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Left atrial maximum volume is a recurrence predictor in lone atrial fibrillation: an acoustic quantification study.

Predictors of recurrence in lone atrial fibrillation have not been clearly identified. Acoustic quantification (AQ) is a promising method in the assessment of left atrial (LA) volumes. The purpose of the present study was to investigate the potential of LA volumes obtained by standard manual tracing and AQ methods in predicting AF-recurrence after restoring the sinus rhythm in patients with lone AF, and to test the agreement between the two approaches. Standard echocardiography combined with AQ was performed in 28 patients with lone AF one hour after the sinus rhythm was regained, and in 10 controls. LA volumes were determined by conventional manual tracing and AQ methods. AQ waveforms of LA were obtained by drawing a region of interest around the LA border. The agreement of the two methods was tested by Bland-Altman analysis. Patients were followed up for 6 months for the occurrence of AF recurrence. A good correlation was observed between AQ and manual tracing methods in determining both minimal (r=0.59) and maximal (r=0.88) LA volumes. Patients with AF recurrence had a significantly larger maximum LA volume as assessed with both methods (P<0.05 for both). M-mode derived LA dimension and isovolumic relaxation time were additional predictors of recurrence in patients with lone AF. In lone AF, patients prone to recurrence could be predicted by determining LA maximum volume assessed either by AQ or manual tracing methods. AQ provides on-line, accurate estimation of LA volumes.

Adult↗

Left atrial appendage Doppler flow patterns: implications on thrombus formation.

The characteristics and clinical implications of left atrial appendage (LAA) flow have not been clearly analyzed. Thirty-nine consecutive patients underwent a transesophageal echocardiographic (TEE) color Doppler study to correlate the LAA pulsed Doppler flow pattern with echocardiographic variables and the cardiac rhythm of each patient. Three different LAA flow patterns were identified. Type I flow, characterized by a biphasic pattern (waves of filling and emptying), was found in 17 patients, all in sinus rhythm; it was not associated with LAA spontaneous contrast or thrombus. Mean peak velocities of the filling and emptying waves were, respectively: 28 +/- 12 cm/sec and 31 +/- 9 cm/sec. Type II sawtooth active flow (eight patients) (mean peak velocity: 49 +/- 12 cm/sec) was only detected in atrial fibrillation (AF) and dilated LAA (LAA area: 421 +/- 40 mm2) but without thrombus or significant LAA spontaneous echocardiographic contrast. Type III flow pattern was noted in 14 patients with AF and a very dilated LAA (LAA area: 619 +/- 96 mm2). This flow pattern was characterized by the absence of identifiable flow waves and was associated with the presence of LAA spontaneous contrast; the majority (six of seven) had evidence of thrombus. We concluded that the LAA is a dynamic structure in which TEE study identified three flow patterns with different implications. AF is associated with two LAA flow types (II and III) with a larger LAA size as well as a higher incidence of LAA clots in type III flow.

Atrial Fibrillation↗

Veratridine-induced intoxication in the isolated left atrium of the rat: effects of some anti-ischemic compounds.

Veratridine-induced Na+ and Ca2+ uptake was used as a simulation of ischemia-induced Na+ and Ca2+ uptake. Therefore, electrically driven (1 Hz) isolated left atria of the rat were intoxicated with veratridine and the 45Ca2+ uptake was determined. Veratridine (10(-4) mol/l) increased the 45Ca2+ uptake from 575 +/- 13 to 2320 +/- 86 dpm/mg ww (n = 20). The total tissue content of 45Ca was elevated from 4328 +/- 132 to 5136 +/- 303 dpm/mg ww (n = 13). The veratridine-induced 45Ca2+ uptake was completely suppressed by tetrodotoxin (10(-7) and 10(-6) mol/l), whereas amiloride (6.10(-6) mol/l) and phentolamine (10(-6) and 10(-5) mol/l) exhibited no effect on the veratridine-induced 45Ca2+ uptake. Nifedipine (10(-7) and 10(-6) mol/l) was ineffective on veratridine-induced 45Ca2+ uptake. Verapamil (10(-5) mol/l) suppressed the veratridine-induced 45Ca2+ uptake, but the 45Ca2+ uptake in the absence of veratridine was also suppressed by verapamil (10(-6) and 10(-5) mol/l). The novel anti-ischemic compounds R 56865 (10(-8)-10(-5) mol/l) and R 59494 (10(-8)-10(-5) mol/l) totally abolished veratridine-induced 45Ca2+ uptake. It is speculated that Ca2+ enters the cell via a Na+ channel which changes its selectivity upon veratridine treatment. Consequently, R 56865 and R 59494 could display their protective effect by either inhibiting the modified Na+ channel or preventing the transition of the normal Na+ channel to its altered state.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Non-linear fluid-coupled computational model of the mitral valve.

