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Dynamic left ventricular outflow tract obstruction secondary to catecholamine excess in a normal ventricle
International Journal of Cardiology 112 (2006) 393 – 396 www.elsevier.com/locate/ijcard
Letter to the Editor
Dynamic left ventricular outflow tract obstruction secondary to catecholamine excess in a normal ventricle S. Mingo *, A. Benedicto, M.C. Jimenez, M.A. Pe´rez, M. Montero Hospital Virgen de Alarcos, Ciudad Real, Spain Received 22 July 2005; accepted 25 July 2005 Available online 14 November 2005
Abstract Hypertrophic cardiomyopathy (HCM) is the most common cause of left ventricular outflow tract (LVOT) obstruction. The LVOT obstruction is a consequence of the asymmetric septal hypertrophy and the mitral systolic anterior motion (SAM), causing both of them a dynamic gradient in LVOT. LVOT obstruction has been observed also in other conditions like hypertensive hypertrophy, dehydration, sepsis, vasodilatation, excessive sympathetic stimulation, pericardial tamponade, and after mitral valve repair and aortic valve replacement for aortic stenosis. We report in this document the case of two patients who developed a significant gradient at LVOT in the context of amine treatment during their admission into the intensive unit care. In both, cases there were no gradient, significant hypertrophy or SAM at baseline cardiac evaluation. We have met only one case reported in the literature matching those conditions. In order to treat this type of patients properly, it is essential to take in consideration this pathology. D 2005 Elsevier Ireland Ltd. All rights reserved. Keywords: LVOT obstruction; Amine treatment; Normal ventricle
1. Introduction HCM is the most common etiology of LVOT obstruction. HCM is a genetic disease with an autosomal dominant pattern of inheritance [1], with variable penetrancy. It is characterized by hypertrophy of the left ventricle (LV), with variable morphologic and haemodynamic abnormalities. In nearly 50% of the patients, the site and extent of cardiac hypertrophy results in different degrees of LVOT obstruction. Significant LVOT obstruction is present in some patients at rest; meanwhile, in other cases, it only appears under certain clinical or pharmacological conditions. This condition should be related to a reduction in preload, afterload, or to an increase in left ventricular inotropism. LVOT obstruction also occurs in other clinical conditions as concentric LVOT hypertrophy in hypertension [2], after * Corresponding author. C/Oce´ano Atla´ntico no. 3, 28760 Tres Cantos, Spain. Tel.: +34 91 803 81 50. E-mail address: [email protected] (S. Mingo). 0167-5273/$ - see front matter D 2005 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2005.07.075
aortic valve replacement for aortic valve stenosis [3], in the setting of acute myocardial infarction [4], mitral valve repair, and also in patients with structurally normal heart during the treatment with catecholamines [5]. In this report, we present the case of two patients without significant left ventricular hypertrophy and with basal septal thickness mild hypertrophy (12 mm), who developed severe dynamic LVOT obstruction and SAM during haemodynamic deterioration in the context of catecholamine treatment.
