Culprit Coronary Artery Research Articles

Quantification and Visualization of CT Myocardial Perfusion Imaging to Detect Ischemia-Causing Coronary Arteries.

Coronary computed tomography angiography (cCTA) has poor specificity to identify coronary stenosis that limit blood flow to the myocardial tissue. Integration of dynamic CT myocardial perfusion imaging (CT-MPI) can potentially improve the diagnostic accuracy. We propose a method that integrates cCTA and CT-MPI to identify culprit coronary lesions that limit blood flow to the myocardium. Coronary arteries and left ventricle surfaces were segmented from cCTA and registered to CT-MPI. Myocardial blood flow (MBF) was derived from CT-MPI. A ray-casting approach was developed to project volumetric MBF onto the left ventricle surface. MBF volume were divided into coronary-specific territories based on proximity to the nearest coronary artery. MBF and normalized MBF were computed for the myocardium and each of the coronary artery. Projection of MBF onto cCTA allowed for direct visualization of perfusion defects. Normalized MBF had higher correlation with ischemic myocardial territory compared to MBF (MBF: R2=0.81 and Index MBF: R2=0.90). There were 18 vessels that showed angiographic disease (stenosis >50%); however, normalized MBF demonstrated only 5 coronary territories to be ischemic. These findings demonstrate that cCTA and CT-MPI can be integrated to visualize myocardial defects and detect culprit coronary arteries responsible for perfusion defects. These methods can allow for non-invasive detection of ischemia-causing coronary lesions and ultimately help guide clinicians to deliver more targeted coronary interventions.

Right bundle branch block in suspected acute coronary syndromes: Diagnostic challenges, treatment and prognosis

BackgroundThere is still conflicting evidence regarding the prognostic implications of right bundle branch block (RBBB) in the general population but also in patients with heart diseases like acute coronary syndromes (ACS). In accordance with current guidelines, RBBB in ACS patients is considered as STEMI equivalent. However, recent studies indicate that further differentiation is necessary in this group, as we will outline below. Methods and resultsA literature search was conducted in PubMed and Google Scholar.In previous studies, RBBB in the general population were mostly considered benign changes of the electrical conduction system. However, recent studies indicate that both complete and incomplete RBBB are associated with increased cardiovascular morbidity and mortality. In addition, among unselected patients with suspected ACS presenting to the emergency department, the prevalence of RBBB was 3 % and it was associated with elevated mortality. The subsequent angiographic identification of a culprit coronary artery stenosis leading to stent implantation was similar at approximately 2 % regardless of the initial ECG presentation with narrow QRS complexes, left bundle branch block (LBBB), or RBBB.Finally, in a group of high-risk patients for ST-elevation myocardial infarction (STEMI), the prevalence of RBBB was 12 %. While RBBB was associated with poor outcome compared to non-BBB and LBBB patients, diagnostic accuracy of STEMI criteria was not affected by the presence of RBBB. However, RBBB patients without distinct STEMI signs in ECG often showed acute STEMI on angiography indicating a potential benefit from immediate transfer to the cardiac catheterization laboratory. ConclusionIn the general population, patients with RBBB and risk factors may need further evaluation. Regarding ACS patients, recent studies support current guidelines that recommend acute invasive evaluation for high-risk ACS patients with RBBB, regardless of ST-T deviations. However, in an unselected group of ACS patients, differential diagnoses should also be investigated through additional diagnostic procedures.

The role of colchicine on ventricular remodelling following myocardial infarction and ischemia-reperfusion injury: article review

Acute myocardial infarction (AMI) is a major cause of cardiac dysfunction, arrhythmias, and a poor prognosis. Even though new technologies have been developed to aid in opening the culprit coronary artery and correcting ischemia-related stenosis by percutaneous coronary intervention (PCI), the ventricular remodelling that induces cardiac failure as a consequence of AMI remains unchanged. Colchicine, a versatile anti-inflammatory medication, has been documented in mitigating cardiac remodelling and enhancing cardiac function following AMI. This article provides an in-depth review of the processes by which colchicine affects ventricular remodeling after AMI, highlighting the potential role of inflammation in the pathogenesis and progression of ventricular dysfunction. Keyword: Colchicine, Ischemia-Reperfusion Injury, Myocardial Infarction, Ventricular Remodelling

