TLR4 inactivation and rBPI(21) block burn-induced myocardial contractile dysfunction.
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Both large burns and severe gram-negative sepsis are associated with acute myocardial contractile dysfunction. Because others have reported that burn injury may be followed by transient endotoxemia, we hypothesized that bacterial endotoxin induces contractile impairment after burn trauma. We tested this hypothesis in two rodent models. In each model, postburn myocardial contractility was assessed using Langendorff preparations of excised hearts. In the first model, mice expressing either a mutant form of or no Toll-like receptor 4 (TLR4), a critical element of the mammalian endotoxin receptor, were resistant to postburn myocardial contractile dysfunction. In the second model, starting 30 min or 4 h after burn injury, rats were infused with recombinant bactericidal/permeability-increasing protein (rBPI(21)), a protein that binds and neutralizes endotoxin. Hearts from rBPI(21)-treated animals were completely protected from postburn contractile impairment. Because burn-induced contractile dysfunction can be prevented either by blocking signaling through the endotoxin receptor or by neutralizing circulating LPS, bacterial endotoxin may contribute to impaired myocardial contractility after burn injury. (+info)
Preload-adjusted maximal power of right ventricle: contribution of end-systolic P-V relation intercept.
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To assess whether preload-adjusted maximal power (PAMP), which is calculated as W(max)/V (where W(max) is maximal power and V(ed) is end-diastolic volume with beta = 2) is an index of right ventricular (RV) contractility, we measured RV pressure (P) and volume (V) and pulmonary artery pressure and flow in 10 dogs at baseline and after inotropic stimulation. PAMP was derived from steady-state data, whereas the slope (E(es)) and intercept (V(d)) of the end-systolic P-V relationship were derived from data obtained during vena caval occlusion. Inotropic stimulation increased E(es) (from 0.96 +/- 0.25 to 1.62 +/- 0.28 mmHg/ml; P < 0.001) and V(d) (from -3.0 +/- 17.2 to 12.4 +/- 10.8 ml; P < 0.05) but not PAMP (from 0.24 +/- 0.10 to 0.36 +/- 0.22 mW/ml(2); P = 0.09). We found a strong relationship between the optimal beta-factor for preload adjustment and V(d). A corrected PAMP, PAMP(c) = W(max)/(V(ed) - V(d))(2), which incorporated the V(d) dependency, was sensitive to the inotropic changes (from 0.23 +/- 0.12 to 0.54 +/- 0.17 mW/ml(2); P < 0.001) with a good correlation with E(es) (r = 0.88; P < 0.001). (+info)
Magnetic resonance imaging to assess the hemodynamic effects of pulmonary valve replacement in adults late after repair of tetralogy of fallot.
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BACKGROUND: Pulmonary regurgitation (PR) late after total correction for tetralogy of Fallot may lead to progressive right ventricular (RV) dilatation and an increased incidence of severe arrhythmias and sudden death. Timing of pulmonary valve replacement (PVR) is subject to discussion, because the effect of PVR on RV function in adults is unclear. In this study, MRI was used to assess the effect of PVR on RV function and PR. Clinical improvement was established by means of the NYHA classification. METHODS AND RESULTS: Twenty-six adult patients were included. Cardiac MRI was performed at a median of 5.1+/-3.4 months before and 7.4+/- 2.4 months after PVR. Mean preoperative PR was 46+/-10% (range, 25% to 64%). After PVR, 20 of 26 patients (77%) showed no residual PR, 5 patients showed mild residual PR, and 1 patient showed moderate PR. RV end-diastolic volume (RV-EDV) decreased from 305+/-87 to 210+/-62 mL (P<0.001), and RV end-systolic volume (RV-ESV) decreased from 181+/-67 to 121+/-58 mL (P<0.001). No significant change was found in RV-EF (42% versus 42%). However, RVEF corrected for regurgitations and shunting increased from 25.2+/-8.0% to 43.3+/-13.7% (P<0.001). Mean validity class improved from 2.0 to 1.3 (P<0.001). CONCLUSIONS: In adult patients with PR and RV dilatation, late after total correction of tetralogy of Fallot, MRI measurements show remarkable hemodynamic improvement of RV function after PVR and improvement of validity. We therefore advocate a less restrictive management concerning PVR in these patients. (+info)
Continuous assessment of left ventricular shape in man.