2. Case 1 The first case describes a 63-year-old woman, with past history of HTA, hypercholesterolemia, and hepatitis C. She was admitted to the hospital due to acute coronary syndrome without persistent ST segment elevation and with ST depression from V4 to V6 on the ECG. Troponin I was elevated until 0.84 ng/ml. On admission cardiopulmonary physical examination was unremarkable and Rx thorax was
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S. Mingo et al. / International Journal of Cardiology 112 (2006) 393 – 396
normal. Transthoracic echocardiographic evaluation revealed a mild basal septal hypertrophy (12 mm) and normal ventricular thickness in the other segments. LV dimensions and function were normal, without segmental wall motion abnormalities. There was no gradient in LVOT at rest. Aortic and mitral valves showed mild calcification with normal function. Coronariography was performed within the hospitalization period, revealing no major coronary stenosis. It was performed in another hospital and the patient was transferred to our institution during the same day. When she arrived, she developed severe haemodynamic deterioration, with hypotension (BP 85/45) and sinus tachycardia (120 bpm). Physical examination revealed a systolic murmur in the left esternal border and an important haematoma on the femoral punction site. In this situation, she was treated with large volumes of fluid and with dopamine. Haemogram showed haemoglobin value of 5 g/dl, so she required blood transfusion. After treatment with cathecholamines, the patient developed haemodynamic deterioration. Due to this deterioration and the appearance of a new murmur in the physical examination, a new echocardiography was performed. Transthoracic and also transesophagic echocardiogram were carried out, under sedation. Two-dimensional echocardiography revealed the SAM of the anterior mitral valve leaflet with dynamic LVOT obstruction. The peak pressure gradient measured with continuous Doppler in LVOT was 64 mm Hg at rest, and it rose up to 116 mm Hg with the Valsalva’s maneuver (Fig. 1). Color Doppler image showed flow acceleration in the LVOT and moderate mitral insufficiency (Fig. 2). Treatment with blood and fluid transfusion, cessation of amine therapy, and mechanical compression of the puncture
site solved the patient’s situation. Transthoracic echocardiography repeated some days after stabilization was similar to the basal one, with complete resolution of SAM and without LVOT obstruction. The patient was discharged from the hospital some days later with medical treatment (Verapamil and ARAII).
3. Case 2 The second case describes a 70-year-old man, with previous history of diabetes mellitus and hypertension. He was admitted to the hospital because of diabetic descompensation in the context of a respiratory tract infection. On admission, cardiopulmonary examination was normal. The ECG was in sinus rithm, with Q wave in V1 an V2, and without left ventricular hypertrophy. He was treated with antibiotics but he worsened and developed septic shock in few days, so he was admitted to the intensive care unit where he needed mechanical ventilation and catecholamine treatment (dopamine and norepinephrine). The patient did not improve in spite of this treatment and the resolution of the fever and infection with antibiotics. The transthoracic echocardiogram showed SAM and severe LVOT obstruction with mild basal hypertrophy (Fig. 3); the peak pressure gradient in LVOT at rest was 90 mm Hg; it rose up to 130 mm Hg post-extrasystole; left ventricular function and contractility were normal. Color Doppler imaging demonstrated also mild mitral regurgitation in relation with SAM. The catecholamine treatment was slowly reduced and the patient improved and tolerated the increasing dosage of
Fig. 1. The peak pressure gradient measured with continuous Doppler in LVOT was 64 mm Hg at rest rising to 116 mm Hg with the Valsalva’s maneuver.
S. Mingo et al. / International Journal of Cardiology 112 (2006) 393 – 396
395
Fig. 2. Color Doppler image showed flow acceleration in the LVOT and moderate mitral insufficiency.
betablockers, and he was moved to the hospitalization cardiology unit in a few days. The echocardiogram was repeated before discharge and it showed mild basal hypertrophy with a basal gradient at LVOT of 14 mm Hg, under betablocker treatment.
4. Discussion Hypertrophic obstructive cardiomyopathy (HCM) is the most common cause of LVOT obstruction; however, other
etiologies have been reported, including the catecholamine therapy in a basal normal heart [5]. There is a recently published article demonstrating that mild basal septal hypertrophy may also produce LVOT obstruction in hypertensive patients who underwent stress echocardiography with dobutamine usual dosage [6]. In this study, LVOT velocities were gradually increased with increasing stress and reached more than 3 m/s g corresponding to a gradient level of 36 mm Hg. Maximum LVOT velocities and gradients were similar in basal septal hypertrophy patients (BSH) and controls at rest. At peak
Fig. 3. A transthoracic echocardiogram showed SAM and severe LVOT obstruction with mild basal hypertrophy.