Computed tomography for the detection of myocardial hypoperfusion in acute myocardial infarction and the associated CT-to-catheter time

Emergency computed tomography (CT) often does not allow for comprehensive coronary artery assessment. However, CT may reveal pathological myocardial hypoperfusion suggestive of acute myocardial infarction (AMI), especially in patients presenting with a different diagnostic hypothesis. CT hypoperfusion is known to be associated with myocardial infarction, however the diagnostic value of CT hypoperfusion for the detection of AMI is still not well evaluated. This was a single-centre retrospective study including patients who underwent invasive coronary angiography (ICA) due to suspected AMI based on incidental perfusion defects upon emergency CT imaging between 2018 and 2023. A total of 22 patients (mean age 66.3 ± 10.8 years, 11 female) were included in this analysis. The diagnosis of AMI was established in all cases leading to ICA. Culprit coronary artery lesions with an indication of percutaneous coronary intervention were detected in all patients who underwent ICA. Spearmann correlation for hypoperfused segments on CT imaging and the corresponding vascular territory upon ICA was significantly substantial (ρ = 0.73, p = < 0.001). The higher the number of affected myocardial segments, the faster ICA was initiated. Mean time between the suspicion of AMI on CT imaging and ICA was 196 (29–4044) minutes. Myocardial hypoperfusion on emergency CT imaging should be considered as AMI until proven otherwise, independent of the clinical scenario leading to performance of CT imaging and whether imaging was performed for the exclusion of non-cardiac pathologies. Early initiation of further diagnostic workup may potentially avoid delays to invasive treatment and reduce the CT-to-catheter-time. Our study explicitly underlines that myocardial hypoperfusion upon contrast enhanced CT imaging needs to be considered as sign of acute myocardial infarction and indicates targeted clinical workup to rule out this diagnosis and to shorten the timeframe from imaging diagnosis to interventional treatment.

Circulating Interleukin-22 in Patients with Acute Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention.

Acute coronary syndrome (ACS) represents an important clinical manifestation of coronary artery disease (CAD) and is characterized by a particularly poor prognosis. Myocardial reperfusion through primary percutaneous coronary intervention (PPCI) is imperative in the event of acute ST elevation myocardial infarction (STEMI). Interleukin-22 (IL-22) regulates immune and inflammatory responses. This interleukin has been described in the scenario of the CAD, but there are no data in patients with STEMI undergoing PPCI. Objectives: The goals of this study were to investigate the differences in circulating IL-22 levels between patients with STEMI undergoing PPCI and healthy controls and to determine whether these differences were associated with the culprit coronary artery, door-to-balloon time (DBT), final angiographic result, CAD classification, and presence of diabetes mellitus (DM). Methods: A total of 280 participants were recruited, comprising 210 STEMI cases and 70 healthy controls. Participants underwent clinical and angiographic evaluations, and serum IL-22 levels were measured using an enzyme-linked immunosorbent assay (ELISA). Data analysis was performed using the Mann-Whitney and Fisher tests, with p < 0.05 indicating significance. Results: Serum IL-22 levels were lower in cases (149.63, 84.99-294.56) than in the controls (482.67, 344.33-641.00); p < 0.001. Lower IL-22 levels were associated with the right coronary artery (RCA) (144.57, 70.84-242.43; 146.00, 63.60-279.67; 191.71, 121.80-388.97); p = 0.033. IL-22 was lower with shorter DBT (≤60 min, 106.00, 49.60-171.71; >60 min, 153.00, 88.86-313.60); p = 0.043. Conclusions: IL-22 levels were significantly lower in patients with STEMI than in healthy controls.

Acute Hyperglycemia-Induced Injury in Myocardial Infarction.

Acute hyperglycemia is a transient increase in plasma glucose level (PGL) frequently observed in patients with ST-elevation myocardial infarction (STEMI). The aim of this review is to clarify the molecular mechanisms whereby acute hyperglycemia impacts coronary flow and myocardial perfusion in patients with acute myocardial infarction (AMI) and to discuss the consequent clinical and prognostic implications. We conducted a comprehensive literature review on the molecular causes of myocardial damage driven by acute hyperglycemia in the context of AMI. The negative impact of high PGL on admission recognizes a multifactorial etiology involving endothelial function, oxidative stress, production of leukocyte adhesion molecules, platelet aggregation, and activation of the coagulation cascade. The current evidence suggests that all these pathophysiological mechanisms compromise myocardial perfusion as a whole and not only in the culprit coronary artery. Acute hyperglycemia on admission, regardless of whether or not in the context of a diabetes mellitus history, could be, thus, identified as a predictor of worse myocardial reperfusion and poorer prognosis in patients with AMI. In order to reduce hyperglycemia-related complications, it seems rational to pursue in these patients an adequate and quick control of PGL, despite the best pharmacological treatment for acute hyperglycemia still remaining a matter of debate.

