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Evaluation of left atrial appendage stasis in patients with atrial fibrillation using transesophageal echocardiography with an intravenous albumin-contrast agent.

To assess stasis in the left atrial appendage in patients with atrial fibrillation and to identify patients at increased risk for thromboembolism, we performed transesophageal echocardiography with an intravenous albumin contrast agent (Albunex) in 25 patients with atrial fibrillation and in 22 patients in sinus rhythm. We demonstrated that the absence of opacification in the left atrial appendage after Albunex administration implies a high risk of left atrial thrombus and cardiogenic thromboembolism.

Adult↗

A pitfall in ultrafast CT scanning for the detection of left atrial thrombi.

We studied 41 patients with mitral stenosis by ultrafast CT (UFCT) and transesophageal echocardiography to detect left atrial thrombi. Cardiac UFCT was performed twice after contrast medium injection to obtain early (during injection lasting 40-60 s) and late (approximately 5 min after beginning injection) phase images. There were 10 patients (24%) in whom a filling defect detected in the early phase disappeared in the late phase. The site of filling defects was the left atrial appendage in nine patients and the left atrium in one patient. All of the filling defects were in the ventral side of the left atrium. Furthermore, all of those patients had chronic atrial fibrillation. Transesophageal echocardiography revealed no thrombus in the area of the filling defect in the early phase. We believe that blood stasis existed in those patients. This finding leads to a false-positive result when only early phase images are obtained. The diagnosis of thrombi should be made only when a filling defect is observed in both phases. Late phase scanning is necessary in the diagnosis of left atrial thrombi.

Adult↗

Pulmonary venous pressure: relationship to pulmonary artery, pulmonary wedge, and left atrial pressure in normal, lightly sedated dogs.

Because pulmonary venous pressure has never been measured, it is unclear whether pulmonary wedge pressure measures left atrial pressure, as commonly assumed, or pressure more upstream in the pulmonary venous or capillary beds. Fluid-filled mean pulmonary artery and pulmonary wedge pressure were compared with pulmonary venous and left atrial pressure obtained with high-fidelity micromanometer catheters in eight lightly sedated dogs over a physiologic range of filling pressures. In all conditions, mean pulmonary wedge pressure was virtually identical (r = 0.99) to mean left atrial pressure (slope = 0.99; intercept = -0.46 mm Hg). At the same time, mean pulmonary venous pressure (17.1 +/- 6.5 mm Hg) was intermediate between mean pulmonary artery pressure (20.2 +/- 6.2 mm Hg) and mean pulmonary wedge pressure (13.3 +/- 6.2 mm Hg; P < 0.0001) or mean left atrial pressure (13.4 +/- 6.3 mm Hg; P < 0.0001). These relationships were maintained over normal and increased pressure ranges. As measured by conventional flow-directed pulmonary catheters, mean pulmonary wedge pressure accurately reflects left atrial pressure in lightly sedated, spontaneously breathing normal dogs.

Animals↗

Heart rate variability in isolated rabbit hearts.

The presence of heart rate variability (HRV) in patients with cardiac denervation after heart transplantation raised our interest in HRV of isolated, denervated hearts. Hearts from seven adult white ELCO rabbits were transferred to a perfusion apparatus. All hearts were perfused in the working mode and in the Langendorff mode for 20 minutes each. HRV was analyzed in the frequency domain. A computer simulated test ECG at a constant rate of 2 Hz was used for error estimation of the system. In the isolated, denervated heart, HRV was of random, broadband fluctuations, different from the well-characterized oscillations at specific frequencies in intact animals. Mean NN was 423 +/- 51 ms in the Langendorff mode, 406 +/- 33 ms in the working heart mode, and 500 ms in the test ECG. Total power was 663 +/- 207 ms2, 817 +/- 318 ms2, and 3.7 ms2, respectively. There was no significant difference in any measure of HRV between Langendorff and working heart modes. The data provide evidence for the presence of HRV in isolated, denervated rabbit hearts. Left atrial and ventricular filling, i.e., the working heart mode, did not alter HRV, indicating that left atrial or ventricular stretch did not influence the sinus nodal discharge rate.

