Challenges for the Management of Pregnancy-Related Spontaneous Coronary Artery Dissection

    

    

    Figure 1:  Coronary angiography findings. Cranial left anterior (A) and
right anterior (B) oblique angiographic projections showing amid-to-distal
subocclusive LAD dissection (black arrows) with distal dye stasis (arrowhead).
LAD: left anterior descending coronary artery.
    
    

Subsequently, due to the risk of acute fetal distress and considering the patient’s gestational age, emergency cesarean section was performed. After cesarean delivery, the baby was referred to Neonatal Unit, while the mother was transferred to Coronary Intensive Care Unit for monitoring.

Troponin I concentration was 0.029ng/mL in the blood sample at admission, while the peak value reached 71.6ng/mL (normal range: 0-0.045ng/mL).

Five days later, Coronary Computed Tomography (CT) showed a partial vessel recanalization, with a remaining narrowing of the middle LAD and a hypodense surrounding soft tissue beyond the origin of the first diagonal branch, compatible as an Intramural Hematoma (IMH) (Figure 2 A,B).

The rest of clinical stay was uneventful, and the patient was discharged with a1-year dual antiplateled therapy (aspirin 100mg and clopidogrel 75mg), pantoprazole 40 mg, bisoprolol 1.2 mg, ramipril 2.5mg and atorvastatin 40mg.

A subsequent one-month follow-up CT revealed a near total dissection healing, without residual significant stenosis and a progressive IMH reabsorption (Figure 2 C,D).

Discussion

SCAD is an under-recognized cause of ACS, accounting for 0.7- 1.1% in published angiographic series [2]. It mainly affects young and otherwise healthy women, with a higher prevalence during peripartum (26-38% of all SCAD, of which approximately one third in late pregnancy and two thirds in the early puerperal period) [1,3]. Patients with pregnancy-related SCAD tend to have more sinister presentation, larger infarcted area and worse left ventricular function compared with those with SCAD related to other etiologies [4].

Although the role of pregnancy in the pathogenesis of SCAD is still unclear, hormonal and hemodynamic changes seem to play a pivotal role in modifying the normal arterial wall architecture, leading to coronary dissection [5]. Estrogen and progesterone surges are thought to drive structural connective tissue changes, including impaired collagen synthesis, increased medial mucopolysaccharide content and fragmentation of the elastic fibers, resulting in weakened media and susceptibility to SCAD [3,4]. On the other hand, the risen cardiac output and circulatory volume may increase hemodynamic shear forces, which predispose to SCAD [5,6]. Furthermore, concomitant driving pathways, such as fibro muscular dysplasia, may favor arterial beds to injury in non-atherosclerotic SCAD, including pregnancy-related coronary dissections [4,7].

Despite coronary angiography is considered the first line diagnostic approach, occasionally it may be difficult to recognize SCAD [2,8]. Particularly in no atherosclerotic SCAD, the dissection plane lies in the outer one-third of the media, leading to a no communicating IMH, which may successively access the true lumen forcing the medial-intimal layer [2].

In the present case, the ambiguous subocclusive stenosis of the middle LAD with a distal dye stasis and the otherwise remaining normal coronary arteries, raised the suspicion of SCAD, which was confirmed by further additional angiographic views (Figure 1).

Currently, there are no specific recommendations for the management of SCAD [3]. Treatment should be individualized, considering the site and extent of the dissection, number of vessels involved, the patient’s hemodynamics and availability of therapeutic facilities [1]. In hemodynamically stable patients, with distal vessel involvement and restored coronary flow, conservative treatment has resulted in a good long-term clinical outcome, especially because the majority of SCAD heal spontaneously [4,8]. Moreover, in case of distal dissected coronary segments, of small caliper, or with extensive dissections, percutaneous revascularization is hardly practicable, and over possible, it requires longer stents application, thus increasing the risk of intra-stent restenosis [6].

In our patient, considering the lack of symptoms, stable hemodynamics, and the extent and caliper of dissected LAD, we preferred to carry on adopting a conservative strategy, with medical therapy and close monitoring by non-invasive coronary CT. The patient’s uneventful course and the spontaneous vessel recanalization ruled in favor of such choice (Figure 2).

    

    

    Figure 2:  Non-invasive imaging assessment at the follow-up. Curved
multiplanar projection and 3D volume rendering CT at five-day (A;B) and onemonth
follow-up (C;D) showing a spontaneous vessel recanalization, with
progressive IMH reabsorption (yellow arrows). CT: computed tomography;
IMH: intramural hematoma.