Positron emission tomography (PET) imaging has evolved over the last 20 years to a powerful tool for assessing vascular biology. The incidental uptake of PET tracers to the vessel wall provided the substrate for creating dedicated protocols and introducing novel agents for molecular imaging that targeted specific pathobiological mechanisms involved in the atherosclerotic process. Preliminary work with 18F-FDG underscored its efficacy to detect macrophage-rich inflammation, while, subsequent studies using 18F-NaF demonstrated its ability to detect active microcalcification and high-risk plaques. These encouraging results lead to the development of a new generation of tracers targeting macrophage receptors, chemokine signalling, angiogenesis, endothelial activation, and mitochondrial activity that have been validated against histology in animal models, endarterectomy, and autopsy tissue. This review provides an overview in the field describing the evolution of PET imaging in the study of atherosclerosis. It summarises the existing and emerging tracers, presents the biological processes that have been targeted by PET agents and collates the evidence from studies for vulnerable-plaque detection. Finally, it outlines technical hurdles and the current limitations of PET imaging that need to be addressed for clinical translation.

Background and aims:This article aims to develop and validate a methodology for realistic anatomical reconstruction of stented segments from optical coherence tomography (OCT) and angiographic images and the computation of local haemodynamic forces using computational fluid dynamics, towards a more realistic haemodynamic characterisation in coronary atherosclerotic lesions post-PCI. Methods:Three-dimensional anatomical models of stented vessels (6 silicone models in vitro and 16 patient models) were reconstructed from OCT and angiography, using a new methodology called REFINED, which relies on the separate reconstruction of the lumen and the stent; these two are then fused in a single model. Blood flow simulations were performed using the anatomical models to calculate the endothelial shear stress (ESS) and shear rate (SR). The models were geometrically and haemodynamically evaluated against those reconstructed using conventional models. Results:The reconstruction error distance was smaller with the REFINED approach than with the conventional approach, in both the silicone and patient models [8 (2-15) μm vs 23 (10-54) μm, p < 0.001, and 19 (9-32) μm vs 19 (7-36) μm, p < 0.001]. The REFINED method depicted higher ESS at the top of the struts in both the silicone (8.01 (4.21-14.92) Pa vs 5.54 (2.96-9.63) Pa; p < 0.001) and patient models [2.41 (1.41-3.65) Pa vs 1.44 (0.77-2.52) Pa; p < 0.001], and a more spatially heterogeneous SR compared to the conventional approach (p < 0.001 for all analyses). Conclusions:The REFINED approach outperforms the conventional method in reconstructing stent geometry and has been shown to be effective in facilitating a high-fidelity computation of the highly disturbed local haemodynamic environment. This demonstrates its potential role in examining device failure.

BACKGROUND:The incorporation of side branches in vessel geometry influences wall shear stress (WSS) distribution. However, complete vessel reconstruction is time-consuming, and there is no evidence that its WSS estimations better predict atherosclerotic disease progression compared with the output of the conventional single-vessel reconstruction (SVR). METHODS:Patients who had baseline and 1-year follow-up intravascular ultrasound imaging (n=40 vessels), and patients with neoatherosclerotic lesions (n=13 vessels) on optical coherence tomography were included. All the studied vessels had at least one side branch with a diameter >1 mm; 3-dimensional complete vessel reconstruction and SVR were performed, and the time-averaged WSS and multidirectional WSS were computed. The performance of both methods in predicting disease progression in intravascular ultrasound and optical coherence tomography models was assessed. RESULTS:The incorporation of side branches in 3-dimensional geometry resulted in lower minimum predominant time-averaged WSS in the intravascular ultrasound (1.09 versus 1.58 Pa, P<0.001) and optical coherence tomography-based reconstructions (0.68 versus 1.33 Pa, P<0.001) and influenced the multidirectional WSS distribution. In native segments, complete vessel reconstruction-derived WSS metrics demonstrated superior predictive performance for disease progression-defined as lumen area reduction and plaque burden increase-compared with SVR, as evidenced by improved out-of-sample accuracy (leave-one-out information criterion: 429 versus 551), discrimination (C statistic: 0.725 versus 0.651), calibration (Brier score: 0.172 versus 0.226), and explained variance (27.8% versus 20.7%). Consistent findings were observed in stented segments, where complete vessel reconstruction-derived WSS metrics more accurately predicted neointimal proliferation than SVR-derived metrics. CONCLUSIONS:Incorporating side branches into vessel reconstruction influences WSS distribution and enables more accurate prediction of atherosclerotic disease progression in native and stented segments than SVR.

