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Right ventricular systolic pressure

S100A4 Overexpression Enhanced tumour development and metastasis Increased right ventricular systolic pressure, right ventricular hypertrophy, reduced ventricular elastance and decreased cardiac output. [Pg.101]

Abdelmoneim SS, Bernier M, Scott C, Dhoble A, Ness SAC, Hageen M, Moir S, McCully RB, Pellikka PA, Mulvagh SL. Echocardiography in patients with elevated right ventricular systolic pressure a cohort study. Circ Cardiovasc Lnag 2010 3 240-8. [Pg.760]

The literature includes eight case reports of pulmonary hypertension in AL amyloidosis attributed to pulmonary vascular amyloid deposition (Table 2). Autopsies confirmed pulmonary artery amyloid deposits in four out of four cases. The prevalence of restrictive cardiomyopathy and diastolic dysfunction in AL patients predisposes them to secondary forms of pulmonary vascular disease. Direct measurements of pulmonary artery pressures (PAP) were obtained in five cases (3 pulmonary arteriograms, 2 right heart catheterizations) however, only two reports include direct measures of left atrial filling pressures. Echocardio-graphic estimates of elevated right ventricular systolic pressures and normal diastolic function were reported in all cases. [Pg.794]

Fig. 1. Hemodynamic effects of anandamide in anesthetized mice. Representative recordings ofthe effects of anandamide [20 mg/kg i.v., W-arachidonoyl-ethanolamine (/1 4)] on mean arterial pressure (iW/iP, top panel, cardiac contractility (left ventricular systolic pressure LVSP and dP/df (dPdt) middle panel and pressure-volume relations (bottom panel in a pentobarbital-anesthetized C57BL6 mouse. The five parts of the and bottom panels represent baseline conditions (BI, phase I (/), phase II (//), and phase III (III ofthe anandamide response, and recovery 10 min following the injection. The arrow indicates the injection ofthe drug. The decrease ofthe amplitude of PV loops and shift to the right indicate decrease of cardiac contractile performance... Fig. 1. Hemodynamic effects of anandamide in anesthetized mice. Representative recordings ofthe effects of anandamide [20 mg/kg i.v., W-arachidonoyl-ethanolamine (/1 4)] on mean arterial pressure (iW/iP, top panel, cardiac contractility (left ventricular systolic pressure LVSP and dP/df (dPdt) middle panel and pressure-volume relations (bottom panel in a pentobarbital-anesthetized C57BL6 mouse. The five parts of the and bottom panels represent baseline conditions (BI, phase I (/), phase II (//), and phase III (III ofthe anandamide response, and recovery 10 min following the injection. The arrow indicates the injection ofthe drug. The decrease ofthe amplitude of PV loops and shift to the right indicate decrease of cardiac contractile performance...
Ghio S, Gavazzi A, Campana C, et al. Independent and additive prognostic value of right ventricular systolic function and pulmonary artery pressure in patients with chronic heart failure. J Am Coll Cardiol 2001 37(1) 183—8. [Pg.162]

Cardiovascular Heart weight, wall thickness, left ventricular (LV) and right ventricular (RV) end-diastolic and end-systolic lumen volumes (EDV and ESV, respectively), cardiac output (CO), heart rate, and LV diastolic filling pressure Magnetic resonance imaging Dog Opie189... [Pg.267]

Rats fed 15 mg vanadium/kg as ammonium vanadate for 2 months showed increased right ventricular pressure and pulmonary hypertension, but no changes in systemic circulation (Susie and Kentera 1986). This laboratory also showed that sodium orthovanadate in the food for 6 months did not alter heart rate or blood pressure, but did induce vasoconstriction (Susie and Kentera 1988). Rats that had one kidney removed had increased systolic blood pressure within 7 weeks of consuming 5 mg/kg/day of vanadium in the diet (Steffen et al. 1981). [Pg.21]

