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Mediastinal Histoplasmosis with Abscess
t
y
T-41 ;// ',
E. P. _ __.__
__._ _ _.::...a_ _.....__ _ __.__ ___.,,___.....__ _.....:_......__..___ _~~-
2. Another continuous recording of standard lead 1. Slowing of the sinus rhythm seen in the upper strip (a) is due to pressure on the eye ball (Aschner's test). Details are discussed in the text. F=fusion beat; other abbreviations same as in Figure 1.
FIGURE
E junction. Then, the third sinus impulse ( Sa) will penetrate into and discharge the parasystolic focus before occurrence of the predicted parasystolic impulse, because the sinus impulse ( Sa) arises within 1.15 sec ( the parasystolic cycle length) after the first sinus impulse ( S,) . Thus, the upper strip of Figure 1 suggests the possibility that a 2:1 entrance block may be present at the V -E junction, as shown in the diagram below. DISCUSSION
Temporary failure of entrance block has been reported by several investigators 2 • 3 as a mechanism of intermittent parasystole. However, intermittent parasystole due to 2:1 entrance block has never been reported before. The observations in this paper suggest the existence of a 2:1 entrance block in intermittent ventricular parasystole. According to the definition of ordinary ventricular parasystole, 4 entrance block at the ventricular-ectopic (V-E) junction protects the ectopic pacemaker from other impulses during all phases of the ectopic cycle, ie, during both the refractory phase and the nonrefractory phase of the ventricular muscle. On the other hand, in idioventricular rhythm or ventricular escape rhythm, there is no protection from other impulses. In this rhythm, whenever a sinus impulse is conducted to the ventricles without causing a ventricular fusion beat, it penetrates into the ectopic pacemaker, and results in discharge and resets the rhythm. This phenomenon indicates that the refractory period of the V-E junction in idioventricular rhythm never exceeds that of the ventricular muscle excluding the V-E junction. In the other junctions, for example, in the atrioventricular junction, there is second degree block between normal conduction and complete block. In the same way, it is expected that second degree entrance block will be found between escape rhythm and continuous parasystole. The presence of a second degree entrance block is indicated in the present case, where the absolute refractory period of the V-E junction is markedly longer than that of the ventricular muscle except the V-E junction, but shorter than the whole length of the ectopic cycle. Recently, Cohen, Langendorf, and Pick 3 reported such a refractory period in cases of intermittent ventricular
CHEST, 67: 2, FEBRUARY, 1975
parasystole. In their cases, however, it appeared that, during a late phase of the parasystolic cycle, parasystolic centers were also protected from other impulses by diastolic depolarization, though this feature was not clearly demonstrated in some of the cases. In our case, such a late zone of protection is not seen in any stage of the parasystolic cycle, as indicated in Figures 1 and 2. As a result, we are convinced that the observations in the present report demonstrate the presence of a "pure" second degree entrance block without any other mechanism of protection.
1 Scherf D, Bornemann C: Parasystole with a rapid ventricular center. Am Heart J 62:320-331, 1961 2 Steffens TG: Intermittent ventricular parasystole due to entrance block failure. Circulation 44:442-445, 1971 3 Cohen H, Langendorf R, Pick A: Intermittent parasystole -mechanism of protection. Circulation 48:761-774, 1973 4 Schamroth L: The Disorders of Cardiac Rhythm. Oxford and Edinburgh, Blackwell Scientific Publications, 1971, p 151
Mediastinal Histoplasmosis with Abscess* Richard D. Schneider, M.D., and John D. Reid, M.D.
A mediastinal mass of cinically undetermined nature was found at autopsy to be an enormous abscess due to secondary infection in granulomatous caseating mediastiDal nodes caused by Histoplasma capsulatum. Other comp6cations of mediastinal histoplasmosis are briefly reviewed.
