Early Comprehensive Cardiovascular Magnetic Resonance Imaging in Patients With Myocardial Infarction With Nonobstructive Coronary Arteries.

OBJECTIVES: The objective of the SMINC-2 (Stockholm Myocardial Infarction With Normal Coronaries 2) study was to determine if more than 70% of patients with myocardial infarction with nonobstructed coronary arteries (MINOCA), investigated early with comprehensive cardiovascular magnetic resonance (CMR), could receive a diagnosis entirely by imaging. BACKGROUND: The etiology of MINOCA is heterogeneous, including coronary, cardiac, and noncardiac causes. Patients with MINOCA, therefore, represent a diagnostic challenge where CMR is increasingly used. METHODS: The SMINC-2 study was a prospective study of 148 patients with MINOCA imaged with 1.5-T CMR with T1 and extracellular volume mapping early after hospital admission, compared to 150 patients with MINOCA imaged using 1.5-T CMR without mapping techniques from the SMINC-1 study as historic controls. RESULTS: CMR was performed at a median of 3 (SMINC-2) versus 12 (SMINC-1) days after hospital admission. In total, 77% of patients received a diagnosis with CMR imaging in the SMINC-2 study compared to 47% in the SMINC-1 study (p < 0.001). Compared to SMINC-1, CMR in SMINC-2 detected higher proportions of myocarditis (17% vs. 7%; p = 0.01) and takotsubo syndrome (35% vs. 19%; p = 0.002) but similar proportions of myocardial infarction (22% vs. 19%; p = 0.56) and other cardiomyopathies (3% vs. 2%; p = 0.46). CONCLUSIONS: The results of the SMINC-2 study show that 77% of all patients with MINOCA received a diagnosis when imaged early with CMR, including advanced tissue characterization, which was a considerable improvement in comparison to the SMINC-1 study. This supports the use of early CMR imaging as a diagnostic tool in the investigation of patients with MINOCA. (Stockholm Myocardial Infarction With Normal Coronaries [SMINC]-2 Study on Diagnosis Made by Cardiac MRI [SCMINC-2]; NCT02318498).

Plasma catecholamine levels in the acute and subacute stages of takotsubo syndrome: Results from the Stockholm myocardial infarction with normal coronaries 2 study.

AIMS: It is well-accepted that takotsubo syndrome (TS) is characterized by a massive surge of plasma catecholamines despite lack of solid evidence. The objective of this study was to examine the hypothesis of a massive catecholamine elevation in TS by studying plasma-free catecholamine metabolites in patients participating in the Stockholm myocardial infarction (MI) with normal coronaries 2 (SMINC-2) study where TS constituted more than one third of the patients. METHODS AND RESULTS: The patients included in the SMINC-2 study were classified, according to cardiac magnetic resonance (CMR) imaging findings (148 patients), which was performed at a median of 3 days after hospital admission. Plasma-free catecholamine metabolites; metanephrine, normetanephrine, and methoxy-tyramine were measured on day 2-4 after admission. Catecholamine metabolite levels were available in 125 patients. One hundred and ten (88%) of the 125 patients included in SMINC-2 study, and 38 (86.4%) of the 44 patients with TS had completely normal plasma metanephrine and normetanephrine levels. All patients had normal plasma methoxy-tyramine levels. Fourteen (11.2%) of the 125 patients included in SMINC-2 study, and 5 (11.6%) of the 43 patients with TS had mild elevations (approximately 1.2 times the upper normal limits) of either plasma metanephrine or normetanephrine. One patient with pheochromocytoma-triggered TS had marked elevation of plasma metanephrine and mild elevation of plasma normetanephrine. There were no significant differences between the number or degree of catecholamine metabolite elevations between the different groups of patients with CMR imaging diagnosis included in SMINC-2 study. CONCLUSION: There was no evidence of massive catecholamine elevations in the acute and subacute stages of TS apart from one patient with pheochromocytoma-induced TS. Most of the TS patients had normal catecholamine metabolites indicating that blood-borne catecholamines do not play a direct role in the pathogenesis of TS.