Arterial pressure in humans during weightlessness induced by parabolic flights.
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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. (+info)
Changes in left ventricular filling and left atrial function six months after nonsurgical septal reduction therapy for hypertrophic obstructive cardiomyopathy.
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OBJECTIVES: The purpose of this study was to evaluate changes in left ventricular (LV) filling, left atrial (LA) volumes and function six months after nonsurgical septal reduction therapy (NSRT) for hypertrophic obstructive cardiomyopathy (HOCM). BACKGROUND: Patients with HOCM frequently have enlarged left atria, which predisposes them to atrial fibrillation. Nonsurgical septal reduction therapy results in significant reduction in left ventricular outflow tract (LVOT) obstruction and symptomatic improvement. However, its effect on LV passive filling volume, LA volumes and function is not yet known. METHODS: Thirty patients with HOCM underwent treadmill exercise testing as well as 2-dimensional and Doppler echocardiography before and six months after NSRT. Data included clinical status, exercise duration, LVOT gradient, mitral regurgitant (MR) volume, LV pre-A pressure and LA volumes. Left atrial ejection force and kinetic energy (KE) were computed noninvasively and were compared with 12 age-matched, normal subjects. RESULTS: New York Heart Association (NYHA) class was lower and exercise duration was longer (p < 0.05) six months after NSRT. The LVOT gradient, MR volume and LV pre-A pressure were all significantly reduced. HOCM patients had larger atria, which had a higher ejection force and KE, compared with normal subjects (p < 0.01). After NSRT, LV passive filling volume increased (p < 0.01), whereas LA volumes, ejection force and KE decreased (p < 0.01). Reduction in LA maximal volume was positively related to changes in LV pre-A pressure (r = 0.8, p < 0.05) and MR volume (0.4, p < 0.05). Changes in LA ejection force were positively related to changes in LA pre-A volume (r = 0.7, p < 0.01) and KE (r = 0.81, p < 0.01). The increase in exercise duration paralleled the increase in LV passive filling volume (r = 0.85, p < 0.05). CONCLUSIONS: Nonsurgical septal reduction therapy results in an increase in LV passive filling volume and a reduction in LA size, ejection force and KE. (+info)
Mechanical remodeling of the left atrium after loss of atrioventricular synchrony. A long-term study in humans.
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BACKGROUND: Tachycardia-mediated mechanical remodeling of the atrium is considered central to the pathogenesis of thromboembolism associated with chronic atrial fibrillation. Whether atrial mechanical remodeling also occurs in response to atrial stretch induced by chronic asynchronous ventricular pacing in patients with permanent pacemakers is unknown. METHODS AND RESULTS: The study design was a prospective randomized comparison between 21 patients paced chronically in the VVI mode and 11 patients paced chronically in the DDD mode for 3 months. Left atrial appendage (LAA) function and the presence of spontaneous echo contrast (SEC) were determined with transesophageal echocardiography (TEE) within 24 hours of pacemaker implantation and after 3 months. The VVI patients were then programmed to DDD and underwent a third TEE after DDD pacing for an additional 3 months. After chronic VVI pacing, LAA velocity decreased from 82.4+/-29.0 to 42.1+/-25.4 cm/s (P<0.01), LAA fractional area change decreased from 74.9+/-17.2% to 49.8+/-22.0% (P<0.01), and 4 patients (19%) developed left atrial SEC (P<0.05). With the reestablishment of chronic AV synchrony, LAA velocity increased to 61.6+/-18.5 cm/s (P<0.01), LAA fractional area change increased to 76.4+/-18.1% (P<0.01), and SEC resolved. In the 11 patients undergoing chronic DDD pacing, no significant changes in LAA velocity (baseline, 86.0+/-28.8 cm/s versus 3 months, 79.6+/-14. 9 cm/s) or LAA fractional area change (baseline, 76.2+/-19.4% versus 72.5+/-15.7%) were demonstrated, and SEC did not develop. CONCLUSIONS: Chronic loss of AV synchrony induced by VVI pacing is associated with mechanical remodeling of the left atrium, which may reverse after the reestablishment of AV synchrony with DDD pacing. This process may be partly responsible for the higher incidence of thromboembolism observed in patients undergoing VVI pacing compared with AV sequential pacing. (+info)
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.
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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. (+info)
Functional studies in atrium overexpressing A1-adenosine receptors.
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1. Adenosine and the A1-adenosine receptor agonist R-PIA, exerted a negative inotropic effect in isolated, electrically driven left atria of wild-type mice. 2. In left atria of mice overexpressing the A1-adenosine receptor, adenosine and R-PIA exerted a positive inotropic effect. 3. The positive inotropic effect of adenosine and R-PIA in transgenic atria could be blocked by the A1-adenosine receptor antagonist DPCPX. 4. In the presence of isoprenaline, adenosine exerted a negative inotropic effect in wild-type atria but a positive inotropic effect in atria from A1-adenosine receptor overexpressing mice. 5. The rate of beating in right atria was lower in mice overexpressing A1-adenosine receptors compared with wild-type. 6. Adenosine exerted comparable negative chronotropic effects in right atria from both A1-adenosine receptor overexpressing and wild-type mice. 7. A1-adenosine receptor overexpression in the mouse heart can reverse the inotropic but not the chronotropic effects of adenosine, implying different receptor-effector coupling mechanisms. (+info)
Prognostic value of changes over time in exercise capacity and echocardiographic measurements in patients with chronic heart failure.