Animals↗

Factor V Leiden mutation and its relation to left atrial thrombus in chronic nonrheumatic atrial fibrillation.

The genetic defect of coagulation factor V, known as factor V Leiden, produces a resistance to degradation by activated protein C and increased venous thrombosis. However, the role of factor V Leiden in the formation of left atrial thrombus with nonrheumatic atrial fibrillation has not been studied. We investigated whether factor V Leiden is a risk factor for left atrial thrombus in patients with nonrheumatic atrial fibrillation. We analyzed clinical, echocardiographic, and biochemical data in 105 consecutive patients with nonrheumatic atrial fibrillation. These patients were divided into two groups: group A (n = 37) with left atrial thrombus and group B (n = 68) without left atrial thrombus. The study also included 42 control subjects. Left atrial thrombus was investigated by using both transthoracic echocardiography and transesophageal echocardiography. Blood samples from the patients and controls were analyzed for the factor V Leiden mutation by DNA analysis, using the polymerase chain reaction. There was no significant difference in the prevalence of factor V Leiden between the patients and control subjects. The prevalence of factor V Leiden mutation was 8.1% (3/37) in patients with left atrial thrombus, and 8.8% (6/68) in patients without left atrial thrombus. The prevalence of factor V Leiden was 7.1% (3/42) in control subjects. The prevalance of factor V Leiden was 10% (2/20) in patients with spontaneous echo contrast and 8% (7/85) in patients without spontaneous echo contrast. Multivariate analyses showed that left ventricular ejection fraction was an independent predictor of left atrial thrombus. Factor V Leiden mutation is not a risk factor for left atrial thrombus formation and spontaneous echo contrast in patients with nonrheumatic atrial fibrillation.

Adult↗

Assessment of left atrial pressure and volume changes during atrial systole with transesophageal pulsed Doppler echocardiography of transmitral and pulmonary venous flow velocities.

To determine whether transmitral and pulmonary venous flow velocity patterns can be used to evaluate left atrial pressure and volume changes during atrial systole, we performed transesophageal pulsed Doppler echocardiography and right heart catheterization in 85 patients (20 with hypertrophic cardiomyopathy, 20 with dilated cardiomyopathy, 30 with prior myocardial infarction, and 15 with mitral regurgitation), and 35 normal subjects. Pulsed Doppler variables from transmitral and pulmonary venous flow velocities during atrial systole were compared with mean pulmonary capillary wedge pressure (mean PCWP), pressure rise during atrial systole (PCWP-A), and left atrial volume change during atrial systole (delta LAV). The mean PCWP correlated significantly with the peak atrial systolic transmitral flow (r = -0.38, p < 0.05) and pulmonary venous flow (r = 0.40, p < 0.05) velocities in all patients. The PCWP-A correlated significantly with the peak atrial systolic transmitral flow (r = -0.39, p < 0.05) and pulmonary venous flow (r = 0.68, p < 0.0001) velocities in all patients. There was a particularly close correlation between the PCWP-A and the peak atrial systolic pulmonary venous flow velocities. The sum of the time-velocity integral of the atrial systolic transmitral and pulmonary venous flow velocities (TAI) correlated closely with the delta LAV (r = 0.70, p < 0.0001) in all patients. Thus, the peak atrial systolic pulmonary venous flow velocity correlated well with left atrial pressure changes during atrial systole. Furthermore, the sum of the time-velocity integral of the atrial systolic transmitral and pulmonary venous flow velocities correlated well with left atrial volume changes during atrial systole. Therefore, transesophageal echocardiographic measurements of atrial systolic transmitral and pulmonary venous flow velocities are reasonable indicators of left atrial pressure and volume changes during atrial systole.

Adult↗

Abnormalities of pulmonary venous flow in patients with lone atrial fibrillation.

