Compression induced by RV pressure overload decreases regional coronary blood flow in anesthetized dogs

Pulmonary artery constriction (PAC), a model of right ventricular (RV) pressure overload, flattens or inverts the septum and may flatten the left ventricular (LV) free wall. Finite element (FE) analysis predicts that such deformations may cause substantial compression. This study tests the hypothesis that deformation-induced myocardial compressive stress impedes coronary blood flow (CBF). Colored microspheres ( approximately 2 x 10(6)) were injected into the left atrium of 13 open-chest, anesthetized dogs under control conditions and during PAC, which decreased the end-diastolic transseptal pressure gradient (LV - RV) from 1.6 +/- 1.3 to -3.4 +/- 1.7 mmHg. Septal and LV deformation was assessed with the use of two-dimensional echocardiography, and by FE analysis, the hydrostatic component of stress was assessed. Postmortem, a 2.5-cm wide, LV equatorial ring was divided into 16 endocardial and epicardial samples. PAC decreased CBF in the FE-predicted compression zones, areas with the greatest compression having the greatest reductions in CBF. During PAC, compression reached a maximum of 25.3 +/- 1.8 mmHg on the (LV) endocardial sides of the RV insertion points, areas that saw CBF decrease from 1.05 +/- 0.08 to 0.68 +/- 0.05 ml.min(-1).g(-1) (P < 0.001), more than 30%. CBF decreased (from 1.08 +/- 0.07 to 0.81 +/- 0.07 ml.min(-1).g(-1); P < 0.001) on the RV side of the midseptum, an area with as much as 16.0 +/- 1.0 mmHg of compression. Overall, average compressions of 10 mmHg decreased CBF by approximately 30%. We conclude that acute RV pressure overload deforms the septum and LV and induces compressive stresses that reduce CBF substantially. This may help explain why some patients with pulmonary hypertension and no critical coronary disease have chest discomfort indistinguishable from angina pectoris.     

Opening the pericardium during pulmonary artery constriction improves cardiac function.

During acute pulmonary hypertension, both the pericardium and the right ventricle (RV) constrain left ventricular (LV) filling; therefore, pericardiotomy should improve LV function. LV, RV, and pericardial pressures and RV and LV dimensions and LV stroke volume (SV) were measured in six anesthetized dogs. The pericardium was closed, the chest was left open, and the lungs were held away from the heart. Data were collected at baseline, during pulmonary artery constriction (PAC), and after pericardiotomy with PAC maintained. PAC decreased SV by one-half. RV diameter increased, and septum-to-LV free wall diameter and LV area (our index of LV end-diastolic volume) decreased. Compared with during PAC, pericardiotomy increased LV area and SV increased 35%. LV and RV compliance (pressure-dimension relations) and LV contractility (stroke work-LV area relations) were unchanged. Although series interaction accounts for much of the decreased cardiac output during acute pulmonary hypertension, pericardial constraint and leftward septal shift are also important. Pericardiotomy can improve LV function in the absence of other sources of external constraint to LV filling.     

Impaired distensibility of the left ventricle after stiffening of the right ventricle.

Acute and chronic alterations of right ventricular (RV) wall properties can change left ventricular (LV) performance. We investigated whether and how stiffening of the RV free wall alters LV diastolic distensibility. We used cross-circulated isolated hearts, in which the LV and RV were independently controllable. Stiffness of the RV free wall was altered by intramuscular injections of glutaraldehyde into the RV free wall after right coronary artery ligation. We measured circumferential and longitudinal regional lengths in the septum and LV free wall. During data acquisition, RV volume was held constant. After the RV free wall was stiffened by glutaraldehyde, the LV diastolic pressure-volume relation shifted upward and became steeper. Importantly, stiffening of the RV free wall increased the diastolic regional area in the septum and LV free wall under constant LV volume. The augmented regional dimensions may result in enhanced regional tension under constant LV volume and may be related to the observed increase in LV diastolic intracavitary pressure. The impaired LV diastolic distensibility by stiffening of the RV free wall may be at least partly explained by myocardial stretch, probably due to LV deformation.     

