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Background Methods Results Conclusion The clinical relevance of cardiac troponin (cTn) elevation in takotsubo syndrome (TTS) remains uncertain. The present study sought to investigate the role of cardiac troponin (cTn) elevations in mortality prediction of patients with Takotsubo syndrome (TTS).Patients enrolled in the International Takotsubo (InterTAK) Registry from January 2011 to February 2020 with available data on peak cTn levels were included in the analysis. Peak cTn levels during the index hospitalization were used to define clinically relevant myocardial injury. The threshold at which clinically relevant myocardial injury drives mortality at 1 year was identified using restricted cubic spline analysis.Out of 2′938 patients, 222 (7.6%) patients died during 1‐year follow‐up. A more than 28.8‐fold increase of cTn above the upper reference limit was identified as threshold for clinically relevant myocardial injury. The presence of clinically relevant myocardial injury was significantly associated with an increased risk of mortality at 5 years (adjusted HR 1.58, 95% CI 1.18–2.12, p =.002). Clinically relevant myocardial injury was related to an increased 5‐year mortality risk in patients with apical TTS (adjusted HR 1.57, 95% CI 1.21–2.03, p =.001), in presence of physical stressors (adjusted HR 1.60, 95% CI 1.22–2.11, p =.001), and in absence of emotional stressors (adjusted HR 1.49, 95% CI, 1.17–1.89, p =.001).This study for the first time determined a troponin threshold for the identification of TTS patients at excess risk of mortality. These findings advance risk stratification in TTS and assist in identifying patients in need for close monitoring and follow‐up. [ABSTRACT FROM AUTHOR]

Complete revascularization is associated with improved outcomes in patients with myocardial infarction and multivessel coronary artery disease. Quantitative flow ratio (QFR) represents an emerging angiography-based tool for functional lesion assessment. The present study investigated the prognostic impact of QFR-consistent complete revascularization in patients with myocardial infarction and multivessel disease. A total of 792 patients with myocardial infarction and multivessel disease were enrolled in the analysis. Post-hoc QFR analyses of 1,320 nonculprit vessels were performed by investigators blinded to clinical outcomes. The primary endpoint was a composite of all-cause death, nonculprit vessel related nonfatal myocardial infarction, and ischemia-driven revascularization at 2 years after index myocardial infarction. Patients were stratified into a QFR-consistent PCI group (n = 646) and a QFR-inconsistent PCI group (n = 146), based on whether the intervention was congruent with the QFR-determined functional significance of the nonculprit lesions. The primary endpoint occurred in a total of 22 patients (3.4%) in the QFR-consistent PCI group and in 27 patients (18.5%) in the QFR-inconsistent group (HR 0.17, 95% CI 0.10-0.30, P <.001).The difference in the primary endpoint was driven by reduced rates of nonfatal myocardial infarction (2.0% vs. 15.1%; HR 0.13, 95% CI 0.06-0.25; P <.001) and ischemia-driven revascularization (1.2% vs. 5.5%; HR 0.21, 95% CI 0.08-0.57; P =.001) in the QFR-consistent PCI group. Among patients with myocardial infarction and multivessel disease, a QFR-consistent complete revascularization was associated with a reduced risk of all-cause mortality, nonfatal myocardial infarction, and ischemia-driven revascularization. These findings underline the value of angiography-based functional lesion assessment for personalized revascularization strategies. [ABSTRACT FROM AUTHOR]

