Valve In Systole Research Articles

659 LEFT ATRIAL MYXOMA IN A PATIENT PRESENTING WITH ACUTE CORONARY SYNDROME: IS EMBOLISM THE PATHOPHYSIOLOGICAL MECHANISM?

Abstract Background Cardiac myxomas, though uncommon, do represent the most frequent primary cardiac neoplasms in human beings. Their clinical presentation is mainly due to flow obstruction, cytokines hyperincretion or embolism. Coronary embolism related to the tumor is a rare finding. Here we describe the case of a left atrial cardiac myxoma with an acute coronary syndrome presentation. Case presentation A 71 year-old woman referred for chest pain, nausea and vomit. On the previous few months she had developed exertional dyspnea and fatigue. No prior history of cardiovascular diseases was reported. The 12-lead ECG showed no significant alterations. Troponin T values were elevated (224 ng/L, normal assay threshold <14 ng/L). Transthoracic echocardiogram displayed left apical akynesia and a bulky left atrial mass protruding through the mitral valve in systole. Coronary angiography showed complete distal occlusion of the left anterior descending (LAD) coronary artery. Thromboaspiration allowed for the retrieval of small-sized non-thrombotic material in the culprit vessel, without angiographic signs of atherosclerotic disease, thus hinting at the embolic nature of LAD occlusion. The patient was then referred to the surgical theatre for removal of the atrial mass, which showed a 4.3×3.4×3.2 cm translucid, lobulated and gelatinous neoformation attached to the interatrial septum via a 1.5×1.2 cm stalk. The mass was surgically removed and the interatrial septum was repaired with a pericardium patch. Hystology was consistent with left atrial myxoma. The hospitalization course was uneventful. Conclusion We reported a case of acute coronary syndrome due to left atrial myxoma. Coronary embolization induced by a cardiac myxoma is rare; however, it should be suspected in patients presenting with myocardial infarction without adjunctive coronary risk factors.

EP04.40: Case report of Ebstein's anomaly which dynamic slow‐motion display was useful for a diagnosis of the functional pulmonary atresia

A 23-year-old woman was referred for fetal echocardiography at 19 weeks' gestation because of suspected cardiomegaly. Fetal echocardiography demonstrated a cardiomegaly (cardiothoracic area ratio was 45%) and severe tricuspid valve insufficiency in the 4 chambers. We diagnosed Ebstein's anomaly. The pulmonary artery flow was observed in an anterograde direction. At 32 weeks' gestation, fetal echocardiography showed severe cardiomegaly (cardiothoracic area ratio was 55%) and the pulmonary artery flow was observed in a retrograde direction. On more careful investigation of using the dynamic slow-motion display, a little regurgitation flow to a pulmonary valve in end systole could be visualised. Therefore, we diagnosed functional pulmonary atresia. Because the dynamic slow-motion display can depict an image by slow motion without deteriorating, it is useful for a diagnosis of the functional pulmonary atresia.

Role of coaptation imaging of mitral valve on ischemic mitral regurgitation by real-time three-dimensional transesophageal echocardiography

Objective To explore the impact of morphological changes of mitral valve coaptation on ischemic mitral regurgitation (IMR), and observe coaptation image of mitral valve in systole in patients with IMR by using real-time three-dimensional transesophageal echocardiography (RT3D-TEE). Methods RT3D-TEE was performed on 112 patients with IMR and 38 patients without MR as the control. Patients with IMR were divided into group of mild IMR (n=46), group of moderate IMR (n=45) and group of severe IMR (n=21), according to the severity of mitral regurgitation. Mitral valve quantification (MVQ) software of Qlab 8.1 was used for image post-processing of RT3D-TEE. The coaptation parameters was measured, included length of anterior combination(LCA3dlf), length of posterior combination(LCP3dlf), area of anterior combination(A3DTANT) and area of posterior combination(A3DTPOST) at end-systole. Then, these coaptation parameters of mitral valve were compared statistically. Logistic regression assessing was applied for analyzing the results. Results Coaptation line of anterior and posterior leaflets was almost same in normal subjects. With increasing of mitral regurgitation, a tendency to prolong in LCA3dlf and LCP3dlf were observed in IMR (P<0.05). Compared to that in mild and moderate IMR groups, besides A3DTANT and A3DTPOST, LCA3dlf and LCP3dlf were also increased significantly in severe IMR group (P<0.05). LCP3dlf was an independent correlation factor of IMR by Logistic regression analysis. The sensitivity was 73.3% and the specificity was 94.7% when LCP3dlf ≥32 mm was regarded as cut-off point, and the area under the ROC curve was 0.949 (0.900~0.999). Conclusions Abnormal coaptation of anterior and posterior leaflets of mitral valve might be one of main cause of IMR. Involution structure of mitral valve before surgery is helpful for surgeon to select an optical surgical procedure and evaluate effects of treatment in patients with IMR. Key words: Echocardiography, real-time three-dimensional; Echocardiography, transesophageal; Mitral valve insufficiency; Myocardial ischemia

