CASE REPORT SCHOFIELD ET AL LEFT VENTRICULAR DYSFUNCTION AFTER PERICARDIECTOMY
The patient regained consciousness on the same day, and mechanical ventilation was discontinued on the next day. His consciousness became clear, and he recovered partially from the left hemiplegia. No new neurologic deficit was observed. The remaining postoperative course was uneventful.
Comment Malperfusion, especially to the heart or to the brain, is a life-threatening complication of aortic dissection [1]. Emergency aortic operation is often inevitable even in the presence of cerebral malperfusion, although neurologic disorders tend to deteriorate. This case clearly highlighted important aspects of such situations. We encountered a long thrombus in the carotid artery that was undetectable with the duplex scan. Without cannula placement in the carotid artery, this thrombus would have been missed, and severe brain damage may have resulted from more serious hypoperfusion to the right cerebral hemisphere during ECC and from persistent malperfusion or embolization in the distal cerebral arteries after repair of the aorta. Direct carotid artery cannulation prevented further brain damage, although preexisting deficits could not be completely eliminated. In view of this hazardous thrombus, palliative procedures, central aortic repair alone [2], and subclavian or axillary artery cannulation [3] are inappropriate. A cannula must be placed into the obstructed carotid artery, and thrombi, if present, must be removed. To avoid possible recurrent malperfusion, moreover, that carotid artery should be reconstructed separately at the cannulation site. Another problem was the timing and method of recanalization of the carotid artery. Because the brain is highly vulnerable to ischemia, it is unclear whether early reperfusion is beneficial. In our opinion, it should be attempted before the initiation of ECC. The earliest possible timing is just after the induction of general anesthesia in the operating room, because puncturing the obstructed true lumen is very difficult and because recanalizing the carotid artery before removing a potentially lethal thrombus is even dangerous. This method is reliable for removing possible thrombi and for promptly recanalizing the true lumen, and the cannulas, once in place, can be used during the following aortic procedure. Thus, this method is advantageous and represents little difference in surgical invasiveness or operation time. In patients with coexistent pericardial tamponade, however, midline sternotomy and pericardial fenestration should be performed first because systemic heparinization is necessary.
References 1. Cambria RP, Brewster DC, Gertler J, et al. Vascular complications associated with spontaneous aortic dissection. J Vasc Surg 1988;7:199 –209. 2. Hughes JD, Bacha EA, Dodson TF, Martin T, Smith RB III, Chaikof EL. Peripheral vascular complications of aortic dissection. Am J Surg 1995;170:209 –12. 3. Neri E, Massetti M, Capannini G, et al. Axillary artery © 2004 by The Society of Thoracic Surgeons Published by Elsevier Inc
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cannulation in type A aortic dissection operations. J Thorac Cardiovasc Surg 1999;118:324 –9.
Left Ventricular Dysfunction After Pericardiectomy for Constrictive Pericarditis Richard S. Schofield, MD, Steven B. Shoemaker, MD, Eugene G. Ryerson, MD, Gary R. Cooper, MD, and William D. Spotnitz, MD Malcom Randall Veterans Administration Medical Center, and Division of Cardiovascular Medicine, Department of Medicine, Division of Pulmonary Medicine, and Division of Cardiothoracic Surgery, University of Florida College of Medicine, Gainesville, Florida
A 56-year-old man was admitted to our hospital with a diagnosis of suspected constrictive pericarditis. After the diagnosis was confirmed by cardiac catheterization, an elective pericardiectomy was performed without complication. Four days after surgery dyspnea developed in the patient, and he was found to have an acute decrease in left ventricular ejection fraction (LVEF) by echocardiography. The patient’s symptoms and the LVEF improved over time and returned to normal 4 weeks after surgery. Transient hemodynamic dysfunction of the left ventricle has previously been reported after pericardiectomy or pericardiocentesis; however, we know of no reports in the literature that confirm an acute reduction in LVEF by echocardiography after pericardiectomy for constrictive pericarditis. (Ann Thorac Surg 2004;77:1449 –51) © 2004 by The Society of Thoracic Surgeons
C
onstrictive pericarditis is an uncommon postinflammatory disorder characterized by pericardial thickening, myocardial constriction, and impaired diastolic filling. The most common etiologies of this disorder are viral pericarditis, renal failure, tuberculosis, radiation therapy, collagen vascular disease, prior pericardiectomy, and idiopathic constrictive pericarditis. Clinical signs and symptoms are predominantly related to systemic vascular congestion and clinical heart failure. The indolent nature of this disorder typically leads to a delay in diagnosis of approximately 2 years from its onset [1, 2]. Hemodynamic abnormalities have been previously reported after pericardiectomy and are presumed to result from myocyte atrophy and physiologic dysfunction caused by chronic constriction. Prior reports of persistent cardiac dysfunction after pericardiectomy have primarily described abnormalities in intracardiac filling pressures or in echocardiographic measures of diastolic left ventricular (LV) relaxation [3]. Although persistent ab-
Accepted for publication May 5, 2003. Address reprint requests to Dr Schofield, 1600 SW Archer Rd, Box 100277, Gainesville, FL 32610; e-mail:
[email protected].
