Homeometric Autoregulation

Author(s):  
R. G. Monroe ◽  
W. J. Gamble ◽  
C. G. Lafarge ◽  
S. F. Vatner
2020 ◽  
Vol 598 (15) ◽  
pp. 3129-3153 ◽  
Author(s):  
Jan‐Christian Reil ◽  
Gert‐Hinrich Reil ◽  
Árpád Kovács ◽  
Vasco Sequeira ◽  
Mark T. Waddingham ◽  
...  

1960 ◽  
Vol 8 (5) ◽  
pp. 1077-1091 ◽  
Author(s):  
S. J. SARNOFF ◽  
J. H. MITCHELL ◽  
J. P. GILMORE ◽  
J. P. REMENSNYDER

1995 ◽  
Vol 25 (6) ◽  
pp. 1428-1435 ◽  
Author(s):  
Robert Johannes Menno Klautz ◽  
David Frank Teitel ◽  
Paul Steendijk ◽  
Frank van Bel ◽  
Jan Baan

1968 ◽  
Vol 214 (5) ◽  
pp. 1186-1192 ◽  
Author(s):  
RL Clancy ◽  
Graham TP ◽  
J Ross ◽  
EH Sonnenblick ◽  
E Braunwald

1963 ◽  
Vol 34 (4) ◽  
pp. 440-451 ◽  
Author(s):  
Stanley J. Sarnoff ◽  
Joseph P. Gilmore ◽  
Jere H. Mitchell ◽  
John P. Remensnyder

EP Europace ◽  
2021 ◽  
Vol 23 (Supplement_3) ◽  
Author(s):  
H Odland ◽  
S Ross ◽  
LO Gammelsrud ◽  
R Cornelussen ◽  
E Kongsgard

Abstract Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): Norwegian South East heath Authorities Background We investigated the homeometric autoregulation utilizing a stepwise change in heart rate on dP/dtmax and time to peak dP/dt (Td) with biventricular pacing (BIVP) and the LV lead positioned in the apical, anterior and lateral positions. Pacing at low HR (LHR) and high heart rates (HHR) changes contractility through homeometric autoregulation (Bowditch effect) without changing the resynchronization itself. Purpose To determine the effect of a change in contractility through homeometric autoregulation on two different effect measures of resynchronization therapy. Methods Twenty-nine patients in heart failure with LBBB underwent CRT implantation with continuous LV pressure registration. The LV lead was first placed in either apical or anterior position followed by a permanent placement in a lateral position. Sequential BIVP pacing was performed for one minute, at a rate 10% above intrinsic heart rate (LHR = 75 ± 9bpm), before dP/dtmax measurements were recorded, and the sequence was repeated with pacing rate increased by 30% (HHR = 98 ± 11bpm). Td was defined as the time from pacemaker stimuli to peak dP/dt. Mixed linear models were used for statistics, numbers are estimated marginal means ± SEM. Significance was set at p < 0.05. Results DP/dtmax was higher with HHR in lateral position (1036 ± 41mmHg/s) than with LHR (933mmHg/s). The same was observed for all other lead positions. However, there was no difference between lateral position with LHR and apical position with HHR (930 ± 44mmHg/s). There were no differences in Td between LHR and HHR, but Td was shorter with BIVP in lateral position at pacing LHR (158 ± 4ms) and HHR (155 ± 4ms) than in all other positions. Overall dP/dtmax increased by 10% from LHR to HHR (888 ± 41mmHg/s vs. 980 ± 41 mmHg/s), while overall Td decreased by 2.4% from 168 ± 4ms to 164 ± 4ms. We found a linear relationship between Td and dP/dtmax (R = 0.7) with β=-0.07 that would indicate a 6ms reduction in Td going from LHR to HHR. The overall change in Td from LHR to HHR could therefore be attributed to the change in dP/dtmax. Conclusion Homeometric regulation does not influence Td, but Td is sensitive to changes in resynchronization and pacing lead position. Td is shorter with BIVP in lateral position at both high and low HR as would be expected from a biomarker of resynchronization. HR influences dP/dtmax so distinction between optimal and non-optimal positions using dP/dtmax may be difficult without knowledge of homeometric state.


2005 ◽  
Vol 7 (1) ◽  
pp. 29-35 ◽  
Author(s):  
Klara Brixius ◽  
Hannes Reuter ◽  
Wilhelm Bloch ◽  
Robert H.G. Schwinger

2000 ◽  
Vol 278 (1) ◽  
pp. H100-H105 ◽  
Author(s):  
Maartje de Vroomen ◽  
Robbert H. Lopes Cardozo ◽  
Paul Steendijk ◽  
Frank van Bel ◽  
Jan Baan

Pulmonary hypertension results in an increased afterload for the right ventricle (RV). To determine the effects of this increased afterload on RV contractile performance, we examined RV performance before and during 4 h of partial balloon occlusion of the pulmonary artery and again after releasing the occlusion in nine newborn lambs. RV contractile performance was quantified by indexes derived from systolic RV pressure-volume relations obtained by a combined pressure-conductance catheter during inflow reduction. An almost twofold increase of end-systolic RV pressure (from 22 to 38 mmHg) was maintained during 4 h. Cardiac output (CO) (0.74 ± 0.08 l/min) and stroke volume (4.3 ± 0.4 ml) were maintained, whereas end-diastolic volume (7.9 ± 1.3 ml) did not change significantly during this period. RV systolic function improved substantially; the end-systolic pressure-volume relation shifted leftward indicated by a significantly decreased volume intercept (up to 70%), together with a slightly increased slope. In this newborn lamb model, maintenance of CO during increased RV afterload is not obtained by an increased end-diastolic volume (Frank-Starling mechanism). Instead, the RV maintains its output by improving contractile performance through homeometric autoregulation.


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