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Postinfarction Ventricular Septal Defect with Posterior Ventricular Aneurysm
ings. Pediatrics 48 :730-739, 1971 3 Bartman J, Van de Velde RL, Friedman F : Pigmented lipid histiocytosis and susceptibility to infection : Ultrastructure of splenic histiocytes. Pediatrics 40 : 1000-1002, 1967 4 Quie PG : Infections due to neutrophil malfunction. Medicine 52 :411-417, 1973 5 Curnutte JT, Wh itten OM, Babior BM: Defective superoxide production by granulocytes from patients with CGD , N Engl} Med 290 :593-597, 1974 6 Rosenow EC : The spectrum of drug induced pulmonary disease . Ann Intern Med 77 :977-991 ,1972 -; Seal RME, Hapke EJ, Thomas GO , et al . The pathology of the acute and chronic stages of fanner's lung . Thorax 23:469-489, 1968
Postinfarction Ventricular Septal Defect with Posterior Ventricular Aneurysm* Result of a Single Distal Right Coronary Artery Obstruction .\ l ichael S. Chandra , M.D.;oO Richard D. Raines, M.D.;oO Donald B. Doty , M.D. , F.C.C.P.;t and ] . Michael Kioschos, M.D.t
A patient with postinfarction ventricular septal defect, posterior aneurysm, severe congestive heart failure, and significant atherosclerosis in the distal right coronary artery only is reported. Closure of the defect resulted in quick recovery of the patient. We demonstrated that a single significant lesion in one coronary artery can cause rupture of the interventricular septum.
CASE REPORT
A 53-year-old white man was admitted to the Veterans Administration Hospital in Iowa City on June 19, 1973, with pulmonary embolism secondary to thrombophlebitis in the right leg; he was given anticoagulation therapy. On the tenth hospital day , the patient developed an acute inferior-wall myocardial infarction. Seven days after myocardial infarction, he developed diaphoresis and left upper quadrant pain. A wade 5/6 holosystolic murmur at the lower left sternal border was noted for the nrst time . The patient was hypotensive for 24 hours and required norepinephrine infusion to maintain blood pressure. A right cardiac catheterization revealed a step-up of oxygen saturation from 40 percent to 80 percent at the right ventricular level. The patient subsequently developed severe congestive heart failure and pulmonary edema, which improved on medical therapy. Because of the clinical impression of an interventricular septal defect, right and left cardiac catheterization was done, which revealed moderately severe elevation of the right atrial, right ventricular, and pulmonary arterial pressures ; decreased card iac index; and a Qp/Qs ratio of 3.9 : 1. There was a severe occlusive lesion of the right coronary artery system at the bifurcation of the posterior descending artery and the artery to the crux (Fig 1) . A left ventriculogram showed a fllling defect posteriorly in the right ante rior oblique position . In the left anterior oblique position, a large ventricular septal defect and an aneurysmal dilatation at the apex were demonstrated (Fig 2). At cardiac surgery, there was an aneurysm of the left ventricular myocardium involving the superior one-third of the posterior wall adjacent to the septum and the atrioventricular groove. A systolic thrill was palpable over the apex . The aneurysm was opened, and a mural thrombus removed. The ventricular septal defect (Fig 3) was high in the septum near the atr ioventricular groove and near the junction of the posterior wall adjacent to the posterior descending coronary artery. The aneurysm was resected, and the defect (2 ern in diameter) was closed with a Dacron patch . The patient has done well since surgery and is back to full activity.
P
osti nfarction interventricular septal defect with ventricular aneurysm has been summarized in the literature by Daicoff and Rhodes.' Loop and associates" recently described posterior ventricular aneurysm in 11 patients, two of whom had associated interventricular septal defects. Most of the cases described in the literature were associated with severe two-vessel disease shown at necropsy." Significant single-vessel disease in this clinical situation documented by coronary cineangiography has not been reported previously. This report describes a case of postinfarction interventricular septal defect associated with a postventricular aneurysm, which had a significant lesion in the po sterior descending coronary artery and only minimal disease in the re st of the coronary system. °From the Division of Cardiovascular Diseases and Cardiovascular and Thoracic Surgery, University of Iowa Hospital s, Iowa City . Supported by HL 05729 from the National Institute of Health. ° ° Fellow. tA ssociate Professor . Reprint requests: Dr. Chandra, Department of Internal Medicine. University of Iowa, Iowa City 52242
CHEST, 68: 6, DECEMBER, 1975
FIGURE 1. Right coronary artery with single lesion distally at bifurcation of posterior descending artery and artery to crux (arrows) .