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Frame by frame analysis of left ventriculograms has been performed in 10 normal subjects and 40 patients with heart disease. Left ventricular shape index was derived as 4 pi (cavity area)/(perimeter)2, which has a maximum value of 1 when the outline is circular. In normal subjects systole was always associated with progressive reduction in shape index, indicating that the cavity projection had become less circular. This change was smaller in patients with low ejection fraction and also when inferior or anterior hypokinesia was present, even though ejection fraction was normal. During early diastole shape index rose rapidly due to an increase in minor diameter occurring throughout the period of rapid filling. In some cases this preceded any change in long axis, which was due to upward movement of the aortic root as well as outward movement of the apex. These results have functional implications, suggesting in particular that wall movement during filling may be non-uniform and that assumptions about cavity shape used in the derivation of wall properties from estimates of ventricular volume may require modification. (+info)
Attenuated cardiovascular reserve during prolonged submaximal cycle exercise in healthy older subjects.
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OBJECTIVE: The goal of this study was to determine the effect of age on the hemodynamic response to prolonged submaximal aerobic exercise in healthy volunteers. BACKGROUND: Reductions in peak work rate, heart rate (HR), and left ventricular (LV) emptying but higher blood pressure (BP) and systemic vascular resistance occur in healthy older versus younger humans during short bursts of graded maximal aerobic exercise. However, the effect of aging on the cardiovascular response to prolonged exercise at submaximal work rates typical of daily aerobic activities remains unknown. METHODS: We evaluated cardiovascular performance throughout prolonged submaximal upright cycle ergometry in 40 carefully screened healthy untrained volunteers, 8 men and 12 women <50 years old, mean = 37 +/- 8 years (younger), and 10 men and 10 women >/=50 years old, mean = 66 +/- 9 years (older), during upright cycle exercise at 70% of peak cycle oxygen consumption (VO(2)) to exhaustion or a maximum of 120 min. Cardiac volumes were acquired by gated blood pool scans with (99m)Tc at rest and every 10 min throughout exercise. RESULTS: Duration of exercise was similar in younger ([81 +/- 28 min] versus older [71+/- 29 min] subjects, p = NS). At 10 min of exercise in the steady state, older subjects demonstrated lower VO(2) (1.1 +/- 0.2 l/min vs. 1.3 +/- 0.3 l/min) and lower HR (118 +/- 17 vs. 135 +/- 11 beats/min, p < 0.001) but larger end-diastolic (80 +/- 11 ml/m(2) vs. 73 +/- 8 ml/m(2), p = 0.03) and end-systolic volume index (ESVI) 20 +/- 6 ml/m(2) vs. 17 +/- 4 ml/m(2), p < 0.05) than younger ones. Between 10 min and exercise termination, with VO(2) held constant in both groups, increases in HR (14.0 +/- 12.4 beats/min vs. 5.9 +/- 11.5 beats/min, p = 0.04), cardiac index (1.6 +/- 1.0 l/min/m(2) vs. 0.8 +/- 1.1 l/min/m(2), p = 0.03), and LV ejection fraction (7.1 +/- 4.0% vs. 2.9 +/- 4.4%, p = 0.003) were greater in younger than older subjects, respectively, as was the reduction in ESVI (-5.1 +/- 3.0 ml/m(2) vs. -1.8 +/- 3.3 ml/m(2), p = 0.002), despite similar declines in systolic BP (-12.3 +/- 6.3 mm Hg vs. -12.1 +/- 15.0 mm Hg, p = NS). CONCLUSIONS: Thus, age-associated deficits in chronotropic and LV systolic reserve performance occur during prolonged submaximal upright cycle ergometry, analogous to those observed during graded maximal exercise. (+info)
Influence of gender on the response to hemodynamic overload after myocardial infarction.
