Influence of pacing site on canine left ventricular contraction

1986 ◽  
Vol 251 (2) ◽  
pp. H428-H435 ◽  
Author(s):  
D. Burkhoff ◽  
R. Y. Oikawa ◽  
K. Sagawa
Keyword(s):  
Right Ventricular ◽  
Time Course ◽  
Peak Pressure ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Atrial Pacing ◽  
Free Wall ◽  
Ventricular Pacing ◽  
Right Ventricular Free Wall ◽  
Isolated Hearts

We investigated the influence of pacing site on several aspects of left ventricular (LV) performance to test the hypothesis that "effective ventricular muscle mass" is reduced with direct ventricular pacing. All studies were performed on isolated supported canine hearts that were constrained to contract isovolumically. To determine the influence of pacing site on magnitude and time course of isovolumic LV pressure (P) generation, LVP waves were recorded in eight isolated hearts paced at 130 beats/min. Pacing was epicardially from atrium, LV apex, LV free wall, right ventricular free wall (RVF), and endocardially from right ventricular endocardium. In a given heart, peak LVP was greatest with atrial pacing and smallest with RVF pacing, the difference being on average 26 +/- 10% (mean +/- SD) of the former pressure. The other pacing sites produced intermediate peak LVPs. When instantaneous LVP waves, obtained while pacing from each of the five sites, were normalized by their respective amplitudes, they were virtually superimposable up to the time of peak pressure and only slightly different during the remainder of the cardiac cycle. With changes in pacing site there was a linear negative correlation (r = 0.971) between changes in peak pressure and changes in duration of the QRS complex of a bipolar epicardial electrogram with an average slope of -0.51 mmHg/ms. Compared with atrial pacing, the slope of the end-systolic pressure-volume relation, Ees, was decreased with ventricular pacing, but Vo, the volume axis intercept, was relatively constant.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of loading conditions and inotropic state on rapid filling phase of left ventricle

1985 ◽  
Vol 248 (4) ◽  
pp. H523-H533 ◽  
Author(s):  
R. C. Bahler ◽  
P. Martin
Keyword(s):  
Right Ventricular ◽  
Time Course ◽  
Left Ventricular ◽  
Atrial Pacing ◽  
Ventricular Pacing ◽  
Descending Aorta ◽  
Right Ventricular Pacing ◽  
Inotropic State ◽  
Venae Cavae ◽  
Activation Sequence

Afterload, activation sequence, inotropism, and extent of shortening affect the time constant (T) of left ventricular (LV) isovolumic pressure decay, yet it is unknown if they modify peak lengthening velocity of the LV minor axis [(dD/dt)/D]. Accordingly, we studied their effects on (dD/dt)/D, measured by sonomicrometry, in nine anesthetized open-chest dogs during atrial pacing at 2 Hz. Afterload was increased 20-40 mmHg by 1) constricting the ascending aorta and 2) occluding the descending aorta for four beats. Activation was altered by right ventricular pacing. These interventions, plus constriction of venae cavae, were studied during four inotropic states. Aortic stenosis increased (dD/dt)/D (P less than 0.05), whereas occlusion of the descending aorta, vena caval constriction, and right ventricular pacing decreased (dD/dt)/D (P less than 0.05). Left atrial pressure was constant except during vena caval constriction. Alterations in inotropic state modified (dD/dt)/D (P less than 0.001). Extent of shortening and (dD/dt)/D were directly related (r = 0.80, P less than 0.001). Changes in (dD/dt)/D and T were inversely related (r = 0.70, P less than 0.001), and alterations in the interval from -dP/dtpeak to the end of rapid filling were directly related to changes in T (r = 0.75, P less than 0.001). We conclude that (dD/dt)/D can be modified by systolic and diastolic load perturbations, activation sequence, and inotropic interventions. These effects relate to changes in extent of shortening, time course of inactivation, or both.

