Successful negative inotropic treatment of acute left ventricular outflow tract obstruction by elongated mitral valve leaflet

Elongated anterior mitral valve leaflet (EAMVL) has not been reported to cause left ventricular outflow tract obstruction (LVOTO) in the absence of left ventricular hypertrophy. We report the case of an elderly male patient who presented with acute heart failure and severe mitral regurgitation in the setting of dehydration. Echocardiography revealed acute LVOTO secondary to EAMVL. The patient was ineligible for surgery and was treated with negative inotropic agents, which ensured resolution of heart failure and marked improvement in the degree of LVOTO. This case demonstrates that, under certain circumstances, EAMVL without associated left ventricular hypertrophy may produce hemodynamic compromise that can be successfully treated medically. © 2013 Wiley Periodicals, Inc. J Clin Ultrasound 42:245–248, 2014     

Anomalous papillary muscle producing dynamic left ventricular outflow tract obstruction.

A patient with a dynamic left ventricular outflow murmur was shown to have an anomalous anterolateral papillary muscle by transthoracic and transesophageal two-dimensional Doppler echocardiography. High late systolic outflow velocity and systolic anterior motion were demonstrated in the lateral outflow tract near the anomalous muscle, suggesting a role for the Venturi effect. This is the first confirmation by Doppler echocardiography of an anomalous papillary muscle contributing to abnormal left ventricular hemodynamics.     

Intra-aortic balloon pump associated with dynamic left ventricular outflow tract obstruction after valve replacement for aortic stenosis.

An unstable patient with critical aortic stenosis had an intra-aortic balloon pump placed preoperatively for hemodynamic support and alleviation of symptoms. After separation from cardiopulmonary bypass following aortic valve replacement, the patient was hypotensive with increased pulmonary artery pressures. Transesophageal echocardiography revealed left ventricular outflow tract obstruction associated with systolic anterior motion of the mitral valve and severe mitral regurgitation. This pathophysiology was present when ventricular systole was preceded by balloon counterpulsation, but was absent during unassisted systole. This case report demonstrates a potentially significant untoward effect of intra-aortic balloon pump augmentation after aortic valve replacement for aortic stenosis. The timely diagnosis of this iatrogenic condition in the operating room permitted the prompt implementation of appropriate management strategies and avoided unnecessary surgical intervention.     

Echocardiographic diagnosis of left ventricular outflow tract obstruction after mitral valvuloplasty with a flexible Duran ring.

We report on a patient in whom left ventricular outflow obstruction developed after mitral valve repair with a flexible Duran ring. This complication has been reported in 4.5% to 21% of patients when a rigid Carpentier ring was used but was thought to be eliminated with the use of flexible rings.     

Echocardiographic diagnosis of left ventricular outflow tract obstruction caused by an acquired subaortic membrane after mitral valve replacement.

Although an acquired subaortic membrane has been reported as a cause of left ventricular outflow tract (LVOT) obstruction in various clinical settings, it previously has not been reported after mitral valve surgery. We describe 3 cases of acquired LVOT obstruction that resulted from development of a subaortic membrane after mitral valve replacement. This report emphasizes the role of an acquired subaortic membrane in LVOT obstruction after mitral valve replacement, the use of echocardiography in diagnosing this condition, and the importance of early intervention.     

Dobutamine induced dynamic left ventricular outflow tract obstruction in patients with hypertrophic nonobstructive cardiomyopathy

Some patients with hypertrophic nonobstructive cardiomyopathy (HNCM) suffer symptoms resembling those in obstructive type despite no left ventricular outflow tract (LVOT) gradient could be detected on resting echocardiography. To investigate the value of dobutamine stress echocardiography (DSE) in determining the dynamic left ventricular (LV) obstruction of patients with HNCM. The study was conducted on 31 patients who were diagnosed HNCM on resting echocardiography and 9 healthy person as a control group. Intraventricular flow acceleration of > 3 m/sec on DSE was accepted as dynamic LVOT obstruction. Group 1 and 2 included patients without and with dynamic LVOT obstruction, respectively. The occurrence of chest pain and dyspnea seen during DSE was more frequent in group 2 than group 1 and control group. The frequency of SAM was significantly higher (p < 0.05) and the septal angle was significantly lower (p < 0.001) in Group 2. The presence of SAM significantly correlated with the peak gradient (r = 0.61, p < 0.001). The septal angle had significant negative correlations with the peak gradient (r = -0.77, p < 0.001) reached at DSE. The relative risk for peak gradient was highest when septal angle was < or = 100 degrees, with a sensitivity of 93%, specificity of 80%, positive predictive value of 82%, negative predictive value of 92%, and predictive accuracy of 87%. DSE is a reliable tool for the diagnosis of dynamic LV obstruction in patients with HNCM. The presence of SAM together with a low septal angle is highly predictive for the presence of a dynamic LVOT obstruction detected by DSE.     