A 2D finite element model of the interventricular septum under normal and abnormal loading

The interventricular septum is the structure that separates the left and right ventricles of the heart. Under normal loading conditions, it is concave to the left ventricle, but under abnormal loading the septum flattens and occasionally inverts. In the past, the septum has frequently been modelled as integral to the left ventricle with the effects of pressure from the right ventricle being ignored. Under abnormal loading, the septum has been described as behaving equivalent to a "flapping sail". There has been no consideration of structural behaviour under these conditions. A 2-D plane stress FE model of the septum was used to investigate the difference in structural behaviour of the septum during diastole between normal and abnormal loading. The biaxial stress patterns that develop are distinctively disparate. Under normal loading, the septum behaves much like a thick-walled cylinder subject to internal and external pressure, with the resulting stresses being circumferential tension and radial compression, both varying with radius. These stresses are very low throughout most of diastole. However, under abnormal loading, the septum behaves in an arch-like fashion, with high compressive stresses almost circumferential in direction, combined with radial compression. We conclude that right ventricular pressures cause bending effects in the wall of the heart, and that under abnormal loading, the compressive stresses that develop in the septum may lead to an understanding of certain, previously unexplained, pathological conditions.     

A 2D Finite Element Model of the Interventricular Septum Under Normal and Abnormal Loading

Abstract

The interventricular septum is the structure that separates the left and right ventricles of the heart. Under normal loading conditions, it is concave to the left ventricle, but under abnormal loading the septum flattens and occasionally inverts. In the past, the septum has frequently been modelled as integral to the left ventricle with the effects of pressure from the right ventricle being ignored. Under abnormal loading, the septum has been described as behaving equivalent to a “flapping sail”. There has been no consideration of structural behaviour under these conditions. A 2-D plane stress FE model of the septum was used to investigate the difference in structural behaviour of the septum during diastole between normal and abnormal loading. The biaxial stress patterns that develop are distinctively disparate. Under normal loading, the septum behaves much like a thick-walled cylinder subject to internal and external pressure, with the resulting stresses being circumferential tension and radial compression, both varying with radius. These stresses are very low throughout most of diastole. However, under abnormal loading, the septum behaves in an arch-like fashion, with high compressive stresses almost circumferential in direction, combined with radial compression. We conclude that right ventricular pressures cause bending effects in the wall of the heart, and that under abnormal loading, the compressive stresses that develop in the septum may lead to an understanding of certain, previously unexplained, pathological conditions.     

Influence of the pericardium on right and left ventricular filling in the dog

We compared the influence of the pericardium on left and right ventricular (LV, RV) filling by measuring LV and RV pressures and segment lengths (SL, LV free wall, and RV inflow and outflow tracts) in six open-chest, pentobarbital sodium-anesthetized dogs before and after pericardiectomy. End-diastolic pressure (EDP) was varied by partial caval occlusion and dextran infusion. At each site the ln EDP-SL relation was fitted by linear regression and characterized by its slope and 1-Torr EDP intercept. The slope and 1-Torr intercept of the LV ln EDP-SL relation changed variably after pericardiectomy, but in each dog a change occurred that shifted this relation downward. In contrast, the RV inflow tract slope invariably decreased significantly after pericardiectomy, whereas its intercept was unchanged in all but one dog. The RV outflow tract results were similar to the inflow tract but less consistent. By the use of the raw EDP-SL data points, we calculated that the absolute contribution of the pericardium to EDP (i.e., the effective pericardial surface pressure) was similar at the three sites. However, as EDP values increased the proportional contribution of the pericardium to right ventricular end-diastolic pressure (RVEDP) increased, whereas that to left ventricular end-diastolic pressure (LVEDP) remained relatively constant. As a result, at the higher EDP values tested, the pericardium was responsible for a larger proportion of RVEDP than LVEDP.(ABSTRACT TRUNCATED AT 250 WORDS)     

