Sudden Cardiac Death Following Thrombolysis in a Young Woman with Spontaneous Coronary Artery Dissection: A Case Report

Background

Spontaneous coronary artery dissection (SCAD) seems to be more and more recognized compared to few years ago. This is partly due to the large number of cases reports and series on this particular pathology, thereby increasing awareness of cardiologists and especially interventionists.

STEMI is the most common clinical scenario revealing SCAD and may rarely be complicated by sudden cardiac arrest [1,2]. Conservative management is the cornerstone of its treatment except where there are clinical manifestations of ongoing ischemia or hemodynamic instability with left main stem involvement [3,4].

We report a case of cardiac arrest complicating an anterior STEMI related to coronary artery dissection treated initially with thrombolysis in a young woman.

Case Report

A 34-year-old woman, a current smoker, had sudden-onset prolonged constrictive chest pain while at home, which prompted calling the Emergency Medical Service (EMS).

Twelve-lead ECG performed by the EMS team showed anterior ST-segment elevation with reciprocal ST depression in the inferior leads. Pharmacologic reperfusion was immediately started as it was going to take more than 2 h to reach the catheterization laboratory.

She received an intravenous loading dose of 250 mg aspirin and oral P2Y12 inhibitor (clopidogrel 300 mg), low-molecular-weight heparin, and bolus of intravenous 7000 IU of tenecteplase. About 15 min after receiving the thrombolytic bolus, she presented with sudden cardiac arrest resulting from ventricular fibrillation. Cardiopulmonary resuscitation, including electrical defibrillation, was immediately initiated by the EMS. After successful resuscitation, she was given 300 mg of intravenous amiodarone and intubated. She regained a pulse (low-flow 5 min, now-flow 0) and was immediately transported to our center for coronary angiography. Meanwhile, she deteriorated hemodynamically, warranting initiation of dobutamine infusion.

Coronary angiography by radial artery approach revealed an acute occlusion with staining contrast of the ostium of the proximal segment of the left anterior descending coronary artery (LAD) ostium, which persisted despite administration of intra-coronary nitrates. The Thrombolysis in Myocardial Infarction (TIMI) flow was grade 0 (Figure 1A, 1B). The other coronary arteries were normal. An intra-aortic balloon pump (IABP) was then implanted through the right femoral artery. After workhorse wire placement in the distal lumen of the LAD was performed without difficulty, flow was restored into the LAD (TIMI 2). The procedure then was completed by implantation of a long drug-eluting stent (DES) from the left main stem (LMS) toward the proximal LAD covering the LAD lesion, with restoration of TIMI flow grade III (Figure 1C, 1D). Of note, to perform the procedure simply and quickly, we did not protect the LCX. Its ostium was then pinched without flow deterioration after stent deployment. But having an ulterior motive of SCAD, and given the appearance of the occlusion in this young female patient, we decided to stop the procedure without further optimization technique due to the fragility of the coronary arteries. We intended to follow up the patient later, after stabilization, with an eventual proximal optimizing technique (POT) if needed.

The echocardiography, after angioplasty, revealed a severely reduced left ventricular ejection fraction (LVEF) at 20% and severe anterior hypokinesia without mechanical complications or pericardial effusion.

However, despite adequate reperfusion, IABP, and dobutamine infusion, the patient’s hemodynamic state remained precarious; hence, we added low-dose norepinephrine. A closer physical examination revealed very marked paleness associated with abdominal pain and low hemoglobin level. The abdominal computed tomography (CT) scan showed active bleeding of the liver and a massive hemoperitoneum. The dual antiplatelet therapy was suspended. She was temporarily stabilized by blood transfusion and adrenaline infusion and definitely by distal hepatic artery embolization followed by packing. Aspirin was then restarted the following day. Clopidogrel was replaced by ticagrelor introduced 6 days later, after bleeding complication management and patient stabilization.

After 9 days after surgery, the patient was discharged home with guideline-directed medical therapy comprising aspirin, ticagrelor, ACE inhibitor, betablocker, and statin.

Three months later, she remained asymptomatic with no events, and a planned angiography showed a quite normal appearance of the coronary arteries, with TIMI grade III flow (Figure 2A, 2B).