Echocardiography is a noninvasive tool that can provide assessment of possible causes, shunts, left atrial hypertension, left ventricular dysfunction, valvular heart disease, and consequences of pulmonary hypertension. Measurements of RV systolic and diastolic pressures, and associated findings of paradoxical septal motion, diminished IVC collapse, RVH, right atrial (RA) or right ventricular (RV) enlargement, pericardial effusion, and decreased RV ejection time should all be included in the assessment of these patients. The measurement of PA pressures can be done with relative precision and varying degrees of correlation with invasive measures. [Pg.147]

Equation (2) states that, given an end-diastolic volume 5V is inversely proportional to (the line coursing from the lower left to upper right corner of the bottom panel of Figure 1). This rectilinear relation is denoted the ventricular end-systolic pressure-stroke volume relationship (VPSVR) . [Pg.92]

Figure 1. Schematic explanation of coupling the left ventricular contraction with the systemic arterial tree. In the middle left panels, left ventricular contraction is represented by its end-systolic pressure-volume relationship. Given a particular end diastolic volume (EDV), this relationship can be converted into ventricular end-systolic pressure P s) stroke volume (5Vj relationship, which is shown by the rectilinear curve coursing from the lower left to upper right corner in the graph at the bottom. In the right middle panel, the aortic input impedance property is represented by a rectilinear arterial end-systolic pressure fF, )-stroke volume SV) relationship curve (Eq. (5)). See the text for the explanation of this representation. This arterial Pes-SV relationship is transcribed in the bottom panel in superposition with the ventricular Pe -SV relationship. The intersection of the two Pes-SV relationship curves indicates the end-systolic pressure and stroke volume which should result from coupling a left ventricle with the given EDV and the slope parameter with a systemic arterial tree with the slope parameter... Figure 1. Schematic explanation of coupling the left ventricular contraction with the systemic arterial tree. In the middle left panels, left ventricular contraction is represented by its end-systolic pressure-volume relationship. Given a particular end diastolic volume (EDV), this relationship can be converted into ventricular end-systolic pressure P s) stroke volume (5Vj relationship, which is shown by the rectilinear curve coursing from the lower left to upper right corner in the graph at the bottom. In the right middle panel, the aortic input impedance property is represented by a rectilinear arterial end-systolic pressure fF, )-stroke volume SV) relationship curve (Eq. (5)). See the text for the explanation of this representation. This arterial Pes-SV relationship is transcribed in the bottom panel in superposition with the ventricular Pe -SV relationship. The intersection of the two Pes-SV relationship curves indicates the end-systolic pressure and stroke volume which should result from coupling a left ventricle with the given EDV and the slope parameter with a systemic arterial tree with the slope parameter...
Extravascnlar resistance may decrease coronary blood flow, primarily during systole. This effect is much more pronounced in the left ventricle compared with the right ventricle. When the effect of increased contractility is separated from the effect of ventricular pressure, about 75% of extravascnlar resistance is accounted for by passive stretch in equilibrium with ventricular pressure, whereas only 25% results from active myocardial contraction. [Pg.265]


See other pages where Right ventricular systolic pressure is mentioned: [Pg.1320]    [Pg.147]    [Pg.151]    [Pg.758]    [Pg.348]    [Pg.742]    [Pg.1320]    [Pg.147]    [Pg.151]    [Pg.758]    [Pg.348]    [Pg.742]    [Pg.806]    [Pg.143]    [Pg.197]    [Pg.144]    [Pg.54]    [Pg.596]    [Pg.131]    [Pg.1796]    [Pg.1621]    [Pg.404]    [Pg.152]    [Pg.392]    [Pg.95]    [Pg.132]    [Pg.87]    [Pg.88]    [Pg.1566]    [Pg.150]    [Pg.2809]    [Pg.474]    [Pg.523]    [Pg.289]    [Pg.133]    [Pg.318]    [Pg.303]    [Pg.330]   
See also in sourсe #XX -- [ Pg.147 ]




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Systole

Systolic

Systolic pressure

Ventricular

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