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Acute mitral valvular obstruction from infective endocarditis
Acute mitral valvular obstruction from infective endocarditis Echocardiographic diagnosis and report of the second successfully treated case Severe mitral stenosis of rapid onset and progression \l'as observed in a patient with infective endocarditis superimposed upon mild rheumatic mitral valvular stenosis, This severe stenosis resultedfrom large vegetations impinging upon the mitral \'{I1I'e orifice, Preoperative studies indicating mitral stenosis with vegetations and pulmonary edema \l'ere followed by emergency mitral valve replacement, which \l'as successful.
Jack G. Copeland, M.D., Neal W. Salomon, M.D., Edward B. Stinson, M.D.,* Richard L. Popp, M.D.,** and Norman E. Shumway, M.D.,
Stanford, Calif.. and Tucson, Ariz.
T
he usual indications for mitral valve replacement in infective endocarditis have been severe congestive heart failure owing to mitral regurgitation or systemic embolization from vegetations. 1-~ Three cases of mitral valvular obstruction caused by infective endocarditis have been previously reported.v ? In two of these cases": 6 the outcome was fatal and the diagnosis was made on postmortem examination. In the third case" the diagnosis was made antemortem in a 51-year-old man, who was treated for 56 days with anti-staphylococcal therapy prior to the development of acute pulmonary edema, right hemiparesis, a loud rumble of mitral stenosis, and echocardiographic findings suggestive of mitral vegetations. He was subsequently transferred to the Stanford Medical Center and underwent successful mitral valve replacement with a porcine xenograft prosthesis. t A second patient has since been treated sue-
From the Departments of Cardiovascular Surgery and Cardiology. Stanford University Medical Center. Stanford. Calif. 94305. and the Department of Surgery at the Arizona Health Sciences Center. Tucson, Ariz. 85724. Received for publication Nov. 28. 1978. Accepted for publication Jan. 4. 1979. Address for reprints: Jack G. Copeland. M.D .. Surgery Department-Room 4402. Arizona Health Sciences Center. 1501 N. Campbell Ave .. Tucson. Ariz. 85724. *Established Investigator. American Heart Association. **Supported in part by a Research Career Development Award. No. K04HL70439. tHancock Laboratories. Inc.. Anaheim. Calif.
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cessfully at Stanford Medical Center. The patient's preoperati ve diagnostic evaluations and intraoperati ve findings constitute the basis for this report.
Case report A 52-year-old woman. known to have had a murmur of mitral stenosis since childhood, was well until October. 1974. At that time a fever of unknown origin developed, which was unresponsive to treatment with oral tetracycline. One month later congestive heart failure ensued. Upon hospitalization. splinter hemorrhages and a Grade 1/6 apical diastolic rumbling murmur were noted. Shortly thereafter. the patient sustained neurologic deficits consisting of transient right hemiparesis. dysphagia. and dysphonia. Multiple blood cultures were negative and treatment with broad-spectrum antibiotics was initiated. Three weeks later. rapidly progressive pulmonary edema. refractory to medical therapy. developed (Fig. I. chest roentgenogram). Echocardiographic examination at this time revealed decreased motion of the anterior leaflet of the mitral valve and multiple adjacent echoes on the atrial aspect of that leaflet (Figs. 2 and 3). Right-sided cardiac catheterization revealed the following pressures: right atrial mean 4 mm. Hg. right ventricle 55/4 rnrn. Hg. pulmonary artery 55/24 rnrn. Hg with a mean pressure of 26 mrn , Hg. and pulmonary artery wedge mean 24 rnm. Hg. At operation. obstructive vegetations. each 3 by 2 by 2 crn., were found on the atrial surface of the mitral valve in the regions of both commissures (Fig. 4). The valve leaflets were thickened and fibrotic without calcification. The estimated valve orifice area with the vegetations removed was 1.5 sq. em. Cultures of the vegetations were negative. Histologically. these vegetations were composed of thrombus and necrotic debris containing an infiltrate of both chronic and acute inflammatory cells. The postoperative course after valve re-
0022-5223/79/070128+03$00.30/0 © 1979 The C. V. Mosby Co.
Volume 78 Number 1 July, 1979
Fig. 1. Chest roentgenogram illustrates acute pulmonary edema prior to mitral valve replacement.
