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BackgroundMyocardial infarction causes irreversible loss of cardiomyocytes and may lead to loss of ventricular function, morbidity and mortality. Infarct size is a major prognostic factor and reduction of infarct size has therefore been an important objective of strategies to improve outcomes. In experimental studies, glucagon-like peptide 1 and exenatide, a long acting glucagon-like peptide 1 receptor agonist, a novel drug introduced for the treatment of type 2 diabetes, reduced infarct size after myocardial infarction by activating pro-survival pathways and by increasing metabolic efficiency.MethodsThe EXAMI trial is a multi-center, prospective, randomized, placebo controlled trial, designed to evaluate clinical outcome of exenatide infusion on top of standard treatment, in patients with an acute myocardial infarction, successfully treated with primary percutaneous coronary intervention. A total of 108 patients will be randomized to exenatide (5 μg bolus in 30 minutes followed by continuous infusion of 20 μg/24 h for 72 h) or placebo treatment. The primary end point of the study is myocardial infarct size (measured using magnetic resonance imaging with delayed enhancement at 4 months) as a percentage of the area at risk (measured using T2 weighted images at 3-7 days).DiscussionIf the current study demonstrates cardioprotective effects, exenatide may constitute a novel therapeutic option to reduce infarct size and preserve cardiac function in adjunction to reperfusion therapy in patients with acute myocardial infarction.Trial registrationClinicalTrials.gov: NCT01254123

We describe a 59-year-old patient presenting with ST-elevation acute coronary syndrome. Coronary angiography with intravascular ultrasound (IVUS) showed an important nonsignificant atherosclerotic lesion in the proximal left anterior descending artery (LAD) and presence of bridging in the mid-LAD. Our hypothesis was that focal spasm at this site was the cause of transmural ischaemia; therefore, treatment was given by performing a percutaneous coronary intervention (PCI) of the lesion. The patient remained symptom-free which confirmed our conclusion. The myocardial bridging had no clinical implications at this moment.Keywords Coronary spasm . Myocardial bridging . Intravascular ultrasound A 59-year-old negroid male presented to the emergency department with chest pain. His previous medical history consisted of heterozygous alpha thalassaemia type 2, reflux disease and lumbar hernia. A coronary angiogram 6 years ago had shown only slight vessel wall abnormalities. Cardiac risk factors were hypertension, a positive family history for coronary artery disease and nicotine abuse in the past. There was no history of cocaine abuse. During the last 5 months he had been complaining of sudden chest pain occurring at rest, which radiated to the left arm and only lasted for roughly 10 min. He had never had any exerciseinduced symptoms. The pain also reacted swiftly to sublingual nitrate. An exercise test performed in the week before his admission showed no abnormalities. His current medication was acetylsalicylic acid, amlodipine, losartan, bisoprolol, proton pump inhibitor and ranitidine. Blood pressure was 129/79 mmHg with a pulse of 53 beats/min. Further physical examination revealed no abnormalities. The symptom-free electrocardiogram showed sinus rhythm and diffuse repolarisation abnormalities with T-wave inversion in leads II, III and V4 to V6. During chest discomfort, there was ST elevation in leads I, aVL, and V2 to V6 with reciprocal depression in leads III and aVF (Fig. 1). Laboratory tests showed no abnormalities and the cardiac enzymes remained normal. He was treated for an acute coronary syndrome with clopidogrel, fraxiparine and intravenous nitroglycerin. Coronary angiography showed 50 % stenosis of the proximal LAD (Fig. 2), myocardial bridging of the mid LAD, 90 % stenosis of the first and second diagonal branch and 70 % stenosis of margo obtuse and posterolateral branches. The culprit lesion appeared to be the proximal LAD as this could explain the electrographic changes. Due to the fact that this stenosis did not seem to be significant on visual assessment, an FFR measurement was performed. This showed a value of 0.96; therefore, the lesion was not considered to be haemodynamically important and PCI was not performed. Although the angiogram showed no evidence of coronary spasm the clinical evidence started to point in this direction. After discontinuing bisoprolol and under treatment with maximum doses of oral nitrate and calcium antagonist he had recurring short and sudden episodes of chest pain. ...

Aims Heart failure (HF) is a progressive disease in which periods of clinical stability are interrupted by episodes of clinical deterioration known as worsening heart failure (WHF). Patients who develop WHF are at high risk of subsequent death, rehospitalization, and excessive healthcare costs. As such, WHF could be seen as a separate disease stage and precursor of advanced HF. Whether WHF has a substantial health, societal, and economic impact evidence regarding its multifactorial nature and the specific barriers in treatment, including advanced HF therapies, remains scarce. The CHAIN‐HF registry aims to describe the incidence, characteristics, current treatment, and outcomes of WHF. Additionally, it will promote structured regional collaboration and educate on increasing awareness for WHF and describe the implementation of guideline directed medical therapy and utilization of advanced HF therapies in a collaborative network. Methods and results The CHAIN‐HF registry is a prospective, observational, and multicentre study from the collaborating hospitals (Rijnmond HF Network) in the Rotterdam area. Unselected and consecutive patients (irrespective of ejection fraction) with a WHF event will be included. Comprehensive data including demographics, co‐morbidities, treatment, and in‐hospital and post‐discharge outcomes will be collected. Notably, data on socio‐economic status, treatment decisions, and referral for advanced HF therapies will be included. Conclusions CHAIN‐HF will be the first prospective, dedicated WHF registry in a collaborative network of hospitals that will provide robust real‐world evidence on the incidence, characteristics, and outcomes of WHF. Moreover, it will provide information on of the value of regional collaboration to improve awareness and outcomes of WHF.

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