M
ediastinal abscesses are so infrequent that they rarely enter in differential diagnosis. Furthermore they have been caused by a variety of microbiologic agents. °From Cleveland Metropolitan General Hospital, Cleveland. Reprint requests: Dr. Schneider, 17 Stanley Street, New Haven 06511
MEDIASTINAL HISTOPLASMOSIS WJ.TH ABSCESS 237
An example secondary to Histopltzsma capsulatum lymphadenitis is reported. To our knowledge this organism has not previously been incriminated. CASE REPORT
A 58-year-old woman housekeeper had been in good health and working until two months before admission when she noticed a gradual loss of stamina and a slight cough. She had fever and diarrhea, more severe cough, and shortness qf breath, for seven days before she was admitted in February, 1973. She had smoked two to three packs of cigarettes for many years. Digitalis was given for three days but there was no improvement and she was transferred to Cleveland Metropolitan General Hospital. Here she was described as obese and dyspneic; 103 kg in weight; with blood pressure 130/85 mm Hg, pulse 110 and temperature 37.5•C. Physical examination was entirely normal apart from rales at both lung bases. Chest x-ray examination ( Fig 1 ) showed cardiomegaly and bibasilar haziness; an anterior mediastinal mass with hilar adenopathy; and a questionable nodular mass in the right lower lung field. Films were originally interpreted as lymphoma or bronchogenic carcinoma with metastases, but subsequently, because of bubbles and streaks of air in a high voltage chest x-ray film, an abscess was suggested.
Laboratory Findings The hematocrit was 50 percent; white blood cell count 21,400 per cu mm, 80 percent segmented neutrophils, 6 percent bands, 8 percent lymphocytes, 4 percent monocytes, and 2 percent metamyelocytes; VDRL negative; IPPD negative on two occasions. Arterial blood pH was 7.41, Pco2 55 mm, P<>2 47 mm and oxygen saturation 82 percent. When the arterial P02 was raised above 50 mm, she retained C02 with a peak partial pressure of 69 mm. ECG was read as consistent with cor pulmonale. Management consisted of low oxygen by Venti-mask (28
percent to 35 percent), intravenous Lasix, and maintenance digitalis. . After admission, her temperature was normal, but on the seventh hospital day rose to 37.5•C and remained there. Her weight fell to 99 kg. On the 14th hospital day, she developed a productive cough with foul-smelling purulent material, laden with Gram-negative bacilli. A chest x-ray film showed clear lung fields without infiltrates. Barium swallow revealed a normal esophagus without deviation, and the source of the purulent sputum was not discovered. Shortly thereafter, she died. Clinical diagnoses were mediastinal mass, undetermined etiology, with respiratory failure.
Relevant Autopsy Findings There was a large abscess in the anterior and superior mediastinum, containing approximately 400 ml of moderately thick, green pus, from which Streptococcus mitis and Bacteroides melaninogenicus were cultured. Fungal and mycobacterial cultures were not requested. The walls of the abscess were the diaphragm below, the parietal pericardium posteriorly, the pleurae on each side, and the sternum and strap muscles of the neck in front. Superiorly, the abscess surrounded the internal jugular vein, the innominate vein and superior vena cava, and extended upward to the limit of anatomic dissection to the upper margin of the thyroid. Despite careful search, no communication was established between ··the · abscess and the trachea or esophagus. On microscopic examination, the mediastinal aspect of the superior vena cava, lying in the posterior abscess wall revealed a granulomatous tissue reaction and was covered with fibrinous material and necrotic caseous debris. Two mural thrombi were present on the intimal surfaces of the right innominate vein and the superior vena cava. In the caseous material, oval parasites suggestive of degenerating yeast forms of Histoplasma capsulatum were found on staining with silver methenamine. Results of acid-fast stains were negative. The thymus was identified byhistology and appeared to be normal for age. There was a fibrinous and fibrous pericarditis with obliteration of the large amount of anterior and superior parts of the pericardia( cavity. There was an acute laryngitis, tracheitis, and bronchitis, with no evidence of the purulent material described clinically. The lungs were congested and edematous, weighing 1,340 gm together. The left upper lobe showed focal consolidation from which cultures grew Streptococcus mitis. Several inferior and superior tracheobronchial lymph nodes showed large caseating foci, some hyalinized lesions and a few epithelioid granulomas. On silver staining, entirely typical yeast forms of Histoplasma capsulatum were present ID. moderate numbers. The spleen showed numerous calcified granulomata typical of old H capsulatum infection, but no organisms were seen. The heart showed biventricular hypertrophy, but was otherwise unremarkable. DISCUSSION
FIGURE 1. Chest PA film. Widening of the mediastinum and basilar infiltrates are apparent. Dashed circle indicates air seen in high voltage x-ray film.