The first optical coherence tomography (OCT) showed under-expansion of a minor left main stem stent. We performed proximal optimizing technique (POT) with a well-sized non-compliant balloon. The second OCT revealed a well-apposed and expanded stent from the left main stem to the proximal LAD and residual hematoma as a lunar crescent, confirming, a posteriori, LAD spontaneous coronary artery hematoma (Figure 3).

The follow-up echocardiogram showed an improved LVEF at 45% with persistent anterior wall motion abnormalities.

Discussion

We report a case of acute coronary syndrome in a young woman with a single risk factor of active smoking. Recent data suggest that SCAD affects both men and women and is much more prevalent among men and older patients than previously reported [2].

A prolonged coronary artery spasm is a plausible underlying mechanism. However, it was ruled out by intracoronary nitrate administration during angiography, since the LAD occlusion persisted. A plaque rupture leading to STEMI is also a possible mechanism given the history of smoking.

In terms of management, our patient was given thrombolytic therapy, as the estimated time to arrival to the Cath lab was over 120 min, which represents “golden hours” for considering primary PCI according to current American and European recommendations [5,6].

Our case was complicated by sudden cardiac arrest related to ventricular fibrillation, which may reflect a potential intramural hematoma extension favored by thrombolysis.

Our case report adds to the evidence suggesting that thrombolytic therapy leads to poor outcomes in patients with SCAD. As reported by numerous sporadic cases, fibrinolytics has many drawbacks [7,8], even though the hemorrhagic complication seen in our patient might have been due to liver damage and rib fracture caused by the aggressive CPR conducted during cardiac arrest on a patient receiving potent antithrombotic medication, including thrombolytic therapy. This should prompt discussion about contraindication of thrombolytics when SCAD is the most plausible STEMI underlying mechanism owing to the risk of dissection expansion or coronary intramural hematoma formation [9]. In fact, the prevalence of SCAD among women with STEMI is about 20% in women ≤50 years of age, showing the relevance of fibrinolysis [10].

Rescue PCI was then performed because SCAD was highly probable. We did not use OCT because the patient was in an unstable hemodynamic status. Nevertheless, in case of dissection with an obvious radiolucent flap, OCT can be of great help by guiding guidewire placement in the true lumen and choosing the optimal stent size and landing zone in order to cover all the eventual intramural hematoma [11]. A cutting balloon could have been of great help in our patient but it was not available. Its utilization in the distal part of the occlusion has been advocated. It could have reduced the risk of hematoma extension distally or proximally, which occurred in our case, but fortunately, as a tiny shift in ostial LCX. Also, it could have changed the ostial LAD stenosis induced by hematoma and potentially avoided stenting the left main stem.

It is important to emphasize that PCI, in the context of SCAD, is very challenging due to the increased risk of extending the dissection or hematoma progression. There is also a suboptimal success rate of PCI for SCAD compared with atherosclerotic ACS [9]. In addition, PCI for SCAD may be associated with poor outcomes, including higher in-hospital mortality and major cardiac adverse events, compared to conservative management [12,13]. Thus, medical management should be the standard of care and PCI should be performed only on clinically or angiographically high-risk patients, including those with hemodynamic instability, persistent chest pain, or large myocardial involvement.

In our patient’s case, SCAD was formally confirmed 3 months later by OCT, highlighted by the remnants of the intramural hematoma.

PCI was covered by IABP to optimize hemodynamic status, even though current data do not support its routine use. That decision was legitimately questionable.

An important discussion point remains the secondary prevention of SCD in our patient. Of note, there are no published randomized clinical trials comparing medical therapy and ICD for patients with SCAD and SCD. Current data support ICD therapy only for secondary prevention in the absence of reversible causes, but a recent retrospective study did not show a benefit of secondary prevention ICD [14]. Our patient’s left ventricular function was very poor in the short-term and justified an optimal guideline-directed medical therapy to improve LVEF before considering ICD implantation.

An alternative in the acute and subacute phase could be a LifeVest wearable defibrillator, given the severe left ventricular dysfunction.

Conclusions

Spontaneous coronary artery dissection might be revealed by cardiac arrest that may compromise vital prognosis if not managed promptly. With our patient, CA was probably due to the extension of hematoma induced by thrombolysis. Although conservative treatment is the cornerstone in the management of SCAD, PCI must be considered if there is evidence of ongoing ischemia or large amount of jeopardized myocardium.