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Predicting the risk of cardiovascular disease is the key to primary prevention. Machine learning has attracted attention in analyzing increasingly large, complex healthcare data. We assessed discrimination and calibration of pre-existing cardiovascular risk prediction models and developed machine learning-based prediction algorithms. This study included 222,998 Korean adults aged 40–79 years, naïve to lipid-lowering therapy, had no history of cardiovascular disease. Pre-existing models showed moderate to good discrimination in predicting future cardiovascular events (C-statistics 0.70–0.80). Pooled cohort equation (PCE) specifically showed C-statistics of 0.738. Among other machine learning models such as logistic regression, treebag, random forest, and adaboost, the neural network model showed the greatest C-statistic (0.751), which was significantly higher than that for PCE. It also showed improved agreement between the predicted risk and observed outcomes (Hosmer–Lemeshow χ 2  = 86.1, P < 0.001) than PCE for whites did (Hosmer–Lemeshow χ 2  = 171.1, P < 0.001). Similar improvements were observed for Framingham risk score, systematic coronary risk evaluation, and QRISK3. This study demonstrated that machine learning-based algorithms could improve performance in cardiovascular risk prediction over contemporary cardiovascular risk models in statin-naïve healthy Korean adults without cardiovascular disease. The model can be easily adopted for risk assessment and clinical decision making.

Acute coronary syndromes are commonly caused by the rupture of vulnerable plaque, which often appear angiographically not severe. Although pharmacologic management is considered standard therapy for stabilizing plaque vulnerability, the potential role of preventive local treatment for vulnerable plaque has not yet been determined. The PREVENT trial was designed to compare preventive percutaneous coronary intervention (PCI) plus optimal medical therapy (OMT) with OMT alone in patients with functionally nonsignificant high-risk vulnerable plaques. The PREVENT trial is a multinational, multicenter, prospective, open-label, active-treatment-controlled randomized trial. Eligible patients have at least 1 angiographically significant stenosis (diameter stenosis >50% by visual estimation) without functional significance (fractional flow reserve [FFR] >0.80). Target lesions are assessed by intracoronary imaging and must meet at least 2 imaging criteria for vulnerable plaque; (1) minimal lumen area <4.0 mm2; (2) plaque burden >70%; (3) maximal lipid core burden index in a 4 mm segment >315 by near infrared spectroscopy; and (4) thin cap fibroatheroma as determined by virtual histology or optical coherence tomography. Enrolled patients are randomly assigned in a 1:1 ratio to either preventive PCI with either bioabsorbable vascular scaffolds or metallic everolimus-eluting stents plus OMT or OMT alone. The primary endpoint is target-vessel failure, defined as the composite of death from cardiac causes, target-vessel myocardial infarction, ischemic-driven target-vessel revascularization, or hospitalization for unstable or progressive angina, at 2 years after randomization. Enrollment of a total of 1,608 patients has been completed. Follow-up of the last enrolled patient will be completed in September 2023 and primary results are expected to be available in early 2024. The PREVENT trial is the first large-scale, randomized trial to evaluate the effect of preventive PCI on non–flow-limiting vulnerable plaques containing multiple high-risk features that is appropriately powered for clinical outcomes. PREVENT will provide compelling evidence as to whether preventive PCI of vulnerable plaques plus OMT improves patient outcomes compared with OMT alone. URL: https://www.clinicaltrials.gov. Unique identifier: NCT02316886. The PREVENT trial is the first, large-scale randomized clinical trial to evaluate the effect of preventive PCI on non-flow-limiting vulnerable plaque with high-risk features. It will provide compelling evidence to determine whether PCI of focal vulnerable plaques on top of OMT improves patient outcomes.

