|Year : 2019 | Volume
| Issue : 3 | Page : 100-102
Dynamic obstruction of left ventricular outflow tract due to bilateral pulmonary embolism
Xin-Lin Liu1, Yan Wu1, Jun-Xiang Liu1, Xin Zhou2
1 Department of Cardiology, Chinese People's Armed Police Force, Characteristic Medical Center, Tianjin, China
2 Department of Cardiology, Tianjin Medical University General Hospital, Tianjin, China
|Date of Submission||28-Mar-2019|
|Date of Acceptance||18-Jun-2019|
|Date of Web Publication||30-Sep-2019|
Department of Cardiology, Chinese People's Armed Police Force, Characteristic Medical Center, 220, Cheng-Lin Street, Dongli District, Tianjin 300162
Source of Support: None, Conflict of Interest: None
A 68-year-old male patient with a history of nonobstructive hypertrophic cardiomyopathy was admitted to the cardiac intensive care unit due to sudden onset of near syncope and hypotension. The diagnosis of acute bilateral pulmonary embolism was confirmed by pulmonary computed tomographic angiography. On day 2 of admission, left ventricular outflow tract (LVOT) obstruction was demonstrated by increased peak systolic blood flow (454 cm/s) and increased transvalvular pressure gradient (83 mmHg), as well as systolic anterior motion of the mitral valve leaflet. LVOT obstruction underwent a gradual normalization and was completely resolved on day 21 after symptom onset, and the patient was discharged. Acute pulmonary embolism is a rare cause of LVOT obstruction. In this case, the concomitant existence of nonobstructive hypertrophic cardiomyopathy exacerbated LVOT obstruction due to right ventricle overload-induced leftward deviation of interventricular septum and may render the patients at higher risk for sudden death. More active anticoagulation therapy should be considered in this situation.
Keywords: Dynamic obstruction, left ventricular outflow tract obstruction, nonobstructive hypertrophic cardiomyopathy, pulmonary embolism
|How to cite this article:|
Liu XL, Wu Y, Liu JX, Zhou X. Dynamic obstruction of left ventricular outflow tract due to bilateral pulmonary embolism. Cardiol Plus 2019;4:100-2
| Introduction|| |
Left ventricular outflow tract (LVOT) obstruction can independently result from various clinical settings. In the published literature, acute pulmonary embolism is a rare cause of LVOT obstruction. Acute pulmonary embolism usually leads to a significant increase in the right ventricular pressure load and leftward deviation of the interventricular septum, which may further aggravate LVOT obstruction in the presence of nonobstructive hypertrophic cardiomyopathy. Here, we report dynamic LVOT obstruction in a case who suffered from acute pulmonary embolism with previously confirmed nonobstructive hypertrophic cardiomyopathy. Due to the potential high-risk nature of this coexistence, more active anticoagulation therapy should be considered to reduce the risk of sudden death.
| Case Report|| |
A 68-year-old male patient was admitted to the cardiac intensive care unit due to sudden onset of near syncope and hypotension. He was diagnosed with nonobstructive hypertrophic cardiomyopathy 3 years prior and had stayed in bed for 1 week after an accidental fall.
Arterial blood gas analysis showed hypoxemia. The diagnosis of acute pulmonary embolism was confirmed by pulmonary computed tomographic angiography showing bilateral pulmonary embolism [Figure 1], as well as the Doppler ultrasonographic evidence of venous thrombosis in both lower extremities. Anticoagulation therapy by enoxaparin was initiated. On 2nd day of admission, the flow velocity of LVOT was 454 cm/s with a transvalvular pressure gradient of 83 mmHg [Figure 2]a. In addition, parasternal long-axis Mmode echocardiography across the mitral valve showed systolic anterior motion (SAM) of the mitral valve leaflet [Figure 3]a. Re-examination of arterial blood gas analysis on the 3rd day showed normalization of hypoxemia and systemic hypotension. Serial echocardiography performed on the 6th, 13th, and 21st day revealed a gradual decrease of LVOT velocity, as well as the transvalvular pressure gradient [Figure 2]b, [Figure 2]d. Notably, the SAM of the anterior mitral leaflet was completely disappeared on the 21st day [Figure 3]b, [Figure 3]d, and the patient was discharged. The dynamics of LVOT velocity and pressure gradient from symptom onset, as well as right ventricular and right atrial diameter, are shown in [Figure 4].
|Figure 1: Pulmonary computed tomographic angiography demonstrated bilateral pulmonary embolism|
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|Figure 2: Transthoracic echocardiography demonstrated increased transvalvular pressure gradient of left ventricular outflow tract on the 2nd day of admission (a), and gradual normalization of the pressure gradient during the following day of hospitalization (b-d)|
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|Figure 3: Transthoracic echocardiography demonstrated systolic anterior motion of the mitral valve leaflet on the 2nd day of admission (a), which was completely disappeared on the 21st day of hospitalization (b-d)|
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|Figure 4: The dynamic changes in left ventricular outflow tract velocity and pressure gradient (left) and changes in right ventricular and atrial diameter (right) from symptom-onset. Note that on the 1st day of symptom-onset, right atrial diameter was not measured|
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| Discussion|| |
LVOT obstruction can independently result from various clinical settings such as LV hypertrophy (hypertension or sigmoid septum), reduced LV chamber size (dehydration, bleeding, or diuresis), mitral valve abnormalities (redundant, long anterior leaflet), hypercontractility (stress, anxiety, or inotropic agents such as dobutamine), and ST-elevation myocardial infarction., Acute pulmonary embolism is a rare cause of LVOT obstruction. This patient had a history of nonobstructive hypertrophic cardiomyopathy with thickened interventricular septum. Acute pulmonary embolism usually leads to a significant increase in the right ventricular pressure load and leftward deviation of interventricular septum, which may further aggravate LVOT obstruction. The bloodstream causes drag forces and a Venturi effect on the anterior mitral leaflet, which results in SAM of the anterior mitral leaflet. This movement results in the anterior mitral leaflet contacting the septum for a period of systole, effectively obstructing the path of left ventricular outflow. Dynamic LVOT obstruction can mimic cardiogenic shock in an acute-care setting. Therefore, hypertrophic cardiomyopathy patients with pulmonary embolism are also at high risk of sudden death. More active anticoagulation therapy should be given to hypertrophic cardiomyopathy patients with high-risk factors of pulmonary embolism.
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Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2], [Figure 3], [Figure 4]