BACKGROUND AND AIM OF THE STUDY: The dynamics of the mitral valve result from the synergy of left heart geometry, local blood flow and tissue integrity. Herein is presented the first coupled fluid-structure computational model of the mitral valve in which valvular kinematics result from the interaction of local blood flow and a continuum representation of valvular microstructure. METHODS: The diastolic geometry of the mitral valve was assembled from previously published experimental data. Anterior and posterior leaflets were modeled as networks of entangled collagen fibers, embedded in an isotropic matrix. The resulting non-linear continuum description of mitral tissue was implemented in a three-dimensional membrane formulation. Chordal tension-only behavior was defined from experimental tensile tests. The computational model considered the valve immersed in a domain of Newtonian blood, with an experimentally determined viscosity corresponding to a shear rate of 180 s(-1) at 37 degrees C. Ventricular and atrial pressure curves were applied to ventricular and atrial surfaces of the blood domain. RESULTS: Peak closing flow and volume were 51 ml/s and 1.17 ml, respectively. Papillary muscle force ranged dynamically between 0.0 and 2.6 N. Acoustic pressure (RMS) was found to be 3.3 Pa, with a peak frequency of 72 Hz at 0.064 s from the onset of systole. Model predictions showed excellent agreement with available transmitral flow, papillary force and first heart sound (S1) acoustic data. CONCLUSION: The addition of blood flow and an experimentally driven microstructural description of mitral tissue represent a significant advance in computational studies of the mitral valve. This model will be the foundation for future computational studies on the effect of pathophysiological tissue alterations on mitral valve competence.

Algorithms↗

Feasibility and validation of registration of three-dimensional left atrial models derived from computed tomography with a noncontact cardiac mapping system.

OBJECTIVES: The purpose of this study was to determine the feasibility and assess the validity of registering three-dimensional (3D) models from computed tomographic (CT) images using a cardiac mapping system. BACKGROUND: Registration of 3D anatomic models with an interventional system could help identify and navigate mapping and ablation catheters over a complex structure such as the left atrium (LA). METHODS: ECG-gated, contrast-enhanced cardiac CT imaging was performed in 14 patients with atrial fibrillation. Segmentation was used to create 3D models of the LA. The 3D models were registered with the mapping system using a series of fiducial points. Registration was accomplished retrospectively in the first 10 patients, and catheter navigation was visualized from recorded data. In the final four patients, registration was accomplished in real time during electrophysiologic study. The mapping catheter position, as it was navigated inside the LA, was applied to the registered model in real time. For the validation study, temporary pacing leads were implanted in the LA of 10 dogs. Following this, CT scanning, segmentation, LA model importation, and registration was described previously. After registration, a mapping catheter was positioned at the site of each buried lead according to the registered model with no fluoroscopic guidance. A radiofrequency lesion was created at this location, and the dog was sacrificed, the heart removed and stained, and the distance between the buried lead and the lesion measured. RESULTS: During the feasibility study, the location of the catheter in the registered model correlated with fluoroscopy, angiography, and intracardiac electrograms. LA endocardial potentials during sinus rhythm and any premature atrial contractions also were successfully delineated over the registered models. In the validation study, the mean target registration error was 2.0 +/- 3.6 mm. CONCLUSIONS: Registration of CT-derived 3D models of the LA using a cardiac mapping system is feasible and accurate.

Animals↗

Comparison of the pulmonary dysfunction caused by cardiogenic and noncardiogenic pulmonary edema.

