Catheter-Induced Bilateral Coronary Ostium Dissection in a Patient with Long-Term Steroid Therapy

ABSTRACT: Catheter-induced coronary dissection is a very rare and serious complication. We report a case of a 44-year-old man with catheter-induced bilateral coronary dissection that occurred during diagnostic coronary angiography for angina. The coronary dissection was successfully treated by stenting at the left main trunk, the left anterior descending artery, and the right coronary ostium. The patient had been maintained on long-term steroid therapy for nephrotic syndrome. The effect of long-term steroid therapy on bilateral coronary dissection is worthy of discussion.

J INVASIVE CARDIOL 2012;24(11):E305-E307

Key words: iatrogenic bilateral coronary dissection, long-term steroid therapy

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Case Report. A 44-year-old man was admitted to our hospital for morning chest pain. His coronary risk factors were hypertension, dyslipidemia, diabetes, and smoking. He had been diagnosed with nephrotic syndrome and had taken 12.5 mg prednisolone per day for 14 years. Initial electrocardiogram (ECG) showed ST elevation in the inferior leads. The transthoracic ECG showed normal left ventricular ejection fraction at 65.2% and no asynergy. We suspected vasospastic angina. The first injection of the right coronary angiography (CAG) revealed a slight stenosis in the ostial segment (figure not shown), which we judged as catheter-induced spasm. The next injection revealed the progression of stenosis in the right ostial lesion (Figure 1A). However, coronary flow, hemodynamics, and 12-lead ECG remained normal. Since we considered it takes a little time to relieve the spasm spontaneously, a left CAG was performed before the final right CAG. The first injection of the left coronary artery (LCA) showed normal coronary arteries (Figure 2A). However, the last injection of the LCA revealed the catheter-induced dissection of left main trunk (LMT) extending to the mid-portion of the left anterior descending (LAD) artery (Figure 2B).

The patient suddenly began to experience severe chest pain, and ECG showed remarkable ST elevation in precordial leads. Rapidly, the diagnostic catheter was exchanged for a 7 Fr Judkins Left 4 guiding catheter (Medtronic), and emergent percutaneous coronary intervention (PCI) was performed. An intravascular ultrasound (IVUS) confirmed that the Runthrough NS floppy wire (Terumo) had successfully passed through the true lumen of the LAD (Figure 2C). After that, two bare metal stents (Liberte 4.0 x 12 mm for LMT-LAD and Liberte 4.0 x 24 mm for LAD mid-portion, Boston Scientific) were implanted in the LMT-LAD dissected lesion. An intra-aortic balloon pump was inserted because the hemodynamics deteriorated during the PCI. Post-dilatation of the LMT-LAD was performed using the Quantum maverick 4.0 x 8 mm (Boston Scientific). The final left CAG was excellent (Figure 2D), and the post-procedural IVUS also showed good patency. Next, a right CAG was performed to confirm the improvement of coronary spam in the right ostial lesion. However, the right CAG revealed a dissection in the ostial lesion associated with catheter-induced spasm (Figure 1B). We decided to perform PCI immediately. A 7 Fr Judkins Left 4 guiding catheter (Medtronic) was engaged, and the Runthrough NS floppy wire (Terumo) was passed through the true lumen of the RCA and confirmed with IVUS (Figure 1C). We sealed the dissection from origin to end by implanting two bare metal stents (S-stent 4.0 x 8 mm and S-stent 4.0 x 23 mm, Biosensors International). The final CAG and IVUS imaging were satisfactory (Figure 1D) and the subsequent hospital course was uncomplicated.

Discussion. Coronary angiography (CAG) is a very widespread and relatively safe procedure in the clinical practice of cardiology. Of the complications of CAG, catheter-induced coronary dissection is a rare but well-recognized life-threatening complication. In addition, bilateral coronary dissection is extremely rare. Numerous factors can contribute to increased risk for catheter-induced bilateral coronary dissection. Here we reported a case of catheter-induced bilateral coronary dissection in a patient on long-term steroid therapy that was successfully resolved by stenting. To the best of our knowledge, this is the first case of catheter-induced bilateral coronary dissection reported in the English literature.

