Cardiovascular Research

Cardiovascular Research 1999 42(1):80-86; doi:10.1016/S0008-6363(98)00288-0
© 1999 by European Society of Cardiology

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Copyright © 1999, European Society of Cardiology

Right coronary pressure modulates right ventricular systolic stiffness and oxygen consumption

Xiaoming Bian^* and H.Fred Downey

Department of Integrative Physiology, University of North Texas Health Science Center at Fort Worth, Fort Worth TX 76107-2699, USA

^* Corresponding author. Tel.: +1-817-735-2078; fax: +1-817-735-5084.

Received 17 April 1998; accepted 2 September 1998

	Abstract

Top Abstract 1 Introduction 2 Materials and methods 3 Results 4 Discussion References

 
Objective: The low transmural pressure of the thin right ventricular (RV) wall may render it responsive to right coronary (RC) pressure-induced changes in systolic stiffness and account for the dependence of RV MVO₂ on RC pressure (RCP). Methods: In eight dogs anesthetized with pentobarbital and fentanyl, RCP was lowered from the baseline to 30 mmHg in 10 mmHg steps by adjusting an occluder on the proximal RC. Myocardial segment length and isometric developed force were measured, and the slope of the force-length curve during ejection period (F/SL) was used as an index of systolic myocardial stiffness. MVO₂ was calculated from RC flow and arteriovenous O₂ difference. Results: As RCP was varied from 120 to 40 mmHg with positive lactate uptake, RC flow, maximum developed force (F_max), F, and MVO₂ decreased linearly, whereas end-diastolic length, SL, and other hemodynamic variables stayed constant. Thus, RV systolic stiffness fell linearly with RC pressure. When RCP was further lowered from 40 to 30 mmHg, F_max and F continued to fall, end-diastolic segment length and right atrial pressure increased significantly, SL and RV dP/dt_max fell significantly, and F/SL reached its lowest value. RV systolic stiffness was 22% of previously reported left ventricular systolic stiffness for coronary perfusion pressure at 100 mmHg, and varied less steeply with coronary pressure. Conclusions: (1) Reductions in RV systolic stiffness preserve SL as coronary pressure is reduced over a wide range. (2) The resulting increase in RV efficiency reduces oxygen demand as oxygen supply is reduced, so ischemia is avoided. (3) RV systolic stiffness is much less than left ventricular stiffness, consistent with their anatomical and functional differences.

KEYWORDS Contractile function; Coronary circulation; Ischemia; Oxygen consumption; Dog

	1 Introduction

Top Abstract 1 Introduction 2 Materials and methods 3 Results 4 Discussion References

 
Since the ‘Gregg phenomenon’ was described in 1958 [1], many studies have attempted to delineate the mechanism by which a change in coronary perfusion alters ventricular function and oxygen consumption, independent of other determinants of myocardial oxygen demand [2–8]. Hypothesized mechanisms involving coronary pressure or flow-induced changes in oxygen delivery or myocardial fiber length have not been consistently supported by experimental findings [5, 6]. Recently we demonstrated that the Gregg phenomenon was evident in left ventricular myocardium only in the absence of effective left coronary pressure-flow autoregulation [9]. Also associated with poor autoregulation was a pronounced pressure-induced change in coronary vascular volume. This change in vascular volume alters ventricular wall thickness [10–12]but not end-diastolic fiber length [9, 13]. We also demonstrated that altered left coronary perfusion pressure and/or flow affected left ventricular systolic stiffness in hearts with poor autoregulation [13]. Systolic stiffness is an important determinant of ventricular internal work, so changes in systolic stiffness affect the internal/external work ratio and impact on ventricular oxygen utilization efficiency [9, 14–16].

Pressure-flow autoregulation is relatively ineffective in the canine right ventricle [17–21]. Also, the afterload and transmural pressure of the right ventricle are much less than that of the left ventricle. These factors may render the right ventricle particularly more sensitive to factors which alter systolic stiffness.