We designed a series of experiments to compare the pulmonary dysfunction observed in models of cardiogenic and noncardiogenic pulmonary edema in chronically instrumented awake sheep. Cardiogenic pulmonary edema was induced by inflating the balloon of a Foley catheter surgically positioned in the mitral valve orifice causing increased left atrial pressure (increases PLA). Noncardiogenic pulmonary edema was induced by intravenous infusion of Perilla ketone (PK). Calculated microvascular pressure remained constant during PK infusion but increased from 9.4 +/- 0.7 to 42.8 +/- 2.4 cm H2O during increases PLA. Comparable increases in lung lymph flow (QL) were observed in the two protocols (five to seven times baseline). Pulmonary edema as quantified by chest radiograph scores increased from 0 (normal) to 2.9 +/- 0.5 and 3.4 +/- 0.1 in the PK and increases PLA groups, respectively. Room air alveolar to arterial oxygen pressure difference (P[A-a]O2) increased from 24 +/- 3 to 46 +/- 7 mm Hg in the PK group and from 23 +/- 4 to 56 +/- 6 mm Hg in the increases PLA group. Dynamic compliance of the lungs (Cdyn) expressed as the percentage of the baseline value decreased to 53 +/- 7 and 50 +/- 7% in the PK and increases PLA groups, respectively. Resistance to airflow across the lungs (RL) increased from 2.5 +/- 0.6 to 3.3 +/- 0.8 cm H2O.L-1.sec-1 in the PK group and from 1.4 +/- 0.3 to 4.2 +/- 1.1 in the increases PLA group. Significant correlations were observed between changes in the severity of pulmonary edema observed on chest radiographs, Cdyn, delta P(A-a)O2, and QL in both the increases PLA groups. We conclude that similar degrees of pulmonary edema, regardless of the mechanism, are associated with similar changes in QL, Cdyn, and delta P(A-a)O2. Hydrostatic pulmonary edema appeared to cause greater changes in RL than that resulting from increased microvascular permeability.

Animals↗

Moderate and chronic hemodynamic overload of sheep atria induces reversible cellular electrophysiologic abnormalities and atrial vulnerability.

OBJECTIVES: The aim of this study was to evaluate the myocardial consequences of a chronic volume overload of the left atrium (LA). BACKGROUND: Atrial dilation is a major risk factor for atrial fibrillation (AF), but the underlying mechanisms are poorly understood. METHODS: A left-right aorto-pulmonary artery shunt (APS) was created in sheep. The cardiopathy was characterized by echocardiography, electrophysiologic testing, and histologic analysis. Cellular action potential (AP) and calcium current (I(Ca)) were recorded by means of microelectrode and patch clamp techniques. RESULTS: Three to four months after surgery, all animals in the APS state had a dilated LA (146.2 +/- 35.4 cm(2)/m(2) vs. 91.7 +/- 10.4 cm(2)/m(2) in the control state; p = 0.0024) but remained in sinus rhythm. Repetitive atrial firing was triggered by a single extra beat in five of six animals in the APS state and in two of six animals in the control state. Moreover, in two animals in the APS state, a single extra beat triggered sustained AF. Myocytes were enlarged and 39.8% showed some degree of myolysis. In animals in the APS state, the AP had no plateau phase or small amplitude and numerous myocytes were unexcitable. The I(Ca) density was 45.2% lower in APS animals than in control animals. Beta-adrenergic stimulation normalized I(Ca) and restored the plateau phase of the AP. After shunt suppression, the electrophysiologic properties of the atria returned to normal. CONCLUSIONS: The APS induced moderate, isolated LA dilation, which was sufficient to cause major changes in cellular electrophysiologic properties and to render the atria vulnerable to fibrillation. These effects were reversed by shunt suppression.

Action Potentials↗

Cardiac surgery and inhaled nitric oxide: indication and follow-up (2-4 years).