Rapid valve prosthesis deterioration coupled with recurrent giant myxoma in a young asymptomatic adult

An 18-year-old female with no past cardiovascular history was admitted to the emergency room due to dyspnoea, reduced exercise tolerance, and mild systolic murmur along the right sternal border. Bedside echocardiography documented a giant polypoid tumour filling the right ventricle (RV), protruding to the right atrium and occluding tricuspid valve in systole. No tricuspid regurgitation and valve stenosis was recorded (Fig. 1A). A second mass located in the left atrium was attached to the atrial septum. With the diagnosis of myxoma, the patient was referred for computed tomography (Fig. 1B) and subsequent surgery. The masses were excised together with tricuspid valve due to extensive, irreparable damage to the anterior leaflet, and mitral biological pericardial prosthesis was implanted. Due to atrioventricular II-block, the patient required permanent pacemaker implantation. The patient remained asymptomatic and was discharged on the eighth postoperative day. Three months later, elective echocardiography revealed hyperechogenic masses in RV (1.5 × 1 cm), raising suspicion of a substantial thrombus formation (Fig. 1C). Additionally, the concomitant, moderate and centrally-located regurgitation of the valve prosthesis was recorded. A repeated echocardiogram performed after three months of anticoagulative therapy documented enlargement of the tumour diameter to 2.0 × 3.5 cm and a significant progression of prosthesis regurgitation. Second surgical inspection revealed a giant multiple myxoma which was subsequently excised (Fig. 1D, E). Leaflets of the prosthesis were thicker, stiff and shortened (Fig. 1F). Due to rapid biological valve degeneration, mechanical prosthesis was implanted. The postoperative course was uneventful. In 12 months of follow-up, no recurrence of myxoma was recorded. Herein we present a unique case of unexpected rapid biological prosthesis deterioration coupled with a giant RV multiple myxoma, early after surgical tumour excision and valve implantation. This case elucidates the requirement for short-term follow-up in patients with a primary diagnosis of multiple myxoma.

Three-dimensional Echocardiography Is Not Essential for Intraoperative Assessment of Mitral Regurgitation

The problem is not what you see on intraoperative echocardiography; it is what you do not see. Intraoperative transesophageal echocardiography and 3-dimensional (3D) echocardiography provide useful information for the surgeon performing mitral valve surgery, but they are not indispensable. We should consider the outstanding results of the pioneer of mitral valve repair, Professor Alain Carpentier. A report of very late results (>20 years) of the earliest series (1970–1984) of mitral valve repair is informative.1 Even without the availability of intraoperative transesophageal echocardiography, the late results were outstanding. At 20 years, freedom from reoperation was 96.9% for patients with posterior leaflet prolapse and 86.2% for patients with anterior prolapse. At the last follow-up (median, 17 years) 15% had moderate or worse mitral regurgitation. An experienced mitral valve surgeon can achieve durable high-quality results without any echocardiography, so 3D echocardiography is not essential. Response by Tsang and Lang on p 658 What is essential for mitral valve surgery? The fundamental elements from the surgical standpoint are the same whether the procedure is performed through a sternotomy or a minimally invasive incision or is robotically assisted. Achieving good surgical exposure is paramount.2 Numerous surgical techniques, including the type and location of venous cannulation, the atrial incision, retraction of the atrial wall, sutures to help rotate the valve and improve visualization, and occasionally the use of an instrument pushing from outside the heart to facilitate exposure of commissures or the anterior leaflet, are routine practice to optimally visualize the valve. Unless the surgeon is expert in the first step of the procedure, results will be compromised. A perfect 3D echocardiography image of the valve will not compensate for poor exposure. Although real-time 3D color echocardiography is useful, there is nothing more realistic than real-time 3D color visualization through 2.5-power loupes by the …

