Culprit Coronary Lesion Research Articles

Circulating nucleases degrade high-molecular-weight cell-free DNA in coronary vessels during acute myocardial infarction

Abstract Introduction Extracellular cell-free DNA (cfDNA) originates from various biological processes, including cell turnover, apoptosis, necrosis, NETosis, and other forms of cell death. In healthy individuals, highly fragmented cfDNA is elevated in the bloodstream due to infection, cancer, inflammation and thrombosis. In thrombotic vascular diseases, neutrophils release elongated, high-molecular-weight DNA with bioactive and prothrombotic properties in a process termed NETosis. Circulating nucleases are thought to counteract pathogenic properties of NETs. However, attempts to connect total cfDNA concentration to nuclease activity have failed. Purpose We aimed to elucidate the in vivo connection between extracellular DNA and circulating nucleases in thrombotic vascular diseases by investigating DNA length as a potential novel biomarker in cardiovascular disease. Methods Citrated plasma from healthy volunteers (n=363) and from ST-elevation myocardial infarction (MI) coronary aspirates (n=59) and peripheral arterial sites (n=96) were analyzed for DNA concentration, length, and nuclease activity. Total DNA concentration was measured with a fluorescent DNA binding dye, and elongated DNA assessed using qPCR and Agilent bioanalyzer high-sensitivity DNA chip. Nuclease activity was measured by single radial enzyme-diffusion (SRED) assay. Cardiac MRI assessed infarct size acutely and six months after the event. Results Coronary aspirates exhibited an elevation in total DNA, with a significant rise in high-molecular weight cell-free DNA in addition to an increase in sub-nucleosome fragmentation (Figure 1). Peripheral and coronary plasma samples from individuals with myocardial infarction (MI) showed elevated levels of total and elongated cfDNA. When compared to healthy individuals, the integrity of cfDNA was lower in peripheral samples and higher in coronary aspirates. During myocardial infarction, circulating nuclease activity was elevated systemically but low at the coronary culprit lesion site. Elongated high-molecular-weight cfDNA accumulates primarily in coronary vessels but is also elevated systemically. In coronary aspirates, nuclease activity negatively correlated with elongated DNA and DNA integrity (rs=0.6255, p<0.0001). Conclusions Elongated DNA accumulates during MI at the culprit lesion site. Its inverse correlation with nuclease activity underscores the role of nucleases in cleaving elongated DNA to shorter, soluble fragments. This study establishes DNA length and integrity as novel biomarkers in thrombotic cardiovascular disease.Figure 1:Coronary cfDNA lengthFigure 2:Nuclease activity and cfDNA

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.

High-sensitivity troponin T for detection of culprit lesions in patients with out-of-hospital cardiac arrest.

Patients with an out-of-hospital cardiac arrest (OHCA) often undergo coronary angiography, although a culprit lesion is found in only 30%-40% of patients. The aim of this study was to investigate high-sensitivity troponin T (hsTnT) levels in post cardiac arrest patients with and without coronary culprit lesions; factors affecting hsTnT levels after return of spontaneous circulation (ROSC); and the diagnostic ability of hsTnT in identifying patients with culprit lesions. We hypothesized that peak hsTnT levels were higher during the initial 48 h after cardiac arrest in patients with a coronary culprit lesion. This was a retrospective observational study, which included patients admitted to the Intensive Care Unit after an OHCA and who received a coronary angiography. Peak values and dynamic changes in hsTnT were analyzed in relation to the presence of a culprit lesion at coronary angiography. A total of 238 patients were studied, of whom 140 had a culprit lesion. HsTnT levels during the initial 48 h were higher in patients with culprit lesions, longer time to ROSC and an unwitnessed cardiac arrest. At 6 to 12 h after ROSC, a hsTnT cut-off level of 1690 ng/L had a sensitivity of 64% and specificity of 84% to identify a culprit lesion. In patients without ST-elevations, hsTnT measured between 6 and 12 h after ROSC had a specificity above 90%, with a sensitivity of 46%. HsTnT levels after cardiac arrest are higher in patients with coronary culprit lesions. Presence of a culprit lesion, witnessed status and the duration of CPR are important factors affecting hsTnT levels. Repeated measurement of hsTnT within the first 12 h after admission improved diagnostic accuracy but the value of hsTnT as a predictor of culprit lesions early after OHCA is limited.