238 SCHNEIDER, REID
In the preantibiotic era, mediastinal abscesses were associated with an 80 percent mortality rate. Even today prompt treatment remains necessary but this is often hampered by the confusing clinical and radiologic presentations and by multiplicity of causative agents. Review of the literature, reveals no report of an anterior mediastinal abscess due to Histoplasma capsulatum.
CHEST, 67: 2, FEBRUARY, 1975
Other manifestations of mediastinal histoplasmosis are well recognized; these include eight cases of pericarditis ;l-1 11 cases of superior vena cava obstruction with 6brosis; 6 •8 • 11 and one case of recurrent atrial flutter. 6 According to Keefer's 1 2 1938 review approximately 50 percent of all cases of anterior mediastinitis are chronic in nature, with tuberculosis as the most common cause, and syphilis in second place. The anterior mediastinal abscess arose by lymphatic spread from the caseating peritracheal lymph nodes. Keefer established this pathway for tuberculous infection, but in this case tuberculosis was ruled out by negative skin tests and negative histologic stains for acidfast bacilli. In favor of H capsulatum are calci6ed splenic lesions, caseating lymph nodes with the typical yeast form of the organism, and the presence of degenerating H capsulatum forms in the necrotic material in the abscess. Superinfection is a recognized although uncommon complication of histoplasmic or tuberculous cavities; S mitis and B melllninogenicus, which are normally nonpathogenic, are interpreted as secondary invaders in this case.
1 Dix JH, Gurkaynak N: Histoplasmosis with massive pericardia! effusion and systemic involvement. JAMA 182: 687, 1962 2 Gregoriades DG, Langeluttig HV, Polk VN : Pericarditis with massive effusion due to histoplasmosis. JAMA 178: 331, 1961 3 Heiner DC: Diagnosis of histoplasmosis using precipitin reactions in agar gel. Pediatrics 22:616, 1958 4 Kaplan MM, Sherwood LM : Acute pericarditis due to Histoplasma capatdatum. Ann Intern Med 58:862, 1963 5 Owen GE, Scherr SN, Segre EJ : Histoplasmosis involving the heart and great vessels. Am J Med 32:552, 1962 6 Webb WR, Herring JL: Pericarditis due to histoplasmosis. Am Heart J 64:679, 1962 7 Wooley CF, Hosier DM : Constrictive pericarditis due to Histoplasma capsulatum. N Eng! J Med 264:1230, 1961 8 Gillespie JB: Superior vena caval obstruction in childhood. J Pediat 49:320, 1956 9 Marshall RJ, Edmundowicz AC, Andrews CE: Chronic obstruction of the superior vena cava due to histoplasmosis. Circulation 29:604, 1964 10 Miller DB, Allen ST, Amidon EL: Obstruction of superior vena cava presumably due to histoplasmosis. Am Rev Tuberc 77:848, 1958 11 Salyer JM, Harrison HN, Winn DF, eta!: Chronic fibrous mediastinitis and superior vena caval obstruction due to histoplasmosis. Dis Chest 35:364, 1959 12 Keefer CS: Acute and chronic mediastinitis. Arch Intern Med 62:109, 1938
CHEST, 67: 2, FEBRUARY, 1975
Delayed Opening of Beall Mitral Prosthetic Valve Detected by Echocardiography* Nobuyoshi Kawai, M.D., Bernard L. Segal, M .D., F.C.C.P., and Joseph W. Linhart, M.D., F.C.C.P.