Introduction A quarter of breast cancers show human epidermal growth factor-2 (HER2) overexpression, where targeted therapy dramatically improves survival. However, cancer therapy-related cardiac dysfunction (CTRCD) occurs in up to 15% of patients. With the interruption of HER2 therapy, if necessary, and the initiation of heart failure therapy (HFT), HER2 CTRCD recovers in over 80% of cases. The need to continue HFT in ‘recovered’ HER2 CTRCD following completion of HER2 therapy is unclear and there are potential significant impacts on patient’s quality of life (QoL). The Randomised Controlled Trial for the Safety of Withdrawal of Pharmacological Treatment for Recovered HER2 Targeted Therapy Related Cardiac Dysfunction (HER-SAFE) aims to evaluate whether HFT can be safely withdrawn in non-high cardiovascular (CV) risk patients with ‘recovered’ HER2 CTRCD.Methods and analysis This is a multicentre, open-label randomised controlled trial investigating whether withdrawal of HFT is non-inferior to continuation in non-high CV risk, breast cancer survivors with recovered HER2 CTRCD after cancer treatment completion. The primary endpoint is the incidence of guideline-defined cardiac dysfunction or clinical heart failure. Secondary endpoints include changes in cardiac blood biomarkers, cardiovascular magnetic resonance (CMR)-derived strain and tissue mapping and heart failure symptom questionnaires. The study will recruit 90 participants who will undergo serial clinical assessment over 12 months with advanced cardiovascular imaging (CMR scans with automated analysis at baseline, 6 and 12 months), cardiac biomarker measurement (six time points over 12 months), plus complete heart failure QoL and medication disutility questionnaires. This is the first multicentre study to address this significant clinical issue.Ethics and dissemination This study was approved by the research ethics committee (London—London Bridge, 23/LO/0152). The results will be disseminated in peer-reviewed scientific journals.Trial registration number NCT05880160.

Background Complete vessel reconstruction (CVR) with incorporation of side branches is essential for accurate evaluation of wall shear stress (WSS) distribution. However, CVR is time consuming and blood flow simulation is computationally expensive, while there is no evidence that WSS computed by CVR, enables better prediction of disease progression compared to WSS derived from the conventional single vessel reconstruction (SVR). We aim to compare the WSS in models reconstructed using the CVR and SVR methods and examine its ability to predict disease progression. Methods Patients who had baseline and 13-months follow-up intravascular ultrasound (IVUS) imaging (n=19 vessels), and with neoatherosclerotic lesions (n=13 vessels) on optical coherence tomography (OCT) were included in the present analysis. All the studied vessels had at least one side branch with diameter >1mm. 3-dimensional (3D) CVR and SVR were performed and time averaged (TAWSS) and multidirectional WSS were computed using pulsatile blood flow simulation and the performance of both methods in predicting disease progression in IVUS and OCT models were assessed. Results The incorporation of side branches in 3D geometry resulted in lower TAWSS in the IVUS (0.821 vs 1.698Pa, p<0.001) and OCT-based reconstructions (0.682 vs 1.325Pa, p<0.001) and influenced the multidirectional WSS distribution. In native segments, WSS metrics estimated by the CVR enabled better prediction of the lumen and plaque area and burden at follow-up than SVR and disease progression defined as decrease in lumen area and increase in plaque burden (AUC CVR 0.712 vs SVR 0.554). In stented segments, multidirectional WSS was associated with neointima area in both CVR and SVR methods, but TAWSS was only a predictor of neointima area in the CVR method. Conclusions The incorporation of side branches in vessel reconstruction influences WSS distribution and enables more accurate prediction of disease progression in native and stented segments than SVR modelling. Highlights Complete vessel reconstruction (CVR) with incorporation of vessel side branches has been proposed for accurate evaluation of wall shear stress (WSS) distribution compared to the traditional single vessel reconstruction (SVR) method; however, there are no studies comparing the performance of the WSS metrics derived by these methods in predicting atherosclerotic evolution. In vessels with large side branches, the incorporation of the side branches in the vessel geometry reconstructed from angiographic and intravascular imaging data resulted in lower time averaged wall shear stress (TAWSS) and influenced the multidirectional WSS estimations compared to the models reconstructed without the side branches. The WSS metrics estimated in the CVR models enabled better prediction of atherosclerotic disease progression at 13-months follow-up on IVUS than the WSS derived by the SVR. In stented vessels, all the WSS metrics in the CVR and the multidirectional WSS in SVR were associated with neointima tissue development; however, both approaches showed limited efficacy in predicting neointima proliferation.