Left ventricular outflow tract obstruction related to a valve prosthesis: case caused by a low-profile mitral prosthesis

Mechanical and bioprosthetic mitral prostheses may have many potential complications. In patients with isolated mitral stenosis and a small left ventricular cavity, low-profile prostheses are recommended to avoid myocardial impingement that can result from a high-profile valve and lead to possible left ventricular inflow or outflow obstruction or ventricular arrhythmias. This case report illustrates that left ventricular outflow obstruction may also result from a low-profile mitral valve prosthesis. This obstruction was not diagnosed before cardiac catheterization. Assessment of patients with suspected prosthetic valve dysfunction is difficult and may necessitate cardiac catheterization or even direct surgical inspection for conclusive information.     

多巴酚丁胺负荷超声心动图对左心室流出道动力性梗阻的研究

目的 应用多巴酚丁胺负荷超声心动图（DSE）检测左心室流出道血流速度，分析负荷后左心室流出道动力性梗阻的原因及其意义。方法 DSE检查待除外心肌缺血性疾病患者42例，分别于试验前后检测左心室流出道血流速度、压力阶差。试验中监测心电图、血压。试验后脱机分析。结果 DSE检查前42例患者左心室流出道血流速度均在正常范围，DSE达到峰值剂量后左心室流出道血流速度均增快，其中14例左心室流出道血流速度明显增快，大于215cm／s（218～627cm／s），压力阶差大于15mmHg（19．5～627．0mmHg，1mmHg=0．133kPa）。该14例患者均有左心室肥厚，其中不对称性以室间隔基底部肥厚为著者10例，对称性肥厚者4例。DSE试验仅3例同时出现心肌节段缺血改变。有明确高血压病史8例。相关分析显示，室间隔厚度与负荷后左心室流出道血流速度呈显著相关性，以室间隔基底肥厚更为显著（r=0．61，P〈0．001）。结论 DSE检测左心室流出道血流速度和压力阶差可明确左心室流出道梗阻，对基础状态左心室流出道压差正常、心室肥厚、临床症状明显者，DSE是明确左心室流出道动力性梗阻的重要手段。     

Urgent percutaneous transluminal septal myocardial ablation for left ventricular outflow tract obstruction exacerbated after surgical aortic valve replacement

Percutaneous transluminal septal myocardial ablation (PTSMA) is an established procedure for treating symptomatic hypertrophic obstructive cardiomyopathy. We report a case of urgent PTSMA for treating refractory heart failure due to exacerbated obstruction of the left ventricular outflow tract after surgical aortic valvular replacement to treat severe aortic stenosis.     

MRI诊断肥厚型梗阻性心肌病继发感染性心内膜炎二尖瓣穿孔一例

正患者女,56岁,咳嗽、咳痰,发热3个月。患者于2015年1月31日受凉后出现咳嗽、咯黄痰,伴发热,当地诊所给予对症治疗;2015年2月3日因意识障碍,就诊当地医院,测体温达40℃,后出现昏迷,经过抗感染治疗,于2015年2月26日后未出现发热,2015年3月27日再次出现咳嗽、咯黄痰,伴有胸闷,夜间不能平卧来我院就诊。体格     

Provocation of left ventricular outflow tract obstruction in patients with hypertrophic cardiomyopathy