The Relationship Between CHA2DS2-VASc Scores and The Degree of TIMI Flow in Patients with Acute ST-Segment Elevation Myocardial Infarction Who Underwent Primary Percutaneous Coronary Intervention at Dr. Saiful Anwar Malang

Background: Suboptimal reperfusion of the compromised myocardium in the area of the culprit coronary arteries is one of the main problems associated with primary PCI that need reliable risk stratification methods to accurately predict the occurrence of decreased TIMI flow given its complex pathophysiology. Some parameters are included CHA2DS2-VASc score. Objective: To understand the relationship between CHA2DS2-VASc and the decreased TIMI flow in STE-ACS patients who had underwent primary PCI at RSUD dr. Saiful Anwar Malang. Material and Methods: The study was cohort retrospective with the inclusion criteria being all STE-ACS patients who underwent primary PCI in RSUD Dr. Saiful Anwar Malang from January 2018 – August 2023. Patients were assigned to TIMI flow grade &lt;3 group (N =169) and TIMI flow grade 3 (N = 677) according to TIMI Flow degree after primary PCI. All the patient’s angiogram were evaluated for TIMI score and CHA2DS2-VASc score is based on a guideline. We concluded data in SPSS program and used the Spearman test and p value of .05 was considered as significant. Result: From a total sample of 846 patients, the correlation between STE-ACS onset and TIMI flow indicates that a higher number of patients with STE-ACS onset &lt;12 hours was found in the TIMI flow &lt;3 and 3 groups (p=0.000). The cutoff CHA2DS2 VASC score's sensitivity and specificity values were ascertained using ROC analysis with cut off value 2.5. The incidence of decreased TIMI flow rate was more significant in the CHA2DS2-VASc ≥3 group with DM (+) and age ≥64 (OR value 0.156, p=0.000) than in the CHA2DS2-VASc ≥3 group without DM and age &lt; 64. With an OR value of 2.94 (p=0.000), Killip class &gt; 2 is another powerful predictor of lower TIMI flow. Conclusion: The only variables in the CHA2DS2-VASc score component that are most strongly associated with the risk of reducing the degree of TIMI flow are DM, age, and Killip class. Keyword: Acute Coronary Syndrome, CHA2DS2-VASc Score, Intervention, Percutaneous Coronary Slow Flow- No Reflow Phenomena, TIMI Flow Degree.

The outcomes of occlusive vs non-occlusive culprit coronary artery in non-ST-segment elevation acute coronary syndrome (NSTEACS): A descriptive prospective study in a tertiary cardiac centre in Sudan

The outcomes of occlusive vs non-occlusive culprit coronary artery in non-ST-segment elevation acute coronary syndrome (NSTEACS): A descriptive prospective study in a tertiary cardiac centre in Sudan

Correlation between St segment elevation in the 12-lead ECG and the culprit coronary artery in patients with acute stemi undergoing primary PCI

Correlation between St segment elevation in the 12-lead ECG and the culprit coronary artery in patients with acute stemi undergoing primary PCI

International evaluation of an artificial intelligence-powered electrocardiogram model detecting acute coronary occlusion myocardial infarction.