We studied the effect of inhaled nitric oxide (NO) on 80 patients who had undergone cardiac surgery in our center. The indications for receiving NO inhalation and the number of patients were as follows: Pp/Ps > 0.5 for pulmonary hypertension (PH) (n = 32; 21 children and 11 adults), severe PH crisis (n = 9), high pulmonary vascular tone (Glenn pressure more than 18 mm Hg after bidirectional Glenn operation) or arterial oxygen saturation (SaO2) less than 70% despite an FiO2 of 1.0 after Blalock-Taussig shunt (n = 6), mean pulmonary artery pressure (PAP) > 15 mm Hg and transpulmonary gradient (TPG) (mean PAP - left atrial pressure [LAP]) > 8 mm Hg after Fontan-type operation (n = 18), elevated pulmonary vascular tone (mean PAP > 30 mm Hg and left ventricular assist system [LVAS] flow rate < 2.5 L/min/m2) in patients with LVAS (n = 3), and impaired oxygenation (PaO2/FiO2 < 100 under positive end-expiratory pressure [PEEP] > 5 cm H2O) (n = 12). Low dose inhaled NO (10 ppm) had the following effects. In adult PH patients, it significantly reduced the mean PAP (from 37.3 to 27.0 mm Hg; average values are given) and increased the mean systemic arterial pressure (SAP) (64.7 to 75.3 mm Hg). In infant PH patients, it increased the mean SAP (51.8 to 56.1 mm Hg). In patients with a PH crisis, it significantly reduced the central venous pressure (CVP) (13.3 to 8.8 mm Hg) while increasing both the mean SAP (49.4 to 57.9 mm Hg) and PaO2/FiO2 (135 to 206). In patients after a Fontan-type operation, it significantly reduced the mean PAP (16.8 to 13.8 mm Hg) and TPG (9.5 to 5.8 mm Hg). In patients under LVAS, it reduced the CVP (11.7 to 8.0 mm Hg) and mean PAP (32.0 to 24.7 mm Hg). In impaired oxygenation patients, PaO2/FiO2 was increased (75 to 106). Sixty-five patients were all followed for 2.0-4.3 years (average, 3.1 years). All 65 patients remained free from oxygen requirement, and possible chronic adverse effects including the occurrence of malignant tumors or chronic inflammation in the respiratory tract were not observed.

Administration, Inhalation↗

Differential responses in left ventricular diastolic filling dynamics with isometric handgrip versus isotonic treadmill exertion.

Although the hemodynamic responses to isotonic and isometric exercise are different, few data exist comparing the response to left ventricular (LV) diastolic filling dynamics with these two forms of exertion. Therefore we performed Doppler examination before and at the end of isotonic and isometric exercise in 20 normal volunteers to define the differential responses of LV filling to these two forms of exertion. Transmitral inflow velocity signals from the apical view and phonocardiography were recorded before and at the termination of treadmill exercise (TRD) to 11 METs and handgrip (HG) 50% maximal for 2 minutes). Mean blood pressure (mBP), heart rate (HR), early diastolic (E) and late atrial (A) inflow velocities, mean acceleration rate (ACC) of E wave, time velocity integral of inflow (Ti), and isovolumic relaxation time (IRT) from second heart sound to onset mitral inflow were measured. Absolute changes from baseline were significantly different for the two forms of exertion: TRD versus HG: BP = 11 +/- 9 versus 36 +/- 10 mm Hg, HR = 37 +/- 16 versus 16 +/- 9 beats/min, E = 11.6 +/- 11.3 versus -7.0 +/- 9.4 cm/sec, A = 29.9 +/- 14.5 versus 14 +/- 12 cm/sec, ACC = 164 +/- 151 versus -56 +/- 135 cm/sec2, Ti = 1.9 +/- 3.0 versus -1.7 +/- 1.7 cm, and IRT = -12 +/- 9 versus 9 +/- 10 msec, all p < 0.0001 except for A, p < 0.001). Isotonic treadmill exercise resulted in enhanced early diastolic filling manifested by increases in E and ACC and a decreased in IRT. Conversely, isometric handgrip exercise produced evidence of reduced early filling including decreased E and ACC and slightly increased IRT. Thus the response of LV filling dynamics recorded by Doppler differs for isotonic and isometric exertion and likely reflects the variable pressure and flow alterations induced by these two forms of exertion.

Adult↗

Evaluation of the hemodynamic relationship between the left atrium and left ventricle during atrial systole by pulsed tissue Doppler imaging in patients with left heart failure.

