- Email: [email protected]
Unusual presentation of a patient with arrhythmogenic right ventricular dysplasia treated with a Glenn shunt
International Journal of Cardiology 113 (2006) 410 – 413 www.elsevier.com/locate/ijcard
Letter to the Editor
Unusual presentation of a patient with arrhythmogenic right ventricular dysplasia treated with a Glenn shunt Sevket Gorgulu a,*, Zekeriya Nurkalem a, Ahmet Celebi b, Mehmet Salih Bilal c, Yalim Yalcin b, Nihat Cine c, Mehmet Eren a a Cardiology Department, Siyami Ersek Thoracic and Cardiovascular Surgery Center, Istanbul, Turkey Pediatric Cardiology Department, Siyami Ersek Thoracic and Cardiovascular Surgery Center, Istanbul, Turkey Cardiovascular Surgery Department, Siyami Ersek Thoracic and Cardiovascular Surgery Center, Istanbul, Turkey
b c
Received 15 September 2005; accepted 20 September 2005 Available online 5 December 2005
Abstract Clinically, arrhythmogenic right ventricular dysplasia (ARVD) usually presents with ventricular arrhythmias, and unusual presentations were reported as acute coronary syndrome, heart failure and electrical storm. Taking all this different presentations and treatments in to account, we report a case of ARVD presenting with central cyanosis and clubbing simulating congenital heart disease. Besides this unusual presentation, the patient underwent also an unusual operation for this kind of abnormality, which cured the cyanosis completely. D 2005 Elsevier Ireland Ltd. All rights reserved. Keywords: Arrhythmogenic right ventricular dysplasia; Cyanosis; Glenn shunt
Arrhythmogenic right ventricular dysplasia (ARVD) is characterized by progressive fibrofatty replacement of the right ventricular myocardium [1]. Clinically, ARVD usually presents with ventricular arrhythmias [2], and this is also the underlying disease in a substantial number of sudden deaths among apparently healthy individuals [3]. There are also unusual presentations such as acute coronary syndrome, heart failure and electrical storm [4– 6]. With regard to the treatment of ARVD, there are no precise guidelines to determine who are the patients who need to be treated and which is the best management approach. Usually, therapy is directed to prevent and/or treat malignant ventricular tachyarrhythmias with medications, implantable cardioverter defibrillator and radiofrequency ablation in selected cases [7]. In patients in whom ARVD has progressed to severe right ventricular or biventricular * Corresponding author. Kayisdagi cad. Icerenkoy Kiptas KonutlarN A1 Blok D:10, Icerenkoy-Istanbul, Turkey. Tel.: +90 216 5746527, +90 216 3499120 (4089-4186); fax: +90 2165504433. E-mail address: [email protected] (S. Gorgulu). 0167-5273/$ - see front matter D 2005 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2005.09.048
systolic dysfunction, treatment consists of current therapy for heart failure [8]. In case of refractory heart failure, the patients may become candidates for heart transplantation [8]. Taking all this different presentations and treatments in to account, we report a case of ARVD presenting with central cyanosis and clubbing simulating congenital heart disease. Besides the unusual presentation, the patient underwent also an unusual operation for this kind of abnormality, which cured the cyanosis completely. A 16-year-old female with a history of cyanosis for 8 years was referred to our hospital for further evaluation. The patient has been living in the rural area and did not seek any medical attention until she applied for the first time to see a general practitioner due to gastric pain. After referred to several hospitals due to cyanosis, the patient finally sent to our hospital from a chest disease hospital, where she was investigated for pulmonary arterio-venous fistula and was found clear after a thorax magnetic resonance (MR) angiogram. Her main complaint was exercise dyspne, palpitation and fatigue since the day cyanosis had begun.
S. Gorgulu et al. / International Journal of Cardiology 113 (2006) 410 – 413
She had a family history of a 30-year-old uncle who died suddenly with unknown cause. The physical examination revealed central cyanosis, clubbing of digits, a raised jugular venous pressure and haepatomegaly. The presenting ECG showed T wave inversion in the precordial leads exploring the right ventricle (V1 – V3). Right precordial QRS prolongation and epsilon waves were evident. The chest X-ray showed considerable right heart prominence. Pulmonary arteries were normal and lung fields were clear. Haemoglobin was 17.3 g/dl. Blood gases were pH 7.49, PCO2 27 mm Hg, PO2 53 mm Hg and O2 saturation was 87%. Lung function tests (spirometry, lung volumes, flow volume loops and transfer factor) were all normal. The transthoracic echocardiogram (TTE) showed a severely dilated right ventricle (RV). The right atrium (RA) was also dilated. The aneurysmal dilations of the diaphragmatic, apical and infundibular regions (so called ‘‘triangle of dysplasia’’) were conspicuous suggesting ARVD (Fig. 1a,b). RV ejection fraction (EF) was estimated as 10%. Although the tricuspid valve structure was normal, severe tricuspid regurgitation due to annular dilation existed.