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S. Mingo et al. / International Journal of Cardiology 112 (2006) 393 – 396
stress, maximum LVOT velocities were significantly increased in BSH patients compared with normal controls. This findings did not correlate with any clinical nor haemodynamic significant changes. Previous studies demonstrated the presence of LVOT gradient in some patients who underwent dobutamine stress test [7], in some of them with SAM and in the others with dynamic obstruction at the papillary muscles level, with no physiological or clinical significance [8]. We only have found two cases reported of LVOT obstruction and hypotension during dobutamine stress echocardiography [9]. In a group of healthy elderly patients with protruded and angulated septum, an increase in LVOT gradient at peak dobutamine stress also were shown [10]. There is only a case reported in the literature describing a patient with structurally normal heart who developed catecholamine-induced dynamic LVOT obstruction compromised by haemodynamic deterioration [5], similar to our two patients. The use of inotropic agents in shocked patients, despite his etiology, is a common and lifesaving practice at the intensive care unit. In few cases, this can result in haemodynamic deterioration. In those patients, we should think about possible mechanisms of catecholamine-induced deterioration, like ischemic provocation, vasodilation secondary to dobutamine or, like in this two cases, LVOT dynamic obstruction. We can suspect this diagnosis if we found in the examination a new systolic murmur in the left low esternal border that increases with Valsalva maneuver or postextrasystole, with a normal second sound, and normal or bisferiens carotid pulse, mainly if the patient presents history of hypertension. Definitive diagnosis requires performing an echocardiogram as soon as possible, and the solution is the cessation of catecholamine therapy, the treatment of the basal illness, and to maintain blood pressure and urine output with volumes of fluid and colloids if necessary. Sometimes, the patients benefit from betablocker treatment. In our two cases, the cessation of catecholamine therapy, the volume substitution in the first one, and the betablocker therapy in the second, together with the correct therapy of the infection, were the solutions to the haemodynamic deterioration. In both patients, the LVOT obstruction, the SAM and the elevated gradient improved with those measures and the posterior Doppler studies were almost normal.
5. Conclusion The presence of dynamic gradient in LVOT is possible in patients with haemodynamic instability who worsen with catecholamine therapy. Echocardiography is essential to diagnose it accurately. It is important to think in this possibility because the solution depends on the amine withdrawal.
References [1] Wigle ED, Rakowski H, Kimball BP, Williams WG. Hypertrophic cardiomyopathy. Clinical spectrum and treatment. Circulation 1995 (Oct 1);92(7):1680 – 92. [2] Come PC, Bulkley BH, Goodman ZD, et al. Hypercontractile cardiac states simulating hypertrophic cardiomyopathy. Circulation 1977;55: 901 – 8. [3] Aurigemma G, Battista S, Orsinelli D, et al. Abnormal left ventricular intracavitary flow acceleration in patients undergoing aortic valve replacement for aortic stenosis: a marker for high postoperative morbidity and mortality. Circulation 1992;86:929 – 36. [4] Bartunek J, Vanderheyden M, de Bruyne B. Dynamic left ventricular outflow tract obstruction after anterior myocardial infarction: a potential mechanism of myocardial rupture. Eur Heart J 1995;16: 1939 – 42. [5] Auer J, Berent R, Weber T, Lamm G, Eber B. Catecholamine therapy inducing dynamic left ventricular outflow tract obstruction. Int J Cardiol 2005 (May 25);101(2):325 – 8. [6] Yalc¸in F, Muderrisoglu H, Korkmaz ME, Ozin B, Baltali M, Yigit F. The effect of dobutamine stress on left ventricular outflow tract gradients in hypertensive patients with basal septal hypertrophy. Angiology 2004;55:295 – 301. [7] Roldan FJ, Vargas-Barron J, Espinola-Zavaleta N, Keirns C, Romero-Cardenas A. Severe dynamic obstruction of the left ventricular outflow tract induced by dobutamine. Echocardiography 2000 (Jan);17(1):37 – 40. [8] Luria D, Klutstein MW, Rosenmann D, Shaheen J, Sergey S, Tzivoni D. Prevalence and significance of left ventricular outflow gradient during dobutamine echocardiography. Eur Heart J 1999 (Mar);20(5): 386 – 92. [9] Ueda T, Mizushige K, Yukiiri K, Watanabe K, Kohno M. Hypotension and functional left ventricular obstruction during dobutamine stress echocardiography—two case reports. Angiology 2001 (Jul);52(7): 489 – 92. [10] Henein MY, O’Sullivan C, Sutton GC, et al. Stess-induced left ventricular outflow tract obstruction: a potential cause of dyspnea in the elderly. J Am Coll Cardiol 1997;30:1301 – 7.
