Upload
brian
View
214
Download
3
Embed Size (px)
Citation preview
International Journal of Cardiology 180 (2015) 60–62
Contents lists available at ScienceDirect
International Journal of Cardiology
j ourna l homepage: www.e lsev ie r .com/ locate / i j ca rd
Letter to the Editor
Dynamic left ventricular outflow tract obstruction causingmyocardial ischemia
Julie He a, Brian Malm a,b,⁎a Yale University, Section of Cardiovascular Medicine, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT, United Statesb Department of Cardiology, VA Connecticut Healthcare System, West Haven, CT, United States
⁎ Corresponding author at: Department of CardiologSystem, 950, Campbell Avenue, West Haven, CT 06516, U
E-mail address: [email protected] (B. Malm).
http://dx.doi.org/10.1016/j.ijcard.2014.11.1360167-5273/Published by Elsevier Ireland Ltd.
a r t i c l e i n f o
Article history:
Received 10 November 2014Accepted 22 November 2014Available online 26 November 2014Keywords:EchocardiographyLeft ventricular outflow tractSystolic anterior motionMitral valveIschemia
LVOT gradient of 17 mmHg at rest which increased to 84 mmHg im-mediately following exercise (Fig. 3C–D). The patient was managedwith beta-blockers and referred for mitral valve surgery.
We present a case of a patient with exertional angina and induc-ible ischemia in the setting of dynamic left ventricular outflow tractobstruction, systolic anterior motion of the mitral valve (SAM), andnormal coronary arteries. This presentation is common in patientswith hypertrophic cardiomyopathy but has also been reported inother settings, including elderly patients [1] and patients with end-stage renal disease [2]. Abnormalities of the mitral valve can accountfor a significant proportion of LVOT obstruction cases [3]. Dynamic
A 71 year oldmale with hypertension, hyperlipidemia, and diabe-tes presented to an outside hospital with exertional chest pain. Heunderwent an exercise myocardial perfusion study during whichhe developed chest pain and ischemic ECG changes (Fig. 1A–B). Hismyocardial perfusion imaging was normal. A transthoracic echocar-diogram was obtained and interpreted as showing significant aorticstenosis. He was subsequently transferred to our medical center forfurther management. In the interim, he developed atrial fibrillationwith rapid ventricular response. A repeat transthoracic echocardio-gram (Fig. 2 A–B) revealed severe left ventricular outflow tract(LVOT) obstruction with a peak resting gradient of 64 mm Hg, mildconcentric left ventricular hypertrophy with proximal septal thick-ening and preserved ejection fraction. A mobile echodensity wasnoted in the LVOT suggestive of systolic anterior motion of the mitralvalve versus a sub-aortic membrane. The aortic valve was tri-leafletand opened normally. The patient underwent a transesophagealechocardiogram (Fig. 2 C–D) which revealed a myxomatous anteriormitral valve leaflet with mild mitral regurgitation and systolicanterior motion leading to LVOT obstruction. There was no sub-aortic membrane. He was in sinus rhythm during this exam with apeak LVOT gradient of 27 mmHg. Coronary angiography was normal(Fig. 3A–B). He subsequently underwent a treadmill stressechocardiogram which was terminated for chest pain and ischemic
y, VA Connecticut Healthcarenited States.
ECG changes. Continuous-wave Doppler imaging measured an
LVOT obstruction during pharmacologic stress with dobutaminehas been previously described [4]. Although dobutamine may pro-voke SAM [5], only a minority of these patients will go on to developSAMwith physiologic exercise stress testing [6]. Predisposing factorsto developing LVOT obstruction include female gender and hyper-tension [4]. In a study of 300 patients referred for exercise echocardi-ography, Zywica et al. found dynamic LVOT obstruction in 5% ofpatients with 44% also demonstrating signs of ischemia [7]. In thisstudy, independent predictors of exercise-induced LVOT obstructionwere systolic anterior motion of the mitral valve, hyperdynamic LVfunction, small ventricular size, increased septal wall thickness,high peak systolic blood pressure, and interestingly, younger age.The strongest predictor was systolic anterior motion of the mitralvalve, as was seen in our case. In a study of patients with dynamicLVOT obstruction during exercise and normal wall thickness, all pa-tients had structural abnormalities of the mitral valve includingelongated, redundant leaflets and anterior position of the papillarymuscles [8]. Our patient had concentric left ventricular hypertrophy,proximal septal thickening, and SAM, all of which predisposed himto developing dynamic LVOT obstruction.
In summary, in patients with demonstrable myocardial ischemia inthe absence of obstructive coronary disease, exercise induced dynamicLVOT obstruction should be considered. Mitral valve abnormalities arecommon in this setting and are best evaluated with transesophagealechocardiography.
Conflict of interest
The authors report no relationships that could be construed as a con-flict of interest.
Fig. 1. 12-Lead ECG at rest (A) and during exercise (B) demonstrating ST depressions in leads II, III, aVF, V5, and V6 consistent with ischemia.
Fig. 2. Transthoracic echocardiogram showing an echodensity in the left ventricular outflow tract (A, arrow) and a continuous wave Doppler peak velocity of 4 m/s (B). Transesophagealechocardiogram showing systolic anterior motion of the mitral valve (C, arrow) and color Doppler evidence of turbulent flow in the left ventricular outflow tract (D).
61J. He, B. Malm / International Journal of Cardiology 180 (2015) 60–62
Acknowledgments
No funding source was used for this manuscript.
References
[1] M. Henein, C. O'Sullivan, G. Sutton, D. Gibson, A. Coats, Stress-induced left ventricularoutflow tract obstruction: a potential cause of dyspnea in the elderly, J. Am. Coll.Cardiol. 30 (1997) 1301–1307.
[2] R. Sharma, D. Pellerin, D. Gaze, M. Rajnikant, H. Gregson, C. Streather, P. Collinson, S.Brecker, Dynamic left ventricular outflow obstruction: a potential cause of angina inend stage renal disease, Int. J. Cardiol. 112 (2006) 295–301.
[3] B. Maron, Hypertrophic cardiomyopathy: a systematic review, J. Am. Med. Assoc. 287(2002) 1308–1320.
[4] M.J. Sorrentino, et al., Left ventricular outflow tract obstruction as a cause for hypo-tension and symptoms during dobutamine stress echocardiography, Clin. Cardiol.19 (1996) 225–230.
[5] P.A. Pellikka, et al., Dynamic intraventricular obstruction during dobutamine stressechocardiography. A new observation, Circulation 86 (1992) 1429–1432.
[6] P. Meimoun, et al., Significance of systolic anterior motion of the mitral valve duringdobutamine stress echocardiography, J. Am. Soc. Echocardiogr. 18 (2005) 49–56.
Fig. 3.Coronary angiography demonstrating normal left (A) and right (B) coronary arteries. Continuous-wave Dopplermeasuring an LVOT gradient of 17mmHg at rest (C) and 84mmHgfollowing exercise (D).
62 J. He, B. Malm / International Journal of Cardiology 180 (2015) 60–62
[7] K. Zywica, R. Jenni, P. Pellikka, A. Faeh-Gunz, B. Seifert, Jost C. Attenhofer, Dynamic leftventricular outflow tract obstruction evoked by exercise echocardiography: preva-lence and predictive factors in a prospective study, Eur. J. Echocardiogr. 9 (2008)665–671.
[8] E. Alhaj, B. Kim, D. Cantales, S. Uretsky, F. Chaudhry, M. Sherrid, Symptomaticexercise-induced left ventricular outflow tract obstruction without left ventricularhypertrophy, J. Am. Soc. Echocardiogr. 26 (2013) 556–565.