Fig. 1. (a) Arrows showing aneurysmal dilation of the right ventricular (RV) apex and RV inflow tract. RA: right atrium. (b) The aneurysmal dilation of the right ventricular outflow tract (RVOT) is the third component of the ‘‘Marcus triangle’’. PA: pulmonary artery.
411
Fig. 2. Transesophageal echocardiography demonstrating a right to left shunt through a patent foramen ovale (PFO). LA: left atrium, RA: right atrium, RV: right ventricle.
Fig. 3. (a) Cardiac magnetic resonance imaging (MRI) is showing fatty infiltration at the apex (black arrow). ra: right atrium, la: left atrium, rv: right ventricle, lv: left ventricle. (b) MRI obtained at the 15 min after contrast injection indicating fibrosis at the right ventricular lateral wall, apex and the right ventricular side of the septum (arrow). ra: right atrium, la: left atrium, rv: right ventricle, lv: left ventricle.
412
S. Gorgulu et al. / International Journal of Cardiology 113 (2006) 410 – 413
Table 1 Shows data obtained at catheterization
Superior vena cava Inferior vena cava Right atrium Left pulmonary vein Right pulmonary vein Left pulmonary artery Right pulmonary artery Main pulmonary artery Pulmonary capillary wedge Left atrium Aorta
Pressure (mm Hg)
O2 saturation (%)
– – Mean 9 – – 22/10 (mean 12) 23/5 (mean 10) Mean 10 Mean 8 Mean 7 112/74 (mean 96)
60 74 71 99 99 68 – 67 – – 87
The estimated pulmonary artery pressure was 12 (RV systolic pressure) + 20 (estimated RA pressure) = 32 mm Hg. Left ventricular EF and valves were normal. Congenital heart disease such as Ebstein anomaly, atrial septal defect and partial anomalous venous return were especially excluded by TTE. Color Doppler echocardiography showed an inconspicuous right to left shunt through the interatrial septum indicating a possible cause for the present cyanosis. Immediately after TTE, transesophageal echocardiography (TEE) was performed in order to investigate the presence of a patent foramen ovale. Indeed, TEE showed a 0.6-cm separation of septum primum and secundum with an evident right to left shunt (Fig. 2). In order to verify ARVD cardiac MR was also done. Magnetic resonance imaging showed all typical features of an ARVD such as prominent dilation of RA and RV, RV dyskinesis and apical trabeculation, distinctive fatty infiltration at the RV apex and fibrosis at the RV lateral wall and the right side of the interventricular septum (Fig. 3a,b). Holter monitoring showed isolated 18 monomorphic ventricular extrasystoles. Symptom limited exercise test showed an exercise duration of 7.48 min without any ventricular arrhythmias. After the diagnosis of ARVD, the patient was consulted with pediatric cardiologists and cardiovascular surgeons. We agreed that a Glenn shunt along with a Devega would be the most appropriate treatment for this patient. Cardiac catheterization was performed to understand whether the patient would be a good candidate for a Glenn shunt. The data obtained from catheterization are summarized in Table 1. Right ventricular cineangiography showed an aneurysmatic infundibulum with a poorly contracting RV. As the mean pulmonary artery pressure (10 mm Hg) and pulmonary vascular resistance (1 unit) were appropriate, the patient was operated on for a Glenn shunt and a Devega procedure regarding the tricuspid valve was done as well. After the operation, the cyanosis disappeared completely. On the end of the 1 week, the O2 saturation increased from 87% to 97% and the PO2 increased from 53 mm Hg to 85 mm Hg. Finally, the patient was discharged from the hospital with the prescription of 100 mg aspirin and 25 mg beta-blocker.
