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Am J Physiol Heart Circ Physiol 290: H2369-H2375, 2006. First published January 6, 2006; doi:10.1152/ajpheart.01211.2004
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Longitudinal but not circumferential deformation reflects global contractile function in the right ventricle with open pericardium

H. Alex Leather,1 Ruggero Ama',1 Carlo Missant,1 Steffen Rex,1,3 Frank E. Rademakers,2 and Patrick F. Wouters1

Departments of 1Anesthesiology and of 2Cardiology, Katholieke Universiteit Leuven, Leuven, Belgium; and 3Department of Anesthesiology, University Hospital of the Rheinisch-Westfälische Hochschule, Aachen, Germany

Submitted 3 December 2004 ; accepted in final form 3 January 2006


   ABSTRACT
TOP
 ABSTRACT
MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 GRANTS
 REFERENCES
 
The clinical evaluation of right ventricular (RV) contractility is problematic because instantaneous RV volumetry is difficult to achieve. Our aim was to test whether global RV contractility can be assessed by using regional indexes in the longitudinal and/or circumferential axis. Six anesthetized adult ewes were instrumented with a RV conductance catheter and four RV free wall sonomicrometry crystals (interrogating the longitudinal and circumferential axes). Global and regional preload recruitable stroke work (PRSW) were measured by using acute vena cava occlusions at baseline, during esmolol and dobutamine infusion, and during stable low-preload and high-afterload conditions. The agreement between regional and global PRSW was assessed with regression and Bland-Altman analysis. Both regional PRSW indexes correlated well with global PRSW in baseline conditions, during inotropic modulation (R2 = 0.83 and 0.74 for longitudinal and circumferential regional PRSW, respectively), and during preload reduction (R2 = 0.62 and 0.83, respectively), but only longitudinal regional PRSW correlated with global PRSW in increased afterload conditions (R2 = 0.59 and 0.13 for longitudinal and circumferential regional PRSW, respectively). We conclude that in the open-chest, open-pericardium animal model, deformation in the longitudinal axis accurately reflects global RV contractile function in baseline conditions and during acute load modulation, whereas circumferential motion is influenced by changes in afterload.

heart contractility; regional function; preload recruitable stroke work; sheep

RIGHT VENTRICULAR (RV) contractile function is an important predictor of outcome in a wide variety of disease states (10, 27). At present, accurate assessment of RV contractility is difficult in clinical practice. The "gold standard" indexes [such as the slope of the preload recruitable stroke work relationship (PRSW)] require pressure-volume analysis, which is particularly difficult to achieve in the RV because of its geometry. Although the conductance technique has been validated in the RV (5, 8, 9, 32) and is routinely used in the laboratory setting (7, 21, 23, 24, 26), its clinical application remains difficult. Surrogates to the pressure-volume-derived indexes that are often used in the left ventricle (LV), such as ejection fraction, maximal rate of pressure rise, and preload-adjusted maximal power, are unacceptably load dependent (25), particularly in the RV (22). There is hence a need for an index of RV contractility that behaves like the pressure-volume-derived indexes in terms of inotropic sensitivity and load independence but that does not require instantaneous volumetry.

One way of circumventing the problem of instantaneous volumetry is the analysis of regional contractility as a surrogate for global ventricular contractile function. Regional PRSW has been validated as a contractile index in the LV (30) and has been used as a surrogate for global contractile indexes in the RV (12). Surprisingly, however, regional PRSW has not been adequately validated in the RV. To our knowledge, only two studies have addressed this question. In one study, regional PRSW in the longitudinal axis was shown to be sensitive to changes in inotropic state (28); in another study, regional PRSW in the circumferential axis was found to have a weak and possibly load-dependent relationship with global PRSW in baseline and during afterload modulation (17). Unfortunately, neither of these studies was designed to fully assess the regional indexes: loading conditions were not modulated in the former study, and inotropic state was not modulated in the latter.

The aim of the present study was to test whether regional PRSW in the longitudinal and circumferential axes can be used as a substitute for the volume-derived indexes of global RV contractility. We hypothesized that longitudinal and circumferential regional PRSW would be as sensitive to changes in inotropy and as insensitive to changes in loading conditions as global PRSW. To test these hypotheses, we examined the agreement between longitudinal regional PRSW, circumferential regional PRSW, and global PRSW, respectively (measured by using validated, invasive measurement techniques) during modulation of inotropic state, preload, and afterload in open-chest sheep.


