|Year : 2017 | Volume
| Issue : 2 | Page : 154-157
Transient dynamic left ventricular outflow tract obstruction
Gnanavelu Ganesan, Ashok Govindaraj, Venkatesan Sangareddi
Institute of Cardiology, Madras Medical College, Chennai, Tamil Nadu, India
|Date of Web Publication||28-Aug-2017|
Rajiv Gandhi Government General Hospital, Chennai - 600 003, Tamil Nadu
Source of Support: None, Conflict of Interest: None
Dynamic left ventricular outflow (LVOT) obstruction has been classically described in patients with hypertrophic cardiomyopathy (HCM). The hypertrophy of the basal septum and systolic anterior motion of the mitral valve leaflet (SAM) cause dynamic LVOT obstruction. In addition, HCM also shows speckled appearance of myocardium and LVOT obstruction is persistent, although to a varying degree. Several other conditions cause the echocardiographic finding of dynamic LVOT obstruction like postoperative patients with hypovolemia, post aortic valve replacement (AVR) or mitral valve repair, hyperdynamic left ventricle and acute anteroapical myocardial infarction. We report two patients who had transient dynamic left ventricular outflow obstruction one with hypertension, mitral valve prolapse associated with hypovolemia and anaemia and another with vomiting and hypovolemia.
Keywords: Dynamic obstruction, hypertrophic cardiomyopathy, transient obstruction
|How to cite this article:|
Ganesan G, Govindaraj A, Sangareddi V. Transient dynamic left ventricular outflow tract obstruction. J Indian Acad Echocardiogr Cardiovasc Imaging 2017;1:154-7
|How to cite this URL:|
Ganesan G, Govindaraj A, Sangareddi V. Transient dynamic left ventricular outflow tract obstruction. J Indian Acad Echocardiogr Cardiovasc Imaging [serial online] 2017 [cited 2020 Sep 30];1:154-7. Available from: http://www.jiaecho.org/text.asp?2017/1/2/154/213670
| Introduction|| |
Dynamic left ventricular outflow tract (LVOT) obstruction has been classically described in patients with hypertrophic cardiomyopathy (HCM). The hypertrophy of the basal septum and systolic anterior motion (SAM) of the mitral valve leaflet cause a dynamic LVOT obstruction. There are several other conditions that cause the echocardiographic finding of dynamic LVOT obstruction such as postoperative patients with hypovolemia, postaortic valve replacement or mitral valve repair, hyperdynamic left ventricle, and acute anteroapical myocardial infarction. We report two cases of dynamic LVOT obstruction, the first patient with hypertension, mitral valve prolapse, anemia with associated hypovolemia and the second patient with vomiting and hypovolemia.
| Case Reports|| |
A 65-year-old male, hypertensive for 6 years on treatment with metoprolol 25 mg once daily, was admitted under surgical oncology with complaints of persistent vomiting for 20 days with a history of melena and exertional dyspnea for 1 week before admission. He was diagnosed to have esophageal carcinoma. During preoperative cardiac evaluation, he was afebrile, pale with signs of moderate dehydration. Pulse rate was 80 bpm, and blood pressure (BP) was 80/60 mmHg in the right upper limb. Cardiac examination revealed a Grade 2/6 cresendo-decrescendo systolic murmur heard in the left third intercostal space close to the sternum. Except for hemoglobin of 10 g%, other biochemical investigations were within normal limits. Electrocardiogram (ECG) revealed left ventricular (LV) hypertrophy. Echocardiogram revealed SAM of mitral valve leaflet [Figure 1] with a peak gradient of 70 mmHg across LVOT [Figure 2]. Thickness of interventricular septum was 11 mm and posterior wall 11 mm suggesting mild LV hypertrophy. Aortic valve was sclerosed but competent. Mild mitral regurgitation (MR) was noted [Figure 3] due to mitral valve prolapse involving predominantly posterior leaflet. There was no previous history of syncope or other cardiac ailment or family history of sudden death. The patient was treated with intravenous fluids to correct dehydration, and the dose of beta-blocker was increased to 50 mg/day. Echocardiogram was repeated after 5 days which showed mild MR with no evidence of LVOT obstruction or SAM [Figure 4]. His pulse was 66 bpm and BP was 110/80 mmHg.