A Review Paper on Optical Coherence Tomography Evaluation of Coronary Calcification Pattern: Is It Relevant Today?

The process of coronary calcification represents one of the numerous pathophysiological mechanisms involved in the atherosclerosis continuum. Optical coherence tomography (OCT) represents an ideal imaging modality to assess plaque components, especially calcium. Different calcification patterns have been contemporarily described in both early stages and advanced atherosclerosis. Microcalcifications and spotty calcifications correlate positively with macrophage burden and inflammatory markers and are more frequently found in the superficial layers of ruptured plaques in acute coronary syndrome patients. More compact, extensive calcification may reflect a later stage of the disease and was traditionally associated with plaque stability. Nevertheless, a small number of culprit coronary lesions demonstrates the presence of dense calcified plaques. The purpose of the current paper is to review the most recent OCT data on coronary calcification and the interrelation between calcification pattern and plaque vulnerability. How different calcified plaques influence treatment strategies and associated prognostic implications is of great interest.

ACUTE CORONARY SYNDROME IN A PATIENT WITH LEFT SUBCLAVIAN OCCLUSION AND ANTEROLATERAL CORONARY STEAL

Abstract This is a 57–year–old male patient suffering from multiple cardiovascular risk factors: obesity, arterial hypertension, dyslipidemia, type 2 diabetes mellitus, active smoker. Chronic obstructive pulmonary disease. Stage 2 chronic kidney disease. Peripheral vascular disease with previous bilateral thromboendarterectomy and percutaneous revascularization of the lower limbs. Stable angina for which three years ago he underwent Coronary Artery Bypass Graft: left internal mammary artery (LIMA) to left anterior descending artery combined with saphenous vein grafts to the main obtuse marginal branch. The patient presented with Acute Coronary Syndrome non ST–segment elevation myocardial infarction (N–STEMI), intermittent episodes of chest pain due to mild exertion in the previous days. Antero–lateral ST depression and inverted T waves, associated with a mild reduction in left ventricular systolic function due to hypokinesia of the antero–lateral walls and increased troponin values were present. Coronary angiography documented patency of the LIMA graft without evidence of any culprit lesions on the coronary branches. However, selective angiography documented a sub–occlusion of the proximal left subclavian artery (Figure 1). A computed tomography scan confirmed a hyperdense calcified plaque occluding 95% of the origin of the left subclavian artery. The patient then underwent angioplasty with stenting of the left subclavian artery (Figure 2). Subclavian coronary steal syndrome usually presents with exertional angina, but rarely can cause Acute Coronary Syndrome. During coronary angiography performed for Acute Coronary Syndrome and in the absence of detection of clear coronary culprit lesions, selective angiography of the subclavian artery may confirm the suspicion of coronary steal syndrome.

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.

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

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 Coronary Culprit Lesion in ST Elevation Myocardial Infarction by Using Deep Learning.