AIMS: Mechanisms underlying lone atrial fibrillation (LAF) are poorly defined. We sought to investigate indices of left atrial (LA) function in patients with recurrent LAF, in comparison with that in healthy subjects. METHODS AND RESULTS: Investigations were performed in 42 patients aged 51.8 +/- 8.7 at least 30 days after the last episode of LAF and in 38 healthy controls. Each subject underwent echocardiographic evaluation including left ventricular parameters and LA function indices. LA ejection fraction served as a measure of LA systolic performance, and acceleration (SAT) and deceleration time (SDT) of systolic phase of pulmonary venous flow (PVF) corresponded to LA relaxation and compliance, respectively. Patients with LAF showed significantly lower values of SAT (179.1 +/- 63.2 vs. 199.2 +/- 45.1 ms, P < 0.02) and higher values of SDT (250.8 +/- 81.6 vs. 211.7 +/- 57.3 ms, P < 0.01) when compared with controls. No significant differences were found with respect to other measured parameters. The combination of SAT < 185 ms and SDT > 239 ms showed a positive predictive value of 92% in the identification of patients prone to LAF. CONCLUSION: This study suggests that (i) patients with LAF have abnormalities of the systolic phase of PVF and (ii) Doppler estimation of PVF seems to be very valuable in the evaluation of patients with LAF.

Adult↗

Hemodynamic profile of a post-infarct ventricular septal defect: left atrial a-waves rather than v-waves may be a prominent feature.

The presence of prominent left atrial v-waves following interventricular septal rupture in acute myocardial infarction have been reported in the past. Hemodynamic profile obtained in one particular case highlighted some of the varying aspects of pressure wave, oxygen saturation, and compliance abnormalities that may also be present in such cases. The presence of large left atrial a-waves rather than v-waves was one of the findings.

Aged↗

Transesophageal measurement of left atrial refractoriness.

During electrophysiological evaluation of supraventricular arrhythmias the transesophageal (TEEP) approach may be the first step but is limited in information available. One difficulty is in measuring left atrial refractoriness, as left atrial capture is seldom detectable either on ECG or via an esophageal lead. The problem may be eliminated and left atrial refractoriness measured via the esophagus, utilizing two or three extrastimuli to scan diastole to determine whether the atrial refractory period has been entered by the first extrastimulus. Measurement of left atrial and/or atrioventricular node or accessory pathway refractoriness then becomes possible.

Adult↗

Time varying loading of the pulmonary circulation: a model to describe hemodynamic observations in the stiff left atrial syndrome.

OBJECTIVE: To develop a mathematical model that could explain the following observations: that right heart failure can develop in association with no other cardiac abnormality than a severe reduction in the compliance of the left atrium; and that patients with this syndrome have systolic pulmonary hypertension with left atrial v waves in the absence of either mitral regurgitation or left ventricular dysfunction. DESIGN: A model of the pulmonary circulation was designed with a time varying terminal hydraulic load, which was varied between a noncompliant left atrium during systole and a compliant left ventricle/left atrium combination during diastole. Using representative parameters and a pulmonary arterial flow wave as input, pressures in the pulmonary artery and left atrium and right ventricular power output were calculated. RESULTS: Pulmonary arterial and left atrial systolic pressures are increased as left atrial compliance is reduced. The time varying change in terminal load results in an increase in systolic pressures, whereas diastolic pressures remain normal. A decrease in left atrial compliance increases both the nonpulsatile and pulsatile components of pulmonary input impedance, whereas only the nonpulsatile component of right ventricular power output is increased. CONCLUSIONS: The time varying pulmonary load model of the pulmonary circulation, in the presence of a reduced left atrial compliance results in pulmonary, and left atrial pressures similar to those observed in patients with the stiff left atrial syndrome. The resulting increase in right ventricular power output could be an important factor in the development of right heart failure.

Aged↗

The coagulation system is activated in idiopathic cardiomyopathy.

