Delayed recovery of revascularized myocardium after referral for cardiac transplantation

Delayed recovery of revascularized myocardium after referral for cardiac transplantation

668 March 1990 American Heart J . . . . al Brief Communications T a b l e I. H e m o d y n a m i c findings before and after balloon valvuloplasty ...

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668

March 1990 American Heart J . . . . al

Brief Communications

T a b l e I. H e m o d y n a m i c findings before and after balloon valvuloplasty

Hemodynamic findings Heart rate (beats/min) Pressure (mm Hg) Aorta Pulmonary artery Right ventricle (RV) Mean right atrium (RA) RA-RV mean diastolic gradient Cardiac output (L/min) Calculated tricuspid valve area (Gorlin formula, cm 2)

Before

After

85

70

110/70 34/16 10 6.0

105/65 34/16 34/8 6 2.5

2.76 0.93

2.86 4.42

34/6

thesis, whenever possible as in our case, is highly recommended. It obviates the danger of inadvertent passage of the exchange wire into a small cusp hole or perivalvular space of the bioprosthesis, with subsequent ~catastrophic heart damage from balloon introduction and dilatation. Our case does not imply use of balloon valvulopiasty routinely in all patients with stenotic bioprostheses; the anatomy of the degenerative bioprosthesis as well as other variables m u s t be defined before attempting the procedure. 6 Furthermore, the long-term results have not yet been established. Factors t h a t might favor a continued successful outcome in our p a t i e n t are t h a t her degenerative bioprosthesis did not have a regurgitant lesion and there was no evidence of significant calcification or thrombosis. At follow-up 6 months later, she has remained asymptomatic. REFERENCES

o u t p u t values were measured by the thermodilution technique. Coronary arteriography was also performed and was essentially normal. Screening of the tricuspid prosthesis did not reveal any calcification. W i t h the flow-directed p u l m o n a r y artery catheter positioned in the pulmonary artery, an 0.032-inch Teflon-coated exchange wire was passed and the catheter was removed. A No. 10F 23 m m diameter balloon catheter (Cook Inc., Bloomington, Ind.) was passed over this wire and the balloon was centered at the tricuspid prosthesis. T h e balloon was then inflated a total of four times, with a 50:50 mixture of contrast m e d i u m and saline solution, to a peak pressure of 3 to 5 atm for durations of 10 to 20 seconds. Each inflation was accompanied by mild tachycardia and hypotension. Initially there was an indentation in the balloon, b u t this resolved with subsequent inflations (Fig. 2). Hemodynamic findings immediately before and after balloon dilatation are shown in Table I. The reduction in transprosthetic valvular gradient (Fig. 1) and the increase in calculated valve area were significant. A post-balloon dilatation right ventriculogram revealed only minimal tricuspid regurgitation. The patient tolerated the procedure well and was discharged 7 days later with her original medical regimen. She has been followed up for 6 months and has shown m a r k e d l y improved exercise tolerance and decreased peripheral edema. Percutaneous balloon valuloplasty has recently been used for t r e a t m e n t in selected patients with stenotic bioprostheses. 3-6 Its application for stenotic tricuspid bioprostheses has been reported infrequently. 4'5 Our report further illustrates the feasibility of this technique for stenotic tricuspid bioprostheses. W i t h a single-balloon catheter, we were able to achieve a considerable increase in valve area together with a moderate reduction in tricuspid valve gradient. The relatively "normal" right atrial pressure at cardiac catheterization was not unexpected, as our p a t i e n t had been given vigorous diuretic t h e r a p y before the procedure. This would also account for her low cardiac output, which failed to rise considerably after valvuloplasty despite a significant increase in valve area. The use of a flow-directed pulmonary artery catheter rather than an " u n p r o t e c t e d " exchange wire to cross the stenotic biopros-

1. Ionue K, Owani T, Nakamura T, Miyamoto N. Clinical application of transvenous mitral commissurotomy by a new balloon catheter. J Thorac Cardiovasc Surg 1984;87:394-402. 2. Lababidi Z, Jiunn-Ren WU, Walls JT. Percutaneous balloon aortic valvuloplasty: results in 23 patients. Am J Cardiol 1984;53:194-7. 3. Calvo OL, Sobrino N, Gamallo C, Oliver J, Domingve F, Iglesias A. Balloon percutaneous valvuloplasty for stenotic bioprosthetic valves in the mitral position. Am J Cardiol 1987; 60:736-7. 4. Feit F, Stacy PJ, Nachamic MS. Percutaneous balloon valvuloplasty for stenosis of a porcine bioprosthesis in the tricuspid position. Am J Cardiol 1986;58:363-4. 5. Wren C, Hunter S. Balloon dilatation of a stenosed bioprosthesis in the tricuspid valve position. Br Heart J 1989;61:65-7. 6. McKay CR, Waller BF, Hong R, Reid CL, Rubin N, Rahimtoola SH. Problems encountered with catheter balloon valvuloplasty of bioprosthetic aortic valves. AM HEART J 1988; 115:463-5:

Delayed recovery of revascularized myocardium after referral for cardiac transplantation Michael Luu, MD, Lynne W a r n e r Stevenson, MD, Richard C. Brunken, MD, Davis M. Drinkwater, MD, Heinrich R. Schelbert, MD, and J a n H. Tillisch, MD.

