SCMR 22nd Annual Scientific Sessions
Description of Clinical Presentation:
A 53 year old obese male presented with one hour of severe substernal chest pain radiating to his right arm and neck which occurred while eating lunch. Chest pain was associated with nausea. He is a former smoker, treated for hyperlipidemia, with a remote history of former cocaine use. Blood pressure was 154/93 mm Hg, pulse 97. Lungs were clear to auscultation and no murmurs rubs or gallops were present. No dependent edema. ECG on presentation as below demonstrated 1mm ST elevation inferiorly with reciprocal depression in avL (Image1). His troponin on arrival was <0.010 ng/mL. He was taken to the cath lab and invasive angiography revealed normal epicardial coronary arteries (Image2), and normal filling pressures. Day 2 his chest pain had resolved, but troponins had risen to a peak of 2.190 ng/mL, falling to 1.560 ng/mL for the third set. Echocardiography revealed normal LV size and function with no reported regional wall motion abnormalities or valvular disease.
Diagnostic Techniques and Their Most Important Findings:
A Cardiac MRI with and without contrast was performed on a 1.5T MRI (GE Healthcare). Steady state free precision (SSFP) cine imaging revealed normal LVEF 58% with focal dyskinesia of the mid to distal inferior and inferolateral wall. Late gadolinium enhanced images (LGE) revealed two seperate bright foci of hyper-enhancement, subendocardial pattern,near- transmural thickness involving just the mid inferior and inferolateral wall, with associated microvascular obstruction (MVO) demonstrated by a hypo-enhanced core within the myocardial scar in a coronary side branch distribution (Image3), consistent with myocardial infaction. These 2 foci are separated by a slice of normal myocardium.
Learning Points from this Case:
The case highlights the role of CMRI in patients with troponin-positive chest pain and unobstructed arteries also called MINOCA (myocardial infaction with non-obstructive coronary arteries),which occurs in 7-10% of patients with STEMI and 10-15% of patients with NSTEMI. Most cases of MINOCA are caused by acute myocarditis, stess cardiomyopathy, and embolic MI/MI with spontaneous recanalization. Differentiation can be performed using cine imaging with SSFP, assessment of myocardial edema by T2 weighted imaging and patterns of LGE. In this case, the diagnosis of a thrombo-embolic MI was favored given two separate, non-contiguous infarct regions (sub-endocardial pattern) separated by a region of non-infarcted myocardium, the acute onset of pain, lack of prodrome, and the time course of troponins, which were initially normal. Demand and stress cardiomyopathies usually lack LGE, and myocarditis may have LGE but it was not most consisent with integrating patient history and the subendcaordial pattern of LGE. CMRI allows for greater definition of etiology of MINOCA which ultimately drives downstream diagnostic testing and patient management, here the patient underwent a hypercoagulability work-up, continuous telephonic monitoring for atrial fibrillation, and was started on a statin and oral anti-coagulation.