Background Modern coronary physiology in the cardiac catheterization laboratory has evolved from a solely wire-based approach to a broader portfolio that now includes coronary computed tomography angiography, angiography-derived physiology, and microcatheter-derived physiology. Limited data exists on real-world practice patterns and perspectives among interventional cardiologists. Methods A web-based 76-item international survey was distributed to attending interventional cardiologists via email and social media from April to July 2024. Results In total, 206 interventional cardiologists completed the survey. Respondents represented diverse global regions, with 55% based in the United States. Most operators performed both percutaneous coronary intervention (PCI) and structural interventions (34%) or only PCI (25%). Nearly all respondents (98%) had access to invasive coronary physiology tools, with non-hyperemic pressure ratios (NHPR) usage being favored over fractional flow reserve (FFR) by operators (60% vs. 40%), particularly in US centers. Pressure-wire pullback was routinely performed by 44% of operators. Angiography-derived FFR was used by 33%, with lack of access being the primary barrier to adoption. Coronary microvascular dysfunction (CMD) evaluation was performed or referred by 39%, primarily using bolus thermodilution (78%) followed by continuous thermodilution in 22%. Conclusions This multinational survey demonstrates substantial heterogeneity and marked geographic variation in the use of modern coronary physiology tools. Although important advances have broadened the coronary physiology toolkit, their routine use remains limited and inconsistent. These findings provide valuable insights into how novel modalities are being integrated into practice, including notable geographic differences.

BACKGROUND:Spontaneous coronary artery dissection (SCAD) and atherosclerosis may appear similar on coronary imaging. CASE SUMMARY:A 62-year-old woman with fibromuscular dysplasia, dyslipidemia, and diabetes presented with chest discomfort. Coronary computed tomography angiography suggested left anterior descending artery (LAD) SCAD, and invasive coronary angiography (ICA) showed possible type 3 SCAD. Intracoronary imaging (ICI) was not performed, and she was treated medically. DISCUSSION:Recurrent chest pain prompted repeat imaging. Follow-up computed tomography angiography suggested persistent LAD SCAD. Repeat ICA revealed high-grade proximal LAD and first diagonal stenoses, confirmed as atherosclerosis on ICI. Percutaneous coronary intervention with 2 drug-eluting stents relieved symptoms. At 5 months, recurrent symptoms from severe LAD stenosis proximal to the stents were treated with drug-eluting stents, and ICA at 8 months showed in-stent restenosis, managed by balloon angioplasty. TAKE-HOME MESSAGES:ICI is essential when type 3 SCAD is suspected and angiography is indeterminate. Stent-edge disease and in-stent restenosis highlight important causes of recurrent symptoms after percutaneous coronary intervention.

BACKGROUND:Protruding coronary ostial stents can be prohibitive for repeat percutaneous coronary interventions (PCI). METHODS:We retrospectively included 6 consecutive patients who underwent the EXPOSE (extraction of protruding ostial stents with En Snare) technique to previous ostial stents to facilitate subsequent PCI. The indication in all cases was revascularization of the target vessel with failed guide intubation of the stented lumen. The protruding stents had been implanted 5 days to 9 years before extraction. The procedure included a 7-F × 45-cm transfemoral sheath, 7-F guide catheter, and 12- to 20-mm En Snare device. RESULTS:Procedural success was achieved in all patients, and complete stent extraction was achieved in 1 patient. All patients underwent successful PCI; 1 case of acute vessel closure immediately postextraction was rescued promptly with PCI. CONCLUSIONS:Snare extraction of previously implanted, protruding ostial stents is feasible to enable PCI after failure of guide intubation.