Heterogeneous expression of connexin 43 in the myocardium of rabbit right ventricular outflow tract

The right ventricular outflow tract (RVOT) has been demonstrated as an important focus in idiopathic ventricular arrhythmias. However, the role of the gap junction in this region in arrhythmic events has not been fully investigated. The purpose of this study was to evaluate the expression and distribution of the gap junction protein connexin 43 (Cx43) in the myocardium of the RVOT area of normal adult rabbits. Tissue samples were obtained from 6 regions of normal rabbit heart, i.e. the left ventricle (LV) free wall, the LV papillary muscle, the RVOT free wall, and the RVOT septum which was subdivided into the RV side, the central layer, and the LV side. Immunohistochemical analysis was performed to investigate the characteristics of Cx43 distribution in the RVOT area. In the LV free wall and papillary muscle, Cx43 was abundantly, homogeneously, and approximately equally expressed in end-to-end- and side-to-side intercellular connections. In the free wall of the RVOT, Cx43 expression was poor compared to both these LV regions and side-to-side cell connections were predominant. Cx43 was as richly and homogeneously distributed in the central layer and LV side of the RVOT septum as in the two LV regions. However, in the RV side of the RVOT septum, its distribution was scant and an unstained area was noted. The heterogeneous expression of Cx43 in the RVOT area may serve as substrate for idiopathic ventricular arrhythmia.     

Right ventricular pressure and dilation during pressure overload determine dysfunction after pressure overload

Volume expansion and inotropic stimulation are used clinically to augment cardiac output during acute right ventricular (RV) pressure overload. We previously showed that a brief period of RV pressure overload causes RV free wall dysfunction that persists after normal loading conditions have been restored. However, the impact of volume expansion and inotropic stimulation on the severity of RV dysfunction after acute pressure overload is unknown. We hypothesized that the severity of RV dysfunction after RV pressure overload would be related to the level of RV free wall systolic stress during RV pressure overload, rather than to the specific interventions used to augment RV function. Chloralose-anesthetized, open-chest pigs were subjected to 1 h of RV pressure overload caused by pulmonary artery constriction, followed by 1 h of recovery after release of pulmonary artery constriction. A wide range of RV free wall systolic stress during RV pressure overload was achieved by either closing or opening the pericardium (to simulate volume expansion) and by administering or not administering dobutamine. The severity of RV free wall dysfunction 1 h after RV pressure overload was strongly and directly correlated with the values of two hemodynamic variables during RV pressure overload: RV free wall area at peak RV systolic pressure (determined by sonomicrometry) and peak RV systolic pressure, two of the major determinants of peak RV free wall systolic stress. Opening or closing the pericardium, and using or not using dobutamine during RV pressure overload, had no independent effects on the severity of RV dysfunction. The findings suggest that the goal of therapeutic intervention during RV pressure overload should be to achieve the required augmentation of cardiac output with the smallest possible increase in RV free wall systolic stress.     

Left ventricular effects on right ventricular developed pressure.

The possibility that left ventricular (LV) performance might affect right ventricular (RV) function through the myocardium was examined by using isolated, flow-perfused, paced rabbit hearts beating isovolumically. Reducing LV volume from its optimal volume to zero caused a 5.7% decrease (N = 10, P less than 0.001) in right ventricular developed pressure (RVDP). Ligating the anterior ventricular branches of the left coronary artery which in the rabbit supply the LV free wall resulted in an additional 9.3% decrease in RVDP (N = 5, P = 0.05) within 3 min of ligation. Finally, cutting the LV free wall from the atrioventricular orifice to the apex (thereby preventing any developed LV free wall force during systole) caused a 45% further decrease in RVDP (N = 2, P less than 0.02). Cineradiographic study showed that the alterations in RVDP resulting from changes in LV volume and coronary occlusion correlated significantly (N = 5, P less than 0.01) with the magnitude of septal bulging into the RV cavity during systole. The results indicate that alteration in LV free wall function and changes in LV volume can directly effect RVDP through the myocardium.     