Although under resting conditions, the pressure gradient between the two atria is predominantly from left to right, temporary reversals during Valsalva maneuver were demonstrated [9]. Right to left shunting of venous blood through a patent foramen ovale might be the cause of systemic hypoxemia in several pathologic states. Examples of such conditions include severe pulmonary hypertension with right atrial hypertension and tricuspid stenosis [10], right ventricular infarction [11], cardiac tamponade [12] and chronic obstructive pulmonary disease [13]. Clinically, ARVD usually presents with ventricular arrhythmias [2], and unusual presentations were reported as acute coronary syndrome, heart failure and electrical storm [4 –6]. Another unusual presentation is central cyanosis resembling congenital heart disease. Besides our case, this kind of abnormality was also reported by Cubero et al. [14]. Different from our case, the patient had high pulmonary artery pressure and underwent cardiac transplantation due to refractory right heart failure and died 1 week after the operation. Our patient underwent a successful Glenn shunt and discharged from the hospital with complete improvement of the cyanosis. It is well known that right atrial pressure may increase secondary to RV diastolic or systolic dysfunction. This may produce a reversal of the left to right atrium gradient and, consequently, it opens the flap of the foramen ovale causing severe hypoxemia. As in our patient, ARVD could also lead to right ventricular systolic dysfunction and elevated right chamber pressures, causing opening of the flap. Therefore, ARVD should be kept in mind in the differential diagnosis of patients who present with cyanosis and right ventricular dysfunction having normal pulmonary artery pressure without obvious congenital cardiac malformation. Briefly, we consider this case report important by indicating that ARVD may cause severe hypoxemia resembling cyanotic congenital heart disease and by demonstrating that it is treatable by a Glenn shunt.
References [1] Richardson P, McKenna W, Bristow M, et al. Report of the 1995 World Health Organisation/International Society and Federation of Cardiology Task Force on the Definition and Classification of Cardiomyopathies. Circulation 1996;93:841 – 2. [2] Pinamonti B, Di Lenarda A, Sinagra G, Silvestri F, Bussani R, Camerini F. Long-term evolution of right ventricular dysplasiacardiomyopathy. Am Heart J 1995;129:412 – 5. [3] Furlanello F, Bertoldi A, Dallago M, et al. Cardiac arrest and sudden death in competitive athletes with arrhythmogenic right ventricular dysplasia. Pacing Clin Electrophysiol 1998;21:331 – 5. [4] Khalil SI, Kamal A, Ahmad S. Arrhythmogenic right ventricular dysplasia presenting as acute coronary syndrome: a case report. Eur J Echocardiogr 2004;5:394 – 8. [5] Indik JH, Smith DE, Sobonya RE, Marcus FI. Arrhythmogenic right ventricular cardiomyopathy/dysplasia: a case report of identical twins with heart failure. Pacing Clin Electrophysiol 2002;25: 1387 – 90.
S. Gorgulu et al. / International Journal of Cardiology 113 (2006) 410 – 413 [6] Barriales V, Tamargo JA, Aguado MG, Martin M, Rondan J, Posada IS. Electrical storm as initial presentation of arrhythmogenic right ventricular cardiomyopathy in an elderly woman. Int J Cardiol 2004; 94:331 – 3. [7] Frances RJ. Arrhythmogenic right ventricular dysplasia/cardiomyopathy. Int J Cardiol [in press. Electronic Publication, http : //www.ncbi.nlm.nih.gov / entrez /query.fcgi?db = pubmed & cmd = Search&term=%22Frances+RJ%22%5BAuthor%5D]. [8] Corrado D, Basso C, Thiene G. Arrhythmogenic right ventricular cardiomyopathy: diagnosis, prognosis, and treatment. Heart 2000;83: 588 – 95. [9] Gorgulu S, Eksik A, Eren M, et al. Assessment of the effects of various maneuvers on both atrial pressure changes. Int J Cardiol 2003; 92:241 – 5. [10] Gill EA. Definitions and pathophysiology of patent foramen ovale: broad overview. Cardiol Clin 2005;23:1 – 6.
413
[11] Bansal RC, Marsa RJ, Holland D, Beehler C, Gold PM. Severe hypoxemia due to shunting through a patent foramen ovale: a correctable complication of right ventricular infarction. J Am Coll Cardiol 1985;5:188 – 92. [12] Thompson RC, Finck SJ, Leventhal JP, Safford RE. Right-to-left shunt across a patent foramen ovale caused by cardiac tamponade: diagnosis by transesophageal echocardiography. Mayo Clin Proc 1991;66:391 – 4. [13] Begin R, Gervais L, Bureau MA. Patent foramen ovale and hypoxemia in chronic obstructive pulmonary disease. Eur J Respir Dis 1981;62:373 – 5. [14] Cubero JM, Gallego P, Pavon M. Arrhythmogenic right ventricular cardiomyopathy and atrial right-to-left shunt. Acta Cardiol 2002; 57:443 – 5.
