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 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We designed this study to test the hypothesis that in acute mitral regurgitation the mitral regurgitant area (MRA) is a dynamic quantity which varies with the time variation of ventricular volume. Mitral insufficiency was created in five open-chest dogs in which a portion of the anterior leaflet was excised. Phasic aortic and mitral flows were measured electromagnetically, along with left atrial and ventricular pressures. Filling, regurgitant, and stroke volumes, and systolic pressure gradient were determined by digital methods. MRA was calculated from the fluid dynamic equation of motion to give the temporal mean and the instantaneous value at three instants of time and at the time of peak flow (when inertia is negligible). Mean regurgitant fraction was 42 +/- 12% with no indication of left ventricular failure due to volume overload. MRA decreased monotonically with time to 59% of its initial value and closely paralleled the decrease in ventricular volume during systole. In a control study using a tilting-disc prosthesis with a hole 5 mm in diameter in the occluder, the calculated MRA was time invariant and equal to the measured area for regurgitation. We conclude that in acute mitral regurgitation the MRA is a function of ventricular volume.
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PMID:Dynamic changes in the canine mitral regurgitant orifice area during ventricular ejection. 48 30

Echocardiographic aortic root motion in systole was studied in 57 patients: 13 normal subjects, 4 patients with left ventricular (LV) volume overload due to anaemia, 16 patients with mitral incompetence, 13 with aortic incompetence and 11 with mitral stenosis. In normal subjects, patients with mitral stenosis and in patients with LV volume overload, in whom the increased stroke volume was ejected forwards into the ascending aorta (anaemia, aortic incompetence) the amplitude of motion of the posterior aortic wall (vp), the aortic widening fraction (AWF) and total aortic motion (TAM) were increased. In mitral incompetence, however, despite the large increase in total LV stroke index, there was a decrease in vp (P less than 0.01), AWF (P less than 0.001) and TAM (P less than 0.001), and the decrease in aortic motion for a given stroke index was related to the mitral regurgitant fraction, indicating that aortic wall movement in systole depended predominantly on forward ejection of the LV stroke volume. Reduced echocardiographic aortic root motion and widening during systole are useful echocardiographic signs of mitral regurgitation.
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PMID:Echocardiographic aortic root motion in ventricular volume overload and the effect of mitral incompetence. 51 Mar 47

Cross-sectional echocardiograms of the mitral valve orifice were recorded in 37 patients with mitral stenosis. Twenty-seven had pure mitral stenosis, and 10 had associated mitral regurgitation. Mitral valve area in patients with pure mitral stenosis measured from cross-sectional echocardiography was highly correlated (r = 0.89) with that calculated with the Gorlin formula using the pressure gradient and Fick cardiac output. With mitral regurgitation, mitral valve area by cross-sectional echocardiography correlated well (r = 0.90) with that calculated from the pressure gradient and cineangiographic stroke output. In two cases, direct pathologic measurements of mitral valve area agreed exactly with the cross-sectional echocardiographic measurement. Correlation between the mitral E-F slope and mitral valve area by cross-sectional echocardiography (r = 0.56) and catheterization (r = 0.49) was less reliable. Cross-sectional echocardiographic measurement of the mitral valve area correlates well with catheterization in patients with pure mitral stenosis and those with associated regurgitation.
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PMID:Determination of mitral valve area by cross-sectional echocardiography. 62 95

A formula was derived for calculating mitral valve stroke volume (MVSV) using the rate of mitral valve (MV) opening (DE slope on the MV echogram), the vertical disease between the mitral leaflet echoes early in diastole (EE), the electrocardiographic PR interval and heart rate. The formula was tested prospectively on 80 consecutive patients from whom 95 simultaneous MV echograms and either thermodilution (45) or Fick (50) cardiac outputs were obtained. Sixteen patients were normal; 54 had coronary artery disease; three had cardiomyopathy; and seven had nonrheumatic mitral regurgitation (MR). Linear regression for stroke volume was r = 0.90, SEE +/- 6, and for cardiac output r = 0.83, SEE +/- 0.5 liter for the 73 patients without MR. The presence or absence of ventricular dyssynergy did not alter statistical findings. MVSV consistently overestimated forward stroke volume for the seven patients with MR. This study shows that the MV echogram provides an accurate, widely applicable method for calculating MVSV.
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PMID:Stroke volume calculated from the mitral valve echogram in patients with and without ventricular dyssynergy. 64 75