A novel technique for measurement of pericardial pressure

To determine whether pericardial liquid pressure accurately measures pericardial constraint, we developed a technique in which a catheter was positioned perpendicular to the epicardial surface. This device, which occupies little or no pericardial space, couples the thin film of liquid to a transducer. In six open-chest dogs, we also measured left ventricular (LV) end-diastolic pressure (LVEDP) and anteroposterior and septum-to-free wall diameters. LVEDP was raised incrementally to approximately 25 mmHg by saline infusion. With the use of the product of the two diameters as an index of area (A(LV)), LVEDP-A(LV) relationships were obtained with the pericardium closed and again after the pericardium had been widely opened to obtain the isovolumic difference in LVEDP (DeltaLVEDP). In all dogs, the technique yielded values of pericardial pressure equal to DeltaLVEDP as well as equal to that measured using a previously placed balloon transducer in the same location and at the same A(LV). We conclude that, when the pressure of the pericardial liquid is appropriately measured, it (in addition to the balloon-measured contact stress) defines the diastolic constraining effect of the pericardium. Furthermore, we suggest that earlier measurements of pericardial "liquid pressure" were low, due to an artifact of measurement.     

Regional passive ventricular stress-strain relations during development of altered loads in chick embryo

Mechanical load influences embryonic ventricular growth, morphogenesis, and function. However, little is known about changes in regional passive ventricular properties during the development of altered mechanical loading conditions in the embryo. We tested the hypothesis that regional mechanical loads are a critical determinant of embryonic ventricular passive properties. We measured biaxial passive right and left ventricular (RV and LV, respectively) stress-strain relations in chick embryos at Hamburger-Hamilton stages 21 and 27 after conotruncal banding (CTB) to increase biventricular pressure load or left atrial ligation (LAL) to reduce LV volume load and increase RV volume load. In the RV, wall strains at end-diastolic (ED) pressure normalized whereas ED stresses increased after either CTB or LAL during development. In the left ventricle, both ED strain and stress normalized after CTB, whereas both remained reduced with significantly increased myocardial stiffness after LAL. These results suggest that the embryonic ventricle adapts to chronically altered mechanical loading conditions by changing specific RV and LV passive properties. Thus regional mechanical load has a critical role during cardiogenesis.     

Right and left ventricular adaptation to hypoxia: a tissue Doppler imaging study

Hypoxia has been reported to alter left ventricular (LV) diastolic function, but associated changes in right ventricular (RV) systolic and diastolic function remain incompletely documented. We used echocardiography and tissue Doppler imaging to investigate the effects on RV and LV function of 90 min of hypoxic breathing (fraction of inspired O(2) of 0.12) compared with those of dobutamine to reproduce the same heart rate effects without change in pulmonary vascular tone in 25 healthy volunteers. Hypoxia and dobutamine increased cardiac output and tricuspid regurgitation velocity. Hypoxia and dobutamine increased LV ejection fraction, isovolumic contraction wave velocity (ICV), acceleration (ICA), and systolic ejection wave velocity (S) at the mitral annulus, indicating increased LV systolic function. Dobutamine had similar effects on RV indexes of systolic function. Hypoxia did not change RV area shortening fraction, tricuspid annular plane systolic excursion, ICV, ICA, and S at the tricuspid annulus. Regional longitudinal wall motion analysis revealed that S, systolic strain, and strain rate were not affected by hypoxia and increased by dobutamine on the RV free wall and interventricular septum but increased by both dobutamine and hypoxia on the LV lateral wall. Hypoxia increased the isovolumic relaxation time related to RR interval (IRT/RR) at both annuli, delayed the onset of the E wave at the tricuspid annulus, and decreased the mitral and tricuspid inflow and annuli E/A ratio. We conclude that hypoxia in normal subjects is associated with altered diastolic function of both ventricles, improved LV systolic function, and preserved RV systolic function.     