OBJECTIVES: We investigated the plasma levels of molecular markers for platelet activity and the thrombotic and fibrinolytic status in patients with hypertrophic cardiomyopathy and dilated cardiomyopathy to determine the activating site of coagulation in these disorders. BACKGROUND: A thromboembolic event is a serious complication in patients with idiopathic cardiomyopathy. However, the activating site of the coagulation system in idiopathic cardiomyopathy has not been fully investigated. METHODS: We determined the plasma levels of molecular markers for platelet activity (platelet factor 4 and beta-thromboglobulin), thrombotic status (fibrinopeptide A and thrombin-antithrombin III complex) and fibrinolytic status (D-dimer and plasmin-alpha 2-plasmin inhibitor complex) in 13 patients with hypertrophic cardiomyopathy, 17 patients with dilated cardiomyopathy and 20 normal subjects. RESULTS: Plasma levels of platelet factor 4, beta-thromboglobulin and plasmin-alpha 2-plasmin inhibitor complex did not differ significantly among the three groups, whereas plasma levels of fibrinopeptide A and thrombin-antithrombin III complex in both patient groups were significantly higher than those in normal subjects. Plasma levels of D-dimer in patients with dilated cardiomyopathy were significantly higher than those in patients with hypertrophic cardiomyopathy and normal groups. In patients with hypertrophic cardiomyopathy, both fibrinopeptide A and thrombin-antithrombin III complex levels were significantly correlated with left atrial diameter. In patients with dilated cardiomyopathy, fibrinopeptide A and thrombin-antithrombin III complex levels showed a positive correlation with left ventricular end-diastolic volume and a negative correlation with fractional shortening of the left ventricle. CONCLUSIONS: The activated coagulation system in patients with hypertrophic and dilated cardiomyopathy may be triggered by left atrial dilation in hypertrophic cardiomyopathy and left ventricular enlargement and dysfunction in dilated cardiomyopathy.

Antifibrinolytic Agents↗

Left atrial abnormality in acute myocardial infarction.

This study assessed left atrial abnormality by electrocardiogram as a predictor of left ventricular dysfunction during acute myocardial infarction. Hemodynamic, angiocardiographic, echocardiographic, and serial creatine kinase-MB studies revealed the electrocardiogram to be a significant predictor of location of acute myocardial infarction, prevalence of occlusive disease in coronary vessels, myocardial contractility, low ejection fraction, increased left ventricular end-diastolic pressure, and serial creatine kinase-MB.

Adult↗

Reversal of atrial mechanical stunning after cardioversion of atrial arrhythmias: implications for the mechanisms of tachycardia-mediated atrial cardiomyopathy.

BACKGROUND: Atrial mechanical stunning develops on termination of chronic atrial arrhythmias and is implicated in the genesis of thromboembolic complications after cardioversion. The mechanisms responsible for atrial mechanical stunning are unknown. The effects of atrial rate, isoproterenol, and calcium on atrial mechanical function in patients with atrial stunning have not been evaluated, and it is not known if atrial stunning can be reversed. METHODS AND RESULTS: Thirty-five patients with chronic atrial flutter (AFL) undergoing radiofrequency ablation were studied. Fifteen patients in sinus rhythm undergoing ablation for paroxysmal AFL were studied as control for effects of the procedure. Left atrial appendage emptying velocities (LAAEVs) and spontaneous echocardiographic contrast (LASEC) were assessed by transesophageal echocardiography during AFL, after reversion to sinus rhythm, during atrial pacing at cycle lengths of 750 to 250 ms, after a postpacing pause, and with isoproterenol or calcium. With termination of AFL, LAAEV decreased from 59.0+/-3.7 cm/s to 18.8+/-1.4 cm/s (P<0.0001) and LASEC grade increased from 0.9+/-0.1 to 2.2+/-0.2 (P<0.0001). Pacing increased LAAEV to a maximum of 38.4+/-3.2 cm/s (P<0.0001) and reduced LASEC grade to 1.9+/-0.2 (P=0.005). Isoproterenol and calcium reversed atrial mechanical stunning with LAAEV increasing to 89.3+/-12.6 cm/s (P=0.0007) and 50.2+/-10.5 cm/s (P=0.005), respectively, and LASEC grade decreasing to 0.2+/-0.1 (P=0.001) and 1.4+/-0.2 (P=0.01), respectively. The postpacing pause increased LAAEV to 69.3+/-3.7 cm/s (P<0.0001). No change in LAAEV was observed in the paroxysmal AFL group. CONCLUSION: Atrial mechanical stunning can be reversed by pacing at increased rates and through the administration of isoproterenol or calcium. These findings suggest a functional contractile apparatus in the mechanically remodeled atrium as a result of chronic atrial flutter.

