754 Calcium Embolism of the Coronary Arteries Mayo Clin Proc, July 2001, Vol 76 Figure 1. Case 1. Transseptal catheterization with double-balloon infl

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1 Mayo Clin Proc, July 2001, Vol 76 Calcium Embolism of the Coronary Arteries 753 Case Report Calcium Embolism of the Coronary Arteries After Percutaneous Mitral Balloon Valvuloplasty BRIAN D. POWELL, MD; DAVID R. HOLMES, JR, MD; RICK A. NISHIMURA, MD; AND CHARANJIT S. RIHAL, MD Two cases of rare, catastrophic calcium emboli to the coronary arteries immediately after percutaneous mitral balloon valvuloplasty are presented. Preoperative echocardiographic findings may identify patients at risk for this complication. These cases should increase the awareness of calcium emboli and lead to consideration of urgent coronary angiography for patients with signs or symptoms of acute coronary occlusion after valvuloplasty. Mayo Clin Proc. 2001;76: PMBV = percutaneous mitral balloon valvuloplasty; TEE = transesophageal echocardiography In the mid 1980s, percutaneous mitral balloon valvuloplasty (PMBV) became an option for patients with mitral stenosis. Randomized trials have shown similar or superior hemodynamic outcomes and survival for patients undergoing PMBV compared with surgical commissurotomy. 1-4 Advantages of balloon valvuloplasty are lower cost, reduced length of hospital stay, and shorter recovery period. 5,6 Guidelines from the American College of Cardiology and the American Heart Association recommend balloon valvuloplasty for patients in New York Heart Association who have symptomatic, moderate to severe mitral stenosis with suitable valve morphology. 7 Optimal selection of candidates is based on individual patient and valvular characteristics. Valve morphology is the greatest predictor of a successful procedure. 8,9 Embolic events are among the most serious complications that can occur after PMBV. If an atrial thrombus is detected on transesophageal echocardiography (TEE), the patient should undergo anticoagulation for approximately 3 months, and TEE should be repeated before balloon valvuloplasty is performed. 7,10 The following 2 cases present a different type of embolization that cannot be prevented by anticoagulation. Of 296 PMBVs performed at Mayo Clinic since the mid 1980s, only 2 known cases of calcium emboli to the coronary arteries have occurred. Both patients had echocardiographic findings of severe calcification. From the Department of Internal Medicine (B.D.P.) and Division of Cardiovascular Diseases and Internal Medicine (D.R.H., R.A.N., C.S.R.), Mayo Clinic, Rochester, Minn. Individual reprints of this article are not available. Address correspondence to Charanjit S. Rihal, MD, Division of Cardiovascular Diseases, Mayo Clinic, 200 First St SW, Rochester, MN ( rihal@mayo.edu). REPORT OF CASES Case 1 A 67-year-old man with a history of mitral stenosis due to rheumatic fever presented in 1989 because of increasing dyspnea on exertion, ankle edema, and orthopnea of 6 months duration. He denied having chest pain and had no history of myocardial infarction. His medical history was notable for hypertension, type 2 diabetes mellitus, chronic atrial fibrillation, renal insufficiency, and a transient ischemic attack. His medications included warfarin, isosorbide dinitrate, verapamil, furosemide, potassium chloride, prazosin, clonidine, and glyburide. Findings on physical examination of the patient at presentation were hypertension with a blood pressure of 200/ 90 mm Hg, heart rate of 68 beats/min, and respirations of 24/ min. His jugular venous pressure was 12 cm with prominent a and v waves and a hepatojugular reflux. Cardiac examination revealed an irregular rhythm with variable first and second heart sounds and an increased pulmonic closure sound. An apical diastolic rumble was noted. Bibasilar rales were detected, as was mild pedal edema. An echocardiogram revealed a mitral valve area of 0.76 cm 2, moderate mitral valve thickness, and mild calcification of the leaflets and subvalvular structures. The patient s Abascal score was Extensive calcification extended into the posteromedial commissure. No intracardiac thrombi were visualized, and the ejection fraction was 52%. The patient was thought to be a poor surgical candidate because of his multiple comorbidities, including labile hypertension, diabetes, and renal insufficiency (creatinine level, 3.5 mg/dl). Thus, he was referred for PMBV. During PMBV, transseptal catheterization was performed, and balloon catheters were passed across the mitral valve with use of the double-balloon technique (Figure 1). 11,12 After 2 inflations, there was marked reduction in the gradient across the mitral valve. However, after balloon Mayo Clin Proc. 2001;76: Mayo Foundation for Medical Education and Research

