Pseudoaneurysm of the left ventricular outflow tract after cardiac surgery

Pseudoaneurysms of the left ventricular outflow tract (LVOT) are rare entity. We present a case of false aneurysm caused by a chronic bacterial infection after mechanical aortic valve replacement in otherwise healthy and asymptomatic young man.     

Delayed pericardial tamponade after penetrating chest trauma.

Delayed pericardial tamponade (PT) after penetrating heart trauma is now a rare condition as a result of advances in medical and surgical management. We report the case of a 32-year-old man with delayed PT after a stab wound from a knife. The initial evaluation was consistent with a traumatic apical myocardial infarction. After an uneventful initial course, the patient developed acute PT, which required emergency surgery. A thrombus was discovered over a laceration in the mid-segment of the left anterior descending artery and a simple suture was performed.     

Mesenteric thrombosis after penetrating cardiac trauma.

Survival of the severely injured trauma victim through aggressive therapy results in new complications. We report the first instance of mesenteric thrombosis in association with penetrating cardiac trauma. Selective visceral angiography should be obtained early in a patient with persistent abdominal pain following a period of prolonged shock; such cases should have a more favorable prognosis if diagnosed early in view of the limited period of cardiac dysfunction and the younger age group.     

Anteroapical stunning and left ventricular outflow tract obstruction

Dynamic left ventricular outflow tract (LVOT) obstruction is typically observed in the setting of hypertrophic cardiomyopathy. It has also been reported with concentric LV hypertrophy, excessive sympathetic stimulation, and acute myocardial infarction. We describe 3 patients with chest discomfort after emotional stress, who had pronounced abnormalities on electrocardiograms, insignificant obstructive coronary disease and hemodynamic instability with LVOT obstruction, and regional wall motion abnormalities. Suppression of contractility with beta-blockers resulted in resolution of the gradient and in clinical improvement. On follow-up, functional recovery was excellent, and ventricular function had normalized. The conditions and mechanisms that may produce this sequence of events are discussed. The most probable scenario is that an acute ischemic insult secondary to vasospasm, LV stunning, and acute geometric remodeling produced a substrate for LVOT obstruction that was exacerbated by basal LV hypercontractility. The importance of this observation is that routine treatment of cardiogenic shock cannot be used and that conservative management results in excellent prognosis.     

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.     

Obstruction of left ventricular outflow tract by vegetation and periaortic abscess.

Echocardiography is the modality of choice for the noninvasive recognition of vegetations and abscesses that complicate endocarditis. Vegetation size is highly variable, and it has been suggested that large vegetations are related to a more complicated course. The case we present is unusual in that the echocardiographically detected vegetation was very large, highly mobile, and caused severe obstruction of the left ventricular outflow tract, which led to impaction and cardiac arrest.     

Traumatic left ventricular false aneurysm with significant regurgitation from left ventricular outflow tract to left atrium: delineation by two-dimensional and color flow Doppler echocardiography

A 22-year-old man was asymptomatic 23 months after an automobile accident but had clinical evidence of progressive mitral insufficiency. Two-dimensional and color flow Doppler echocardiography demonstrated a false aneurysm adjacent to the left ventricular outflow tract and significant regurgitation of blood through a traumatic channel from the left ventricular outflow tract to the left atrium. The patient underwent successful surgical closure of the false aneurysm and repair of the traumatic left atrial regurgitation.     

Calculation of left ventricular outflow tract area using three-dimensional echocardiography

In 23 patients with aortic valve stenosis (14 male, 9 female, mean age 66 ± 21.5 years) left ventricular outflow tract cross-sectional area was determined in planimetric fashion using three-dimensional echocardiography. The 3-D data-set for each patient had been acquired in the course of a multiplane transesophageal examination. Aortic valve area was determined using the continuity equation. Results obtained were compared to those calculated by continuity equation using to the conventionally determined LVOT area (a = π [d/2]2). As reference method the results were compared to invasive measurements. 3-D planimetric determination of LVOT cross-sectional area was possible in 20 of 23 patients. In three patients, this method failed due to artefacts. The mean difference to the conventionally calculated LVOT area amounted to 0.18 cm2 (SD = 0.46). The comparison of AVA determined by continuity equation and by invasive measurement showed a mean difference of ?0.074 cm2 (SD = 0.21) for the conventionally calculated LVOT area; for the planimetrically determined LVOT area the mean difference of AVA amounted to ?0.03 cm2 (SD = 0.14) (p < 0.05). Planimetric determination of LVOT area using 3-D echocardiography improves the agreement of the continuity equation with invasive measurement.     

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.     

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.     