Letter to the Editor
Unusual presentation of a patient with arrhythmogenic right ventricular dysplasia treated with a Glenn shunt Sevket Gorgulu a,*, Zekeriya Nurkalem a, Ahmet Celebi b, Mehmet Salih Bilal c, Yalim Yalcin b, Nihat Cine c, Mehmet Eren a a Cardiology Department, Siyami Ersek Thoracic and Cardiovascular Surgery Center, Istanbul, Turkey Pediatric Cardiology Department, Siyami Ersek Thoracic and Cardiovascular Surgery Center, Istanbul, Turkey Cardiovascular Surgery Department, Siyami Ersek Thoracic and Cardiovascular Surgery Center, Istanbul, Turkey
b c
Received 15 September 2005; accepted 20 September 2005 Available online 5 December 2005
Abstract Clinically, arrhythmogenic right ventricular dysplasia (ARVD) usually presents with ventricular arrhythmias, and unusual presentations were reported as acute coronary syndrome, heart failure and electrical storm. Taking all this different presentations and treatments in to account, we report a case of ARVD presenting with central cyanosis and clubbing simulating congenital heart disease. Besides this unusual presentation, the patient underwent also an unusual operation for this kind of abnormality, which cured the cyanosis completely. D 2005 Elsevier Ireland Ltd. All rights reserved. Keywords: Arrhythmogenic right ventricular dysplasia; Cyanosis; Glenn shunt
Arrhythmogenic right ventricular dysplasia (ARVD) is characterized by progressive fibrofatty replacement of the right ventricular myocardium [1]. Clinically, ARVD usually presents with ventricular arrhythmias [2], and this is also the underlying disease in a substantial number of sudden deaths among apparently healthy individuals [3]. There are also unusual presentations such as acute coronary syndrome, heart failure and electrical storm [4– 6]. With regard to the treatment of ARVD, there are no precise guidelines to determine who are the patients who need to be treated and which is the best management approach. Usually, therapy is directed to prevent and/or treat malignant ventricular tachyarrhythmias with medications, implantable cardioverter defibrillator and radiofrequency ablation in selected cases [7]. In patients in whom ARVD has progressed to severe right ventricular or biventricular * Corresponding author. Kayisdagi cad. Icerenkoy Kiptas KonutlarN A1 Blok D:10, Icerenkoy-Istanbul, Turkey. Tel.: +90 216 5746527, +90 216 3499120 (4089-4186); fax: +90 2165504433. E-mail address: [email protected] (S. Gorgulu). 0167-5273/$ - see front matter D 2005 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2005.09.048
systolic dysfunction, treatment consists of current therapy for heart failure [8]. In case of refractory heart failure, the patients may become candidates for heart transplantation [8]. Taking all this different presentations and treatments in to account, we report a case of ARVD presenting with central cyanosis and clubbing simulating congenital heart disease. Besides the unusual presentation, the patient underwent also an unusual operation for this kind of abnormality, which cured the cyanosis completely. A 16-year-old female with a history of cyanosis for 8 years was referred to our hospital for further evaluation. The patient has been living in the rural area and did not seek any medical attention until she applied for the first time to see a general practitioner due to gastric pain. After referred to several hospitals due to cyanosis, the patient finally sent to our hospital from a chest disease hospital, where she was investigated for pulmonary arterio-venous fistula and was found clear after a thorax magnetic resonance (MR) angiogram. Her main complaint was exercise dyspne, palpitation and fatigue since the day cyanosis had begun.
S. Gorgulu et al. / International Journal of Cardiology 113 (2006) 410 – 413
She had a family history of a 30-year-old uncle who died suddenly with unknown cause. The physical examination revealed central cyanosis, clubbing of digits, a raised jugular venous pressure and haepatomegaly. The presenting ECG showed T wave inversion in the precordial leads exploring the right ventricle (V1 – V3). Right precordial QRS prolongation and epsilon waves were evident. The chest X-ray showed considerable right heart prominence. Pulmonary arteries were normal and lung fields were clear. Haemoglobin was 17.3 g/dl. Blood gases were pH 7.49, PCO2 27 mm Hg, PO2 53 mm Hg and O2 saturation was 87%. Lung function tests (spirometry, lung volumes, flow volume loops and transfer factor) were all normal. The transthoracic echocardiogram (TTE) showed a severely dilated right ventricle (RV). The right atrium (RA) was also dilated. The aneurysmal dilations of the diaphragmatic, apical and infundibular regions (so called ‘‘triangle of dysplasia’’) were conspicuous suggesting ARVD (Fig. 1a,b). RV ejection fraction (EF) was estimated as 10%. Although the tricuspid valve structure was normal, severe tricuspid regurgitation due to annular dilation existed.