|Figure 1: M-mode echocardiogram showing systolic anterior motion of mitral leaflet|
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|Figure 2: Doppler interrogation across left ventricular outflow tract demonstrating gradient of 70 mmHg|
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|Figure 3: Doppler interrogation of mitral valve demonstrating mild mitral regurgitation|
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|Figure 4: Doppler across left ventricular outflow tract demonstrating reduction in the gradient (14 mmHg) after hydration|
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A 67-year-old female was referred to us with complaints of difficulty in breathing of 1 week duration. She had vomiting 8–10 episodes for the past 3 days. No history of chest pain, syncope, swelling of the legs, and loose stools. She was normotensive with no history of hypertension, diabetes, coronary artery disease, or family history of sudden death. The patient was obese with a body mass index of 31. Complete blood count, urine examination, and renal function tests were normal. She had a history of swelling of legs 2 months back and was evaluated at a nearby hospital, echocardiogram done at that time revealed no regional wall motion abnormalities, normal LV systolic function, and no gradient across the LVOT. Clinical examination revealed a pulse rate of 98/min and a BP of 90/60 mmHg. No significant abnormality was detected during general and cardiovascular examination except for mild degree of dehydration. ECG taken during her present visit showed sinus rthyum with a heart rate of 100/min and no evidence of chamber enlargement. Echocardiogram showed mild basal septal hypertrophy of 12 mm, SAM of mitral valve with severe LVOT obstruction (peak gradient of 64 mmHg) [Figure 5], mild MR was also noted [Figure 6]. LV systolic function was normal with Grade I LV diastolic dysfunction. The patient was treated with antiemetics and other supportive management and advised to review after 1 week. The patient improved symptomatically and repeat echocardiogram showed the absence of outflow tract gradient and MR.
|Figure 5: Doppler across left ventricular outflow tract demonstrating peak gradient of 64 mmHg|
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|Figure 6: Doppler across mitral valve demonstrating mild mid-late mitral regurgitation|
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| Discussion|| |
Dynamic LVOT obstruction is usually described in the context of hypertrophic obstructive cardiomyopathy and has been a hallmark of this condition. Dynamic LVOT obstruction has been reported in conditions such as postoperative states, acute coronary syndrome, following percutaneous coronary intervention, dobutamine stress test, hypovolemia, hypertension, and excess catecholamine with hypercontractility.
Both structural and functional abnormalities contribute to the development of LVOT obstruction. Asymmetric septal hypertrophy, LV hypertrophy (hypertension or sigmoid septum), reduced LV chamber size, e.g., due to dehydration, bleeding or diuresis, mitral valve abnormalities (redundant, long anterior leaflet), and hypercontractility (inotropes, hyperdynamic state) contribute to LVOT obstruction. LVOT obstruction is a dynamic condition that is affected by fluctuations in volume status, autonomic activity, diurnal variations, pharmacotherapy, and exercise.,, Any condition causing hypotension causes increase in sympathetic activity. The high level of catecholamines enhances the inotropic and chronotropic effects – both of which have a significant deleterious effect on LVOT obstruction. Hypercontractility accelerates the blood flow across LVOT and hypovolemia results in less end-diastolic volume which in turn, reduces the LVOT cross-sectional area during systole. This further accelerates blood flow through the narrower LVOT. The resultant high acceleration of blood flow can create a negative pressure below the anterior mitral leaflet that sucks it anteriorly toward the septum [Figure 7]. The SAM of the anterior mitral leaflet toward the septum further obstructs the LVOT. Failure of the anterior mitral leaflet to coapt with the posterior leaflet in systole results in MR. The degree and duration of mitral SAM determine the severity of the dynamic LVOT gradient and MR. As a net result, cardiac output decreases and hypotension worsens which further activates the sympathetic system. This process can continue to deteriorate until the cycle is interrupted.
|Figure 7: Mechanisms of left ventricular outflow tract obstruction during hypovolemia|
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Management of this condition includes increasing intravascular and LV volume by intravenous fluids, thereby reducing the SAM. Beta-blockers will decrease LVOT gradients by reducing basal hypercontractility, increasing LV filling and size and reducing heart rate.
| Conclusion|| |
In patients with dynamic LVOT obstruction, causes other than HCM should be thought of when there is no significant hypertrophy. Simple volume replacement helps in rectifying dynamic LVOT obstruction in such conditions. Inotropic agents which actually aggravate the obstruction should be used cautiously in these conditions. These patients however should not be labeled as HCM in which the dynamic nature of obstruction is present always although in varying severity depending on the drugs, etc., typical asymmetric hypertrophy, and speckled appearance of the septum.
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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], [Figure 5], [Figure 6], [Figure 7]