In the present study, we tested the effects of decreased right coronary pressure on right ventricular mechanical properties (segment length and developed force) in intact, ejecting canine hearts. We estimated changes in systolic ventricular stiffness, and then related these observations to pressure-related changes in myocardial mechanical efficiency. Finally, these results were compared to the effects of altered left coronary perfusion pressure on left ventricular systolic stiffness.

	2 Materials and methods

Top Abstract 1 Introduction 2 Materials and methods 3 Results 4 Discussion References

 
2.1 Surgical preparation
This investigation was approved by the Institutional Animal Care and Use Committee of the University of North Texas Health Science Center at Fort Worth and was conducted in accordance with the Guide for the Care and Use of Laboratory Animals (NIH publication 85–23, revised 1996). Eight adult healthy mongrel dogs of either sex (17.5–27 kg), anesthetized with sodium pentobarbital (30 mg/kg, i.v.), were used in this study. Supplemental fentanyl (10 µg/kg, i.v.) was given as needed to maintain stable anaesthesia and low heart rate. The animals were mechanically ventilated with room air supplemented with oxygen to maintain arterial blood gases normal throughout the experiment. A catheter was inserted into a femoral artery to monitor aortic pressure, and a catheter was inserted into the corresponding femoral vein for infusion of supplemental blood and anaesthetic. A right thoracotomy was performed in the fourth intercostal space, and the heart was suspended in a pericardial cradle. A nonbranching section of the right coronary artery was dissected free for 1–1.5 cm for attachment of a single-crystal Doppler flow probe proximal to a metal screw occluder. A Millar catheter-tip pressure transducer was placed in the right ventricle through the right atrial appendage to measure right ventricular pressure and dP/dt. A catheter was inserted into the right atrium to monitor right atrial pressure.

A pair of piezoelectric crystals were implanted in the mid-myocardium of the right coronary artery perfusion territory to measure myocardial segment lengths. The crystals were positioned 1 cm apart and parallel to the principal axis of shortening [22]. A miniature force transducer was sutured within the right coronary perfusion territory parallel to the piezoelectric crystals to record right ventricular isometric developed force [23–25]. The force transducer was positioned with 3-mm deep 3–0 silk sutures and 1 cm from the crystals. To maintain constant fibre length throughout the cardiac cycle, the feet of the transducer were anchored such that underlying fibers were stretched by about 40–50% of their resting length. The force transducer was sufficiently remote from the piezoelectric crystals that its placement did not affect measurement of segment length shortening. This was documented by removing the force transducer at the conclusion of the experiment and observing no change in measured segment lengths. We have used similar instrumentation to measure left ventricular isometric force and shortening [13].

A 24-gauge i.v. catheter was inserted into a vein draining the area perfused by the right coronary artery. Right coronary arterial and venous blood samples were collected anaerobically. Oxygen content of these samples was measured with an Instrumentation Laboratory model 282 CO-Oximeter. Right ventricular MVO₂ was calculated from the product of right coronary blood flow times the regional arteriovenous oxygen difference.

2.2 Assessment of regional right ventricular myocardial mechanics
Systolic shortening (%) equaled [(EDL–ESL)/EDL]x100, where EDL=end-diastolic segment length and ESL=end-systolic segment length. End-diastole and end-systole were defined as the beginning of the positive upstroke of the right ventricular dP/dt tracing and a point 20 ms before peak negative dP/dt, respectively.

The force-length curve, obtained from segment length and isometric developed force measurements, was used to estimate regional right ventricular systolic stiffness. Force-length loops from the same heart are illustrated in Fig. 1 for baseline and reduced right coronary pressure. At baseline right coronary pressure, right ventricular contraction began at point A. From A to pulmonic valve opening at B, the right ventricle contracted isovolumetricaly, and then from B to C, the right ventricle ejected blood to the pulmonary artery. F is the isometric developed force the right ventricular muscle produced during the ejection period. SL is the shortening of right ventricular muscle during ejection. The slope of line from B to C, i.e., F/SL, was computed. At constant afterload, changes in F/SL reflect alterations in systolic ventricular stiffness [25]. At least three stable beats were analyzed. Variables were calculated for each beat and averaged, and F/SL values were calculated from averaged F and SL.

