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Inability of Intracoronary Stenting to Provide Long-Term Relief for Coronary Compression (Full title below)
Inability of Intracoronary Stenting to Provide Long-Term Relief for Coronary Compression Secondary to Chronic Constrictive Pericarditis
pg. E13 - E15 ABSTRACT: Chronic constrictive pericarditis can result in extrinsic compression of coronary arteries during diastole. We present one such case wherein the coronary compression and the resultant cardiac ischemia developed late after surgical pericardiectomy, and treatment with intracoronary stenting was unsuccessful. Issues pertaining to management of this rare condition are discussed and a case made for surgical treatment for such patients. J INVASIVE CARDIOL 2010;22:E13–E15 Key words: Cardiac ischemia; Extrinsic diastolic coronary compression Diastolic compression of a coronary artery is a rare condition and likely to result in significant coronary ischemia since the major coronary blood flow occurs in diastole.1 Potential etiologies include chronic constrictive pericarditis. As the left ventricle expands during diastole and compresses the coronary artery against a noncompliant pericardium or epicardial scar, a significant dynamic narrowing of the epicardial coronary segment can develop and lead to ischemia in the myocardial territory supplied. The condition is distinct from a myocardial bridge which denotes a segment of epicardial coronary artery embedded within the myocardium and causes systolic compression of the involved coronary segment. There is no consensus in the medical literature about treatment of systolic myocardial bridges; our understanding and management of diastolic coronary compression, in comparison, is even more limited. Case Report. A 57-year-old man with a remote history of effusive-constrictive pericarditis presented with symptoms of exertional dyspnea and recurrent signs of constrictive pericarditis. He had undergone a pericardiectomy 20 years earlier. His co-morbidities included hypertension and peripheral arterial disease. An invasive cardiac evaluation for anginal symptoms 2 years prior to presentation had revealed non-significant diastolic compression of the left anterior descending artery and mild reduction in left ventricular systolic function. At that time he was managed with atenolol, lisinopril, hydrochlorothiazide, nifedipine and clonidine. He had recently returned from a cross-country car ride and presented with orthopnea, paroxysmal nocturnal dyspnea, and lower extremity edema. A spiral computed tomographic scan revealed no evidence of pulmonary embolism, but did show bilateral small pleural effusions and hazy ground glass opacities suggestive of mild congestive heart failure. A transthoracic echocardiogram revealed mildly reduced left ventricular performance, mild left ventricular hypertrophy, and mildly reduced right ventricular performance. These findings were unchanged in comparison with an echocardiogram performed two years earlier. Adenosine myocardial perfusion scintigraphy revealed a mild stress-induced perfusion defect in the anterior wall consistent with ischemia of left anterior descending territory. Invasive cardiac evaluation revealed equalization of diastolic pressures, and inter-dependence of ventricular pressures consistent with a constrictive physiology (Table 1, Figure 1). Coronary angiography revealed no significant coronary artery disease; however the proximal segments of the left anterior descending and ramus intermedius arteries demonstrated focal diastolic compression (Figure 2). Fluoroscopy revealed a significant band of pericardial calcification spanning these sites of compression. Using a 0.014 inch PressureWire (St. Jude Medical, St. Paul, Minnesota), fractional flow reserve in the left anterior descending artery and the ramus interdius branch was calculated to be 0.74 and 0.88, respectively. Magnetic resonance imaging of the heart confirmed a decreased ejection fraction and localized area of epicardial calcification at the base of the heart. Congestive heart failure improved with addition of loop diuretics. Percutaneous and surgical revascularization options for managing his coronary ischemia were discussed and a decision made to attempt percutaneous coronary intervention first. A 3.5 x 13 mm Cypher (Cordis, Miami Lakes, Florida) stent was successfully deployed in the left anterior descending artery at the site of diastolic compression. Control angiogram revealed no diastolic compression of the coronary artery. Symptoms of exertional dyspnea improved, but recurred within 6 weeks. A repeat adenosine myocardial perfusion study revealed significantly worse perfusion in the anterior wall. Coronary angiography confirmed coronary restenosis. Fluoroscopy revealed a significant stent crush at the site of extrinsic compression from the pericardial calcification. Repeat pericardiectomy and single vessel bypass to left anterior descending artery was performed without complications. The patient demonstrated significant improvement in his signs and symptoms and was asymptomatic on his follow-up visit a year later. Discussion. 