Background The burden and pathophysiologic mechanisms of myocardial infarction (MI) in younger patients remain understudied. Prior studies have been limited by selected cohorts and lack of awareness of nonatherothrombotic causes. Objectives We sought to determine the incidence and outcomes of MI according to a unique pathophysiologic mechanism in a large community cohort aged ≤65 years, and to evaluate sex-differences in etiology Methods We identified all residents of Olmsted County, Minnesota, USA, age ≤65 years who experienced an event associated with a cardiac troponin T >99th percentile of upper reference range (≥0.01 ng/mL) from January 2003 to March 2018. Records and imaging were individually scrutinized. Patients classified as MI were assigned to 1 of 6 adjudicated pathophysiologic mechanisms: atherothrombosis, spontaneous coronary artery dissection (SCAD), embolism, vasospasm, myocardial infarction with nonobstructed coronary arteries not meeting another category (MINOCA-U), and supply/demand mismatch secondary myocardial infarction. We determined incidence and long-term all-cause and cardiovascular mortality for each group. Results There were 4,116 myocardial injury events in 2,780 patients (36% women) over 15 years. Excluding periprocedural MI, 1,474 events were classified as index MI, of which 68% were caused by atherothrombosis. The population incidence of MI was much lower in women, particularly in MI caused by atherothrombosis (48 vs 137 per 100,000 person years and 23 vs 105 per 100,000 person-years). Incidence of SCAD was much higher in women (3.2 vs 0.9 per 100,000 person-years) with 55% of cases misclassified as MINOCA or atherothrombosis at index presentation. Women with atherothrombosis were similar in age to men (55 ± 8 years vs 54 ± 8 years), with similar disease extent at angiography but greater burden of risk factors. Proportionately, nonatherothrombotic causes comprised the majority of MI in women (atherothrombosis 47% vs 75%, secondary myocardial infarction [SSDM] 34% vs 19%, SCAD 11% vs 0.7%, embolism 2% vs 2%, vasospasm 3% vs 1%, MINOCA-U 3% vs 2%). The 5-year all-cause mortality was highest after SSDM (SSDM 33%, atherothrombosis 8%, embolism 8%, SCAD 0%) with low cardiovascular mortality in all groups. Conclusions This community-based study demonstrates nonatherothrombotic causes comprise an important burden of acute MI in persons age ≤65 years, particularly women. These cause-specific findings have implications for individualized management and risk stratification and provide epidemiologic benchmarking for future studies.

The primary evaluation of pulmonary embolism (PE) is complicated by the presence of various pre-test clinical probability scores (pCPS) with different cut-offs, all equally recommended by guidelines. This lack of consensus has led to practice variability, unnecessary imaging, and worse patient outcomes. We aim to provide more definitive insights through a holistic comparison of available pCPS. PubMed, Embase and Web of Science, and Google Scholar were searched for studies evaluating pCPS in patients clinically suspected of PE until June 2023. Risk of bias was evaluated using QUADAS-2. Included pCPS were evaluated based on their diagnostic accuracy in: (1) Ruling-out PE (2) Utilization of imaging, and (3) Differentiating between patients needing d-dimer from imaging. Diagnostic test accuracy indices were synthesized using beta-binomial Bayesian methods. Forty studies (37,027 patients) were included in the meta-analysis. Three-tier revised Geneva (RG) and three-tier Wells performed similarly in ruling-out PE (negative likelihood ratio (LR-) [95

BACKGROUND: Coronary microvascular dysfunction (CMD) is a common cause of chest pain (CP) in patients with angina and non-obstructive coronary arteries (ANOCA). Although both CMD and CP have distinct classifications, the relationship between them remains insufficiently understood. AIMS: This study investigated the relationship between CMD and CP patterns and their prognostic impact in ANOCA patients. METHODS: Serial patients with ANOCA who underwent coronary reactivity testing were enrolled. CP patterns were categorised as exertional, resting, or both. Endothelium-dependent CMD was defined as a <50% change in coronary blood flow (CBF) with intracoronary acetylcholine infusion and endothelium-independent CMD as a coronary flow reserve (CFR) <2.5 during adenosine-induced hyperaemia. Microvascular function and prognosis were compared between patients with exertional CP and resting CP. RESULTS: Among 1,264 patients, the median age was 52 years, and 65.3% were women; 23.7% had exertional CP, 27.0% resting CP, and 49.4% both. Exertional CP patients had a lower CFR and a higher prevalence of endothelium-independent CMD compared to resting CP patients (2.8 vs 3.0; p=0.014, 32.1% vs 24.4%; p=0.034). Exertional CP patients showed a significantly lower CBF increase in response to acetylcholine (38.2% vs 50.7%; p=0.015). Survival analysis over a median 7-year follow-up revealed that endothelium-independent CMD significantly increased risk in exertional CP patients (p=0.002) but not in resting CP patients (p=0.388). CONCLUSIONS: ANOCA patients with exertional CP demonstrated worse microvascular function than those with resting CP, with endothelium-independent CMD showing a significant prognostic impact. Exertional CP patients may benefit more from treatment strategies specifically targeting CMD.

