Coronary neovascularization as a specific sign for left atrial appendage thrombus in mitral stenosis.
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BACKGROUND: Left atrial systolic force (LASF) has been recently reported to be associated with prolonged left ventricular (LV) relaxation and concentric LV geometry in a clinical setting. This study analyzes the association of increased LASF to LV geometry and function in hypertensive patients from a population study. METHODS: Doppler echocardiographic findings were examined in 684 subjects with treated hypertension and without prevalent cardiovascular disease from the Hypertension Genetic Epidemiology Network (HyperGEN) Study (426 African American, 448 female, 125 diabetic, 174 obese; age 53.8+/-10.8 years). The LASF was assessed from the mitral orifice area and pulse-wave Doppler peak A flow velocity. The LASF was defined as being high if >14.33 kdynes (90th percentile of the normal distribution in 246 normal adults). RESULTS: The LASF was high in 269 participants (39.3% of study population), who were older and had higher mean body mass index (all P<.01). Participants with high LASF had higher systolic BP and heart rate (both P<.01) but similar diastolic BP. After controlling for covariates, participants with high LASF exhibited higher LV dimensions and mass than those with normal LASF (all P<.01). The prevalence of LV hypertrophy was also higher (P<.001). Participants with high LASF exhibited normal ejection fraction, higher stroke volume, cardiac output, E and A velocities, slower E deceleration, and lower E/A ratio than those with normal LASF (all P<.01). CONCLUSIONS: Enhanced LASF is associated with LV hypertrophy, normal LV chamber function, increased cardiac output, and prolonged relaxation. The LASF is a preload-dependent measure.
INTRODUCTION: Electrophysiologic remodeling is involved in the self-perpetuation of atrial fibrillation. To define whether differences in atrial electrophysiology already are present in patients with increased susceptibility for atrial fibrillation, we compared patients in sinus rhythm with and without heart failure. METHODS AND RESULTS: Atrial specimens were obtained from patients with reduced left ventricular ejection fraction (LVEF; n = 10) and normal LVEF (n = 16) who were undergoing aortocoronary bypass surgery and from donor hearts (n = 4). Enzymatically isolated atrial myocytes were investigated by whole cell, patch clamp techniques. Total outward current was significantly larger in myocytes of hearts with low LVEF than normal LVEF (19.4 +/- 1.3 vs 15.1 +/- 1.2 pA/pF at pulses to +60 mV, respectively). Analysis of inactivation time courses of different outward current components revealed that the observed current difference is due to the transient calcium-independent outward current I(to1) which is twice as large in the low LVEF group than in the normal LVEF group (9.4 +/- 0.9 vs 4.7 +/- 0.4 pA/pF at pulses to +60 mV, respectively). I(to1) recovery from inactivation was significantly more rapid in myocytes of hearts with low LVEF, and action potential plateau in these cells was significantly shorter. The results of I(to1) and action potential measurements in atrial myocytes of donor hearts were very similar to the results of patients with preserved heart function. CONCLUSION: I(to1) in human atrial myocytes of patients with reduced LVEF has an increased density and altered kinetics in sinus rhythm. These differences in outward current may explain the reduced plateau phase of action potentials.
To investigate whether left atrial systolic dysfunction in dilated cardiomyopathy is the result of left atrial dilatation, atrial involvement in the myopathic process, or both, 20 patients with aortic stenosis, 14 patients with idiopathic dilated cardiomyopathy, and 10 normal control subjects were studied. Left atrial volumes (cubic centimeters) were echocardiographically measured at mitral valve opening (maximal), mitral valve closure (minimal), and onset of atrial systole (P wave of the electrocardiogram) with the biplane area-length method. Atrial systolic function was assessed by calculating the active emptying fraction, equal to (volume at onset of atrial systole minus minimal volume)/volume at onset of atrial systole. Heart rate was similar in patients with aortic stenosis and dilated cardiomyopathy (83 +/- 11 vs 86 +/- 15 beats/min, respectively). Maximal volume was similar in patients with aortic stenosis (74.8 +/- 26.4 cm3) and dilated cardiomyopathy (79.7 +/- 25.3 cm3) but greater (p < 0.0001) than in control subjects (46.4 +/- 11.9 cm3). Active emptying fraction was inversely related to volume at onset of atrial systole and to tension at end of atrial systole (aortic stenosis r = -0.61 and r = -0.81, respectively; dilated cardiomyopathy r = -0.79 and r = -0.66, respectively). At any given level of volume at onset of atrial systole and tension at end of atrial systole, however, active emptying fraction was lower in patients with dilated cardiomyopathy compared with those with aortic stenosis.(ABSTRACT TRUNCATED AT 250 WORDS)
