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Spontaneous Regression of Benign Heart Tumor
Table !-Representative Hemodynamic Data lime, hr
Intervention
()
Control Pa0 2 .'53 mm Hg-room air Nitroprusside 30 ~Jog/min IV Hydralazine .5 mg IV Verapamil 6.8 mg IV (0.01 mg/kg) Control Pa02 68-71 mm Hg-2 liters O,.lmin Verapamil 6.8 mg IV (0.01 mg/kg) Verapamil 80 mg PO q6h Nifedipine 20 mg PO q6h
0-1 3-4 10-11 24 25-26 26-50 60-96
BP mm Hg
p
PAP mmHg
PCWP mm Hg
CO Umin
SVRu
PVRu
103
90
60
2
4.63
20.73
12.53
113
77
50
3
5.93
19.38
7.93
103
91
66
3
4.60
21.09
13.70
100
56
46
4
5.65
16.64
7.43
97
93
53
4
4.62
19.69
10.61
97
80
35
6
5.48
16.42
4.93
87
78
49
7
4.43
17.83
9.61
47
4
5.17
17.97
8.51
99 92
BP=mean arterial pressure; P =pulse; PAP= mean pulmonary arterial pressure; PCWP =mean pulmonary capillary wedge pressure; CO= cardiac output; SV_R= systemic vascular resistance; PVR =pulmonary vascular resistance; u = wood units administered for 36 hours with both hemodynamic and symptomatic improvement throughout the study period. He was then maintained on the dose of nifedipine noted in the table in addition to his previous medications, including oxygen. Approximately 18 hours after leaving the intensive care unit, the patient was found unresponsive and bradycardic; he was resuscitated, but died 12 hours later. Autopsy disclosed no pulmonary embolus, myocardial infarction or cerebral vascular accident. Noncaseating granulomas were found in lung parenchyma and lymph nodes, but not in the myocardium. The patient had been monitored while on nifedipine for 36 hours without any arrhythmias, hypotension or congestive heart failure. His death only 18 hours after leaving the intensive care unit and without any change in medication suggests that nifedipine may have contributed to his death. The mechanism is unclear to us, but this event suggests that a longer period of monitoring may be required to disclose the cumulative effects of oral nifedipine on cardiopulmonary hemodynamics in patients with pulmonary hypertension. Additional studies are required before use of this agent for pulmonary hypertension becomes ac<.-epted practice.
Harrison W. Farber, M.D., Pulmonary Fellow, Boston University School of Medicine Pulmonary Medicine Program; joel B. Karlinsky, M.D., Assistant Professor of Medicine, Boston University School of Medicine; L. jack Faling, M.D., F.C.C.P., Associate Professor of Medicine, Tufts University School of Medicine, Boston REFERENCES
2
3
4
5
Mohuiddin SM, Esterbrooks D, Saenz A, O'Donahue W, Moss AN, Runco V. Hemodynamic effects of nifedipine in severe pulmonary hypertension (abstract) Chest 1981; 80:387 Bishop MJ, Gronka B, Cheney FW. Minoxidil and nifedipine inhibit hypoxic pulmonary vasoconstriction (abstract). Chest 1981; 80:388 Simonneau G, Escourrou P, Duroux P, Lockhart A. Inhibition of hypoxic pulmonry vasoconstriction by nifedipine. N Engl J Med 1981; 304:1582-85 Kadowitz PJ, Hyman AL. Hydralazine and the treatment of primary pulmonary hypertension (Editorial). N Eng) J Med 1982; 306:1357-58 Summer W, Michael J, Brinker J. Initial and long-term effects of nifedipine in primary pulmonary hypertension (abstract). Chest 1982; 82:223-24
Spontaneous Regression of Benign Heart Tumor To the Editor: In a recent article entitled "Benign mesenchymal tumor of the heart-spontaneous regression and disappearance of pulmonary artery stenosis (Chest 1982; 82:503-05) the authors state that to their knowledge, spontaneous regression of cardiac tumor has not been reported. I wish to bring to their attention a recent case report published in 1980 by the French authors J. C. Hoeffel et al, "Primary tumors of the heart with spontaneous regression in childhood." Ro Fo 1980; 133: 549-51. They describe circumstances similar to those reported by Lee et al and mention an additional15 cases from the literature. Paul Stark, M.D. University ofTe:r:as Health Science Center at Houston To the Editor: We appreciate the comments of Dr. Stark. The case reported by Hoeffel et al and the additional 15 cases cited in their aritcle were reviewed. There was one patient1 similar to our patient in that the tumor could not be demonstrated on subsequent examination. In four other cases, including the patient reported by Hoeffel et al, the tumor was still present, although symptomatic improvement occurred. One of these patients• was discussed in our article. The remaining patients did not have evidence of spontaneous regression of the cardiac tumor. In fact, one patient died at surgery, some patients were considered inoperable, and no follow-up data were given.