POSTINFARCTION VENTRICULAR SEPTAL DEFECT 837
REFERENCES
FU;UIIE 2. Left ventriculogram in left anterior oblique position demonstrating ventricular septal defect (arrow) and filling of right ventricle (RV) . S, Intraventricular septum ; LV, left ventricle. DISCUSSION
This appears to be the first case report of a massive inferior wall infarction associated with a ventricular sep tal defect and a posterior ventricular aneurysm, which had only one significant lesion in the coronary system as shown by angiography. Loop and associates- stated that all of their patients had severe atherosclerotic obstruction in the right coronary artery or circumflex artery, or both . Jeresaty et al ' reported a patient with postinfarction interventricular septal defect who survived for two years and died of noncardiac causes. At autopsy, there was a 60 percent occlusive lesion of the posterior descending branch of the right coronary artery and minimal atherosclerotic disease in the left coronary artery. In reviewing the literature, we noted that the survival and surgical results in this situation depend upon many factors . These include younger age (less than 55 years) , high cardiac output (more than 3 L/ min), high pulmonary artery pressure, aneurysmectomy at surgery, 1 adequate residual myocardial function, ' and preservation of blood supply to the posterior papillary muscle." Although our patient was in borderline compensated congestive heart failure for six weeks postinfarction, we believe this patient survived the postinfarction period and surgery because of significant residual myocardial function .
1 Daicoff GR, Rhodes ML; Surgical repair of ventricular septal rupture and ventricular aneurysm. JAMA 203;115, 1968 2 Loop FD , Effler DB, Webster JS, et al . Posterior ventricu lar aneurysms ; Etiologic factors and results of surgical treatment. N Engl J Med 288:237, 1973 3 Dubnow MH, Burchell HB, Titu s JL: Post-infarction ventricular aneurysm : A clinicomorphologlc and electrocardiographic study of 80 cases. Am Heart J 70:753, 1965 4 Jeresaty RM, Landry AB [r, Stirsel HC Jr: Post-infarction interventricular septal defects : Report of two cases with long survival, one with surgical repair . Am Heart J 74 : 543, 1967 5 Grobam AF, Stinson EB, Dalby PO, et al . Ventricular septal defects after myocardial infarction : Early operative treatment. JAMA 225:708, 1973
Bone Resorption of the Ribs and Pulmonary Function in Progressive Systemic Sclerosis* James C . Steigerwald. M.D .;oO Martin H. Seifert, M.B.;t May M. CliO. M .D .;! and Thomas A. NeD, M .D .• F.C.C.P.§
We report a case of progressive systemic sclerosis which showed the unusual feature of bone resorption of the ribs associated with pulmonary function abnormalities. This case, to our knowledge, is the first reported in which this bone resorption of the ribs has occurred. progreSSive systemic sclerosis (PSS) is a multisystem disease which frequently causes pulmonary function and chest roentgenogram abnormalities.' Bone resorption is another common finding in PSS, with the distal phalanges, radius, ulna, clavicle, and jaws most often involved . 2 ' < We have recently observed a young woman with PSS who, during the course of her disease, developed marked bone resorption of the ribs along with pulmonary function abnormalities. CASE REpORT
A 25-year-old black woman was first seen at the University of Colorado Medical Center in May 1966 with the chief complaint of increasing tightness of the skin. She had been entirely well until March of 1965 when she first noted arthralgia and arthritis involving the metacarpal phalangeal, and proximal interphalangeal joints of both hands . The results of evaluation at that time had been normal, except for a °From the Department of Internal Medicine, University of Colorado Medical Center and Denver General Hospital, Denver. 00 Assistant Professor of Medicine, Division of Rheumatic Diseases. tFormer Fellow, Division of Rheumatic Diseases. !Associate Professor of Radiology. §Associate Professor of Medicine, Division of Pulmonary Disease.