In Vitro Images of a Double Orifice Mitral Valve in a Reanimated Human Heart

Using Visible Heart® methodologies [1] the heart from a 45 year old male (BMI 30.4, pre-op BP 145/70, HR 107, regular rhythm and normal heart tones), deemed not viable for transplant to a recipient patient, was explanted to an isolated heart apparatus. Briefly, this methodology utilizes a clear Krebs-Henseleit buffer to provide nutrients and oxygen to the heart and allow for native ex-vivo functionality while providing the opportunity to visualize the internal anatomy with endoscopes. Upon reanimation LV and LA pressures were 95/12mmHg and 13/15mmHg respectively during sinus rhythm. The patient’s heart presented with no signs of any other congenital pathology and a pre-operative ultrasound indicated a 65% LV ejection fraction, normal chamber dimensions and trivial mitral regurgitation. The double orifice mitral valve can best be defined as an incomplete bridge, situated toward the superior commissure of the valve and supported by the superolateral (anterolateral) papillary muscle. Shown here is a series of four screenshots of the valve in both systole (Figure 1 A&B) and diastole (Figure 1 C&D) from the left atrium (Figure 1 A&C) and the left ventricle (Figure 1 B&D). These images clearly show the fibrous connection between the mural (posteroinferior) and aortic (anterosuperior) leaflets in the central region. Interestingly, the chronic presence of the fibrous bridge in this patient has had seemingly negligible effect on overall cardiac performance. Functional video footage of the valve can be accessed via the link provided (An accompanying video for this article can be viewed on the Internet at http://ats.ctsnetjournals.org/content/volNUMBER/issueNUMBER/images/data/PAGE/DC1/FILENAME). Figure 1

Imaging Phenotype Versus Genotype in Hypertrophic Cardiomyopathy

Hypertrophic cardiomyopathy (HCM) is a common monogenetic cardiac disease with a prevalence of 0.2%1 that usually is inherited as an autosomal dominant trait with variable penetrance and expression. Clinically, HCM is defined by the presence of left ventricular (LV) hypertrophy (LVH) unexplained by abnormal loading conditions.1 The natural history varies from an asymptomatic course to drug-refractory angina/dyspnea, sudden cardiac death (SCD), and end-stage heart failure. The incidence of HCM-related SCD is approximately 1% to 2% in children and adolescents and 0.5% to 1% in adults.2,3 In this review, we examine the impact of advanced diagnostic imaging technologies on HCM, with particular emphasis on the detection of particular genetic subtypes. In ≈60% of cases, HCM is inherited as an autosomal dominant trait caused by mutations in genes coding for cardiac sarcomere proteins (Figure 1).4–7 Mutations in genes encoding Z-disc proteins and proteins involved in calcium regulation account for <5% of cases. The absence of sarcomeric gene mutations can be explained by limitations of current mutation detection techniques or mutations in as yet unidentified genes, but in some cases, hypertrophy is caused by other diseases that mimic the phenotype of sarcomeric protein disease. Table 1 lists genetic disorders associated with HCM. Figure 1. A schematic illustration of a cardiac sarcomere. View this table: Table 1. Currently Known Genes Implicated in HCM More than 600 different sarcomeric gene mutations are reported in patients with HCM.8–16 The majority are missense mutations, but nonsense, frameshift, and in-frame insertion/deletion mutations also occur. Most mutations are characterized by incomplete penetrance and variable clinical expression likely due to locus heterogeneity and the effect of mutations at different locations within the same gene. Most mutations probably have a dominant negative effect on sarcomere function, but in some cases, haploinsufficiency (ie, only a single functional …