Infective endocarditis
129
Fig. 2. Preoperative echocardiogram. Labeled structures are electrocardiogram (EKG) , intraventricular septum (lVS) , anterior leaflet of mitral valve (MAL), posterior leaflet of mitral valve (MPL) , posterior wall (PW), pericardium (P), and echo from vegetation (VEG). The appearance of this echocardiogram is very similar to that seen in patients with left atrial myxoma. Note a small pericardial effusion is also present between the posterior wall (PW) and the pericardium (P).
EKG
Fig. 3. M-mode echocardiographic beam directed from the aortic valve and left atrium (left) and then angled toward the mitral valve (right). Labeled structures are reference electrocardiogram (EKG) , aorta (AD), left atrium (LA), intraventricular septum (IVS) , region of the mitral valve in diastole (MV), pericardial effusion (EFF) , vegetation behind the anterior leaflet of the mitral valve (VEG), and right ventricle (RV). Note that near the atrium the increased echoes from the vegetation are seen predominantly during systole. As the transducer beam is angled further toward the ventricle, the vegetations are seen both in systole and diastole. placement with a porcine xenograft was unremarkable. At present, the patient has no cardiac disability but retains minimal neurologic dysfunction.
Discussion Both this patient and the patient previously treated surgically at the Stanford Medical Center' presented a
similar syndrome. Infective endocarditis (caused by Staphylococcus in the previously reported case and of unknown origin in this case) developed on mildly stenotic mitral valves that showed gross and microscopic features of chronic rheumatic valvulitis. Several weeks after initiation of antibiotic therapy, rapid clinical deterioration ensued, despite bloodstream sterility. In
The Journal of
I 30 Copeland et al.
Fig. 4. Photograph of excised mitral valve shows vegetations (VEG) attached to both the right and left commissures. The
anterior leaflet (AL) and posterior leaflet (PL) both are thickened and somewhat foreshortened. The vegetations can be seen prolapsing into the stenotic mitral orifice. which is in the center of the valve. addition, neurologic abnormalities, presumably embolic in origin, developed during the same interval. The most noteworthy clinical feature in both cases was rapidly progressive pulmonary edema that did not respond to intensive medical therapy. Prompt diagnostic studies were therefore undertaken. Echocardiograms in both instances showed evidence of mild underlying mitral stenosis and multiple echoes on the atrial side of the anterior leaflet consistent with a mass lesion. The results of right heart catheterization were compatible with severe mitral stenosis. The diagnosis of acute, mechanical mitral valve obstruction by enlarging vegetations was made, and emergency valve replacement was successfully performed. In two previously reported necropsy cases of obstructive endocarditis involving the mitral valve, car-
Thoracic and Cardiovascular Surgery
diac decompensation was also rapid.": 6 In both of these cases there was also mild underlying rheumatic mitral stenosis prior to the development of endocarditis. In neither of these patients, however, was operation attempted. Previous reviews of the surgical treatment of infective endocarditis do not include instances of acute mitral obstruction. 2-~ Such lesions would therefore appear uncommon. Indeed, the two patients treated at our institution are unique in our experience with treatment of infective endocarditis involving native heart valves. 1 Although uncommon, the potential for acute mechanical valvular obstruction from vegetations during the course of endocarditis in patients with underlying mild mitral stenosis must be considered. Prompt diagnosis and operative intervention are necessary to save the patient.
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REFERENCES Stinson EB. Griepp RB. Vosti K. Copeland JG. Shumway NE: Operative treatment of active endocarditis. J THoRAc CARDIOVASC SURG 71:659-665. 1976 Black S. O'Rourke R, Karliner J: Role of surgery in the treatment of primary infective endocarditis. Am J Med 56:357-369. 1974 Crosby IK. Carrell R. Reed WA: Operative management of valvular complications of bacterial endocarditis. J THoRAc CARDIOVASC SURG 64:235-246. 1972 Okies J. Bradshaw M. Williams T: Valve replacement in bacterial endocarditis. Chest 63:898-904. 1973 Reve R. Saki J. Matula G. Lawson W: Mitral obstruction by vegetations of staphylococcal endocarditis. JAMA 228:75. 1974 Roberts W. Ewy G. Glancy D. Marcus F: Valvular stenosis produced by active infective endocarditis. Circulation 36:449-451, 1967 Matula G. Karpman L. Frank S. Stinson E: Mitral obstruction from staphylococcal endocarditis. corrected surgically. JAMA 233:58-59. 1975
Jack G. Copeland, M.D., Neal W. Salomon, M.D., Edward B. Stinson, M.D.,* Richard L. Popp, M.D.,** and Norman E. Shumway, M.D.,
Stanford, Calif.. and Tucson, Ariz.