A majority of acute coronary syndromes (ACS) present without typical ST elevation. One-third of non-ST-elevation myocardial infarction (NSTEMI) patients have an acutely occluded culprit coronary artery [occlusion myocardial infarction (OMI)], leading to poor outcomes due to delayed identification and invasive management. In this study, we sought to develop a versatile artificial intelligence (AI) model detecting acute OMI on single-standard 12-lead electrocardiograms (ECGs) and compare its performance with existing state-of-the-art diagnostic criteria. An AI model was developed using 18 616 ECGs from 10 543 patients with suspected ACS from an international database with clinically validated outcomes. The model was evaluated in an international cohort and compared with STEMI criteria and ECG experts in detecting OMI. The primary outcome of OMI was an acutely occluded or flow-limiting culprit artery requiring emergent revascularization. In the overall test set of 3254 ECGs from 2222 patients (age 62 ± 14 years, 67% males, 21.6% OMI), the AI model achieved an area under the curve of 0.938 [95% confidence interval (CI): 0.924-0.951] in identifying the primary OMI outcome, with superior performance [accuracy 90.9% (95% CI: 89.7-92.0), sensitivity 80.6% (95% CI: 76.8-84.0), and specificity 93.7 (95% CI: 92.6-94.8)] compared with STEMI criteria [accuracy 83.6% (95% CI: 82.1-85.1), sensitivity 32.5% (95% CI: 28.4-36.6), and specificity 97.7% (95% CI: 97.0-98.3)] and with similar performance compared with ECG experts [accuracy 90.8% (95% CI: 89.5-91.9), sensitivity 73.0% (95% CI: 68.7-77.0), and specificity 95.7% (95% CI: 94.7-96.6)]. The present novel ECG AI model demonstrates superior accuracy to detect acute OMI when compared with STEMI criteria. This suggests its potential to improve ACS triage, ensuring appropriate and timely referral for immediate revascularization.

A machine learning algorithm to predict a culprit lesion after out of hospital cardiac arrest

Abstract Background Between 50-90% of patients suffering from out-of-hospital cardiac arrest (OHCA) have a primary cardiac aetiology of arrest with the presence of a culprit coronary lesion. However, recent trials have failed to show a benefit from an early invasive angiographic approach following OHCA. Identification of patients with high likelihood of a culprit lesion may enable selection of patients likely to benefit from direct conveyance to cardiac arrest centres and for an early invasive approach. However, electrocardiogram (ECG) following return of spontaneous circulation, the current gold-standard, is a poor predictor of presence of a culprit lesion. Purpose We aimed to develop a machine learning algorithm to predict the presence of a culprit lesion in patients with OHCA. Methods We used a retrospective cohort of 398 patients admitted with primary cardiac aetiology OHCA to a tertiary cardiology centre in the United Kingdom, between May 2012 and December 2017. The primary outcome was the presence of a culprit coronary artery lesion, for which a Gradient Boosting model was optimised to predict. The algorithm was then validated in two independent European cohorts comprising 568 patients (346 and 222 patients respectively). Results The development cohort consisted of 398 patients (median age 64.3 years [IQR 53.3-75.4], 74.6% male), and the two validation cohorts consisted of 346 patients (median age 63.0 years [IQR 55.0-73.0], 81.5% male) and 222 patients (median age 63.0 years [IQR 52.0-74.0], 77.0% male). Of all patients, 85.6% had a witnessed arrest, 69.6% received bystander cardiopulmonary resuscitation, and 77.3% had an initial shockable rhythm. A culprit lesion was observed in 67.4% patients receiving early coronary angiography in the development cohort, and 67.9% and 61.1% in the two validation cohorts respectively. A Gradient Boosting model yielded an algorithm, named KOCAR Culprit Predictor, incorporating nine variables including age, a localising feature on ECG (≥2mm of ST change in contiguous leads), regional wall motion abnormality, history of vascular disease and initial shockable rhythm. This model had an AUC of 0.89 in the development and 0.83/0.81 in the validation cohorts with good calibration (Figure 1), and outperformed the current gold-standard ECG alone (AUC 0.69/0.67/0/67). Conclusions A novel simple machine learning derived algorithm (Figure 2) combining nine variables which are readily available to clinicians can be applied to patients with OHCA to predict a culprit coronary artery lesion with high accuracy. The algorithm, KOCAR Culprit Predictor, outperforms the current gold-standard ECG alone.Figure 1Figure 2

Abstract 17298: Deep Learning Electrocardiogram Detecting Acute Coronary Occlusion in Myocardial Infarction Presenting Without ST-Elevation