A 47-year-old woman in normal sinus rhythm developed frequent pulse defidta, immediately following mitral valve replacement with a Beall disc prosthesis. Emergency bedside simultaneous tradDg of ecbocardiognm, phon. cardlognm ud arterial pulse revealed a delayed opening of tbe disc with vuious timing Intervals in diastole, and sugested some form of interference with normal disc motion. An interfering papillary muscle remDDt was later confirmed and corrected by reoperatioa. techniques at the bedside are an acceptable Ultrasonic noninvasive means to evaluate the function of a
disc-type mitral prosthesis.l-8 A decreased excursion and opening velocity of the disc has been proposed as indicating valve dysfunction in the presence of thrombus formation within the prosthetic cage. 2 This report describes a patient with frequent pulse deficits associated with an abnormally delayed opening of the disc immediately following mitral valve replacement with a Beall disc prosthesis. The delayed opening was caused by the interference of a papillary muscle remnant with normal disc excursion. This condition, clearly detected at the bedside by simultaneous tracings of echocardiogram, phonocardiogram, and arterial pulse, was later confirmed by reoperation. CASE
REPoRT
A 47 -year-old white woman was referred to Hahnemann Medical College and Hospital for evaluation of shortness of breath, episodes of palpitations, and occasional chest pain. For two months before admission, the patient had been administered digoxin, 0.25 mg daily, and a diuretic. On admission, the patient was not acutely distressed. Vital signs were normal. Pertinent cardiovascular examination disclosed no neclc-vein distention. There was moderate cardiomegaly, with a palpable left ventricular heaving impulse over the sixth intercostal space at the anterior axillary line. On auscultation, murmurs and sounds indicating moderate to severe mitral insufficiency and mild aortic insufficiency were heard. Both lungs were clear on auscultation except for slight expiratory prolongation. No signs of right ventricular failure were observed. Chest x-ray examination revealed moderate enlargment of the left atrium and the left ventricle, and slight calcification of mitral valve leaflets, but there was no lung congestion. The electrocardiogram showed atrial fibrillation, with a ventricular response of 70 beats per minute, with left ventricular hypertrophy, and nonspecific ST-T wave abnormalities. The phonocardiogram, the echocardiogram and cardiac catheter•From the Division of Cardiology Department of Medicine, Hahnemann Medical College and Hospital, Philadelphia. Reprint requests: Dr. Linhart, Hahnemann Medical College and Hospital, Philadelphia 19102
DELAYED OPENING OF BEALL MITRAL PROSTHETIC VALVE 239
y
T-41 ;// ',
E. P. _ __.__
__._ _ _.::...a_ _.....__ _ __.__ ___.,,___.....__ _.....:_......__..___ _~~-
2. Another continuous recording of standard lead 1. Slowing of the sinus rhythm seen in the upper strip (a) is due to pressure on the eye ball (Aschner's test). Details are discussed in the text. F=fusion beat; other abbreviations same as in Figure 1.
FIGURE
E junction. Then, the third sinus impulse ( Sa) will penetrate into and discharge the parasystolic focus before occurrence of the predicted parasystolic impulse, because the sinus impulse ( Sa) arises within 1.15 sec ( the parasystolic cycle length) after the first sinus impulse ( S,) . Thus, the upper strip of Figure 1 suggests the possibility that a 2:1 entrance block may be present at the V -E junction, as shown in the diagram below. DISCUSSION
Temporary failure of entrance block has been reported by several investigators 2 • 3 as a mechanism of intermittent parasystole. However, intermittent parasystole due to 2:1 entrance block has never been reported before. The observations in this paper suggest the existence of a 2:1 entrance block in intermittent ventricular parasystole. According to the definition of ordinary ventricular parasystole, 4 entrance block at the ventricular-ectopic (V-E) junction protects the ectopic pacemaker from other impulses during all phases of the ectopic cycle, ie, during both the refractory phase and the nonrefractory phase of the ventricular muscle. On the other hand, in idioventricular rhythm or ventricular escape rhythm, there is no protection from other impulses. In this rhythm, whenever a sinus impulse is conducted to the ventricles without causing a ventricular fusion beat, it penetrates into the ectopic pacemaker, and results in discharge and resets the rhythm. This phenomenon indicates that the refractory period of the V-E junction in idioventricular rhythm never exceeds that of the ventricular muscle excluding the V-E junction. In the other junctions, for example, in the atrioventricular junction, there is second degree block between normal conduction and complete block. In the same way, it is expected that second degree entrance block will be found between escape rhythm and continuous parasystole. The presence of a second degree entrance block is indicated in the present case, where the absolute refractory period of the V-E junction is markedly longer than that of the ventricular muscle except the V-E junction, but shorter than the whole length of the ectopic cycle. Recently, Cohen, Langendorf, and Pick 3 reported such a refractory period in cases of intermittent ventricular
CHEST, 67: 2, FEBRUARY, 1975
parasystole. In their cases, however, it appeared that, during a late phase of the parasystolic cycle, parasystolic centers were also protected from other impulses by diastolic depolarization, though this feature was not clearly demonstrated in some of the cases. In our case, such a late zone of protection is not seen in any stage of the parasystolic cycle, as indicated in Figures 1 and 2. As a result, we are convinced that the observations in the present report demonstrate the presence of a "pure" second degree entrance block without any other mechanism of protection.
