Showing papers by "Walter Paulus published in 1987"

Post-reextension force decay of relaxing cardiac muscle.

Abstract: Residual active cardiac muscle force during ventricular filling causes deviations of the pressure-volume and pressure-segment length relations from passive left ventricular compliance curves. A possible interaction at the myocardial level between muscle reextension and subsequent active force decay has not yet been investigated. We therefore studied the relation between isolated cat papillary muscle reextension, load during reextension, and isometric force decay after isotonic reextension. Both timing and extent of the isotonic muscle reextension phase were altered while load during reextension was lowered, subsequent residual isometric force was decreased. The extent of reextension or the final muscle length did not alter residual active isometric force after isotonic reextension at an identical load. Moreover, irrespective of the loading history of the shortening phase of the contraction, equal loads during reextension resulted in superimposable subsequent isometric force decay traces. From these results it therefore appears that residual isometric force after isotonic reextension is determined by the load during reextension. Extrapolation of these results to the filling ventricle implies the existence of a dynamic interaction between instantaneous extent of filling, wall stress, and residual force development.

Failure of Inactivation of Hypertrophied Myocardium: A Cause of Impaired Left Ventricular Filling in Hypertrophic Cardiomyopathy and Aortic Stenosis

Abstract: Impaired left ventricular filling has been observed in hypertrophic cardiomyopathy [1–5] and in pressure overload hypertrophy [1, 4, 6–12] This impairment of left ventricular filling has been related to slow left ventricular pressure decay [13, 14], which prolongs isovolumic relaxation and impedes left ventricular inflow [15, 16] A slow left ventricular pressure decay, persisting into the left ventricular filling phase can be explained by a failure of myocardial inactivation [17, 18], which causes incomplete myoplasmic calcium reuptake and favors persistent diastolic cross-bridge interaction and contractile tension generation A failure of myocardial inactivation of the hypertrophied left ventricle could be induced by a shift of certain critical proteins involved in excitation-contraction coupling towards isomeric forms with slower enzyme kinetics and an altered calcium sensitivity [19, 20]

Dilatation of stenotic aortic valves through a temporary vascular prosthesis on the subclavian artery

Abstract: Percutaneous valve dilatation recently has been proposed as an alternative palliative procedure for valve replacement in the elderly patient with valvular aortic stenosis (AS). 1,2 The current technique is hampered by a number of technical problems such as a lack of suitable introducer sheaths, obstructive peripheral vascular disease, elongation or dilation of the aortic root and lack of a profiled balloon catheter, all of which may preclude smooth advance of the balloon catheter over the guidewire. In addition, in the presence of a tight AS, crossing the valve with the balloon catheter may become impossible due to dissipation of the forward forces through loss of catheter support in tortuous iliac arteries. The alternative approach through the brachial artery may alleviate some of these problems. However, arterial tortuosities in the lower neck and the small sizes of the brachial artery, especially in women, might also increase failure rate. In our first 15 aortic valvuloplasties, crossing the aortic valve with the balloon catheter was impossible in 2 patients due to the combination of tight AS and extreme tortuosity of the iliac artery. Both patients were elderly woman and the size of the brachial artery was anticipated to be too small to accept the larger dilatation balloon catheters. Therefore, valvuloplasty was attempted through a temporary graft mounted on the subclavian artery. Since then, this new technique was successfully used in 2 more patients in whom severe peripheral vascular disease precluded the standard femoral approach.