Catheterization and Cardiovascular Interventions 65:271–275 (2005)
Diastolic Coronary Artery Compression in a Cardiac Transplant Recipient: Treatment With a Stent Ravi K. Garg,
MD,
Allen S. Anderson,
MD,
and Neeraj Jolly*
MD
Myocardial bridges, with resultant systolic compression of the coronary artery, are common inborn anomalies that generally have a benign course. Diastolic compression of the coronary artery, however, is a rare finding that is believed to be an acquired lesion. It can be hypothesized that during diastole, when left ventricular filling occurs, the coronary artery is compressed against epicardial scar tissue or a noncompliant pericardium. This can then lead to diminished intracoronary blood flow. We present a case of functionally significant diastolic coronary artery compression in a cardiac transplant recipient who was successfully treated with intracoronary stent placement. ' 2005 Wiley-Liss, Inc. Key words: stents; heart transplantation; coronary vessel anomalies
INTRODUCTION
Myocardial bridges are detected in 0.5–16% of coronary angiograms [1]. These occur when a portion of the normally epicardial coronary artery is embedded within the myocardium, resulting in systolic compression of the vessel [2]. The presence of a myocardial bridge, with resultant systolic compression, is a common inborn coronary anomaly that generally has a benign course because coronary artery blood flow occurs predominantly during diastole. Diastolic compression of the coronary artery, however, is a rare and most likely an acquired finding [3]. It can be theorized that during the diastolic filling phase, the left ventricle (LV) expands and compresses the coronary artery against a noncompliant pericardium or against an epicardial scar resulting in diminished coronary blood flow. We describe a case of a cardiac transplant recipient who presented for routine annual cardiac catheterization and was found to have hemodynamically significant diastolic compression of a major diagonal artery. The patient was treated successfully with a selfexpanding intracoronary stent that ameliorated the coronary ischemia. CASE REPORT
A 34-year-old male status post cardiac transplantation for a dilated cardiomyopathy presented for an annual right and left heart catheterization to evaluate for cellular rejection and cardiac allograft vasculopathy. His immediate post transplant course had been complicated by acute, grade IIIA cellular rejection, with clinical manifestation that included congestive heart failure, pericardial effusion, and tachyarrthymias (atrial fibrilla' 2005 Wiley-Liss, Inc.
tion, atrial flutter, and nonsustained ventricular tachycardia). Right heart pressures at that time were mildly elevated but no evidence of tamponade or constrictive physiology was present. A transthoracic echocardiogram had demonstrated normal LV systolic function, mild pulmonary hypertension, and a small pericardial effusion without tamponade or constrictive physiology. This episode of rejection was successfully treated with murine monoclonal anti-CD3 antibodies, and the patient was maintained on tacrolimus, mycophenolate, and prednisone. Over the subsequent 2 years, he underwent periodic endomyocardial biopsies and did have occasional episodes of mild, acute grade IA-IB cellular rejection, treated successfully with dose adjustments in his immunosuppressive regimen. The patient at the time of his follow-up annual catheterization was asymptomatic with normal vital signs and physical examination. The electrocardiogram showed normal sinus rhythm with a heart rate of 83 beats/min and an incomplete right bundle branch block. Transthoracic echocardiogram and routine laboratory measurements were unremarkable. The right
Section of Cardiology, Department of Medicine, University of Chicago, Chicago, Illinois *Correspondence to: Dr. Neeraj Jolly, Section of Cardiology, University of Chicago Hospitals, 5841 S. Maryland Avenue, MC 5076, Chicago, IL 60637. E-mail:
[email protected] Received 4 August 2004; Revision accepted 27 January 2005 DOI 10.1002/ccd.20349 Published online 14 May 2005 in Wiley InterScience (www.interscience. wiley.com).