BACKGROUND:The Universal Definition classifies myocardial infarction (MI) by etiology, but its prognostic implications are uncertain. OBJECTIVES:The goal was to compare the rate and risk of recurrent MI or cardiovascular death among patients with myocardial injury and infarction classified according to the Universal Definition. METHODS:A systematic search of MEDLINE, EMBASE, Central, and Web of Science from January 1, 2007 to July 1, 2025 was performed to identify prospective studies where cardiac troponin was measured for suspected acute coronary syndrome, diagnoses were adjudicated using the Universal Definition, and both MI and cause-specific mortality were reported at a minimum of 1 year. Subdistribution HRs were derived to account for the competing risk of noncardiovascular death. Meta-analysis was performed with random-effects models. The primary outcome was major adverse cardiovascular events (MACE), defined as MI or cardiovascular death. The secondary outcome was noncardiovascular death. RESULTS:We identified 17 studies of 9 cohorts from 9 countries, with individual patient-level data available in 8 cohorts. Among 120,734 patients (median age: 61.0 years; 45.8% women), type 1 MI occurred in 9.4% (n = 11,298), type 2 MI in 3.0% (n = 3,609), acute myocardial injury in 4.9% (n = 5,864), and chronic myocardial injury in 4.7% (n = 5,625). In patients with type 1 and type 2 MI, the MACE rate was 55.2 and 51.7 per 1,000 patient-years and the noncardiovascular death rate was 25.7 and 60.1 per 1,000 patient-years, respectively. Compared with those without myocardial injury, the risk of MACE (subdistribution HR) was 4.82 (95% CI: 3.55-6.57; I2 = 84%) and 3.36 (95% CI: 2.92-3.86; I2 = 0%), respectively. In patients with acute and chronic myocardial injury, the MACE rate was 47.1 and 44.9 per 1,000 patient-years and the noncardiovascular death rate was 67.0 and 46.9 per 1,000 patient-years, respectively. The risk of MACE was 3.24 (95% CI: 2.41-4.36; I2 = 59%) and 3.03 (95% CI: 2.53-3.62; I2 = 20%), respectively. CONCLUSIONS:All patients with myocardial injury and infarction are at increased risk of future cardiovascular events. However, in type 2 MI, this apparent risk is reduced by a substantially greater competing risk of noncardiovascular death. (PROSPERO Registration: CRD42023464836).

AIMS:Type 2 myocardial infarction due to myocardial oxygen supply-demand imbalance is associated with poor outcomes. There are no guidelines to inform care for these patients. The consensus on the assessment and management of type 2 myocardial infarction is gained. METHODS AND RESULTS:An international e-Delphi study including experts in type 2 myocardial infarction identified through systematic review was conducted. Participants were asked to describe their approach to (i) definition and diagnosis, (ii) risk stratification, (iii) assessment of coronary artery disease and cardiac function, (iv) specialty management, (v) treatment and secondary prevention, and (vi) communication and rehabilitation. Statements generated in round one were circulated, with consensus defined a priori as ≥70% agreement on a 5-point Likert scale. Where no consensus was reached, statements were amended and recirculated for a final round. The response rate was 56% (38/68), 54% (37/68), and 72% (49/68) in the first, second, and third rounds, respectively. Following the first round, 67 unique statements were generated across six domains. Overall, consensus was achieved on 64% (43/67) of statements. Consensus was achieved for 42% (5/12) of statements on the diagnosis of type 2 myocardial infarction, 75% (3/4) on risk stratification, 50% (9/18) on the assessment of coronary artery disease and cardiac function, 60% (6/10), on specialty management, 100% (9/9) on treatment and secondary prevention, and 79% (11/15) on communication and rehabilitation. CONCLUSION:Consensus was obtained across a number of domains for the assessment and management of patients with type 2 myocardial infarction. However, there was limited agreement amongst experts on the diagnostic criteria, which may benefit from refinement.

Background We tested whether biologic age, as estimated by deficits, functional impairments, or Age‐Gap or their combination, provide improved estimation of cause‐specific death as compared with chronological age. Methods Cardiovascular and noncardiovascular deficits, functional impairments, and Age‐Gap were prospectively collected in 535 patients aged ≥55 years undergoing percutaneous coronary interventions between August 1, 2014, and March 31, 2018. Age‐Gap was calculated as the difference between chronological age and age estimated by artificial intelligence ECG using a convolutional neural network. The full biological age model included deficits, functional impairments, and Age‐Gap >2 SD. A multivariable reduced model with the least number of variables was also created to provide a comparable C index to the full model. Results The average chronological age was 72.1±9.5 years, and there were 68% of men. During a median follow‐up of 2.61 years, 124 (23%) patients died. There was a modest correlation between Age‐Gap and biological age (r=0.28 [95% CI, 0.20–0.35]; P<0.001). When modeled with chronologic age as a covariate, Age‐Gap predicted all‐cause (hazard ratio [HR], 1.07 [95% CI, 1.04–1.10]; P<0.001) and cardiovascular (HR, 1.07 [95% CI, 1.04–1.11]; P<0.001) mortality. As compared with chronological age, the full biological age model noted significant improvement in the prediction of long‐term overall (95% CI, 0.65–0.78), cardiovascular (95% CI, 0.69–0.77), and noncardiovascular (95% CI, 0.55–0.86) mortality. In the reduced models, most prognostic information for noncardiovascular mortality (C index: 0.79) was obtained by subjective difficulty in performing tasks, whereas the deficit‐based estimation predicted cardiovascular mortality (C index: 0.72). Conclusions Estimated biological age from deficits and functional impairments was superior to chronological age in predicting long‐term cause‐specific mortality following percutaneous coronary interventions.