OBJECTIVE: Gaseous microemboli during cardiac surgery have been implicated as a potential cause of postoperative neurologic injury. Any monitoring technique that exposes the systemic circulation to atmospheric pressure could introduce gaseous microemboli, causing cerebral microembolization. The incidence of carotid artery gaseous microemboli was studied during left atrial catheter insertion. DESIGN: Prospective clinical study. SETTING: Tertiary care university hospital. PARTICIPANTS: Twelve patients undergoing elective cardiac surgery. INTERVENTIONS: Perioperatively, a 5-MHz continuous wave Doppler probe was positioned over the left carotid artery to maximally record blood flow signals. The criteria used for detecting a gaseous microembolus were a sudden increase in the amplitude of the visual signal by 30% and a characteristic audible sound. MEASUREMENTS AND MAIN RESULTS: Numbers of microemboli at three timepoints (before and during left atrial catheter insertion and during catheter flushing) were assessed using the Friedman test. No emboli were detected before left atrial catheter insertion. When compared with the preinsertion time period, statistically (p < 0.05) significant numbers of gaseous microemboli were found in six patients during catheter insertion (3 +/- 1 microemboli; range 1 to 7 microemboli) and in five patients during catheter flushing (5 +/- 2 microemboli; range 1 to 12 microemboli). There was a tendency for patients with lower filling pressures to entrain more microemboli during insertion (r = 0.44; p = 0.149). No patient showed evidence of gross neurologic dysfunction postoperatively, although sensitive neurologic testing was not performed. CONCLUSIONS: Left atrial catheter insertion and flushing can cause systemic gaseous microemboli in more than 50% of patients. Although the number of microemboli introduced is relatively small, extreme care should be used during left atrial catheter insertion.
The possible mechanisms of the indirect negative inotropic responses to the P1-receptor agonist, L-phenylisopropyladenosine (L-PIA) were evaluated in electrically paced (2 Hz, 5 ms pulse width, voltage 50% above threshold) left atria and papillary muscles of guinea pigs. The responses were compared in naive tissues (direct effects) or after prestimulation with submaximal concentrations of either cAMP-dependent positive inotropes (isoprenaline or forskolin) or the cAMP-independent inotrope Bay K 8644. Cumulative concentration-response curves were obtained in naive or prestimulated preparations for L-PIA or the potassium channel activator, cromakalim, for comparison. L-PIA and cromakalim exerted negative inotropy in naive atrial tissues, whereas only cromakalim was active in naive papillary muscles. In atria prestimulated with isoprenaline (31 nM) or forskolin (1.4 microM), the negative inotropy of L-PIA was enhanced compared with naive tissues. In contrast, prestimulation with Bay K 8644 (1 microM) exerted a significant functional antagonism of the response to L-PIA. In the case of cromakalim, prestimulation with isoprenaline exerted a functional antagonistic effect. In papillary muscles, an indirect negative inotropic effect of L-PIA was only seen in tissues prestimulated with the cAMP-dependent inotropes isoprenaline (31 nM) or forskolin (2.4 microM), and not in naive tissues or those prestimulated by Bay K 8644 (333 nM). As with atria, prestimulation with isoprenaline exerted a functional antagonistic effect on the response to cromakalim. These results suggest that the P1-receptor agonist, L-PIA, exerts its indirect negative inotropic effects in left atria by two mechanisms.2+ with cAMP-dependent positive inotropes.(ABSTRACT TRUNCATED AT 250 WORDS)
OBJECTIVES: The objective of this study was to evaluate the effect of a transpulmonary contrast agent on Doppler flow signals in the left heart chambers. BACKGROUND: Echo contrast agents are good ultrasound reflectors and could be used as Doppler signal enhancers. Sonicated albumin microbubbles are transpulmonary echo contrast agents and could enhance left heart Doppler signals after peripheral venous injection. METHODS: Thirty-one patients with various heart diseases without intracardiac shunts were assessed with Doppler echocardiography before and after injection of sonicated albumin. RESULTS: After an intravenous injection, pulsed Doppler signals of transmitral flow became more intense in all 16 patients examined, although flow velocity itself was not changed. In Doppler color flow imaging, the maximal mitral regurgitant signal area increased from 312 +/- 405 mm2 to 434 +/- 465 mm2, an average increase of 59 +/- 40% in all 17 patients with mitral regurgitation (p < 0.01). These effects were considered to be due to improvement of signal to noise ratio by the enhancement of Doppler flow signals. The duration of enhancement of pulsed Doppler transmitral flow signals was significantly longer than that of the left ventricular echocardiographic opacification (44 +/- 11 s vs. 17 +/- 7 s, p < 0.01). CONCLUSIONS: Intravenous injection of sonicated albumin can enhance the Doppler flow signals in the left heart chambers. This effect may be useful to improve the sensitivity of the Doppler system for detecting abnormalities of left heart blood flow such as mitral regurgitation.