Los Angeles, Calif.

The shortage of donor hearts limits cardiac transplantation to a minority of the patients referred, necessitating careful From the Divisionof Cardiology,Department of Medicine;and Divisionof NuclearMedicineand Biophysics,Department of RadiologicalSciencesand Department of Surgery, UCLA Medical Center. Dr. Stevenson is a Clinician-Scientistof the American Heart Association, Greater Los AngelesAffiliate.Dr Brunken is the recipient of a ClinicalInvestigator Award (HL-02002-01) from the National Institutes of Health, Bethesda, Md. Reprint requests: Lynne Warner Stevenson MD, Division of Cardiology, 47-123 CHS, UCLA School of Medicine,Los Angeles,CA 90024. 4/4/18125

Volume 119 Number 3, Part

1

Fig. 1. Three contiguous cross-sectional images of rela-

tive blood flow and glucose metabolism (F-18 deoxyglucose [lSFDG]) obtained prior to coronary bypass surgery. The left ventricle points toward the upper right-hand side of each image. On the single photon emission computed tomography thallium-201 (SPECT 2oiTl) images, obtained 24 hours following the intravenous administration of thallium-201 chloride, there are extensive perfusion defects in the septal, anterolateral, apical, and inferior segments. In contrast, glucose metabolism is well preserved in these segments on the positron-emission tomography (PET) metabolic study with lSFDG, indicating residual tissue viability.

evaluation for potentially reversible left ventricular dysfunction. This report describes a patient with an ejection fraction of 0.16, initially attributed to toxic cardiomyopathy, in whom severe coronary artery disease with regions of metabolically active myocardium was later demonstrated. Coronary artery bypass graft surgery led to delayed improvement in ventricular function and exercise performance and the patient's return to work without cardiac transplantation. The patient is a 45-year-old white man with a history of non-Hodgkin's lymphoma, successfully treated 10 years previously with mediastinal radiation and doxorubicin. He also described 5 years of heavy alcohol consumption that was discontinued 4 years prior to presentation. He was asymptomatic until the gradual onset of dyspnea 5 months prior to evaluation. At that time, an endomyocardial biopsy revealed fibrosis and myocyte hypertrophy without lym-

Brief Communications

669

Fig. 2. Follow-up positron-emission tomography (PET) study obtained 2 months after coronary revascularization. In the N-13 ammonia (13NH3) images of flow, improvement in perfusion is noted, indicating a beneficial effect from coronary revascularization. Prominent myocardial uptake of F-18 deoxyglucose (18FDG) is again identified, indicating active tissue glucose metabolism.

phocytic infiltrates. After three further hospitalizations for congestive heart failure without any history of chest discomfort, he was referred for cardiac transplantation evaluation for presumed toxic cardiomyopathy. At that time, his exercise tolerance was limited to walking 20 feet, and physical examination revealed jugular venous pressure elevation to the angle of the jaw, cardiomegaly with a third heart sound and mitral regurgitation murmur, hepatomegaly, ascites, and peripheral edema. The electrocardiogram showed T wave inversion in the inferior leads, and poor R wave progression from leads V1 to V3. The echocardiogram showed global left ventricular hypokinesis with apical dyskinesis and left ventricular enlargement (Table I). Radionuclide ventriculography revealed a resting ejection fraction of 16%. During 15 W bicycle exercise, the patient developed several minutes of chest tightness that had not previously been experienced. Coronary arteriography was performed, revealing triple-vessel coronary artery disease. Tomographic thallium-201 scintigraphy demonstrated extensive, fixed perfusion defects in the inferior, septal, and anteroapical regions of the ventricle (Fig. 1). Positron emission tomography demonstrated prominent uptake of F-18 deoxyglucose in the hypoperfused ventricular regions,

670

March 1990 American Heart Journal

Brief Communications

Table I. Left ventricular function before and after coronary

artery bypass grafting

Time Initial 4 weeks postoperative 6 months postoperative

Radionuclide Left ventricular ejection fraction end-diastolic Doppler dimension mitral Rest Exercise (mm) regurgitation (%) (%) 66 68