T
he usual indications for mitral valve replacement in infective endocarditis have been severe congestive heart failure owing to mitral regurgitation or systemic embolization from vegetations. 1-~ Three cases of mitral valvular obstruction caused by infective endocarditis have been previously reported.v ? In two of these cases": 6 the outcome was fatal and the diagnosis was made on postmortem examination. In the third case" the diagnosis was made antemortem in a 51-year-old man, who was treated for 56 days with anti-staphylococcal therapy prior to the development of acute pulmonary edema, right hemiparesis, a loud rumble of mitral stenosis, and echocardiographic findings suggestive of mitral vegetations. He was subsequently transferred to the Stanford Medical Center and underwent successful mitral valve replacement with a porcine xenograft prosthesis. t A second patient has since been treated sue-
From the Departments of Cardiovascular Surgery and Cardiology. Stanford University Medical Center. Stanford. Calif. 94305. and the Department of Surgery at the Arizona Health Sciences Center. Tucson, Ariz. 85724. Received for publication Nov. 28. 1978. Accepted for publication Jan. 4. 1979. Address for reprints: Jack G. Copeland. M.D .. Surgery Department-Room 4402. Arizona Health Sciences Center. 1501 N. Campbell Ave .. Tucson. Ariz. 85724. *Established Investigator. American Heart Association. **Supported in part by a Research Career Development Award. No. K04HL70439. tHancock Laboratories. Inc.. Anaheim. Calif.
128
cessfully at Stanford Medical Center. The patient's preoperati ve diagnostic evaluations and intraoperati ve findings constitute the basis for this report.
Case report A 52-year-old woman. known to have had a murmur of mitral stenosis since childhood, was well until October. 1974. At that time a fever of unknown origin developed, which was unresponsive to treatment with oral tetracycline. One month later congestive heart failure ensued. Upon hospitalization. splinter hemorrhages and a Grade 1/6 apical diastolic rumbling murmur were noted. Shortly thereafter. the patient sustained neurologic deficits consisting of transient right hemiparesis. dysphagia. and dysphonia. Multiple blood cultures were negative and treatment with broad-spectrum antibiotics was initiated. Three weeks later. rapidly progressive pulmonary edema. refractory to medical therapy. developed (Fig. I. chest roentgenogram). Echocardiographic examination at this time revealed decreased motion of the anterior leaflet of the mitral valve and multiple adjacent echoes on the atrial aspect of that leaflet (Figs. 2 and 3). Right-sided cardiac catheterization revealed the following pressures: right atrial mean 4 mm. Hg. right ventricle 55/4 rnrn. Hg. pulmonary artery 55/24 rnrn. Hg with a mean pressure of 26 mrn , Hg. and pulmonary artery wedge mean 24 rnm. Hg. At operation. obstructive vegetations. each 3 by 2 by 2 crn., were found on the atrial surface of the mitral valve in the regions of both commissures (Fig. 4). The valve leaflets were thickened and fibrotic without calcification. The estimated valve orifice area with the vegetations removed was 1.5 sq. em. Cultures of the vegetations were negative. Histologically. these vegetations were composed of thrombus and necrotic debris containing an infiltrate of both chronic and acute inflammatory cells. The postoperative course after valve re-
0022-5223/79/070128+03$00.30/0 © 1979 The C. V. Mosby Co.
Volume 78 Number 1 July, 1979
Fig. 1. Chest roentgenogram illustrates acute pulmonary edema prior to mitral valve replacement.
Infective endocarditis
129
Fig. 2. Preoperative echocardiogram. Labeled structures are electrocardiogram (EKG) , intraventricular septum (lVS) , anterior leaflet of mitral valve (MAL), posterior leaflet of mitral valve (MPL) , posterior wall (PW), pericardium (P), and echo from vegetation (VEG). The appearance of this echocardiogram is very similar to that seen in patients with left atrial myxoma. Note a small pericardial effusion is also present between the posterior wall (PW) and the pericardium (P).