The objective of the present study was to evaluate the hemodynamic relationship between the left atrium (LA) and left ventricle (LV) during atrial systole in the presence of an elevated left ventricular end-diastolic pressure (LVEDP) and LV failure using pulsed tissue Doppler imaging (TDI). Fifty-three patients with LV systolic dysfunction and no regional LV asynergy were divided into 3 groups: relaxation failure group (RF, n=20) with a ratio of peak early diastolic to atrial systolic velocity of the transmitral flow (E/A) < or = 1; pseudonormalization group (PN, n=19) with 1 or =2. In addition, 20 normal patients (E/A > or = 1) were studied as a control group. The transmitral and pulmonary venous flow velocities were recorded by transesophageal pulsed Doppler echocardiography. The wall motion velocity patterns were recorded at the middle portion of the LV posterior wall (LVPW) and at the mitral annulus (MA) of the LVPW site in the apical LV long-axis view by transthoracic pulsed TDI. The LVEDP was significantly greater in the PN and RS groups than in the RF and control groups. The moan pulmonary capillary wedge pressure was greatest in the RS group. The percent fractional change of the LA area during atrial systole determined by 2-dimensional echocardiography was significantly lower in the RS group than in the PN group. The peak atrial systolic pulmonary venous flow velocity was significantly greater in the PN group than in the RS group. The peak atrial systolic motion velocity (Aw) at the LVPW was significantly lower in the PN and RS groups than in the RF and control groups. The Aw at the MA was significantly lower in the RS group than in the other groups. There was no significant difference in Aw between the LVPW and MA in the RS group, whereas Aw at the MA was significantly greater than that at the LVPW in the PN group. In conclusion, the measurements of Aw at the LVPW and MA can be used to noninvasively evaluate the hemodynamic relationship between the LA and LV during atrial systole in patients with LV failure.

Adult↗

Noninvasive estimation of the instantaneous first derivative of left ventricular pressure using continuous-wave Doppler echocardiography.

BACKGROUND: The complete continuous-wave Doppler mitral regurgitant velocity curve should allow reconstruction of the ventriculoatrial (VA) pressure gradient from mitral valve closure to opening, including left ventricular (LV) isovolumic contraction, ejection, and isovolumic relaxation. Assuming that the left atrial pressure fluctuation is relatively minor in comparison with the corresponding LV pressure changes during systole, the first derivative of the Doppler-derived VA pressure gradient curve (Doppler dP/dt) might be used to estimate the LV dP/dt curve, previously measurable only at catheterization (catheter dP/dt). METHODS AND RESULTS: This hypothesis was examined in an in vivo mitral regurgitant model during 30 hemodynamic stages in eight dogs. Contractility and relaxation were altered by inotropic stimulation and hypothermia. The Doppler mitral regurgitant velocity spectrum was recorded along with simultaneously acquired micromanometer LV and left atrial pressures. The regurgitant velocity profiles were digitized and converted to VA pressure gradient curves using the simplified Bernoulli equation. The instantaneous dP/dt of the VA pressure gradient curve was then derived. The instantaneous Doppler-derived VA pressure gradients, instantaneous Doppler dP/dt, dP/dtmax, and -dP/dtmax were compared with corresponding catheter measurements. This method of estimating dP/dtmax from the instantaneous dP/dt curve was also compared with a previously proposed Doppler method of estimating dP/dtmax using the Doppler-derived mean rate of LV pressure rise over the time period between velocities of 1 and 3 m/sec on the ascending slope of the Doppler velocity spectrum. Both instantaneous Doppler-derived VA pressure gradients (r = 0.95, p less than 0.0001) and Doppler dP/dt (r = 0.92, p less than 0.0001) correlated well with corresponding measurements by catheter during systolic contraction and isovolumic relaxation (pooled data). The Doppler dP/dtmax (1,266 +/- 701 mm Hg/sec) also correlated well (r = 0.94) with the catheter dP/dtmax (1,200 +/- 573 mm Hg/sec). There was no difference between the two methods for measurement of dP/dtmax (p = NS). Although Doppler -dP/dtmax was slightly lower than the catheter measurement (961 +/- 511 versus 1,057 +/- 540 mm Hg/sec, p less than 0.01), the correlation between measurements by Doppler and catheter was excellent (r = 0.93, p less than 0.0001). The alternative method of mean isovolumic pressure rise (896 +/- 465 mm Hg/sec) underestimated the catheter dP/dtmax (1,200 +/- 573 mm Hg/sec) significantly (on average, 25%; p less than 0.001). CONCLUSIONS: The present study demonstrated an accurate and reliable noninvasive Doppler method for estimating instantaneous LV dP/dt, dP/dtmax, and -dP/dtmax.

Animals↗

Validation of the noncontact mapping system in the left atrium during permanent atrial fibrillation and sinus rhythm.