Early revascularization of the occluded coronary artery in patients with ST elevation myocardial infarction (STEMI) has been demonstrated to decrease mortality and morbidity. Currently, physicians rely on features of electrocardiograms (ECGs) to identify the most likely location of coronary arteries related to an infarct. We sought to predict these culprit arteries more accurately by using deep learning. A deep learning model with a convolutional neural network (CNN) that incorporated ECG signals was trained on 384 patients with STEMI who underwent primary percutaneous coronary intervention (PCI) at a medical center. The performances of various signal preprocessing methods (short-time Fourier transform [STFT] and continuous wavelet transform [CWT]) with different lengths of input ECG signals were compared. The sensitivity and specificity for predicting each infarct-related artery and the overall accuracy were evaluated. ECG signal preprocessing with STFT achieved fair overall prediction accuracy (79.3%). The sensitivity and specificity for predicting the left anterior descending artery (LAD) as the culprit vessel were 85.7% and 88.4%, respectively. The sensitivity and specificity for predicting the left circumflex artery (LCX) were 37% and 99%, respectively, and the sensitivity and specificity for predicting the right coronary artery (RCA) were 88.4% and 82.4%, respectively. Using CWT (Morlet wavelet) for signal preprocessing resulted in better overall accuracy (83.7%) compared with STFT preprocessing. The sensitivity and specificity were 93.46% and 80.39% for LAD, 56% and 99.7% for LCX, and 85.9% and 92.9% for RCA, respectively. Our study demonstrated that deep learning with a CNN could facilitate the identification of the culprit coronary artery in patients with STEMI. Preprocessing ECG signals with CWT was demonstrated to be superior to doing so with STFT.

Factors predicting cardiac arrest in acute coronary syndrome patients under 50: A state-wide angiographic and forensic evaluation of outcomes

BackgroundAn uncertain proportion of patients with acute coronary syndrome (ACS) also experience out-of-hospital cardiac arrest (OHCA). Predictors of OHCA in ACS remain unclear and vulnerable to selection bias as pre-hospital deceased patients are usually not included. MethodsData on patients aged 18–50 years from a percutaneous coronary intervention (PCI) and OHCA registry were combined to identify all patients experiencing OHCA due to ACS (not including those managed medically or who proceeded to cardiac surgery). Clinical, angiographic and forensic details were collated. In-hospital and post-discharge outcomes were compared between OHCA survivors and non-OHCA ACS patients. ResultsOHCA occurred in 6.0% of ACS patients transported to hospital and 10.0% of all ACS patients. Clinical predictors were non-diabetic status (p = 0.015), non-obesity (p = 0.004), ST-elevation myocardial infarction (p < 0.0001) and left main (p < 0.0002) or left anterior descending (LAD) coronary artery (p < 0.0001) as culprit vessel. OHCA patients had poorer in-hospital clinical outcomes, including longer length of stay and higher pre-procedural intubation, cardiogenic shock, major adverse cardiovascular events, bleeding, and mortality (p < 0.0001 for all). At 30 days, OHCA survivors had equivalent cardiac function and return to premorbid independence but higher rates of anxiety/depression (p = 0.029). ConclusionOHCA complicates approximately 10% of ACS in the young. Predictors of OHCA are being non-diabetic, non-obese, having a STEMI presentation, and left main or LAD coronary culprit lesion. For OHCA patients surviving to PCI, higher rates of in-hospital complications are observed. Despite this, recovery of pre-morbid physical and cardiac function is equivalent to non-OHCA patients, apart from higher rates of anxiety/depression.

Assessment of Papillary Muscle Infarction with Dark-Blood Delayed Enhancement Cardiac MRI in Canines and Humans.