AbstractAimsThe long‐term outcomes of the intracoronary delivery of autologous bone marrow‐derived cells (BMCs) after acute myocardial infarction are not well established. Following the promising 1 year results of the REGENERATE‐AMI trial (despite it not achieving its primary endpoint), this paper presents the analysis of the 5 year clinical outcomes of these acute myocardial infarction patients who were treated with an early intracoronary autologous BMC infusion or placebo.Methods and resultsA 5 year follow‐up of major adverse cardiac events (defined as the composite of all‐cause death, recurrent myocardial infarction, and all coronary revascularization) and of rehospitalization for heart failure was completed in 85 patients (BMC n = 46 and placebo n = 39). The incidence of major adverse cardiac events was similar between the BMC‐treated patients and the placebo group (26.1% vs. 18.0%, P = 0.41). There were no cases of cardiac death in either group, but an increase in non‐cardiac death was seen in the BMC group (6.5% vs. 0%, P = 0.11). The rates of recurrent myocardial infarction and repeat revascularization were similar between the two groups. There were no cases of rehospitalization for heart failure in either group.ConclusionThis 5 year follow‐up analysis of the REGENERATE‐AMI trial did not show an improvement in clinical outcomes for patients treated with cell therapy. This contrasts with the 1 year results which showed improvements in the surrogate outcome measures of ejection fraction and myocardial salvage index.

Background Intravascular imaging has been used to assess the morphology of lesions causing an acute coronary syndrome (ACS) in native vessels (NV) and identify differences between plaques that ruptured (PR) and caused an event and those that ruptured without clinical manifestations. However, there is no data about the morphological and physiological characteristics of neoatherosclerotic plaques that ruptured (PR-NA) which constitute a common cause of stent failure. Methods We retrospectively analyzed data from patients admitted with an acute myocardial infarction that had optical coherence tomography (OCT) imaging of the culprit vessel before balloon pre-dilation. OCT pullbacks showing PR were segmented at every 0.4 mm. The extent of the formed cavity, lipid and calcific tissue, thrombus, and macrophages were measured, and the fibrous cap thickness (FCT) and the incidence of micro-channels and cholesterol crystals were reported. These data were used to reconstruct a representative model of the native and neoatherosclerotic lesion geometry that was processed with computational fluid dynamics (CFD) techniques to estimate the distribution of the endothelial shear stress and plaque structural stress. Result Eighty patients were included in the present analysis: 56 had PR in NV (PR-NV group) and 24 in NA segments (PR-NA group). The PR-NV group had a larger minimum lumen area (2.93 ± 2.03 vs. 2.00 ± 1.26 mm2, p = 0.015) but similar lesion length and area stenosis compared to PR-NA group. The mean FCT (186 ± 65 vs. 232 ± 80 μm, p = 0.009) and the lipid index was smaller (16.7 ± 13.8 vs. 25.9 ± 14.1, p = 0.008) while the of calcific index (8.3 ± 9.5 vs. 2.2 ± 1.6%, p = 0.002) and the incidence of micro-channels (41.4 vs. 12.5%, p = 0.013) was higher in the PR-NV group. Conversely, there was no difference in the incidence of cholesterol crystals, thrombus burden or the location of the rupture site between groups. CFD analysis revealed higher maximum endothelial shear stress (19.1 vs. 11.0 Pa) and lower maximum plaque structural stress (38.8 vs. 95.1 kPa) in the PR-NA compared to the PR-NV model. Conclusion We reported significant morphological and physiological differences between culprit ruptured plaques in native and stented segments. Further research is needed to better understand the causes of these differences and the mechanisms regulating neoatherosclerotic lesion destabilization.

