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High altitude pulmonary hypertension with severe right ventricular dysfunction
International Journal of Cardiology 168 (2013) e89–e90
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
High altitude pulmonary hypertension with severe right ventricular dysfunction Abdirashit Maripov a,b,⁎, Argen Mamazhakypov b, Gulnura Karagulova a, Akylbek Sydykov a,c, Akpay Sarybaev a,b a b c
Department of Pulmonary Hypertension and Mountain Medicine, National Center of Cardiology and Internal Medicine, Bishkek, Kyrgyzstan Kyrgyz-Indian Mountain Biomedical Research Center, Bishkek, Kyrgyzstan University of Giessen and Marburg Lung Center (UGMLC), Department of Internal Medicine, Justus Liebig University of Giessen, Giessen, Germany
a r t i c l e
i n f o
Article history: Received 9 July 2013 Accepted 13 July 2013 Available online 1 August 2013 Keywords: High altitude Pulmonary hypertension Right ventricular dysfunction
Long-term high altitude residence leads to development of pulmonary hypertension and in some individuals to right ventricular (RV) hypertrophy and failure [1]. As the high altitude pulmonary hypertension is in most cases of mild to moderate degrees, an exaggerated pulmonary hypertension during mild exercise associated with daily activity has been suggested as underlying cause of RV failure in patients with chronic mountain sickness [2]. However, recent echocardiography studies failed to show clear evidence of RV dysfunction in patients with chronic mountain sickness despite obvious pulmonary arterial hypertension and right heart dilatation [3,4]. Furthermore, no imaging studies of RV function have been reported in subjects with RV failure due to high altitude-induced pulmonary hypertension yet [5]. Therefore, we sought to present a case of high altitude pulmonary hypertension with severe RV dysfunction evaluated by conventional echocardiography and tissue Doppler imaging. We describe a 64-year-old male herdsman resident at the altitude of 3200 m who was referred to our department (760 m) for the evaluation of abnormal electrocardiographic findings suggesting RV hypertrophy (Fig. 1). His main complaints were of dyspnea on mild exertion, dry cough, and peripheral edema. Secondary causes of pulmonary hypertension were excluded by a routine work-up. Transthoracic echocardiographic examination revealed dilated right-sided chambers with interatrium and interventricular septa bulging toward left cavities (Fig. 2A and B). Right ventricular chamber dimensions including the basal and the mid-cavity diameters and the distance from the tricuspid valve annulus to the RV apex in the apical four-chamber view at end diastole were measured at 5.5, 5.7 and 7.8 cm, respectively. The RV ⁎ Corresponding author at: National Center of Cardiology and Internal Medicine, T.Moldo street 3, 720040 Bishkek, Kyrgyzstan. Tel.: + 996 312 625679; fax: + 996 312 660387. E-mail address: [email protected] (A. Maripov). 0167-5273/$ – see front matter © 2013 Elsevier Ireland Ltd. All rights reserved. http://dx.doi.org/10.1016/j.ijcard.2013.07.129
outflow tract from the parasternal projection was measured at 5.4 cm (Fig. 2C). There was a large tricuspid regurgitation with a maximal pressure gradient between the right ventricle and the right atrium of 78 mm Hg and a moderate pulmonary regurgitation with an enddiastolic pressure gradient of 42 mm Hg (Fig. 2D–G). The inferior vena cava was dilated to 2.26 cm at expiration with loss of inspiratory decrease in diameter (Fig. 2H). With an assumption of right atrial pressure of 15 mm Hg, systolic pulmonary artery pressure was estimated to be approximately 93 mm Hg. The pulmonary flow pattern showed a midsystolic notching pattern with the acceleration time of 76 ms (Fig. 2I). The tricuspid inflow E wave peak velocity was measured at 98 mm/s consistent with severe tricuspid regurgitation (Fig. 2J). The ratio of early tricuspid inflow to annular diastolic velocity E/E(a), as a noninvasive estimation of RV filling pressure, was increased at 6.1. Right ventricular systolic function was severely impaired with tricuspid annular plane systolic excursion of 1.07 cm and peak systolic velocity at the lateral tricuspid annulus of 8.7 cm/s (Fig. 2K and L). Improvement of acute high altitude induced right ventricular dysfunction has been reported upon descent of the patient to sea level [6]. Therefore, we assume that the echocardiographic examination would reveal even more severe impairment of the RV function in this patient if it were performed at the place of his usual residence at high altitude. In summary, chronic high altitude pulmonary hypertension may lead to RV dysfunction in some individuals as illustrated in this case report. Right ventricular dysfunction is associated with