Severe Moderate

16 26

15 24

52

Mild

33

34

suggesting tissue viability. T h e p a t i e n t underwent a triple saphenous vein bypass grafting. The postoperative course was complicated by severe biventricular failure requiring an intra-aortic balloon p u m p and high-dose intravenous inotropic support for the first 4 days. The p a t i e n t was placed on the waiting list for cardiac transplantation. An echocardiogram done at 4 days revealed some i m p r o v e m e n t in wall motion of the anterior and lateral wall without decrease in ventricular size. Elevated filling pressure required intravenous afterload reduction, which was later replaced by an oral regimen prior to discharge. At 1 m o n t h the ejection fraction had improved to 26 %, with some decrease in mitral regurgitation (Table I). On study with positron tomography 2 months after coronary revascularization, improved myocardial perfusion was noted on the N-13 ammonia flow study. P r o m i n e n t myocardial u p t a k e of F-18 deoxyglucose was again noted on the metabolic study, indicating active tissue glucose metabolism (Fig. 2). Severe congestive symptoms and serum sodium < 130 m E q / d l persisted several months after discharge, resulting in two rehospitalizations. However, the p a t i e n t improved gradually, with decreasing congestive symptoms and increasing exercise tolerance. A t 9 months, his peak oxygen u p t a k e was 18 ml/kg, and he returned to his previous full-time employment in public relations. A t t h a t time he requested t h a t he be removed from the waiting list for transplantation. By 12 months, his echocardiographic left ventricular dimension had decreased to 52 m m from 66 m m (Table I), his ejection fraction was 40%, and he had no edema or jugular venous pressure elevation. In patients presenting with global hypokinesis and ejection fraction <25 %, the noninvasive identification of coronary disease can be difficult, as apical wall motion abnormalities I and electrocardiographic anterior infarction p a t t e r n s also occur in nonischemic dilated cardiomyopathy. Chest discomfort m a y be absent in the p a t i e n t with coronary artery disease 2 and present in up to 52 % of card i o m y o p a t h y patients without epicardial coronary artery disease. 3 After identifying coronary artery disease, the potential benefit from revascularization must be assessed. Although patients with ejection fraction <25 % have been considered unlikely to benefit when congestive s y m p t o m s predominate, 4 widespread ischemia may lead to "hibernating myocardium," in which systolic function can im-

prove significantly with better coronary perfusion. 5 Preserved glucose metabolism frequently identifies regions of reversible dysfunction 6 not always evident from delayed thallium images. In this p a t i e n t referred for cardiac transplantation, metabolic imaging with positron emission tom o g r a p h y revealed substantial viable myocardium in hypoperfused regions, p r o m p t i n g performance of coronary artery bypass grafting despite an ejection fraction of 16 % and severe symptoms of congestive h e a r t failure. 7 Delayed recovery of myocardial function has been demo n s t r a t e d after myocardial infarction and coronary artery bypass grafting in patients with milder left ventricular dysfunction, s Despite a small improvement in ejection fraction early after revascularization, this patient had persistent congestive s y m p t o m s of sufficient severity to place him on the t r a n s p l a n t waiting list for several months. Fortunately, the donor shortage allowed sufficient waiting time for further myocardial recovery to occur. His current functional status with his native heart is equivalent to t h a t of the majority of patients following cardiac transplantation. 9 This has allowed him to resume his previous activity without assuming the risk of rejection and infection associated with cardiac transplantation. W i t h the current donor shortage limiting cardiac t r a n s p l a n t a t i o n to only 10% of eligible patients, I~ the vigorous search for reversible ischemia is necessary in order to reserve donor hearts for those patients who truly have no other option. REFERENCES

1. Medina R, Panidis IP, Morganroth J, Kotler MN, Mintz GS. The value of echocardiographic regional wall motion abnormalities in detecting coronary artery disease. AM HEART J 1985;109:799-803. 2. Quyyumi AA, Wright CM, Mockus LJ, Fox KM. How important is a history of chest pain in determining the degree of ischemia in patients with angina pectoris? Br Heart J 1985;54: 22-6. 3. Massumi RA, Rios JC, Gooch AS, Nutter D, Devita VT, Datlow DW. Primary myocardial disease. Report of fifty cases and review of the subject. Circulation 1965;31:19-41. 4. Detre KM, Peduzzi P, Hammermeister KE, Murphy ML, Hultgren HN, Takaro T. Five-year effect of medical and surgical therapy on resting left ventricular function in stable angina: Veterans Administration Cooperative Study. Am J Cardiol 1984;53:444-50. 5. Braunwald E, Rutherford JD. Reversible ischemic left ventricular dysfunction: evidence for "hibernating myocardium." J Am Coll Cardiol 1986;8:1467-70. 6. Tillisch J, Brunken R, Marshall R, Schwaiger M, Mandelkern M, Phelps M, Schelbert H. Reversibility of cardiac wall motion abnormalities predicted by positron tomography. N Engl J Med 1986;314:884-8. 7. Shearn DL, Brent BN. Coronary artery bypass surgery in patients withleft ventricular dysfunction. Am J Med 1986;80:40511. 8. Mintz LJ, Ingels NB Jr, Daughters GT II, Stinson EB, Alderman EL. Sequential studies of left ventricular function and wall motion after coronary arterial bypass surgery. Am J Cardiol 1980;45:210-6. 9. Kavanaugh T, Yacoub MH, Merlens DJ, Kennedy J, Campbell RB, Sawyer P. Cardiorespiratory responses to exercise training after orthotopic cardiac transplant. Circulation 1988;77:162-8. 10. Evans RW, Manninen DL, Garrison LP, Maier AM. Donor availability as the primary determinant of the future of heart transplantation. JAMA 1986;225:1892-8.