   MATERIALS AND METHODS
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 ABSTRACT
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 GRANTS
 REFERENCES
 
This investigation conforms to the Guide for the Care and Use of Laboratory Animals published by the National Institutes of Health (NIH Publication No. 85–23, Revised 1996) and was approved by the ethics committee of the Katholieke Universiteit Leuven.

Instrumentation

Six adult ewes (weight 55 ± 6 kg) were included in this study. The animals were premedicated with ketamine hydrochloride (10 mg/kg). Anesthesia was induced with intravenous pentobarbital sodium (8 mg/kg) and piritramide (1 mg/kg) and maintained with pentobarbital sodium (3 mg·kg–1·h–1) and piritramide (1 mg·kg–1·h–1). The lungs were mechanically ventilated with a mixture of oxygen and room air to maintain normocapnia and normoxia. Lactated Ringer solution was administered at a rate of 5 ml·kg–1·h–1. A triple-lumen catheter was inserted in the right jugular vein. A fluid-filled catheter was advanced into the proximal aorta via the right carotid artery for monitoring of systemic arterial pressure. Via a midline sternotomy, a tourniquet was placed around the inferior vena cava (IVC) for controlled alterations of preload. The pericardium was opened, and a 20-mm perivascular flow probe (Transonic Systems, Ithaca, NY) and a tourniquet were placed around the main pulmonary artery. A combined pressure-conductance catheter (Millar Instruments, Houston, TX) was inserted into the RV through a small stab wound in the pulmonary outflow tract. A pair of sonomicrometry crystals (Sonometrics, London, Ontario, Canada) was sutured to the RV free wall in the axis perpendicular to the atrial groove (along an imaginary line extending to the apex), with the basal crystal 10–15 mm from the atrial groove (intercrystal distance 24 ± 5 mm). A second pair of crystals was sutured at right angles to the first pair.

Data Acquisition and Analysis

The conductance catheter was connected to a signal-processing unit (Sigma 5 DF, CDLeycom, Zoetermeer, The Netherlands). Parallel conductance and blood resistivity were measured at regular intervals by using the hypertonic saline method (injection of 5 ml of 10% NaCl into the right atrium) and the CDLeycom resistivity meter, respectively. The correction factor {alpha} was recalculated for each measurement. The sonomicrometry crystals were connected to a sonomicrometry system (Sonometrics). All parameters were digitized at 960 Hz and stored for off-line analysis (Cardiosoft, Sonometrics). Global RV contractility was quantified by using global PRSW (11). Regional stroke work and maximal regional segment length were calculated beat by beat during caval vein occlusion. Linear regression lines were fitted to the resulting data sets by using Excel (Microsoft); the slope of the regression line was defined as regional PRSW.

Experimental Protocol

Two subprotocols were performed in random order.

Inotropic sensitivity. After completion of instrumentation and calibration and achievement of hemodynamic steady state, baseline measurements were performed with the ventilation suspended at end expiration. Data were acquired during steady-state conditions (for general hemodynamics) and during a brief period of IVC occlusion (for the calculation of global and regional PRSW). After baseline measurements, esmolol was administered intravenously (bolus followed by infusion titrated to achieve a decrease in heart rate of ~25%; mean dose 66 µg·kg–1·min–1). Measurements were performed at least 15 min after the start of the infusion, after stabilization of heart rate. The esmolol infusion was then stopped. After the heart rate had returned to baseline values, dobutamine was administered at 1.5 and 3 µg·kg–1·min–1 iv consecutively. Measurements were performed at least 15 min after the start of each infusion, after stabilization of heart rate.

Sensitivity to alterations in preload and afterload. After achievement of hemodynamic steady state, baseline measurements were performed. Preload reduction and afterload increase were then imposed in random order. For preload reduction, the IVC was partially occluded to achieve a new hemodynamic steady state. A tourniquet was gradually adjusted until end-diastolic RV volumes shown on the oscilloscope decreased to approximately 75% or 50% of baseline values. This position was maintained while hemodynamics were allowed to stabilize for at least 5 min. All measurements, including a brief period of IVC occlusion for the calculation of global and regional PRSW, were performed at two degrees of preload reduction in a random order. For afterload increase, the main pulmonary artery was partially occluded with a tourniquet to obtain an increase of systolic pulmonary artery pressures to approximately 25% or 50% of baseline values. The tourniquet was fixed in this position, and hemodynamics were allowed to stabilize for at least 5 min. Measurements were performed at two degrees of increased afterload in a random order.

