Tabla 1. Current classification and modification proposal.

Figura 1. Cine coronary arteriography at baseline and after treatment. Angiography of a 52-year-old ...

Figura 2. Coronary computed tomography angiography. Panel A shows the left coronary artery with st...

Figura 3. Angiography at baseline and follow-up. During baseline angiography, panel A shows dissect...

INTRODUCTION

Spontaneous coronary artery dissection (SCAD) is a leading cause of myocardial infarction in young women and is still underdiagnosed. Its management can be different from the acute coronary syndrome (ACS) due to ruptured or eroded atherosclerotic plaque in epicardial arteries.

This is the case of a young woman with anterior myocardial infarction treated with bypass angioplasty revascularization with stent and 5-month follow-up.

CASE REPORT

This is the case of a 53-year-old woman without a past medical cardiovascular history or routine medication admitted with typical precordial pain of maximum intensity after a “once-in-a-lifetime” argument with a relative. The patient remained alert and normotensive at admission with oppressive precordial pain and no traits of heart failure. The ECG reveals the presence of ST-segment elevation of V3 to V6 and DI and avL that is interpreted as an ST-segment elevation acute coronary syndrome (STEACS). An emergency angiography was performed. A 6-Fr introducer sheath was inserted via right radial puncture. The cine coronary arteriography performed revealed no significant lesions in the right coronary artery with total occlusion of the middle third of the left anterior descending coronary artery (LAD) and spontaneous coronary artery dissection of circumflex arteries (type 2B Yip-Saw classification) and LAD diagnonal branch (type 2A) as shown on figure 1. Because of the compromised territory and the patient’s hemodynamic status it was decided to use a Terumo® Runthrough NS PTCA 0.014 in guidewire (Tokyo, Japan) towards the LAD. Afterwards, three 2.25 mm x 16 mm, 2.5 mm x 16 mm, and 3.0 mm x 16 mm Translumina® Yukon Chrome PC drug-eluting stents (Munich, Germany) were implanted directly and at nominal pressure from distal to middle third direction to cover the entire length of the dissection leaving 5 mm proximal and distal with good final outcomes and TIMI grade-3 flow. It was decided to use a conservative strategy in the same procedure with the left circumflex artery and LAD diagonal branch lesions to prevent possible complications. Patient’s progression was stable with an ejection fraction of 45% and apical cap on the Doppler echocardiogram at admission. She was discharged from the hospital 5 days later on prasugrel 10 mg/day, aspirin 100 mg/day, bisoprolol 2.5 mg/day, losartan 50 mg/day, spironolactone 25 mg/day, empagliflozin 10 mg/day, and rosuvastatin 40 mg/day.

The patient remained with intermittent, variable, and precordial pain with different functional class at the outpatient follow-up with no ECG changes or elevated cardiac biomarkers. The patient started cardiovascular rehabilitation. The ECG-gated SPECT performed revealed no signs of ischemia with an improved ejection fraction with respect to infarction. Due to the presence of persistent precordial pain, a coronary computed tomography angiography was performed 5 months after the index episode (figure 2) that revealed no signs of dissection to the LAD diagonal branch. Due to distal stent restenosis located at the LAD, a coronary angiography was performed (figure 3) that revealed the presence of a left circumflex artery without signs of SCAD and a partially normal LAD diagonal branch. The patient’s clinical progression was good without any signs of pump failure or ECG changes. Currently, she remains on cardiovascular rehabilitation with good functional class.

DISCUSSION

SCAD is defined as the acute separation of coronary artery layers not due to trauma or iatrogenesis. It is not associated with atherosclerotic disease of epicardial arteries and compromises coronary flow (1). The prevalence of SCAD is between 2% and 4% of all acute coronary syndromes (ACS). However, when categorized by sex and age group in the registries already published, it is responsible for 25% to 35% of all ACSs diagnosed in women between 45 and 53 years old (2).

Although, at the beginning, this entity was associated with pregnancy and rarely appeared in a few isolated case reports, the arrival of TUS and early angiography for the management of SCAD facilitated the detection of this condition (3). Currently, it is widely accepted that only 10% of all SCADs reported occur in pregnant or postpartum women. Within this group, the leading cause of infarction is a ruptured plaque even though SCAD would be responsible for 25% of all acute coronary syndromes reported (4-6). The main hypothesis of SCAD is the so-called “outside-in” hypothesis where the bleeding of vasa vasorum towards the tunica media layer leads to the formation of an intramural hematoma and the corresponding compression of the vessel lumen that eventually causes the disruption or tear of the intima layer resulting in the classic dissection tear (1,3).

There are several predisposing and triggering factors that can be found in almost all the series published to this date. Getting to know them allows us to perform the differential diagnosis of this entity among the different subgroups of patients. Age (45 to 55 years-old) and feminine sex are leading factors that should be taken into consideration and, although certain susceptible genes have been identified, collagenopathies (Ehler-Danlos syndrome, Marfan syndrome), systemic diseases (systemic lupus erythematous, Crohn’s disease), and migraine have been discussed as predisposing factors (1,2,6,7). We should mention that there is a clear association between fibromuscular dysplasia and SCAD. In the largest registry published to this date, half the women with a diagnosis of SCAD also showed dysplasia in the carotid, renal or femoral territories, which is consistent with the findings made by former studies. Therefore, screening is advised (2,7). The main triggering factor is stress—both physical and emotional—in over 50% of the cases (2,7)

In all the case series reported, the most common clinical sign was precordial pain while the classic presentation is an ACS (2, 8). It has been reported that up to 60% of the cases can be STEACS, and 7% to 8% complex ventricular arrhythmias (7,8).

