Reduced Microvascular Blood Volume as a Driver of Coronary Microvascular Disease in Patients With Non-obstructive Coronary Artery Disease: Rationale and Design of the MICORDIS Study

Background: Ischemia with non-obstructive coronary arteries (INOCA) is part of the ischemic heart disease spectrum, and is particularly observed in women. INOCA has various mechanisms, such as coronary vasospasm and coronary microvascular dysfunction (CMD). A decreased coronary flow reserve (CFR) and-or increased myocardial resistance (MR) are commonly used to diagnose CMD. However, CFR and MR do not describe all pathophysiological mechanisms underlying CMD. Increased myocardial oxygen consumption (MVO2) normally increases myocardial blood volume (MBV), independently from myocardial blood flow (MBF). In addition insulin enhances MBV in healthy skeletal muscle, and this effect is impaired in INOCA-related conditions such as diabetes and obesity. Therefore, we propose that MBV is reduced in INOCA patients.Aim: To assess whether myocardial blood volume (MBV) is decreased in INOCA patients, at baseline, during hyperinsulinemia and during stress.Design: The MICORDIS-study is a single-center observational cross-sectional cohort study (identifier NTR7515). The primary outcome is MBV, compared between INOCA patients and matched healthy controls. The patient group will undergo coronary function testing using a Doppler guidewire, intracoronary adenosine and acetylcholine to measure CFR and coronary vasospasm. Both the patient- and the control group will undergo myocardial contrast echocardiography (MCE) to determine MBV at baseline, during hyperinsulinemia and during stress. Subsequently, cardiac magnetic resonance (CMR) will be evaluated as a new and noninvasive diagnostic tool for CMD in INOCA patients. Microvascular endothelial function is a determinant of MBV and will be evaluated by non-invasive microvascular function testing using EndoPAT and by measuring NO production in circulating endothelial cells (ECFCs).

On the Precipice of Disaster – Fulminant Acute Myocarditis Mimicking ST-Elevation Myocardial Infarction in a Young Patient

Although acute myocarditis and coronary vasospasm are common differential diagnoses in the case of young patients with persistent ST elevation, the association of coronary vasospasm and acute fulminant myocarditis is a rare situation. We present the case of a 21 year-old male who presented with chest pain, ECG changes and biomarker levels initially interpreted as ST elevation myocardial infarction (STEMI), in which severe coronary vasospasm was identifi ed. Shortly after, he developed cardiogenic shock and fulminant acute myocarditis was suspected.

Proteasome inhibitor-induced coronary vasospasm in multiple myeloma: a case report

Background Coronary vasospasm is an increasingly recognized cause of myocardial infarction or myocardial ischaemia in patients without obstructive coronary artery disease. A thorough medication review may identify drugs or toxins that could trigger coronary vasospasm. This case provides mechanistic insight into the off-target effect of proteasome inhibition leading to coronary vasospasm in a patient referred with chest pain consistent with typical angina. Case summary A 72-year-old lady presented with anginal chest pain at rest with electrocardiogram evidence of myocardial ischaemia who was referred for invasive coronary angiography. This demonstrated minor coronary disease without an obstructive lesion. Vasoreactivity testing revealed diffuse coronary vasospasm of the left anterior descending artery. Carfilzomib was identified as the trigger for coronary vasospasm. Symptoms resolved without recurrence after appropriate treatment including cessation of the triggering agent. Conclusion Coronary spasm is a rare but important adverse reaction to proteasome inhibitors. This case supports the clinical utility of invasive coronary vasoreactivity testing in patients with ischaemia with no obstructive coronary artery disease.

Misoprostol-induced Coronary Vasospasm Complicated by Takotsubo Cardiomyopathy and Cardiac Arrest

Misoprostol is a synthetic E1 prostaglandin commonly used to induce abortion in the United States and elsewhere. There is limited literature on the cardiovascular adverse effects of misoprostol, and, to the best of our knowledge, very few such events have been reported. We describe the case of 52-year-old woman who was given misoprostol for cervical softening before endometrial ablation and experienced a cardiac arrest due to coronary vasospasm. She was successfully resuscitated and echocardiography showed features consistent with Takotsubo cardiomyopathy. Coronary angiography revealed coronary artery spasm which responded to nitroglycerin. Our case adds to the limited literature on this life-threatening adverse event of misoprostol.