Patients with unprotected left main coronary artery stenosis were assigned to either CABG or PCI with sirolimus-eluting stents. At 1 year, with a wide prespecified noninferiority margin, PCI was found to be noninferior to CABG. Anumber of registry reports, as well as a substudy from a large, randomized trial, have indicated that percutaneous coronary intervention (PCI) may be an acceptable alternative to coronary-artery bypass grafting (CABG) in some patients with unprotected left main coronary artery stenosis. 1 – 11 Recent clinical guidelines have accordingly stated that elective PCI can be considered for patients who have unprotected left main coronary artery disease, although they suggest that the aggregated evidence favors CABG. 12 , 13 Whether the outcomes after PCI are similar to those after CABG remains uncertain, however, owing to the lack of large, randomized clinical trials. Registry results have . . .

Atherosclerosis is an inflammatory process, and inflammatory biomarkers have been identified as useful predictors of clinical outcomes. The prognostic value of leukocyte count in patients with ST-segment elevation myocardial infarctions who undergo primary percutaneous coronary intervention is not clearly defined. In 325 patients with STEMIs treated with primary percutaneous coronary intervention, total and differential leukocyte counts, once at admission and 24 hours thereafter, were measured. The neutrophil/lymphocyte ratio (NLR) was calculated as the ratio of neutrophil count to lymphocyte count. The primary end point was all-cause death. Twenty-five patients (7.7%) died during follow-up (median 1,092 days, interquartile range 632 to 1,464). The total leukocyte count decreased (from 11,853 ± 3,946/μl to 11,245 ± 3,979/μl, p = 0.004) from baseline to 24 hours after admission. Patients who died had higher neutrophil counts (9,887 ± 5,417/μl vs 8,399 ± 3,639/μl, p = 0.061), lower lymphocyte counts (1,566 ± 786/μl vs 1,899 ± 770/μl, p = 0.039), and higher NLRs (8.58 ± 7.41 vs 5.51 ± 4.20, p = 0.001) at 24 hours after admission. Baseline leukocyte profile was not associated with outcomes. The best cut-off value of 24-hour NLR to predict mortality was 5.44 (area under the curve 0.72, 95% confidence interval [CI] 0.52 to 0.82). In multivariate analysis, a 24-hour NLR ≥5.44 was an independent predictor of mortality (hazard ratio 3.12, 95% CI 1.14 to 8.55), along with chronic kidney disease (hazard ratio 4.23, 95% CI 1.62 to 11.1) and the left ventricular ejection fraction (hazard ratio 0.94 for a 3% increase, 95% CI 0.76 to 0.93). In conclusion, NLR at 24 hours after admission can be used for risk stratification in patients with STEMIs who undergo primary PCI. Patients with STEMIs with 24-hour NLRs ≥5.44 are at increased risk for mortality and should receive more intensive treatment.

Ischemia–reperfusion (IR) injury accelerates myocardial injury sustained during the myocardial ischemic period and thus abrogates the benefit of reperfusion therapy in patients with acute myocardial infarction. We investigated the efficacy of intracoronary ethylenediaminetetraacetic acid (EDTA) administration as an adjunctive treatment to coronary intervention to reduce IR injury in a swine model. We occluded the left anterior descending artery for 1 h. From the time of reperfusion, we infused 50 mL of EDTA-based chelating agent via the coronary artery in the EDTA group and normal saline in the control group. IR injury was identified by myocardial edema on echocardiography. Tetrazolium chloride assay revealed that the infarct size was significantly lower in the EDTA group than in the control group, and the salvage percentage was higher. Electron microscopy demonstrated that the mitochondrial loss in the cardiomyocytes of the infarcted area was significantly lower in the EDTA group than in the control group. Echocardiography after 4 weeks showed that the remodeling of the left ventricle was significantly less in the EDTA group than in the control group: end-diastolic dimension 38.8 ± 3.3 mm vs. 43.9 ± 3.7 mm (n = 10, p  = 0.0089). Left ventricular ejection fraction was higher in the EDTA group (45.3 ± 10.3 vs. 34.4 ± 11.8, n = 10, respectively, p  = 0.031). In a swine model, intracoronary administration of an EDTA chelating agent reduced infarct size, mitochondrial damage, and post-infarct remodeling. This result warrants further clinical study evaluating the efficacy of the EDTA chelating agent in patients with ST-segment elevation myocardial infarction.