Background The relationship between papillary muscle infarction (papMI) and the culprit coronary lesion has not been fully investigated. Delayed enhancement cardiac MRI may detect papMI, yet its accuracy is unknown. Flow-independent dark-blood delayed enhancement (FIDDLE) cardiac MRI has been shown to improve the detection of myocardial infarction adjacent to blood pool. Purpose To assess the diagnostic performance of delayed enhancement and FIDDLE cardiac MRI for the detection of papMI, and to investigate the prevalence of papMI and its relationship to the location of the culprit coronary lesion. Materials and Methods A prospective canine study was used to determine the accuracy of conventional delayed enhancement imaging and FIDDLE imaging for detection of papMI, with pathology-based findings as the reference standard. Participants with first-time myocardial infarction with a clear culprit lesion at coronary angiography were prospectively enrolled at a single hospital from 2015 to 2018 and compared against control participants with low Framingham risk scores. In canines, diagnostic accuracy was calculated for delayed enhancement and FIDDLE imaging. Results In canines (n = 27), FIDDLE imaging was more sensitive (100% [23 of 23] vs 57% [13 of 23], P < .001) and accurate (100% [54 of 54] vs 80% [43 of 54], P = .01) than delayed enhancement imaging for detection of papMI. In 43 participants with myocardial infarction (mean age, 56 years ± 16 [SD]; 28 men), the infarct-related artery was the left anterior descending coronary artery (LAD), left circumflex coronary artery (LCX), and right coronary artery in 47% (20 of 43), 26% (11 of 43), and 28% (12 of 43), respectively. The prevalence of anterior papMI was lower than posterior papMI (37% [16 of 43 participants] vs 44% [19 of 43 participants]) despite more LAD culprit lesions. Culprits leading to papMI were restricted to a smaller "at-risk" portion of the coronary tree for anterior papMI (subtended first diagonal branch of the LAD or first marginal branch of the LCX) compared with posterior (subtended posterior descending artery or third obtuse marginal branch of the LCX). Culprits within these at-risk portions were predictive of papMI at a similar rate (anterior, 83% [15 of 18 participants] vs posterior, 86% [18 of 21 participants]). Conclusion Flow-independent dark-blood delayed enhancement cardiac MRI, unlike conventional delayed enhancement cardiac MRI, was highly accurate in the detection of papillary muscle infarction (papMI). Anterior papMI was less prevalent than posterior papMI, most likely due to culprit lesions being restricted to a smaller portion of the coronary tree rather than because of redundant, dual vascular supply. © RSNA, 2022 Online supplemental material is available for this article. See also the editorial by Kawel-Boehm and Bremerich in this issue.

Coronary angiographic findings for out-of-hospital cardiac arrest survivors presenting with nonshockable rhythms and no ST elevation post resuscitation

BackgroundRecent guidelines suggest that coronary angiography (CAG) should be considered for out-of-hospital cardiac arrest (OHCA) survivors, including those without ST elevation (STE) and without shockable rhythms. However, there is no prospective data to support CAG for survivors with nonshockable rhythms and no STE post resuscitation. MethodsThis was a re-analysis of the PEARL study (randomized OHCA survivors without STE to early CAG versus not). Patients were subdivided by initial rhythm as nonshockable (Nsh) vs shockable (Sh). The primary outcome was coronary angiographic evidence of acute culprit lesion, with secondary outcomes being survival to hospital discharge and neurological recovery. ResultsThe PEARL study included 99 patients with OHCA from a presumed cardiac etiology, 24 with nonshockable and 75 with shockable rhythms. There was no difference in the frequency of CAG between the two groups [71% (Nsh) and 75% (Sh); p = 0.79], presence of CAD [81% (Nsh) and 68% (sh); p = 0.37, or culprit lesions identified in each group [50% (Nsh) and 45% (Sh); p = 0.78. Nonshockable patients had worse discharge survival [33% (Nsh) vs 57% (Sh); p = 0.04] and those survived, had worse neurological recovery [30% (Nsh) vs 54% (Sh); p = 0.02] compared to shockable patients. ConclusionsOHCA survivors presenting with nonshockable rhythms and no STE post resuscitation had similar prevalence of culprit coronary lesions to those with shockable rhythms. CAG may be considered in patients with OHCA without STE regardless of initial presenting rhythm. There was no benefit of emergent CAG both in shockable and non-shockable rhythms.