Yu-Chen Lee, M.D.; Robert T. Singleton, M.D.; Chik-Kwan Tang, M.D.; University of Maryland Hospital, Baltimore REFERENCES
Khattar H, Guerin R, Fouron JC, Stanley P, Kratz C, Davignon A. Les tumeurs cardiaques chez I'enfant Rapport de 3 observations avec evolution spontanement favorable. Arch mal coeur 1975; 419-29 2 Hoen AG, Ellia EJ. Intramural fibroma of the heart. Am J Cardiol 1960; 17:579-84 CHEST I 83 I 4 I April, 1983
709
Intervention
()
Control Pa0 2 .'53 mm Hg-room air Nitroprusside 30 ~Jog/min IV Hydralazine .5 mg IV Verapamil 6.8 mg IV (0.01 mg/kg) Control Pa02 68-71 mm Hg-2 liters O,.lmin Verapamil 6.8 mg IV (0.01 mg/kg) Verapamil 80 mg PO q6h Nifedipine 20 mg PO q6h
0-1 3-4 10-11 24 25-26 26-50 60-96
BP mm Hg
p
PAP mmHg
PCWP mm Hg
CO Umin
SVRu
PVRu
103
90
60
2
4.63
20.73
12.53
113
77
50
3
5.93
19.38
7.93
103
91
66
3
4.60
21.09
13.70
100
56
46
4
5.65
16.64
7.43
97
93
53
4
4.62
19.69
10.61
97
80
35
6
5.48
16.42
4.93
87
78
49
7
4.43
17.83
9.61
47
4
5.17
17.97
8.51
99 92
BP=mean arterial pressure; P =pulse; PAP= mean pulmonary arterial pressure; PCWP =mean pulmonary capillary wedge pressure; CO= cardiac output; SV_R= systemic vascular resistance; PVR =pulmonary vascular resistance; u = wood units administered for 36 hours with both hemodynamic and symptomatic improvement throughout the study period. He was then maintained on the dose of nifedipine noted in the table in addition to his previous medications, including oxygen. Approximately 18 hours after leaving the intensive care unit, the patient was found unresponsive and bradycardic; he was resuscitated, but died 12 hours later. Autopsy disclosed no pulmonary embolus, myocardial infarction or cerebral vascular accident. Noncaseating granulomas were found in lung parenchyma and lymph nodes, but not in the myocardium. The patient had been monitored while on nifedipine for 36 hours without any arrhythmias, hypotension or congestive heart failure. His death only 18 hours after leaving the intensive care unit and without any change in medication suggests that nifedipine may have contributed to his death. The mechanism is unclear to us, but this event suggests that a longer period of monitoring may be required to disclose the cumulative effects of oral nifedipine on cardiopulmonary hemodynamics in patients with pulmonary hypertension. Additional studies are required before use of this agent for pulmonary hypertension becomes ac<.-epted practice.
Harrison W. Farber, M.D., Pulmonary Fellow, Boston University School of Medicine Pulmonary Medicine Program; joel B. Karlinsky, M.D., Assistant Professor of Medicine, Boston University School of Medicine; L. jack Faling, M.D., F.C.C.P., Associate Professor of Medicine, Tufts University School of Medicine, Boston REFERENCES
2
3
4
5
Mohuiddin SM, Esterbrooks D, Saenz A, O'Donahue W, Moss AN, Runco V. Hemodynamic effects of nifedipine in severe pulmonary hypertension (abstract) Chest 1981; 80:387 Bishop MJ, Gronka B, Cheney FW. Minoxidil and nifedipine inhibit hypoxic pulmonary vasoconstriction (abstract). Chest 1981; 80:388 Simonneau G, Escourrou P, Duroux P, Lockhart A. Inhibition of hypoxic pulmonry vasoconstriction by nifedipine. N Engl J Med 1981; 304:1582-85 Kadowitz PJ, Hyman AL. Hydralazine and the treatment of primary pulmonary hypertension (Editorial). N Eng) J Med 1982; 306:1357-58 Summer W, Michael J, Brinker J. Initial and long-term effects of nifedipine in primary pulmonary hypertension (abstract). Chest 1982; 82:223-24
Spontaneous Regression of Benign Heart Tumor To the Editor: In a recent article entitled "Benign mesenchymal tumor of the heart-spontaneous regression and disappearance of pulmonary artery stenosis (Chest 1982; 82:503-05) the authors state that to their knowledge, spontaneous regression of cardiac tumor has not been reported. I wish to bring to their attention a recent case report published in 1980 by the French authors J. C. Hoeffel et al, "Primary tumors of the heart with spontaneous regression in childhood." Ro Fo 1980; 133: 549-51. They describe circumstances similar to those reported by Lee et al and mention an additional15 cases from the literature. Paul Stark, M.D. University ofTe:r:as Health Science Center at Houston To the Editor: We appreciate the comments of Dr. Stark. The case reported by Hoeffel et al and the additional 15 cases cited in their aritcle were reviewed. There was one patient1 similar to our patient in that the tumor could not be demonstrated on subsequent examination. In four other cases, including the patient reported by Hoeffel et al, the tumor was still present, although symptomatic improvement occurred. One of these patients• was discussed in our article. The remaining patients did not have evidence of spontaneous regression of the cardiac tumor. In fact, one patient died at surgery, some patients were considered inoperable, and no follow-up data were given.
Yu-Chen Lee, M.D.; Robert T. Singleton, M.D.; Chik-Kwan Tang, M.D.; University of Maryland Hospital, Baltimore REFERENCES
Khattar H, Guerin R, Fouron JC, Stanley P, Kratz C, Davignon A. Les tumeurs cardiaques chez I'enfant Rapport de 3 observations avec evolution spontanement favorable. Arch mal coeur 1975; 419-29 2 Hoen AG, Ellia EJ. Intramural fibroma of the heart. Am J Cardiol 1960; 17:579-84 CHEST I 83 I 4 I April, 1983
709