Atrial Flutter↗

Echocardiographic findings in mild and severe forms of sickle cell anemia.

M-mode echocardiographic findings were compared between sickle cell anemic and healthy children. Patients were composed of two groups; Group 1: mild group with no crises, no blood transfusions at the ages of 5.0 to 13.0, total of 12 children; Group 2: severe group, with frequent crises with requirement of blood transfusions at the ages of 3.0 to 13.0 years, total of 18 children. Control group was composed of 12 healthy children aged 5.0 to 13.0. When M-mode echocardiographic findings were compared, important findings were as follows: Mean left atrium dimension was increased both in the mild and severe groups (P < 0.001) compared with controls. This finding also supports the increase in the left ventricle end-diastolic dimension in both the severe and mild groups as compared with controls (P < 0.001). The increase in end-diastolic left ventricle dimension could be due to anemia present in the patients, but there was no difference between the two patient groups. Posterior left ventricle thickness and left ventricle mass was increased in both the mild and severe groups compared with controls (P < 0.001, P < 0.05), respectively. Left ventricular fractional shortening was more or less the same with controls. In spite of left ventricular volume load and dilatation, left ventricular contraction was good and systolic function was normal, and there was no correlation between the ECHO findings and hematological indices.

Adolescent↗

Comparison of clinical and echocardiographic determinations of left ventricular dimension during weaning from cardiopulmonary bypass.

Twenty patients (age 45 to 78 years) were studied with ethical committee approval and informed patient consent during coronary artery bypass grafting. Transesophageal echocardiography (TEE) was used to validate a clinical measure of preload: inspection of the line of contact between the heart (acute margin) and the diaphragm. Immediately before going on cardiopulmonary bypass (CPB), with the cannulas and stay sutures in place, a small mark was made with the cautery on the diaphragm at the line of contact. After CPB the patients were transfused from the extracorporeal circuit to exactly the same level. At these two times, TEE recordings of the short axis of the left ventricle were performed and stored on videotape for later blinded evaluation off-line. The left ventricle short-axis area in end-diastole measured after CPB showed a close correlation to that measured before CPB, r = 0.88, P < 0.001. The regression line was close to the line of identity. The conclusion was that inspection of the line of contact between the heart and the diaphragm can be used clinically during weaning from bypass to obtain the same left ventricular end-diastolic volume as before CPB.

Aged↗

Relationship of auscultatory fourth heart sound to the quantitated left atrial filling fraction.

The fourth heart sound (S4) has been associated with vigorous atrial contraction. However, the presence of S4 has not been previously correlated with quantitated left atrial filling fraction. In this study, the presence of an auscultatory S4 was compared with the Doppler echocardiographically quantitated left atrial filling fraction in 41 consecutive patients in whom S4 was judged to be present or absent according to the consensus of cardiologists. Left atrial filling fraction in patients with S4 was 49% and was significantly greater than 33% found in patients without S4 (p less than 0.005). Using atrial filling fraction of 35% as a dividing line, S4 had a sensitivity of 84% and a specificity of 75% for determining left atrial filling fraction greater than or equal to 35%. Furthermore, of 25 patients with S4, 21 (84%) had atrial filling fraction greater than or equal to or less than 35%, and of 16 patients without S4, 12 (75%) had atrial filling fraction less than 35%. Thus, the presence or the absence of S4 is quantitatively related to the left atrial filling fraction and appears to predict atrial filling fraction greater than or equal to or less than 35% reasonably well.

Adult↗