greater morbidity and mortality and represents a major public health problem in mountainous regions around the world. Therefore, more studies are needed to determine the true prevalence and features of high altitude-induced RV failure. We certify that we comply with the Principles of Ethical Publishing in the International Journal of Cardiology. References [1] Mirrakhimov M, Winslow R. The cardiovascular system at high altitude. In: Blatties CM, Fregly MJ, editors. Handbook of Physiology: Section 4: Environmental Physiology. American Physiological SocietyOxford: Oxford University Press; 1996. p. 1241–58. [2] Stuber T, Sartori C, Schwab M, et al. Exaggerated pulmonary hypertension during mild exercise in chronic mountain sickness. Chest 2010;137(2):388–92. [3] Maignan M, Rivera-Ch M, Privat C, Leon-Velarde F, Richalet JP, Pham I. Pulmonary pressure and cardiac function in chronic mountain sickness patients. Chest 2009;135(2):499–504. [4] Huez S, Faoro V, Guenard H, Martinot JB, Naeije R. Echocardiographic and tissue Doppler imaging of cardiac adaptation to high altitude in native highlanders versus acclimatized lowlanders. Am J Cardiol 2009;103(11):1605–9. [5] Naeije R, Dedobbeleer C. Pulmonary hypertension and the right ventricle in hypoxia. Exp Physiol 2013;98(8):1247–356. [6] Huez S, Faoro V, Vachiery JL, Unger P, Martinot JB, Naeije R. Images in cardiovascular medicine. High-altitude-induced right-heart failure. Circulation 2007;115(9):e308–9.
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A. Maripov et al. / International Journal of Cardiology 168 (2013) e89–e90
Fig. 1. 12-lead ECG showing right ventricular hypertrophy.
Fig. 2. A and B, Apical four-chamber and parasternal short-axis view, demonstrating severe right ventricular enlargement and displacement of the interatrium and interventricular septa toward left cavities. C, RV outflow tract at subpulmonary region from the parasternal short-axis view. D, Apical four-chamber view showing significant tricuspid regurgitation. E, Maximal tricuspid regurgitant jet velocity, measured from the spectral profile of the tricuspid regurgitation jet in the apical four-chamber view. F, Dilated inferior vena cava from the subcostal view. G, Tricuspid annular plane systolic excursion using M-mode of the tricuspid annulus in the apical four-chamber view. H, Midsystolic notching of the pulse wave Doppler profile in the right ventricular outflow tract. I, Lateral tricuspid annular motion velocity using pulsed wave tissue Doppler imaging.
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
High altitude pulmonary hypertension with severe right ventricular dysfunction Abdirashit Maripov a,b,⁎, Argen Mamazhakypov b, Gulnura Karagulova a, Akylbek Sydykov a,c, Akpay Sarybaev a,b a b c
Department of Pulmonary Hypertension and Mountain Medicine, National Center of Cardiology and Internal Medicine, Bishkek, Kyrgyzstan Kyrgyz-Indian Mountain Biomedical Research Center, Bishkek, Kyrgyzstan University of Giessen and Marburg Lung Center (UGMLC), Department of Internal Medicine, Justus Liebig University of Giessen, Giessen, Germany
a r t i c l e
i n f o
Article history: Received 9 July 2013 Accepted 13 July 2013 Available online 1 August 2013 Keywords: High altitude Pulmonary hypertension Right ventricular dysfunction
Long-term high altitude residence leads to development of pulmonary hypertension and in some individuals to right ventricular (RV) hypertrophy and failure [1]. As the high altitude pulmonary hypertension is in most cases of mild to moderate degrees, an exaggerated pulmonary hypertension during mild exercise associated with daily activity has been suggested as underlying cause of RV failure in patients with chronic mountain sickness [2]. However, recent echocardiography studies failed to show clear evidence of RV dysfunction in patients with chronic mountain sickness despite obvious pulmonary arterial hypertension and right heart dilatation [3,4]. Furthermore, no imaging studies of RV function have been reported in subjects with RV failure due to high altitude-induced pulmonary hypertension yet [5]. Therefore, we sought to present a case of high altitude pulmonary hypertension with severe RV dysfunction evaluated by conventional echocardiography and tissue Doppler imaging. We describe a 64-year-old male herdsman resident at the altitude of 3200 m who was referred to our department (760 m) for the evaluation of abnormal electrocardiographic findings suggesting RV hypertrophy (Fig. 1). His main complaints were of dyspnea on mild exertion, dry cough, and peripheral edema. Secondary causes of pulmonary hypertension were excluded by a routine work-up. Transthoracic echocardiographic examination revealed dilated right-sided chambers with interatrium and interventricular septa bulging toward left cavities (Fig. 2A and B). Right ventricular chamber dimensions including the basal and the mid-cavity diameters and the distance from the tricuspid valve annulus to the RV apex in the apical four-chamber view at end diastole were measured at 5.5, 5.7 and 7.8 cm, respectively. The RV ⁎ Corresponding author at: National Center of Cardiology and Internal Medicine, T.Moldo street 3, 720040 Bishkek, Kyrgyzstan. Tel.: + 996 312 625679; fax: + 996 312 660387. E-mail address: [email protected] (A. Maripov). 0167-5273/$ – see front matter © 2013 Elsevier Ireland Ltd. All rights reserved. http://dx.doi.org/10.1016/j.ijcard.2013.07.129
