Asian Cardiovasc Thorac Ann 2007;15:441-443
© 2007 Asia Publishing EXchange Ltd
Benefits of a ß-Blocker for Intractable Hemolysis due to Paraprosthetic Leakage
Shigeaki Aoyagi, MD,
Shuji Fukunaga, MD,
Eiki Tayama, MD,
Eiji Nakamura, MD,
Noriko Egawa, MD,
Yukio Hosokawa, MD
Department of Surgery, Kurume University School of Medicine, Kurume, Japan
For reprint information contact: Shigeaki Aoyagi, MD, Tel: 81 94 235 3311, Fax: 81 94 235 8967, Email: aoyagi{at}med.kurume-u.ac.jp, Department of Surgery (2), Kurume University School of Medicine, 67 Asahi-machi, Kurume 830-0011, Japan.
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ABSTRACT
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We describe a 58-year-old man who was successfully treated with a ß-adrenergic receptor blocking agent for intractable hemolysis due to paraprosthetic leakage. After replacement of a mitral prosthetic valve with another mechanical valve, the patient suffered intractable intravascular hemolysis resulting from recurrent paraprosthetic leakage. With oral administration of a ß-adrenergic receptor blocker, betaxolol hydrochloride, for 3 months, the hemoglobin value increased from 9.7 g·dL–1 to 12.4 g·dL–1, although glutamic oxaloacetic transaminase and lactic dehydrogenase values remained elevated.
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INTRODUCTION
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Paraprosthetic valve leakage is a serious complication of valve replacement, and often causes intractable intravascular hemolysis due to the shearing stress generated between the foreign body surface (sewing cuff) and the erythrocyte.1–3 In such cases, hemolysis rarely resolves spontaneously, and usually requires a further operation to prevent occurrence of lethal complications.
In this paper, we describe a patient who developed intractable intravascular hemolysis after replacement of a mitral prosthetic valve, and emphasize the benefits of a ß-adrenergic receptor blocker for the treatment of intractable hemolysis due to paraprosthetic valve leakage.
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CASE REPORT
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A 58-year-old man was transferred to our hospital for treatment of congestive heart failure and hemolytic anemia. The patient had undergone aortic and mitral valve replacement with a Bjork-Shiley valve (Shiley, Irvine, CA, USA) and Carpentier-Edwards (CE) porcine valve (Edwards Lifescience, Irvine, CA, USA) 23 years previously. Subsequently, the mitral CE valve had been replaced with a St. Jude Medical (SJM) valve (St. Jude Medical Inc., St. Paul, MN, USA) 5 years after the initial valve replacement. Until he developed a low grade fever one month before admission, his cardiac condition was well controlled with oral administration of furosemide (20 mg·day–1) and digitoxin (0.05 mg·day–1). With intravenous injection of an antibiotic and additional oral administration of furosemide at a local hospital, he became afebrile but anemic and severely dyspneic. Blood cultures were not performed at the local hospital. On admission to our hospital, he was afebrile but slightly anemic, icteric, and edematous. In addition to clear closing clicks of the prosthetic valves, a grade 3 systolic ejection murmur was heard at the 2nd right sternal border and moist rales were audible on both lower lung fields.
A chest X-Ray showed cardiomegaly (cardiothoracic ratio: 0.56) with pulmonary congestion and pleural effusion. Transthoracic echocardiography (TTE) revealed no dilatation of the left ventricle, and normal ventricular contraction. Transthoracic echocardiography did not delineate paravalvular leakage (PVL) but transesophageal echocardiography (TEE) demonstrated moderate PVL around the mitral prosthetic valve. Laboratory examination revealed serum hemoglobin of 8.5 g·dL–1, glutamic oxaloacetic transaminase (GOT) of 163 units·L–1 (normal range: 13–33 units·L–1), and lactic dehydroxygenase (LDH) of 3848 Wroblewski units (normal range; 100–400 Wroblewski units). Total bilirubin (TB) level was 3.05 mg·dL–1. Blood cultures and Coombs test were negative. A blood smear revealed fragmentation of the erythrocytes. Concentrations of folic acid and vitamin B12 were within normal range.
On the basis of these findings, a diagnosis of PVL of the mitral SJM valve resulting from infective endocarditis and hemolytic anemia was made, although blood culture was negative. During re-operation, the left atrium (LA) was opened through a transseptal approach. No vegetations or thrombi were found on the prosthetic valve and a paraprosthetic valve dehiscence of 5 mm in diameter was found on the posteromedial mitral annulus. After removal of the SJM valve, an Advancing The Standard (ATS) valve (ATS Medical Inc., Minneapolis, MN, USA) was fixed on the native mitral annulus.
