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Background Acute myocardial infarction (AMI) with in‐hospital onset (AMI‐IHO) has poor prognosis but is clinically underappreciated. Whether its occurrence has changed over time is uncertain. Methods and Results Since 1987, the ARIC (Atherosclerosis Risk in Communities) study has conducted adjudicated surveillance of AMI hospitalizations in 4 US communities. Our analysis was limited to patients aged 35 to 74 years with symptomatic AMI. Patients with symptoms initiating after hospital arrival were considered AMI‐IHO. A total of 26 678 weighted hospitalizations (14 276 unweighted hospitalizations) for symptomatic AMI were identified from 1995 to 2014, with 1137 (4%) classified as in‐hospital onset. The population incidence rate of AMI‐IHO increased in the 4 ARIC communities from 1995 through 2004 to 2005 through 2014 (12.7—16.9 events per 100 000 people; P for 20‐year trend P for 20‐year trend =0.03). The 10‐year proportions were stable for patients aged 35 to 64 years (3.0%–3.4%; P for 20‐year trend =0.3) but increased for patients aged ≥65 years (4.6%–7.8%; P for 20‐year trend =0.008; P for interaction by age group =0.04). AMI‐IHO had a more severe clinical course with lower use of AMI therapies or invasive strategies and higher in‐hospital (7% versus 3%), 28‐day (19% versus 5%), and 1‐year (29% versus 12%) mortality ( P< 0.0001 for all). Conclusions In this population‐based community surveillance, AMI‐IHO increased from 2005 to 2014, particularly among older patients. Quality initiatives to improve recognition and management of AMI‐IHO should be especially focused on hospitalized patients aged >65.

Introduction: Shock index (SI), defined as the ratio of heart rate (HR) to systolic blood pressure (SBP), is easily obtained and has been reported to predict all-cause mortality in acute myocardial infarction (AMI) hospitalizations, primarily among patients with STEMI. Large-scale investigations examining the prognostic value of SI in patients with NSTEMI are lacking. Methods: Hospitalizations for acute myocardial infarction were sampled from 4 US areas by the ARIC Study and classified by physician review. HR and SBP at first presentation were abstracted from the medical record. Pulseless patients, those with unobtainable SBP, and transfer patients were excluded. An SI value ≥0.7 was considered high. The TIMI risk score for NSTE-ACS was calculated using the established algorithm. Predictions of all-cause 28-day mortality were analyzed using receiver operating characteristics (ROC). Results: From 2000-2014, 18,301 weighted hospitalizations for NSTEMI patients were sampled and had vitals successfully obtained. Of these, 5753 (31%) had high SI (≥0.7). Patients with high SI were more often female (46% vs 39%) and older (65 vs 63 years), with more prevalent chronic kidney disease (40% vs. 32%), pneumonia (16% vs 8%), and complication by acute heart failure (42% vs 30%). However, the TIMI risk score was comparable for the 2 groups (4.3 vs. 4.2). Angiography (36% vs 58%), revascularization (19% vs 41%), and guideline-directed medications were less often administered to patients with high SI, and the 28-day mortality was nearly 3 times higher (13% vs 5%). Continuous values of SI were more predictive of 28-day mortality than the TIMI risk score, both overall (ROC-AUC: 0.68 vs 0.54; P P Conclusion: The SI outperformed the TIMI risk score for prediction of short-term mortality in patients hospitalized with NSTEMI, and may be useful for risk stratification in emergency settings.

Objective— Transplant-associated arteriosclerosis manifests as progressive vascular neointimal expansion throughout the arterial system of allografted solid organs, and eventually compromises graft perfusion and function. Allografts placed in colony stimulating factor (CSF)-1-deficient osteopetrotic ( Csf1 op /Csf1 op ) mice develop very little neointima, a finding attributed to impaired recipient macrophage function. We examined how CSF-1 affects neointima-derived vascular smooth muscle cells, tested the significance of CSF-1 expressed in donor tissue, and evaluated the contribution of secreted versus cell surface CSF-1 isoforms in transplant-associated arteriosclerosis. Methods and Results— CSF-1 activated specific signaling pathways to promote migration, survival, and proliferation of cultured vascular smooth muscle cells. Tumor necrosis factor-α addition increased CSF-1 and CSF-1 receptor expression, and tumor necrosis factor-α-driven proliferation was blocked by anti-CSF-1 antibody. In a mouse vascular allograft model, lack of recipient or donor CSF-1 impaired neointima formation; the latter suggests local CSF-1 function within the allograft. Moreover, reconstitution of donor or recipient cell surface CSF-1, without secreted CSF-1, restored neointimal formation. Conclusion— Vascular smooth muscle cells activation, including that mediated by tumor necrosis factor-α, can be driven in an autocrine/juxtacrine manner by CSF-1. These studies provide evidence for local function of CSF-1 in neointimal expansion, and identify CSF-1 signaling in vascular smooth muscle cells, particularly cell surface CSF-1 signaling, as a target for therapeutic strategies in transplant-associated arteriosclerosis.

Background Major advances have been made in the treatment of ST ‐elevation myocardial infarction ( STEMI ) in outpatients. In contrast, little is known about outcomes in STEMI that occur in patients hospitalized for a noncardiac condition. Methods and Results This was a retrospective, single‐center study of inpatient STEMI s from January 1, 2007, to July 31, 2011. Forty‐eight cases were confirmed to be inpatient STEMI s of a total of 139 410 adult discharges. These patients were older and more often female and had higher rates of chronic kidney disease and prior cerebrovascular events compared with 227 patients with outpatient STEMI s treated during the same period. Onset of inpatient STEMI was heralded most frequently by a change in clinical status (60%) and less commonly by patient complaints (33%) or changes on telemetry. Coronary angiography and percutaneous coronary intervention were performed in 71% and 56% of patients, respectively. The median time to obtain ECG (41 [10, 600] versus 5 [2, 10] minutes; P ECG to angiography time (91 [26, 209] versus 35 [25, 46] minutes; P ECG to first device activation ( FDA ) (129 [65, 25] versus 60 [47, 76] minutes; P STEMI . Survival to discharge was lower for inpatient STEMI (60% versus 96%; P Conclusions Patients who develop a STEMI while hospitalized for a noncardiac condition are older and more often female, have more comorbidities, have longer ECG ‐to‐ FDA times, and are less likely to survive than patients with an outpatient STEMI .