Fig. 1. (a) Arrows showing aneurysmal dilation of the right ventricular (RV) apex and RV inflow tract. RA: right atrium. (b) The aneurysmal dilation of the right ventricular outflow tract (RVOT) is the third component of the ‘‘Marcus triangle’’. PA: pulmonary artery.
411
Fig. 2. Transesophageal echocardiography demonstrating a right to left shunt through a patent foramen ovale (PFO). LA: left atrium, RA: right atrium, RV: right ventricle.
Fig. 3. (a) Cardiac magnetic resonance imaging (MRI) is showing fatty infiltration at the apex (black arrow). ra: right atrium, la: left atrium, rv: right ventricle, lv: left ventricle. (b) MRI obtained at the 15 min after contrast injection indicating fibrosis at the right ventricular lateral wall, apex and the right ventricular side of the septum (arrow). ra: right atrium, la: left atrium, rv: right ventricle, lv: left ventricle.
412
S. Gorgulu et al. / International Journal of Cardiology 113 (2006) 410 – 413
Table 1 Shows data obtained at catheterization
Superior vena cava Inferior vena cava Right atrium Left pulmonary vein Right pulmonary vein Left pulmonary artery Right pulmonary artery Main pulmonary artery Pulmonary capillary wedge Left atrium Aorta
Pressure (mm Hg)
O2 saturation (%)
– – Mean 9 – – 22/10 (mean 12) 23/5 (mean 10) Mean 10 Mean 8 Mean 7 112/74 (mean 96)
60 74 71 99 99 68 – 67 – – 87
The estimated pulmonary artery pressure was 12 (RV systolic pressure) + 20 (estimated RA pressure) = 32 mm Hg. Left ventricular EF and valves were normal. Congenital heart disease such as Ebstein anomaly, atrial septal defect and partial anomalous venous return were especially excluded by TTE. Color Doppler echocardiography showed an inconspicuous right to left shunt through the interatrial septum indicating a possible cause for the present cyanosis. Immediately after TTE, transesophageal echocardiography (TEE) was performed in order to investigate the presence of a patent foramen ovale. Indeed, TEE showed a 0.6-cm separation of septum primum and secundum with an evident right to left shunt (Fig. 2). In order to verify ARVD cardiac MR was also done. Magnetic resonance imaging showed all typical features of an ARVD such as prominent dilation of RA and RV, RV dyskinesis and apical trabeculation, distinctive fatty infiltration at the RV apex and fibrosis at the RV lateral wall and the right side of the interventricular septum (Fig. 3a,b). Holter monitoring showed isolated 18 monomorphic ventricular extrasystoles. Symptom limited exercise test showed an exercise duration of 7.48 min without any ventricular arrhythmias. After the diagnosis of ARVD, the patient was consulted with pediatric cardiologists and cardiovascular surgeons. We agreed that a Glenn shunt along with a Devega would be the most appropriate treatment for this patient. Cardiac catheterization was performed to understand whether the patient would be a good candidate for a Glenn shunt. The data obtained from catheterization are summarized in Table 1. Right ventricular cineangiography showed an aneurysmatic infundibulum with a poorly contracting RV. As the mean pulmonary artery pressure (10 mm Hg) and pulmonary vascular resistance (1 unit) were appropriate, the patient was operated on for a Glenn shunt and a Devega procedure regarding the tricuspid valve was done as well. After the operation, the cyanosis disappeared completely. On the end of the 1 week, the O2 saturation increased from 87% to 97% and the PO2 increased from 53 mm Hg to 85 mm Hg. Finally, the patient was discharged from the hospital with the prescription of 100 mg aspirin and 25 mg beta-blocker.