Introduction: One third of Non-ST-elevation myocardial infarction (NSTEMI) patients present with an acutely occluded culprit coronary artery (OMI), associated with poor short and long-term outcomes due to delayed identification and consequent delayed invasive management. Hypothesis: We sought to develop and validate an artificial intelligence (AI) model detecting OMI on single standard 12-lead electrocardiograms (ECGs) and compare its performance to existing standard criteria. Methods: An AI model was developed using 18,616 ECGs from 10,692 unique contacts (22.9% OMI) of 10,543 patients (age 66±14 years, 65.9% males) with acute coronary syndrome (ACS) from an international cohort. This AI model was tested on an international test set of 3,254 ECGs from 2,263 unique contacts (20% OMI) of 2,222 patients (age 62±14 years, 67% males) and compared with STEMI criteria and annotations of ECG experts in detecting OMI on 12-lead ECGs using sensitivity, specificity, predictive values and time to OMI diagnosis. OMI was based on a combination of angiographic and biomarker outcomes. Results: The AI model achieved an area under the curve (AUC) of 0.941 (95% CI: 0.926-0.954) in identifying the primary outcome of OMI, with superior performance (accuracy 90.7% [95% CI: 89.5-91.9], sensitivity 82.6% [95% CI: 78.9-86.1], specificity 92.8 [95% CI: 91.5-93.9]) compared to STEMI criteria (accuracy 84.9% [95% CI: 83.5-86.3], sensitivity 34.4% [95% CI: 30.0-38.8], specificity 97.6% [95% CI: 96.8-98.2]) and similar performance compared to ECG experts (accuracy 91.2% [95% CI: 90.0-92.4], sensitivity 75.9% [95% CI: 71.9-80.0], specificity 95.0 [95% CI: 94.0-96.0]) ( Figure 1 ). Conclusions: The present novel ECG AI model demonstrates superior accuracy in detecting acute OMI when compared to the STEMI criteria. Its external and international validation suggests its potential to improve ACS patient triage with timely referral for immediate revascularization.

The role of cardiac pericytes in health and disease: therapeutic targets for myocardial infarction.

Millions of cardiomyocytes die immediately after myocardial infarction, regardless of whether the culprit coronary artery undergoes prompt revascularization. Residual ischaemia in the peri-infarct border zone causes further cardiomyocyte damage, resulting in a progressive decline in contractile function. To date, no treatment has succeeded in increasing the vascularization of the infarcted heart. In the past decade, new approaches that can target the heart's highly plastic perivascular niche have been proposed. The perivascular environment is populated by mesenchymal progenitor cells, fibroblasts, myofibroblasts and pericytes, which can together mount a healing response to the ischaemic damage. In the infarcted heart, pericytes have crucial roles in angiogenesis, scar formation and stabilization, and control of the inflammatory response. Persistent ischaemia and accrual of age-related risk factors can lead to pericyte depletion and dysfunction. In this Review, we describe the phenotypic changes that characterize the response of cardiac pericytes to ischaemia and the potential of pericyte-based therapy for restoring the perivascular niche after myocardial infarction. Pericyte-related therapies that can salvage the area at risk of an ischaemic injury include exogenously administered pericytes, pericyte-derived exosomes, pericyte-engineered biomaterials, and pharmacological approaches that can stimulate the differentiation of constitutively resident pericytes towards an arteriogenic phenotype. Promising preclinical results from in vitro and in vivo studies indicate that pericytes have crucial roles in the treatment of coronary artery disease and the prevention of post-ischaemic heart failure.

Trombosit Dağılım Genişliği Akut Koroner Sendrom Şiddeti ve Koroner Trombüs Yükü ile İlişkili mi?

Aim: Platelets play a pivotal role in the pathogenesis of acute coronary syndrome (ACS), and platelet distribution width (PDW) shows the activities of platelets in circulation. The purpose of this study was to determine the association of PDW with the ACS severity and angiographic intracoronary thrombus burden and Thrombolysis In Myocardial Infarction (TIMI) flow grade.&#x0D; Materials and Methods: One hundred forty-nine consecutive patients who were diagnosed as having ACS were retrospectively evaluated. Global Registry of Acute Coronary Events (GRACE) scores were calculated from the clinical and laboratory data for ACS severity. TIMI flow grades and thrombus grades of the culprit coronary arteries were calculated for each patient. Patients were grouped into two groups according to their PDW values: high PDW and low PDW. The SPSS 17.0 software was used for statistical analysis. &#x0D; Results: PDW was found to be correlated with GRACE scores (P