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AIMS: This study sought to examine the predictive values of changes over time in exercise capacity and echocardiographic measurements of ventricular dimensions or function in predicting mortality in patients with chronic heart failure. METHODS AND RESULTS: Sixty-two patients with chronic heart failure (58 men, mean [+/-SD] age 60+/-10 years, mean peak oxygen consumption (VO(2)) 18.2+/- 5.9 ml. kg(-1). min(-1), mean left ventricular ejection fraction 38.9+/-15. 8%) who underwent both treadmill exercise testing and echocardiographic examination on two occasions, separated by 19+/-15 months were followed-up for a mean of 17 months (interquartile range 9-30 months). During the follow-up period, 19 patients (30%) died and three (4.8%) underwent heart transplantation. Of measurements taken at a single time-point (visit 2) exercise duration, peak VO(2), ventilatory response to exercise (VE/VCO(2)), left atrial diameter and left ventricular ejection fraction were found, by Cox proportional-hazard analysis, to predict the outcome in these patients (all P<0.05). Of the changes in parameters between visit 1 to visit 2, only changes in peak VO(2)per year (P=0.026) predicted non-transplanted survival (independent of changes in left ventricular ejection fraction and VE/VCO(2)). In Kaplan-Meier survival analysis patients with increased peak VO(2)over time (n=28) showed a better prognosis at 2 years (cumulative survival 75% [95% confidence interval: 56-95%] than those with a decrease in peak VO(2)(n=34, cumulative survival 50% [95% confidence interval: 31-68%]). CONCLUSIONS: Although single estimates of peak VO(2), VE/VCO(2)and left ventricular ejection fraction have significant prognostic importance in patients with chronic heart failure, when monitoring changes over time only peak VO(2)remains a significant predictor of outcome. (+info)
Lipoprotein(a), left atrial appendage function and thromboembolic risk in patients with chronic nonvalvular atrial fibrillation.
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Lipoprotein(a) (Lp(a)) has a prothrombotic effect by modulating the fibrinolytic system. The purpose of the present study was to determine whether serum Lp(a) levels are associated with an increased risk of thromboembolism in chronic nonvalvular atrial fibrillation (NVAF). Clinical, laboratory and transesophageal echocardiographic data were collected in 172 consecutive, non-anticoagulated patients with chronic NVAF. Thirty-four patients (thromboembolic group) had a recent (<1 month) embolic event and/or a left atrial thrombus on transesophageal echocardiography. The thromboembolic group had a higher frequency of spontaneous echo contrast (94 vs. 58%, p<0.0001), increased concentrations of Lp(a) (median: 31.5 vs. 15.5 mg/dl, p<0.0001) and fibrinogen (median: 352 vs. 314 mg/dl, p = 0.0015), larger left atrial dimensions (median: 5.1 vs. 4.8cm, p = 0.0078), and reduced left atrial appendage (LAA) flow velocities (median: 9.5 vs. 21.2 cm/s, p<0.0001) than the nonthromboembolic group. Multivariate analysis identified 3 independent predictors of thromboembolism: Lp(a) level > or =30 mg/dl (odds ratio (OR) 9.5, 95% confidence interval (CI) 4.4-20.4, p<0.0001), LAA flow velocity of <20 cm/s (OR 8.7, 95% CI 3.3-23.0, p = 0.0003) and a fibrinogen concentration of <377mg/dl (OR 3.2, 95% CI 1.5-6.9, p = 0.0201). The Lp(a) elevations and reduced LAA flow velocities are independently associated with thromboembolism in chronic NVAF. (+info)
Left atrial volume assessed by transthoracic three dimensional echocardiography and magnetic resonance imaging: dynamic changes during the heart cycle in children.
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OBJECTIVE: To assess the dynamic changes in left atrial volume by transthoracic three dimensional echocardiography and compare the results with those obtained by magnetic resonance imaging (MRI). DESIGN AND PATIENTS: 30 healthy children (15 boys and 15 girls, aged 8 to 13 years) underwent examination by three dimensional echocardiography and MRI. METHODS: Three dimensional echocardiography of the left atrium was performed using rotational acquisition of planes at 18 degrees intervals from the parasternal window with ECG gating and without respiratory gating. Volume estimation by MRI was performed with a slice thickness of 4-8 mm and ECG triggering during breath holding in deep inspiration. A left atrial time-volume curve was reconstructed in each child. RESULTS: Left atrial maximum and minimum volumes averaged 24.0 ml/m(2) and 7. 6 ml/m(2) by three dimensional echocardiography, and 22.1 ml/m(2) and 11.9 ml/m(2) by MRI. The greater left atrial minimum volume in the latter was at least in part a result of breath holding. Dynamic changes in left atrial volume during the heart cycle were detectable by both methods. The higher temporal resolution of three dimensional echocardiography allowed a more precise evaluation of different phases. CONCLUSIONS: Three dimensional echocardiography and MRI were both useful methods for studying the physiological volume changes in the left atrium in children. These methods may be used for further study of the systolic and diastolic function of the heart. (+info)