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Fig. 1. A: Coronary angiography demonstrating no significant coronary artery disease and no evidence of diagonal artery compression during systole (arrow). B: Pronounced diastolic compression of the mid portion of the diagonal branch (arrow). LCx, left circumflex artery; LAD, left anterior descending artery.
heart pressures and endomyocardial biopsy results were normal. Coronary angiography revealed no significant coronary artery disease; however, the mid segment of the first diagonal branch demonstrated marked dynamic diastolic compression (Fig. 1). A 6 Fr Judkins Left 4 (JL4) guiding coronary catheter was placed in the ostium of the left main coronary artery and a 0.014@, 175 cm PressureWire (Radi Medical, Uppsala, Sweden) was advanced through the catheter and into the diagonal coronary artery. Intracoronary (IC) pressures were obtained proximal, within, and distal to the compressed segment. IC pressures were similar throughout the cardiac cycle in the aorta and proximal diagonal branch. The PressureWire was advanced to within the compressed diagonal segment (Fig. 2) and a dramatic rise in diastolic pressure was observed consistent with the transmitted compressive forces of the coronary artery on the transducer. The transducer was subsequently advanced distal to the area of compression in the diagonal branch and mild systolic attenuation and a more pronounced diastolic decrease in pressure was observed, as compared with the aorta; 40 mg of IC adenosine was administered and a marked reduction in diastolic pressure distal to the compression was observed with a calculated fractional flow reserve (FFR) of 0.71 (Fig. 3). The patient underwent a pharmacological stress myocardial perfusion study the following day. He achieved 93% of age-predicted maximal heart rate with dobutamine infusion of 30 mg/kg/min. The stress electrocardiogram revealed no evidence of myocardial ischemia; however, scintigraphy revealed a significant moderate-sized stress-induced perfusion defect in the
anterolateral distribution consistent with ischemia in the diagonal territory. The resting LV ejection fraction was normal without regional wall motion abnormalities. The patient returned to the catheterization laboratory the subsequent day and underwent percutaneous intervention at the site of diastolic diagonal artery compression based on the data from intracoronary pressure recording and stress myocardial perfusion imaging. A self-expanding 3.0 20 mm Radius Intracoronary Stent (Boston Scientific, Natick, MA) was advanced over a 0.014@, 300 cm Balance Middleweight Guide Wire (Guidant, Indianapolis, IN) and positioned across the diagonal branch at the site of compression. The stent was deployed without difficulty and repeat angiography revealed no residual diastolic compression (Fig. 4). The patient was discharged the next day with the addition of aspirin and clopidogrel to his medical regimen. Follow-up pharmacological stress myocardial perfusion study was performed 5 months later and demonstrated significant improvement in the stress myocardial perfusion to the diagonal artery territory. Repeat angiography 1 year after stent deployment demonstrated no significant restenosis (Fig. 5). The remaining coronary arteries were unchanged. DISCUSSION
Myocardial bridges can result in systolic compression of the epicardial coronary artery and are a common inborn anomaly occurring in 0.5–16% of all angiographic cases [1]. These bridges result in systolic
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Fig. 2. A and B: Intracoronary PressureWire placement in the compressed diagonal segment. C: Pressure tracings in the aorta and from within the compressed segment of the diagonal branch. Marked increase in pressure within the compressed diagonal branch during diastole. This is in contrast with the nearly equivalent pressure tracings just proximal to the compressed segment.
compression of the epicardial artery, but because the majority of epicardial coronary blood flow occurs during diastole, they generally have a benign course. Pathophysiologic studies have shown that, especially in the setting of tachycardia, reduction of diastolic filling time combined with a lag in reopening of the coronary bed distally after systolic compression can lead to reduced coronary perfusion and ischemia [4,5]. There have been reports of ischemic syndromes [6], myocardial infarctions [7,8], tachyarrhythmias [9], bradyarrhythmias [10], and sudden death [11,12] linked with myocardial bridges. Despite the aforementioned mechanisms for ischemia, the vast majority of patients with myocardial bridges are clinically unaffected. Two large prospective series have documented the excellent longterm prognosis in those patients with isolated bridges found during angiography [13,14]. Diastolic compression of the epicardial coronary artery, unlike myocardial bridging and systolic compression, is probably an acquired lesion that has not been well reported. Our patient demonstrated nearobliteration of the diagonal lumen during diastole without evidence of systolic compression. Patients who
undergo cardiac transplantation often lack ischemic symptoms because the heart is denervated. Objective evidence of impaired coronary blood flow and resultant ischemia in the diagonal artery territory by both myocardial perfusion imaging and fractional flow reserve was demonstrated. A plausible link between diastolic compression and ischemic syndromes can be made because greater than three-fourths of coronary blood flow occurs during diastole. Goldberg et al. [3] reported the case of a patient with documented history of tuberculous pericarditis and a heavily calcified pericardium who presented with symptomatic cardiac constriction without angina. Right heart catheterization demonstrated diastolic equalization of pressures, and coronary angiography showed complete diastolic obliteration of the obtuse marginal branch of the left circumflex artery without other coronary stenoses. After pericardiotomy, his symptoms resolved. Follow-up angiography was not performed. The authors theorized that diastolic filling of the left ventricle seemed to ‘‘stretch and obliterate’’ the affected vessel against the fixed noncompliant pericardium.