0003-4975/04/$30.00 doi:10.1016/S0003-4975(03)01151-2
CASE REPORTS
Ann Thorac Surg 2004;77:1449 –51
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CASE REPORT SCHOFIELD ET AL LEFT VENTRICULAR DYSFUNCTION AFTER PERICARDIECTOMY
Table 1. Right Heart Pressures (in mm Hg) at Baseline (Preoperative) and on the Day of Postoperative Heart Failure Decompensation
RA RV PA PAW
Preoperative
Postoperative
15 32/15 32/19 17
22 50/22 50/30 30
RA ⫽ right atrium; RV ⫽ right ventricle; PAW ⫽ pulmonary arterial wedge pressure.
PA ⫽ pulmonary artery;
normalities of Doppler filling have been noted after pericardial release, acute reductions in LVEF by echocardiography have not been described. We describe a case of severe reduction in echocardiographic LVEF after pericardiectomy that spontaneously improved over time.
CASE REPORTS
A 56-year-old man was admitted to our hospital for evaluation of suspected constrictive pericarditis. He had an 18-month history of worsening shortness of breath, fatigue, and weight loss of 80 lb. An evaluation for pulmonary and liver failure was undertaken by his outside physicians and was unrevealing for the cause of his symptoms. A liver biopsy specimen confirmed signs of hepatic congestion with sinusoidal dilation and mild cholestasis but no evidence of cirrhosis. Right and left heart catheterization 8 months before presentation to our hospital revealed elevated right heart pressures; however, the diagnosis of constrictive pericarditis was not confirmed. At the time of presentation, the patient required supplemental oxygen and was dyspneic with walking even a few feet, consistent with New York Heart Association class IV heart failure. Physical examination confirmed severe jugular venous distention with the crest of the Fig 1. Preoperative left ventricular (LV) and right ventricular (RV) pressure tracings in our patient with constrictive pericarditis. There is a characteristic rapid increase in RV pressure during diastole, the “dip and plateau” pattern typical of constrictive pericarditis.
Ann Thorac Surg 2004;77:1449 –51
jugular pressure wave at the angle of the mandible with the patient sitting upright at 90 degrees. An intermittent pericardial knock was noted during diastole, as were significant ascites and hepatomegaly, with the liver edge palpable 6 cm inferior to the costal margin. Lower extremity edema was absent; however, the patient had been on long-term therapy with high doses of loop diuretics and had recently undergone a large-volume paracentesis for tense ascites. The electrocardiogram confirmed sinus rhythm with a right bundle branch block and left atrial enlargement. A skin test for tuberculosis was negative. A computed tomographic scan of the chest revealed a thickened pericardium without calcification as well as pleural effusions and hepatic congestion. A transthoracic echocardiogram showed paradoxical motion of the interventricular septum, normal LVEF, no pericardial effusion, and a dilated inferior vena cava. Repeat right and left heart catheterization showed elevated right atrial pressure with a prominent Y descent and a rapid increase of diastolic pressure during right ventricular filling (Table 1, Fig 1). Coronary angiography was normal. After a phrenic-to-phrenic pericardiectomy, the elevated wedge and right atrial pressures normalized. The pericardium was noted to be thickened and adherent to the anterior structures of the heart. Pericardial biopsy confirmed fibrosis without evidence of infectious, neoplastic, or autoimmune disease. The patient was recovering uneventfully when on postoperative day 4 he complained of worsening shortness of breath. A repeat 12-lead electrocardiogram revealed loss of R wave amplitude across the anterior leads without ST segment elevation or depression. Urgent repeat cardiac catheterization was performed and again showed normal coronary arteries with new evidence of combined right and LV hemodynamic dysfunction (Table 1). Repeat echocar-
Ann Thorac Surg 2004;77:1451– 4
Comment We describe the first known case of a severe, transient decrease in echo-derived LVEF after pericardiectomy for constrictive pericarditis. Our patient had an unexplained, abrupt decrease in LVEF noted early postoperatively that gradually improved over the next 4 weeks. Associated with this abrupt decrease in LVEF was a corresponding loss of anterior lead R wave amplitude demonstrated on the electrocardiogram and hemodynamic evidence of LV failure. Similar findings of reduced LVEF have been noted after pericardiocentesis in patients with cardiac tamponade related to malignant pericardial effusion but not in those with constrictive pericarditis [4]. Prior investigators have surmised that postpericardiotomy cardiac dysfunction is related to myocardial damage from chronic constriction, leading to myocyte atrophy [5, 6]. Release of the pericardium at surgery leads to a rapid increase in LV volume and an abrupt change in LV geometry. These rapid changes may stress the chronically dysfunctional myocardium, leading to cardiac failure. Because the myocardium remains viable and capable of repair, however, gradual improvement in global cardiac function can be expected over time in many cases [6]. Patients with more severe degrees of constriction and more prolonged preoperative clinical courses may be more predisposed to this type of postoperative myocardial dysfunction. Our patient had a fairly long prodrome of heart failure symptoms (18 months) and was profoundly symptomatic at the time of presentation, factors that may have contributed to the development of LV systolic failure after pericardiectomy. McCaughan and colleagues [7] have described hemodynamic abnormalities after pericardiectomy in the largest case series available (231 patients). These investigators noted a 28% incidence of low cardiac output syndrome postoperatively in their patients, with many of the perioperative deaths occurring in this low cardiac output group. No relationship was found between low cardiac output and the type of surgical approach undertaken or the extent of the pericardial resection. Those patients with low cardiac output syndrome appeared to go on to have a normal long-term survival if they sur© 2004 by The Society of Thoracic Surgeons Published by Elsevier Inc
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vived the immediate postoperative period. In their case series, however, low cardiac output was defined by right heart catheterization or clinical observation alone. LVEF was not measured. The development of postpericardiotomy hemodynamic abnormalities and/or clinical heart failure is not uncommon in patients with constrictive pericarditis. This is a potentially serious consequence of pericardiectomy and warrants prompt recognition and aggressive treatment for heart failure. Appropriate therapy for heart failure often results in improvement in LV function over time.
