Cardiac MRI in myocardial infarction without obstructive coronary artery disease (MINOCA) helps arrive at correct diagnosis - A case report and discussion

Abstract

Myocardial infarction without obstructive coronary artery disease (MINOCA) is a common condition with estimated prevalence of 5 to 15 %. It is not a benign condition and diagnosing the exact underlying etiology can be challenging, but it is important to ensure appropriate management of MINOCA patients. Cardiac magnetic resonance imaging (CMRI) can be a valuable and non-invasive test to identify the underlying etiology, as well as to risk-stratify such patients. Both the European Society of Cardiology and the American Heart Association recommend CMRI in diagnostic work up of MINOCA patients. We report a case of an 83-year-old man who presented to the emergency department with atypical chest pain but had significantly elevated cardiac troponin levels, with non-obstructive coronary artery disease on left heart catheterization. Subsequent CMRI led to the diagnosis of acute myocarditis. He was medically managed with good clinical outcomes. We discuss this case in detail and highlight the role of CMRI in MINOCA patients. As our understanding of troponin elevation and its various mechanisms continues to evolve, cardiac MRI has a significant role in diagnosis and management, as demonstrated in our case.

Learning objectives

• 1.Illustrate the clinical relevance and diagnosis of myocardial infarction without obstructive coronary artery disease (MINOCA).
• 2.Explain the role of cardiac magnetic resonance imaging in diagnosis and management of MINOCA.

Introduction

Myocardial infarction can occur in the absence of hemodynamically significant obstructive coronary artery disease (CAD). The term myocardial infarction without obstructive coronary artery disease (MINOCA) was coined to include patients with acute myocardial infarction with evidence of atherosclerosis that is not adequately severe to compromise myocardial blood flow [1]. MINOCA is defined by three major criteria: 1. Patients with acute myocardial infarction (AMI) as defined by the fourth universal definition of myocardial infarction; 2. presence of non-obstructive CAD with no lesions ≥ 50 % of major epicardial vessel; and 3. no other alternative cause for the acute presentation. Thus, MINOCA is a working diagnosis that should be considered at the time of cardiac catheterization and needs further assessment to identify specific diagnosis. Diagnosing the specific underlying cause of MINOCA is important but can be challenging and may require multiple diagnostic modalities including echocardiography, cardiac magnetic resonance imaging (CMRI), coronary vascular imaging including intravascular ultrasonography, coronary optical coherence tomography, and invasive coronary imaging and functional testing [1].

CMRI has emerged as an important diagnostic and prognostication tool in cases of MINOCA owing to its safety, accuracy, and inter-observer consistency and reliability to characterize the myocardium [1]. Studies have shown that CMRI can lead to specific diagnosis in 74 % [2] to 84 % [3] of MINOCA patients. CMRI can promptly diagnose several conditions responsible for MINOCA and allows early initiation of tailored therapies [1]. Furthermore, CMRI allows risk stratification of MINOCA patients [3]. CMRI is recommended by both the European Society of Cardiology (ESC) and the American Heart Association (AHA) in the diagnostic work up of MINOCA patients [1], [4].

We discuss a case of acute myocarditis mimicking acute coronary syndrome where CMRI played a significant role in the diagnosis and subsequent management. We discuss current literature on the utility of CMRI in similar cases of MINOCA to further emphasize the role of CMRI in MINOCA patients.

Case report

An 83-year-old man with medical history of CAD and previous percutaneous intervention to right coronary artery, mitral regurgitation, hyperlipidemia, supraventricular tachycardia, and benign prostatic hyperplasia presented with complains of retrosternal chest pain that radiated to his left arm and associated with shortness of breath and diaphoresis. At presentation, his blood pressure was 112/54 mm Hg, pulse 55, temperature of 97.6 °F and respiratory rate of 20/min. He was saturating at 98 % in room air. Electrocardiography showed sinus rhythm with premature atrial contractions and non-specific ST-T wave changes (Fig. 1). Initial troponin was within normal limit, but subsequent troponin trended to as high as 22, 981 ng/L. Computed tomography angiography of the chest was negative for pulmonary embolism but showed patchy bibasilar opacities concerning for pneumonia. Coronavirus disease 2019 and upper respiratory polymerase chain reaction were negative. Laboratory results were notable for white cell count of 17.2 × 1000/μL, hemoglobin of 13.2 g/dL, platelets 473 × 1000/μL, and blood urea nitrogen of 20 mg/dL with serum creatinine of 1.5 mg/dL, creatine phosphokinase 1124 U/L, erythrocyte sedimentation rate 22 mm/h, high sensitivity C-reactive protein 1.25 mg/dL. He was started on antibiotics, IV nitroglycerin and IV heparin and IV morphine with improvement in chest pain. He underwent cardiac catheterization which revealed 50 % proximal left anterior descending (LAD) lesion, 40 % mid-LAD lesion, and patent right coronary artery as well as left circumflex artery. Transthoracic echocardiogram (TTE) showed normal ejection fraction 62 % with no significant wall motion abnormalities. Left ventricular relaxation was impaired. There was no evidence of myocardial wall edema or pericardial effusion. Trace mitral regurgitation and trace pulmonary regurgitation was noted. Working diagnosis of MINOCA was made and patient subsequently had CMRI on day 3 of admission. T2 sequence imaging showed mild increased signal in the inferolateral wall suggestive of edema and delayed enhancement imaging showed multiple dense patches of subepicardial delayed enhancement in the entire inferolateral and apical lateral wall. In addition, normal left ventricle cavity size with mild concentric hypertrophy with no regional wall motion abnormalities was seen with calculated left ventricular ejection fraction (LVEF) of 60 % (Fig. 2, Fig. 3). Based on CMRI findings, a diagnosis of acute myocarditis was made. He responded well to medical management including antibiotics for pneumonia, aspirin, and low-dose beta-blocker. He was seen in the clinic for follow up within 2 weeks during which he was found to have sinus bradycardia and beta-blocker was stopped. He was otherwise doing well.