Real time three-dimensional transthoracic echocardiographic segmental volume analysis: quantitative and objective tool for assessing regional wall motion abnormalities in ischemic heart disease

Abstract Funding Acknowledgements Type of funding sources: None. Background Evaluation of regional wall motion abnormality (RWMA) by 2D echocardiography (2DE) plays an important role in the diagnosing ischemic heart disease (IHD). However, 2DE is disadvantaged by being subjective, semi-quantitative, and expert-dependent. Recently, a method of measuring LV segmental volume by 3DE has been introduced, which enabled volume changes in LV regional to be measured. This study aimed to demonstrate the clinical usefulness of 3DE segmental volume analysis as an objective and quantitative tool for assessing RWMA in patients with IHD. Methods 33 patients with ischemic heart disease confirmed by coronary aniography and showing single vessel territory RWMA by 2DE were retrospectively enrolled. In the 2DE study, RWMAs were evaluated visually by and experienced physicians, and 17-segment bull's-eye polar maps were generated using a two-point scale, viz. 'normal' (showing normal contractility) or 'abnormal' (showing hypokinesis or akinesis). Culprit vessel territories were specified by a physician based on typical coronary artery distributions. In the 3DE study, two independent observers analyzed data using QLAB 3D quantification advanced software (version 10.0, Philips Healthcare). Segmental volumes of 17 LV segments were measured using a predetermined algorithm, and segmental volume ejection fractions (SVEFs) were calculated. Receiver operating characteristic (ROC) curve analysis was used to determine the SVEF cut-off value that best differentiated 'normal' and 'abnormal'. Using this cut-off value, 17-segment bull's-eye polar maps were generated. Reliability of correct predicting the culprit coronary arteries by 3DE bull's-eyes compared to 2DE ones was evaluated using Cohen's kappa co-efficients, which were also used for inter- and intra-observer variability analysis of 3DE bull's-eye derived culprit coronary artery predictions. Results Mean 3DE SVEFs were significantly lower for segments showing RWMA by 2DE. Additionally, among the segments determined to be normal by 2DE, 3D basal segmental EF is statistically lower than mid- and apical ones. The optimum SVEF cut-off value was 44%, with a sensitivity of 75.0% and a specificity of 73.9% (AUC = 0.801, 95% CI 0.763–0.838, p&amp;lt;0.001). The reliability of 3DE bull's-eye derived culprit coronary artery predictions was 81.8% (kappa = 0.672, 95% CI 0.555–0.789, p&amp;lt;0.001). Inter- and intra-observer variabilities of 3DE bull's-eye derived culprit coronary artery predictions were 97.0% (kappa = 0.947, 95% CI 0.894–0.100, p&amp;lt;0.001) and 93.9% (kappa = 0.897, 95% CI 0.827–0.967, p&amp;lt;0.001), respectively. Conclusion Assessment of RWMA using 3D echocardiographic segmental volume analysis was found to be feasible and reproducible, and its predictions of culprit coronary arteries well matched those of 2DE. 3DE segmental volume analysis could be used as a quantitative and objective tool for assessing RWMA in ischemic heart disease patients.

Peripheral atherosclerosis in acute coronary syndrome patients with plaque rupture vs plaque erosion: A prospective coronary optical coherence tomography and peripheral ultrasound study

Plaque rupture (PR) and plaque erosion (PE) are two distinct, different, and most common culprit lesion morphologies responsible for acute coronary syndrome (ACS). However, the prevalence, distribution, and characteristics of peripheral atherosclerosis in ACS patients with PR vs PE has never been studied. The aim of this study was to assess peripheral atherosclerosis burden and vulnerability evaluated by vascular ultrasound in ACS patients with coronary PR versus PE identified by optical coherence tomography (OCT). Between October 2018 and December 2019, 297 ACS patients who underwent preintervention OCT examination of the culprit coronary artery were enrolled. Peripheral ultrasound examinations of carotid, femoral, and popliteal arteries were performed before discharge. Overall, 265/297 (89.2%) patients had at least one atherosclerotic plaque in a peripheral arterial bed. Compared with coronary PE, patients with coronary PR had a higher prevalence of peripheral atherosclerotic plaques (93.4% vs 79.1%, P<0.001), regardless of location: carotid, femoral, or popliteal arteries. The number of peripheral plaques per patient was significantly larger in the coronary PR group than coronary PE (4 [2-7] vs 2 [1-5], P<0.001). Additionally, there was a greater prevalence of peripheral vulnerable characteristics including plaque surface irregularity, heterogeneous plaque, and calcification in patients with coronary PR versus PE. Peripheral atherosclerosis exists commonly in patients presenting with ACS. Patients with coronary PR had greater peripheral atherosclerosis burden and more peripheral vulnerability compared to those with coronary PE, suggesting that comprehensive evaluation of peripheral atherosclerosis and multidisciplinary cooperative management maybe necessary, especially in patients with PR. clinicaltrials.gov (NCT03971864).