The 2017 American College of Cardiology/American Heart Association (ACC/AHA) hypertension guideline lowered the threshold defining hypertension and treatment target from 140/90 mmHg to 130/80 mmHg. We compared the 2017 ACC/AHA guideline and the Eighth Joint National Committee (JNC8) report with regard to the current status of hypertension using the Korean National Health and Nutrition Examination Survey. The association between blood pressure (BP) control and long-term major cardiovascular outcomes (MACEs) was analyzed using the Korea National Health Insurance Service cohort. In the cross-sectional study with 15,784 adults, the prevalence of hypertension was expected to be 49.2 ± 0.6% based on the definition suggested by the 2017 ACC/AHA guideline versus 30.4 ± 0.6% based on the JNC8 report. In a longitudinal analysis with 373,800 hypertensive adults for the median follow-up periods of 11.0 years, the adults meeting the target goal BP goal of 2017 ACC/AHA guideline were associated with 21% reduced risk of MACEs compared with adults, not meeting 2017 ACC/AHA BP goal but meeting JNC8 target goal. In conclusion, substantial increase of prevalence of hypertension is expected by the 2017 ACC/AHA guideline. This study also suggests endorsing the aggressive approach would lead to an improvement in cardiovascular care.

ST-segment elevation myocardial infarction (STEMI) is characterized by thrombotic coronary artery occlusions caused by atherosclerotic plaque rupture. The gut microbiome potentially contributes to the pathogenesis of coronary artery diseases. This study investigated the microbial diversity and composition of coronary thrombi in STEMI patients and the composition of the thrombus microbiome relative to that of the oral and gut microbiomes. A case–control study was performed with 22 STEMI patients and 20 age- and sex-matched healthy controls. Coronary thrombi were acquired from STEMI patients via manual thrombus aspiration during primary coronary intervention. Oral swab and stool samples were collected from both groups, and 16S rRNA sequencing and metagenomic microbiome analyses were performed. Microbial DNA was detected in 4 of 22 coronary thrombi. Proteobacteria (p) and Bacteroidetes (p) were the most abundant phyla. The oral and gut microbiomes significantly differed between patients and healthy controls. The patient group presented microbial dysbiosis, as follows: a higher relative abundance of Proteobacteria (p) and Enterobacteriaceae (f) in the gut microbiome and a lower abundance of Firmicutes (p) and Haemophilus (g) in the oral microbiome. Furthermore, 4 significantly abundant genera were observed in the coronary thrombus in the patients: Escherichia, 1.25%; Parabacteroides, 0.25%; Christensenella, 0.0%; and Bacteroides, 7.48%. The present results indicate that the relative abundance of the gut and oral microbiomes was correlated with that of the thrombus microbiome.Heart disease: microbiome linked to heart attackDisruption to microbiome composition and functioning may contribute to heart attacks. The most serious form of heart attack is ST-segment elevation myocardial infarction (STEMI), where the coronary artery is blocked by ruptured plaques. Previous research has linked cardiovascular diseases with disruption to the microbiome, but links between STEMI and the microbiome are not yet clear. Si-Hyuck Kang at Seoul National University in Seongnam-si, South Korea, and co-workers analyzed oral, fecal, and coronary thrombus (blood clot) microbial samples from 22 STEMI patients and 20 healthy controls. They found significant differences in oral and gut microbiome composition between the two groups, including increased Proteobacteria phylum and Enterobacteriaceae species and decreased Firmicutes phylum in STEMI patients. Microbes matching patients’ oral and gut bacteria were present in four thrombus samples, suggesting that microbes may influence clot formation and plaque rupture.