Effects of free wall ischemia and bundle branch block on systolic ventricular interaction in dog hearts

1994 ◽  
Vol 266 (3) ◽  
pp. H1087-H1094 ◽  
Author(s):  
H. Yaku ◽  
B. K. Slinker ◽  
S. P. Bell ◽  
M. M. LeWinter
Keyword(s):  
Right Ventricular ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Stroke Work ◽  
Free Wall ◽  
Ventricular Pacing ◽  
Aortic Constriction ◽  
Bundle Branch Block ◽  
Ventricular Interaction ◽  
Right Ventricular Stroke Volume

Systolic direct ventricular interaction is thought to occur via the ventricular septum and the coordinated contraction of common fibers shared by both ventricles. The purpose of the present study was to evaluate the effects of transient free wall ischemia and bundle branch block, which disrupt the coordinated contraction of shared common fibers, on left-to-right systolic ventricular interaction. We produced transient right and left ventricular free wall ischemia by 2-min coronary artery occlusions and bundle branch block by ventricular pacing in nine in situ dog hearts. To eliminate any confounding effect of series interaction, we used an abrupt hemodynamic perturbation (aortic constriction), and we measured systolic interaction gain (IG) as delta right ventricular peak systolic pressure/delta left ventricular peak systolic pressure (IG(peak)) and instantaneous delta right ventricular pressure/delta left ventricular pressure at matched data sampling times (IG(inst)), along with changes in right ventricular stroke volume and stroke work before and on the beat immediately after the aortic constriction. To achieve equivalence of the interventricular septal pressure transmission contribution to ventricular interaction, the delta left ventricular peak systolic pressure produced by the aortic constriction was matched under all experimental conditions [average increase: 64 +/- 19 (SD) mmHg]. Control IG(peak) was 0.12 +/- 0.05, and control IG(inst) was 0.11 +/- 0.05. These values did not change with either free wall ischemia or ventricular pacing, with or without an intact pericardium. The changes in right ventricular stroke volume and stroke work produced by the aortic constriction were not different from zero, during either ischemia or ventricular pacing, with or without an intact pericardium.(ABSTRACT TRUNCATED AT 250 WORDS)

Differential regional gene expression from cardiac dyssynchrony induced by chronic right ventricular free wall pacing in the mouse

2006 ◽  
Vol 26 (2) ◽  
pp. 109-115 ◽  
Author(s):  
Kenneth C. Bilchick ◽  
Sudip K. Saha ◽  
Ed Mikolajczyk ◽  
Leslie Cope ◽  
Will J. Ferguson ◽  
...  
Keyword(s):  
Gene Expression ◽  
Right Ventricular ◽  
Differential Expression ◽  
Stem Cell Differentiation ◽  
Left Ventricular ◽  
Ventricular Free Wall ◽  
Free Wall ◽  
Right Ventricular Free Wall ◽  
Cardiac Dyssynchrony ◽  
Clinical Prognosis

Routine clinical right ventricular pacing generates left ventricular dyssynchrony manifested by early septal shortening followed by late lateral contraction, which, in turn, reciprocally stretches the septum. Dyssynchrony is disadvantageous to cardiac mechanoenergetics and worsens clinical prognosis, yet little is known about its molecular consequences. Here, we report the influence of cardiac dyssynchrony on regional cardiac gene expression in mice. Mice were implanted with a custom-designed miniature cardiac pacemaker and subjected to 1-wk overdrive right ventricular free wall pacing (720 beats/min, baseline heart rate 520–620 beats/min) to generate dyssynchrony (pacemaker: 3-V lithium battery, rate programmable, 1.5 g, bipolar lead). Electrical capture was confirmed by pulsed-wave Doppler and dyssynchrony by echocardiography. Gene expression from the left ventricular septal and lateral wall myocardium was assessed by microarray (dual-dye method, Agilent) using oligonucleotide probes and dye swap. Identical analysis was applied to four synchronously contracting controls. Of the 22,000 genes surveyed, only 18 genes displayed significant ( P < 0.01) differential expression between septal/lateral walls >1.5 times that in synchronous controls. Gene changes were confirmed by quantitative PCR with excellent correlations. Most of the genes ( n = 16) showed greater septal expression. Of particular interest were seven genes coding proteins involved with stretch responses, matrix remodeling, stem cell differentiation to myocyte lineage, and Purkinje fiber differentiation. One week of iatrogenic cardiac dyssynchrony triggered regional differential expression in relatively few select genes. Such analysis using a murine implantable pacemaker should facilitate molecular studies of cardiac dyssynchrony and help elucidate novel mechanisms by which stress/stretch stimuli due to dyssynchrony impact the normal and failing heart.