Strain Rate Changes during Stress Echocardiography Are the Most Accurate Predictors of Significant Coronary Artery Disease in Patients with Previously Treated Acute Coronary Syndrome.

Dobutamine stress echocardiography (DSE) is a well-established non-invasive investigation for the detection of ischemic myocardial dysfunction. The aim of this study was to evaluate the accuracy of myocardial deformation parameters measured by speckle tracking echocardiography (STE) in predicting culprit coronary artery lesions in patients with prior revascularization and acute coronary syndrome (ACS). We prospectively studied 33 patients with ischemic heart disease, a history of at least one episode of ACS and prior revascularization. All patients underwent a complete stress Doppler echocardiographic examination, including the myocardial deformation parameters of peak systolic strain (PSS), peak systolic strain rate (SR) and wall motion score index (WMSI). The regional PSS and SR were analyzed for different culprit lesions. The mean age of patients was 59 ± 11 years and 72.7% were males. At peak dobutamine stress, the change in regional PSS and SR in territories supplied by the LAD showed smaller increases compared to those in patients without culprit LAD lesions (p < 0.05 for all). Likewise, the regional parameters of myocardial deformation were reduced in patients with culprit LCx lesions compared to those with non-culprit LCx lesions and in patients with culprit RCA legions compared to those with non-culprit RCA lesions (p < 0.05 for all). In the multivariate analysis, the △ regional PSS (1.134 (CI = 1.059-3.315, p = 0.02)) and the △ regional SR (1.566 (CI = 1.191-9.013, p = 0.001)) for LAD territories predicted the presence of LAD lesions. Similarly, in a multivariable analysis, the △ regional PSS and the △SR predicted LCx culprit lesions and RCA culprit lesions (p < 0.05 for all). In an ROC analysis, the PSS and SR had higher accuracies compared to the regional WMSI in predicting culprit lesions. A △ regional SR of -0.24 for the LAD territories was 88% sensitive and 76% specific (AUC = 0.75; p < 0.001), a △ regional PSS of -1.20 was 78% sensitive and 71% specific (AUC = 0.76, p < 0.001) and a △ WMSI of -0.35 was 67% sensitive and 68% specific (AUC = 0.68, p = 0.02) in predicting LAD culprit lesions. Similarly, the △ SR for LCx and RCA territories had higher accuracies in predicting LCx and RCA culprit lesions. The myocardial deformation parameters, particularly the change in regional strain rate, are the most powerful predictors of culprit lesions. These findings strengthen the role of myocardial deformation in increasing the accuracy of DSE analyses in patients with prior cardiac events and revascularization.

A machine learning algorithm to predict a culprit lesion after out of hospital cardiac arrest.

We aimed to develop a machine learning algorithm to predict the presence of a culprit lesion in patients with out-of-hospital cardiac arrest (OHCA). We used the King's Out-of-Hospital Cardiac Arrest Registry, a retrospective cohort of 398 patients admitted to King's College Hospital between May 2012 and December 2017. The primary outcome was the presence of a culprit coronary artery lesion, for which a gradient boosting model was optimized to predict. The algorithm was then validated in two independent European cohorts comprising 568 patients. A culprit lesion was observed in 209/309 (67.4%) patients receiving early coronary angiography in the development, and 199/293 (67.9%) in the Ljubljana and 102/132 (61.1%) in the Bristol validation cohorts, respectively. The algorithm, which is presented as a web application, incorporates nine variables including age, a localizing feature on electrocardiogram (ECG) (≥2 mm of ST change in contiguous leads), regional wall motion abnormality, history of vascular disease and initial shockable rhythm. This model had an area under the curve (AUC) of 0.89 in the development and 0.83/0.81 in the validation cohorts with good calibration and outperforms the current gold standard-ECG alone (AUC: 0.69/0.67/0/67). A novel simple machine learning-derived algorithm can be applied to patients with OHCA, to predict a culpritcoronary artery disease lesion with high accuracy.