Coronary Angiographic Findings in Survivors of Sudden Cardiac Arrest at Nicvd Karachi

Background: The most recent guidelines advocate an immediate coronary angiography [1] for those who have survived a cardiac arrest and are still exhibiting electrocardiographic indications of ischemia. Recovered cardiac patients who don't show signs of ongoing ischemia may nonetheless need an emergency angiography, according to the same recommendations. Conventional ECG is ineffective in diagnosing if coronary culprit lesions are present during an angiography, according to earlier study [2]. As a result, some believe that all patients who are resuscitated after a cardiac arrest should undergo an urgent cardiac catheterization. [3]. Objective: To determine the frequency of coronary angiographic findings in survivors of sudden cardiac arrest. Materials and methods: We included all patients who satisfied the study's criteria and visited the NICVD in Karachi for treatment. After a thorough explanation of the study's procedures, risks, and benefits, participants agreed to participate. The results of coronary angiography were recorded for each patient. The form at the end contained all of the information that had been acquired and was used electronically for research purposes. Results: Mean ± SD of age was 51.4±10.6 years. In distribution of gender, 142 (67.6%) were male while 68 (32.4%) were female. left anterior descending (LAD) as noted in 104 (49.5%) patients, left circumflex artery (LCX) in 31 (14.8%), 52 (24.8%) had right coronary artery (RCA) while left main artery (LMA) was found in 23 (10.9%) patients. Conclusion: It is to be concluded that left anterior descending noted as most common coronary angiographic finding followed by right coronary artery and left circumflex artery. Epidemiological and research data should be expanded by further studies to validate the current findings. Keywords: Acute Coronary Syndrome, Angiographic Findings, CABG, Cardiac, Arrest, Survivors, Percutaneous Coronary Intervention

Analysis of the Guiding Role of CYP2C19 Gene Combined With Platelet Function Detection in Antiplatelet Therapy in Patients With Complex Coronary Artery Disease After PCI.

ObjectiveTo explore the influence of CYP2C19 gene combined with platelet function test on clinical prognosis of patients with complex coronary artery disease receiving antiplatelet therapy after PCI.MethodsA total of 200 patients undergoing PCI in our hospital due to complex coronary artery disease from February 2019 to February 2021 were selected and divided into the control group and the observation group according to whether CYP2C19 gene detection was performed. The control group was treated with dual antiplatelet therapy of classical aspirin combined with clopidogrel, and the observation group was treated with individual antiplatelet therapy. The patients in the two groups were followed up for 1 year after PCI, and their quality of life was assessed using the Seattle Angina Questionnaire (SAQ score). The occurrence of major adverse cardiovascular events (MACE) during the follow-up period was also recorded.ResultsThe incidence of total MACE events in the observation group was slightly less than that in the control group, and the difference was statistically significant (P = 0.040). In particular, the observation group was superior to the control group in reducing the readmission rate of recurrent unstable angina pectoris, and the difference was statistically significant (P = 0.023). The location of coronary culprit lesions with recurrent ischemic events was commonly seen in non-interventional target lesions (interventional/non-interventional target sites: 12.9%: 77.1%). The SAQ score in the observation group was larger than that in the control group, and the difference was statistically significant (P = 0.012). There was no statistical difference in the incidence of major bleeding between the two groups (P = 0.352).ConclusionUsing CYP2C19 genotype combined with platelet function test to guide individualized antiplatelet therapy after complex coronary artery PCI is beneficial to reducing ischemic events in a short period (1 year), mainly due to reducing the risk of readmission for recurrent unstable angina pectoris, and improving the quality of daily life of patients without increasing the risk of massive hemorrhage, which can improve clinical prognosis.