Left atrial (LA) adaptation during the development of left ventricular (LV) dysfunction is not fully understood. We performed echocardiographic assessment of LA volumes simultaneously with recordings of pulmonary wedge pressures in 60 patients. Twenty patients had no structural or functional LV abnormalities, 20 had a recent myocardial infarction with LV dysfunction, and 20 suffered from congestive heart failure (CHF). Pressure-volume loops were obtained at baseline and during increases in LA pressure produced by normal saline infusion. LA afterload was estimated by the effective LV elastance (E(LV)). Atrioventricular coupling was calculated by the E(LV)/E(es) ratio (where E(es) is the end-systolic elastance). E(es) increased in patients with myocardial infarction (0.80 +/- 0.09 mm Hg/ml, p <0.001), whereas it decreased in patients with CHF (0.22 +/- 0.05 mm Hg/ml, p <0.001) compared with controls (0.61 +/- 0.07 mm Hg/ml). Similarly, stroke workload increased in patients with myocardial infarction (60.7 +/- 7.3 mm Hg x ml, p <0.001), whereas it decreased in patients with CHF (25.4 +/- 2.2 mm Hg x ml, p <0.001) compared with controls (44.8 +/- 5.5 mm Hg x ml). In all patients LA stiffness (slope of the relation of the filling portion of the pressure-volume loop) was increased compared with controls (controls: 0.13 +/- 0.04, patients with myocardial infarction: 0.22 +/- 0.05, and patients with CHF: 0.27 +/- 0.05 mm Hg/ml, p <0.001 for both comparisons). Moreover, the E(LV)/E(es) ratio increased gradually as LV function deteriorated (controls: 1.06 +/- 0.10, patients with myocardial infarction: 1.35 +/- 0.16, and patients with CHF: 6.90 +/- 0.84, p <0.001). Thus, early in heart failure, LA pump function is augmented but LA stiffness increases and work mismatch occurs. With further progression of LV dysfunction, LA pump function decreases as a result of increased afterload imposed on the LA myocardium.
BACKGROUND: Normal healthy aging results in changes in Doppler indexes of diastolic function. One widely accepted explanation for these alterations that is based on animal data is an age-associated impairment of myocardial relaxation resulting from abnormal myocyte calcium handling. However, an alternative theory based on altered left atrial compliance with aging has been proposed in which early left atrial pressure could be low in the aged heart but rise rapidly during atrial diastole, resulting in a higher late atrial pressure and thus a normal mean pressure. We sought to explore this issue directly by performing a detailed analysis of the pulmonary capillary wedge pressure waveform obtained by right-heart catheterization during 5 different loading conditions. METHODS AND RESULTS: Twelve healthy elderly sedentary subjects (mean age, 69.8+/-3 years) were recruited for the seniors group. An additional 12 young sedentary subjects (mean age, 35+/-8 years) made up the young group. All subjects were rigorously screened for comorbidities. All subjects underwent transthoracic echocardiography to determine Doppler variables of early and late transmitral filling (E and A velocities) and isovolumetric relaxation time. Each subject also underwent pulmonary artery catheterization with measurement of pulmonary capillary wedge pressure waveform during 5 different loading conditions: baseline, lower-body negative pressures of -15 and -30 mm Hg, and rapid saline infusions of 10 to 15 and 20 to 30 mL/kg. Pressure was measured at 6 points of the waveform: point 1, peak of the atrial contraction (a wave); point 2, the left atrial pressure during the start of ventricular systole; point 3, peak of atrial filling (v wave); point 4, earliest left atrial pressure during ventricular filling; and the line between points 5 and 6, pressure during diastasis. Aging resulted in a decrease in the E/A ratio (P<0.001) and a prolongation of the isovolumetric relaxation time (P<0.001) as assessed by echocardiography, but there was no effect of age on pulmonary capillary wedge pressure at any point throughout the cardiac cycle (P=0.290). Specifically, at no measured point at any level of cardiac filling volume was the pulmonary capillary wedge pressure of the seniors lower than that of the young subjects. CONCLUSIONS: We conclude that the age-related echocardiographic change of decreasing E/A ratio is not the result of a lowering of early diastolic left atrial pressure.