Several provocation maneuvers are described in hypertrophic cardiomyopathy to Doppler echocardiographically distinguish the obstructive from the non obstructive type. No data are available about the value of orthostasis testing in comparison with nitrate application in this disease. In this study, 16 consecutive patients with hypertrophic cardiomyopathy were examined. 11 patients with hypertrophic cardiomyopathy were classified as obstructive, 5 patients with hypertrophic cardiomyopathy as non obstructive. Normal left ventricular outflow tract velocities as detected by the Doppler method were defined as < 2,0 m/s. Doppler echocardiographic measurements were performed after 10 minutes in supine position, within 10 minutes after head-up tilt and again, within 10 minutes in supine position. If systolic blood pressure during this examination exceeded 100 mm Hg 2,5 mg isosorbiddinitrate were sprayed sublingually. Measurements were done after 20 minutes in supine position and within 10 minutes after head-up tilt. Only in 7 of the 11 patients with hypertrophic obstructive cardiomyopathy maximal left ventricular outflow tract velocity in supine position measured > 2,0 m/s (2,2 ± 0,8). During head-up tilt, all patients showed increased values (3,8 ± 1,2 m/s). No differences in maximal left ventricular outflow tract velocity between head-up tilt and nitrate application in supine position (3,5 ± 1,4 m/s) were present. All patients with hypertrophic non obstructive cardiomyopathy showed maximal left ventricular outflow tract velocities < 2,0 m/s in every step of the examination. Consequently, orthostasis testing was able to identify all patients with hypertrophic obstructive cardiomyopathy and demonstrated a diagnostic value similar to nitrate application.     

Relationship between mitral regurgitation and left ventricular outflow obstruction in hypertrophic cardiomyopathy

To clarify the relationship between mitral regurgitation and left ventricular outflow obstruction, Doppler and two-dimensional echocardiographic studies were performed in 62 patients with hypertrophic cardiomyopathy (22 with and 40 without obstruction caused by mitral systolic anterior motion with septal contact). Pulsed Doppler echocardiography with color Doppler flow imaging demostrated that in 20 of the 22 patients with obstruction, mitral regurgitation occurred mainly during midsystole from the onset to the end of mitral-septal contact. Such midsystolic mitral regurgitation was not observed in patients without obstruction, except in three of 25 patients with mild mitral systolic anterior motion without septal contact. Furthermore, that regurgitation developed or disappeared together with the obstruction during follow-up periods or pharmacologic interventions. Two-dimensional echocardiography showed that in 21 of the 22 patients with obstruction, a distal residual portion of the "anterior" mitral leaflet moved anteriorly in early systole and protruded into the outflow tract during midsystole to cause the obstruction. In the other patient with obstruction, who had only early systolic mitral regurgitation, a distal residual "posterior" leaflet moved similary. These results may indicate that the midsystolic mitral regurgitation is hydrodynamically induced by the midsystolic pressure gradient across the protruding distal residual anterior mitral leaflet.     

Dynamic left ventricular outflow tract obstruction induced by dobutamine stress echocardiography leading to myocardial ischemia and infarction

Left ventricular outflow tract (LVOT) obstruction occurring during dobutamine stress echocardiography (DSE) occurs in approximately 15-20% of patients undergoing DSE. The clinical significance and mechanism of LVOT obstruction has been debated, but is now generally felt to result from the pharmacological effects of dobutamine in increasing inotropy and causing peripheral vasodilation. It must be realized that in rare instances, ischemia may occur and lead to wall motion abnormalities and eventually myocardial infarction. We present the case of a 70-year-old asymptomatic woman who underwent a routine pre-operative cardiac stress evaluation and was found to develop a dynamic outflow tract obstruction leading to myocardial ischemia and infarction.     

4D flow MRI left atrial kinetic energy in hypertrophic cardiomyopathy is associated with mitral regurgitation and left ventricular outflow tract obstruction

To noninvasively assess left atrial (LA) kinetic energy (KE) in hypertrophic cardiomyopathy (HCM) patients using 4D flow MRI and evaluate coupling associations with mitral regurgitation (MR) and left ventricular outflow tract (LVOT) obstruction. Twenty-nine retrospectively identified patients with HCM underwent 4D flow MRI. MRI-estimated peak LVOT pressure gradient (?P_MRI) was used to classify patients into non-obstructive and obstructive HCM. Time-resolved volumetric LA kinetic energy (KE_LA) was computed throughout systole. Average systolic (KE_LA-avg) and peak systolic (KE_LA-peak) KE_LA were compared between non-obstructive and obstructive HCM groups, and associations to MR severity and LVOT ?P_MRI were tested.The study included 15 patients with non-obstructive HCM (58.6 [45.9, 65.2] years, 7 females) and 14 patients with obstructive HCM (51.9 [47.6, 62.6] years, 6 females). Obstructive HCM patients demonstrated significantly elevated instantaneous KE_LA over all systolic time-points compared to non-obstructive HCM (P?<?0.05). Obstructive HCM patients also demonstrated higher KE_LA-avg (14.8 [10.6, 20.4] J/m³ vs. 33.4 [23.9, 61.3] J/m³, P?<?0.001) and KE_LA-peak (22.1 [15.9, 28.7] J/m³ vs. 57.2 [44.5, 121.4] J/m³, P?<?0.001) than non-obstructive HCM. MR severity was significantly correlated with KE_LA-avg (rho?=?0.81, P?<?0.001) and KE_LA-peak (rho?=?0.79, P?<?0.001). LVOT ?P_MRI was strongly correlated with KE_LA metrics in obstructive HCM (KE_LA-avg: rho?=?0.86, P?<?0.001; KE_LA-peak: rho?=?0.85, P?<?0.001).In HCM patients, left atrial kinetic energy, by 4D flow MRI, is associated with MR severity and the degree of LVOT obstruction.