Clinical Significance of Early Echocardiographic Changes after Resuscitated Out-of-Hospital Cardiac Arrest

BackgroundLeft Ventricular Systolic Dysfunction (LVSD) is common after out-of-hospital cardiac arrest (OOHCA) and can manifest globally or regionally, although its clinical significance has not been robustly studied. This study evaluates the association between LVSD, extent of coronary artery disease (CAD) and outcome in those undergoing early echocardiography and coronary angiography after OOHCA. MethodsTrans-thoracic echocardiography (TTE) was performed in OOHCA patients on arrival to our centre between May 2012 and December 2017. Rates of cardiogenic shock and extent of CAD, respectively classified by SCAI grade and the SYNTAX score, were measured. The primary end-point was 12-month mortality. ResultsFrom 398 patients in the King’s Out of Hospital Cardiac Arrest Registry (KOCAR), 266 patients (median age 61 [53–71], 76% male) underwent both TTE and coronary angiography on arrival. 96 patients (36%) had significant LVSD (Left Ventricular Ejection Fraction [LVEF] <40%) and 139 (52.2%) patients had regional wall motion abnormalities (RWMAs). Patients with LVEF <40% had more SCAI grade C-E shock (65.3% vs. 34.5%, p <0.001) and higher 12-month mortality (55.2% vs 31.8%, p <0.001) which was more likely to be due to a cardiac aetiology (27.3% vs 5.3%, p <0.001). Patients with RWMAs had higher median SYNTAX scores (14.75 vs 7, p=0.001), culprit coronary lesions (83.5% vs. 45.3%, p <0.001) and lower 12-month mortality (29.5% vs 52%, p <0.001). ConclusionsPatients with LVEF <40% at presentation have an increased mortality, driven by cardiac aetiology death, while the presence of RWMAs is associated with a higher rate of culprit coronary lesions, representing a potentially reversible cause of the arrest, and improved survival at 1 year.

Impact of triglyceride levels on plaque characteristics in patients with coronary artery disease

BackgroundHigh triglyceride (TG) levels have been demonstrated to be a risk factor for coronary artery disease. This study aimed to clarify the impact of TG levels on the characteristics of coronary plaques. MethodsA total of 850 consecutive patients who underwent optical coherence tomography (OCT) imaging of the culprit lesion were included. The morphologies of culprit plaques were compared between the higher TG group (nonfasting TG levels ≥150 mg/dL, n = 337) and the lower TG group (nonfasting TG <150 mg/dL, n = 513). ResultsThe prevalence of lipid-rich plaques (43% vs. 33%, p = 0.005), thin-cap fibroatheromas (TCFAs) (24% vs. 17%, p = 0.015) and macrophages (40% vs. 31%, p = 0.006) was significantly higher in the higher TG group than in the lower TG group. In addition to a high low-density lipoprotein cholesterol (LDL-C) level (≥140 mg/dL), high TGs (≥150 mg/dL) were identified as an independent factor for the presence of TCFAs (odds ratio 1.465, 95% confidence interval 1.004–2.137, p = 0.048). Among patients with lower LDL-C levels (<100 mg/dL), the prevalence of macrophages (38% vs. 26%, p = 0.007) and layered plaques (48% vs. 38%, p = 0.019) was significantly higher in the higher TG group than in the lower TG group. ConclusionsHigher TG levels were associated with a higher prevalence of TCFAs in culprit coronary lesions. The prevalence of macrophages and layered plaques was more frequently observed in patients with higher TGs than those with lower TGs among patients with LDL-C < 100 mg/dL.

Longitudinal change in cardiac structure and function following acute coronary syndrome according to culprit coronary artery lesion.

