Rapid Improvements in Physical Activity and Sedentary Behavior in Patients With Acute Myocardial Infarction Immediately Following Hospital Discharge.

Background Little is known about changes in physical activity (PA) and sedentary behavior (SB) patterns in the acute phase of a myocardial infarction (MI). We objectively assessed PA and SB during hospitalization and the first week after discharge. Methods and Results Consecutively admitted patients hospitalized with an MI were approached to participate in this prospective cohort study. SB, light-intensity PA, and moderate-vigorous intensity PA were objectively assessed for 24 h/d during hospitalization and up to 7 days after discharge in 165 patients. Changes in PA and SB from the hospital to home phase were evaluated using mixed-model analyses, and outcomes were stratified for predefined subgroups based on patient characteristics. Patients (78% men) were aged 65±10 years and diagnosed with ST-segment-elevation MI (50%) or non-ST-segment-elevation MI (50%). Sedentary time was high during hospitalization (12.6 [95% CI, 11.8-13.7] h/d) but substantially decreased following transition to the home environment (-1.8 [95% CI, -2.4 to -1.3] h/d). Furthermore, the number of prolonged sedentary bouts (≥60 minutes) decreased between hospital and home (-1.6 [95% CI, -2.0 to -1.2] bouts/day). Light-intensity PA (1.1 [95% CI, 0.8-1.6] h/d) and moderate-vigorous intensity PA (0.2 [95% CI, 0.1-0.3] h/d) were low during hospitalization but significantly increased following transition to the home environment (light-intensity PA: 1.8 [95% CI, 1.4-2.3] h/d; moderate-vigorous intensity PA: 0.4 [95% CI, 0.3-0.5] h/d; both P<0.001). Improvements in PA and SB were similar across groups, except for patients who underwent coronary artery bypass grafting and who did not improve their PA patterns after discharge. Conclusions Patients with MI demonstrate high levels of SB and low PA volumes during hospitalization, which immediately improved following discharge at the patient's home environment. Registration URL: trialsearch.who.int/; Unique identifier: NTR7646.

Acute rule-out of non-ST-segment elevation acute coronary syndrome in the (pre)hospital setting by HEART score assessment and a single point-of-care troponin: rationale and design of the ARTICA randomised trial.

INTRODUCTION: Because of the lack of prehospital protocols to rule out a non-ST-segment elevation acute coronary syndrome (NSTE-ACS), patients with chest pain are often transferred to the emergency department (ED) for thorough evaluation. However, in low-risk patients, an ACS is rarely found, resulting in unnecessary healthcare consumption. Using the HEART (History, ECG, Age, Risk factors and Troponin) score, low-risk patients are easily identified. When a point-of-care (POC) troponin measurement is included in the HEART score, an ACS can adequately be ruled out in low-risk patients in the prehospital setting. However, it remains unclear whether a prehospital rule-out strategy using the HEART score and a POC troponin measurement in patients with suspected NSTE-ACS is cost-effective. METHODS AND ANALYSIS: The ARTICA trial is a randomised trial in which the primary objective is to investigate the cost-effectiveness after 30 days of an early rule-out strategy for low-risk patients suspected of a NSTE-ACS, using a modified HEART score including a POC troponin T measurement. Patients are included by ambulance paramedics and 1:1 randomised for (1) presentation at the ED (control group) or (2) POC troponin T measurement (intervention group) and transfer of the care to the general practitioner in case of a low troponin T value. In total, 866 patients will be included. Follow-up will be performed after 30 days, 6 months and 12 months. ETHICS AND DISSEMINATION: This trial has been accepted by the Medical Research Ethics Committee region Arnhem-Nijmegen. The results of this trial will be disseminated in one main paper and in additional papers with subgroup analyses. TRIAL REGISTRATION NUMBER: Netherlands Trial Register (NL7148).

Temporal Pattern of Growth Differentiation Factor-15 Protein After Acute Coronary Syndrome (From the BIOMArCS Study).