Statistical Analysis

The effects of alterations in inotropic state and loading conditions on the measured parameters were analyzed by using ANOVA for repeated measurements with Statview 5.0 (SAS Institute, Cary, NC). Fisher's protected least significant difference test was used as a post hoc test. The agreement between the regional indexes and global PRSW in the various conditions was analyzed by using linear regression analysis and Bland-Altman analysis (1). Aggregate data are expressed as means ± SD.


   RESULTS
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 ABSTRACT
 MATERIALS AND METHODS
 RESULTS
DISCUSSION
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Inotropic Sensitivity

Global PRSW and longitudinal regional PRSW both decreased during esmolol administration and increased in a dose-related fashion during dobutamine administration (Table 1). Circumferential regional PRSW increased in a dose-related fashion during dobutamine administration but did not change in response to esmolol. Regression analysis of the regional indexes vs. global PRSW showed a strong linear correlation between both longitudinal and circumferential regional PRSW and global PRSW (Fig. 1). Bland-Altman analysis of longitudinal regional PRSW vs. global PRSW showed a bias of 2 mmHg, with limits of agreement of 10 and –7 mmHg. Circumferential regional PRSW had a bias of 2 mmHg, with limits of agreement of 11 and –8 mmHg (Fig. 1).


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  		Table 1. General hemodynamics and contractile indexes during inotropic modulation

 

Figure 1
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  		Fig. 1. Regression and Bland-Altman analysis of regional preload recruitable stroke work (PRSW) vs. global PRSW during baseline and inotropic modulation. Scatterplot with regression analysis (A) and Bland-Altman analysis (B) of longitudinal regional (Long Reg) PRSW vs. global PRSW; scatterplot with regression analysis (C) and Bland-Altman analysis (D) of circumferential regional (Circ Reg) PRSW vs. global PRSW. PRSW, slope of the preload recruitable stroke work relationship. In A and C, the thick line represents the linear regression line. In B and D, the thick line represents the bias, and the dotted lines represent the limits of agreement.

 
Sensitivity to Alterations in Preload and Afterload

The changes in end-diastolic volume produced by acute alterations of RV loading correlated better with longitudinal than with circumferential changes of end-diastolic segment length (r2 = 0.73 vs. 0.30). Similarly, loading-induced changes in RV stroke volume correlated better with longitudinal than with circumferential changes of segment shortening (r2 = 0.81 vs. 0.33) (Fig. 2).


Figure 2
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  		Fig. 2. Regression analysis of volume changes vs. changes in regional deformation during acute modulation of right ventricular (RV) loading conditions. A and C: longitudinal deformation. B and D: circumferential deformation. A and B show changes from baseline in end-diastolic volume vs. end-diastolic segment length during lowering of preload ({triangleup}) and elevation of afterload (bullet). C and D display stroke volume and segment shortening. Longitudinal deformation (A and C) consistently shows higher coefficients of determination compared with circumferential deformation (B and D).

 
Global PRSW and longitudinal and circumferential regional PRSW did not change significantly in response to preload reduction (Table 2). Both regional indexes maintained a strong correlation with PRSW, but regression analysis suggested an overestimation by circumferential regional PRSW at high contractile states and an underestimation at low contractile states (Fig. 3). Longitudinal regional PRSW displayed a bias of 0 mmHg, with limits of agreement of 8 and –7 mmHg. Circumferential regional PRSW displayed a bias of 0 mmHg, with limits of agreement of 7 and –6 mmHg (Fig. 3).


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  		Table 2. General hemodynamics and contractile indexes during preload reduction

 

Figure 3
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  		Fig. 3. Preload reduction protocol. Scatterplot with regression analysis (A) and Bland-Altman analysis (B) of longitudinal regional PRSW vs. global PRSW; scatterplot with regression analysis (C) and Bland-Altman analysis (D) of circumferential regional PRSW vs. global PRSW. In A and C, the thick line represents the linear regression line. In B and D, the thick line represents the bias, and the dotted lines represent the limits of agreement.