Aims Coronary microevaginations (CMEs) represent an outward bulge of coronary plaques and have been introduced as a sign of adverse vascular remodelling following coronary device implantation. However, their role in atherosclerosis and plaque destabilization in the absence of coronary intervention is unknown. This study aimed to investigate CME as a novel feature of plaque vulnerability and to characterize its associated inflammatory cell–vessel–wall interactions. Methods and results A total of 557 patients from the translational OPTICO-ACS study programme underwent optical coherence tomography imaging of the culprit vessel and simultaneous immunophenotyping of the culprit lesion (CL). Two hundred and fifty-eight CLs had a ruptured fibrous cap (RFC) and one hundred had intact fibrous cap (IFC) acute coronary syndrome (ACS) as an underlying pathophysiology. CMEs were significantly more frequent in CL when compared with non-CL (25 vs. 4%, P < 0.001) and were more frequently observed in lesions with IFC-ACS when compared with RFC-ACS (55.0 vs. 12.7%, P < 0.001). CMEs were particularly prevalent in IFC-ACS-causing CLs independent of a coronary bifurcation (IFC-ICB) when compared with IFC-ACS with an association to a coronary bifurcation (IFC-ACB, 65.4 vs. 43.7%, P = 0.030). CME emerged as the strongest independent predictor of IFC-ICB (relative risk 3.36, 95% confidence interval 1.67–6.76, P = 0.001) by multivariable regression analysis. IFC-ICB demonstrated an enrichment of monocytes in both culprit blood analysis (culprit ratio: 1.1 ± 0.2 vs. 0.9 ± 0.2, P = 0.048) and aspirated culprit thrombi (326 ± 162 vs. 96 ± 87 cells/mm2, P = 0.017), while IFC-ACB confirmed the accumulation of CD4+ T cells, as recently described. Conclusion This study provides novel evidence for a pathophysiological involvement of CME in the development of IFC-ACS and provides first evidence for a distinct pathophysiological pathway for IFC-ICB, driven by CME-derived flow disturbances and inflammatory activation involving the innate immune system. Trial registration Registration of the study at clinicalTrials.gov (NCT03129503). [ABSTRACT FROM AUTHOR]

Convergent experimental and clinical evidence have established the pathophysiological importance of pro-inflammatory pathways in coronary artery disease. Notably, the interest in treating inflammation in patients suffering acute myocardial infarction (AMI) is now expanding from its chronic aspects to the acute setting. Few large outcome trials have proven the benefits of anti-inflammatory therapies on cardiovascular outcomes by targeting the residual inflammatory risk (RIR), i.e. the smouldering ember of low-grade inflammation persisting in the late phase after AMI. However, these studies have also taught us about potential risks of anti-inflammatory therapy after AMI, particularly related to impaired host defence. Recently, numerous smaller-scale trials have addressed the concept of targeting a deleterious flare of excessive inflammation in the early phase after AMI. Targeting different pathways and implementing various treatment regimens, those trials have met with varied degrees of success. Promising results have come from those studies intervening early on the interleukin-1 and -6 pathways. Taking lessons from such past research may inform an optimized approach to target post-AMI inflammation, tailored to spare 'The Good' (repair and defence) while treating 'The Bad' (smouldering RIR) and capturing 'The Ugly' (flaming early burst of excess inflammation in the acute phase). Key constituents of such a strategy may read as follows: select patients with large pro-inflammatory burden (i.e. large AMI); initiate treatment early (e.g. ≤12 h post-AMI); implement a precisely targeted anti-inflammatory agent; follow through with a tapering treatment regimen. This approach warrants testing in rigorous clinical trials. [ABSTRACT FROM AUTHOR]

In Switzerland, about 20 000 people experience an acute coronary syndrome (ACS) event each year. Acute coronary syndromes comprise ST-segment elevation myocardial infarction (STEMI), non-ST-segment elevation myocardial infarction (NSTEMI), and unstable angina. The diagnosis is made based on the clinical presentation, a rise in cardiac biomarkers, and ischemic ECG changes. In patients with acute STEMI, urgent coronary angiography with primary percutaneous coronary intervention (PCI) to open the occluded artery is indicated. In patients with NSTEMI and unstable angina, the timing of coronary angiography and PCI is based on the clinical presentation and on a comprehensive and individualized risk stratification. Optimal secondary prevention and aggressive cardiovascular risk factor control are important following the acute event. [ABSTRACT FROM AUTHOR]