Stroke Caused by Left Ventricular Myxoma

![Figure][1] ![Figure][1] [![Graphic][3] ][3] Transthoracic Echocardiography, Long-Axis Parasternal View A large mass is seen in the left ventricle with grapelike clusters measuring 53 × 34 × 29 mm, almost protruding through the aortic valve in systole. ![Figure][1]</img

Left ventricular myxoma in a child: a case report

Left ventricular myxoma are quite rare and have not been reported in children. We report a left ventricular myxoma arising from interventricular septum in a 12-year-old girl who presented with history of single episode of syncope while playing in school. General examination of the child did not reveal any abnormality except a grade II/VI systolic murmur in left parasternal area. Transthoracic echocardiography revealed a round pedunculated mass (18 × 30 mm) in left ventricle arising from middle of interventricular septum with a pedicle measuring 4 mm at its base. The tumour was projecting through aortic valve in systole. Syncope in this case was probably due to obstruction of left ventricular outflow tract by myxoma leading to a decrease in cardiac output. Complete excision of myxoma was done through transmitral approach.

Gestation-specific reference intervals for fetal cardiac Doppler indices for the left heart from 12 to 40 weeks of gestation

ObjectivesThe authors aimed to establish gestation specific reference intervals for Doppler indices of fetal cardiac function from 12 to 40 weeks of pregnancy.MethodsIn a cross-sectional observational study of singleton pregnancies,...

Gestation-specific reference intervals for fetal cardiac Doppler indices for the right heart from 12 to 40 weeks of gestation

ObjectivesThe authors aimed to establish gestation specific reference intervals for Doppler indices of fetal cardiac function from 12 to 40 weeks of pregnancy.MethodsIn a cross-sectional observational study of singleton pregnancies,...

Echocardiographic variables affecting surgical outcome in patients undergoing closed mitral commissurotomy

We studied, by transthoracic cross-sectional echocardiography, the influence of subvalvar pathology on the early hemodynamic result of closed mitral commissurotomy in 132 patients with severe rheumatic mitral stenosis (56 males, 76 females, mean age 25.2 yr, range 10–55) in our tertiary care hospital in North India from July 89 to December 91. The mitral subdistance ratio was calculated by dividing the distance between the papillary muscle tip and mitral valve in systole (apical 4-chamber view) by left ventricular diastolic length (apical long axis view). Nineteen patients with mild subvalvar pathology (mitral subdistance ratio > 0.18) and 71 patients with moderate, achieved a larger valve area (2.26 cm 2 SD 0.54) than 42 patients with severe subvalvar pathology (mitral subdistance ratio < 0.12, postoperative valve area 2.09 cm 2 SD 0.6, p < 0.05). In addition, 9 of these 42 patients (21%) developed significant mitral regurgitation (4 deaths), in contrast to 1 19 with mild and 6 17 with moderate subvalvar pathology. We conclude that echocardiography identifies patients with severe subvalvar pathology who fare poorly after closed mitral commissurotomy. However, this procedure would still be practised in developing countries like ours due to financial constraints.

Flow Velocity Acceleration in the Left Ventricle: A Useful Doppler Echocardiographic Sign of Hemodynamically Significant Mitral Regurgitation

