scholarly journals Effects of abnormal activation on the time course of the left ventricular pressure pulse in dilated cardiomyopathy

Heart ◽  
1992 ◽  
Vol 68 (10) ◽  
pp. 403-407 ◽  
Author(s):  
H. B Xiao ◽  
S. J D Brecker ◽  
D. G Gibson
1993 ◽  
Vol 265 (3) ◽  
pp. H899-H909 ◽  
Author(s):  
D. Burkhoff ◽  
P. P. De Tombe ◽  
W. C. Hunter

This study focuses on elucidating how ventricular afterloading conditions affect the time course of change of left ventricular pressure (LVP) throughout the cardiac cycle, with particular emphasis on revealing specific limitations in the time-varying elastance model of ventricular dynamics. Studies were performed in eight isolated canine hearts ejecting into a simulated windkessel afterload. LVP waves measured (LVPm) during ejection were compared with those predicted (LVPpred) according to the elastance theory. LVPm exceeded LVPpred from a time point shortly after the onset of ejection to the end of the beat. The instantaneous difference between LVPm and LVPpred increased steadily as ejection proceeded and reached between 45 and 65 mmHg near end ejection. This was in large part due to an average 35-ms prolongation of the time to end systole (tes) in ejecting compared with isovolumic beats. The time constant of relaxation was decreased on ejecting beats so that, despite the marked prolongation of tes, the overall duration of ejecting contractions was not greater than that of isovolumic beats. The results demonstrate a marked ejection-mediated enhancement and prolongation of ventricular pressure-generating capacity during the ejection phase of the cardiac cycle with concomitant acceleration of relaxation. None of these factors are accounted for by the time-varying elastance theory.


2013 ◽  
Vol 115 (11) ◽  
pp. 1672-1682 ◽  
Author(s):  
Ellyce Stehlin ◽  
Simon C. Malpas ◽  
David M. Budgett ◽  
Carolyn J. Barrett ◽  
Daniel McCormick ◽  
...  

Measurements of left ventricular pressure (LVP) in conscious freely moving animals are uncommon, yet could offer considerable opportunity for understanding cardiovascular disease progression and treatment. The aim of this study was to develop surgical methods and validate the measurements of a new high-fidelity, solid-state pressure-sensor telemetry device for chronically measuring LVP and dP/d t in rats. The pressure-sensor catheter tip (2-Fr) was inserted into the left ventricular chamber through the apex of the heart, and the telemeter body was implanted in the abdomen. Data were measured up to 85 days after implant. The average daytime dP/d t max was 9,444 ± 363 mmHg/s, ranging from 7,870 to 10,558 mmHg/s ( n = 7). A circadian variation in dP/d t max and heart rate (HR) was observed with an average increase during the night phase in dP/d t max of 918 ± 84 mmHg/s, and in HR of 38 ± 3 bpm. The β-adrenergic-agonist isoproterenol, β1-adrenergic agonist dobutamine, Ca2+ channel blocker verapamil, and the calcium sensitizer levosimendan were administered throughout the implant period, inducing dose-dependent time course changes and absolute changes in dP/d t max of −6,000 to +13,000 mmHg/s. The surgical methods and new technologies demonstrated long-term stability, sensitivity to circadian variation, and the ability to measure large drug-induced changes, validating this new solution for chronic measurement of LVP in conscious rats.


1990 ◽  
Vol 258 (5) ◽  
pp. H1348-H1356
Author(s):  
W. P. Miller ◽  
S. H. Nellis ◽  
A. J. Liedtke

In intact hearts the beat-to-beat left ventricular systolic pressure-length relationship is not uniquely defined, but rather is history dependent and appears hysteretic. The purpose of these studies was to assess the time course of this phenomenon. In an open chest swine heart preparation, left ventricular pressure, regional lengths, and wall thickness were measured. Loading conditions were altered by the infusion of volume into the left ventricle to increase peak systolic pressure approximately 30 mmHg. The resultant interbeat systolic pressure-dimension relationships were hysteretic. The first part of the study (n = 13) was to test whether the myocardium exhibited a long-term memory of prior mechanical events. Measurements obtained 30 and 120 s after volume loading revealed no residual differences in pressure or dimension compared with preinjection values. Thus the phenomenon was transient and complete (reversible) by 30 s. To better characterize this event, the temporal effects of myocardial loading were studied (n = 8). A randomized comparison of two different rates of volume infusions (27 +/- 2 vs. 56 +/- 2 ml/s, P less than 0.001) was performed. Varying the volume loading resulted in similar increases in peak left ventricular pressure (35 +/- 3 vs. 31 +/- 3 mmHg) but at different increments of development, i.e., greater than 5-7 cardiac cycles at the slower rate of volume infusion vs. greater than 2-3 cardiac cycles (P less than 0.001) at the faster rate. The isochronal systolic pressure-dimension relationships were quantitated by measuring the area of the hysteretic relationship and its slope.(ABSTRACT TRUNCATED AT 250 WORDS)


1960 ◽  
Vol 199 (2) ◽  
pp. 328-330 ◽  
Author(s):  
John W. Remington

An accurate record of the left ventricular pressure pulse in the dog is difficult to register, and often cannot be recognized unless a comparison with a simultaneously recorded pulse from the ascending aorta is made. What seem reliable records usually indicate a transient pressure excess over the aortic level when ejection presumably is beginning. Hence, there is a lag of some 5 msec. between the time when the ventricular pressure reaches the aortic diastolic pressure level and the start of the aortic pulse. The timing of the latter is coincident with an inflection on the slope of ventricular pressure rise. The start of the pulse requires little, if any, transmission lag for the first part of the ascending aorta, but does for the descending aorta. The incisura, in contrast, shows a propagation delay from the very mouth of the aorta. The initial steep slope of the aortic pulse, and the height of the inflection, are not necessarily related to the slope of the ventricular pulse, or the excess ventricular pressure height-initiating ejection.


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