Determination of left ventricular wall thickness by angiocardiography

Hugenholtz, Paul G.; Kaplan, Ernest N.; Hull, E I

doi:10.1016/0002-8703(69)90486-4

Cited by 156 publications

(43 citation statements)

References 8 publications

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“…LV wall thickness was estimated throughout the cardiac cycle from the equation of Hugenholtz and colleagues, 9 and LV mass was calculated by the method of Rackley and colleagues. 10 Circumferential stresses were calculated by the method of Mirsky.…”

Section: Discussionmentioning

confidence: 99%

Effects of β-Adrenergic Blocking Therapy on Left Ventricular Diastolic Relaxation Properties in Patients With Dilated Cardiomyopathy

et al. 1999

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Background-The hemodynamic mechanism for the improvement in left ventricle (LV) end-diastolic pressure in cardiomyopathy patients treated with ␤-adrenergic blocking agents is controversial. We hypothesized that the salutary effect of this kind of therapy on LV end-diastolic pressure would be indicative of an improvement in late, passive diastolic relaxation properties. Methods and Results-We studied 14 cardiomyopathy patients in normal sinus rhythm with no arteriographic evidence of coronary artery disease and an LV ejection fraction of Յ40% by radionuclide angiography both before and after 6 months of metoprolol therapy with simultaneous micromanometry and biplane cineventriculography. Four comparable patients who were not treated with metoprolol were studied in a similar fashion and served as control subjects. In those receiving metoprolol, LV end-diastolic pressure decreased (Pϭ0.001). The isovolumic relaxation index, ln , shortened (Pϭ0.03). In a similar fashion, the LV chamber stiffness constant, , decreased (Pϭ0.02), LV volume elastance improved (Pϭ0.04), and the myocardial stiffness constant, e , decreased (Pϭ0.02). A multiple regression analysis revealed that the decrease in LV end-diastolic pressure was indicative of significant improvements in ln and e with the relationship: LV end-diastolic pressureϭϪ4.73ϩ0.27 ln ϩ0.54 e (rϭ0.81, PϽ0.0001). These LV diastolic relaxation properties did not change or worsened in the control cardiomyopathy patients. Conclusions-We conclude that the decrease in LV end-diastolic pressure in cardiomyopathy patients treated with metoprolol is an indicator of improvement in LV diastolic properties resulting from more complete myocardial relaxation. (Circulation. 1999;100:729-735.)

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Section: Discussionmentioning

confidence: 99%

Effects of β-Adrenergic Blocking Therapy on Left Ventricular Diastolic Relaxation Properties in Patients With Dilated Cardiomyopathy

et al. 1999

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“…End-systolic wall thickness was calculated from end-diastolic wall thickness using the amount of shortening and the assumption that left ventricular wall mass is constant throughout systole. 13 Echocardiograms were available in 20 of the 39 patients for corroboration of measured end-diastolic wall thickness. Angiographically determined anterior wall thickness and echocardiographically determined posterior wall thickness were remarkably concordant and did not vary by more than 1 mm in the 16 patients in whom echocardiographic wall thickness was discernible.…”

Section: Methodsmentioning

confidence: 99%

“…Ejection fraction, VcF, and stress data allowed for construction of the stress-shortening relationship. [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16] Pressures were recorded nonsimultaneously just before ventriculography. In patients in atrial fibrillation, RR intervals preceding the beats used for volume determination were matched to similar RR intervals from the pressure tracings.…”

Section: Methodsmentioning

confidence: 99%

Hemodynamic predictors of outcome in patients undergoing valve replacement.

Carabello¹,

Williams²,

Gash³

et al. 1986

Circulation

133

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“…The systolic increase in wall thickness was then calculated using the assumption that left ventricular mass remains constant throughout the cardiac cycle (18). Circumferential wall stress was calculated frame by frame using Mirsky's (19) formula.…”

Section: Patient Studiesmentioning

confidence: 99%

Mechanism of decreased forward stroke volume in children and swine with ventricular septal defect and failure to thrive.

Corin¹,

Swindle²,

Spann³

et al. 1988

J. Clin. Invest.

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Children with ventricular septal defect (VSD) often demonstrate failure to thrive (Ff1'). Such patients usually have reduced systemic cardiac output which has been postulated as a cause for their growth retardation. This study was conducted to ascertain the mechanism of the reduced cardiac output in children with VSD and FT1'1 and also in a porcine model of VSD. Forward stroke volume was reduced in VSD-F'IT children, 31±8 ml/m2, compared to normal children, 49±15 ml/m2 (P < 0.05), but was not reduced in children with VSD and normal growth and development (41±16 ml/m2). Forward stroke volume was also reduced in swine with VSD compared to controls. Contractility assessed by mean velocity of circumferential shortening (Vd) corrected for afterload was similar in normals and VSD-FT'I children. Contractile performance was also similar in normal and VSD swine. Afterload assessed as systolic stress was similar in FIT-VSD children and normal subjects. Preload assessed as end-diastolic stress was increased in the VSD-FI' group. End-diastolic volume was not larger in the VSD-FTI' group. We conclude that the reduced stroke volume seen in VSD-FT'I children and VSD-swine was not due to reduced contractility, increased afterload or reduced preload. The reduced stroke volume may have been due to failure of end-diastolic volume to increase adequately.

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Determination of left ventricular wall thickness by angiocardiography

Cited by 156 publications

References 8 publications

Effects of β-Adrenergic Blocking Therapy on Left Ventricular Diastolic Relaxation Properties in Patients With Dilated Cardiomyopathy

Effects of β-Adrenergic Blocking Therapy on Left Ventricular Diastolic Relaxation Properties in Patients With Dilated Cardiomyopathy

Hemodynamic predictors of outcome in patients undergoing valve replacement.

Mechanism of decreased forward stroke volume in children and swine with ventricular septal defect and failure to thrive.

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