Doppler echocardiography is a sensitive method to detect mitral regurgitation in patients with both native and prosthetic valves. However, estimates of the amount of mitral regurgitation remain semiquantitative, and even severe mitral regurgitation may be underestimated in the presence of markedly eccentric regurgitant jets or acoustic shadowing of the left atrium by mitral or aortic prostheses. This report describes the Doppler findings in 10 patients with severe native valve mitral regurgitation (angiographic grade III or IV) and in 15 patients with severe bioprosthetic mitral regurgitation that required valve replacement. An increase in peak mitral flow velocity above normal values was seen in eight of 10 patients with severe native valve mitral regurgitation (greater than or equal to 130 cm per second) and 11 of 15 patients with severe prosthetic valve mitral regurgitation (greater than or equal to 210 cm per second). One of 10 patients with a native valve and four of 15 patients with a bioprosthetic valve appeared to have only a localized left atrial systolic flow disturbance, incorrectly suggesting that the mitral regurgitation was mild. However, in all patients with severe mitral regurgitation, a low velocity (less than 100 cm per second) flow signal could be recorded in the left ventricle that was directed toward the mitral valve in systole. This flow signal showed a gradual increase in velocity as the sample volume was moved toward the mitral valve, with an abrupt further increase on entry into the left atrium. This signal was continuous with antegrade mitral flow and had the same orientation as mitral regurgitation recorded by continuous wave technique from the apex. A similar flow signal was not recorded in the left ventricle of any individual in a control group of 30 patients who had no mitral regurgitation or who had angiographic grade I or II mitral regurgitation. These findings suggest that acceleration of left ventricle flow toward the mitral valve in systole is only recorded when there is hemodynamically significant mitral regurgitation that is approximately equal to angiographic grade III or IV. Recognition of this Doppler finding may help in the estimation of mitral regurgitation severity, especially in difficult diagnostic situations.

Diagnosing tricuspid regurgitation by direct imaging of the regurgitant flow in the right atrium using contrast echocardiography

To determine whether tricuspid regurgitation (TR) can be diagnosed by direct imaging of regurgitant flow in the right atrium (RA) using contrast echocardiography, echocardiography was performed in 35 patients using peripheral intravenous injections of 5% dextrose solution. Fifteen patients had TR judged by v-wave synchronous contrast appearance on the inferior vena cava echogram (a previously validated method for diagnosing TR), 5 of whom had clinically obvious TR. Twenty patients had no TR on inferior vena cava contrast echocardiography, 9 of whom were normal volunteers. On subsequent blind review, 13 of the 15 patients with TR were correctly identified on the basis of the regurgitant contrast flow just posterior to the tricuspid valve in the RA. Of the 20 without TR, 19 were correctly identified and there was 1 false-positive result. Using different criteria for the diagnosis (insisting on imaging of flow across the tricuspid valve in systole), another blinded observer correctly diagnosed only 8 of the 15 patients as having TR, but had no false-positive results. To avoid false-positive results, it is important to realize that there are 2 regions where retrograde flow can normally be seen in the RA: (1) briefly at the onset of systole coincident with tricuspid valve closure, and (2) in the posterior RA, as distinct from the anterior RA area just behind the tricuspid valve where TR is diagnosed in this study. It is concluded that direct imaging of regurgitant flow in the RA just posterior to the tricuspid valve is an accurate method for diagnosing or excluding TR and is ideally complementary to inferior vena cava contrast echocardiography in making this diagnosis.

Incidence of Ruptured Chordae Tendineae in the Mitral Valvular Prolapse Syndrome: An Echocardiographic Study

Echocardiographic studies were performed in 190 consecutive patients with mitral valvular prolapse. All patients had either midsystolic posterior motion of the mitral valve or holosystolic hammock-like movement of the valve in systole. Thirteen patients (7 percent) were noted to have ruptured chordae tendineae. In four patients, a combination of abnormalities was observed. Five patients had clinical and bacteriologic evidence of infective endocarditis, two of whom had severe intractable pulmonary edema consequent to acute mitral regurgitation which required mitral valvular replacement. At surgery, one of these patients had ruptured chordae tendineae to both leaflets, and the other had chordal rupture of the posterior leaflet. The other patients probably had spontaneous rupture of the chordae tendineae. A spectrum of clinical findings was noted. Six patients had marked mitral regurgitation, while two had isolated systolic clicks. Thus, chordal rupture does not always result in severe hemodynamic deterioration. Serial echocardiographic studies will be of value in studying the natural history and progression of disease in patients with chordal rupture.

Echocardiographic, angiocardiographic, and surgical correlations in right ventricular myxoma simulating valvar pulmonic stenosis.