EKG
Fig. 3. M-mode echocardiographic beam directed from the aortic valve and left atrium (left) and then angled toward the mitral valve (right). Labeled structures are reference electrocardiogram (EKG) , aorta (AD), left atrium (LA), intraventricular septum (IVS) , region of the mitral valve in diastole (MV), pericardial effusion (EFF) , vegetation behind the anterior leaflet of the mitral valve (VEG), and right ventricle (RV). Note that near the atrium the increased echoes from the vegetation are seen predominantly during systole. As the transducer beam is angled further toward the ventricle, the vegetations are seen both in systole and diastole. placement with a porcine xenograft was unremarkable. At present, the patient has no cardiac disability but retains minimal neurologic dysfunction.
Discussion Both this patient and the patient previously treated surgically at the Stanford Medical Center' presented a
similar syndrome. Infective endocarditis (caused by Staphylococcus in the previously reported case and of unknown origin in this case) developed on mildly stenotic mitral valves that showed gross and microscopic features of chronic rheumatic valvulitis. Several weeks after initiation of antibiotic therapy, rapid clinical deterioration ensued, despite bloodstream sterility. In
The Journal of
I 30 Copeland et al.
Fig. 4. Photograph of excised mitral valve shows vegetations (VEG) attached to both the right and left commissures. The
anterior leaflet (AL) and posterior leaflet (PL) both are thickened and somewhat foreshortened. The vegetations can be seen prolapsing into the stenotic mitral orifice. which is in the center of the valve. addition, neurologic abnormalities, presumably embolic in origin, developed during the same interval. The most noteworthy clinical feature in both cases was rapidly progressive pulmonary edema that did not respond to intensive medical therapy. Prompt diagnostic studies were therefore undertaken. Echocardiograms in both instances showed evidence of mild underlying mitral stenosis and multiple echoes on the atrial side of the anterior leaflet consistent with a mass lesion. The results of right heart catheterization were compatible with severe mitral stenosis. The diagnosis of acute, mechanical mitral valve obstruction by enlarging vegetations was made, and emergency valve replacement was successfully performed. In two previously reported necropsy cases of obstructive endocarditis involving the mitral valve, car-
Thoracic and Cardiovascular Surgery
diac decompensation was also rapid.": 6 In both of these cases there was also mild underlying rheumatic mitral stenosis prior to the development of endocarditis. In neither of these patients, however, was operation attempted. Previous reviews of the surgical treatment of infective endocarditis do not include instances of acute mitral obstruction. 2-~ Such lesions would therefore appear uncommon. Indeed, the two patients treated at our institution are unique in our experience with treatment of infective endocarditis involving native heart valves. 1 Although uncommon, the potential for acute mechanical valvular obstruction from vegetations during the course of endocarditis in patients with underlying mild mitral stenosis must be considered. Prompt diagnosis and operative intervention are necessary to save the patient.
2
3
4 5
6
7
REFERENCES Stinson EB. Griepp RB. Vosti K. Copeland JG. Shumway NE: Operative treatment of active endocarditis. J THoRAc CARDIOVASC SURG 71:659-665. 1976 Black S. O'Rourke R, Karliner J: Role of surgery in the treatment of primary infective endocarditis. Am J Med 56:357-369. 1974 Crosby IK. Carrell R. Reed WA: Operative management of valvular complications of bacterial endocarditis. J THoRAc CARDIOVASC SURG 64:235-246. 1972 Okies J. Bradshaw M. Williams T: Valve replacement in bacterial endocarditis. Chest 63:898-904. 1973 Reve R. Saki J. Matula G. Lawson W: Mitral obstruction by vegetations of staphylococcal endocarditis. JAMA 228:75. 1974 Roberts W. Ewy G. Glancy D. Marcus F: Valvular stenosis produced by active infective endocarditis. Circulation 36:449-451, 1967 Matula G. Karpman L. Frank S. Stinson E: Mitral obstruction from staphylococcal endocarditis. corrected surgically. JAMA 233:58-59. 1975