Coronary luminal dimensions change during the cardiac cycle. However, contemporary volumetric intravascular ultrasound (IVUS) analysis is performed in non-gated images as existing methods to acquire gated or to retrospectively gate IVUS images have failed to dominate in research. We developed a novel deep learning (DL)-methodology for end-diastolic frame detection in IVUS and compared its efficacy against expert analysts and a previously established methodology using electrocardiographic (ECG)-estimations as reference standard. Near-infrared spectroscopy-IVUS (NIRS-IVUS) data were prospectively acquired from 20 coronary arteries and co-registered with the concurrent ECG-signal to identify end-diastolic frames. A DL-methodology which takes advantage of changes in intensity of corresponding pixels in consecutive NIRS-IVUS frames and consists of a network model designed in a bidirectional gated-recurrent-unit (Bi-GRU) structure was trained to detect end-diastolic frames. The efficacy of the DL-methodology in identifying end-diastolic frames was compared with two expert analysts and a conventional image-based (CIB)-methodology that relies on detecting vessel movement to estimate phases of the cardiac cycle. A window of ± 100 ms from the ECG estimations was used to define accurate end-diastolic frames detection. The ECG-signal identified 3,167 end-diastolic frames. The mean difference between DL and ECG estimations was 3 ± 112 ms while the mean differences between the 1st-analyst and ECG, 2nd-analyst and ECG and CIB-methodology and ECG were 86 ± 192 ms, 78 ± 183 ms and 59 ± 207 ms, respectively. The DL-methodology was able to accurately detect 80.4%, while the two analysts and the CIB-methodology detected 39.0%, 43.4% and 42.8% of end-diastolic frames, respectively (P < 0.05). The DL-methodology can identify NIRS-IVUS end-diastolic frames accurately and should be preferred over expert analysts and CIB-methodologies, which have limited efficacy.

OBJECTIVE:Fractional flow reserve (FFR) is regarded as the gold standard for the physiological assessment of intermediate coronary artery stenoses. However, FFR does not allow assessment of plaque morphology and lesion geometry. Intracoronary imaging techniques such as intravascular ultrasound (IVUS) and optical coherence tomography (OCT) can help treatment planning by optimising stent implantation, which can improve patient outcomes. The aim of this meta-analysis is to compare the efficacy of IVUS and OCT-derived metrics in detecting flow limiting stenoses in non-left main stem lesions.METHODS:A systematic review of PubMed, Medline, and Cochrane databases was performed and identified studies examining the diagnostic accuracy of IVUS and OCT in detecting significant stenoses when compared to FFR.RESULTS:A total of 33 (7537 lesions) studies (24 IVUS, 7 OCT and 2 IVUS & OCT studies) were included in the meta-analysis. Pooled analysis showed that IVUS- and OCT-derived minimum lumen area (MLA) had a similar sensitivity in predicting haemodynamically significant lesions (IVUS-MLA: 0.747 vs OCT-MLA 0.732, p = 0.519). However, OCT-MLA had a higher specificity (0.763 vs 0.665, p < 0.001) and diagnostic accuracy in detecting flow-limiting stenoses than IVUS-MLA (AUC 0.810 vs 0.754, p = 0.045). Sub-analysis of the studies with the clinically significant FFR cut-off value of 0.80 yielded similar results demonstrating that OCT-MLA has a better accuracy than IVUS-MLA in detecting haemodynamically significant stenoses (AUC 0.809 vs 0.750, p = 0.034).CONCLUSIONS:OCT with its superior image resolution appears to be the preferable intravascular imaging modality for the detection of haemodynamically significant stenoses in non-left main stem lesions.

BACKGROUNDAttenuation-compensated (AC) technique was recently introduced to improve the plaque characterization of optical coherence tomography (OCT). Histological validation demonstrated promising results but the efficacy and reproducibility of this technique for assessing in-vivo tissue composition remains unclear.Methods and Results:OCT images portraying native (n=200) and stented (n=200) segments and 31 histological cross-sections were analyzed. AC-OCT appeared superior to conventional (C)-OCT in detecting the external elastic lamina (EEM) borders (76% vs. 65.5%); AC-OCT enabled larger EEM arc detection compared with C-OCT (174.2±58.7° vs. 137.5±57.9°; P<0.001). There was poor agreement between the 2 techniques for detection of lipid in native and lipid and calcific tissue in stented segments (κ range: 0.164-0.466) but the agreement of C-OCT and AC-OCT was high for calcific tissue in native segments (κ=0.825). Intra and interobserver agreement of the 2 analysts was moderate to excellent with C-OCT (κ range: 0.681-0.979) and AC-OCT (κ range: 0.733-0.892) for all tissue types in both native and stented segments. Ex-vivoanalysis demonstrated that C-OCT was superior to AC-OCT (κ=0.545 vs. κ=0.296) for the detection of the lipid component in native segments.CONCLUSIONSThe AC technique allows better delineation of the EEM but it remains inferior for lipid pool detection and neointima characterization. Combined AC- and C-OCT imaging may provide additional value for complete assessment of plaque and neointima characteristics.