Ventricular systolic interdependence: volume elastance model in isolated canine hearts

1987 ◽  
Vol 253 (6) ◽  
pp. H1381-H1390 ◽  
Author(s):  
W. L. Maughan ◽  
K. Sunagawa ◽  
K. Sagawa
Keyword(s):  
Left Ventricle ◽  
Right Ventricle ◽  
Cross Talk ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Ventricular Free Wall ◽  
Free Wall ◽  
Right Ventricular Free Wall ◽  
Systolic Volume ◽  
The Right

To analyze the interaction between the right and left ventricle, we developed a model that consists of three functional elastic compartments (left ventricular free wall, septal, and right ventricular free wall compartments). Using 10 isolated blood-perfused canine hearts, we determined the end-systolic volume elastance of each of these three compartments. The functional septum was by far stiffer for either direction [47.2 +/- 7.2 (SE) mmHg/ml when pushed from left ventricle and 44.6 +/- 6.8 when pushed from right ventricle] than ventricular free walls [6.8 +/- 0.9 mmHg/ml for left ventricle and 2.9 +/- 0.2 for right ventricle]. The model prediction that right-to-left ventricular interaction (GRL) would be about twice as large as left-to-right interaction (GLR) was tested by direct measurement of changes in isovolumic peak pressure in one ventricle while the systolic pressure of the contralateral ventricle was varied. GRL thus measured was about twice GLR (0.146 +/- 0.003 vs. 0.08 +/- 0.001). In a separate protocol the end-systolic pressure-volume relationship (ESPVR) of each ventricle was measured while the contralateral ventricle was alternatively empty and while systolic pressure was maintained at a fixed value. The cross-talk gain was derived by dividing the amount of upward shift of the ESPVR by the systolic pressure difference in the other ventricle. Again GRL measured about twice GLR (0.126 +/- 0.002 vs. 0.065 +/- 0.008). There was no statistical difference between the gains determined by each of the three methods (predicted from the compartment elastances, measured directly, or calculated from shifts in the ESPVR). We conclude that systolic cross-talk gain was twice as large from right to left as from left to right and that the three-compartment volume elastance model is a powerful concept in interpreting ventricular cross talk.

Adverse effects of atrioventricular synchronous right ventricular pacing on left ventricular sympathetic activity, efficiency, and hemodynamic status

2006 ◽  
Vol 291 (5) ◽  
pp. H2377-H2379 ◽  
Author(s):  
Abdul Al-Hesayen ◽  
John D. Parker
Keyword(s):  
Heart Failure ◽  
Right Ventricular ◽  
Sympathetic Activity ◽  
Left Ventricular ◽  
Right Atrial ◽  
Lv Function ◽  
Atrial Pacing ◽  
Ventricular Pacing ◽  
Rv Pacing ◽  
Norepinephrine Spillover

Right ventricular (RV) pacing is now recognized to play a role in the development of heart failure in patients with and without underlying left ventricular (LV) dysfunction. We used the cardiac norepinephrine spillover method to test the hypothesis that RV pacing is associated with cardiac sympathetic activation. We studied 8 patients with normal LV function using temporary right atrial and ventricular pacing wires. All measurements were carried out during a fixed atrial pacing rate. The radiotracer norepinephrine spillover technique was employed to measure total body and cardiac sympathetic activity while changes in LV performance were evaluated with a high-fidelity manometer catheter. Atrioventricular synchronous RV pacing, compared with atrial pacing alone, was associated with a 65% increase in cardiac norepinephrine spillover, an increase in LV end-diastolic pressure, and a reduction in myocardial efficiency. These responses may play a role in the development of heart failure and poor outcomes that are associated with chronic RV pacing.