Intracoronary pressure gradients and translesional flow patterns have been correlated with coronary plaque progression and lesion destabilization. In this study, we aimed to determine the relationship between endothelial shear stress and plaque progression and to evaluate the effect of shear forces on coronary plaque features. A systematic review was conducted in medical on-line databases. Selected were studies including human participants who underwent coronary anatomy assessment with computational fluid dynamics (CFD)-based wall shear stress (WSS) calculation at baseline with anatomical evaluation at follow-up. A total of six studies were included for data extraction and analysis. The meta-analysis encompassed 31′385 arterial segments from 136 patients. Lower translesional WSS values were significantly associated with a reduction in lumen area (mean difference −0.88, 95% CI −1.13 to −0.62), an increase in plaque burden (mean difference 4.32, 95% CI 1.65 to 6.99), and an increase in necrotic core area (mean difference 0.02, 95% CI 0.02 to 0.03) at follow-up imaging. Elevated WSS values were associated with an increase in lumen area (mean difference 0.78, 95% CI 0.34 to 1.21) and a reduction in both fibrofatty (mean difference −0.02, 95% CI −0.03 to −0.01) and fibrous plaque areas (mean difference −0.03, 95% CI −0.03 to −0.03). This meta-analysis shows that WSS parameters were related to vulnerable plaque features at follow-up. These results emphasize the impact of endothelial shear forces on coronary plaque growth and composition. Future studies are warranted to evaluate the role of WSS in guiding clinical decision-making. Effect of translesional shear forces on coronary plaques. Wall shear stress (WSS) impacts on plaque evolution through its influence on plaque composition and progression. While lower WSS values promote plaque growth and reduce lumen area, higher WSS values, despite preserving lumen area, may adversely affect plaque stability by thinning its fibrous components. Understanding these complex interactions between WSS and plaque evolution may help to identify vulnerable plaques and guide clinical decision-making. [Display omitted] • Meta-analysis links WSS to coronary plaque progression in 31,385 segments. • Low WSS increases plaque burden and necrotic core, impacting evolution. • High WSS boosts lumen area, reduces fibrofatty/fibrous plaque areas. • WSS represents a diagnostic marker for high-risk coronary plaques. • WSS could lead clinical decisions and targeted therapies, more research granted. [ABSTRACT FROM AUTHOR]

Coronary hemodynamics impact coronary plaque progression and destabilization. The aim of the present study was to establish the association between focal vs. diffuse intracoronary pressure gradients and wall shear stress (WSS) patterns with atherosclerotic plaque composition. Prospective, international, single-arm study of patients with chronic coronary syndromes and hemodynamic significant lesions (fractional flow reserve [FFR] ≤ 0.80). Motorized FFR pullback pressure gradient (PPG), optical coherence tomography (OCT), and time-average WSS (TAWSS) and topological shear variation index (TSVI) derived from three-dimensional angiography were obtained. One hundred five vessels (median FFR 0.70 [Interquartile range (IQR) 0.56–0.77]) had combined PPG and WSS analyses. TSVI was correlated with PPG (r = 0.47, [95% Confidence Interval (95% CI) 0.30–0.65], p < 0.001). Vessels with a focal CAD (PPG above the median value of 0.67) had significantly higher TAWSS (14.8 [IQR 8.6–24.3] vs. 7.03 [4.8–11.7] Pa, p < 0.001) and TSVI (163.9 [117.6–249.2] vs. 76.8 [23.1–140.9] m−1, p < 0.001). In the 51 vessels with baseline OCT, TSVI was associated with plaque rupture (OR 1.01 [1.00–1.02], p = 0.024), PPG with the extension of lipids (OR 7.78 [6.19–9.77], p = 0.003), with the presence of thin-cap fibroatheroma (OR 2.85 [1.11–7.83], p = 0.024) and plaque rupture (OR 4.94 [1.82 to 13.47], p = 0.002). Focal and diffuse coronary artery disease, defined using coronary physiology, are associated with differential WSS profiles. Pullback pressure gradients and WSS profiles are associated with atherosclerotic plaque phenotypes. Focal disease (as identified by high PPG) and high TSVI are associated with high-risk plaque features. https://clinicaltrials,gov/ct2/show/NCT03782688 Central illustration – Interplay between wall shear stress and intracoronary pressure patterns and their association with plaque phenotypes. In the present investigation of the Precise PCI Plan (P3) Study, 105 vessels with invasive fractional flow reserve (FFR) ≤ 0.80 underwent combined assessment of intracoronary pressure gradients with motorized hyperemic pullback pressure gradients (PPG), angiography-derived computational fluid dynamics simulation with the calculation of the topological shear variation index (TSVI, i.e. a measure of the variability of the wall shear stress contraction/expansion action on the endothelium), and plaque analysis before percutaneous coronary intervention (PCI) with optical coherence tomography (OCT). Vessels were classified as presenting either a predominantly diffuse or focal pressure drop pattern according to their PPG-Index (below or higher than the median value of the population, respectively). Low-PPG vessels (panels on the left) exhibited moderate flow disturbances, as quantified by lower TSVI values at the level of the lesion throat, with less dysplastic plaque, lower prevalence of thin-cap fibrous atheroma (TCFA) and subclinical plaque rupture. On the contrary, high-PPG vessels (panels on the right) exhibited flow disturbances quantified by elevated TSVI values over the mid portion of the lesion, associated with the OCT finding of vulnerable or even ruptured plaques. [Display omitted] • The study explored key relationship between intravascular hemodynamic forces and plaque composition. • Higher TAWSS and TSVI were found in vessels with focal versus diffuse disease. • Focal disease and increased shear forces linked to high-risk plaque phenotypes. • Diffuse disease vessels showed milder local flow disruptions and fewer signs of plaque vulnerability. [ABSTRACT FROM AUTHOR]