Identification of Optical Coherence Tomography-Defined Coronary Plaque Erosion by Preprocedural Computed Tomography Angiography.

Background A previous coronary computed tomography (CT) angiographic study failed to discriminate optical coherence tomography-defined intact fibrous cap culprit lesions (IFC group) from those with ruptured fibrous caps (RFC group) in patients with coronary artery disease. This study aimed to evaluate the diagnostic efficacy of preprocedural coronary CT imaging in identifying subsequently performed optical coherence tomography-defined plaque rupture or erosion at culprit lesions in patients with non-ST-segment-elevation acute myocardial infarction. Methods and Results This study used data from 2 recently published studies that tested the hypothesis that coronary CT angiography (CCTA) before percutaneous coronary intervention may provide diagnostic information on the high-risk atherosclerotic burden in patients with non-ST-segment-elevation acute myocardial infarction. In the analysis of 186 patients, optical coherence tomography identified 106 RFC plaques and 80 IFC plaques as the culprit lesions. On CT, the prevalence of low-attenuation plaque, positive remodeling, napkin-ring sign, and spotty calcification were all significantly lower in the IFC group. The culprit vessel pericoronary adipose tissue inflammation and coronary artery calcium scores were significantly lower in the IFC group than in the RFC group. The absence of low-attenuation plaque, napkin-ring sign, zero coronary artery calcium, and low pericoronary adipose tissue inflammation were independent predictors of IFC. When stratified into 5 subgroups according to the number of these 4 CT factors, the prevalence of IFC was 8.3%, 20.8%, 44.6%, 75.6%, and 100% (P<0.001), respectively. Conclusions Preprocedural comprehensive coronary CT imaging, including coronary artery calcium and pericoronary adipose tissue inflammation assessment, can accurately and noninvasively identify optical coherence tomography-defined IFC or RFC culprit lesions.

Characterization of Systemic and Culprit-Coronary Artery miR-483-5p Expression in Chronic CAD and Acute Myocardial Infarction Male Patients.

Coronary artery disease (CAD) is the leading cause of mortality worldwide. In chronic and myocardial infarction (MI) states, aberrant levels of circulating microRNAs compromise gene expression and pathophysiology. We aimed to compare microRNA expression in chronic-CAD and acute-MI male patients in peripheral blood vasculature versus coronary arteries proximal to a culprit area. Blood from chronic-CAD, acute-MI with/out ST segment elevation (STEMI/NSTEMI, respectively), and control patients lacking previous CAD or having patent coronary arteries was collected during coronary catheterization from peripheral arteries and from proximal culprit coronary arteries aimed for the interventions. Random coronary arterial blood was collected from controls; RNA extraction, miRNA library preparation and Next Generation Sequencing followed. High concentrations of microRNA-483-5p (miR-483-5p) were noted as 'coronary arterial gradient' in culprit acute-MI versus chronic-CAD (p = 0.035) which were similar to controls versus chronic-CAD (p < 0.001). Meanwhile, peripheral miR-483-5p was downregulated in acute-MI and chronic-CAD, compared with controls (1.1 ± 2.2 vs. 2.6 ± 3.3, respectively, p < 0.005). A receiver operating characteristic curve analysis for miR483-5p association with chronic CAD demonstrated an area under the curve of 0.722 (p < 0.001) with 79% sensitivity and 70% specificity. Using in silico gene analysis, we detected miR-483-5p cardiac gene targets, responsible for inflammation (PLA2G5), oxidative stress (NUDT8, GRK2), apoptosis (DNAAF10), fibrosis (IQSEC2, ZMYM6, MYOM2), angiogenesis (HGSNAT, TIMP2) and wound healing (ADAMTS2). High miR-483-5p 'coronary arterial gradient' in acute-MI, unnoticed in chronic-CAD, suggests important local mechanisms for miR483-5p in CAD in response to local myocardial ischemia. MiR-483-5p may have an important role as a gene modulator for pathologic and tissue repair states, is a suggestive biomarker, and is a potential therapeutic target for acute and chronic cardiovascular disease.