RelJrint requests : Dr. Ste igerwald, Denver General Hospital , Denver 80204
838 STEIGERWALD ET AL
CHEST, 68: 6, DECEMBER. 1975
Postinfarction Ventricular Septal Defect with Posterior Ventricular Aneurysm* Result of a Single Distal Right Coronary Artery Obstruction .\ l ichael S. Chandra , M.D.;oO Richard D. Raines, M.D.;oO Donald B. Doty , M.D. , F.C.C.P.;t and ] . Michael Kioschos, M.D.t
A patient with postinfarction ventricular septal defect, posterior aneurysm, severe congestive heart failure, and significant atherosclerosis in the distal right coronary artery only is reported. Closure of the defect resulted in quick recovery of the patient. We demonstrated that a single significant lesion in one coronary artery can cause rupture of the interventricular septum.
CASE REPORT
A 53-year-old white man was admitted to the Veterans Administration Hospital in Iowa City on June 19, 1973, with pulmonary embolism secondary to thrombophlebitis in the right leg; he was given anticoagulation therapy. On the tenth hospital day , the patient developed an acute inferior-wall myocardial infarction. Seven days after myocardial infarction, he developed diaphoresis and left upper quadrant pain. A wade 5/6 holosystolic murmur at the lower left sternal border was noted for the nrst time . The patient was hypotensive for 24 hours and required norepinephrine infusion to maintain blood pressure. A right cardiac catheterization revealed a step-up of oxygen saturation from 40 percent to 80 percent at the right ventricular level. The patient subsequently developed severe congestive heart failure and pulmonary edema, which improved on medical therapy. Because of the clinical impression of an interventricular septal defect, right and left cardiac catheterization was done, which revealed moderately severe elevation of the right atrial, right ventricular, and pulmonary arterial pressures ; decreased card iac index; and a Qp/Qs ratio of 3.9 : 1. There was a severe occlusive lesion of the right coronary artery system at the bifurcation of the posterior descending artery and the artery to the crux (Fig 1) . A left ventriculogram showed a fllling defect posteriorly in the right ante rior oblique position . In the left anterior oblique position, a large ventricular septal defect and an aneurysmal dilatation at the apex were demonstrated (Fig 2). At cardiac surgery, there was an aneurysm of the left ventricular myocardium involving the superior one-third of the posterior wall adjacent to the septum and the atrioventricular groove. A systolic thrill was palpable over the apex . The aneurysm was opened, and a mural thrombus removed. The ventricular septal defect (Fig 3) was high in the septum near the atr ioventricular groove and near the junction of the posterior wall adjacent to the posterior descending coronary artery. The aneurysm was resected, and the defect (2 ern in diameter) was closed with a Dacron patch . The patient has done well since surgery and is back to full activity.
P
osti nfarction interventricular septal defect with ventricular aneurysm has been summarized in the literature by Daicoff and Rhodes.' Loop and associates" recently described posterior ventricular aneurysm in 11 patients, two of whom had associated interventricular septal defects. Most of the cases described in the literature were associated with severe two-vessel disease shown at necropsy." Significant single-vessel disease in this clinical situation documented by coronary cineangiography has not been reported previously. This report describes a case of postinfarction interventricular septal defect associated with a postventricular aneurysm, which had a significant lesion in the po sterior descending coronary artery and only minimal disease in the re st of the coronary system. °From the Division of Cardiovascular Diseases and Cardiovascular and Thoracic Surgery, University of Iowa Hospital s, Iowa City . Supported by HL 05729 from the National Institute of Health. ° ° Fellow. tA ssociate Professor . Reprint requests: Dr. Chandra, Department of Internal Medicine. University of Iowa, Iowa City 52242
CHEST, 68: 6, DECEMBER, 1975
FIGURE 1. Right coronary artery with single lesion distally at bifurcation of posterior descending artery and artery to crux (arrows) .