Coronary dissection can occur spontaneously¹ or can be iatrogenic^2,3 as in this case. The incidence of iatrogenic left main coronary artery dissection was reported to be about 0.07%.^4,5 According to Eshtehardi et al, 51,452 coronary catheterization procedures have been performed: 35,789 CAGs and 15,663 PCIs. In all, 38 iatrogenic left main dissections (0.07% of coronary catheterization procedures) have been diagnosed, 22 during CAG (0.06% of CAGs) and 16 during PCI (0.01% of PCIs).⁵ The most frequent causes of dissection were diagnostic catheter-induced (58%), deep intubation of the guiding catheter during balloon retrieval (26%), and guiding catheter-induced during PCI (16%).⁵ A number of factors are associated with increased risk for catheter-induced coronary dissection. These includes atherosclerotic LMT disease, the use of Amplatz-shaped catheters, catheterization for acute myocardial infarction, unskilled catheter manipulations, rapid contrast injection, deep intubation of the catheter within the coronary artery, and abnormal anatomy of the coronary ostia.⁶ In this case, both the mechanical trauma due to catheter manipulation and the vascular tissue changes resulting from long-term steroid therapy may have contributed to the initiation of dissection.

It is well known that the long-term use of steroids is associated with atherosclerosis of arteries.⁷ Steroid therapy often induces coronary risk factors, namely obesity, diabetes, dyslipidemia, and hypertension. In this case, the patient had hypertension, dyslipidemia, and diabetes. However, coronary atherosclerosis did not appear to be advanced, as the IVUS demonstrated. Coronary dissection is very unique and interesting in this case, because the patient had few atherosclerotic lesions in spite of long-term steroid therapy. The dissection flap of the LMT extended to the 3rd diagonal branch. It means that the absence of atherosclerosis is a risk factor for propagation of coronary dissection, because atheroma may lead to atrophy and scarring, which prevents propagation of dissection.⁸

It is known that long-term steroid therapy has adverse effects on the connective tissue of arteries. That is, steroids inhibit the formation of the chondroitin sulfate and granulation tissue, and this leads to medial degeneration and necrosis of the medial aortic wall.⁹ There have been previous reports, one of aortic dissection and another of spontaneous rupture of pulmonary artery, both in females with long-term steroid therapy.^9,10 However, it is unknown whether this can happen to the coronary artery. We speculate that the fragility of coronary arterial wall due to long-term steroid therapy may be the cause of this catheter-induced bilateral coronary dissection.

Iatrogenic coronary dissection has been treated successfully with conservative therapy,¹ PCI,^2,11 or coronary artery bypass graft surgery.¹² Recently, it was reported that successful bail-out stenting resulted in good long-term survival.^2,4,11 Therefore, we also opted for PCI, and it was successfully completed. On the other hand, when the dissection is seen angiographically without obstruction to flow such as the RCA of this case, the choice of stenting versus conservative management is made on a case-by-case basis.^6,13 The interventional cardiologists should keep in mind the possibility of this complication in the patients with long-term steroid therapy even during CAG.

Acknowledgments. The authors thank Dr. Toshiyuki Aokage, Dr. Hiroshige Murata, Dr. Hiroomi Suzuki, Dr. Yusuke Hosokawa, Dr. Ryo Munakata, Dr. Koichi Akutsu, and Dr. Naoki Sato for their assistance in taking care of this patient and Dr. Takeshi Yamamoto for his review of this manuscript.

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From Nippon Medical School Hospital, Intensive and Cardiac Care Unit, Tokyo, Japan.
Disclosure: The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. The authors report no conflicts of interest regarding the content herein.
Manuscript submitted April 16, 2012, provisional acceptance given May 16, 2012, final version accepted May 30, 2012.
Address for correspondence: Hideki Miyachi MD, Intensive and Cardiac Care Unit, Nippon Medical School Hospital, 1-1-5 Sendagi, Bunkyo-ku, Tokyo, Japan 113-8603. Email: hidep-@nms.ac.jp