OBJECTIVES: The aim of this study was to validate noncontact mapping (NCM) in the left atrium (LA) during sinus rhythm and atrial fibrillation (AF). BACKGROUND: Understanding the mechanisms of AF is crucial to the development of novel and effective treatments. Noncontact mapping records global electrical activation simultaneously and therefore has the potential to elucidate these mechanisms. METHODS: Patients underwent catheter ablation of permanent AF guided by NCM. Virtual and contact unipolar electrograms were recorded simultaneously during sinus rhythm and AF from sites spanning the LA and their morphology, amplitude, and timing were compared. The impact of distance from the array to the endocardial surface and electrogram amplitude were analyzed. RESULTS: A total of 22 patients age 52 +/- 9 (mean +/- SD) years were studied. During sinus rhythm, the median (range) morphology correlation and timing difference between contact and virtual atrial electrograms were 0.81 (0.27 to 0.98) and 4.2 (0 to 18.3) ms, respectively. These results were significantly worse than the corresponding far field individual ventricular electrograms; 0.91 (0.53 to 1.0) and 1.7 (0 to 18.3) ms (p < 0.001). For endocardial sites >40 mm from the array, the correlation was significantly worse than sites <40 mm: 0.73 (0.48 to 0.95) versus 0.87 (0.27 to 0.98) (p < 0.001). The correlation during AF was 0.72 (0.24 to 0.98), which deteriorated with increasing distance from the array. In the presence of adenosine induced atrioventricular block the correlation deteriorated 0.67 +/- 0.16 versus 0.79 +/- 0.11 (p < 0.001). CONCLUSIONS: Noncontact mapping can be performed in human LA; however, the accuracy of reconstructed electrograms is poor >40 mm from the center of the array, particularly during AF. Care must be taken interpreting isopotential maps if the entire endocardial surface of the LA is not close to the array.

Adenosine↗

Effect of radiofrequency catheter ablation for atrial fibrillation on left atrial cavity size.

Left atrial (LA) remodeling is associated with atrial fibrillation (AF). Radiofrequency catheter ablation offers a good treatment option for AF, with reasonable long-term results. The purpose of the present study was to assess whether LA reverse remodeling occurs after successful catheter ablation. Fifty-seven consecutive patients (45 men; age 53 +/- 8 years) with symptomatic drug-refractory AF were treated with radiofrequency catheter ablation. The patients were divided into 2 groups on the basis of AF recurrence as determined by Holter monitoring and 12-lead electrocardiographic findings at 6 weeks and 3 months of follow-up (sinus rhythm [SR] group, no recurrence; AF group, AF recurrence). At baseline and 3 months of follow-up, 2-dimensional echocardiography was performed to assess LA size and dimensions. Furthermore, LA volumes were measured at end-systole and end-diastole. After 3 months, 39 of 57 patients (68%) maintained SR. At 3 months of follow-up, the LA anteroposterior diameter showed a significant reduction in the SR group (4.5+/- 0.3 vs 4.2 +/- 0.2 cm, p <0.01), and an additional increase was observed in the AF group (4.5+/- 0.3 vs 4.8 +/- 0.3 cm, p <0.05). Furthermore, the LA end-systolic and end-diastolic volumes decreased significantly in the SR group from baseline to follow-up (59 +/- 12 vs 50 +/- 11 ml, p <0.01, and 37 +/- 9 vs 31 +/- 7 ml, p <0.01, respectively). However, a tendency toward an increase in LA volumes was observed in the AF group. In conclusion, the results of this study have demonstrated that LA reverse remodeling occurs after successful radiofrequency catheter ablation for AF.

Atrial Fibrillation↗

Clinical and echocardiographic predictors of left atrial appendage dysfunction in patients with mitral stenosis in sinus rhythm.