1 Scherf D, Bornemann C: Parasystole with a rapid ventricular center. Am Heart J 62:320-331, 1961 2 Steffens TG: Intermittent ventricular parasystole due to entrance block failure. Circulation 44:442-445, 1971 3 Cohen H, Langendorf R, Pick A: Intermittent parasystole -mechanism of protection. Circulation 48:761-774, 1973 4 Schamroth L: The Disorders of Cardiac Rhythm. Oxford and Edinburgh, Blackwell Scientific Publications, 1971, p 151
Mediastinal Histoplasmosis with Abscess* Richard D. Schneider, M.D., and John D. Reid, M.D.
A mediastinal mass of cinically undetermined nature was found at autopsy to be an enormous abscess due to secondary infection in granulomatous caseating mediastiDal nodes caused by Histoplasma capsulatum. Other comp6cations of mediastinal histoplasmosis are briefly reviewed.
M
ediastinal abscesses are so infrequent that they rarely enter in differential diagnosis. Furthermore they have been caused by a variety of microbiologic agents. °From Cleveland Metropolitan General Hospital, Cleveland. Reprint requests: Dr. Schneider, 17 Stanley Street, New Haven 06511
MEDIASTINAL HISTOPLASMOSIS WJ.TH ABSCESS 237
An example secondary to Histopltzsma capsulatum lymphadenitis is reported. To our knowledge this organism has not previously been incriminated. CASE REPORT
A 58-year-old woman housekeeper had been in good health and working until two months before admission when she noticed a gradual loss of stamina and a slight cough. She had fever and diarrhea, more severe cough, and shortness qf breath, for seven days before she was admitted in February, 1973. She had smoked two to three packs of cigarettes for many years. Digitalis was given for three days but there was no improvement and she was transferred to Cleveland Metropolitan General Hospital. Here she was described as obese and dyspneic; 103 kg in weight; with blood pressure 130/85 mm Hg, pulse 110 and temperature 37.5•C. Physical examination was entirely normal apart from rales at both lung bases. Chest x-ray examination ( Fig 1 ) showed cardiomegaly and bibasilar haziness; an anterior mediastinal mass with hilar adenopathy; and a questionable nodular mass in the right lower lung field. Films were originally interpreted as lymphoma or bronchogenic carcinoma with metastases, but subsequently, because of bubbles and streaks of air in a high voltage chest x-ray film, an abscess was suggested.
Laboratory Findings The hematocrit was 50 percent; white blood cell count 21,400 per cu mm, 80 percent segmented neutrophils, 6 percent bands, 8 percent lymphocytes, 4 percent monocytes, and 2 percent metamyelocytes; VDRL negative; IPPD negative on two occasions. Arterial blood pH was 7.41, Pco2 55 mm, P<>2 47 mm and oxygen saturation 82 percent. When the arterial P02 was raised above 50 mm, she retained C02 with a peak partial pressure of 69 mm. ECG was read as consistent with cor pulmonale. Management consisted of low oxygen by Venti-mask (28
percent to 35 percent), intravenous Lasix, and maintenance digitalis. . After admission, her temperature was normal, but on the seventh hospital day rose to 37.5•C and remained there. Her weight fell to 99 kg. On the 14th hospital day, she developed a productive cough with foul-smelling purulent material, laden with Gram-negative bacilli. A chest x-ray film showed clear lung fields without infiltrates. Barium swallow revealed a normal esophagus without deviation, and the source of the purulent sputum was not discovered. Shortly thereafter, she died. Clinical diagnoses were mediastinal mass, undetermined etiology, with respiratory failure.