Growth differentiation factor-15 (GDF-15) has appeared as a promising biomarker with strong predictive abilities in acute coronary syndrome (ACS). However, studies are solely based on single measurements in the acute phase of an ACS event. The way GDF-15 patterns in post-ACS patients behave on the long term is largely unknown. We conducted a nested case-control study within our multicenter, prospective, observational biomarker study (BIOMArCS) of 844 ACS patients. Following an index ACS event, high-frequency blood sampling was performed during 1-year of follow-up. GDF-15 was determined batchwise by electrochemiluminescence immunoassays in 37 cases with a recurrent event during 1-year follow-up, and in 74 event-free controls. Cases and controls had a mean ± standard deviation age of 66.9 ± 11.3 years and 81% were men. From 30 days onwards, patients showed stable levels, which were on average 333 (95% confidence interval 68 to 647) pg/mL higher in cases than controls (1704 vs 1371 pg/mL; p value 0.013). Additionally, in the post 30-day period, GDF-15 showed low within-individual variability in both cases and controls. In conclusion, post-ACS patients experiencing a recurrent event had stable and systematically higher GDF-15 levels during 30-day to 1-year follow-up than their event-free counterparts with otherwise similar clinical characteristics. Thus, postdischarge blood sampling might be used throughout the course of 1 year to improve prognostication, whereas, in view of the low within-individual variation, the number of repeated sampling moments might be limited.

Cohort profile of BIOMArCS: the BIOMarker study to identify the Acute risk of a Coronary Syndrome-a prospective multicentre biomarker study conducted in the Netherlands.

PURPOSE: Progression of stable coronary artery disease (CAD) towards acute coronary syndrome (ACS) is a dynamic and heterogeneous process with many intertwined constituents, in which a plaque destabilising sequence could lead to ACS within short time frames. Current CAD risk assessment models, however, are not designed to identify increased vulnerability for the occurrence of coronary events within a precise, short time frame at the individual patient level. The BIOMarker study to identify the Acute risk of a Coronary Syndrome (BIOMArCS) was designed to evaluate whether repeated measurements of multiple biomarkers can predict such 'vulnerable periods'. PARTICIPANTS: BIOMArCS is a multicentre, prospective, observational study of 844 patients presenting with ACS, either with or without ST-elevation and at least one additional cardiovascular risk factor. METHODS AND ANALYSIS: We hypothesised that patterns of circulating biomarkers that reflect the various pathophysiological components of CAD, such as distorted lipid metabolism, vascular inflammation, endothelial dysfunction, increased thrombogenicity and ischaemia, diverge in the days to weeks before a coronary event. Divergent biomarker patterns, identified by serial biomarker measurements during 1-year follow-up might then indicate 'vulnerable periods' during which patients with CAD are at high short-term risk of developing an ACS. Venepuncture was performed every fortnight during the first half-year and monthly thereafter. As prespecified, patient enrolment was terminated after the primary end point of cardiovascular death or hospital admission for non-fatal ACS had occurred in 50 patients. A case-cohort design will explore differences in temporal patterns of circulating biomarkers prior to the repeat ACS. FUTURE PLANS AND DISSEMINATION: Follow-up and event adjudication have been completed. Prespecified biomarker analyses are currently being performed and dissemination through peer-reviewed publications and conference presentations is expected from the third quarter of 2016. Should identification of a 'vulnerable period' prove to be feasible, then future research could focus on event reduction through pharmacological or mechanical intervention during such periods of high risk for ACS. TRIAL REGISTRATION NUMBER: NTR1698 and NTR1106.

Troponin I release at rest and after exercise in patients with hypertrophic cardiomyopathy and the effect of betablockade

PURPOSE OF THE WORK: In patients with hypertrophic cardiomyopathy ischemia may occur due to massive heart weight, myocyte disarray or small vessel disease. We detected elevated troponin levels in some of these patients and hypothesized that troponin release would rise after exercise and diminish after betablockade. METHODS AND RESULTS: In 5 of 7 young patients (6 males) with hypertrophic cardiomyopathy and no overt coronary artery disease we found elevated troponin levels after physical exercise; the peak was between 6 and 9 hours and levels returned to pre-exercise values within 24 hours. Troponin release was consistently diminished after use of a betablocker. CONCLUSIONS: Increased troponin release may be present in patients with hypertrophic cardiomyopathy and is temporarily enhanced by exercise and diminishes with betablockade.

Troponin I release at rest and after exercise in patients with hypertrophic cardiomyopathy and the effect of betablockade.

PURPOSE OF THE WORK: In patients with hypertrophic cardiomyopathy ischemia may occur due to massive heart weight, myocyte disarray or small vessel disease. We detected elevated troponin levels in some of these patients and hypothesized that troponin release would rise after exercise and diminish after betablockade. METHODS AND RESULTS: In 5 of 7 young patients (6 males) with hypertrophic cardiomyopathy and no overt coronary artery disease we found elevated troponin levels after physical exercise; the peak was between 6 and 9 hours and levels returned to pre-exercise values within 24 hours. Troponin release was consistently diminished after use of a betablocker. CONCLUSIONS: Increased troponin release may be present in patients with hypertrophic cardiomyopathy and is temporarily enhanced by exercise and diminishes with betablockade.