左室流出道室性心律失常的射频消融治疗

目的 探讨起源于左室流出道少见部位的室性心动过速和/或频发室性早搏的心电图特点和射频消融治疗.方法 3例左室流出道室速和/或室早患者,术中进行激动和起搏标测,同时结合冠状动脉造影或三维电解剖标测系统(CARTO)定位.结果 3例患者中2例体表心电图特点类似右室流出道间隔部室速及室早,经腔内电生理证实起源于主动脉根部右冠窦内.1例起源于主动脉瓣-二尖瓣连接区(AMC),该部位室速及室早特有的典型心电图表现为II、III、aVF及所有胸前导联QRS波均呈R形.3例患者消融后观察2~24个月,均无复发.结论 右冠窦和AMC是左室流出道室速和/或室早的少见特殊起源部位,根据体表心电图形态,结合多种腔内标测技术及冠脉造影,能进行准确定位及成功消融.     

Delayed presentation of thoracic esophageal perforation after blunt trauma

Thoracic esophageal perforation after blunt trauma is a rare injury with high mortality. Prompt recognition and aggressive treatment are paramount to survival. We report a case of delayed presentation that emphasizes the diagnostic difficulties in this traumatic injury. A review of the prevalence, diagnosis, and management is also discussed.     

Left ventricular outflow tract presystolic flow velocity--another marker of left ventricular diastolic function

Left ventricular outflow tract (LVOT) presystolic flow velocities were studied using pulse doppler echocardiography in 30 normal persons. Thirty patients of mild hypertension with transmitral flow velocity pattern suggestive of impaired relaxation were also studied. Transmitral flow velocity pattern was correlated with LVOT presystolic flow velocities in the two groups. Hypertensive patients had significantly higher transmitral A wave velocity (p < 0.001) and significantly lower transmitral E wave/A wave velocity ratio (p < 0.001) as compared to normal group. LVOT presystolic flow velocities had significant direct correlation with transmitral A wave velocity (p < 0.01) and significant inverse relation with transmitral E wave/A wave velocity ratio (p < 0.05). Our observations suggest that increased LVOT presystolic flow peak velocity can also be used as another marker of impaired left ventricular compliance during atrial contraction. More work is needed to establish exact status of this preliminary observation.     

Delayed enhancement cardiac MR imaging in noncompaction of left ventricular myocardium.

A 49-year-old female with a history of paroxysmal atrial fibrillation, presented with worsening dyspnea on minimal exertion. During the follow-up period, transthoracic echocardiography and cardiac magnetic resonance imaging (CMR) were consistent with the diagnosis of noncompaction of the left ventricle. Delayed-enhancement CMR demonstrated hyperenhancement of the prominent trabeculations located at the mid and apical portions of the left ventricle, suggesting areas of fibrosis. Although previous cases of left ventricular noncompaction diagnosed with CMR have been described in the literature, this is the first case to describe the utility of delayed-enhancement imaging in the pathohistological confirmation of myocardial fibrosis and scarring in the hypertrabeculated myocardium.     

Doppler characteristics of late-diastolic flow in the left ventricular outflow tract

This study characterizes the relationship between late-diastolic Doppler detected forward flow in the left ventricular outflow tract and diastolic transmitral flow. Pulsed-wave Doppler interrogation of the left ventricular outflow tract, in a prospective consecutive series (n = 137), revealed the presence of end-diastolic forward flow in 83% of the patients studied. Further quantification of both flow signals was performed in 67 patients. Pulsed-wave mapping demonstrated that peak velocity of the end-diastolic left ventricular outflow tract signal (J wave) was maximal, 2.6 +/- 0.7 cm from the aortic valve anulus, and occurred 48 +/- 34 milliseconds after the peak transmitral atrial velocity flow signal. Peak J velocity ranged from 25 to 118 cm per second and correlated with peak A velocity (r = 0.69, p less than 0.001). Peak J velocity was inversely related to left ventricular end-diastolic dimension (r = -0.53, p less than 0.0001) and left ventricular end-diastolic volume (r = -0.43, p less than 0.004). There was no relationship between J wave velocity and early diastolic filling. We concluded that a late-diastolic forward flow signal is commonly observed in the left ventricular outflow tract. It is a manifestation of transmitral atrial systolic flow in the left ventricular outflow tract and is determined predominantly by peak transmitral atrial velocity and left ventricular size.     

Left ventricular apicoaortic valved conduit for treating obstruction of the left ventricular outflow tract

The left ventricular-aortic conduit provides one solution to the problem of a congenital obstruction of the left ventricular outflow tract, which may result from a wide variety of conditions. The creation of a double-outlet left ventricle successfully relieves left ventricular hypertension and its sequelae. This case demonstrates one long-term complication of the left ventricular-aortic conduit--stenosis at the point of origin of the graft in the left ventricle due to endothelial proliferation, which necessitated replacement of the graft.