Early detection and treatment of cardiotoxicity from cancer therapies is key to preventing a rise in adverse cardiovascular outcomes in cancer patients. Over-diagnosis of cardiotoxicity in this context is however equally hazardous, leading to patients receiving suboptimal cancer treatment, thereby impacting cancer outcomes. Accurate screening therefore depends on the widespread availability of sensitive and reproducible biomarkers of cardiotoxicity, which can clearly discriminate early disease. Blood biomarkers are limited in cardiovascular disease and clinicians generally still use generic screening with ejection fraction, based on historical local expertise and resources. Recently, however, there has been growing recognition that simple measurement of left ventricular ejection fraction using 2D echocardiography may not be optimal for screening: diagnostic accuracy, reproducibility and feasibility are limited. Modern cancer therapies affect many myocardial pathways: inflammatory, fibrotic, metabolic, vascular and myocyte function, meaning that multiple biomarkers may be needed to track myocardial cardiotoxicity. Advanced imaging modalities including cardiovascular magnetic resonance (CMR), computed tomography (CT) and positron emission tomography (PET) add improved sensitivity and insights into the underlying pathophysiology, as well as the ability to screen for other cardiotoxicities including coronary artery, valve and pericardial diseases resulting from cancer treatment. Delivering screening for cardiotoxicity using advanced imaging modalities will however require a significant change in current clinical pathways, with incorporation of machine learning algorithms into imaging analysis fundamental to improving efficiency and precision. In the future, we should aspire to personalized rather than generic screening, based on a patient's individual risk factors and the pathophysiological mechanisms of the cancer treatment they are receiving. We should aspire that progress in cardiooncology is able to track progress in oncology, and to ensure that the current 'one size fits all' approach to screening be obsolete in the very near future.

Opinion statement Early detection and treatment of cardiotoxicity from cancer therapies is key to preventing a rise in adverse cardiovascular outcomes in cancer patients. Over-diagnosis of cardiotoxicity in this context is however equally hazardous, leading to patients receiving suboptimal cancer treatment, thereby impacting cancer outcomes. Accurate screening therefore depends on the widespread availability of sensitive and reproducible biomarkers of cardiotoxicity, which can clearly discriminate early disease. Blood biomarkers are limited in cardiovascular disease and clinicians generally still use generic screening with ejection fraction, based on historical local expertise and resources. Recently, however, there has been growing recognition that simple measurement of left ventricular ejection fraction using 2D echocardiography may not be optimal for screening: diagnostic accuracy, reproducibility and feasibility are limited. Modern cancer therapies affect many myocardial pathways: inflammatory, fibrotic, metabolic, vascular and myocyte function, meaning that multiple biomarkers may be needed to track myocardial cardiotoxicity. Advanced imaging modalities including cardiovascular magnetic resonance (CMR), computed tomography (CT) and positron emission tomography (PET) add improved sensitivity and insights into the underlying pathophysiology, as well as the ability to screen for other cardiotoxicities including coronary artery, valve and pericardial diseases resulting from cancer treatment. Delivering screening for cardiotoxicity using advanced imaging modalities will however require a significant change in current clinical pathways, with incorporation of machine learning algorithms into imaging analysis fundamental to improving efficiency and precision. In the future, we should aspire to personalized rather than generic screening, based on a patient’s individual risk factors and the pathophysiological mechanisms of the cancer treatment they are receiving. We should aspire that progress in cardiooncology is able to track progress in oncology, and to ensure that the current ‘one size fits all’ approach to screening be obsolete in the very near future.