BACKGROUND:Coronary vasomotor dysfunction (CVDys) can be comprehensively classified on the basis of anatomy and functional mechanisms. OBJECTIVES:The aim of this study was to evaluate the association between different CVDys phenotypes and outcomes in patients with angina and nonobstructive coronary artery disease (ANOCA). METHODS:Patients with ANOCA who underwent coronary reactivity testing using an intracoronary Doppler guidewire to assess microvascular and epicardial coronary endothelium-dependent and endothelium-independent function were enrolled. Endothelium-dependent microvascular and epicardial coronary dysfunction were defined as a <50% change in coronary blood flow in response to intracoronary acetylcholine (Ach) infusion and a <-20% change in coronary artery diameter in response to Ach. Endothelium-independent microvascular and epicardial coronary dysfunction were defined as coronary flow reserve < 2.5 during adenosine-induced hyperemia and change in cross-sectional area in response to intracoronary nitroglycerin administration < 20%. Major adverse cardiac and cerebrovascular events (cardiovascular death, nonfatal MI, heart failure, stroke, and late revascularization) served as clinical outcomes. RESULTS:Among the 1,196 patients with ANOCA, the prevalence of CVDys was 24.5% and 51.8% among those with endothelium-independent and endothelium-dependent microvascular dysfunction, respectively, and 47.4% and 25.4% among those with endothelium-independent and endothelium-dependent epicardial coronary dysfunction, respectively. During 6.3 years (Q1-Q3: 2.5-12.9 years) of follow-up, patients with endothelium-dependent microvascular dysfunction, endothelium-dependent epicardial coronary dysfunction, or endothelium-independent microvascular dysfunction showed significantly higher event rates compared with those without (19.5% vs 12.0% [P < 0.001], 19.7% vs 14.6% [P = 0.038] and 22.2% vs 13.8% [P = 0.001], respectively). Coronary flow reserve (HR: 0.757; 95% CI: 0.604-0.957) and percentage change in coronary blood flow in response to Ach infusion (HR: 0.998; 95% CI: 0.996-0.999) remained significant predictors of major adverse cardiac and cerebrovascular event after adjustment for conventional risk factors. CONCLUSIONS:CVDys phenotype is differentially associated with worse outcomes, and endothelium-dependent and endothelium-independent microvascular function provide independent prognostic information in patients with ANOCA.

Background: Coronary microvascular disease (CMD) may be endothelium-independent (coronary flow reserve, CFR<2.5) or endothelium-dependent (<50% increase in coronary blood flow in response to acetylcholine). Endothelium-independent CMD has been subclassified into structural and functional groups based on hyperemic microvascular resistance (hMR, mmHg/cm/s). We hypothesized that endothelium-dependent CMD also has these subtypes. Methods: Patients with non-obstructive coronary artery disease who underwent coronary catheterization of the left anterior descending artery were included (n=112). Pressure and flow were recorded at rest, with adenosine, and with acetylcholine. Patients were classified by endothelial type and functional CMD (hMR<2.5) or structural CMD (hMR>2.5). Wave intensity analysis was performed and cumulative separated wave intensity (Joules/m 2 ) was calculated by standard formulae. Three dominant waves were analyzed (forward compression wave, FCW; backward compression wave, BCW; backward expansion wave, BEW). Results: Seventy-four of 109 patients had CMD, of which 59 had endothelium-independent and 38 had endothelium-dependent CMD (23 had both). Functional and structural subgroups were identified (Figure 1). All CMD subtypes had significantly different wave intensities at rest, adenosine, and acetylcholine (p<0.05). Comparing subtypes, there was no difference in wave intensities at rest. However, wave intensities significantly differed between all CMD subtypes with adenosine and acetylcholine, with higher energy waves in the endothelium-independent and functional groups (p<0.05, Figure 2). Conclusions: CMD is a heterogenous condition with distinct subtypes. Functional and structural groups exist in both endothelium-dependent and endothelium-independent CMD. These subgroups have distinct hemodynamic profiles as measured by wave intensity. A patient-specific approach to first line medical therapy may be improved by subgroup classification.