Letter to the Editor
Dynamic left ventricular outflow tract obstruction secondary to catecholamine excess in a normal ventricle S. Mingo *, A. Benedicto, M.C. Jimenez, M.A. Pe´rez, M. Montero Hospital Virgen de Alarcos, Ciudad Real, Spain Received 22 July 2005; accepted 25 July 2005 Available online 14 November 2005
Abstract Hypertrophic cardiomyopathy (HCM) is the most common cause of left ventricular outflow tract (LVOT) obstruction. The LVOT obstruction is a consequence of the asymmetric septal hypertrophy and the mitral systolic anterior motion (SAM), causing both of them a dynamic gradient in LVOT. LVOT obstruction has been observed also in other conditions like hypertensive hypertrophy, dehydration, sepsis, vasodilatation, excessive sympathetic stimulation, pericardial tamponade, and after mitral valve repair and aortic valve replacement for aortic stenosis. We report in this document the case of two patients who developed a significant gradient at LVOT in the context of amine treatment during their admission into the intensive unit care. In both, cases there were no gradient, significant hypertrophy or SAM at baseline cardiac evaluation. We have met only one case reported in the literature matching those conditions. In order to treat this type of patients properly, it is essential to take in consideration this pathology. D 2005 Elsevier Ireland Ltd. All rights reserved. Keywords: LVOT obstruction; Amine treatment; Normal ventricle
1. Introduction HCM is the most common etiology of LVOT obstruction. HCM is a genetic disease with an autosomal dominant pattern of inheritance [1], with variable penetrancy. It is characterized by hypertrophy of the left ventricle (LV), with variable morphologic and haemodynamic abnormalities. In nearly 50% of the patients, the site and extent of cardiac hypertrophy results in different degrees of LVOT obstruction. Significant LVOT obstruction is present in some patients at rest; meanwhile, in other cases, it only appears under certain clinical or pharmacological conditions. This condition should be related to a reduction in preload, afterload, or to an increase in left ventricular inotropism. LVOT obstruction also occurs in other clinical conditions as concentric LVOT hypertrophy in hypertension [2], after * Corresponding author. C/Oce´ano Atla´ntico no. 3, 28760 Tres Cantos, Spain. Tel.: +34 91 803 81 50. E-mail address: [email protected] (S. Mingo). 0167-5273/$ - see front matter D 2005 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2005.07.075
aortic valve replacement for aortic valve stenosis [3], in the setting of acute myocardial infarction [4], mitral valve repair, and also in patients with structurally normal heart during the treatment with catecholamines [5]. In this report, we present the case of two patients without significant left ventricular hypertrophy and with basal septal thickness mild hypertrophy (12 mm), who developed severe dynamic LVOT obstruction and SAM during haemodynamic deterioration in the context of catecholamine treatment.
2. Case 1 The first case describes a 63-year-old woman, with past history of HTA, hypercholesterolemia, and hepatitis C. She was admitted to the hospital due to acute coronary syndrome without persistent ST segment elevation and with ST depression from V4 to V6 on the ECG. Troponin I was elevated until 0.84 ng/ml. On admission cardiopulmonary physical examination was unremarkable and Rx thorax was
394
S. Mingo et al. / International Journal of Cardiology 112 (2006) 393 – 396
normal. Transthoracic echocardiographic evaluation revealed a mild basal septal hypertrophy (12 mm) and normal ventricular thickness in the other segments. LV dimensions and function were normal, without segmental wall motion abnormalities. There was no gradient in LVOT at rest. Aortic and mitral valves showed mild calcification with normal function. Coronariography was performed within the hospitalization period, revealing no major coronary stenosis. It was performed in another hospital and the patient was transferred to our institution during the same day. When she arrived, she developed severe haemodynamic deterioration, with hypotension (BP 85/45) and sinus tachycardia (120 bpm). Physical examination revealed a systolic murmur in the left esternal border and an important haematoma on the femoral punction site. In this situation, she was treated with large volumes of fluid and with dopamine. Haemogram showed haemoglobin value of 5 g/dl, so she required blood transfusion. After treatment with cathecholamines, the patient developed haemodynamic deterioration. Due to this deterioration and the appearance of a new murmur in the physical examination, a new echocardiography was performed. Transthoracic and also transesophagic echocardiogram were carried out, under sedation. Two-dimensional echocardiography revealed the SAM of the anterior mitral valve leaflet with dynamic LVOT obstruction. The peak pressure gradient measured with continuous Doppler in LVOT was 64 mm Hg at rest, and it rose up to 116 mm Hg with the Valsalva’s maneuver (Fig. 1). Color Doppler image showed flow acceleration in the LVOT and moderate mitral insufficiency (Fig. 2). Treatment with blood and fluid transfusion, cessation of amine therapy, and mechanical compression of the puncture
site solved the patient’s situation. Transthoracic echocardiography repeated some days after stabilization was similar to the basal one, with complete resolution of SAM and without LVOT obstruction. The patient was discharged from the hospital some days later with medical treatment (Verapamil and ARAII).
