Quantitative left ventricular angiocardiographic findings in mitral stenosis

Curry, George C.; Elliott, Larry P.; Ramsey, Howard W.

doi:10.1016/0002-9149(72)90162-2

Cited by 75 publications

(15 citation statements)

References 24 publications

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“…The myocardialfactor is often blamed for the depresxd left ventricular function in rheumatic mitral stenosis (Ferrer et Curry has already shown that LVF impairment occurs with high right ventricular volumes, suggesting a probable interplay between the two ventricles (Curry and Elliott, 1972). In this study, we investigated such a possible relationship.…”

Section: Discussionmentioning

confidence: 85%

“…Nevertheless, global LVF impairment has already been treated in many publications (Bolen et al, 1975;Curry and Elliott, 1972;Linhart, 1972;Ross and Braunwald, 1964), despite a recent controversy (Grbic, 1982;Sigwart and Reid, 1976).…”

Section: Discussionmentioning

confidence: 99%

“…Some recent publications have pointed out the high incidence of contraction abnormality in pure mitral stenosis, such as posterobasal or anterolateral hypokinesis. It has been suggested that a regional contraction abnormality could be responsible for global LV function impairments (Bolen et af., 1975;Curry and Elliott, 1972;Heller and Carleton, 1970).…”

Section: Introductionmentioning

confidence: 99%

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Global left ventricular function and regional wall motion in pure mitral stenosis‐Left ventricular function in pure mitral stenosis

Colle

Rahal

Ohayon

et al. 1984

Clinical Cardiology

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Summary:Global left ventricular function (LVF) and segmental wall motion of the left ventricle are registered in 113 patients presenting a pure mitral stenosis (MS) and in a control group of 50 individuals. The segmental wall motion is measured on the end-diastolic-end-systolic frames of the left ventricle, obtained from right anterior oblique (RAO) monoplane cineangiography . Measurement of the segmental wall shortening is performed using the Stanford method. Group 1 includes 68 patients (60% of the total number of patients studied). These patients show no pathological contraction abnormality. In this group, the global LVF is not different from the control group. Group 2 includes 45 patients (40% of the total) for whom contraction abnormalities are present: anterior hypokinesis in 20% of the cases (anterior area mean shortening (AAS) = 18f8%; p

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Section: Discussionmentioning

confidence: 85%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Global left ventricular function and regional wall motion in pure mitral stenosis‐Left ventricular function in pure mitral stenosis

Colle

Rahal

Ohayon

et al. 1984

Clinical Cardiology

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“…In addition to coronary artery disease, it is well known that many other cardiac diseases may involve segmental contractile abnormalities (such as mitral valve prolapse, or mitral stenosis) (Curry and Eliott, 1972;Gulotta et N / . , 1974;Heller et al, 1970;Honvitz ef a/.…”

Section: Introductionmentioning

confidence: 99%

Untitled

1986

Clinical Cardiology

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Summary:This work attempted to study the segmental wall motion on left ventriculograms, in terms of segmental shortening, velocity of segmental shortening, and temporal sequences of various events in systole as well as in diastole. The ability of such a method to characterize pat-(ems of normal regional wall motion and to detect mild abnormalities such as isolated asynchronisms, was tested on two groups of patients. Group I included 25 patients presenting evidence of a normal left ventricle (LV) after left heart catheterization. Group I1 consisted of 21 patients suffering from an isolated pure idiopathic mitral valve prolapse (MVP), with no mitral insufficiency and with an unaffected global LV function. In all patients left ventnculography was filmed in the right anterior oblique view at a rate of 50 frames/s. For each patient a cycle was chosen, distant from any premature beat, with acceptably contrasted outlines, and a quantitative frame by frame study ofthe motion of 10 segments was performed using a semiautomated method derived from the Stanford method. In the control group (Group I), analysis of the segmental motion by means of this method demonstrates a mild nonuniformity of the normal wall motion. This is prin- vs. Ok0.48 circ/s in Group I, p

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“…'-5 Immobilization of the left ventricular posterobasal area due to a rigid "mitral complex" and impaired contractility of the anterolateral left ventricular wall of uncertain etiology have been observed radiographically and suggested as causes of left ventricular dysfunction.2 4 Ventricular function curves constructed using angiotensin,' isometric handgrip,5 or atrial pacing3 have been interpreted as indicative of abnormal left ventricular function in significant numbers of mitral stenosis patients as compared to normals. 2 Previous reports'13 5 suggest that not all patients with mitral stenosis have detectable radiographic or function abnormalities.…”

mentioning

confidence: 99%

Analysis of left ventricular function in response to afterload changes in patients with mitral stenosis.

Bolen¹,

Lopes²,

Harrison³

et al. 1975

Circulation

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SUMMARYIn order to assess left ventricular function in patients with rheumatic mitral stenosis, left ventricular function curves (plotting stroke work index vs left ventricular end-diastolic pressure) were June 20, 1975. tion curves were constructed by afterload elevation with angiotensin and reduction by nitroprusside. The over-all hemodynamic response of patients with mitral stenosis to these afterload changes was also examined.Methods Fourteen patients with isolated mitral stenosis were included in the study. Informed consent was obtained from all participants. Patients with other valvular disease were excluded by physical examination, echocardiography, and by the results of catheterization. Any patient exhibiting more than trivial mitral regurgitation at the time of left ventricular angiography was excluded.Resting cardiac catheterization was performed after premedication with 100 mg secobarbital intramuscularly. Wedge or NIH catheters with Statham P23Db transducers were employed for right-sided pressures, and 6.7 polyethylene end-hole catheters with Micron MP-15 transducers for left-sided pressures. Cardiac outputs were determined either by the direct Fick method or by duplicate indocyanine green dye dilution techniques. Pressures, mitral valve gradients, and stroke work indices were computerdetermined" and checked manually. Mitral valve area was calculated according to a modified Gorlin formula,7 using the mean pulmonary artery wedge-left ventricular pressure difference as the mitral valve gradient and an empirical constant of 44.5. The use of 44.5 reflects our reservations concerning the precision of constants derived from operative measurements of orifice size and preference for standardization with aortic valve measurements.Resting left ventricular angiography was performed using a 6.7F angiographic catheter passed retrogradely across the aortic valve, and with the patient in the 300 right anterior oblique position. End-diastolic and end-systolic left ventricular volumes and ejection fraction were determined by Circulation, Volume 52, November I975

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Quantitative left ventricular angiocardiographic findings in mitral stenosis

Cited by 75 publications

References 24 publications

Global left ventricular function and regional wall motion in pure mitral stenosis‐Left ventricular function in pure mitral stenosis

Global left ventricular function and regional wall motion in pure mitral stenosis‐Left ventricular function in pure mitral stenosis

Untitled

Analysis of left ventricular function in response to afterload changes in patients with mitral stenosis.

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