Artificial Intelligence-Enabled Quantitative Coronary Plaque and Hemodynamic Analysis for Predicting Acute Coronary Syndrome.

BACKGROUND: A lesion-level risk prediction for acute coronary syndrome (ACS) needs better characterization. OBJECTIVES: This study sought to investigate the additive value of artificial intelligence-enabled quantitative coronary plaque and hemodynamic analysis (AI-QCPHA). METHODS: Among ACS patients who underwent coronary computed tomography angiography (CTA) from 1 month to 3 years before the ACS event, culprit and nonculprit lesions on coronary CTA were adjudicated based on invasive coronary angiography. The primary endpoint was the predictability of the risk models for ACS culprit lesions. The reference model included the Coronary Artery Disease Reporting and Data System, a standardized classification for stenosis severity, and high-risk plaque, defined as lesions with ≥2 adverse plaque characteristics. The new prediction model was the reference model plus AI-QCPHA features, selected by hierarchical clustering and information gain in the derivation cohort. The model performance was assessed in the validation cohort. RESULTS: Among 351 patients (age: 65.9 ± 11.7 years) with 2,088 nonculprit and 363 culprit lesions, the median interval from coronary CTA to ACS event was 375 days (Q1-Q3: 95-645 days), and 223 patients (63.5%) presented with myocardial infarction. In the derivation cohort (n = 243), the best AI-QCPHA features were fractional flow reserve across the lesion, plaque burden, total plaque volume, low-attenuation plaque volume, and averaged percent total myocardial blood flow. The addition of AI-QCPHA features showed higher predictability than the reference model in the validation cohort (n = 108) (AUC: 0.84 vs 0.78; P < 0.001). The additive value of AI-QCPHA features was consistent across different timepoints from coronary CTA. CONCLUSIONS: AI-enabled plaque and hemodynamic quantification enhanced the predictability for ACS culprit lesions over the conventional coronary CTA analysis. (Exploring the Mechanism of Plaque Rupture in Acute Coronary Syndrome Using Coronary Computed Tomography Angiography and Computational Fluid Dynamics II [EMERALD-II]; NCT03591328).

Impact of Aortomitral Continuity Calcification on Need for Permanent Pacemaker After Transcatheter Aortic Valve Replacement.

BACKGROUND: By virtue of its proximity to structures vital to cardiac conduction, aortomitral continuity calcification (AMCC) may help identify patients at highest risk for developing atrioventricular conduction disease requiring permanent pacemaker implantation (PPMI). We aim to determine the association of AMCC and need for PPMI after transcatheter aortic valve replacement. METHODS: Of 614 patients who underwent transcatheter aortic valve replacement (11.8% PPMI rate), we included 136 patients (age 85±8 years, 47% male) without a preexisting intracardiac device or prior valve surgery who underwent preprocedural computed tomography. We analyzed for the presence of AMCC, aortic valve calcification, and mitral annular calcification as well as quantified AMCC and aortic valve calcification score using the Agatston method. We further stratified AMCC score into 3 categories: 0, 1 to 300, and >300. End point was PPMI at 1 month after transcatheter aortic valve replacement. RESULTS: There were 51 (38%) new PPMIs (median time to PPMI, 5 days). Patients who underwent PPMI had a higher prevalence of AMCC than patients without PPMI (69% versus 32%; P<0.0001), as well as higher median AMCC score (263 versus 0; P<0.0001). There was no difference in aortic valve calcification and mitral annular calcification between patients with and without PPMI (all P≥0.09). Patients with AMCC had a 4-fold increase in odds for PPMI compared with those without (adjusted odds ratio, 4.0; P=0.0026). Compared with patients with an AMCC score of 0, patients with an AMCC score >300 had greater than a 5-fold increased odds for PPMI (adjusted odds ratio, 5.7; P=0.0016). CONCLUSIONS: Presence of AMCC, particularly with AMCC score >300, is associated with the need for PPMI after transcatheter aortic valve replacement.

Precision Medicine and Men's Health.

Precision medicine can greatly benefit men's health by helping to prevent, diagnose, and treat prostate cancer, benign prostatic hyperplasia, infertility, hypogonadism, and erectile dysfunction. For example, precision medicine can facilitate the selection of men at high risk for prostate cancer for targeted prostate-specific antigen screening and chemoprevention administration, as well as assist in identifying men who are resistant to medical therapy for prostatic hyperplasia, who may instead require surgery. Precision medicine-trained clinicians can also let couples know whether their specific cause of infertility should be bypassed by sperm extraction and in vitro fertilization to prevent abnormalities in their offspring. Though precision medicine's role in the management of hypogonadism has yet to be defined, it could be used to identify biomarkers associated with individual patients' responses to treatment so that appropriate therapy can be prescribed. Last, precision medicine can improve erectile dysfunction treatment by identifying genetic polymorphisms that regulate response to medical therapies and by aiding in the selection of patients for further cardiovascular disease screening.

PFO Closure for Cryptogenic Stroke: A Review and Clinical Treatment Algorithm.

With a high prevalence in the general population of approximately 25%, and a prevalence in the cryptogenic stroke population approaching 40%, the propensity of a patent foramen ovale (PFO) to precipitate or enable stroke, especially in young, otherwise healthy individuals, has been the subject of much debate. With proof of concept achieved via imaging modalities documenting thrombus-in-transit, and the development of minimally-invasive percutaneous approaches to closure, multiple observational studies and, more recently, several completed randomized controlled trials have sought to answer the question of when and in whom PFO closure should occur. We describe the historical context of PFO closure and review the observational and randomized control trial evidence in this field, culminating in the recent Food and Drug Administration approval of the first dedicated closure device for PFO. Guidelines and consensus statements are discussed, and a novel treatment algorithm is proposed. Future directions in PFO closure will include new devices, further data from completed and upcoming clinical trials, and potential expansion into other disease states associated with PFO.