Relevant Autopsy Findings There was a large abscess in the anterior and superior mediastinum, containing approximately 400 ml of moderately thick, green pus, from which Streptococcus mitis and Bacteroides melaninogenicus were cultured. Fungal and mycobacterial cultures were not requested. The walls of the abscess were the diaphragm below, the parietal pericardium posteriorly, the pleurae on each side, and the sternum and strap muscles of the neck in front. Superiorly, the abscess surrounded the internal jugular vein, the innominate vein and superior vena cava, and extended upward to the limit of anatomic dissection to the upper margin of the thyroid. Despite careful search, no communication was established between ··the · abscess and the trachea or esophagus. On microscopic examination, the mediastinal aspect of the superior vena cava, lying in the posterior abscess wall revealed a granulomatous tissue reaction and was covered with fibrinous material and necrotic caseous debris. Two mural thrombi were present on the intimal surfaces of the right innominate vein and the superior vena cava. In the caseous material, oval parasites suggestive of degenerating yeast forms of Histoplasma capsulatum were found on staining with silver methenamine. Results of acid-fast stains were negative. The thymus was identified byhistology and appeared to be normal for age. There was a fibrinous and fibrous pericarditis with obliteration of the large amount of anterior and superior parts of the pericardia( cavity. There was an acute laryngitis, tracheitis, and bronchitis, with no evidence of the purulent material described clinically. The lungs were congested and edematous, weighing 1,340 gm together. The left upper lobe showed focal consolidation from which cultures grew Streptococcus mitis. Several inferior and superior tracheobronchial lymph nodes showed large caseating foci, some hyalinized lesions and a few epithelioid granulomas. On silver staining, entirely typical yeast forms of Histoplasma capsulatum were present ID. moderate numbers. The spleen showed numerous calcified granulomata typical of old H capsulatum infection, but no organisms were seen. The heart showed biventricular hypertrophy, but was otherwise unremarkable. DISCUSSION
FIGURE 1. Chest PA film. Widening of the mediastinum and basilar infiltrates are apparent. Dashed circle indicates air seen in high voltage x-ray film.
238 SCHNEIDER, REID
In the preantibiotic era, mediastinal abscesses were associated with an 80 percent mortality rate. Even today prompt treatment remains necessary but this is often hampered by the confusing clinical and radiologic presentations and by multiplicity of causative agents. Review of the literature, reveals no report of an anterior mediastinal abscess due to Histoplasma capsulatum.
CHEST, 67: 2, FEBRUARY, 1975
Other manifestations of mediastinal histoplasmosis are well recognized; these include eight cases of pericarditis ;l-1 11 cases of superior vena cava obstruction with 6brosis; 6 •8 • 11 and one case of recurrent atrial flutter. 6 According to Keefer's 1 2 1938 review approximately 50 percent of all cases of anterior mediastinitis are chronic in nature, with tuberculosis as the most common cause, and syphilis in second place. The anterior mediastinal abscess arose by lymphatic spread from the caseating peritracheal lymph nodes. Keefer established this pathway for tuberculous infection, but in this case tuberculosis was ruled out by negative skin tests and negative histologic stains for acidfast bacilli. In favor of H capsulatum are calci6ed splenic lesions, caseating lymph nodes with the typical yeast form of the organism, and the presence of degenerating H capsulatum forms in the necrotic material in the abscess. Superinfection is a recognized although uncommon complication of histoplasmic or tuberculous cavities; S mitis and B melllninogenicus, which are normally nonpathogenic, are interpreted as secondary invaders in this case.
