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IMPORTANCE: Stem and progenitor cells mobilize from the bone marrow in response to myocardial ischemia. However, the association between the change in circulating progenitor cell (CPC) counts and disease prognosis among patients with ischemia is unknown. OBJECTIVE: To investigate the association between the change in CPC counts during stress testing and the risk of adverse cardiovascular events in patients with stable coronary artery disease (CAD). DESIGN, SETTING, AND PARTICIPANTS: This prospective cohort study included a population-based sample of 454 patients with stable CAD who were recruited between June 1, 2011, and August 15, 2014, at Emory University-affiliated hospitals and followed up for 3 years. Data were analyzed from September 15, 2018, to October 15, 2018. EXPOSURES: Myocardial perfusion imaging with technetium Tc 99m sestamibi at rest and 30 to 60 minutes after conventional stress testing. MAIN OUTCOMES AND MEASURES: Circulating progenitor cells were enumerated with flow cytometry as CD34-expressing mononuclear cells (CD45med/CD34+), with additional quantification of subsets coexpressing the chemokine (C-X-C motif) receptor 4 (CD34+/CXCR4+). Changes in CPC counts were calculated as poststress minus resting CPC counts. Cox proportional hazards regression models were used to identify factors associated with the combined end point of cardiovascular death and myocardial infarction after adjusting for clinical covariates, including age, sex, race, smoking history, body mass index, and history of heart failure, hypertension, dyslipidemia, and diabetes. RESULTS: Of the 454 patients (mean [SD] age, 63 [9] years; 76% men) with stable CAD enrolled in the study, 142 (31.3%) had stress-induced ischemia and 312 (68.7%) did not, as measured by single-photon emission computed tomography. During stress testing, patients with stress-induced ischemia had a mean decrease of 20.2% (interquartile range [IQR], −45.3 to 5.5; P < .001) in their CD34+/CXCR4+ counts, and patients without stress-induced ischemia had a mean increase of 3.2% (IQR, −20.6 to 35.1; P < .001) in their CD34+/CXCR4+ counts. Twenty-four patients (5.2%) experienced adverse events. After adjustment, baseline CPC counts were associated with worse adverse outcomes, but this association was not present after stress-induced ischemia was included in the model. However, the change in CPC counts during exercise remained significantly associated with adverse events (hazard ratio, 2.59; 95% CI, 1.15-5.32, per 50% CD34+/CXCR4+ count decrease), even after adjustment for clinical variables and the presence of ischemia. The discrimination of risk factors associated with incident adverse events improved (increase in C statistic from 0.72 to 0.77; P = .003) with the addition of the change in CD34+/CXCR4+ counts to a model that included clinical characteristics, baseline CPC count, and ischemia. CONCLUSIONS AND RELEVANCE: In this study of patients with CAD, a decrease in CPC counts during exercise is associated with a worse disease prognosis compared with the presence of stress-induced myocardial ischemia. Further studies are needed to evaluate whether strategies to improve CPC responses during exercise stress will be associated with improvements in the prognosis of patients with CAD.

Current practice guidelines recommend antibiotic prophylaxis in patients with high-risk congenital heart conditions, including those with Prosthetic heart valves and prosthetic material, including annuloplasty rings or clips undergoing invasive dental procedures. However, there is limited clinical data on the burden of infective endocarditis (IE) following Mitral TEER. This study investigated temporal trends of very early IE immediately after TEER using National Inpatient Sample from 2016 - 2020. It showed that the rate of very early TEER-related IE was relatively low over the five years of analysis and that there was a downward trend of very early IE after TEER.

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ABSTRACTBackground:Data on clinical or symptomatic leaflet thrombosis after transcatheter aortic valve replacement (TAVR) are limited. Whether clinical leaflet thrombosis has significance beyond peri-TAVR stroke or transient ischemic attacks (TIA) is yet to be elucidated.Methods:Between January 2012 and October 2015, we searched the MAUDE database for all entries with the identifier code, “NPT,” designated by the U.S. FDA to identify TAVR-related adverse events (AEs). Selected entries were searched further for the terms “leaflet,” “central aortic regurgitation,” and “aortic stenosis” to capture all events related to leaflet thrombosis causing structural valve dysfunction (SVD). Presentation of leaflet thrombosis (aortic stenosis or regurgitation or mixed valve lesion), mode of diagnosis (echocardiography, computed tomography, surgical explantation, or autopsy), and timing of presentation after TAVR were recorded. For all AEs of SVD due to leaflet thrombosis, the following outcomes were recorded: stroke or TIA, cardiogenic shock, and death from any cause.Results:A total of 5691 TAVR-related AEs were reported in the MAUDE database. SVD due to leaflet thrombosis was reported in 30 cases. Most cases (n = 18/30, 60.0%, 95% CI 0.41–0.77) occurred in the first year following TAVR. SVD manifested as either aortic stenosis (n = 16/30, 53.3%, 95% CI 0.34–0.72), or regurgitation (n = 7/30, 23.3%, 95% CI 0.10–0.42), or both (n = 4/30, 13.3%, 95% CI 0.04–0.31). Interventions to address leaflet thrombosis included either escalation of antiplatelet or anticoagulant therapy (n = 9/30, 30.0%, 95% CI 0.15–0.49), valve-in-valve TAVR (n = 5/30, 16.7%, 95% CI 0.06–0.35), or surgery (n = 14/30, 46.7%, 95% CI 0.28–0.66), or their combination. Outcome following leaflet thrombosis included stroke/TIA (n = 3/30, 10.0%, 95% CI 0.02–0.27), cardiogenic shock (n = 2/30, 6.7%, 95% CI 0.01–0.22), and death (n = 9/30, 30.0%, 95% CI 0.15–0.49).Conclusion:Clinically manifest leaflet thrombosis was associated with serious manifestations that included stroke, cardiogenic shock, and death.

Mental stress–induced (MSIMI) or physical stress–induced (PSIMI) myocardial ischemia portends a worse prognosis in patients with coronary artery disease (CAD). Vitamin D insufficiency is associated with adverse cardiovascular outcomes, but its relationship to myocardial ischemia remains unclear. We hypothesized that vitamin D insufficiency will be associated with a higher prevalence of myocardial ischemia in patients with CAD.

Traditional cardiovascular risk factors lead to endothelial injury and activation of leukocytes and platelets that initiate and propagate atherosclerosis. We proposed that clopidogrel therapy in patients with stable coronary artery disease imparts a pleiotropic effect that extends beyond antiplatelet aggregation to other atheroprotective processes.

Mental stress provokes myocardial ischemia in many patients with stable coronary artery disease (CAD). Mental stress–induced myocardial ischemia (MSIMI) portends a worse prognosis, independent of standard cardiac risk factors or outcome of traditional physical stress testing. Angiotensin II plays a significant role in the physiological response to stress, but its role in MSIMI remains unknown. Our aim was to evaluate whether the use of angiotensin-converting enzyme inhibitors (ACEIs) is associated with a differential effect on the incidence of MSIMI compared with ischemia during physical stress.