Cholesterol crystals (CCs) represent a feature of advanced atherosclerotic plaque and may be assessed by optical coherence tomography (OCT). Their impact on cardiovascular outcomes in patients presenting with acute coronary syndromes (ACS) is yet unknown. The culprit lesion (CL) of 346 ACS-patients undergoing preintervention OCT imaging were screened for the presence of CCs and divided into two groups accordingly. The primary end-point was the rate of major adverse cardiac events plus (MACE+) consisting of cardiac death, myocardial infarction, target vessel revascularization and re-hospitalization due to unstable or progressive angina at two years. Among 346 patients, 57.2% presented with CCs at the CL. Patients with CCs exhibited a higher prevalence of ruptured fibrous caps (RFC-ACS) (79.8% vs. 56.8%; p < 0.001) and other high-risk features such as thin cap fibroatheroma (80.8% vs. 64.9%; p = 0.001), presence of macrophages (99.0% vs. 85.1%; p < 0.001) as well as a greater maximum lipid arc (294.0° vs. 259.3°; p < 0.001) at the CL as compared to patients without CCs. MACE+ at two years follow-up occurred more often in CC-patients (29.2% vs. 16.1%; p = 0.006) as compared to patients without CCs at the culprit site. Multivariable cox regression analysis identified CCs as independent predictor of MACE+ (HR 1.705; 1.025–2.838 CI, p = 0.040). CCs were associated with conventional high-risk plaque features and associated with increased MACE+-rates at two years follow up. The identification of CCs might be useful as prognostic marker in patients with ACS and assist "precision prevention" in the future. • Cholesterol crystals (CCs) are a frequently occurring feature of advanced atherosclerotic plaque • They are associated with classical high-risk plaque features in acute coronary syndrome (ACS). • They are associated with enhanced inflammation(increased peripheral CRP-levels and local macrophage accumulation). • They are associated with increased cardiovascular event-rates at two years follow-up. • CCs may therefore facilitate risk stratification after ACS. [ABSTRACT FROM AUTHOR]

Introduction and Objectives: Multivessel percutaneous coronary intervention (MV-PCI) is recommended in patients with ST-segment elevation myocardial infarction (STEMI) and multivessel coronary artery disease (CAD) without cardiogenic shock. The present network meta-analysis investigated the optimal timing of MV-PCI in this context., Methods: We pooled the aggregated data from randomized trials investigating stable STEMI patients with multivessel CAD treated with a strategy of either MV-PCI or culprit vessel-only PCI. The primary outcome was all-cause death. The main secondary outcomes were cardiovascular death, myocardial infarction, and unplanned ischemia-driven revascularization., Results: Among 11 trials, a total of 10 507 patients were randomly assigned to MV-PCI (same sitting, n=1683; staged during the index hospitalization, n=3460; staged during a subsequent hospitalization within 45 days, n=3275) or to culprit vessel-only PCI (n=2089). The median follow-up was 18.6 months. In comparison with culprit vessel-only PCI, MV-PCI staged during the index hospitalization significantly reduced all-cause death (risk ratio, 0.73; 95%CI, 0.56-0.92; P=.008) and ranked as possibly the best treatment option for this outcome compared with all other strategies. In comparison with culprit vessel-only PCI, a MV-PCI reduced cardiovascular mortality without differences dependent on the timing of revascularization. MV-PCI within the index hospitalization, either in a single procedure or staged, significantly reduced myocardial infarction and unplanned ischemia-driven revascularization, with no significant difference between each other., Conclusions: In patients with STEMI and multivessel CAD without cardiogenic shock, multivessel PCI within the index hospitalization, either in a single procedure or staged, represents the safest and most efficacious approach. The different timings of multivessel PCI did not result in any significant differences in all-cause death. This study is registered at PROSPERO (CRD42023457794)., (Copyright © 2024 Sociedad Española de Cardiología. Published by Elsevier España, S.L.U. All rights reserved.)