 
Global PRSW and longitudinal regional PRSW increased in response to increased afterload, while circumferential regional PRSW did not change significantly (Table 3). Longitudinal regional PRSW maintained a good agreement with global PRSW during afterload modulation (bias 1 mmHg, limits of agreement 8 and –6 mmHg) although the slope of the regression line did decrease (Fig. 4). In contrast, the agreement between circumferential regional PRSW and global PRSW deteriorated severely. Linear regression no longer reported a significant correlation between circumferential regional PRSW and global PRSW. Although the bias only increased slightly (to 4 mmHg), the limits of agreement became unacceptably high (29 and –22 mmHg).


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  		Table 3. General hemodynamics and contractile indexes during afterload increase

 

Figure 4
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  		Fig. 4. Afterload increase protocol. Scatterplot with regression analysis (A) and Bland-Altman analysis (B) of longitudinal regional PRSW vs. global PRSW; scatterplot with regression analysis (C) and Bland-Altman analysis (D) of circumferential regional PRSW vs. global PRSW. In A and C, the thick line represents the linear regression line. In B and D, the thick line represents the bias, and the dotted lines represent the limits of agreement.

 

   DISCUSSION
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 ABSTRACT
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
GRANTS
 REFERENCES
 
Our findings suggest that, in the ovine RV, regional contractility in the longitudinal axis accurately reflects global contractile function while data derived from the circumferential axis are unreliable when loading conditions vary.

The slope of the global PRSW relationship accurately reflects contractility in both the LV (11) and the RV (18). It has been previously shown that the relationship between end-diastolic segment length and segmental stroke work is also linear (30), allowing the quantification of regional PRSW relationships in any dimension of the ventricle. However, the fact that the relationship between end-diastolic segment length and segmental stroke work is linear does not automatically imply that the slope of this relationship is a reliable contractile index.

In the present study, longitudinal regional PRSW displayed a strong agreement with global PRSW during modulation of inotropic state and loading conditions, suggesting that, like global PRSW, longitudinal regional PRSW is inotropically sensitive and relatively load independent. Our data therefore suggest that longitudinal regional PRSW is a robust index of global RV contractile function. Circumferential regional PRSW did not detect the esmolol-induced decrease in contractility (P = 0.43). Most importantly, in response to increased afterload, circumferential regional PRSW became inaccurate compared with global PRSW. Our findings therefore suggest that circumferential regional PRSW is unreliable in settings where loading conditions, and particularly afterload, may fluctuate.

While the present study does not provide information as to why the longitudinal axis provides a better approximation to global RV contractile function than the circumferential axis, our findings are compatible with historical observations (3) and more recent insights in global cardiac mechanics. Although the RV shares four (bulbospiral and sinospiral) muscle bundles with the LV (2), which run in the circumferential direction, it has been suggested that the heart can be described as a single functional muscle band arranged in a dual-helix form (33). There is evidence that, during systole, contraction of the basal segment causes the entire heart to mimic a stiff cylinder, which then shortens (in the base-to-apex direction) because of contraction of the descending segment, leading to ventricular ejection. In other words, this suggests that volume displacement during the heart cycle is mainly thanks to longitudinal deformation. This is in agreement with our findings that global contractile function in the ejection phase is assessed more accurately by regional deformation in the longitudinal axis than by regional deformation in the circumferential axis. There is indeed increasing evidence that RV longitudinal deformation provides reliable information concerning global ventricular function both in the experimental and clinical setting (4, 13, 14, 16, 20, 29, 34).

Our findings concerning regional PRSW are in agreement with several previous studies. Nicolosi and coworkers (28) previously showed that RV longitudinal regional PRSW increases in response to calcium administration and decreases in response to administration of pentobarbital in bolus. Unfortunately, they did not mathematically analyze the agreement between longitudinal regional PRSW and global PRSW in their study. Karunanithi and Feneley (17) examined the relationship between RV circumferential regional PRSW and global PRSW at baseline, during increased RV afterload, and during increased LV afterload. They reported a weak relationship between circumferential regional PRSW and global PRSW at baseline (R2 = 0.25). Moreover, circumferential regional PRSW but not global PRSW decreased during pulmonary artery constriction (according to multiple linear regression analysis).

