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| CASE REPORT |
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| Year : 2006 | Volume
: 7
| Issue : 4 | Page : 146-149 |
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Intracoronary stenting of sponraenous left main coronary artery dissection using drug-eluting stent
Prashanth Panduranga1, Mohammed K Mukhaini2
1 Specialist Cardiologist, Department of Cardiology, Royal Hospital, Muscat, Oman
2 Consultant Cardiologist, Department of Cardiology, Royal Hospital, Muscat, Oman
| Date of Web Publication | 17-Jun-2010 |
Correspondence Address:
Prashanth Panduranga
Specialist Cardiologist, Department of Cardiology, Royal Hospital, Muscat-111
Oman
 Source of Support: None, Conflict of Interest: None  | Check |
How to cite this article:
Panduranga P, Mukhaini MK. Intracoronary stenting of sponraenous left main coronary artery dissection using drug-eluting stent. Heart Views 2006;7:146-9 |
How to cite this URL:
Panduranga P, Mukhaini MK. Intracoronary stenting of sponraenous left main coronary artery dissection using drug-eluting stent. Heart Views [serial online] 2006 [cited 2023 Dec 8];7:146-9. Available from: https://www.heartviews.org/text.asp?2006/7/4/146/63898 |
 Introduction | |  |
Spontaneous coronary artery dissection (SCAD) is rare. Only 224 cases have been reported in the literature [1] . It is the result of an intimal tear and intramural hematoma in the media of the arterial wall that creates a false lumen. Expansion of this lumen through blood or clot accumulation along with dissection flap leads to compression of the true lumen and myocardial ischemia presenting as acute coronary syndromes or sudden death. We present a case of SCAD treated with drug eluting stent.
| Case Presentation | | |
A 25-year Omani lady presented to our emergency department with a history of prolonged retrosternal chest pain radiating to the left arm. The pain started at rest and lasted about 30 min. The pain was associated with vomiting and brief syncopal episode. She has no history of any coronary risk factors, nor had she used oral contraceptive pills or illicit drugs. Physical examination revealed a blood pressure of 105/72 mmHg, a pulse rate of 80/minute and normal cardiovascular examination. Initial ECG showed sinus rhythm with transient 1 mm ST elevation in V1-V3, I, AVL followed by normalization of ST with minor T inversion in V1-V6 and AVL. Troponin I was positive at 1.83 ng/ml (normal range < 0.04 ng/ml).
She was admitted to the Coronary Care Unit with a diagnosis of acute coronary syndrome. She was started on aspirin, clopidogrel, enoxaparin, nitrates, and atenolol. She underwent coronary angiography via right femoral artery approach on the third hospital day.. Left coronary (LCA) injection demonstrated linear dissection of the left main coronary artery starting from the mid-segment and extending into the left anterior descending artery (LAD), which looked narrowed proximally up to Diagonal 1 (D1) followed by a long well-delineated dissection flap in the mid LAD with TIMI 3 distal flow. [Figure 1].
The left main coronary artery had a clear cut intimal flap with double lumen and the diameter of the LAD was decreased at the proximal portion. There was a dissection flap at mid-portion with an endoluminal cap. The circumflex and right coronary arteries appeared normal.
Following the coronary angiogram, the patient started complaining of chest pain with drop in blood pressure to 90/60mmHg. Inotropes were started and proceeded to angioplasty after discussion with the surgeons.
A diagnosis of spontaneous coronary artery dissection was made. The dissection involved the left main and LAD up to mid third. The cardiac surgeons' opinion was sought and it was concluded that, as the patient was unstable, immediate stenting would be a better option than surgery. Angioplasty and stenting with a drug eluting stent (DES) was therefore performed.
A temporary pacing wire was placed in the right ventricle through left femoral vein approach. After positioning JL3.5 7 French guiding catheter using 0.014 inch Galeo floppy (Biotronik) guide wire the true lumen was crossed and the wire placed in the distal LAD with free movement of the tip. Direct stenting of the left main was done; 3.5 x 32 mm TAXUS (Boston scientific) stent was deployed at 10 atm. into left main and proximal LAD up to D1 with complete sealing of dissection flap. [Figure 2].
The mid LAD dissection was initially treated with prolonged dilatation using 2.75 x 20 mm World Pass Balloon (Cordis Corporation) at 8 atm attempting to 'glue' the dissection and to avoid another stent but this was unsuccessful. This was followed by a 2.75 x 16 mm TAXUS stent deployed at 16 atm overlapping with the proximal stent followed by high pressure dilatation of overlapping segment to 16 atm. Final results showed no residual dissection and there was TIMI 3 flow in the LAD. [Figure 3]. Patient received peri-procedural intravenous heparin and bolus dose of tirofiban.