     

Obstructive left ventricular hypertrophy. Reversibility of outflow tract obstruction by drug therapy.

We report the cases of four patients with secondary left ventricular hypertrophy (three due to hypertension and one to aortic stenosis) in whom Doppler echocardiography showed dynamic left ventricular outflow tract obstruction and marked impairment of diastolic filling. Each patient derived marked symptomatic benefit from treatment with either a beta-blocker (atenolol) or calcium antagonist (verapamil). Repeat Doppler studies in three patients revealed a substantial improvement in systolic and diastolic flow abnormalities. Ventricular outflow tract obstruction should be recognized as occurring in a subgroup of patients with secondary left ventricular hypertrophy, and its presence should be sought by Doppler echocardiography before embarking on therapy. Negatively inotropic or positively lusitropic agents such as beta-blockers and rate-limiting calcium antagonists appear to be logical therapy for this condition.     

Contribution of mitral valve leaflet length and septal wall thickness to outflow tract obstruction in patients with hypertrophic cardiomyopathy

We sought to examine whether elongation of the mitral valve leaflets in patients with hypertrophic cardiomyopathy (HCM) is synergistic to septal wall thickness (SWT) in the development of left ventricular outflow tract obstruction (LVOTO). HCM is a common genetic cardiac disease characterized by asymmetric septal hypertrophy and predisposition towards LVOTO. It has been reported that elongation of the mitral valve leaflets may be a primary phenotypic feature and contribute to LVOTO. However, the relative contribution of this finding versus SWT has not been studied. 152 patients (76 with HCM and 76 non-diseased age, race and BSA-matched controls) and 18 young, healthy volunteers were studied. SWT and the anterior mitral valve leaflet length (AMVLL) were measured using cine MRI. The combined contribution of these variables (SWT × AMVLL) was described as the Septal Anterior Leaflet Product (SALP). Peak LVOT pressure gradient was determined by Doppler interrogation and defined as “obstructive” if?≥?30 mmHg. Patients with HCM were confirmed to have increased AMVLL compared with controls and volunteers (p?<?0.01). Among HCM patients, both SWT and SALP were significantly higher in patients with LVOTO (N?=?17) versus without. SALP showed modest improvement in predictive accuracy for LVOTO (AUC?=?0.81) among the HCM population versus SWT alone (AUC?=?0.77). However, in isolated patients this variable identified patients with LVOTO despite modest SWT. Elongation of the AMVLL is a primary phenotypic feature of HCM. While incremental contributions to LVOTO appear modest at a population level, specific patients may have dominant contribution to LVOTO. The combined marker of SALP allows for maintained identification of such patients despite modest increases in SWT.     

Cyclic appearance of left ventricular outflow tract dynamic obstruction during mechanical ventilation: evidence for a preload dependent phenomenon

The cyclic appearance of dynamic left ventricular outflow tract obstruction during mechanical ventilation, according to the phasic changes in preload, is described in this article. Hemodialysis-induced fluid removal resulted in preload dependence as evidenced by the pulse pressure variation in a 56-year-old critically ill patient. The clinical picture was suggestive of myocardial failure. Transthoracic echocardiography disclosed dynamic left ventricular outflow tract obstruction associated with systolic anterior motion of the mitral valve. Progressive fluid restitution resulted in a parallel decrease in both the degree of dynamic obstruction and pulse pressure variation. During fluid loading, dynamic obstruction disappeared at first during the inspiratory phase of intermittent positive pressure ventilation corresponding to the phasic increase in left ventricular preload. Further fluid loading resulted in the disappearance of dynamic obstruction during both inspiratory and expiratory phase of intermittent positive pressure ventilation. This is the first reported case clearly relating left ventricular outflow tract dynamic obstruction to preload dependence during mechanical ventilation in a critically ill patient without predisposing anatomical factor.