Colin Berry

Aims: Rest late gadolinium enhancement cardiovascular magnetic resonance (LGE-CMR) identifies infarct-pattern scar but does not assess coronary anatomy. We estimated the prevalence of angiographic coronary artery disease (CAD) among adults with heart failure and reduced ejection fraction (HFrEF) or otherwise unexplained left ventricular systolic dysfunction without infarct-pattern LGE. Methods and results: MEDLINE, Embase, CENTRAL, and ClinicalTrials.gov were searched to 27 July 2026. Eligible studies provided separable scar-negative denominators and corresponding angiographic CAD counts from invasive coronary angiography (ICA). Scar-negative was defined as the absence of subendocardial or transmural LGE in a coronary distribution. Random-effects logit meta-analysis used restricted maximum likelihood and Hartung-Knapp confidence intervals. Twenty-two reports representing 20 studies included 2,236 paired LGE-CMR and ICA. 818 patients had infarct-pattern scar, and 1,418 were scar-negative. Eight studies contributed 44 CAD cases among 468 scar-negative patients for ≥50% stenosis, giving a pooled prevalence of 10.8% (95% confidence interval [CI] 7.4–15.4). Five studies contributed 19 CAD cases among 271 scar-negative patients for ≥70% stenosis, giving a pooled prevalence of 7.6% (95% CI 4.4–12.6). Seven studies contributed 33 CAD cases among 679 scar-negative patients for high-risk-pattern CAD, giving a pooled prevalence of 4.9% (95% CI 2.2–10.6) and a 95% prediction interval of 0.8–24.8%. These strata represented different study subsets and were not nested. Conclusion: Among selected adults with HFrEF or otherwise unexplained LVSD who underwent paired LGE-CMR and ICA, absence of infarct-pattern LGE did not exclude angiographic CAD. Further coronary assessment should be considered when resolving that uncertainty would alter diagnosis or management.

Background: Older adults with non-ST-segment elevation myocardial infarction (NSTEMI) and cognitive impairment experience higher cardiovascular risk than patients with normal cognition. It remains unclear how cognition should influence whether older adults receive an invasive or conservative treatment strategy. Objectives: To compare an invasive and conservative treatment strategy among older adults with NSTEMI and cognitive impairment. Methods: This study is a pre-specified analysis of the SENIOR-RITA randomised controlled trial. Cognition was measured at randomisation using the Montreal Cognitive Assessment (MoCA). Patients were followed up for a median of 4.1 years postrandomisation. The primary outcome was a composite of time to cardiovascular death or nonfatal myocardial infarction (MI). Results: MoCA was available for 1455 patients (95.8%) who underwent randomisation. Within the cognitively impaired group (909 patients), the primary outcome occurred in 116 patients (26.8%) in the invasive group and in 141 patients (29.6%) in the conservative group (hazard ratio [HR], 0.85; 95% confidence interval [CI], 0.66 to 1.10; P = 0.20). Nonfatal MI occurred in 48 patients (11.1%) in the invasive group and in 75 patients (15.8%) in the conservative group (HR 0.64; 95% CI, 0.44 to 0.92). However, there was no interaction between treatment strategy and cognition. Conclusions: Among those with evidence of cognitive impairment at randomisation, an invasive treatment strategy did not reduce the primary composite outcome of cardiovascular death or nonfatal MI, and there was no evidence of treatment effect heterogeneity based on cognition. The reduction in nonfatal MI events among those with cognitive impairment should be interpreted as an exploratory finding.

Aims: Among women with suspected ischaemia and non-obstructive coronary artery disease (INOCA), the temporal effect of combination intensive medical treatment (IMT) with angiotensin-converting enzyme inhibitors or receptor blockers, statins, and aspirin on coronary plaque composition is not known. This prospective ancillary study examined changes in atherosclerotic plaque volumes and composition (percentage of total plaque volume) over time between IMT and usual care (UC). Methods and results: Participants from the randomized WARRIOR trial with the presence of plaque on their first coronary computed tomography angiography (CCTA) were enrolled for a follow-up CCTA at least 2 years after randomization. Volumes and volumetric composition (percentage of total plaque volume) of non-calcified plaque (NCP), low-density NCP (LD-NCP, defined as NCP <30 HU), and calcified plaque (CP) were quantified over the coronary tree in the serial scans. Participants (n = 186) completed both scans with good image quality (94 IMT arm and 92 UC arm). Overall mean age was 61.0 years (SD ±10.9), and there were no statistically significant differences in baseline risk factors, plaque volumes, or statin treatment between the arms. There was a greater bi-annualized increase in CP volume [ΔCP volume (mm3)] in the IMT arm, 6.2 (SD ±15.5) compared to the UC arm, 3.9 (SD ±16.0), P = 0.013, and a consistent greater reduction in NCP composition [ΔNCP composition (%)] in the IMT arm, −3.9 (SD ±7.7) compared to the UC arm, −1.5 (SD ±5.8), P = 0.003, with no increase in total plaque volume. Conclusion: In women with suspected INOCA, IMT reduces NCP volumetric composition to a greater extent than UC and may promote plaque stabilization.