End-systolic pressure length relations of stunned right and left ventricles after inotropic stimulation

1993 ◽  
Vol 265 (6) ◽  
pp. H2099-H2109 ◽  
Author(s):  
R. Krams ◽  
L. K. Soei ◽  
E. O. McFalls ◽  
E. A. Winkler Prins ◽  
L. M. Sassen ◽  
...  
Keyword(s):  
Right Ventricle ◽  
Right Ventricular ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Segment Length ◽  
Atrial Pacing ◽  
Regression Equations ◽  
External Work ◽  
Left And Right ◽  
The Right

Regional end-systolic pressure-segment length relationships (ESPSLR) were used to compare the degree of right and left ventricular stunning induced by a 10-min occlusion of the left anterior descending coronary artery and the response to subsequent atrial pacing (50 beats/min above intrinsic heart rate) without and with dobutamine (2 micrograms.kg-1.min-1) in nine anesthetized open-chest pigs. From the ESPSLR, the slope (Ees) (at 100 mmHg for the left and 25 mmHg for the right ventricle) and the total area of the pressure-length relationship (PLA) were determined. From the latter, the distribution into external work (EW) and potential energy (PE) as well as the efficiency of energy transfer (EET = EW/PLA) were calculated. In both the stunned left and right ventricular myocardium Ees and EW were reduced according to the same linear regression equations (delta Ees = 0.7 Ees,baseline - 11.4, r2 = 0.86 and delta EW = 0.4 EWbaseline + 2.3, r2 = 0.67), where Ees,baseline and EWbaseline are Ees and EW at baseline, respectively. EET of the stunned left and right ventricular segments decreased as PLA remained unchanged, due to an increase in PE. EET decreased from 0.84 +/- 0.02 to 0.71 +/- 0.03 (P < 0.05) in the stunned right ventricular segment and from 0.71 +/- 0.02 to 0.44 +/- 0.03 (P < 0.05) in the stunned left ventricular segment. Atrial pacing did not affect EET with respect to stunning levels, whereas the additional infusion of dobutamine restored Ees, EW, and PE and consequently EET to baseline values. In conclusion, the right ventricle is susceptible to stunning. During atrial pacing the EET was lower than expected from the Ees, which could, in agreement with the time-varying elastance concept, be explained by an increase in afterload (a consequence of the decrease in stroke volume). Dobutamine not only increased Ees, EW, and EET but also restored the relationship between Ees and EET in both ventricular stunned segments.

scholarly journals Right Ventricular Free Wall Strain and Congestive Hepatopathy in Patients with Acute Worsening of Chronic Heart Failure: A CATSTAT-HF Echo Substudy

2020 ◽  
Vol 9 (5) ◽  
pp. 1317
Author(s):  
Josip A. Borovac ◽  
Duska Glavas ◽  
Zora Susilovic Grabovac ◽  
Daniela Supe Domic ◽  
Lada Stanisic ◽  
...  
Keyword(s):  
Heart Failure ◽  
Right Ventricular ◽  
Hepatic Dysfunction ◽  
Total Bilirubin ◽  
Systolic Pressure ◽  
Liver Function Tests ◽  
International Normalized Ratio ◽  
Free Wall ◽  
Right Ventricular Free Wall ◽  
Rv Function

Right ventricular (RV) function is an important predictor of prognosis in patients with heart failure. However, the relationship of the RV free wall longitudinal strain (RV FWS) and the degree of hepatic dysfunction during the acute worsening of heart failure (AWHF) is unknown. We sought to determine associations of RV FWS with laboratory liver function tests and parameters of RV function including tricuspid annular plane systolic excursion (TAPSE), RV fractional area change (RV FAC), maximal tricuspid jet velocity (TR Vmax), RV S′ velocity, and estimated RV systolic pressure (RVSP). A total of 42 AWHF patients from the CATSTAT-HF study were stratified in two groups by the RV FWS median (−16.5%). Patients < RV FWS median had significantly prolonged international normalized ratio (INR; p = 0.002), increased total bilirubin (p < 0.001) and alkaline phosphatase (ALP; p = 0.020), and decreased albumin (p = 0.005) and thrombocytes (p = 0.017) compared to patients > RV FWS median. RV FWS independently correlated to total bilirubin (β = 0.457, p = 0.004), ALP (β = 0.556, p = 0.002), INR (β = 0.392, p = 0.022), albumin (β = −0.437, p = 0.013), and thrombocytes (β = −404, p = 0.038). Similarly, TAPSE, RV FAC, and RV S′ significantly correlated with RV FWS. In conclusion, RV impairment, reflected in reduced RV FWS, is independently associated with a higher degree of hepatic dysfunction among patients with AWHF (CATSTAT-HF ClinicalTrials gov number, NCT03389386).

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