Effect of the pericardium on atrial systolic function.

The effect of pericardial constraint on atrial systolic function was investigated in nine acutely instrumented anesthetized dogs. Left and right atrial pressures were recorded by high-fidelity catheters; auricular diameters and free wall segment lengths were measured by sonomicrometry. Atrial function curves were constructed by relating atrial systolic dimensional shortening to atrial end-diastolic pressure during progressive volume loading. With the pericardium closed, the function curves were shifted markedly downward and rightward, such that atrial systolic shortening was reduced at any given pressure. There was a concomitant leftward and upward shift of the atrial end-diastolic pressure-dimension relationship. The relationship between atrial systolic shortening and atrial end-diastolic dimension was not shifted. These results suggest that the apparent depression of atrial systolic function with the pericardium closed is due to a restrictive effect of the pericardium on atrial filling. In conclusion, in the acutely dilated heart, the pericardium restricts atrial filling and thus causes a reduction in atrial systolic contribution to ventricular filling.     

Dynamic effects of positive-pressure ventilation on canine left ventricular pressure-volume relations.

Positive-pressure ventilation (PPV) may affect left ventricular (LV) performance by altering both LV diastolic compliance and pericardial pressure (Ppc). We measured the effect of PPV on LV intraluminal pressure, Ppc, LV volume, and LV cross-sectional area in 17 acute anesthetized dogs. To account for changes in lung volume independent of changes in Ppc and differences in contractility, measures were made during both open- and closed-chest conditions, during closed chest with and without chest wall binding, and after propranolol-induced acute ventricular failure (AVF). Apneic end-systolic pressure-volume relations (ESPVR) were generated by inferior vena caval occlusions. With the open chest, PPV had no effects. With the chest closed, PPV inspiration decreased LV end-diastolic volume (EDV) along its diastolic compliance curve and decreased end-systolic volume (ESV) such that the end-systolic pressure-volume domain was shifted to a point left of the LV ESPVR, even when referenced to Ppc. The decrease in EDV was greater in control than in AVF conditions, whereas the shift of the ESV to the left of the ESPVR was greater with AVF than in control conditions. We conclude that the hemodynamic effects of PPV inspiration are due primarily to changes in intrathoracic pressure and that the inspiration-induced decreases of LV EDV reflect direct effects of intrathoracic pressure on LV filling. The decreases in LV ESV exceed the amount explained solely by a reduction in LV ejection pressure.     

Effects of sequential biventricular pacing during acute right ventricular pressure overload

Temporary sequential biventricular pacing (BiVP) is a promising treatment for postoperative cardiac dysfunction, but the mechanism for improvement in right ventricular (RV) dysfunction is not understood. In the present study, cardiac output (CO) was optimized by sequential BiVP in six anesthetized, open-chest pigs during control and acute RV pressure overload (RVPO). Ventricular contractility was assessed by the maximum rate of increase of ventricular pressure (dP/dt(max)). Mechanical interventricular synchrony was measured by the area of the normalized RV-left ventricular (LV) pressure diagram (A(PP)). Positive A(PP) indicates RV pressure preceding LV pressure, whereas zero indicates complete synchrony. In the control state, CO was maximized with nearly simultaneous stimulation of the RV and LV, which increased RV (P = 0.006) and LV dP/dt(max) (P = 0.002). During RVPO, CO was maximized with RV-first pacing, which increased RV dP/dt(max) (P = 0.007), but did not affect LV dP/dt(max), and decreased the left-to-right, end-diastolic pressure gradient (P = 0.023). Percent increase of RV dP/dt(max) was greater than LV dP/dt(max) (P = 0.014). There were no increases in end-diastolic pressure to account for increases in dP/dt(max). In control and RVPO, RV dP/dt(max) was linearly related to A(PP) (r = 0.779, P < 0.001). The relation of CO to A(PP) was curvilinear, with a peak in CO with positive A(PP) in the control state (P = 0.004) and with A(PP) approaching zero during RVPO (P = 0.001). These observations imply that, in our model, BiVP optimization improves CO by augmenting RV contractility. This is mediated by changes in mechanical interventricular synchrony. Afterload increases during RVPO exaggerate this effect, making CO critically dependent on simultaneous pressure generation in the RV and LV, with support of RV contractility by transmission of LV pressure across the interventricular septum.     