Although under resting conditions, the pressure gradient between the two atria is predominantly from left to right, temporary reversals during Valsalva maneuver were demonstrated [9]. Right to left shunting of venous blood through a patent foramen ovale might be the cause of systemic hypoxemia in several pathologic states. Examples of such conditions include severe pulmonary hypertension with right atrial hypertension and tricuspid stenosis [10], right ventricular infarction [11], cardiac tamponade [12] and chronic obstructive pulmonary disease [13]. Clinically, ARVD usually presents with ventricular arrhythmias [2], and unusual presentations were reported as acute coronary syndrome, heart failure and electrical storm [4 –6]. Another unusual presentation is central cyanosis resembling congenital heart disease. Besides our case, this kind of abnormality was also reported by Cubero et al. [14]. Different from our case, the patient had high pulmonary artery pressure and underwent cardiac transplantation due to refractory right heart failure and died 1 week after the operation. Our patient underwent a successful Glenn shunt and discharged from the hospital with complete improvement of the cyanosis. It is well known that right atrial pressure may increase secondary to RV diastolic or systolic dysfunction. This may produce a reversal of the left to right atrium gradient and, consequently, it opens the flap of the foramen ovale causing severe hypoxemia. As in our patient, ARVD could also lead to right ventricular systolic dysfunction and elevated right chamber pressures, causing opening of the flap. Therefore, ARVD should be kept in mind in the differential diagnosis of patients who present with cyanosis and right ventricular dysfunction having normal pulmonary artery pressure without obvious congenital cardiac malformation. Briefly, we consider this case report important by indicating that ARVD may cause severe hypoxemia resembling cyanotic congenital heart disease and by demonstrating that it is treatable by a Glenn shunt.
References [1] Richardson P, McKenna W, Bristow M, et al. Report of the 1995 World Health Organisation/International Society and Federation of Cardiology Task Force on the Definition and Classification of Cardiomyopathies. Circulation 1996;93:841 – 2. [2] Pinamonti B, Di Lenarda A, Sinagra G, Silvestri F, Bussani R, Camerini F. Long-term evolution of right ventricular dysplasiacardiomyopathy. Am Heart J 1995;129:412 – 5. [3] Furlanello F, Bertoldi A, Dallago M, et al. Cardiac arrest and sudden death in competitive athletes with arrhythmogenic right ventricular dysplasia. Pacing Clin Electrophysiol 1998;21:331 – 5. [4] Khalil SI, Kamal A, Ahmad S. Arrhythmogenic right ventricular dysplasia presenting as acute coronary syndrome: a case report. Eur J Echocardiogr 2004;5:394 – 8. [5] Indik JH, Smith DE, Sobonya RE, Marcus FI. Arrhythmogenic right ventricular cardiomyopathy/dysplasia: a case report of identical twins with heart failure. Pacing Clin Electrophysiol 2002;25: 1387 – 90.
S. Gorgulu et al. / International Journal of Cardiology 113 (2006) 410 – 413 [6] Barriales V, Tamargo JA, Aguado MG, Martin M, Rondan J, Posada IS. Electrical storm as initial presentation of arrhythmogenic right ventricular cardiomyopathy in an elderly woman. Int J Cardiol 2004; 94:331 – 3. [7] Frances RJ. Arrhythmogenic right ventricular dysplasia/cardiomyopathy. Int J Cardiol [in press. Electronic Publication, http : //www.ncbi.nlm.nih.gov / entrez /query.fcgi?db = pubmed & cmd = Search&term=%22Frances+RJ%22%5BAuthor%5D]. [8] Corrado D, Basso C, Thiene G. Arrhythmogenic right ventricular cardiomyopathy: diagnosis, prognosis, and treatment. Heart 2000;83: 588 – 95. [9] Gorgulu S, Eksik A, Eren M, et al. Assessment of the effects of various maneuvers on both atrial pressure changes. Int J Cardiol 2003; 92:241 – 5. [10] Gill EA. Definitions and pathophysiology of patent foramen ovale: broad overview. Cardiol Clin 2005;23:1 – 6.
413
[11] Bansal RC, Marsa RJ, Holland D, Beehler C, Gold PM. Severe hypoxemia due to shunting through a patent foramen ovale: a correctable complication of right ventricular infarction. J Am Coll Cardiol 1985;5:188 – 92. [12] Thompson RC, Finck SJ, Leventhal JP, Safford RE. Right-to-left shunt across a patent foramen ovale caused by cardiac tamponade: diagnosis by transesophageal echocardiography. Mayo Clin Proc 1991;66:391 – 4. [13] Begin R, Gervais L, Bureau MA. Patent foramen ovale and hypoxemia in chronic obstructive pulmonary disease. Eur J Respir Dis 1981;62:373 – 5. [14] Cubero JM, Gallego P, Pavon M. Arrhythmogenic right ventricular cardiomyopathy and atrial right-to-left shunt. Acta Cardiol 2002; 57:443 – 5.