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After myocardial infarction (MI), the left ventricle (LV) undergoes ventricular remodeling characterized by progressive global dilation, infarct expansion, and compensatory hypertrophy of the noninfarcted myocardium. Little attention has been given to the response of remodeling myocardium to additional hemodynamic overload. Studies have indicated that gender may influence remodeling and the response to both MI and hemodynamic overload. We therefore determined 1) structural and function consequences of superimposing hemodynamic overload (systemic hypertension) on remodeling myocardium after a MI and 2) the potential influence of gender on this remodeling response. Male and female Dahl salt-sensitive and salt-resistant rats underwent coronary ligation, resulting in similar degrees of MI. One week post-MI, all rats were placed on a high-salt diet. Four groups were then studied 4 wk after initiation of high-salt feeding: MI female, MI female + hypertension, MI male, and MI male + hypertension. Hypertension-induced pressure overload resulted in additional comparable degrees of myocardial hypertrophy in both females and males. In females, hypertension post-MI resulted in concentric hypertrophy with no additional cavity dilation and no measurable scar thinning. In contrast, in males, hypertension post-MI resulted in eccentric hypertrophy, further LV cavity dilation, and scar thinning. Physiologically, concentric hypertrophy in post-MI hypertensive females resulted in elevated contractile function, whereas eccentrically hypertrophied males had no such increase. Female gender influences favorably the remodeling and physiological response to hemodynamic overload after large MI. (+info)
Left ventricular pressure-volume relationship in a murine model of congestive heart failure due to acute viral myocarditis.
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OBJECTIVES: This study, performed in a murine model of encephalomyocarditis virus myocarditis, used a new Millar 1.4F conductance-micromanometer system for the in vivo determination of the left ventricular (LV) pressure-volume relationship (PVR). BACKGROUND: Viral myocarditis is an important cause of congestive heart failure and may lead to dilated cardiomyopathy. However, the hemodynamic changes associated with its acute phase have not been analyzed in detail. METHODS: Four-week-old DBA/2 mice were inoculated with EMCV (day 0). Serial hemodynamic measurements, compared with uninfected control mice were made on days 0, 1, 3, 4, 5, 7, 9, 12, and 14. RESULTS: On day 1, the hearts of infected mice manifested enhanced contractile function, decreased LV compliance, and abnormal diastolic function with increased LV end-diastolic pressure (EDP). Mean stroke index, ejection fraction (EF), and cardiac index (CI) were significantly higher than in uninfected control mice (p < 0.05). Contractile function decreased from days 4 to 14. On day 7, when hemodynamic abnormalities consistent with heart failure culminated, end-diastolic volume (EDV), EDP, and EDPVR were significantly higher, and CI, EF, end-systolic pressure (ESP), and ESPVR significantly lower in the infected than in control mice. Heart rate remained comparable in both groups. Although heart failure receded between day 9 and day 14, ESPVR, ESP, and EF remained significantly depressed up to day 14, and EDV and EDP remained significantly higher. CONCLUSIONS: These hemodynamic data provide new insights into the pathophysiology of acute viral myocarditis and may be useful in the development of therapeutic interventions. (+info)
Left ventricular mass: reliability of M-mode and 2-dimensional echocardiographic formulas.
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The study of left ventricular (LV) hypertrophy is hindered by problems with LV mass measurement by echocardiography. Both the M-mode and 2D area-length formulas for calculating LV mass assume a fixed geometric shape, which may be a source of error. We examined this hypothesis by using cardiovascular magnetic resonance images to eliminate the confounding effects of acoustic access and image quality. LV mass was measured directly in 212 healthy subjects by means of a standard 3D cardiovascular magnetic resonance technique. LV mass was also calculated by using the cube-function and area-length formulas with measurements from the magnetic resonance images. A comparison of serial measurements was made by examining the changes in LV mass by all 3 techniques in those completing an exercise program (n=140). The cube-function technique showed a consistent underestimation of LV mass of 14.3 g, and there were wide 95% limits of agreement (+/-57.6 g and +/-46.3 g for cube-function and area-length techniques, respectively) when compared with 3D measurement. There were similarly wide limits of agreement for the change in mass (+/-55.2 g and +/-44.8 g for cube-function and area-length, respectively). The assumption of geometric shape in the cube-function and area-length formulas resulted in significant variation in LV mass estimates from direct measurement by using a 3D technique. The technique cannot be recommended either at a single time point or for serial studies in small populations; 3D imaging techniques, such as cardiovascular magnetic resonance, are preferable. (+info)