Acute coronary syndrome (ACS) may lead to adverse remodelling and impaired cardiac function. Limited data exists on the effect of culprit coronary artery lesion site and impact on longitudinal cardiac remodelling. The present study included a total of 299 patients suffering from ACS treated with percutaneous coronary intervention (PCI). All patients had two echocardiographic examinations. The first echocardiography was median 2(IQR: 1;3) days following PCI, while the follow-up echocardiography (FUE) was median 257(IQR: 96;942) days following the first. Patients were grouped based on coronary artery PCI location; left anterior descending artery (LAD), right coronary artery (RCA) or circumflex artery (Cx). Patients with multiple lesions were excluded. Mean age was 63 ± 11years and 77% were male. At FUE, mean left ventricular ejection fraction was 42 ± 9% and global longitudinal strain (GLS) was -13 ± 4%. PCI treatment was allocated as 168 LAD lesions, 95 RCA lesions, and 36 Cx lesions. Linear regression analysis showed that patients with a LAD lesion displayed worsening in E/A (mean ∆ = 0.05, β = -0.196, p = 0.001) and a larger increase in LVEDV (mean ∆ = 33.18mL, β = 0.135, p = 0.012). Meanwhile patients with Cx lesion were significantly associated with a larger decrease in E/e' (mean ∆ = 2.6, β = -0.120, p = 0.028). Patients with Cx lesion were observed to have elevated E/e' at baseline, which normalized at FUE. The present study suggests that culprit coronary artery lesion has a differential impact on myocardial remodelling. This information may potentially aid in understanding the pathophysiological differences in cardiac structure and function amongst patients with ACS.

Abstract 13573: Prediction of Culprit Lesions in Acute Coronary Syndrome Based Upon Myocardial Mass At-Risk From Coronary CT Angiography

Introduction: Stratifying patients with coronary artery disease (CAD) remains challenging. Assessing CAD using myocardial mass at-risk may help identify patients at higher risk of acute coronary syndrome. Hypothesis: This study investigated whether quantitative myocardial mass at-risk (MMAR) can improve prognostication of future culprit coronary lesions at the time of acute coronary syndrome (ACS) events. Methods: From the multicenter, international ICONIC study, 49 patients suspected of coronary artery disease (CAD) going coronary CT angiography imaging (CCTA) were followed to the occurrence of the first ACS. At the time of ACS, culprit lesion was adjudicated by invasive coronary angiography by a group of cardiologists blinded to the previously acquired CCTA. MMAR was calculated for each lesion using the minimum-cost path technique, a previously validated method for calculating myocardial perfusion territories. Left ventricle myocardial segmentation and coronary centerline extraction was performed and used to calculate MMAR distal to all identifiable culprit and non-culprit coronary lesions. Results: In the study sample, 243 coronary lesions were identified on CCTA (194 non-culprit lesions; 49 culprit lesions). The mean MMAR, as a percentage of total left ventricle myocardial mass, for all lesions was 24.6±12.4%. The mean MMAR was 23.1±12.5% and 30.3±10.3% for non-culprit and culprit lesions, respectively (p&lt;0.05). Receiver operating characteristic curve analysis was performed to determine the value of MMAR in predicting a culprit lesion, with an area-under-the-curve analysis for MMAR predicting a culprit lesion of 0.68. Conclusions: MMAR is larger for lesions that will versus will not become culprit at the time of future ACS. The addition of MMAR in the assessment of CAD on CCTA may help stratify the risk of individual coronary lesions.

Atypical ST-Segment-Elevation Myocardial Infarction Presentation in Patients With COVID-19 at a High-Volume Center in New York City.

Atypical presentations of ST-segment-elevation myocardial infarction (STEMI) have been reported in patients who have COVID-19. We have seen this occurrence in our center in Bronx, New York, where multitudes of patients sought treatment for the coronavirus. We studied the prevalence of atypical STEMI findings among patients with COVID-19 who presented during the first 2 months of the pandemic. Consistent with previous reports, 4 of our 10 patients with COVID-19 and STEMI had no identifiable culprit coronary lesion; rather, they often had diffuse ST-segment elevations on surface electrocardiograms along with higher levels of D-dimer and inflammatory markers. In contrast, 32 of 33 patients without COVID-19 (97%) had a culprit lesion. The patients with COVID-19 and a culprit lesion more often needed thrombectomy catheterization and administration of glycoprotein IIb/IIIa inhibitors. Our study confirms that patients with COVID-19 often have atypical STEMI presentations, including the frequent absence of a culprit coronary lesion. Our findings can help clinicians prepare for these atypical clinical presentations.