Purpose: The invasive British Cardiovascular Intervention Society Jeopardy Score (iBCIS-JS) is a simple angiographic scoring system, enabling quantification of the extent of jeopardized myocardium related to clinically significant coronary artery disease (CAD). The purpose of this study was to develop and validate the coronary CT angiography-based BCIS-JS (CT-BCIS-JS) against the iBCIS-JS in patients with suspected or stable CAD., Materials and Methods: Patients who underwent coronary CT angiography followed by invasive coronary angiography, within 90 days were retrospectively included. CT-BCIS-JS and iBCIS-JS were calculated, with a score ≥ 6 indicating extensive CAD. Correlation between the CT-BCIS-JS and iBCIS-JS was searched for using Spearman's coefficient, and agreement with weighted Kappa (κ) analyses., Results: A total of 122 patients were included. There were 102 men and 20 women with a median age of 62 years (Q1, Q3: 54, 68; age range: 19-83 years). No differences in median CT-BCIS-JS (4; Q1, Q3: 0, 8) and median iBCIS-JS (4; Q1, Q3: 0, 8) were found (P = 0.18). Extensive CAD was identified in 53 (43.4%) and 52 (42.6%) patients using CT-BCIS-JS and iBCIS-JS, respectively (P = 0.88). CT-based and iBCIS-JS showed excellent correlation (r = 0.98; P < 0.001) and almost perfect agreement (κ = 0.93; 95% confidence interval: 0.90-0.97). Agreement for identification of an iBCIS-JS ≥ 6 was almost perfect (κ = 0.94; 95 % confidence interval: 0.87-0.99)., Conclusion: The CT-BCIS-JS represents a feasible, and accurate method for quantification of CAD, with capabilities not different from those of iBCIS-JS. It enables simple, non-invasive identification of patients with anatomically extensive CAD., Competing Interests: Declaration of Competing Interest AC has consultancy agreements with Medyria and Nanoflex. DCB reports payments from Amgen, Pfizer and Philips Healthcare, and research support from Philips Healthcare, Spectrum Dynamics and MIM Software Inc. BS has been supported by the H.H. Sheikh Khalifa bin Hamad Al-Thani Research Programme; BS has received grants to the institution from the OPO Foundation, the Iten-Kohaut Foundation, the German Center for Cardiovascular Research (DZHK), the German Heart Research Foundation, the B. Braun Foundation, Boston Scientific, and Edwards Lifesciences. The University Hospital of Zurich holds a research agreement with GE Healthcare. All other authors report no personal conflicts of interests in relation with this study., (Copyright © 2023 The Author(s). Published by Elsevier Masson SAS.. All rights reserved.)