3. Case 2 The second case describes a 70-year-old man, with previous history of diabetes mellitus and hypertension. He was admitted to the hospital because of diabetic descompensation in the context of a respiratory tract infection. On admission, cardiopulmonary examination was normal. The ECG was in sinus rithm, with Q wave in V1 an V2, and without left ventricular hypertrophy. He was treated with antibiotics but he worsened and developed septic shock in few days, so he was admitted to the intensive care unit where he needed mechanical ventilation and catecholamine treatment (dopamine and norepinephrine). The patient did not improve in spite of this treatment and the resolution of the fever and infection with antibiotics. The transthoracic echocardiogram showed SAM and severe LVOT obstruction with mild basal hypertrophy (Fig. 3); the peak pressure gradient in LVOT at rest was 90 mm Hg; it rose up to 130 mm Hg post-extrasystole; left ventricular function and contractility were normal. Color Doppler imaging demonstrated also mild mitral regurgitation in relation with SAM. The catecholamine treatment was slowly reduced and the patient improved and tolerated the increasing dosage of
Fig. 1. The peak pressure gradient measured with continuous Doppler in LVOT was 64 mm Hg at rest rising to 116 mm Hg with the Valsalva’s maneuver.
S. Mingo et al. / International Journal of Cardiology 112 (2006) 393 – 396
395
Fig. 2. Color Doppler image showed flow acceleration in the LVOT and moderate mitral insufficiency.
betablockers, and he was moved to the hospitalization cardiology unit in a few days. The echocardiogram was repeated before discharge and it showed mild basal hypertrophy with a basal gradient at LVOT of 14 mm Hg, under betablocker treatment.
4. Discussion Hypertrophic obstructive cardiomyopathy (HCM) is the most common cause of LVOT obstruction; however, other
etiologies have been reported, including the catecholamine therapy in a basal normal heart [5]. There is a recently published article demonstrating that mild basal septal hypertrophy may also produce LVOT obstruction in hypertensive patients who underwent stress echocardiography with dobutamine usual dosage [6]. In this study, LVOT velocities were gradually increased with increasing stress and reached more than 3 m/s g corresponding to a gradient level of 36 mm Hg. Maximum LVOT velocities and gradients were similar in basal septal hypertrophy patients (BSH) and controls at rest. At peak
Fig. 3. A transthoracic echocardiogram showed SAM and severe LVOT obstruction with mild basal hypertrophy.