The present study has two main implications. First, it may be feasible to calculate regional PRSW in the longitudinal axis as an alternative to the volume-dependent indexes in the clinical setting, by integrating a RV pressure signal with noninvasively acquired echocardiographic deformation data and performing minor load modifications (for instance, by altering the position of the patient). A second and more important implication of this study is that it confirms a train of thought that clinicians have held for decades (19) but that has not been adequately validated: that regional RV contractile function is accurately reflected by motion in the longitudinal axis but not in the circumferential axis. This information therefore confirms that future investigations into less invasive RV contractile indexes should probably focus on longitudinal function.

Limitations of this study include the fact that the data were obtained in an acutely instrumented open-chest, open-pericardium model, which is relevant primarily for the intraoperative setting during cardiac surgery. However, hemodynamic data obtained in open-chest anesthetized animal models may differ considerably from those obtained in conscious animals with intact pericardium (15, 31). Particularly the shape of the RV may change when the constraints of a closed pericardium are no longer present. Therefore, these data should not be transposed to the intact organism without further validation. Finally, the current study was performed in normal animals, and additional studies are required to examine the effects of chronic pathological states (including chronic changes in loading conditions) on the regional contractile indexes. An intrinsic limitation of any regional index that is used to describe global function is the fact that it cannot be used in diseases with a regional effect on contractile performance, such as myocardial ischemia. Our observation that an increase in afterload caused an increase in contractility as assessed by using global PRSW is in agreement with previous studies (6, 7, 26) and most probably reflects the physiological phenomenon of homeometric autoregulation (26). Alternatively, we cannot exclude sympathetic activation as a possible cause of this effect because the autonomic nervous system was left intact in our animals. In this respect, previous studies in autonomically blocked animals have shown global PRSW to be relatively afterload independent (18, 22). Regardless of the mechanism, the increase in PRSW during acute augmentation of afterload should not be confused with load-induced errors in the index itself. Because the aim of the present study was to examine the agreement between the regional indexes and the gold standard, global PRSW, in different conditions, this physiological behavior does not constitute a limitation to the present observations.

We conclude that in an experimental model with open chest and opened pericardium, longitudinal regional deformation accurately reflects global RV contractile function, while circumferential motion responds differently to changes in afterload. Regional PRSW in the longitudinal axis is a reliable alternative to global, volumetry-dependent RV PRSW.


   GRANTS
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 ABSTRACT
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 GRANTS
REFERENCES
 
This study was supported by grants from the Fund for Scientific Research-Flanders, Belgium (1.5.156.02 [EC] ) and the Research Fund Katholieke Universiteit Leuven (P. F. Wouters). H. A. Leather is a research assistant for the Fund for Scientific Research-Flanders, Belgium.


   ACKNOWLEDGMENTS
 
We thank Kevin Lathouwers for technical assistance.


   FOOTNOTES
 

Address for reprint requests and other correspondence: P. F. Wouters, Dept. of Anesthesiology, Univ. Hospitals Katholieke Universiteit Leuven, Herestraat 49, B-3000 Leuven, Belgium (e-mail: patrick.wouters{at}uz.kuleuven.ac.be)

The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.


   REFERENCES
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 ABSTRACT
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 GRANTS
 REFERENCES
 