View larger version (18K): [in this window] [in a new window] [Download PowerPoint slide]   Fig. 1 Example of right ventricular force-length loops recorded in the same heart with baseline (120 mmHg; A, B, C) and reduced (40 mmHg; A', B', C') right coronary pressure (RCP). Muscle contraction began at A, and a line from A to B reflects isovolumetric contraction. A line from B to C reflects ejection. The slope of line B–C (F/SL) was used as an index of systolic ventricular stiffness.

 
2.3 Experimental protocols
Baseline right coronary pressure varied from 100 to 120 mmHg. Coronary pressure, flow, segment length, and developed force were recorded at baseline right coronary pressure and as right coronary pressure was reduced from baseline to 30 mmHg in 10 mmHg steps. At least 60 s were allowed for right coronary blood flow to stabilize at each pressure before hemodynamic and right ventricular function data were recorded and arterial and right coronary venous samples were collected.

2.4 Statistics
Values are expressed as mean±SEM. The effects of altering right coronary pressure were evaluated by repeated measures analysis of variance (ANOVA). Variables which varied significantly with right coronary pressure according to ANOVA were further examined with the Student-Newman-Kuels test or by linear regression analysis. Probability (P) values <0.05 were taken to indicate statistically significant differences.

	3 Results

Top Abstract 1 Introduction 2 Materials and methods 3 Results 4 Discussion References

 
Systemic hemodynamic variables are summarized in Table 1. Heart rate, systolic and diastolic systemic arterial blood pressures, mean right atrial pressure, and right ventricular systolic pressure and dP/dt_max were not affected by changes in right coronary artery pressure from 120 to 40 mmHg. Thus, reducing right coronary pressure over this range did not affect systemic hemodynamics or global right ventricular preload, afterload, or contractile function. At 30 mmHg, right atrial pressure was significantly elevated, and right ventricular dP/dt_max was significantly depressed.

View this table: [in this window] [in a new window]   Table 1 Summary of systemic haemodynamic variables

 
The effects of stepwise decreases in right coronary perfusion pressure on right coronary blood flow and right ventricular MVO₂ are shown in Table 2. Right coronary flow decreased significantly with each reduction in perfusion pressure, and a significant linear relationship with pressure was evident from 120 to 30 mmHg (P<0.01, r²=0.93). Right ventricular MVO₂ decreased significantly with right coronary pressure, and a significant linear relationship with pressure was evident from 120 to 30 mmHg (P<0.01, r²=0.95).

View this table: [in this window] [in a new window]   Table 2 Right coronary blood flow, right ventricular myocardial oxygen consumption, and right ventricular lactate uptake

 
Representative right ventricular force-length loops recorded at baseline and reduced right coronary pressure are shown in Fig. 1. Right ventricular function variables are summarized in Figs. 2–5. Decreasing right coronary pressure from 120 to 40 mmHg produced no significant change in end-diastolic segment length (Fig. 2); only at 30 mmHg did end-diastolic segment length significantly increase. End-systolic segment length was unchanged at pressures greater than 40 mmHg (Fig. 2). At 40 mmHg, end-systolic segment length increased significantly; at 30 mmHg, end-systolic segment length increased further (P<0.05). Segment shortening was also constant at right coronary pressures greater than 40 mmHg (Fig. 3). At 40 mmHg, segment shortening decreased significantly; at 30 mmHg, segment shortening decreased further (P<0.05). SL, right ventricular segment shortening during ejection, was unchanged at right coronary pressures greater than 30 mmHg; at 30 mmHg, SL fell significantly (Fig. 3). Thus, a lower right coronary pressure was required to cause an increase in diastolic segment length (Fig. 2) and to depress SL (Fig. 3). Fig. 4 shows that F_max and F followed a different pattern; F_max and F fell continuously as right coronary pressure was reduced (linear trend, P<0.01). The decrease in F_max was due essentially to the pressure related decrease in F. Although SL was not significantly affected as right coronary pressure was reduced to 40 mmHg (Fig. 3), the fall in F (Fig. 4) produced significant reductions in systolic stiffness (F/SL) from 6.6 g mm^{– 1} at 120 mmHg to 0.8 g mm^–1 at 40 mmHg (linear trend, P<0.01; Fig. 5). The marked effect of right coronary pressure on right ventricular systolic stiffness is clearly evident from the representative force-length loops shown in Fig. 1. When right coronary pressure was further reduced to 30 mmHg, no further decrease in F/SL occurred due to decreases in both SL and F.

