- Email: [email protected]
Central cyanosis following coronary artery bypass graft surgery
101
block develops which is more commonly associated with aortic valve endocarditis this carries a grave prognosis [2-41. The aetiology of the chest pain and heart block in this patient was thought to be due to extension of the infection into the conducting system from the aortic valve [4,5]. Since sudden death and heart failure are the main causes of death among patients with complete heart block complicating infective endocarditis, early pacing is essential in their management [4]. In addition as the QTc was prolonged (Fig. 1) (possibly due to cerebral emboli), ventricular tachyarrhythmias were likely to be suppressed by ventricular pacing.
References 1 Stewart JA, Silimperi D, Harris P, Wise NK, Fraker TD Jr, Kisslo JA. Echocardiographic documentation of vegetative lesions in infective endocarditis: Clinical implications. Circulation 1980;61:374-380. 2 Roberts NK, Somerville J. Pathological significance of electrocardiographic changes in aortic valve endocarditis. Br Heart J 1969;31:395-396. 3 Oakley CM. Infective endocarditis. Br J Hosp Med 1980;24:232-243. 4 Wang K, Gobel F, Gleason DF, Edwards JE. Complete heart block complicating bacterial endocarditis. Circulation 1972;46:939-947. 5 Mildvan D, Goldberg E, Berger M, Altchek MR, Lukban SB. Diagnosis and successful management of septal myocardial abscess: a complication of bacterial endocarditis. Am J Med Sci 1977;274:311-316.
IJC 0089F
Central cyanosis following coronary artery bypass graft surgery David Lipkin, Robert Morris and Kim Fox National Heart Hospital, Westmoreland Street, London, WIM 8BA, U.K.
(Received 29 July 1983; accepted 2 August 1983)
A case of central cyanosis occurring after coronary artery bypass graft surgery is described. This was due to the development of a right ventricular infarction which facilitated shunting from right to left through a previously undiagnosed patent foramen ovale or small atrial septal defect. Central cyanosis usually occurs as a consequence of congenital heart disease or pulmonary disease. When it occurs acutely, severe rapidly progressive lung disease (e.g. pneumonia) or
Correspondence to: Dr. Kim Fox, National U.K.
Heart Hospital,
International Journal of Cardiology, 5 (1984) 101-103 0 Elsevier Science Publishers B.V.
Westmoreland
Street, London,
WlM
8BA,
102
arteribvenous shunting (e.g. pulmonary embolism) are usually the causes. Intracardiac shunting though well known to cause long-standing central cyanosis is not usually considered a common cause of cyanosis that occurs acutely. We report a patient who developed a right-to-left intracardiac shunt following coronary artery bypass graft surgery. Case Report A 60-year-old man underwent coronary artery bypass graft surgery following the failure of medical therapy to control his angina. He had not had a previous myocardial infarction and his chest X-ray was normal. Grafts were made to the left anterior descending and right coronary artery, and although his post-operative recovery was uncomplicated it was noted that his electrocardiogram had altered, showing evidence of true posterior infarction. He was admitted 1 month after discharge with shortness of breath and noted for the first time to be centrally cyanosed (PO, 60 mm Hg, 89% saturated). Chest X-ray was normal and there was no evidence of pulmonary embolism on ventilation perfusion scanning. It was noted, however, on cross-sectional echocardiography that there were increased ethos from the free wall of the right ventricle, compatible with myocardial fibrosis; there was also reduced motion of the inferior wall. Injection of 10 ml of normal saline into the antecubital vein produced bubbles that were seen on cross-sectional echocardiography to pass from the right atrium to the left atrium across either a small defect in the atria1 septum or a patent foramen ovale. Gated blood pool studies showed normal left ventricular function (ejection fraction SOS), but there was reduced right ventricular function (ejection fraction 35%). Cardiac catheterization confirmed these findings and revealed a right-to-left shunt of 1.6 : 1 and in addition showed that although the left anterior descending graft was widely patent, the graft to the right coronary artery was blocked with complete obstruction of the native vessel. Comment This patient developed a right-to-left shunt either through a patent foramen ovale or through a small previously undetected atria1 septal defect. It is likely that the shunt developed because the right ventricle became “stiff” or relatively noncompliant as compared to the left ventricle following coronary artery bypass graft surgery; probably as a consequence of a right ventricular infarction that occurred at the time of surgery. A patent foramen ovale is a common finding in the normal population, occurring in approximately 25% [l] of individuals at post mortem. Right ventricular infarction is not common, but is becoming increasingly recognised [2,3] and although it may be a difficult diagnosis to make clinically, should be considered in patients with an inferior or true posterior infarction who have evidence of right heart failure in the absence of left heart failure. Our case would suggest that the recent development of cyanosis in patients with right ventricular infarction, particularly in the absence of evidence of pulmonary embolism, should alert one to the possibility of intracardiac shunting at atria1 level. In a single previous case report, hypoxia was described in a patient with myocardial infarction who had a patent foramen ovale, but who did not have right ventricular failure [4]. Treatment is difficult and it may be necessary to consider closure of the defect if the cyanosis and the symptoms are severe.
