Myocardial infarction with non-obstructive coronary artery disease

Abstract

As a result of the increased use of coronary angiography in acute myocardial infarction in the last two decades, myocardial infarction with non-obstructive coronary arteries (MINOCA) has received growing attention in everyday clinical practice. At the same time, research interest in MINOCA has increased significantly. MINOCA is a heterogeneous disease entity seen in 5-10% of all patients with myocardial infarction, especially in women. Clinically, MINOCA may be difficult to distinguish from other non-ischaemic conditions that can cause similar symptoms and myocardial injury. There is still some confusion around the diagnosis, investigation and management of patients with MINOCA. The present review summarises the current knowledge of MINOCA regarding epidemiology, pathophysiology, investigation, and treatment, with a special focus on imaging modalities. In addition, remaining important knowledge gaps are highlighted.

Central illustration

Schematic illustration of different conditions that cause myocardial injury, based on whether there is an ischaemic or non-ischaemic cause of the injury. A) In theory, ischaemic and non-ischaemic conditions are clearly separated. B) In clinical practice, the delimitation of the different conditions is sometimes unclear and difficult to determine.

Figure 1

Schematic illustration of the relation between myocardial infarction with non-obstructive coronary arteries (MINOCA) and ST-elevation myocardial infarction (STEMI)/non-ST-elevation myocardial infarction (NSTEMI) and type 1 myocardial infarction (MI)/type 2 MI, respectively.

Figure 2

Examples of findings on cardiac magnetic resonance (CMR) and coronary angiography in patients with an initial working diagnosis of MINOCA. A) A 77-year-old female with hypertension, admitted due to chest pain. ECG with T-wave inversions in precordial leads. Hs-Troponin I elevation up to 8,000 ng/L. Coronary angiogram on day 1 showed non-obstructed coronary arteries. Ventriculography revealed a distal apical hypo/dyskinesia, raising suspicion of Takotsubo syndrome. CMR on day 12 showed a normal-sized left ventricle with regional akinesia limited to one apical segment of the anterolateral wall and globally normal systolic function (left ventricular end-diastolic volume [LVEDV] 64 ml/m², ejection fraction [EF] 62%) (steady-state free precession [SSFP] sequence). In the corresponding area, an increased signal in T2wSTIR sequence suggestive of oedema, and a transmural contrast enhancement in LGE sequence, suggestive of a cell membrane damage/scarring, were seen. Final diagnosis was acute myocardial infarction limited to a small area, suggestive of an embolic genesis. The apical segment with respective pathologies indicated by blue arrows. B) A 60-year-old female admitted due to acute chest pain and dizziness, with acute onset during physical activity. Ongoing hormone therapy and radiotherapy after mastectomy two months previously for breast cancer. ECG showed ST-elevations, predominantly in precordial leads. Hs-troponin elevation up to 6,300 ng/L. Coronary angiogram on day 1 showed non-obstructed coronary arteries. Ventriculography was not performed; however, echocardiography revealed an apical dyskinesia suggestive for Takotsubo syndrome. CMR on day 15 showed a normal-sized left ventricle with basal hyperkinesia and apical hypokinesia mainly in the anterolateral wall and a globally normal systolic function (LVEDV 78 ml/m², EF 58%). T2wSTIR sequence showed a clear increased oedema signal in all apical segments. No contrast enhancement was observed in LGE sequences. Final diagnosis was Takotsubo syndrome. C) A 61-year-old male without any cardiovascular risk factors admitted due to a chest pain. ECG showed generalised ST-elevations. Acute coronary angiogram showed non-obstructed coronary arteries. Hs-Troponin I elevation up to >50,000 ng/L. CMR on day 4 revealed a normal-sized left ventricle with regional hypokinesia in mid-apical lateral wall and in mid anterior wall and globally mildly impaired systolic function (LVEDV 89 ml/m², EF 51%) (SSFP sequence). Oedema sequences (T2wSTIR) showed an increased signal in the entire anterolateral wall and in basal-midventricular inferior wall, which also could be confirmed by prolonged native T1-time in T1-mapping sequence. Viability sequences (LGE) show widespread subepicardial and mid-wall signal increase throughout the anterolateral wall, in basal inferior wall, and mid-wall in apical septum. The pattern was suggestive of acute myocarditis.

Figure 3

Examples of findings at coronary angiography and OCT imaging in MINOCA. A) A patient admitted with chest pain and anterior ST depression on ECG. Angiography (left panel) shows an intermediate narrowing in the mid left anterior descending artery. OCT showed an atherosclerotic plaque with thin fibrous cap (dotted arrow), a small fibrous cap ulceration (arrowhead) and minimal luminal irregularities due to thrombus remnant (solid arrow). The OCT longitudinal view shows the plaque architecture and plaque ulceration. The findings on OCT confirm the diagnosis of MINOCA. B) A patient admitted to the chest unit for a hypertensive crisis with concomitant anterior ST depression on ECG. Angiography shows an intermediate narrowing in the proximal left anterior descending artery (arrow in the left panel). OCT shows an atherosclerotic plaque with calcific components (solid arrow) in the reference cross sections. At the most narrowed site a small lumen area (less than 3.0 mm²) is present (dotted arrow). The findings on OCT are compatible with a diagnosis of MINOCA due to oxygen supply-demand mismatch (secondary ischaemia).

Figure 4

Three types of SCAD. Left panels. Schematic figure of the three different types of dissections. Reprinted with permission from. Right panel: OCT image illustrating a type 3 dissection with vessel haematoma (asterisks) and the presence of the inner three vessel layer at the site of dissection (dotted arrow).