View larger version (65K): [in this window] [in a new window] [Download PowerPoint slide]   Fig. 2 Effect of reducing right coronary pressure (RCP) from baseline (120 mmHg) to 30 mmHg on right ventricular segment lengths (RV SL). EDL=end diastolic length, ESL=end systolic length. Error bars=SEM, n=8. * P<0.05 vs. all values at higher RCP; P<0.05 vs. all values at RCP50 mmHg.

 

View larger version (46K): [in this window] [in a new window] [Download PowerPoint slide]   Fig. 3 Effect of reducing right coronary pressure (RCP) from baseline (120 mmHg) to 30 mmHg on percent segment shortening (SS) and on the change of segment length during ejection period (SL). Error bars=SEM, n=8. * P<0.05 vs. all values at higher RCP.

 

View larger version (35K): [in this window] [in a new window] [Download PowerPoint slide]   Fig. 4 Effect of reducing right coronary pressure (RCP) from baseline (120 mmHg) to 30 mmHg on maximal developed force (Fmax) and on developed force during ejection period (F). Error bars=SEM, n=8.

 

View larger version (20K): [in this window] [in a new window] [Download PowerPoint slide]   Fig. 5 Effect of reducing right coronary pressure (RCP) from baseline (120 mmHg) to 30 mmHg on right ventricular systolic stiffness (F/SL). Error bars=SEM, n=8.

 
In Fig. 6, right ventricular systolic stiffness is compared with our previously reported values of left ventricular systolic stiffness [13]. Coronary perfusion pressure ranged from 40 to 120 mmHg in the current right ventricle study and from 60 to 180 mmHg in the left ventricle study. Right ventricular systolic stiffness was 15% of left ventricular systolic stiffness at coronary pressure of 60 mmHg (the lowest pressure at which measurements were made in both ventricles) and 22% of left ventricular systolic stiffness at 100 mmHg. Stiffness varied more steeply with coronary pressure in the left ventricle (P<0.01).

View larger version (17K): [in this window] [in a new window] [Download PowerPoint slide]   Fig. 6 Comparison of right and left ventricular systolic stiffness (F/SL) as functions of coronary perfusion pressure (CPP). LV=left ventricle, RV=right ventricle. Error bars=SEM, n=8. * P<0.01 vs. LV at the same CPP. Left ventricular data from a previous report of our laboratory [13].

 

	4 Discussion

Top Abstract 1 Introduction 2 Materials and methods 3 Results 4 Discussion References

 
This report describes the first measurements of systolic stiffness of the in situ, working right ventricle. As right coronary pressure was decreased from baseline, isometric force during right ventricular ejection fell, although segment shortening during ejection stayed constant. Thus, right ventricular systolic stiffness fell, and this may explain the previously described direct dependence of right ventricular MVO₂ on right coronary pressure. These findings may also account for the remarkable ability of the right ventricle to maintain external work and cytosolic energetics in the face of moderately reduced coronary blood flow and right ventricular MVO₂ [15]. Finally, the lesser systolic stiffness of the right ventricle compared to the left ventricle may explain important differences in right and left ventricular function and myocardial energetics.