Abstract Background There is increasing awareness of cardiotoxicity arising from cancer treatments. Early diagnosis and treatment is key, to ensure patients receive optimal oncological management. Cardiovascular magnetic resonance (CMR) offers gold standard measurement of cardiac function, alongside tissue characterisation and myocardial perfusion, thereby potentially providing additive value in the context of cardio-oncology. Purpose We sought to understand the clinical value of CMR in cardio-oncology at a tertiary cardio-oncology centre. Methods We retrospectively reviewed CMR scans requested in cardio-oncology patients at our institution within a ten-month period. We categorised clinical indications and assessed the impact on clinical management using previously-published criteria. Results 102 CMR studies were requested in 93 cardio-oncology patients (mean age 56 (range 18 to 82), 49% male) between (March to December 2018). 41% of patients had haematological malignancies, 59% solid tumours. 15% of requests were for risk stratification prior to initiation of cancer therapy, 21% for screening for cardio-toxicity in patients currently receiving cardiotoxic agents (3% anthracyclines, 13% HER2 monoclonal antibodies, 4% fluoropyrimidines), 15% for investigation of patients with cardiac complications during cancer treatment, 35% assessment for late effects post cancer treatment, and 14% for cardiac malignancies/ infiltration. The most common indications for CMR were monitoring of left ventricular ejection fraction (LVEF) in patients where quantification by echocardiography was non-diagnostic or significantly different between imaging studies (39%) and ischaemia assessment including for patients due to receive fluoropyrimidines (26%). Others were aetiology of LV dysfunction/cardiomyopathy (13%) and tissue characterisation (23%), including assessment for cardiac AL amyloid (11 patients), myocarditis (2), cardiac metastases (1), cardiac masses (6), and cardiac iron loading (1). CMR findings had clinical impact in 61% of patients and assisted in adjudicating a new diagnosis in 29% of patients. 88% of patients were able to continue anthracycline/anti-HER2 therapies based on CMR findings of stable LVEF (93% of whose echocardiograms had suggested reductions). LVEF had reduced significantly in 12% of patients meaning chemotherapy was held/discontinued. 3 patients were recommended to receive non-fluoropyrimidine chemotherapy based on perfusion CMR (pCMR) findings, with one patient permitted to receive capecitabine following normal pCMR. Conclusion CMR provides a comprehensive assessment of myocardial structure and function with utility within the context of cardio-oncology for risk stratification pre-chemotherapy, screening for cardiotoxicity during treatment and investigation of cardiac complications of cancer treatment. The additional information derived from CMR generally provides reassurance enabling administration of optimal cancer therapies.

Background: In ST-elevation myocardial infarction (STEMI) patients with multivessel (MV) disease, after primary percutaneous coronary intervention (PCI), emerging evidence suggests that significant disease in non–infarct-related coronary arteries (IRAs) should be routinely stented. Whether this procedure should be guided by angiography alone or ischemia testing is unclear. Methods: All STEMI patients treated with primary PCI between January 1, 2005, and December 31, 2012, at a tertiary cardiology center were reviewed retrospectively. Inclusion criterion is patients with at least 70% stenosis in non-IRAs. There were 3 treatment groups: (1) angiography-guided MV-PCI, (2) ischemia-guided PCI, and (3) medical therapy. Primary endpoint is all-cause mortality, and secondary end point is major adverse cardiovascular events (MACE), including death, acute coronary syndrome, revascularization, or stent thrombosis. Event-free survivals were compared using multivariate Cox proportional-hazards analysis. A propensity score–adjusted analysis was performed. Results: Four hundred forty-seven STEMI patients had >70% stenosis in non-IRAs. For all-cause mortality, the 3 strategies did not differ. For MACE, ischemia-guided PCI was associated with the lowest MACE rate, followed by angiography-guided PCI and medical therapy, which was associated with the highest MACE rate, driven by death and myocardial infarction. Hazard ratios (HRs) for MACE: angiography-guided MV-PCI versus ischemia-guided MV-PCI: HR = 2.23 [95% confidence interval (CI), 1.11–4.48; P = 0.023]; medical therapy versus angiography-guided MV-PCI: HR = 1.58 (95% CI, 0.99–2.63; P = 0.062); medical therapy versus ischemia-guided MV-PCI: HR = 1.72 (95% CI, 1.08–2.74; P = 0.022). Propensity score–adjusted analysis yielded similar results. Conclusions: After primary PCI, complete revascularization in STEMI multivessel disease is associated with lower MACE rates than medical therapy. However, ischemia-testing–guided rather than angiography-guided revascularization was associated with the lowest MACE. This study provides preliminary data and hypotheses for future randomized controlled studies.

To understand the variety of conditions in which the pericardium may be affected in cancer patients.