A Novel Approach to Standard Techniques in the Assessment and Quantification of the Interventricular Systolic Relationship

A 51-year-old female undergoing an outpatient stress echocardiogram to evaluate atypical chest pain developed acute ST elevation in the anterior precordial leads on electrocardiogram following exercise. Echocardiography revealed a severe rise in pulmonary artery systolic pressure (PASP) with marked right ventricular (RV) enlargement and interventricular septum flattening. Subsequently, cardiac catherization confirmed an exercise-induced elevation in PASP and diagnosed pulmonary arterial hypertension without evidence of coronary artery disease. This case suggests that an acute elevation in pulmonary artery pressure with RV dilation may be a potential cause of acute ST elevation during stress testing.     

Time course of right ventricular remodeling in rats with experimental myocardial infarction

Right ventricular (RV) weight increases dependent on time after myocardial infarction (MI) and on MI size. The sequential changes in RV volume and hemodynamics and their relations to left ventricular (LV) remodeling after MI are unknown. We therefore examined the time course of RV remodeling in rats with LV MI. MI was produced by left coronary artery ligation. Four, eight, and sixteen weeks later, LV and RV hemodynamic measurements were performed and pressure-volume curves were obtained. For serial measurement of RV volumes and performance, cine-MRI was performed 2 and 8 wk after MI. The ratios of beta-myosin heavy chain (MHC) to alpha-MHC and skeletal to cardiac alpha-actin were determined for the RV and LV after large MI or sham operation. RV weight increased in rats with MI, as did RV volume. RV pressure-volume curves were shifted toward larger volumes 16 wk after large MI. RV systolic pressure increased gradually over time; however, the gain in RV weight was always in excess of RV systolic pressure. The ratios of skeletal to cardiac alpha-actin and beta-MHC to alpha-MHC were increased after MI in both ventricles in a similar fashion. Because RV wall stress was not increased after infarction, mechanical factors may not conclusively explain hypertrophy, which maintained balanced loading conditions for the RV even after large LV infarction.     

Differential effects of left ventricular pacing sites in an acute canine model of contraction dyssynchrony

The goal of the present study was to assess the effects of left ventricular (LV) pacing sites (apex vs. free wall) on radial synchrony and global LV performance in a canine model of contraction dyssynchrony. Ultrasound tissue Doppler imaging and hemodynamic (LV pressure-volume) data were collected in seven anesthetized, opened-chest dogs. Right atrial (RA) pacing served as the control, and contraction dyssynchrony was created by simultaneous RA and right ventricular (RV) pacing to induce a left bundle-branch block-like contraction pattern. Cardiac resynchronization therapy (CRT) was implemented by adding simultaneous LV pacing to the RV pacing mode at either the LV apex (CRTa) or free wall (CRTf). A new index of synchrony was developed via pair-wise cross-correlation analysis of tissue Doppler radial strain from six midmyocardial cross-sectional regions, with a value of 15 indicating perfect synchrony. Compared with RA pacing, RV pacing significantly decreased radial synchrony (11.1 +/- 0.8 vs. 4.8 +/- 1.2, P < 0.01) and global LV performance (cardiac output: 2.0 +/- 0.3 vs. 1.4 +/- 0.1 l/min and stroke work: 137 +/- 22 vs. 60 +/- 14 mJ, P < 0.05). Although both CRTa and CRTf significantly improved radial synchrony, only CRTa markedly improved global function (cardiac output: 2.1 +/- 0.2 l/min and stroke work: 113 +/- 13 mJ, P < 0.01 vs. RV pacing). Furthermore, CRTa decreased LV end-systolic volume compared with RV pacing without any change in LV end-systolic pressure, indicating an augmented global LV contractile state. Thus, LV apical pacing appears to be a superior pacing site in the context of CRT. The dissociation between changes in synchrony and global LV performance with CRTf suggests that regional analysis from a single plane may not be sufficient to adequately characterize contraction synchrony.     