2 754 Calcium Embolism of the Coronary Arteries Mayo Clin Proc, July 2001, Vol 76 Figure 1. Case 1. Transseptal catheterization with double-balloon inflation across the stenotic mitral valve. Figure 2. Case 1. Angiogram showing a filling defect in the left main coronary artery with minimal contrast dye passing beyond the obstructing lesion. deflation, the patient developed bilateral arm discomfort. A left ventriculogram documented no pronounced mitral insufficiency and reasonably well-preserved left ventricular function. Subsequently, cardiogenic shock and electromechanical dissociation occurred. Cardiopulmonary resuscitation was initiated; an emergent echocardiogram showed no evidence of cardiac tamponade. As cardiopulmonary resuscitation was continued, an angiogram was obtained that revealed a large obstruction in the left main coronary artery (Figure 2). Balloon catheters were maneuvered past the obstruction, inflated, and pulled back in an attempt to dislodge the obstructing material. Repeated attempts were unsuccessful, and the patient died. Autopsy findings revealed an irregular, calcified mass lodged at the bifurcation of the left main coronary artery (Figure 3). Inspection of the mitral valve disclosed prominent calcification in the posteromedial commissure, which was presumed to be the source of calcium embolism. No mural thrombus was evident within the heart at autopsy. Case 2 A 69-year-old woman with a history of rheumatic heart disease presented in 1996 with progressively increasing dyspnea on exertion over several months. She had no orthopnea, paroxysmal nocturnal dyspnea, or peripheral edema. Her medical history was remarkable for mitral stenosis, transient ischemic attacks, and atrial fibrillation, for which she took long-term warfarin and digoxin. She denied having a history of diabetes, hypertension, or myocardial infarction. Figure 3. Case 1. Gross autopsy photographs. Left, Mitral valve viewed from left atrial aspect showing presumed source of embolus from exposed calcium near the posteromedial commissure (arrow). AML = anterior mitral leaflet. Right, Unroofed left main coronary artery at the bifurcation of the left anterior descending and circumflex arteries showing occlusion by a large calcific embolus (arrow).

3 Mayo Clin Proc, July 2001, Vol 76 Calcium Embolism of the Coronary Arteries 755 Figure 4. Case 2. Left, Short-axis image of transthoracic echocardiogram showing a large protruding area of mitral valvular calcification, approximately 8 mm in diameter, along the medial commissure. Right, Artist representation of echocardiographic image. AML = anterior mitral leaflet; C = calcification; PML = posterior mitral leaflet. Cardiac examination revealed atrial fibrillation with adequate rate control. A grade 2 apical diastolic rumble was detected along with a grade 2 systolic murmur at the apex. Her jugular venous pressure was 6 cm with an absent hepatojugular reflux. A chest x-ray film showed cardiomegaly with marked enlargement of the left atrium. Mitral valve calcification was also noted. The lung fields revealed increased interstitial markings at the bases, consistent with pulmonary edema. Transthoracic echocardiography was performed to assess the degree of mitral stenosis. The mitral valve was thickened with extensive calcification of the medial commissure (Figure 4). The anterolateral commissure was noncalcified. Doppler examination revealed a mitral valve area of 0.8 cm 2 and a mean gradient of 16 mm Hg. Mild to moderate mitral regurgitation was noted, and the ejection fraction was 52%. With this information, an echocardiographic score of 8 to 9 was assigned to the mitral valve, and PMBV was planned. Four days before the planned procedure, the patient discontinued use of warfarin, and heparin was given intravenously until the procedure. TEE the day before valvuloplasty showed no signs of intracardiac thrombus. The patient underwent PMBV via transseptal left atrial catheterization. An Inoue balloon was passed across the stenotic mitral valve, with moderate difficulty. A series of inflations reduced the mean gradient from 16 mm Hg to 6 mm Hg. However, the patient experienced hypotension and bradycardia with balloon inflations. Subsequently, chest pain developed. Atropine was given, and a temporary pacemaker was placed. An urgent coronary angiogram showed acute occlusion of the obtuse marginal artery (Figure 5). A radiodense intraluminal filling defect occluded the artery. An emergency echocardiogram confirmed that no pericardial effusion or hemorrhage was evident. A guidewire was passed by the occlusion, and angioplasty was performed. After a series of inflations, patency and normal flow in the obtuse marginal artery were restored. The radiodense filling defect did not efface with balloon inflations, and restoration of patency was due to stretching of the vessel wall. The patient s chest pain and bradycardia resolved. Cardiac enzymes during the following 24 hours peaked with a creatine kinase level of 1526 U/L and creatine kinase-mb of 355 ng/ml. A small cerebellar stroke, confirmed by magnetic resonance imaging, resulted in dysarthria and ataxia that gradually diminished during her 4-day hospitalization. Before dismissal, a follow-up echocardiogram demonstrated an increased mitral valve area from 0.8 cm 2 to 1.4 cm 2 and a mean gradient of 6 mm Hg. The patient was subsequently discharged home and was taking warfarin. Although pathologic confirmation of the diagnosis of calcium embolization was not available, fluoroscopic characteristics and response of the obstructing mass to balloon angioplasty were consistent with a calcific embolus. DISCUSSION These 2 cases illustrate the potential complication of calcium embolization during PMBV. A review of the Mayo Clinic PMBV database from 1987 to 2000 (unpublished data) shows an overall procedural death rate of 1.0% (of