BACKGROUND: Mitral stenosis (MS) causes left atrial (LA) appendage (LAA) dysfunction resulting in reduced LAA flow velocities. Low LAA peak emptying velocity (PEV), determined by transesophageal echocardiography, is a risk for thrombus formation and systemic embolism. OBJECTIVE: We sought to investigate various clinical and echocardiographic predictors of low LAA blood flow velocities. METHODS: A total of 44 patients with newly diagnosed MS were classified into two groups on the basis of the presence of high (PEV > or = 46 cm/s) or low (PEV < 46 cm/s) LAA flow profile on Doppler transesophageal echocardiography. LAA flow velocities were measured to be 27.38 +/- 8.17 cm/s in patients with LAA dysfunction and 70.75 +/- 16.71 cm/s in high-flow profile (P <.0001). Simultaneous 12-lead electrocardiogram was used to measure P waves. RESULTS: P maximum, P dispersion, and LA diameter were significantly higher in patients with low LAA PEV (n = 32) than in those with high LAA PEV (111.87 +/- 16.93 vs 96.66 +/- 14.97, P =.0084; 73.12 +/- 20.7 vs 49.16 +/- 9.96, P <.0001; 46.06 +/- 4.384 vs 38.08 +/- 7.42 mm, P =.004; respectively). Patients with MS and low LAA blood flow had smaller mitral valve area compared with those with high LAA blood flow velocity (1.48 +/- 0.431 vs 1.85 +/- 0.442 cm(2), P =.02). Male sex, spontaneous echocontrast, and thrombus were more frequent in patients with low LAA PEV [7 [21.87%] vs 5 [41.66%], P =.026; 21 [65.62%] vs 4 [33.3%], P =.088; 4 [12.5%] vs none; respectively]. Mild MS was more frequent in patients with high blood flow velocity [6 [27.2%] vs 14 [63.6%], P =.03]. CONCLUSION: At linear regression analysis, only P-wave dispersion and LA diameter predicted the LAA mechanical dysfunction reflected as low LAA PEVs.

Atrial Function, Left↗

Prognostic value of left atrial enlargement in patients with idiopathic dilated cardiomyopathy and ischemic cardiomyopathy.

Previous studies have shown that abnormal mitral flow patterns and left atrial (LA) enlargement are independently associated with survival in patients with left ventricular (LV) dysfunction. However, it is not known whether these outcome indicators can provide different information in patients of various age groups. This study was designed to assess the prognostic value of the restrictive mitral flow pattern (RMFP) and increased LA size in patients with LV dysfunction (ejection fraction <45%) grouped into those < or = 70 years old (n = 102; mean age 61) and those >70 years old (n = 105; mean age 78). Echocardiographic and Doppler indexes were recorded in patients with LV systolic dysfunction due to dilated cardiomyopathy who were followed up for 22 plus minus 14 months. In patients >70 years, indexed LA size (>26 mm/m(2)) was the single best predictor of death (hazard ratio [HR] 3.0, p = 0.018) and emerged as the most important outcome variable of the combined end point (HR 2.2, p = 0.016) on multivariate analysis. In patients < or =70 years, RMFP, characterized by an early wave deceleration time <140 ms, was independently associated with cardiac death or heart failure hospitalization (HR 5.7, p = 0.0013). When demographics, clinical, echocardiographic, and Doppler measurements were analyzed in hierarchical order, indexed LA size yielded the most valuable contribution in predicting the combined end point in older patients (global chi-square from 11.5 to 18.7). RMFP was associated with the higher additional prognostic value in younger patients (global chi-square from 14.4 to 24.1). These data suggest that LA enlargement has an independent and additional prognostic value in elderly patients with LV dysfunction.

Aged↗

Mechanism of altered patterns of left ventricular filling during the development of congestive heart failure.

BACKGROUND: The mechanism of the alterations in the pattern of left ventricular (LV) filling during the development of congestive heart failure (CHF) is not fully understood. METHODS AND RESULTS: We studied six conscious dogs instrumented to measure LV and left atrial (LA) pressures and LV volume as CHF was induced by rapid pacing. Diastolic filling dynamics were serially measured over 4 weeks during normal sinus rhythm. Four days after we initiated pacing, the peak early diastolic filing rate decreased from 108 +/- 24 to 88 +/- 27 mL/s (P < .05) as the maximal early diastolic LA-LV pressure gradient decreased associated with a slowing of the rate of LV relaxation. Subsequently, the peak early filling rate progressively increased, returning to control at 1 week, and by the fourth week, it had increased to 168 +/- 39 mL/s (P < .05). These changes in early filling rates occurred as the maximal early diastolic LA-LV pressure gradient increased in association with a progressive increase in LV pressure despite further progressive slowing of the rate of LV relaxation. Throughout the development of CHF, peak early filling rate and the maximal LA-LV pressure gradient correlated (r = .99, P < .001). The early filling deceleration rate increased and deceleration time progressively decreased over the 4 weeks as LV stiffness and net LA plus LV stiffness increased (P < .05). As predicted by a theoretical analysis, the deceleration time was linearly related to the reciprocal of the square root of LV stiffness (r = .94, P < .01). CONCLUSIONS: Early in CHF, slowing of LV relaxation reduces the maximal early diastolic LA-LV pressure gradient, decreasing the peak early filling rate. As CHF progresses, this is overcome by an increase in LA pressure that augments the early diastolic LA-LV pressure gradient, increasing peak early filling rate. Increasing LV stiffness during the development of CHF progressively shortens the early filling deceleration time and augments the early filling deceleration rate. These observations suggest that the early filling deceleration time reflects LV stiffness.