Post procedure, the patient remained hypotensive, was resuscitated with intravenous fluids, inotropes and intra-aortic balloon pump for 12 hrs. Final check injection showed no residual dissection with TIMI 3 flow [Figure 4]. She developed right groin haematoma with drop in hemoglobin requiring blood transfusion. She was gradually weaned from supports and the rest of her stay was uneventful.
Her echocardiogram showed nondilated left ventricle with septal hypokinesia, good LV systolic function and trace pericardial effusion .On hospital discharge, she was advised to continue post-stent antithrombotic regimen (oral aspirin/clopidrogel) in addition to beta blockers. She was also advised to come for follow up coronary angiogram at 3 and 6 months.
| Discussion | | |
The incidence of SCAD occurs at rates of 0.1 to 0.28% of all angiographic studies [2],[3] . The majority of cases, about 70-75% [2],[4] are diagnosed post-mortem. Mortality is due to sudden death in 50% of cases. Twenty percent (20%) die in the hours following the dissection 5. In those surviving the initial event, the survival rate is reported to be 82% [4] .
SCAD is the result of an intimal tear and intramural hematoma in the media of the arterial wall that creates a false lumen. Expansion of this lumen through blood or clot accumulation along with dissection flap leads to compression of the true lumen and myocardial ischemia presenting as acute coronary syndromes or sudden death.
Most reports novolve apparently healthy, young to middle aged women (78%; mean age 40 years) without overt risk for coronary artery disease and without severe coronary atheromatosis2. One-third of women with SCAD are in the peripartum state [1] .
The etiology is poorly defined, but many studies have identified 3 types of risk factors, namely atherosclerotic disease, pregnancy or peri-partum period and an idiopathic cause [1],[2],[4] . SCAD has also been associated with oral contraceptive ingestion, cocaine use, blunt trauma, Marfan's syndrome, cystic medical necrosis, hypersensitivity vasculitis, coronary spasm, hypertension, fibromuscular dysplasia, after intense physical exercise and autoimmune thyroiditis [1],[6] .
The condition is generally discovered on coronary angiography, which may reveal dissections in single or multiple coronary arteries with or without left main coronary artery involvement. Men are more likely to have SCAD in the right coronary artery system than women (50.8 versus 13.0%), whereas women had a higher proportion of LAD artery involvement (46.6 versus 25.4%) and left main artery involvement (14.9 versus 3.2%). The circumflex artery was infrequently involved in men and women [1] .
The angiogram may show narrowing or compression of coronary arteries with decreased diameters and compromised coronary blood flow which may range from TIMI 0-3. Dissection flaps may or may not be seen6. When seen, double lumen may be noted with contrast staining of false lumen. IVUS has been used to diagnose and assess SCAD [7],[13] .
Treatment strategy in SCAD is on a case-by-case basis and based on clinical and angiography results. Medical treatment can be considered in asymptomatic patients [2],[5],[8] . Medical treatment includes antiplatelet treatment with aspirin and clopidrogel to prevent platelet-rich thrombus formation. There are few data on the use of low molecular weight heparin or glycoprotein IIb/IIIa inhibitors [8],[9],[10] . Thrombolytic agents were used in the past [2] , but are contraindicated as they may worsen the dissection process. Beta Blockers are also used for their effects on heart rate, coronary blood flow, and vessel wall shear stress.
Percutaneous intervention has been increasingly performed for SCAD depending upon location and extent of dissection. In the absence of severe LV impairment, symptomatic patients with single vessel dissection not involving the left main coronary artery have benefited from primary coronary stenting [11],[12] . The deployment of a stent tacks back the dissection flap but very long stents may be necessary when the dissection flap is extensive, although the use of drug eluting stents may reduce this concern as in our case. Recently there was a report on the use of drug-eluting stents in SCAD deployed in the LAD [13] .
CABG is generally recommended as first-line treatment when several coronary vessels are involved [4],[5],[14] and in left main stem dissection[15]. But in our case as there was a long dissection starting from the left main with extension to mid LAD we went ahead with stenting of left main and LAD dissection with excellent final results. CABG was also an option but there was a high chance of propagation of this dissection to the distal LAD, hence to limit the dissection immediate stenting was considered the first choice of management.
| Conclusion | | |
In conclusion, to the best of our knowledge, this is the only case report describing intracoronary drug eluting stent implantation of spontaneous left main dissection in a young patient with acute coronary syndrome. This report supports the proposition that percutaneous coronary intervention with use of drug eluting stents must be the treatment of choice for single vessel dissection. Patients with multivessel dissection should go for coronary artery bypass grafting.
| References | | |
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[Figure 1], [Figure 2], [Figure 3], [Figure 4]
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