Incidental Spontaneous Coronary Dissection: An Interventionist's Dilemma.

Spontaneous coronary artery dissection (SCAD) is an uncommon entity, frequently presenting as ST-elevation myocardial infarction (MI) or sudden cardiac death. It is usually reported in association with pregnancy and has a high mortality. We present here a case of asymptomatic dissection of the right coronary artery, incidentally detected, in a young normotensive male when coronary angiography was done following acute anterior wall MI. This patient had none of the risk factors to which SCAD is generally ascribed. While management of the infarct-related artery was clear-cut, whether or not to intervene for this nonocclusive dissection was a difficult decision. A conservative approach was finally adopted for the spontaneous dissection and the patient is faring well till date.

INTRODUCTION

Spontaneous coronary artery dissection (SCAD) is an uncommon entity, frequently presenting as ST-elevation myocardial infarction (MI) or sudden cardiac death. Usually, it is reported in pregnant females. Case fatality rate as high as 80% has been reported.[1] We present here a case of incidental finding of coronary artery dissection in noninfarct-related artery in a young normotensive male with acute anterior wall MI.

CASE REPORT

A 34-year-old male presented to the emergency with severe chest pain 1-day back associated with diaphoresis and multiple episodes of syncope over the past few hours. Smoking was the only atherosclerotic risk factor present.

Physical examination revealed hypotension (systolic blood pressure of 60 mmHg), bradycardia (pulse rate 20/min), and basal crepitations. There was no murmur on auscultation. Electrocardiogram (ECG) revealed complete heart block with a broad QRS escape of q with Right Bundle Branch Block (qRBBB) morphology [Figure 1]. On regaining sinus rhythm, ST-segment elevation in leads V1 through V5 and qRBBB morphology was evident; suggestive of anterior wall MI [Figure 2]. Echocardiogram demonstrated hypokinesia in the left anterior descending (LAD) territory with left ventricle (LV) ejection fraction of 39%.

Figure 1

Presentation electrocardiogram showing complete heart block with qRBBB morphology escape rhythm

Figure 2

Electrocardiogram after regain of sinus rhythm showing qRBBB with ST elevation in precordial leads

The patient underwent temporary transvenous pacing and vasopressor support was initiated. Standard anti-platelet and anti-ischemic therapy in accordance with current guidelines was given. Pressures stabilized soon after pacing, and the rhythm reverted to sinus thereafter.

The patient was taken up for angiography with intent to revascularize. The left coronary angiography showed a significant stenosis in the mid-segment of LAD [Figure 3]. The right coronary angiogram revealed presence of a nonocclusive dissection in the proximal right coronary artery (RCA) with maintained thrombolysis in myocardial infarction 3 (TIMI 3) flow [Figure 4]. There was no evidence of dissection in the LAD.

Figure 3

Left coronary angiogram. Right anterior oblique view with cranial angulation showing severe stenosis in the middle segment of left anterior descending artery

Figure 4

Right coronary angiogram. Left anterior oblique view showing nonocclusive dissection in the proximal right coronary artery. This was managed conservatively

As the LAD was the infarct-related artery, the LAD lesion was addressed with balloon angioplasty followed by implantation of a drug-eluting stent. A conservative approach was adopted for the incidentally diagnosed RCA dissection. The patient had an uneventful convalescence and is currently in our follow-up.

DISCUSSION

Spontaneous coronary artery dissection is a little-studied entity, encountered primarily in females with a male to female ratio of 1:4.[23] While it was earlier believed to be exceedingly rare, a recent study using optical coherence tomography has ascribed as many as 4% cases of acute coronary syndrome to SCAD.[4] While up to a quarter of patients with SCAD may have involvement of more than one vessel, and recurrence rates as high as 20% have been described, the finding of SCAD in noninfarct-related artery when the infarct is resulting from atherosclerotic disease has not been described earlier.

Another remarkable finding in this patient was the absolutely silent nature of this dissection, in an individual with none of the many ascribed risk factors for SCAD – female sex, peripartum state, hypertension, preceding heavy exertion, autoimmune disease, connective tissue disease or cocaine intake.[5] It is tempting to argue that the dissection may have been precipitated by the hyperadrenergic state accompanying acute anterior wall MI, and its pain at that stage may have been concealed by the pain of the anterior wall MI. However, with no ECG or echocardiographic manifestation, the timing of the dissection is at best a matter of conjecture.

There is little consensus regarding the ideal management of SCAD. In their analysis of 440 reported cases of SCAD, Shamloo et al. concluded that an aggressive management with percutaneous or surgical intervention yielded better results.[6] However, extrapolating this inference to an asymptomatic patient with a nonocclusive dissection would be naïve. It is clear that percutaneous interventions for SCAD have a higher likelihood of getting complicated than when these are done for unstable plaques, and select cases may fare better with conservative management.[2] Furthermore, the golden rule is to leave the noninfarct related vessel untouched as far as possible. As mentioned earlier, our patient's blood pressure had stabilized, and the rhythm had reverted to sinus when he was taken up for the procedure. Hence, in view of the asymptomatic and nonocclusive nature of the dissection with preserved TIMI 3 flow as well as its presence in a noninfarct-related artery we opted for a conservative strategy for the RCA, while going ahead and stenting the LAD.