Assessment of Right Ventricular Structure and Function in Mouse Model of Pulmonary Artery Constriction by Transthoracic Echocardiography

Emerging clinical data support the notion that RV dysfunction is critical to the pathogenesis of cardiovascular disease and heart failure^1-3. Moreover, the RV is significantly affected in pulmonary diseases such as pulmonary artery hypertension (PAH). In addition, the RV is remarkably sensitive to cardiac pathologies, including left ventricular (LV) dysfunction, valvular disease or RV infarction⁴. To understand the role of RV in the pathogenesis of cardiac diseases, a reliable and noninvasive method to access the RV structurally and functionally is essential.A noninvasive trans-thoracic echocardiography (TTE) based methodology was established and validated for monitoring dynamic changes in RV structure and function in adult mice. To impose RV stress, we employed a surgical model of pulmonary artery constriction (PAC) and measured the RV response over a 7-day period using a high-frequency ultrasound microimaging system. Sham operated mice were used as controls. Images were acquired in lightly anesthetized mice at baseline (before surgery), day 0 (immediately post-surgery), day 3, and day 7 (post-surgery). Data was analyzed offline using software.Several acoustic windows (B, M, and Color Doppler modes), which can be consistently obtained in mice, allowed for reliable and reproducible measurement of RV structure (including RV wall thickness, end-diastolic and end-systolic dimensions), and function (fractional area change, fractional shortening, PA peak velocity, and peak pressure gradient) in normal mice and following PAC.Using this method, the pressure-gradient resulting from PAC was accurately measured in real-time using Color Doppler mode and was comparable to direct pressure measurements performed with a Millar high-fidelity microtip catheter. Taken together, these data demonstrate that RV measurements obtained from various complimentary views using echocardiography are reliable, reproducible and can provide insights regarding RV structure and function. This method will enable a better understanding of the role of RV cardiac dysfunction.     

Differential modulation of right ventricular strain and right atrial mechanics in mild vs. severe pressure overload

Increased right atrial (RA) and ventricular (RV) chamber volumes are a late maladaptive response to chronic pulmonary hypertension. The purpose of the current investigation was to characterize the early compensatory changes that occur in the right heart during chronic RV pressure overload before the development of chamber dilation. Magnetic resonance imaging with radiofrequency tissue tagging was performed on dogs at baseline and after 10 wk of pulmonary artery banding to yield either mild RV pressure overload (36% rise in RV pressure; n = 5) or severe overload (250% rise in RV pressure; n = 4). The RV free wall was divided into three segments within a midventricular plane, and circumferential myocardial strain was calculated for each segment, the septum, and the left ventricle. Chamber volumes were calculated from stacked MRI images, and RA mechanics were characterized by calculating the RA reservoir, conduit, and pump contribution to RV filling. With mild RV overload, there were no changes in RV strain or RA function. With severe RV overload, RV circumferential strain diminished by 62% anterior (P = 0.04), 42% inferior (P = 0.03), and 50% in the septum (P = 0.02), with no change in the left ventricle (P = 0.12). RV filling became more dependent on RA conduit function, which increased from 30 ± 9 to 43 ± 13% (P = 0.01), than on RA reservoir function, which decreased from 47 ± 6 to 33 ± 4% (P = 0.04), with no change in RA pump function (P = 0.94). RA and RV volumes and RV ejection fraction were unchanged from baseline during either mild (P > 0.10) or severe RV pressure overload (P > 0.53). In response to severe RV pressure overload, RV myocardial strain is segmentally diminished and RV filling becomes more dependent on RA conduit rather than reservoir function. These compensatory mechanisms of the right heart occur early in chronic RV pressure overload before chamber dilation develops.