IMPORTANCE High-sensitivity cardiac troponin I testing is widely used to evaluate patients with suspected acute coronary syndrome. A cardiac troponin concentration of less than 5 ng/L identifies patients at presentation as low risk, but the optimal threshold is uncertain. OBJECTIVE To evaluate the performance of a cardiac troponin I threshold of 5 ng/L at presentation as a risk stratification tool in patients with suspected acute coronary syndrome.

Cut-off values for hs-cTnI measurements are determined which allow a similar diagnostic classification as compared with hs-cTnT. Importantly, for a rule-out paradigm this cut-off value is unmistakably lower than the upper reference limit.

AimsThe study aimed to compare the addition of felodipine to metoprolol, and of the replacement of metoprolol by felodipine, with continuation of metoprolol, in patients with angina pectoris despite optimal betablockade. Methods and resultsThe study was double-blind, parallel, randomized and controlled, and comprised 363 patients from 27 outpatient cardiology clinics in the Netherlands. The patients had angina and positive bicycle exercise tests despite optimal beta-blockade (resting heart rate <65 beats . min~ '). Randomization was to three treatment groups: continuation of metoprolol (control), addition of felodipine to metoprolol, and replacement of metoprolol by felodipine. Exercise tests were repeated after 2 and 5 weeks. The main outcome measure was: exercise result after 5 weeks, compared with baseline, betweengroup comparison of changes vs control. There were no significant differences in exercise duration and onset of chest pain vs control. The addition of felodipine increased time until 1 mm ST depression (43 s, 95% confidence interval 20-65 s), and decreased both ST depression at highest comparable work load (0-46 mm, 95% confidence interval 0-19-0-72), and maximal ST depression (0-49 mm, 95% confidence interval 0-23-0-74). Exercise results after replacement of metoprolol by felodipine were not different from control, apart from a significant increase in rate pressure product. Significantly more patients experienced adverse events in the felodipine monotherapy group. ConclusionCombination of metoprolol and felodipine is to be preferred to felodipine monotherapy in patients who have signs and symptoms of myocardial ischaemia despite optimal beta-blockade.

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. ...