We have examined left ventricular systolic stiffness with the same approach used in this study [13]. Comparison of the data from both studies shows that right ventricular stiffness is much less than left ventricular stiffness. Right ventricular systolic stiffness increases with coronary pressure as does left ventricular stiffness, although less steeply. These differences in systolic stiffness are consistent with the anatomical and functional differences between the ventricles, since the thinner right ventricular wall produces only 20% as much systolic pressure as the left ventricle. Since baseline right ventricular systolic stiffness is so low, changes in coronary pressure produce proportionally greater changes in right ventricular stiffness compared to the left ventricle. This may explain why changes in coronary perfusion pressure produce more marked changes in MVO₂ in the right ventricle than in the left ventricle.

Right ventricular MVO₂ is highly dependent on right coronary artery pressure [15, 17, 19]. From one point of view, this pressure-related effect on right ventricular oxygen demand could account for the poor pressure-flow autoregulation of the right coronary circulation apparent in this study and in previous reports [17–21], i.e., right coronary flow is adjusted in response to alter oxygen demand rather than to maintain constant flow. On the other hand, if the right coronary circulation were capable of more effective autoregulation, changes in coronary pressure might not have such a pronounced effect on right ventricular oxygen demand. In support of this view, we demonstrated that left coronary vascular volume is highly pressure dependent only in poorly autoregulating preparations, and only in those poorly autoregulating left coronary circulations did left ventricular MVO₂ vary with pressure [9]. Recently, we have observed marked changes in right coronary vascular volume that correlated with right ventricular MVO₂ [26]. Thus, we propose that in the poorly autoregulating right coronary circulation, reduced coronary pressure unloads the coronary hydraulic skeleton and reduces right ventricular systolic stiffness. The current findings of pressure-induced changes in right ventricular stiffness and MVO₂ are clearly consistent with this explanation. Systolic ventricular stiffness is an important determinant of ventricular internal work, so reduced systolic stiffness at low coronary perfusion pressure would improve the ratio of external to total work. This would decrease myocardial oxygen demand as oxygen supply is reduced, so ventricular oxygen supply/demand balance is maintained. Maintenance of this balance is evident from the absence of lactate production, although right ventricular MVO₂ fell by 45% as right coronary perfusion pressure was reduced from 120 to 40 mmHg. Furthermore, in a previously reported study, we found that right ventricular contractile function and high energy reserves were uncompromised, although MVO₂ fell when right coronary pressure was reduced to 60 mmHg [15].

Systolic stiffness was computed from the ratio of isometric force (F) and nearby segment shortening (SL) during right ventricular ejection [25]. It must be recognized that this approach can provide only an approximation of systolic stiffness, since isometric rather than auxotonic force was measured. More precise methods for measuring regional, dynamic ventricular stiffness, such as the relation between the indentation stress and indentation strain during high frequency indentations [27], are not readily applied to the in vivo, working heart.

The ratio F/SL fell with pressure, since F decreased, and SL was unchanged. While the hydraulic effects of altered coronary vascular volume would permit similar shortening during ejection with less potentially available force, this investigation does not address the important question of why F falls with coronary pressure. It is tempting to postulate a feedback loop such that F is modulated to maintain constant SL despite changes in stiffness, but at present a stiffness sensor required for this loop is not apparent. An alternative hypothesis would be that F is directly modulated by coronary pressure [7], and the decrease in stiffness fortuitously results in constant SL with reduced MVO₂. Clearly this topic merits further research.

In this investigation, right ventricular mechanics were examined in the perfusion territory of the right coronary artery. In the canine heart, this artery perfuses approximately 60% of the right ventricular free wall, and none of the interventricular septum [28]. Thus, it is possible to perturb contractile function of this portion of the right ventricular wall with little impact on global right ventricular contractile function [29]. Since we found that right ventricular SL was uncompromised until right coronary pressure was reduced below 40 mmHg, it is not surprising that measured indices of global right ventricular function did not fall. At 30 mmHg, however, regional systolic shortening fell and global right ventricular function was also adversely affected.

Time for primary review 35 days.

	Acknowledgements

 
We thank Arthur G. Williams, Jr., and Min Fu for expert technical assistance. This study was supported by NIH grant HL 35027.

	References

Top Abstract 1 Introduction 2 Materials and methods 3 Results 4 Discussion References

 

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