103
References 1 Pomerance A, Davies M. Pathology of the heart. London: Blackwell, 1975. 2 Croft CH, Nicod P, Corbett JR, et al. Detection of acute right ventricular infarction by right precordial leads. Am J Cardiol 1982;50:421-427. 3 Sharpe DN, Botvinick EH, Shames DM, et al. The non-invasive diagnosis of right ventricular infarction. Circulation 1978;57:483-490. 4 Morris AL, Donen N. Hypoxia and intracardiac right to left shunt: complicating infarction with right ventricular extension. Arch Intern Med 1978;139:1405-1406.
inferior myocardial
IJC 0089G
Premature closure of the foramen ovale and hypoplasia of the left heart Stewart A. Schall ’ and Frederic G. Dalldorf 2 Departments
of
’ Pediatrics and ’ Pathology, University of North Carolina School of Medicine, Chapel Hill, North Carolina (Received and accepted 8 August 1983)
Although premature closure of the foramen ovale has been proposed as a possible cause of hypoplastic left heart syndrome, very few such cases have been described. We have seen two examples of the combination and no associated malformations. In both the foramen was firmly closed on its left atrial aspect and the dimensions of the left sided structures were well below normal values. Premature closure of the foramen ovale has been proposed as one possible cause of hypoplasia of the left heart [l]. As logical as this concept appears, very few cases of pure premature closure associated with left hypoplasia have been reported. In the majority of cases there are other severe malformations of the left heart such as endocardial fibroelastosis, mitral stenosis or aortic atresia that could in themselves result in hypoplasia [2,3]. We recently had an opportunity to examine the hearts from two infants who had premature closure of the foramen ovale and associated hypoplastic but otherwise normal left hearts. Case Reports Case 1 was a full-term baby boy who weighed 3402 g at birth. The pregnancy was normal but delivery failed to progress and a Cesarean section was performed. Meconium aspiration
Correspondence to: Dr. Steward A. SchaB, Department School of Medicine, Chapel Hill, NC 27514, U.S.A.
International Journal of Cardiology, 5 (1984) 103-107 0 Elsevier Science Publishers B.V.
of Pediatrics,
University
of North Carolina
block develops which is more commonly associated with aortic valve endocarditis this carries a grave prognosis [2-41. The aetiology of the chest pain and heart block in this patient was thought to be due to extension of the infection into the conducting system from the aortic valve [4,5]. Since sudden death and heart failure are the main causes of death among patients with complete heart block complicating infective endocarditis, early pacing is essential in their management [4]. In addition as the QTc was prolonged (Fig. 1) (possibly due to cerebral emboli), ventricular tachyarrhythmias were likely to be suppressed by ventricular pacing.
References 1 Stewart JA, Silimperi D, Harris P, Wise NK, Fraker TD Jr, Kisslo JA. Echocardiographic documentation of vegetative lesions in infective endocarditis: Clinical implications. Circulation 1980;61:374-380. 2 Roberts NK, Somerville J. Pathological significance of electrocardiographic changes in aortic valve endocarditis. Br Heart J 1969;31:395-396. 3 Oakley CM. Infective endocarditis. Br J Hosp Med 1980;24:232-243. 4 Wang K, Gobel F, Gleason DF, Edwards JE. Complete heart block complicating bacterial endocarditis. Circulation 1972;46:939-947. 5 Mildvan D, Goldberg E, Berger M, Altchek MR, Lukban SB. Diagnosis and successful management of septal myocardial abscess: a complication of bacterial endocarditis. Am J Med Sci 1977;274:311-316.
IJC 0089F
Central cyanosis following coronary artery bypass graft surgery David Lipkin, Robert Morris and Kim Fox National Heart Hospital, Westmoreland Street, London, WIM 8BA, U.K.
(Received 29 July 1983; accepted 2 August 1983)
A case of central cyanosis occurring after coronary artery bypass graft surgery is described. This was due to the development of a right ventricular infarction which facilitated shunting from right to left through a previously undiagnosed patent foramen ovale or small atrial septal defect. Central cyanosis usually occurs as a consequence of congenital heart disease or pulmonary disease. When it occurs acutely, severe rapidly progressive lung disease (e.g. pneumonia) or
Correspondence to: Dr. Kim Fox, National U.K.
Heart Hospital,
International Journal of Cardiology, 5 (1984) 101-103 0 Elsevier Science Publishers B.V.