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Fig. 3. Intracoronary pressure measurements in the aorta and distal diagonal branch after 40 mg IC adenosine administration. A marked decrease in the distal diagonal branch diastolic pressure is present with FFR of 0.71. Ao, aorta; Dia, diagonal artery; Pc, intracoronary pressure; Pao, aortic pressure; FFR, fractional flow reserve.
Subsequent to this report, Jain et al. [15] reported the de novo appearance of a myocardial bridge in an asymptomatic heart transplant recipient. Intravascular ultrasound (IVUS) and quantitative coronary angiography (QCA) demonstrated both systolic and diastolic compression of the mid left anterior descending artery, with luminal reductions of 62% and 42%, respectively. Atherosclerosis was absent within the bridged segment. Intracoronary Doppler flow studies revealed elevated velocities within the bridged segment during both systole and diastole. Notably, the precatheterization myocardial perfusion scan was normal. The patient was discharged without intervention or adjustment in medical regimen. Finally, Akasaka et al. [16] have shown derangements in coronary flow reserve (CFR) in the left anterior descending artery in patients with documented constrictive pericarditis (compared with normal controls and patients with restrictive cardiomyopathy). While none of the patients in this series exhibited systolic or diastolic compression on coronary angiography, QCA demonstrated evidence of reduced arterial compliance via a lack of significant coronary dilation after end-diastole. It is possible that any process affecting the pericardium (incision, inflammation, or calcification) could lead to local or global scarring with reduced pericardial compliance. As the myocardium relaxes and fills during diastole, a portion of an epicardial coronary artery could become compressed between the myocardium and pericardium, impeding forward blood flow. In cardiac transplant recipients, pericardial inflammation and constriction can be associated with cellular
Fig. 4. A and B: Coronary angiography showing deployment of a self-expanding intracoronary stent across the compressed diagonal artery segment.
rejection [17]. Given the relative frequency with which an inflammatory process may involve the pericardium in this population, it is surprising that the phenomenon of diastolic compression has not been seen more frequently. The choice of a self-expanding stent in this case was deliberate. These stents, unlike balloon-expanded stents, exert constant outward radial expansive force after deployment [18,19]. Theoretically, this should avoid the effect of cyclic compressive forces on the artery. Improvement in myocardial perfusion imaging was demonstrated 5 months later and there was no evidence of restenosis at a 15-month follow-up angiogram. In summary, myocardial bridges are commonly seen and can occasionally be associated with clinical syndromes of cardiac ischemia. Diastolic compression of a coronary artery, on the other hand, is rare. Diastolic
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Fig. 5. Coronary angiography performed 15 months after intracoronary stent placement. There was no evidence of compression and no significant in-stent restenosis.
compression is likely due to entrapment of an epicardial coronary artery between relaxing myocardium and a noncompliant pericardium. We present the first reported case of diastolic coronary artery compression producing objective evidence of myocardial ischemia in a cardiac transplant recipient. This patient was successfully treated with intracoronary stent placement. REFERENCES 1. Kalaria VG, Koradia N, Breall JA. Myocardial bridge: a clinical review. Catheter Cardiovasc Interv 2002;57:552–556. 2. Angelini P, Trivellato M, Donis J, Leachman RD. Myocardial bridges: a review. Prog Cardiovasc Dis 1983;26:75–88. 3. Goldberg E, Stein J, Berger M, Berdoff RL. Diastolic segmental coronary artery obliteration in constrictive pericarditis. Cathet Cardiovasc Diagn 1981;7:197–202. 4. Krawczyk JA, Dashkoff N, Mays A, Klocke FJ. Reduced coronary flow in a canine model of ‘‘muscle bridge’’ with inflow occlusion extending into diastole: possible role of downstream vascular closure. Trans Assoc Am Physicians 1980;93:100–109. 5. Rouleau JR, Dumesnil JG, Roy L, Dagenais GR. How does systolic coronary artery compression cause myocardial ischemia in dogs? Am J Cardiol 1981;47:473.
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