Large left atrium (LA) and LA appendage (LAA) dysfunction are known to relate to cardiogenic thromboembolism, so the present study investigated the relation of the atrial fibrillatory wave (F wave) amplitude to hemostatic markers and LAA function. Transthoracic and transesophageal echocardiographic studies were performed in 82 consecutive patients with chronic, nonrheumatic atrial fibrillation (AF). Patients were divided into 2 groups according to F wave amplitude in lead V1 on the 12-lead ECG: coarse AF (the greatest amplitude of F wave > or =1 mm, n=44) and fine AF (<1 mm, n=38). Plasma levels of thrombin-antithrombin III complex, D-dimer, platelet factor 4 and beta-thromboglobulin were determined. Compared with patients with coarse AF, those with fine AF had lower LAA peak flow velocity (p<0.05) and higher prevalence of embolic cerebral infarction (50% vs 27%, p<0.05). Platelet activity did not differ between the 2 groups; however, plasma levels of thrombin-antithrombin III complex and D-dimer were significantly higher in patients with fine AF than in those with coarse AF (p<0.05). Multiple logistic regression analysis showed that fine AF was independently associated with cerebral embolism. Therefore, the presence of fine F wave in V1 would be a useful marker of LAA dysfunction and hypercoagulability, and indicate a risk for cerebral embolism in patients with chronic, nonrheumatic AF.
BACKGROUND: Large-scale clinical trials have demonstrated that patients with atrial fibrillation (AF), when treated with a rhythm-control strategy, are still at risk for embolic events. We hypothesized that left atrial (LA) dysfunction persisted even after successful maintenance of sinus rhythm for > 3 months. METHODS: A total of 93 patients with AF and satisfactory rhythm control for > 3 months were included. Satisfactory rhythm control was defined as being free of AF based on patient-reported symptoms, monthly ECG follow-up, and ambulatory Holter ECG if needed. Among the 93 patients, 25 patients had sustained AF that was terminated by electrical or pharmacologic cardioversion, while 68 patients had paroxysmal AF under good medical control. Clinical data were obtained, and transthoracic and transesophageal echocardiography were performed after satisfactory rhythm control for > 3 months. RESULTS: Among the 93 patients, 34 patients (37%) had LA dysfunction, defined as LA appendage (LAA) peak emptying velocity < 40 cm/s or spontaneous echo contrast and/or thrombus in the LA or LAA. When compared to the other 59 patients without LA dysfunction, they had larger LA dimension (40 +/- 6 mm vs 36 +/- 8 mm [+/- SD], p = 0.018) but did not differ significantly regarding the left ventricular (LV) chamber size, LV ejection fraction, mitral or tricuspid inflow, and ratio of the amplitude of the waves created by early diastolic filling and atrial contraction. We also analyzed the relationship between LA function and clinical risk factors for stroke, including hypertension, diabetes mellitus, coronary artery disease, age > 65 years, and prior cerebral vascular accident. LA dysfunction was found in 10 of 17 patients (59%) with three or more risk factors. The odds ratio for having LA dysfunction was 3.1 (p = 0.04; 95% confidence interval, 1.1 to 9.1) when compared with patients with less than three risk factors. CONCLUSIONS: LA dysfunction was present in more than one third of AF patients after satisfactory rhythm control for > 3 months. Patients with higher burden (three or more) of clinical risk factors were more likely to have impaired LA function.
The purpose of this study was to determine analytically the hemodynamic factors that affect the closing velocity of the disc of Björk-Shiley convexo-concave (BSCC) prosthetic mitral valves. The motion of the BSCC disk was modelled by Newton's second law written in the form of a second order differential equation which expressed the instantaneous angle of the disc with respect to the valve ring as a function of the instantaneous pressure drop across the mitral valve, delta P(t), and the angle of the pressure gradient vector acting upon the disc during closure. The disc closes in response to the negative pressure drop created by the crossover of left atrial and left ventricular (LV) pressures. The rate of closure depends on the rate of development of the pressure drop across the valve, d delta P/dt, which is largely dependent upon the rate of change of left ventricular pressure during isovolumic contraction, LV dP/dt. The closure rate is also strongly dependent on the initial angle of the pressure drop vector with respect to the disc. The disc was predicted to reach its highest velocity at the moment of impact, based on the Runge-Kutta solution. Modelling suggests that a high LV dP/dt during valve closure or distorted LV geometry, causing the angle between the fully open disc and the pressure drop vector to shift, will cause the valve to have a high velocity at the moment of impact and may produce high impact loads.