To assess the association of transaortic flow-rate (TFR) with symptom-driven aortic valve replacement (AVR) in asymptomatic patients with moderate to severe aortic stenosis (AS). PRIMID was a prospective, multi-centre observational study. Patients with asymptomatic moderate to severe AS underwent transthoracic echocardiography (TTE), cardiopulmonary exercise testing and stress cardiovascular magnetic resonance (CMR) imaging. TFR was calculated as stroke volume divided by left ventricular ejection time. Patients were followed-up for a minimum of one-year initially. The primary outcome was symptom-driven AVR. Long-term follow-up data was obtained through electronic health records. The secondary outcome was long-term major adverse cardiovascular events (MACE) defined as cardiovascular mortality and hospitalisation with heart failure, myocardial infarction, syncope or arrhythmia. We included 171 individuals: mean age 66.21±3.43 years, 76% male, mean aortic valve area 1.12±0.31cm2. At one-year (median: 366 days, IQR: 312-437) there were 47 symptom-driven AVRs. Over long-term follow-up of 6.52 years (IQR: 5.23-7.22), there were 95 symptom-driven AVRs and 47 MACE events. In multivariable models, TFR was associated with symptom-driven AVR at one-year (HR: 0.12, 95%CI: 0.04-0.39, p<0.01), independent of a positive exercise tolerance test and CMR-measured myocardial perfusion reserve. Age (HR: 1.05, 95%CI: 1.01-1.10, p=0.01) and NT-pro-BNP (HR: 1.46, 95%CI: 1.12-1.89, p<0.01) predicted long-term MACE events, while TFR did not (HR: 0.48, 95%CI: 0.13, 1.74, p=0.26). TFR is independently associated with symptom-driven AVR in initially asymptomatic individuals with moderate to severe AS at one-year. TFR may be useful in identifying individuals who will undergo symptom-driven intervention, but prospective randomised data are needed to assess clinical utility.

BackgroundAngina with no obstructive coronary artery disease (ANOCA) is a prevalent cause of chest pain. We assessed angiographic characteristics by ANOCA endotype.MethodsWe conducted a prospective, multicenter, blinded study. Patients undergoing clinically indicated coronary computed tomography angiography (CCTA) for suspected angina were screened and individuals with unobstructive coronary arteries post-CCTA were invited to undergo further investigation based on informed consent.Functional coronary angiography was performed including fractional flow reserve (FFR), bolus thermodilution (coronary flow reserve (CFR), index of microvascular resistance (IMR), resistance reserve ratio (RRR), microvascular resistance reserve (MRR)), and intracoronary infusion of acetylcholine (graded doses, followed by bolus) to assess vasospasm. Cumulative stenotic plaque burden (Gensini Score), myocardial bridging, and coronary tortuosity (Inflection Count Metric) were assessed by central blinded review.ResultsAmong 231 participants without flow-limiting coronary artery disease (FFR≥0.80), 127(55.0%) had microvascular angina, 27(11.7%) vasospastic angina, 17(7.4%) both, and 60(26.0%) had no abnormality. Diagnostic guidewire testing was performed in the left anterior descending artery in 96.5% of cases. The median Gensini score was 1.5(0.0-5.0).Reduced CFR (p=0.002), RRR (p=0.009), and MRR (p=0.010) were independently associated with an increased cumulative plaque burden.Myocardial bridging (OR 2.542 [95% CI 1.001-6.451], p=0.050), and a smoking history (OR 2.086 [95% CI 1.039-4.189], p=0.039) were independently associated with epicardial, but not microvascular vasospasm. Increased coronary tortuosity was associated with microvascular spasm (OR 1.180 [95% CI 1.030-1.352], p=0.017).ConclusionsANOCA endotypes associate with atherosclerosis burden, myocardial bridging, and vascular tortuosity. These findings link pathophysiology with the rationale for preventive therapy.