The echocardiographic, angiographic and surgical correlations in a patients with a right ventricular myxoma simulating valvar pulmonic stenosis are presented. A dense mass of echoes was seen in the body of the right ventricle in diastole; in the right ventricular outflow tract throughout the cardiac cycle; and within the pulmonic valve in systole. These echocardiographic findings suggested the presence of a mass high in the right ventricle, which moved throught the pulmonic valve in systole. This impression was confirmed by angiography and surgery. A 53 mmHg gradient across the pulmonic valve was noted at cardiac catheterization. At operation a myxoma which originated above the crista supraventricularis was found. The tumor moved into the main pulmonary artery in systole. Surgical removal of the tumor resulted in the disappearance of the abnormal echoes.

Echocardiographic detection of tricuspid valve prolapse.

The echocardiographic findings in 12 patients with tricuspid valve prolapse are presented. Eight of these patients had associated mitral valve prolapse. Only one of the above patients had the characteristic physical signs of tricuspid incompetence. Two types of abnormality were noted on the echocardiogram of the tricuspid valve. In eight patients, the systolic segment of the tricuspid valve showed an initial horizontal motion followed by a posterior motion in midsystole. Four patients exhibited posterior motion of the tricuspid valve in early systole, which reached a maximum in midsystole, and this was followed by an anterior motion, thus producing a hammock-like configuration. We conclude that echocardiography is useful in the diagnosis of tricuspid valve prolapse. Since this condition may be associated with clinically significant tricuspid incompetence or bacterial endocarditis, its recognition is of clinical importance.

Echocardiography of the tricuspid valve in congenital left ventricular-riht atrial communication.

Two patients, ages 14 and 18, with congenital left ventricular-right atrial communication through a defect in the tricuspid valve were studied by echocardiography. Proof was obtained by angiocardiography and surgery in one and ultrasonic contrast injection and angiocardiography in the other. Both presented clinically as uncomplicated ventricular septal defects. Echocardiography consistently demonstrated a high frequency, low amplitude flutter of the tricuspid valve in systole and none in diastole. Following surgical correction of the defect in one patient, there was complete disappearance of the systolic flutter. Systolic flutter has not been observed with tricuspid incompetence nor with other forms of ventricular septal defects. Fistulous communication from the aorta to the right atrium just above the tricuspid valve did not demonstrate systolic flutter in one patient studies. Tricuspid valve systolic flutter appears to be caused by the passage of the left ventricular jet blood into the right atrium through a defect in the tricuspid valve. Echocardiographic study of the tricuspid valve is of value in the recognition of the congenital left ventricular-right atrial communication.

Use of echocardiography in patients with prolapsed mitral valve.

The echocardiographic findings are described for five patients who had the prolapsed mitral valve syndrome, proven by cardiac catheterization and angiocardiography. In all five patients, the echocardiograms demonstrated posterior displacement of the posterior mitral leaflet during systole. In four of the patients there was also posterior displacement of the anterior leaflet. Four of the five patients had mitral insufficiency, demonstrated by cineangiography. These four patients demonstrated echocardiographic separation of the anterior and posterior leaflets of the mitral valve in late systole. The fifth patient did not show this separation, and she had no mitral insufficiency by selective cineangiography. Two patients were given amyl nitrite during the echocardiographic examination, and the echogram showed earlier separation of the anterior and posterior leaflets as well as lengthening of the murmur. Echocardiography should be a very useful noninvasive, yet direct, method for diagnosing, studying, and following patients with prolapse of the mitral valve.

Use of echocardiography in patients with prolapsed mitral valve

The echocardiographic findings are described for five patients who had the prolapsed mitral valve syndrome, proven by cardiac catheterization and angiocardiography. In all five patients, the echocardiograms demonstrated posterior displacement of the posterior mitral leaflet during systole. In four of the patients there was also posterior displacement of the anterior leaflet. Four of the five patients had mitral insufficiency, demonstrated by cineangiography. These four patients demonstrated echocardiographic separation of the anterior and posterior leaflets of the mitral valve in late systole. The fifth patient did not show this separation, and she had no mitral insufficiency by selective cineangiography. Two patients were given amyl nitrite during the echocardiographic examination, and the echogram showed earlier separation of the anterior and posterior leaflets as well as lengthening of the murmur. Echocardiography should be a very useful noninvasive, yet direct, method for diagnosing, studying, and following patients with prolapse of the mitral valve.