Although epidemiology-based clinical suspicion is required to achieve diagnosis, it is often achieved by discard, which is why based on the coronary angiography findings, the approach can be invasive or conservative (1-3,9). The angiographic classification used was proposed by Yip-Saw. However, not all SCADs fall within this classification. It identifies type 1 (showing dual lumen on the angiography), type 2A (presence of long, anfractuous, symmetric, and narrow lesion that, distally, goes back to its normal diameter), and type 2B SCADs (similar but distally continuous without going back to its original diameter). Type 3 SCADs mimic a classic atherosclerotic lesion. Intracoronary imaging modalities are required to differentiate it (10). Currently, different changes have been proposed to the former classification because in 25% of the cases, patients present with more than just 1 dissection. We hereby propose adding 2 extra types: type 4 (total occlusions ending in a “flute lip plate” appearance), and type 5 SCADs (occurring in several coronary territories where different types of SCADs often coexist) (2,5,11). It is our understanding that only types 4 and 5 should be revascularized—only when type 4 lesions are found—and in the absence of hemodynamic instability or certain alarming signs shown on table 1.

Currently, acute treatment is conservative since the different case series published show good long-term results. Invasive treatment, however, is spared for cases of total occlusions or TIMI grade-0-1 flow in a vessel compromising most of the territory, hemodynamic instability or in situations of cardiogenic shock, persistent ischemia or complex ventricular arrhythmias (3,9). In the real world, the angioplasty is the method of choice sparing surgery for bailout situations (2,3,7,9). The complications described during invasive procedures are varied including risk of iatrogenic dissection, guidewire passage to false lumen, distal or proximal false lumen spread to stenting, persistent distal dissection, and secondary branch occlusion due to hematoma spreading. Among other strategies suggested, it is advised to use a Floppy guidewire, avoid guide catheter cannulation, keep coaxiality, limit the strength of contrast injection, try direct stenting at nominal pressure to avoid pre- and post-dilatation, and consider that the length of the sent should cover 5 mm pre- and post-lesion to avoid hematoma spreading (2,3,9,11). Since in an acute episode we run the risk of ACS and SCAD related complications per se like new dissections, referral to the coronary care unit for 3 to 5 days is advised. (2)

Long-term prognosis is good. Precordial pain can persist up to 3 years, but despite being reported in patients with angiographic follow-up, 95% of the patients heal without invasive treatment (7,3). There is no consensus on the optimal medical therapy that should be used. The use of dual antiplatelet therapy is controversial and is associated with stenting or the dissection imaging provided by IVUS or OCT (2). Anticoagulant drugs should be spared for very specific cases while the use of ACE inhibitors/ARA2, anti-aldosterone drugs, beta-blockers or calcium channel blockers should be administered based on the myocardial sequela. Their use in patients with preserved ventricular function is still more controversial. All the current evidence comes from registries and expert consensus documents (2). The same thing happens with the use of statins. Data on medical follow-up and pregnancies in women with pregnancy-related SCADs are limited, which is why management should be handled by a heart team (2,5).

It is our understanding that widening the current angiographic classification will allow us to establish the existence of multiple and simultaneously different types of clinical signs of the disease to select the most appropriate revascularization strategy while not always taking the same approach in all the lesions.

CONCLUSION

SCAD is a challenging situation when it comes to the clinical and interventional management of this entity regarding diagnosis and long-term acute treatment. Getting to know this entity is of paramount importance to approach this group of young patients.

1. Saw J, Mancini J, Humphries KH. Contemporary Review on Spontaneous Coronary Artery Dissection J Am Coll Cardiol 2016;68:297-312.

2. Adlam D, Alfonso F, Maas A, et al. European Society of Cardiology, acute cardiovascular care association, SCAD study group: a position paper on spontaneous coronary artery dissection. European Heart Journal (2018) 39,3353-68.

3. Krittanawong C, Gulati R, Eitzman D, Jneid H. Revascularization in Patients With Spontaneous Coronary Artery Dissection: Where Are We Now? J Am Heart Assoc 2021;10:e018551.

4. Singh T, Chapman AR, Dweck MR; Mills NL; Newby DE. MINOCA: a heterogenous group of conditions associated with myocardial damage. Heart 2021;107:1458-64.

5. Tweet MS; Hayes SN; Codsi E; Gulati R; Rose CH; Best PJM. Spontaneous Coronary Artery Dissection Associated With Pregnancy. J Am Coll Cardiol 2017;70:426–35

6. Hayes SN, Tweet MS, Adlam D, et al. JACC State-of-the-Art Review. Spontaneous Coronary Artery Dissection. J Am Coll Cardiol 2020;76:961-84.

7. Saw J, Starovoytov A, Aymong E, et al. Canadian Spontaneous Coronary Artery Dissection Cohort Study: 3-Year Outcomes. J Am Coll Cardiol 2022;80:1585-97.

8. Kim E. Spontaneous Coronary-Artery Dissection. N Engl J Med 2020;383:2358-70.

9. Kotecha D, Garcia-Guimaraes M, Premawardhana D, et al. Risks and benefits of percutaneous coronary intervention in spontaneous coronary artery dissection. Heart 2021;0:1–9.

10. Yip A, Saw J. Spontaneous coronary artery dissection—a review. Cardiovasc Diagn Ther 2015;5:37-48.

11. Adlam D, Tweet M, Gulati R, et al. Spontaneous Coronary Artery Dissection Pitfalls of Angiographic Diagnosis and an Approach to Ambiguous Cases. J Am Coll Cardiol Intv 2021;14:1743-56.

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Anterior infarction as the clinical presentation of a 53-year-old woman with spontaneous coronary artery dissection

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