In patients with valvular heart disease the initial systolic ejection rate was determined in an attempt to characterize ventricular function in pressure and volume overload. By means of left ventricular cineangiography, the volume change during the initial third of the ejection phase was determined and the mean ejection rate of this period was calculated. A total of 40 patients were examined, 7 patients without heart disease, 15 patients with pure aortic regurgitation, 9 patient with pure aortic stenosis and 9 patients with pure mitral regurgitation. In patients with pure aortic regurgitation and high-normal values for ejection fraction and mean velocity of circumferential fiber shortening (mVcf) a significant increase in initial systolic ejection rate when compared to the group of normals was observed. The distribution of the stroke volume for each third of the ejection phase corresponded to the normal pattern. In contrast, in patients with low-normal values for ejection fraction and mVcf, a decrease in the initial systolic ejection rate below the normal value was observed, along with a pathological distribution of the stroke volume during the ejection phase. This finding was also noted in all patients with pure mitral regurgitation and pure aortic stenosis. In aortic stenosis, the decline in initial systolic ejection rate was regarded as a consequence of the outflow tract obstruction, whereas in volume overload, this was regarded as a sign of a decline in ventricular function which is not recognized with global parameters such as ejection fraction and mVcf.
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PMID:[Initial systolic ejection rate as a parameter of ventricular function in valvular heart disease (author's transl)]. 65 6

The severity of mitral regurgitation is, in part, determined by aortic impedance to left ventricular outflow. Sodium nitroprusside acutely decreases regurgitant flow, but the importance of its dual vasodilating effects, the lowering of peripheral vascular resistance and increasing of venous capacitance, is unclear. We studied the hemodynamic response to intravenous hydralazine, which selectively acts on the arteriolar resistance bed, in 10 patients with severe mitral regurgitation. Hydralazine produced a 50% increase in forward stroke volume (22 +/- 2 to 33 +/- 3 ml/m2, P less than 0.001) and a 33% reduction in regurgitant stroke volume (40 +/- 6 to 27 +/- 6 ml/m2, P less than 0.001), with a resultant fall in pulmonary capillary wedge v wave and mean pressures. Unlike nitroprusside, it did not alter left ventricular end-diastolic volume or pressure. Oral hydralazine maintained this hemodynamic improvement for at least 48 hours and, in three patients, provided more sustained clinical improvement. We conclude that hydralazine, by virtue of its selective lowering of aortic impedance, reduces the amount of mitral regurgitation and thus may be a useful mode of interim or chronic therapy in selected patients.
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PMID:Beneficial effects of hydralazine in severe mitral regurgitation. 66 75

The hemodynamic effects of the site of the artificial cardiac stimulation were studied in 17 open chest dogs. The right atrium and five ventricular sites (the inflow and outflow tracts and apex of the right ventricle, apex and lateral wall of the left ventricle) were stimulated electronically at a given rate, ranging from 130 to 190 per min. When cardiac performance during ventricular pacing was compared with those during right atrial pacing, the former uniformly caused a diminution of cardiac output and systemic blood pressure, without reduction of left ventricular end-diastolic pressure. Ventricular function curves, in which left ventricular stroke work was related to left ventricular end-diastolic pressure, shifted downwards and to the right during ventricular pacing. Stimulation frequency did not alter these variables. It was considered that the left ventricular dysfunction in ventricular pacing resulted from the absence of atrial contribution to ventricular filling, mitral regurgitation present and asynchronous ventricular contraction. No significant difference of cardiac performance was demonstrated by changing the site of ventricular pacing, suggesting that the mode of ventricular depolarization itself was not relevant to a decrease in cardiac performance.
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PMID:Effects of varying pacemaker sites on left ventricular performance. 101 96