Animals↗

Relationship between flow dynamics in the left atrium and hemostatic abnormalities in patients with nonvalvular atrial fibrillation.

To investigate the relationship between left atrial (LA) flow dynamics and hemostatic markers in nonvalvular atrial fibrillation (AF), 45 patients with nonvalvular AF who had not received anticoagulants were evaluated by transesophageal echocardiography. We determined the LA appendage flow and the presence of LA spontaneous echo contrast (SEC) or thrombus. We measured plasma levels of thrombin-antithrombin III complex (TAT), fibrinopeptide A, D-dimer, beta-thromboglobulin, and platelet factor 4 in peripheral blood as hemostatic markers. The patients were divided into a low-velocity group (n = 19; sum of peak emptying and filling LA appendage flow velocities < 40 cm/s) and a high-velocity group (n = 26; > or = 40 cm/s). The maximum LA diameter was significantly greater and the LA expansion fraction was significantly smaller in the low-velocity group than in the high-velocity group. LA SEC or thrombus was observed in 11 patients (58%) in the low-velocity group, but not in any patients in the high-velocity group (p < 0.001). The plasma levels of TAT, fibrinopeptide A, D-dimer, beta-thromboglobulin, and platelet factor 4 were significantly higher in the low-velocity group than in the high-velocity group. The plasma levels of TAT, fibrinopeptide A, beta-thromboglobulin, and platelet factor 4 were significantly higher in 8 patients without LA SEC or thrombus in the low-velocity group than in 26 patients in the high-velocity group. Patients with nonvalvular AF accompanied by an enlarged and dysfunctioning LA and a decreased LA appendage flow velocity had increased intravascular coagulation-fibrinolysis activity and platelet activation. These abnormalities may be closely related to the thrombogenetic state in patients with nonvalvular AF.

Adult↗

Peak early diastolic filling velocity may decrease with preload augmentation: effect of concomitant increase in the rate of left atrial pressure drop in early diastole.

Doppler-determined transmitral flow velocity pattern has been shown to depend on transmitral pressure gradient, and left atrial (LA) pressure has been considered to be important in determining transmitral pressure gradient in early diastole and peak early diastolic filling velocity (E). In recent studies in human beings, however, it was proved that E did not necessarily change with LA pressure. This may be because concomitant changes in other factors masked the effect of LA pressure. To investigate the relation between transmitral flow velocity pattern and hemodynamic parameters during preload intervention over the wide range of LA pressure, pulsed Doppler transmitral flow velocity pattern and high-fidelity LA and left ventricular (LV) pressures were simultaneously recorded during rapid volume loading to the LA. Data at three stages, at control, at moderate volume loading (the median LA-to-LV crossover pressure during the volume loading), and at advanced volume loading (the maximal crossover pressure during the volume loading), were compared with one another in 11 dogs. A mean value of E increased with the crossover pressure up to moderate volume loading but did not further increase at advanced volume loading. In the data pooled from all experimental stages in all dogs, the changes in E did not correlate with those in the crossover pressure, but correlated weakly with those in the difference between the crossover pressure and LV minimum pressure (r = 0.45, p < 0.05). E decreased at advanced volume loading in three of 11 dogs with a steep LA pressure drop in early diastole although the changes in the difference between the crossover pressure and LV minimum pressure in the three dogs were similar to those in the other eight dogs. The changes in a rate of LA pressure drop in early diastole associated with advanced volume loading inversely correlated with those in E (r = -0.79, p < 0.01). Thus, E may decrease with an extreme increase in LA pressure; this change may be due to an associated increase in a rate of LA pressure drop in early diastole. This finding suggests that at high LA pressure the increased rate of LA pressure drop in early diastole appears to decrease LV filling and hence to reduce stroke volume.

Animals↗