.9%), HFpEF higher in women (11.5% vs 6.4%).
- Eight modifiable factors accounted for 71% of incident HFrEF in women (60% in men).
- Hypertension and hypercholesterolemia were strongest for HFrEF; hypertension and obesity for HFpEF.
Methodological Strengths
- Longitudinal community cohort with 25 years of follow-up and adjudicated HF phenotypes
- Sex-specific lifetime risk and population attributable fraction analyses
Limitations
- Hospital record-based HF ascertainment may miss subclinical cases
- Cohort demographics may limit generalizability beyond European populations
Future Directions: Interventional prevention trials targeting high-PAF factors (hypertension, obesity, lipids) with sex-specific endpoints; integration with polygenic and biomarker risk to refine prediction.
BACKGROUND AND AIMS: Current estimates for the lifetime risk to develop heart failure with either a reduced (HFrEF) or preserved ejection fraction (HFpEF) and their associated risk factors are derived from two studies from the USA. The sex-specific lifetime risk and population attributable fraction of potentially modifiable risk factors for incident HFpEF and HFrEF are described in a large European community-based cohort with 25 years of follow-up. METHODS: A total of 8558 participants from the PREVEND cohort were studied at baseline from 1997 onwards and followed until 2022 for cases of new-onset HFrEF (ejection fraction < 50%) and HFpEF (ejection fraction ≥ 50%) by assessment of hospital records. RESULTS: A total of 804 cases of new-onset HF were identified (534 HFrEF and 270 HFpEF) during 25 years of follow-up. The mean age at baseline was 50 years for men and 47 years for women. The mean age at onset of HF was 72.1 years in men and 74.2 years in women. The overall lifetime risk of developing HF was 24.5% in men compared to 23.3% in women. The lifetime risk of HFrEF was lower in women compared with men (11.9% vs. 18.1%), while the lifetime risk of HFpEF was higher in women compared with men (11.5% vs. 6.4%). In women, 71% of incident HFrEF cases were attributable to eight risk factors (hypertension, hypercholesterolaemia, obesity, smoking, atrial fibrillation, chronic kidney disease, myocardial infarction, and diabetes mellitus) and 60% in men. In women, 64% of incident HFpEF cases were attributable to those risk factors, whereas this was 46% in men. More specifically, in both men and women, hypertension and hypercholesterolaemia were the strongest risk factors for HFrEF, whereas hypertension and obesity were the strongest risk factors for HFpEF. CONCLUSIONS: In this European cohort, the lifetime risk of developing HFrEF was greater in men than in women, while women were at greater risk of developing HFpEF. Eight directly and indirectly modifiable risk factors substantially accounted for the risk of developing HFrEF and HFpEF, particularly in women.