396
S. Mingo et al. / International Journal of Cardiology 112 (2006) 393 – 396
stress, maximum LVOT velocities were significantly increased in BSH patients compared with normal controls. This findings did not correlate with any clinical nor haemodynamic significant changes. Previous studies demonstrated the presence of LVOT gradient in some patients who underwent dobutamine stress test [7], in some of them with SAM and in the others with dynamic obstruction at the papillary muscles level, with no physiological or clinical significance [8]. We only have found two cases reported of LVOT obstruction and hypotension during dobutamine stress echocardiography [9]. In a group of healthy elderly patients with protruded and angulated septum, an increase in LVOT gradient at peak dobutamine stress also were shown [10]. There is only a case reported in the literature describing a patient with structurally normal heart who developed catecholamine-induced dynamic LVOT obstruction compromised by haemodynamic deterioration [5], similar to our two patients. The use of inotropic agents in shocked patients, despite his etiology, is a common and lifesaving practice at the intensive care unit. In few cases, this can result in haemodynamic deterioration. In those patients, we should think about possible mechanisms of catecholamine-induced deterioration, like ischemic provocation, vasodilation secondary to dobutamine or, like in this two cases, LVOT dynamic obstruction. We can suspect this diagnosis if we found in the examination a new systolic murmur in the left low esternal border that increases with Valsalva maneuver or postextrasystole, with a normal second sound, and normal or bisferiens carotid pulse, mainly if the patient presents history of hypertension. Definitive diagnosis requires performing an echocardiogram as soon as possible, and the solution is the cessation of catecholamine therapy, the treatment of the basal illness, and to maintain blood pressure and urine output with volumes of fluid and colloids if necessary. Sometimes, the patients benefit from betablocker treatment. In our two cases, the cessation of catecholamine therapy, the volume substitution in the first one, and the betablocker therapy in the second, together with the correct therapy of the infection, were the solutions to the haemodynamic deterioration. In both patients, the LVOT obstruction, the SAM and the elevated gradient improved with those measures and the posterior Doppler studies were almost normal.
5. Conclusion The presence of dynamic gradient in LVOT is possible in patients with haemodynamic instability who worsen with catecholamine therapy. Echocardiography is essential to diagnose it accurately. It is important to think in this possibility because the solution depends on the amine withdrawal.
References [1] Wigle ED, Rakowski H, Kimball BP, Williams WG. Hypertrophic cardiomyopathy. Clinical spectrum and treatment. Circulation 1995 (Oct 1);92(7):1680 – 92. [2] Come PC, Bulkley BH, Goodman ZD, et al. Hypercontractile cardiac states simulating hypertrophic cardiomyopathy. Circulation 1977;55: 901 – 8. [3] Aurigemma G, Battista S, Orsinelli D, et al. Abnormal left ventricular intracavitary flow acceleration in patients undergoing aortic valve replacement for aortic stenosis: a marker for high postoperative morbidity and mortality. Circulation 1992;86:929 – 36. [4] Bartunek J, Vanderheyden M, de Bruyne B. Dynamic left ventricular outflow tract obstruction after anterior myocardial infarction: a potential mechanism of myocardial rupture. Eur Heart J 1995;16: 1939 – 42. [5] Auer J, Berent R, Weber T, Lamm G, Eber B. Catecholamine therapy inducing dynamic left ventricular outflow tract obstruction. Int J Cardiol 2005 (May 25);101(2):325 – 8. [6] Yalc¸in F, Muderrisoglu H, Korkmaz ME, Ozin B, Baltali M, Yigit F. The effect of dobutamine stress on left ventricular outflow tract gradients in hypertensive patients with basal septal hypertrophy. Angiology 2004;55:295 – 301. [7] Roldan FJ, Vargas-Barron J, Espinola-Zavaleta N, Keirns C, Romero-Cardenas A. Severe dynamic obstruction of the left ventricular outflow tract induced by dobutamine. Echocardiography 2000 (Jan);17(1):37 – 40. [8] Luria D, Klutstein MW, Rosenmann D, Shaheen J, Sergey S, Tzivoni D. Prevalence and significance of left ventricular outflow gradient during dobutamine echocardiography. Eur Heart J 1999 (Mar);20(5): 386 – 92. [9] Ueda T, Mizushige K, Yukiiri K, Watanabe K, Kohno M. Hypotension and functional left ventricular obstruction during dobutamine stress echocardiography—two case reports. Angiology 2001 (Jul);52(7): 489 – 92. [10] Henein MY, O’Sullivan C, Sutton GC, et al. Stess-induced left ventricular outflow tract obstruction: a potential cause of dyspnea in the elderly. J Am Coll Cardiol 1997;30:1301 – 7.