Westmoreland
Street, London,
WlM
8BA,
102
arteribvenous shunting (e.g. pulmonary embolism) are usually the causes. Intracardiac shunting though well known to cause long-standing central cyanosis is not usually considered a common cause of cyanosis that occurs acutely. We report a patient who developed a right-to-left intracardiac shunt following coronary artery bypass graft surgery. Case Report A 60-year-old man underwent coronary artery bypass graft surgery following the failure of medical therapy to control his angina. He had not had a previous myocardial infarction and his chest X-ray was normal. Grafts were made to the left anterior descending and right coronary artery, and although his post-operative recovery was uncomplicated it was noted that his electrocardiogram had altered, showing evidence of true posterior infarction. He was admitted 1 month after discharge with shortness of breath and noted for the first time to be centrally cyanosed (PO, 60 mm Hg, 89% saturated). Chest X-ray was normal and there was no evidence of pulmonary embolism on ventilation perfusion scanning. It was noted, however, on cross-sectional echocardiography that there were increased ethos from the free wall of the right ventricle, compatible with myocardial fibrosis; there was also reduced motion of the inferior wall. Injection of 10 ml of normal saline into the antecubital vein produced bubbles that were seen on cross-sectional echocardiography to pass from the right atrium to the left atrium across either a small defect in the atria1 septum or a patent foramen ovale. Gated blood pool studies showed normal left ventricular function (ejection fraction SOS), but there was reduced right ventricular function (ejection fraction 35%). Cardiac catheterization confirmed these findings and revealed a right-to-left shunt of 1.6 : 1 and in addition showed that although the left anterior descending graft was widely patent, the graft to the right coronary artery was blocked with complete obstruction of the native vessel. Comment This patient developed a right-to-left shunt either through a patent foramen ovale or through a small previously undetected atria1 septal defect. It is likely that the shunt developed because the right ventricle became “stiff” or relatively noncompliant as compared to the left ventricle following coronary artery bypass graft surgery; probably as a consequence of a right ventricular infarction that occurred at the time of surgery. A patent foramen ovale is a common finding in the normal population, occurring in approximately 25% [l] of individuals at post mortem. Right ventricular infarction is not common, but is becoming increasingly recognised [2,3] and although it may be a difficult diagnosis to make clinically, should be considered in patients with an inferior or true posterior infarction who have evidence of right heart failure in the absence of left heart failure. Our case would suggest that the recent development of cyanosis in patients with right ventricular infarction, particularly in the absence of evidence of pulmonary embolism, should alert one to the possibility of intracardiac shunting at atria1 level. In a single previous case report, hypoxia was described in a patient with myocardial infarction who had a patent foramen ovale, but who did not have right ventricular failure [4]. Treatment is difficult and it may be necessary to consider closure of the defect if the cyanosis and the symptoms are severe.
103
References 1 Pomerance A, Davies M. Pathology of the heart. London: Blackwell, 1975. 2 Croft CH, Nicod P, Corbett JR, et al. Detection of acute right ventricular infarction by right precordial leads. Am J Cardiol 1982;50:421-427. 3 Sharpe DN, Botvinick EH, Shames DM, et al. The non-invasive diagnosis of right ventricular infarction. Circulation 1978;57:483-490. 4 Morris AL, Donen N. Hypoxia and intracardiac right to left shunt: complicating infarction with right ventricular extension. Arch Intern Med 1978;139:1405-1406.
inferior myocardial
IJC 0089G
Premature closure of the foramen ovale and hypoplasia of the left heart Stewart A. Schall ’ and Frederic G. Dalldorf 2 Departments
of
’ Pediatrics and ’ Pathology, University of North Carolina School of Medicine, Chapel Hill, North Carolina (Received and accepted 8 August 1983)
Although premature closure of the foramen ovale has been proposed as a possible cause of hypoplastic left heart syndrome, very few such cases have been described. We have seen two examples of the combination and no associated malformations. In both the foramen was firmly closed on its left atrial aspect and the dimensions of the left sided structures were well below normal values. Premature closure of the foramen ovale has been proposed as one possible cause of hypoplasia of the left heart [l]. As logical as this concept appears, very few cases of pure premature closure associated with left hypoplasia have been reported. In the majority of cases there are other severe malformations of the left heart such as endocardial fibroelastosis, mitral stenosis or aortic atresia that could in themselves result in hypoplasia [2,3]. We recently had an opportunity to examine the hearts from two infants who had premature closure of the foramen ovale and associated hypoplastic but otherwise normal left hearts. Case Reports Case 1 was a full-term baby boy who weighed 3402 g at birth. The pregnancy was normal but delivery failed to progress and a Cesarean section was performed. Meconium aspiration
Correspondence to: Dr. Steward A. SchaB, Department School of Medicine, Chapel Hill, NC 27514, U.S.A.
International Journal of Cardiology, 5 (1984) 103-107 0 Elsevier Science Publishers B.V.
of Pediatrics,
University
of North Carolina