Acute coronary syndrome and sudden cardiac death are often caused by rupture and thrombosis of lipid-rich atherosclerotic coronary plaques (known as vulnerable plaques), many of which are non-flow-limiting. The safety and effectiveness of focal preventive therapy with percutaneous coronary intervention of vulnerable plaques in reducing adverse cardiac events are unknown. We aimed to assess whether preventive percutaneous coronary intervention of non-flow-limiting vulnerable plaques improves clinical outcomes compared with optimal medical therapy alone. PREVENT was a multicentre, open-label, randomised controlled trial done at 15 research hospitals in four countries (South Korea, Japan, Taiwan, and New Zealand). Patients aged 18 years or older with non-flow-limiting (fractional flow reserve >0·80) vulnerable coronary plaques identified by intracoronary imaging were randomly assigned (1:1) to either percutaneous coronary intervention plus optimal medical therapy or optimal medical therapy alone, in block sizes of 4 or 6, stratified by diabetes status and the performance of percutaneous coronary intervention in a non-study target vessel. Follow-up continued annually in all enrolled patients until the last enrolled patient reached 2 years after randomisation. The primary outcome was a composite of death from cardiac causes, target-vessel myocardial infarction, ischaemia-driven target-vessel revascularisation, or hospitalisation for unstable or progressive angina, assessed in the intention-to-treat population at 2 years. Time-to-first-event estimates were calculated with the Kaplan–Meier method and were compared with the log-rank test. This report is the principal analysis from the trial and includes all long-term analysed data. The trial is registered at ClinicalTrials.gov, NCT02316886, and is complete. Between Sept 23, 2015, and Sept 29, 2021, 5627 patients were screened for eligibility, 1606 of whom were enrolled and randomly assigned to percutaneous coronary intervention (n=803) or optimal medical therapy alone (n=803). 1177 (73%) patients were men and 429 (27%) were women. 2-year follow-up for the primary outcome assessment was completed in 1556 (97%) patients (percutaneous coronary intervention group n=780; optimal medical therapy group n=776). At 2 years, the primary outcome occurred in three (0·4%) patients in the percutaneous coronary intervention group and in 27 (3·4%) patients in the medical therapy group (absolute difference –3·0 percentage points [95% CI –4·4 to –1·8]; p=0·0003). The effect of preventive percutaneous coronary intervention was directionally consistent for each component of the primary composite outcome. Serious clinical or adverse events did not differ between the percutaneous coronary intervention group and the medical therapy group: at 2 years, four (0·5%) versus ten (1·3%) patients died (absolute difference –0·8 percentage points [95% CI –1·7 to 0·2]) and nine (1·1%) versus 13 (1·7%) patients had myocardial infarction (absolute difference –0·5 percentage points [–1·7 to 0·6]). In patients with non-flow-limiting vulnerable coronary plaques, preventive percutaneous coronary intervention reduced major adverse cardiac events arising from high-risk vulnerable plaques, compared with optimal medical therapy alone. Given that PREVENT is the first large trial to show the potential effect of the focal treatment for vulnerable plaques, these findings support consideration to expand indications for percutaneous coronary intervention to include non-flow-limiting, high-risk vulnerable plaques. The CardioVascular Research Foundation, Abbott, Yuhan Corp, CAH-Cordis, Philips, and Infraredx, a Nipro company.

Electrocardiogram (ECG) changes after primary percutaneous coronary intervention (PCI) in ST-segment elevation myocardial infarction (STEMI) patients are associated with prognosis. This study investigated the feasibility of predicting left ventricular (LV) dysfunction in STEMI patients using an artificial intelligence (AI)-enabled ECG algorithm developed to diagnose STEMI. Serial ECGs from 637 STEMI patients were analyzed with the AI algorithm, which quantified the probability of STEMI at various time points. The time points included pre-PCI, immediately post-PCI, 6 h post-PCI, 24 h post-PCI, at discharge, and one-month post-PCI. The prevalence of LV dysfunction was significantly associated with the AI-derived probability index. A high probability index was an independent predictor of LV dysfunction, with higher cardiac death and heart failure hospitalization rates observed in patients with higher indices. The study demonstrates that the AI-enabled ECG index effectively quantifies ECG changes post-PCI and serves as a digital biomarker capable of predicting post-STEMI LV dysfunction, heart failure, and mortality. These findings suggest that AI-enabled ECG analysis can be a valuable tool in the early identification of high-risk patients, enabling timely and targeted interventions to improve clinical outcomes in STEMI patients.