POSTINFARCTION VENTRICULAR SEPTAL DEFECT 837
REFERENCES
FU;UIIE 2. Left ventriculogram in left anterior oblique position demonstrating ventricular septal defect (arrow) and filling of right ventricle (RV) . S, Intraventricular septum ; LV, left ventricle. DISCUSSION
This appears to be the first case report of a massive inferior wall infarction associated with a ventricular sep tal defect and a posterior ventricular aneurysm, which had only one significant lesion in the coronary system as shown by angiography. Loop and associates- stated that all of their patients had severe atherosclerotic obstruction in the right coronary artery or circumflex artery, or both . Jeresaty et al ' reported a patient with postinfarction interventricular septal defect who survived for two years and died of noncardiac causes. At autopsy, there was a 60 percent occlusive lesion of the posterior descending branch of the right coronary artery and minimal atherosclerotic disease in the left coronary artery. In reviewing the literature, we noted that the survival and surgical results in this situation depend upon many factors . These include younger age (less than 55 years) , high cardiac output (more than 3 L/ min), high pulmonary artery pressure, aneurysmectomy at surgery, 1 adequate residual myocardial function, ' and preservation of blood supply to the posterior papillary muscle." Although our patient was in borderline compensated congestive heart failure for six weeks postinfarction, we believe this patient survived the postinfarction period and surgery because of significant residual myocardial function .
1 Daicoff GR, Rhodes ML; Surgical repair of ventricular septal rupture and ventricular aneurysm. JAMA 203;115, 1968 2 Loop FD , Effler DB, Webster JS, et al . Posterior ventricu lar aneurysms ; Etiologic factors and results of surgical treatment. N Engl J Med 288:237, 1973 3 Dubnow MH, Burchell HB, Titu s JL: Post-infarction ventricular aneurysm : A clinicomorphologlc and electrocardiographic study of 80 cases. Am Heart J 70:753, 1965 4 Jeresaty RM, Landry AB [r, Stirsel HC Jr: Post-infarction interventricular septal defects : Report of two cases with long survival, one with surgical repair . Am Heart J 74 : 543, 1967 5 Grobam AF, Stinson EB, Dalby PO, et al . Ventricular septal defects after myocardial infarction : Early operative treatment. JAMA 225:708, 1973
Bone Resorption of the Ribs and Pulmonary Function in Progressive Systemic Sclerosis* James C . Steigerwald. M.D .;oO Martin H. Seifert, M.B.;t May M. CliO. M .D .;! and Thomas A. NeD, M .D .• F.C.C.P.§
We report a case of progressive systemic sclerosis which showed the unusual feature of bone resorption of the ribs associated with pulmonary function abnormalities. This case, to our knowledge, is the first reported in which this bone resorption of the ribs has occurred. progreSSive systemic sclerosis (PSS) is a multisystem disease which frequently causes pulmonary function and chest roentgenogram abnormalities.' Bone resorption is another common finding in PSS, with the distal phalanges, radius, ulna, clavicle, and jaws most often involved . 2 ' < We have recently observed a young woman with PSS who, during the course of her disease, developed marked bone resorption of the ribs along with pulmonary function abnormalities. CASE REpORT
A 25-year-old black woman was first seen at the University of Colorado Medical Center in May 1966 with the chief complaint of increasing tightness of the skin. She had been entirely well until March of 1965 when she first noted arthralgia and arthritis involving the metacarpal phalangeal, and proximal interphalangeal joints of both hands . The results of evaluation at that time had been normal, except for a °From the Department of Internal Medicine, University of Colorado Medical Center and Denver General Hospital, Denver. 00 Assistant Professor of Medicine, Division of Rheumatic Diseases. tFormer Fellow, Division of Rheumatic Diseases. !Associate Professor of Radiology. §Associate Professor of Medicine, Division of Pulmonary Disease.
RelJrint requests : Dr. Ste igerwald, Denver General Hospital , Denver 80204
838 STEIGERWALD ET AL
CHEST, 68: 6, DECEMBER. 1975