1. Extrinsic compression of coronary arteries as a cause of cardiac ischemia: Systolic compression of an epicardial coronary artery because of a myocardial bridge is seen in 0.5–16% of coronary angiograms.2,3 Myocardial bridges have been causally related to development of acute coronary syndromes,4 coronary spasm,5 ventricular septal rupture,6 arrhythmias (including supraventricular tachycardia and ventricular tachycardia),7,8 exercise-induced atrioventricular conduction block,9 myocardial stunning,10 transient ventricular dysfunction,11 early death after cardiac transplantation,12 and sudden cardiac death.13–15 Despite the possibility of these adverse outcomes, two prospective natural history studies of systolic myocardial bridging suggest that most patients have a benign long term course.16,17 Diastolic coronary artery compression is an acquired condition that has not been well reported. Goldberg et al1 have described a patient with calcific tuberculous pericarditis who demonstrated complete “diastolic obliteration” of an obtuse marginal branch of the left circumflex artery. The patient underwent pericardiectomy with complete resolution of his symptoms. In this case a repeat coronary angiogram was not performed, but it was hypothesized that diastolic filling of the left ventricle “stretched and obliterated” the vessel against the fixed noncompliant pericardium. We have reported a heart transplant recipient who developed diastolic coronary compression of his major diagonal branch. Coronary ischemia was demonstrated on myocardial perfusion imaging. A self-expanding coronary stent was used to relieve the extrinsic compression on the coronary artery with a sustained improvement on long-term follow-up. It was theorized that this patient may have had pericardial scarring as a remnant of the episode of cellular rejection.18 In a study of patients with constrictive pericarditis, derangements in coronary flow reserve were demonstrated in the left anterior descending artery. Though none of these patients had signs of systolic or diastolic coronary artery compression on routine coronary angiography, quantitative coronary angiography demonstrated decreased coronary artery compliance due to a lack of significant coronary dilatation following end-diastole.19 Pericardial constriction, therefore, can lead to coronary ischemia because of extrinsic compression of epicardial coronary arteries during diastole. 2. Recurrence of pericardiac constriction following pericardiectomy: The definitive treatment of chronic constrictive pericarditis is pericardiectomy.20 While partial decortication, limited to the anterior and lateral surface of the ventricles, is advocated by some to achieve better results; others believe that an extensive pericardiectomy should be performed to obtain as complete a decompression of the two ventricles as possible. A review of the few reports in literature about repeat operations for recurrent pericardial constriction, reveals that all of the reported cases were as a result of partial pericardiectomy with residual pericardium in the posterior surface of the heart. In this case there were signs of calcification near the base of the heart along the anterior surface.20–23 Our patient had much of his parietal pericardium removed, as a pericardiectomy had been performed nearly 20 years prior. The cardiac MRI suggested that there was a small area of scar tissue at the base of heart, which corresponded to the area of diastolic compression. 3. Intracoronary stenting versus repeat pericardiectomy for extrinsic coronary artery compression: Given the noncompliant nature of the scar tissue causing the compression, it can be argued whether a self expanding stent made of nitinol would be a better device than a balloon expandable stent. In the absence of a Nitinol stent for this application, a balloon expandable stainless steel stent was used in this case and resulted in a stent fracture within a span of 2 months. Stent fractures, although rare, have been mainly reported to complicate stenting in peripheral arterial distributions. It has, however, been reported to affect stents deployed across a systolic myocardial bridge,24 a clinical situation similar to that of this case. Caution is, therefore, appropriate when considering stents for any stenotic lesion because of an extrinsic coronary compression. From the University of Chicago Medical Center, Chicago, Illinois The authors report no conflicts of interest regarding the content herein. Manuscript submitted July 24, 2009, provisional acceptance given August 4, 2009, final version accepted August 13, 2009. Address for correspondence: Dr. Neeraj Jolly, MD, DM, University of Chicago Medical Center, 5841 S Maryland Avenue, MC 5076, Chicago, IL 60637. E-mail: njolly@medicine.bsd.uchicago.edu2. Angelini P, Trivellato M, Donis J, Leachman RD. Myocardial bridges: A review. Prog Cardiovasc Dis 1983;26:75‚Äì88.
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