  1. Bland JM and Altman DG. Statistical methods for assessing agreement between two methods of clinical measurement. Lancet 1: 307–310, 1986.[CrossRef][ISI][Medline]
  2. Brecher GA and Galletti PM. Functional anatomy of cardiac pumping. In: Handbook of Physiology. Circulation Washington, DC: Am. Physiol. Soc., 1963, sect. 2, vol. I, chapt. 23, p. 759–798.
  3. Carlsson E. Experimental studies on ventricular mechanics in dogs using the tantalum-labeled heart. Fed Proc 25: 1324–1329, 1969.
  4. Dambrauskaite V, Herbots L, Claus P, Verleden G, Van Raemdonck D, Delcroix M, and Sutherland GR. Differential changes in regional right ventricular function before and after a bilateral lung transplantation: an ultrasonic strain and strain rate study. J Am Soc Echocardiogr 16: 432–436, 2003.[CrossRef][ISI][Medline]
  5. Danton MH, Greil GF, Byrne JG, Hsin M, Cohn L, and Maier SE. Right ventricular volume measurement by conductance catheter. Am J Physiol Heart Circ Physiol 285: H1774–H1785, 2003.[Abstract/Free Full Text]
  6. de Vroomen M, Cardozo RH, Steendijk P, van Bel F, and Baan J. Improved contractile performance of right ventricle in response to increased RV afterload in newborn lamb. Am J Physiol Heart Circ Physiol 278: H100–H105, 2000.[Abstract/Free Full Text]
  7. De Vroomen M, Steendijk P, Lopes Cardozo RH, Brouwers HH, Van Bel F, and Baan J. Enhanced systolic function of the right ventricle during respiratory distress syndrome in newborn lambs. Am J Physiol Heart Circ Physiol 280: H392–H400, 2001.[Abstract/Free Full Text]
  8. Dickstein ML, Yano O, Spotnitz HM, and Burkhoff D. Assessment of right ventricular contractile state with the conductance catheter technique in the pig. Cardiovasc Res 29: 820–826, 1995.[CrossRef][ISI][Medline]
  9. Erb TO, Craig DM, Gaskin PM, Cheifetz IM, Resai Bengur A, and Sanders SP. Preload recruitable stroke work relationship in the right ventricle: simultaneous assessment using conductance catheter and sonomicrometry. Crit Care Med 30: 2535–2541, 2002.[CrossRef][ISI][Medline]
  10. Gavazzi A, Berzuini C, Campana C, Inserra C, Ponzetta M, Sebastiani R, Ghio S, and Recusani F. Value of right ventricular ejection fraction in predicting short-term prognosis of patients with severe chronic heart failure. J Heart Lung Transplant 16: 774–785, 1997.[ISI][Medline]
  11. Glower DD, Spratt JA, Snow ND, Kabas JS, Davis JW, Olsen CO, Tyson GS, Sabiston DC Jr, and Rankin JS. Linearity of the Frank-Starling relationship in the intact heart: the concept of preload recruitable stroke work. Circulation 71: 994–1009, 1985.[Abstract/Free Full Text]
  12. Greyson C, Xu Y, Cohen J, and Schwartz GG. Right ventricular dysfunction persists following brief right ventricular pressure overload. Cardiovasc Res 34: 281–288, 1997.[Abstract/Free Full Text]
  13. Herbots L, Kowalski M, Vanhaecke J, Hatle L, and Sutherland GR. Characterizing abnormal regional longitudinal function in arrhythmogenic right ventricular dysplasia. The potential clinical role of ultrasonic myocardial deformation imaging. Eur J Echocardiogr 4: 101–107, 2003.[CrossRef][Medline]
  14. Hughes ML, Shekerdemian LS, Brizard CP, and Penny DJ. Improved early ventricular performance with a right ventricle to pulmonary artery conduit in stage 1 palliation for hypoplastic left heart syndrome: evidence from strain Doppler echocardiography. Heart 90: 191–194, 2004.[Abstract/Free Full Text]
  15. Ihara T, Shannon PR, Komamura K, Pasipoularides A, Patrick T, Shen YT, and Vatner SF. Effects of anaesthesia and recent surgery on diastolic function. Cardiovasc Res 28: 325–336, 1994.[Abstract/Free Full Text]
  16. Jamal F, Bergerot C, Argaud L, Loufouat J, and Ovize M. Longitudinal strain quantitates regional right ventricular contractile function. Am J Physiol Heart Circ Physiol 285: H2842–H2847, 2003.[Abstract/Free Full Text]
  17. Karunanithi MK and Feneley MP. Limitations of unidimensional indexes of right ventricular contractile function in conscious dogs. J Thorac Cardiovasc Surg 120: 302–312, 2000.[Abstract/Free Full Text]
  18. Karunanithi MK, Michniewicz J, Copeland SE, and Feneley MP. Right ventricular preload recruitable stroke work, end-systolic pressure-volume, and dP/dtmax-end-diastolic volume relations compared as indexes of right ventricular contractile performance in conscious dogs. Circ Res 70: 1169–1179, 1992.[Abstract/Free Full Text]