4 756 Calcium Embolism of the Coronary Arteries Mayo Clin Proc, July 2001, Vol 76 Figure 5. Case 2. Angiogram showing occlusion of the obtuse marginal artery. 296 patients, 3 died). All 3 deaths occurred during the early era of PMBV from 1987 to 1989, and no mortality has occurred during the past 12 years, during which time more than 250 procedures have been performed. One of the procedural deaths was due to calcium embolization of the left main coronary artery, whereas the other 2 were a result of left ventricular perforation. The left ventricular perforations occurred with use of a dual-balloon technique, which is no longer used in our laboratory. In our experience, clinically important acute embolic events have occurred in only 3 patients, including the 2 described herein. The acute embolic event rate was 1.0% (3 of 296 cases). The third patient had a nonfatal cerebrovascular accident during the procedure. Of note, all 3 of these patients had a history of transient ischemic attacks before PMBV. In other series the embolic rate has been reported to be from 1% to 5% and thought to be due to dislodgement of thrombus from the left atrium. 13 We have had no further embolic events since routinely using TEE before PMBV to exclude the presence of a thrombus. Although the echocardiographic characteristics presented by Abascal et al 9 and Wilkins et al 14 provide some guidance in selecting patients who should have excellent short- and long-term results from this procedure, the echocardiographic score may not accurately predict a patient at risk for calcium embolization. Our 2 patients had Abascal echocardiographic scores greater than 8, placing them at high risk for poor outcomes from the procedure. However, review of the echocardiograms of these 2 patients revealed similar patterns of valvular calcification. Both had 8- to 10-mm areas of anterior mitral leaflet calcification extending to the posteromedial commissure. In retrospect, protruding leaflet calcification may pose a substantial risk for embolization. In a review of the Mayo Clinic experience of echocardiographic valvular calcification characteristics and outcome after PMBV, Cannan et al 8 and Tuzcu et al 15 found that the presence of commissural calcium was superior to the Abascal score in predicting outcomes 1 to 3 years after balloon valvuloplasty. Analyzing 149 consecutive cases of PMBV, they found that patients with commissural calcium had a significantly lower survival rate and a higher need for mitral valve replacement or repeated PMBV. Embolic complications were not reported separately. In 1 case report, an autopsy showed valvular debris in a coronary artery after PMBV. 16 Drobinski et al 17 reported their experience of systemic embolization after PMBV. Of their 80 patients, 3 (3.8%) had clinically significant embolization, 1 of whom had a calcific embolism. Similar to our 2 cases, the calcific embolism was thought to have detached from the mitral valve leaflet. To our knowledge, only 1 other case report has previously described angioplasty for coronary embolism after PMBV. 13 Our first patient had such a large calcified embolus in the left main coronary artery that it was not susceptible to compression or extraction with use of a balloon catheter. In contrast, our second patient responded well to urgent angioplasty. Our 2 cases should help to increase the awareness of this infrequent complication. Calcium embolism should be considered in the risk stratification of valvuloplasty candidates with pronounced valvular calcification. If a patient develops signs or symptoms of acute coronary occlusion after valvuloplasty, urgent angiography can provide an opportunity for intervention if a coronary embolism is present. We thank Dr William D. Edwards for providing pathology photographs and Kim M. Andreen for providing data on PMBV. REFERENCES 1. Reyes VP, Raju BS, Wynne J, et al. Percutaneous balloon valvuloplasty compared with open surgical commissurotomy for mitral stenosis. N Engl J Med. 1994;331: Turi ZG, Reyes VP, Raju BS, et al. Percutaneous balloon versus surgical closed commissurotomy for mitral stenosis: a prospective, randomized trial. Circulation. 1991;83: Ben Farhat M, Ayari M, Maatouk F, et al. Percutaneous balloon versus surgical closed and open mitral commissurotomy: sevenyear follow-up results of a randomized trial. Circulation. 1998; 97: Ommen SR, Nishimura RA, Grill DE, Holmes DR Jr, Rihal CS. Comparison of long-term results of percutaneous mitral balloon valvotomy with closed transventricular mitral commissurotomy at a single North American institution. Am J Cardiol. 1999;84:

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