Variability of left and right atrial and left ventricular bloodflow was studied using transthoracic and transesophageal Doppler echocardiography and related to pacemaker mode preference during everyday activity. Bloodflow variability was less at all sites during dual chamber pacing compared to single chamber pacing. However, in patients suffering from pacemaker syndrome and who prefer DDDR pacing, significantly increased variability of left atrial antegrade (but not retrograde) bloodflow during VVIR pacing compared to DDDR pacing was noted, which was not evident in patients tolerating VVIR mode pacing. This effect was not detected at any other site and suggests that adverse left atrial hemodynamics may result in intolerance to VVI/R mode pacing and might cause pacemaker syndrome.
BACKGROUND: Abnormal flow patterns in the left atrium in atrial fibrillation or mitral stenosis are associated with an increased risk of thrombosis and systemic embolisation; the characteristics of normal atrial flow that avoid stasis have not been well defined. OBJECTIVES: To present a three dimensional particle trace visualisation of normal left atrial flow in vivo, constructed from flow velocities in three dimensional space. METHODS: Particle trace visualisation of time resolved three dimensional magnetic resonance imaging velocity measurements was used to provide a display of intracardiac flow without the limitations of angle sensitivity or restriction to imaging planes. Global flow patterns of the left atrium were studied in 11 healthy volunteers. RESULTS: In all subjects vortical flow was observed in the atrium during systole and diastolic diastasis (mean (SD) duration of systolic vortex, 280 (77) ms; and of diastolic vortex, 256 (118) ms). The volume incorporated and recirculated within the vortices originated predominantly from the left pulmonary veins. Inflow from the right veins passed along the vortex periphery, constrained between the vortex and the atrial wall. CONCLUSIONS: Global left atrial flow in the normal human heart comprises consistent patterns specific to the phase of the cardiac cycle. Separate paths of left and right pulmonary venous inflow and vortex formation may have beneficial effects in avoiding left atrial stasis in the normal subject in sinus rhythm.
Post-operative data have been presented in seven patients with atrial septal defect. In five of them, residual patency of the atrial septum was found at cardiac catheterization, but in two the defect had been closed. All showed evidence of 'left-sided dysfunction', expressed either as an increase in the pulmonary arterial wedge pressure or the left ventricular end-diastolic pressure or both. The reasons for these findings are not clear, though in several there were indications of impaired right ventricular compliance and possible transmission of raised right-sided pressures to the left side of the heart through a still patent atrial septum. This could not, however, be the mechanism in all cases, and dysfunction of the left ventricle has been seen in two patients in whom the defect was securely closed. The cause of this phenomenon in these selected cases remains obscure.
Results from our laboratory have indicated that, compared with those of the 1-G supine (Sup) position, left atrial diameter (LAD) and transmural central venous pressure increase in humans during weightlessness (0 G) induced by parabolic flights (R. Videbaek and P. Norsk. J. Appl. Physiol. 83: 1862-1866, 1997). Therefore, because cardiopulmonary low-pressure receptors are stimulated during 0 G, the hypothesis was tested that mean arterial pressure (MAP) in humans decreases during 0 G to values below those of the 1-G Sup condition. When the subjects were Sup, 0 G induced a decrease in MAP from 93 +/- 4 to 88 +/- 4 mmHg (P < 0.001), and LAD increased from 30 +/- 1 to 33 +/- 1 mm (P < 0.001). In the seated position, MAP also decreased from 93 +/- 6 to 87 +/- 5 mmHg (P < 0.01) and LAD increased from 28 +/- 1 to 32 +/- 1 mm (P < 0.001). During 1-G conditions with subjects in the horizontal left lateral position, LAD increased compared with that of Sup (P < 0.001) with no further effects of 0 G. In conclusion, MAP decreases during short-term weightlessness to below that of 1-G Sup simultaneously with an increase in LAD. Therefore, distension of the heart and associated central vessels during 0 G might induce the hypotensive effects through peripheral vasodilatation. Furthermore, the left lateral position in humans could constitute a simulation model of weightlessness.
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BACKGROUND: Left ventricular diastolic dysfunction, with secondary atrial pressure elevation, is a well-known concept. On the contrary, effect of left atrial compliance on pulmonary pressure is rarely considered. CASE PRESENTATION: We report the echocardiographic case of a 9-year-old child who presented severe rheumatic mitral valve regurgitation with a giant left atrium, in contrast to a normal artery pulmonary pressure, testifying of the high left atrial compliance. CONCLUSION: Left atrial compliance is an important determinant of symptoms and pulmonary artery pressure in mitral valve disease.