Mechanical factors that can modify the peak transvalvar pressure differences (delta P) in aortic stenosis were evaluated in a model. A latex rubber sac simulated the ventricle. Expansion of the walls of the sac by means of a negative pressure applied to its outer wall introduced a measure volume into the sac and placed the wall materials under tension. The stretched sac was then permitted to contract and to expel its contents through "aortic valvar" orifices of various severities of stenosis, into an aortic standpipe of selected diameters (compliances). Factors that increased the peak delta P included the strength (thickness) of the ventricular wall, the rate at which it mobilized and applied its tensile force to compress the sac contents, the unstressed volume of the sac, the total volume in the sac at onset of contraction, the severity of the valvar stenosis, the compliance of the aorta, the rate of arterial run-off, and the aortic diastolic pressure. Loss of forward stroke volume due to mitral regurgitation lowered the peak delta P. Elevations in diastolic arterial pressure also lowered delta P. All of these mechanical factors should be considered in the analysis of the severity of clinical aortic valvar stenosis and in decisions for medical therapy and surgical correction. The several factors which do not depend directly on the orifice area or on the forward stroke volume vitiate the sole use of the orifice formula in the analysis of the dynamics of aortic stenosis. The application of this approach in related problems is indicated.
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PMID:Factors affecting the transvalvar pressure difference in a hydraulic model of aortic stenosis. 101 94

Determination of cardiac output by impedance cardiography exhibited perfect agreement with determinations performed by the Fick principle (r = 0.905; p less than 0.001); the measurements were carried out on 11 patients without valvular disease, 15 patients with mitral stenosis, 5 patients with aortic stenosis and 4 patients with combined aortic valvular disease. Impedance cardiography tends to give an underestimate of the cardiac output in patients with mitral insufficiency (N = 7) and in cases with combined mitral valvular disease (N = 9); in patients suffering from aortic insufficiency (N = 6), combined valvular disease (N = 5) and left to right shunts (N = 10) the cardiac output is often overestimated. Impedance cardiography is also suitable for determination of the cardiac output under exercise testing conditions up to submaximum ranges. This was demonstrated on 30 well-trained sportsmen, in a comperison and oxygen consumption testing (r = 0.937; p less than 0.001). Zo impedance does not change in healthy persons during exercise testing. Pharmacological investigations can be performed using impedance cardiography; a reduction in pressure values in pulmonary hypertension was demonstrated under the influence of nitroprusside. The stroke volume of a single cardiac revolution was, more over, measured in 12 patients with implanted pacemakers. P-ST intervals were 70--200 msec. The increase in cardiac output by 33% indifies the opinion that in certain cases, especially in young people, atrial synchronous pacemaker systems should be tried, despite the reported pitfalls and lack of success to date.
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PMID:[Impedance cardiography (author's transl)]. 106 5

To determine the effects of myocardial revascularization on decreased left ventricular diastolic compliance consequent to chronic stable coronary artery disease, 15 patients with patent coronary artery bypass grafts (Group I) were compared with 8 patients with occluded grafts (Group II) studied before and after operation. In addition, eight normal patients served as controls. Left ventricular diastolic compliance was assessed by: (1) total observed diastolic compliance: stroke volume (V) related to left ventricular diastolic pressure (P) change (deltaV/deltaP) normalized for end-systolic volume; (2) left ventricular stiffness index of passive elastic modulus (a equals slope of deltaP/deltaV related to mean left ventricular diastolic pressure); and (3) fractional pattern of left ventricular filling. All patients had normal sinus rhythm and none had preoperative or postoperative mitral regurgitation. The two groups with coronary disease were well matched preoperatively for ventricular function, volumes, mass, segmental contraction and compliance. Ejection fraction increased in Group I (0.56 preoperatively to 0.65 postoperatively, P less than 0.05) but was unchanged in Group II (0.63 To 0.61, P greater 0.05). Postoperative indexes of left ventricular compliance improved in Group I: (1) 0.110 to 0.150 (P less 0.05); (2) 0.030 TO 0.019 (P less 0.05); and (3) 37 to 30 percent filling during last one third of diastole (P less 0.05). These indexes were unchanged postoperatively in Group II: (1) 0.109 to 0.102 (P greater 0.05); (2) 0.033 to 0.039 (P greater than 0.05); and (3) 36 to 41 percent (P greater 0.05). Compliance indexes were not altered (P greater 0.05) in a subset of seven patients in Group I with preoperative or intercurrent myocardial infarction. Thus, this investigation demonstrates the relatively reversible nature of abnormal left ventricular compliance after successful coronary artery bypass surgery in certain patients with ischemic heart disease.
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PMID:Improvement of reduced left ventricular diastolic compliance in ischemic heart disease after successful coronary artery bypass surgery. 107 48


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