The follow-up of myocardial injury and left ventricular function after spontaneous coronary artery dissection

Abstract

Monitoring patients with spontaneous coronary dissection (SCAD) is critical in their care, as there are no accepted recommendations. To this end, finding clinical or imaging predictors of recurrent events in these patients is essential for predicting adverse events and guiding treatment decisions between conservative medical therapy and percutaneous coronary intervention. Myocardial injury and left ventricular function after SCAD can be variable parameters that require monitoring. Echocardiography and cardiac magnetic resonance are two useful imaging techniques to do so. This review aims to analyze previously published results on monitoring myocardial injury and left ventricular function in SCAD patients while highlighting the potential benefits of contemporary imaging techniques that could further improve patient care in the future.

Keywords: cardiac magnetic resonance; echocardiography; follow-up; left ventricular function; myocardial injury; spontaneous coronary artery dissection.

Figure 1

Proposed algorithm for evaluation of patients with recurrent chest pain following previous SCAD episode [Designed according to reference (12)]. ACS, acute coronary syndrome; CMR, cardiac magnetic resonance; CTCA, computer tomography coronary angiography; hs-troponin, high-sensitivity troponin; ICA, invasive coronary angiography; OCT, optical coherence tomography; IVUS, Intravascular ultrasound; SCAD, spontaneous coronary artery dissection.

Figure 2

A 42-year-old woman presented as STEMI anterior localization SCAD on left anterior artery type 4 and TIMI flow 0, treated with percutaneous transluminal coronary angioplasty (PTCA) without implantation of stents. Late gadolinium enhancement (LGE) was seen in the sub-endocardium in the medio-apical part of the septum apical parts of inferior and posterior walls and transmural in the apical part of the septum and anterolateral walls of LV. Post-contrast T1 mapping identified the zone of fibrosis, which was the zone of infarction and was also present in apical segments of LV. In addition, the peri-infarct area had a high T1 signal. The size of fibrosis (infarct size) was 13%.

Figure 3

A 43-year-old woman presented as STEMI anterior localization, SCAD on left anterior artery type 3, and TIMI flow 0, treated with percutaneous coronary intervention (PCI) and implanted four stents guided with intravascular ultrasound (IVUS). LGE was seen in the medio-apical part of the septum, apical parts of the anterior wall transmurally, and in the medial parts of the anterior wall in the sub-endocardial layer. Using post-contrast T1 mapping, the zone of fibrosis, which was the zone of infarction, was also present in the same segments. The size of fibrosis (infarct size) was 17%.

Figure 4

A 55-year-old woman presented STEMI anterior localization, SCAD on left anterior artery type 2A, and TIMI flow 2, treated with conservative medical therapy. There was no LGE in the myocardium of LV. Using post-contrast T1 mapping, the values were normal. The infarct size was 0%.

Figure 5

A young woman presented with STEMI anterior localization and SCAD type 4 on the left anterior artery. She underwent treatment with PTCA. The baseline GLS and regional longitudinal strain were measured, and the baseline LVEF was found to be 38% (A). GLS and regional longitudinal strain in follow-up after 1 month were presented in one young woman in part (B). The control LVEF value was 48%.

Figure 6

The baseline GLS and regional longitudinal strain in one young woman with SCAD type 3 presented as STEMI anterior localization who was treated with PCI and implanted four stents. The baseline LVEF was 43% (A). The improved GLS and regional longitudinal strain were seen in the follow-up of the patient after 1 month (B). The control LVEF value was 53%.

Figure 7

Patient with SCAD type 2A of left anterior artery treated with medical therapy. The baseline LVEF was 52% (A). Slightly improved GLS and regional longitudinal strain were seen in the follow-up of the patient after 1 month (B). The control LVEF was 65%.