The postoperative course was difficult because of systemic hypotension with low systemic vascular resistance and elevated pulmonary artery pressure. With intravenous administration of vasopressin and inhalation of nitric oxide, the patient’s hemodynamic condition improved. Transthoracic echocardiography performed on the 18th postoperative day revealed recurrence of PVL. Thereafter, hemolytic anemia resulting from mechanical hemolysis gradually became obvious. Blood smear showed fragmentation of the erythrocytes. Changes in hemoglobin, GOT, LDH, and TB levels are summarized in Table 1
. One month after discharge from our hospital, oral administration of a ß-adrenergic receptor blocker (betaxolol hydrochloride: Kerlong® 2.5 mg·day–1) was started. Three months later, no significant changes in left ventricular systolic function were apparent, as evaluated by echocardiography. Left ventricular ejection fraction and fractional shortening before and after treatment were 54% and 56%, 0.28 and 0.29, respectively. However, a remarkable decrease (27.1%) in heart rate from 96 to 70 beats·min–1 was observed.
Consequently, oral administration of low dose betaxolol hydrochloride achieved a remarkable decrease of hemolysis without aggravation of symptoms and signs of congestive heart failure. The hemoglobin value reached 12.4 g·dL–1, while GOT and LDH were still high at 53 units·L–1 and 1197 IU·L–1, respectively, as shown in Table 1
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DISCUSSION
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Since the early days of valve surgery, frank hemolysis following mechanical valve replacement has been a well-recognized phenomenon. This mechanical hemolysis is usually attributed to shearing stress on the erythrocytes in turbulent flow1 which can occur with elevated transvalvular pressure gradients, paravalvular leakage or increased cardiac output. Shearing stress is directly proportional to the square of the velocity of blood flow through the stenosed area.4 An experimental study demonstrated that a shearing stress of more than 3,000 dynes·cm2 could significantly increase hemolysis.1 Although mechanical hemolysis associated with paravalvular leakage has occurred predominantly in aortic valve replacement,5 severe mechanical hemolysis has also been reported in mitral valve replacement.2
Okita and colleagues2 emphasized that the shearing stress is considered to be greater in mitral paravalvular leakage because the left ventricular contractile forces can directly strike the leak during systole. In addition, the pressure gradient between the left ventricle and the left atrium during systole is greater than that between the aorta and left ventricle during diastole. On the other hand, knitted Dacron double-velour fabric, which is used for the sewing cuff of both SJM and ATS valves, shows an irregular, shaggy surface structure in surface-scanning electron microscopic images.2 This non-smooth surface structure can also generate greater vortices and shearing stress once PVL occurs.
Considering the mechanism of mechanical hemolysis resulting from PVL after valve replacement, decreases could theoretically be achieved by slowing the velocity of the blood flow through the paraprosthetic leakage. ß-adrenergic receptor blocking agents such as propranolol2 or betaxolol principally reduce left ventricular contractile forces which results in decreasing the velocity and blood flow across the paraprosthetic leakage. In addition, ß-adrenergic receptor blockers also slow down the heart rate. Consequently, shearing stress is considered to be lowered by administration of the ß-adrenergic receptor blocker. In the present patient, significant changes in left ventricular systolic function were not demonstrated by echocardiography probably because of administration of a low dose of betaxolol hydochloride. However, a remarkable decrease in the heart rate was observed on oral administration of a low dose of betaxolol hydrochloride, in addition to surprising decreases of hemolysis as shown by an increase of serum hemoglobin and decrease of LDH. Although the use of ß-blocking drugs is not a fundamental treatment for intractable hemolysis due to paraprosthetic leakage, we believe that ß-adrenergic receptor blockers may be effective in reducing the severity of intractable mechanical hemolysis, and in preventing the occurrence of lethal complications.
In conclusion, we report a patient who developed intractable intravascular hemolysis after replacement of a mitral prosthetic valve and discuss the benefits of a ß-adrenergic receptor blocking agent for treatment of mechanical hemolysis due to PVL.
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REFERENCES
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- Nevaril CG, Lynch EC, Alfrey CP Jr, Hellums JD. Erythrocyte damage and destruction induced by shearing stress. J Lab Clin Med 1968;71;784–90.[Medline]
- Okita Y, Miki S, Kusuhara K, Ueda Y, Tahata T, Tsukamoto Y, et al. Intractable hemolysis caused by perivalvular leakage following mitral valve replacement with St. Jude Medical prosthesis. Ann Thorac Surg 1988;46:89–92.[Abstract]
- Okita Y, Miki S, Kusuhara K, Ueda Y, Tahata T, Yamada K. Propranolol for intractable hemolysis after open heart operation. Ann Thorac Surg 1991;52:1158–60.[Abstract]
- Nevaril CG, Lynch EC, Alfrey CP, Hellums JD. Erythrocte damage and destruction induced by shearing stress. J Lab Clin Med 1968;71:784–790.[Medline]
- Rodgers BM, Sabiston DC Jr. Hemolytic anemia following prosthetic valve replacement. Circulation 1969;39(5 Suppl 1):I155–61.[Medline]
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ABSTRACT
INTRODUCTION
