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Proximal Right Coronary Artery Diverticulum Resulting in Recurrent Distal Embolization

Igor Shkolnik, MD and Samer Salka, MD

Igor Shkolnik, MD and Samer Salka, MD

ABSTRACT: This is a case of a right coronary artery (RCA) diverticulum. We highlight the complications of distal embolization and recurrent myocardial infarctions (MI), and the successful closure with a covered stent.

A 33-year-old Khat user experienced non-ST elevation MI (non-STEMI) 3 times over 2 years. His first cardiac catheterization showed a proximal RCA ulceration. The last catheterization revealed a proximal RCA diverticulum containing a thrombus, and a thrombus at the distal PDA. A covered Jomed® stent (Jomed International AB) was placed into the proximal RCA, closing the diverticulum, and preventing future embolizations.

Patient’s atherosclerotic ulceration led to diverticular disease that resulted in blood flow stasis, thrombi, distal embolization, and repeat acute coronary events.

J INVASIVE CARDIOL 2011;23:E249-E250

Key words: covered stent, thrombus, thrombectomy

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To date, coronary artery segmental aberrations have been limited to aneurysmal disease.1 We present a case of a diverticulum of the right coronary artery (RCA) that to our knowledge has not been reported. The clinical value of this report is to highlight the potential complications of distal embolization and recurrent myocardial infarctions (MI), as well as the successful closure with a covered stent.

Case Report. A 33-year-old male Yemenite with history of smoking, hyperlipidemia, and Khat-use experienced 3 non-ST elevation MI’s (non-STEMI) over 2 years. Cardiac catheterization of his initial presentation revealed left anterior descending (LAD) coronary artery 30% stenosis and mild proximal RCA ulceration. The second occurrence showed posterior descending artery (PDA) thrombosis with near total occlusion, and mild proximal disease of the RCA with eccentric ectasia/deeper ulceration. Patient was successfully treated with balloon angioplasty to the PDA. In the interim between each MI, the patient was placed on aspirin, atorvastatin, and metoprolol tartrate, which maintained stable blood pressure and cholesterol control. The third catheterization revealed a proximal RCA diverticulum containing thrombus, plus an occlusive thrombus (embolus) at the distal PDA, without worsening LAD stenosis.

Possis AngioJet® (Medrad Medical, Inc.) thrombectomy of the distal PDA was performed without residual stenosis. A 3.5 x 16 mm covered Jomed® (Jomed International AB) stent was placed into the proximal RCA closing the diverticulum. Since then, the patient has not experienced acute cardiac events for over 7 years.

Discussion. To our knowledge and upon searching PubMed and Ovid MEDLINE (1947 to November 2010), this is the first case of a coronary artery diverticulum presented in literature. Arterial segmental aberrations stem from arterial wall weaknesses caused by atherosclerosis or congenital defects.2,3 Clearly our patient had risk factors for atherosclerosis and endothelial dysfunction, including a history of smoking and hyperlipidemia.4 The patient had no other coexisting comorbidities. He also used Khat, a chewable amphetamine-like leaf that has been linked to MI, due to transient vasospasms by its active ingredient cathinone. Heavy Khat users carry a 39-fold increased risk of acute MI development, secondary to increased myocardial oxygen demands from coronary vasoconstriction and positive ionotropic effect of cathinone induced norepinephrine release from peripheral stores.5 Vasospasm from Khat, as well as atherosclerosis, resulting in arterial ulceration/eventual diverticulum formation may all have been contributing factors to the patient’s 3 myocardial events. The larger size of the ulceration leading to diverticulum formation resulted in thromboembolism from the ulceration/diverticulum to the distal PDA. The deepening of the ulceration leading to diverticular formation, most appreciated on the last catheterization, suggests that atherosclerosis probably played a significant role in the evolution of the diverticulum. An initial medial thinning or necrosis at that spot may have been initiated by a genetic mechanism, unreported trauma, or sudden elevation of blood pressure from Khat-use. It is unknown to what extent Khat-use contributed to the evolution of the diverticulum, but cocaine, another cardiac stimulant, has been linked to coronary artery aneurysm formation.6

This case emphasizes the importance of educating Khat users regarding potential serious complications of their habit. Moreover, it highlights the significance of including Khat-use in the differential of acute MI and coronary ectasia. The thrombus noted in the distal PDA appears to have been initiated at the site of the diverticulum, since there was no atherosclerosis at that site, no residual after thrombectomy, and no recurrent events after closure of the diverticulum. This case demonstrates that utilization of covered stents for coronary ulcerations/pseudoaneurysms/diverticula can prevent future cardiac events linked to such coronary aberrations.

References

  1. Swaye PS, Fisher LD, Litwin P, et al. Aneurysmal coronary artery disease. Circulation. 1983;67(1):134-138.
  2. Iwai-Takano M, Oikawa M, Yamaki T, et al. A case of recurrent myocardial infarction caused by a giant right coronary artery aneurysm. J Am Soc Echocard. 2007;20(11):1318.e5-e8.
  3. Maldonado JA, Henry T, Gutiérrez FR. Congenital thoracic vascular anomalies. Radiol Clin North Am. 2010;48(1):85-115. 
  4. Hoffman R, Benz EJ, Shattil SJ, et al. Epidemiology and prevention of atherosclerosis. In: Hematology: Basics Principles and Practice. 5th ed. Philadelphia, Pa: Elsevier Churchill Livingstone; 2008:chap 136.
  5. Magdum S. An Overview of Khat. Addictive Disorders & Their Treatment. 2011;10(2):72-83.
  6. Satran A, Bart BA, Henry CR, et al. Increased prevalence of coronary artery aneurysms among cocaine users. Circulation. 2005;111(19):2424-2429.

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From the Premier Cardiovascular Specialists, PC and Oakwood Hospital Medical Center, Dearborn, Michigan.
Disclosure: The author has completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. The author reports no conflicts of interest regarding the content herein.
Manuscript submitted February 25, 2011, provisional acceptance given March 21, 2011, final version accepted May 25, 2011.
Address for correspondence: Samer Salka, MD, FACC, 15120 Michigan Avenue, Dearborn, MI 48126. Email: samersalka@gmail.com