Aims: Coronary microevaginations (CMEs) represent an outward bulge of coronary plaques and have been introduced as a sign of adverse vascular remodelling following coronary device implantation. However, their role in atherosclerosis and plaque destabilization in the absence of coronary intervention is unknown. This study aimed to investigate CME as a novel feature of plaque vulnerability and to characterize its associated inflammatory cell-vessel-wall interactions., Methods and Results: A total of 557 patients from the translational OPTICO-ACS study programme underwent optical coherence tomography imaging of the culprit vessel and simultaneous immunophenotyping of the culprit lesion (CL). Two hundred and fifty-eight CLs had a ruptured fibrous cap (RFC) and one hundred had intact fibrous cap (IFC) acute coronary syndrome (ACS) as an underlying pathophysiology. CMEs were significantly more frequent in CL when compared with non-CL (25 vs. 4%, P < 0.001) and were more frequently observed in lesions with IFC-ACS when compared with RFC-ACS (55.0 vs. 12.7%, P < 0.001). CMEs were particularly prevalent in IFC-ACS-causing CLs independent of a coronary bifurcation (IFC-ICB) when compared with IFC-ACS with an association to a coronary bifurcation (IFC-ACB, 65.4 vs. 43.7%, P = 0.030). CME emerged as the strongest independent predictor of IFC-ICB (relative risk 3.36, 95% confidence interval 1.67-6.76, P = 0.001) by multivariable regression analysis. IFC-ICB demonstrated an enrichment of monocytes in both culprit blood analysis (culprit ratio: 1.1 ± 0.2 vs. 0.9 ± 0.2, P = 0.048) and aspirated culprit thrombi (326 ± 162 vs. 96 ± 87 cells/mm2, P = 0.017), while IFC-ACB confirmed the accumulation of CD4+ T cells, as recently described., Conclusion: This study provides novel evidence for a pathophysiological involvement of CME in the development of IFC-ACS and provides first evidence for a distinct pathophysiological pathway for IFC-ICB, driven by CME-derived flow disturbances and inflammatory activation involving the innate immune system., Trial Registration: Registration of the study at clinicalTrials.gov (NCT03129503)., Competing Interests: Conflict of interest: D.M.L. received lecture honoraria from Amgen, Abbott Vascular, AstraZeneca, and Novo Nordisk. M.J. received consulting fees from Biotronik, TriCares, Veryan, and Shockwave, and is in the Steering Committee of Biotronik and Edwards Lifesciences. T.D.T. received payment honoraria from Novartis, AstraZeneca, Berlin Chemie, Abbott, NeoVasc, and Amgen. U.L. reports lecture and advisory honorary from Abbott. All other authors report no conflicts of interest., (© The Author(s) 2023. Published by Oxford University Press on behalf of the European Society of Cardiology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Background: Spontaneous coronary artery dissection (SCAD) has been described as an infrequent cause of acute coronary syndrome (ACS). Knowledge about the disease is still limited and SCAD might still be underdiagnosed., Objectives: Trends in incidence, presentation, angiographic appearance, management, and outcomes of SCAD over 25 years were analyzed., Methods: Patients with SCAD between 1997 and 2021 at the University Hospital Zurich, Switzerland, were included. Incidences were assessed as total numbers and proportions of ACS cases. Clinical data were collected from medical records and angiographic findings were reviewed. Major adverse cardiac events (MACE) were defined as the composite of all-cause death, cardiac arrest, SCAD recurrence or progression, other myocardial infarction, and stroke., Results: One hundred fifty-six SCAD cases were included in this study. The incidence increased significantly in total (p < 0.001) and relative to ACS cases (p < 0.001). This was based on an increase of shorter lesions (p = 0.004), SCAD type 2 (p < 0.001), and lesions in side branches (p = 0.014), whereas lesions in the left main coronary artery and proximal segments were decreasing (p-values 0.029 and < 0.001, respectively). There was an increase in conservative therapy (p < 0.001). The rate of MACE (24%) was stable, however, there was a reduced proportion of patients with a need for intensive care treatment (p = 0.017)., Conclusions: SCAD represents an important entity of ACS that still might be underappreciated. The increasing incidence of SCAD is likely based on better awareness and familiarity with the disease. A lower need for intensive care treatment suggests positive effects of the increasing implementation of conservative management., (Copyright © 2023 The Authors. Published by Elsevier B.V. All rights reserved.)

Introduction: In Switzerland, about 20 000 people experience an acute coronary syndrome (ACS) event each year. Acute coronary syndromes comprise ST-segment elevation myocardial infarction (STEMI), non-ST-segment elevation myocardial infarction (NSTEMI), and unstable angina. The diagnosis is made based on the clinical presentation, a rise in cardiac biomarkers, and ischemic ECG changes. In patients with acute STEMI, urgent coronary angiography with primary percutaneous coronary intervention (PCI) to open the occluded artery is indicated. In patients with NSTEMI and unstable angina, the timing of coronary angiography and PCI is based on the clinical presentation and on a comprehensive and individualized risk stratification. Optimal secondary prevention and aggressive cardiovascular risk factor control are important following the acute event. Keywords., Competing Interests: Es bestehen keine Interessenskonflikte., (© 2024 Aerzteverlag medinfo AG.)