1 Dix JH, Gurkaynak N: Histoplasmosis with massive pericardia! effusion and systemic involvement. JAMA 182: 687, 1962 2 Gregoriades DG, Langeluttig HV, Polk VN : Pericarditis with massive effusion due to histoplasmosis. JAMA 178: 331, 1961 3 Heiner DC: Diagnosis of histoplasmosis using precipitin reactions in agar gel. Pediatrics 22:616, 1958 4 Kaplan MM, Sherwood LM : Acute pericarditis due to Histoplasma capatdatum. Ann Intern Med 58:862, 1963 5 Owen GE, Scherr SN, Segre EJ : Histoplasmosis involving the heart and great vessels. Am J Med 32:552, 1962 6 Webb WR, Herring JL: Pericarditis due to histoplasmosis. Am Heart J 64:679, 1962 7 Wooley CF, Hosier DM : Constrictive pericarditis due to Histoplasma capsulatum. N Eng! J Med 264:1230, 1961 8 Gillespie JB: Superior vena caval obstruction in childhood. J Pediat 49:320, 1956 9 Marshall RJ, Edmundowicz AC, Andrews CE: Chronic obstruction of the superior vena cava due to histoplasmosis. Circulation 29:604, 1964 10 Miller DB, Allen ST, Amidon EL: Obstruction of superior vena cava presumably due to histoplasmosis. Am Rev Tuberc 77:848, 1958 11 Salyer JM, Harrison HN, Winn DF, eta!: Chronic fibrous mediastinitis and superior vena caval obstruction due to histoplasmosis. Dis Chest 35:364, 1959 12 Keefer CS: Acute and chronic mediastinitis. Arch Intern Med 62:109, 1938
CHEST, 67: 2, FEBRUARY, 1975
Delayed Opening of Beall Mitral Prosthetic Valve Detected by Echocardiography* Nobuyoshi Kawai, M.D., Bernard L. Segal, M .D., F.C.C.P., and Joseph W. Linhart, M.D., F.C.C.P.
A 47-year-old woman in normal sinus rhythm developed frequent pulse defidta, immediately following mitral valve replacement with a Beall disc prosthesis. Emergency bedside simultaneous tradDg of ecbocardiognm, phon. cardlognm ud arterial pulse revealed a delayed opening of tbe disc with vuious timing Intervals in diastole, and sugested some form of interference with normal disc motion. An interfering papillary muscle remDDt was later confirmed and corrected by reoperatioa. techniques at the bedside are an acceptable Ultrasonic noninvasive means to evaluate the function of a
disc-type mitral prosthesis.l-8 A decreased excursion and opening velocity of the disc has been proposed as indicating valve dysfunction in the presence of thrombus formation within the prosthetic cage. 2 This report describes a patient with frequent pulse deficits associated with an abnormally delayed opening of the disc immediately following mitral valve replacement with a Beall disc prosthesis. The delayed opening was caused by the interference of a papillary muscle remnant with normal disc excursion. This condition, clearly detected at the bedside by simultaneous tracings of echocardiogram, phonocardiogram, and arterial pulse, was later confirmed by reoperation. CASE
REPoRT
A 47 -year-old white woman was referred to Hahnemann Medical College and Hospital for evaluation of shortness of breath, episodes of palpitations, and occasional chest pain. For two months before admission, the patient had been administered digoxin, 0.25 mg daily, and a diuretic. On admission, the patient was not acutely distressed. Vital signs were normal. Pertinent cardiovascular examination disclosed no neclc-vein distention. There was moderate cardiomegaly, with a palpable left ventricular heaving impulse over the sixth intercostal space at the anterior axillary line. On auscultation, murmurs and sounds indicating moderate to severe mitral insufficiency and mild aortic insufficiency were heard. Both lungs were clear on auscultation except for slight expiratory prolongation. No signs of right ventricular failure were observed. Chest x-ray examination revealed moderate enlargment of the left atrium and the left ventricle, and slight calcification of mitral valve leaflets, but there was no lung congestion. The electrocardiogram showed atrial fibrillation, with a ventricular response of 70 beats per minute, with left ventricular hypertrophy, and nonspecific ST-T wave abnormalities. The phonocardiogram, the echocardiogram and cardiac catheter•From the Division of Cardiology Department of Medicine, Hahnemann Medical College and Hospital, Philadelphia. Reprint requests: Dr. Linhart, Hahnemann Medical College and Hospital, Philadelphia 19102
DELAYED OPENING OF BEALL MITRAL PROSTHETIC VALVE 239