References 1. Myers RBH, Spodick DH. Constrictive pericarditis: clinical and pathophysiologic characteristics. Am Heart J 1999;138: 219 –32. 2. Ling LH, Oh JK, Schaff HV, et al. Constrictive pericarditis in the modern era: evolving clinical spectrum and impact on outcome after pericardiectomy. Circulation 1999;100:1380 –6. 3. Senni M, Redfield MM, Ling LH, Danielson GK, Tajik AJ, Oh JK. Left ventricular systolic and diastolic function after pericardiectomy in patients with constrictive pericarditis: Doppler echocardiographic findings and correlation with clinical status. J Am Coll Cardiol 1999;33:1182–8. 4. Wolfe MW, Edelman ER. Transient systolic dysfunction after relief of cardiac tamponade. Ann Intern Med 1993;119:42–4. 5. Dines DE, Edwards JE, Burchell HB. Myocardial atrophy in constrictive pericarditis. Staff Meetings Mayo Clin 1958;33: 93–9. 6. Roberts JT, Beck CS. The effect of chronic cardiac compression on the size of the heart muscle fibers. Am Heart J 1941;22:314 –9. 7. McCaughan BC, Schaff HV, Piehler JM, et al. Early and late results of pericardiectomy for constrictive pericarditis. J Thorac Cardiovasc Surg 1985;89:340 –50.
Successful Off-Pump Coronary Artery Bypass for Behcet’s Disease Min-Ho Song, MD, PhD, Takashi Watanabe, MD, PhD, and Hajime Nakamura, MD, PhD Division of Cardiovascular Surgery, Shizuoka Saiseikai General Hospital, Shizuoka, Japan
A 66-year-old woman with a 30-year history of Behcet’s disease was referred for coronary surgery because of restenosed stent and crescendo angina. We succeeded in operating on her by off-pump coronary bypass with bilateral internal mammary arteries, which were anastomosed to the left anterior descending artery and diagonal artery. The grafts were patent postoperatively and she became free from angina. Coronary surgery for Behcet’s disease is extremely rare and this experience prompted us to report this case. (Ann Thorac Surg 2004;77:1451– 4) © 2004 by The Society of Thoracic Surgeons Accepted for publication April 29, 2003. Address reprint requests to Dr Song, Division of Cardiovascular Surgery, Shizuoka Saiseikai General Hospital, 1-1-1 Oshika, Shizuoka-shi, Shizuoka 422-8527, Japan; e-mail:
[email protected].
0003-4975/04/$30.00 doi:10.1016/S0003-4975(03)00752-5
CASE REPORTS
diography now revealed severe LV systolic dysfunction with the LVEF estimated to be 0.25. Multiple anterior, septal, and apical wall motion abnormalities were noted and were new compared with the baseline preoperative echocardiogram. Right ventricular systolic function was also newly depressed. Serial cardiac enzymes were negative for ischemic myocardial injury. Treatment for heart failure with loop diuretics, digoxin, and an angiotensinconverting enzyme inhibitor was begun with gradual resolution of symptoms. A repeat echocardiogram performed 3 days after the initial decompensation revealed improvement in the LVEF to 0.40 with only mild global hypokinesis noted. The patient continued to improve, and at 4 weeks after surgery a repeat echocardiogram showed a normal LVEF of 0.60, no wall motion abnormalities, and the right heart pressure estimation was normal. A repeat 12-lead electrocardiogram showed a return of the anterior R wave amplitude to baseline levels.
CASE REPORT SONG ET AL OPCAB FOR BEHCET’S DISEASE