Fig. 1.

EKG at presentation: Sinus rhythm, with premature atrial contraction and borderline ST elevation in lateral leads.

Fig. 2.

Cardiac MRI (Trufi image)-Mild increased signal in the inferolateral wall suggestive of edema.

Fig. 3.

Cardiac MRI (four chamber stack) — Multiple dense patches of subepicardial delayed enhancement in the entire inferolateral and apical lateral wall suggestive of myocarditis as clinically questioned.

Discussion

MINOCA is not a benign condition. A meta-analysis by Pasupathy et al. [5] showed 4.7 % (95 % CI, 2.6 %–6.9 %) 12-month all-cause mortality for patients with MINOCA which is significantly lower compared with those with MI-CAD. However, MINOCA patients were found to have poorer prognosis compared to patients with stable chest pain and nonobstructive CAD. There are several etiological possibilities for MINOCA with different underlying mechanisms including coronary spasm, coronary dissection, coronary microvascular dysfunction, spontaneous coronary thrombosis and emboli, as well as myocarditis and infiltrative diseases. Moreover, various other cardiac and non-cardiac conditions can result in elevated cardiac enzymes due to myocardial injury, mimicking an MI and often being misclassified as MINOCA [5]. Therefore, MINOCA should be considered a working diagnosis that requires further evaluation to identify potential underlying cause as it has therapeutic and prognostic implications.

CMRI has emerged as an important diagnostic tool to investigate the underlying etiology of MINOCA patients and aid in definitive management. In one prospective study, Pathik et al., were able to identify a specific diagnosis in 87 % of MINOCA patient (37 % with acute myocarditis, 27 % with takotsubo cardiomyopathy, 21 % with AMI, and 1 % atypical hypertrophy and 2 % with dilated cardiomyopathy) [2]. In another study by Dastidar et al., CMRI identified etiology of MINOCA in 74 % of the patients (25 % myocarditis, 25 % MI, and 25 % cardiomyopathy), whereas a normal CMRI was only identified in 26 % of cases. CMRI was able also to provide important prognostic information. Cardiomyopathy seen on CMRI was associated with the worst prognosis (15 % mortality) followed by MI (4 % mortality) and myocarditis (2 % mortality). Cardiomyopathy group in this study was a heterogenous group with takotsubo cardiomyopathy being the most common (43 % of the cardiomyopathy group) and it was associated with worst prognosis when compared with any other CMRI diagnosis. The study also showed that CMRI use in MINOCA led to a change in 54 % of diagnosis and 41 % of management, further highlighting its utility [3]. The difference in diagnostic rates between these two studies could potentially be attributed to the timing of the CMRI, as the median time between CMRI and admission was 6 days in Pathik's study and 37 days in Dastidar's study. This highlights the need to perform CMRI earlier after presentation preferably within 7 days. Pathik et al. also showed poor concordance between clinical and CMRI diagnosis in MINOCA patients. In only 32 % of patients, did all three cardiologists have the same diagnosis as CMRI and in 25 % cases, none of the three cardiologists had a diagnosis consistent with CMRI diagnosis despite the availability of all pertinent clinical details, electrocardiogram, cardiac troponin T, angiography, and echocardiography results [2]. This finding emphasizes the role of CMR as an objective tool to aid clinicians' decision making.

In the absence of explanatory stenotic lesions on cardiac catheterization, CMRI can non-invasively diagnose AMI if there is late gadolinium enhancement (LGE) in a subendocardial or transmural pattern corresponding to a vascular territory. T2 weighted imaging with a high regional signal may suggest perilesional edema, indicative of an acute event. Test sensitivity can reach up to 99 % for detecting AMI and 94 % for detecting chronic MI based on the delayed-enhancement magnetic resonance imaging trial [6]. In the presence of LGE, correct location and culprit artery can be identified in 97–100 % of cases [7]. CMRI diagnosis of acute myocarditis can be made if two of the three Lake Louise Criteria are met: 1. Presence of myocardial edema; 2. capillary leaks and hyperemia; and 3. necrosis/fibrosis. Lake Louise Criteria approach consists of late enhancement sequences, T2-weighted edema images, and T1-weighted sequences before and after contrast injection (early enhancement) [8].

CMRI may fail to elicit etiology in up to 26 % of cases depending on the timing of the test [4]. Delay in performing CMRI may lessen the diagnostic yield. Often, the lesions and damage caused by acute MI may be too small to be detected by CMRI. Similarly, vasospastic angina or CAD or coronary embolism or pulmonary embolism may have normal CMRI findings [9]. Often, patient-related factors such as morbid obesity, advanced chronic kidney disease, claustrophobia, presence of metal hardware implants, and MRI incompatible pacemakers/defibrillators, and clinical instability may preclude the CMRI in MINOCA patients. Also, CMRI may not be readily available in some centers, could be costly and time consuming. Despite these limitations, CMRI should be considered when available to obtain valuable information that aids in diagnosis, risk stratification, and treatment individualization. Prompt utilization of CMRI in patients such as ours, in whom coronary markers were suggestive of significant myocardial injury should be considered sooner than later, as it is likely to direct us toward the correct diagnosis and appropriate management.

Declaration of competing interest

The authors declare that there is no conflict of interest.