outflow tract from the parasternal projection was measured at 5.4 cm (Fig. 2C). There was a large tricuspid regurgitation with a maximal pressure gradient between the right ventricle and the right atrium of 78 mm Hg and a moderate pulmonary regurgitation with an enddiastolic pressure gradient of 42 mm Hg (Fig. 2D–G). The inferior vena cava was dilated to 2.26 cm at expiration with loss of inspiratory decrease in diameter (Fig. 2H). With an assumption of right atrial pressure of 15 mm Hg, systolic pulmonary artery pressure was estimated to be approximately 93 mm Hg. The pulmonary flow pattern showed a midsystolic notching pattern with the acceleration time of 76 ms (Fig. 2I). The tricuspid inflow E wave peak velocity was measured at 98 mm/s consistent with severe tricuspid regurgitation (Fig. 2J). The ratio of early tricuspid inflow to annular diastolic velocity E/E(a), as a noninvasive estimation of RV filling pressure, was increased at 6.1. Right ventricular systolic function was severely impaired with tricuspid annular plane systolic excursion of 1.07 cm and peak systolic velocity at the lateral tricuspid annulus of 8.7 cm/s (Fig. 2K and L). Improvement of acute high altitude induced right ventricular dysfunction has been reported upon descent of the patient to sea level [6]. Therefore, we assume that the echocardiographic examination would reveal even more severe impairment of the RV function in this patient if it were performed at the place of his usual residence at high altitude. In summary, chronic high altitude pulmonary hypertension may lead to RV dysfunction in some individuals as illustrated in this case report. Right ventricular dysfunction is associated with greater morbidity and mortality and represents a major public health problem in mountainous regions around the world. Therefore, more studies are needed to determine the true prevalence and features of high altitude-induced RV failure. We certify that we comply with the Principles of Ethical Publishing in the International Journal of Cardiology. References [1] Mirrakhimov M, Winslow R. The cardiovascular system at high altitude. In: Blatties CM, Fregly MJ, editors. Handbook of Physiology: Section 4: Environmental Physiology. American Physiological SocietyOxford: Oxford University Press; 1996. p. 1241–58. [2] Stuber T, Sartori C, Schwab M, et al. Exaggerated pulmonary hypertension during mild exercise in chronic mountain sickness. Chest 2010;137(2):388–92. [3] Maignan M, Rivera-Ch M, Privat C, Leon-Velarde F, Richalet JP, Pham I. Pulmonary pressure and cardiac function in chronic mountain sickness patients. Chest 2009;135(2):499–504. [4] Huez S, Faoro V, Guenard H, Martinot JB, Naeije R. Echocardiographic and tissue Doppler imaging of cardiac adaptation to high altitude in native highlanders versus acclimatized lowlanders. Am J Cardiol 2009;103(11):1605–9. [5] Naeije R, Dedobbeleer C. Pulmonary hypertension and the right ventricle in hypoxia. Exp Physiol 2013;98(8):1247–356. [6] Huez S, Faoro V, Vachiery JL, Unger P, Martinot JB, Naeije R. Images in cardiovascular medicine. High-altitude-induced right-heart failure. Circulation 2007;115(9):e308–9.
e90
A. Maripov et al. / International Journal of Cardiology 168 (2013) e89–e90
Fig. 1. 12-lead ECG showing right ventricular hypertrophy.
Fig. 2. A and B, Apical four-chamber and parasternal short-axis view, demonstrating severe right ventricular enlargement and displacement of the interatrium and interventricular septa toward left cavities. C, RV outflow tract at subpulmonary region from the parasternal short-axis view. D, Apical four-chamber view showing significant tricuspid regurgitation. E, Maximal tricuspid regurgitant jet velocity, measured from the spectral profile of the tricuspid regurgitation jet in the apical four-chamber view. F, Dilated inferior vena cava from the subcostal view. G, Tricuspid annular plane systolic excursion using M-mode of the tricuspid annulus in the apical four-chamber view. H, Midsystolic notching of the pulse wave Doppler profile in the right ventricular outflow tract. I, Lateral tricuspid annular motion velocity using pulsed wave tissue Doppler imaging.