  19. Kaul S, Tei C, Hopkins JM, and Shah PM. Assessment of right ventricular function using two-dimensional echocardiography. Am Heart J 107: 526–531, 1984.[CrossRef][ISI][Medline]
  20. Koyama J, Davidoff R, and Falk RH. Longitudinal myocardial velocity gradient derived from pulsed Doppler tissue imaging in AL amyloidosis: a sensitive indicator of systolic and diastolic dysfunction. J Am Soc Echocardiogr 17: 36–44, 2004.[CrossRef][ISI][Medline]
  21. Leather HA, Segers P, Berends N, Vandermeersch E, and Wouters PF. Effects of vasopressin on right ventricular function in an experimental model of acute pulmonary hypertension. Crit Care Med 30: 2548–52, 2002.[CrossRef][ISI][Medline]
  22. Leather HA, Segers P, Sun YY, De Ruyter HA, Vandermeersch E, and Wouters PF. The limitations of preload-adjusted maximal power as an index of right ventricular contractility. Anesth Analg 95: 798–804, 2002.[Abstract/Free Full Text]
  23. Leather HA, Ver Eycken K, Segers P, Herijgers P, Vandermeersch E, and Wouters PF. Effects of levosimendan on right ventricular function and ventriculovascular coupling in open chest pigs. Crit Care Med 31: 2339–2343, 2003.[CrossRef][ISI][Medline]
  24. Leeuwenburgh BP, Helbing WA, Steendijk P, Schoof PH, and Baan J. Biventricular systolic function in young lambs subject to chronic systemic right ventricular pressure overload. Am J Physiol Heart Circ Physiol 281: H2697–H2704, 2001.[Abstract/Free Full Text]
  25. Little WC, Cheng CP, Mumma M, Igarashi Y, Vinten-Johansen J, and Johnston WE. Comparison of measures of left ventricular contractile performance derived from pressure-volume loops in conscious dogs. Circulation 80: 1378–1387, 1989.[Abstract/Free Full Text]
  26. Lopes Cardozo RH, Steendijk P, Baan J, Brouwers HA, De Vroomen M, and Van Bel F. Right ventricular function in respiratory distress syndrome and subsequent partial liquid ventilation. Homeometric autoregulation in the right ventricle of the newborn animal. Am J Respir Crit Care Med 162: 374–379, 2000.[Abstract/Free Full Text]
  27. Monchi M, Bellenfant F, Cariou A, Joly LM, Thebert D, Laurent I, Dhainaut JF, and Brunet F. Early predictive factors of survival in the acute respiratory distress syndrome. A multivariate analysis. Am J Respir Crit Care Med 158: 1076–1081, 1998.[Abstract/Free Full Text]
  28. Nicolosi AC, Hettrick DA, and Warltier DC. Assessment of right ventricular function in swine using sonomicrometry and conductance. Ann Thorac Surg 61: 1381–1387, 1996.[Abstract/Free Full Text]
  29. Nikitin NP, Witte KK, Thackray SD, de Silva R, Clark AL, and Cleland JG. Longitudinal ventricular function: normal values of atrioventricular annular and myocardial velocities measured with quantitative two-dimensional color Doppler tissue imaging. J Am Soc Echocardiogr 16: 906–921, 2003.[CrossRef][ISI][Medline]
  30. Pagel PS, Kampine JP, Schmeling WT, and Warltier DC. Comparison of end-systolic pressure-length relations and preload recruitable stroke work as indices of myocardial contractility in the conscious and anesthetized, chronically instrumented dog. Anesthesiology 73: 278–290, 1990.[ISI][Medline]
  31. Pasipoularides AD, Shu M, Shah A, and Glower DD. Right ventricular diastolic relaxation in conscious dog models of pressure overload, volume overload, and ischemia. J Thorac Cardiovasc Surg 124: 964–972, 2002.[Abstract/Free Full Text]
  32. Stamato TM, Szwarc RS, and Benson LN. Measurement of right ventricular volume by conductance catheter in closed-chest pigs. Am J Physiol Heart Circ Physiol 269: H869–H876, 1995.[Abstract/Free Full Text]
  33. Torrent-Guasp F, Ballester M, Buckberg GD, Carreras F, Flotats A, Carrio I, Ferreira A, Samuels LE, and Narula J. Spatial orientation of the ventricular muscle band: physiologic contribution and surgical implications. J Thorac Cardiovasc Surg 122: 389–392, 2001.[Free Full Text]
  34. Vogel M, Schmidt MR, Kristiansen SB, Cheung M, White PA, Sorensen K, and Redington AN. Validation of myocardial acceleration during isovolumic contraction as a novel noninvasive index of right ventricular contractility: comparison with ventricular pressure-volume relations in an animal model. Circulation 105: 1693–1699, 2002.[Abstract/Free Full Text]



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