Ventricular Interaction Research Articles

2007 Laennec Clinician/Educator Lecture—Unraveling the Mysteries of Diastology

Diastolic dysfunction plays a critical role in the pathophysiology of producing signs and symptoms of heart failure. Heart failure with a normal ejection fraction (HFnlEF) is one of the leading causes of hospital admissions today and is associated with significant morbidity and mortality. It is thus important to understand the pathophysiology of diastolic dysfunction, which itself is a complex series of multiple interrelated events, including relaxation, suction, ventricular interaction, ventricular arterial coupling, pericardial restraint, and myocardial viscoelastic forces. It was difficult for the clinician to understand “diastology” in the past. Initial studies were limited to complex equations derived from animal models and were difficult to apply to patient care. The development of radionuclide angiography and Doppler echocardiography allowed noninvasive rapid assessment of volumetric filling and flow velocity curves, which began to provide insight into the complex process of diastolic filling for the clinician. As our understanding of diastology evolved over the past 2 decades, it has become clear that we now need to pursue new areas to understand this fascinating subject and apply it to patient care. These areas include the underlying mechanism HFnlEF (ventricular-vascular coupling versus true myocardial stiffness), relationship of rest versus exercise hemodynamics, and the complex ventricular fiber “twisting and shortening” of both contraction and relaxation.

Time-dependent response of both ventricles after septal ablation: Implications for biventricular support after left ventricular assist device placement

An ovine model of septal ablation was studied to elucidate the mechanisms involved in right ventricular failure when commencing left ventricular mechanical assistance. The disruption of ventricular interdependence after acute and chronic septal injury was examined. Twelve sheep underwent percutaneous transluminal septal myocardial ablation using 0.6 mL ethanol. Twelve other sheep underwent a sham procedure. Left ventricular and right ventricular pressure and volume (conductance) response 15 minutes and 4 weeks postinjury were measured. Ultrasonic crystals measured chamber dimensions and wall movement. Areas at risk and infarct zones were quantified. Compared with sham, ablation chronically reduced systolic interventricular septal thickening (18.4% +/- 5.8% vs 7.3% +/- 3.1%; P < .001) and acutely increased right ventricular ejection fraction (37.6% +/- 8.5% vs 69.9% +/- 7.2%; P < .001), preload recruitable stroke work (42.0 +/- 4.4 erg x 10(3) vs 48.7 +/- 2.0 erg x 10(3), P < .001), end-systolic elastance (1.03 +/- 0.19 mm Hg mL(-1) vs 1.31 +/- 0.18 mm Hg mL(-1); P < .001), and Tau (24.9 +/- 3.8 ms vs 29.6 +/- 8.2 ms; P < .001). In contrast, for left ventricular ejection fraction (55.5% +/- 5.9% vs 38.9% +/- 7.7%; P < .001), preload recruitable stroke work (85.9 +/- 10.6 mm Hg vs 66.5 +/- 9.6 mm Hg; P < .001) and elastance (2.13 +/- 0.51 mm Hg mL(-1) vs 1.81 +/- 0.44 mm Hg mL(-1); P < .001) were reduced, but Tau increased (22.0 +/- 3.5 ms vs 28.9 +/- 5.8 ms; P < .001) and remained elevated at 4 weeks compared with sham. The area at risk was the same between groups, and injury was limited to the septum (17.2% +/- 2.7% vs 2.9% +/- 5.8%; P < .001). Acute and chronic hemodynamic responses are distinctly different after septal injury; the acute response demonstrates a paradoxical motion. Resolution of this motion at 4 weeks is suggestive of reduced septal compliance and buttressing. Ventricular interactions after placement of a left ventricular assist device will vary depending on the injury duration.

Acute Changes in Pulmonary Artery Pressures Due to Exercise and Exposure to High Altitude Do Not Cause Left Ventricular Diastolic Dysfunction

Altitude-induced pulmonary hypertension has been suggested to cause left ventricular (LV) diastolic dysfunction due to ventricular interaction. In this study, we evaluate the effects of exercise- and altitude-induced increase in pulmonary artery pressures on LV diastolic function in an interventional setting investigating high-altitude pulmonary edema (HAPE) prophylaxis. Among 39 subjects, 29 were HAPE susceptible (HAPE-S) and 10 served as control subjects. HAPE-S subjects were randomly assigned to prophylactic tadalafil (10 mg), dexamethasone (8 mg), or placebo bid, starting 1 day before ascent. Doppler echocardiography at rest and during submaximal exercise was performed at low altitude (490 m) and high altitude (4,559 m). The ratio of early transmitral inflow peak velocity (E) to atrial transmitral inflow peak velocity (A), pulmonary venous flow parameters, and tissue velocity within the septal mitral annulus during early diastole (E') were used to assess LV diastolic properties. LV filling pressures were estimated by E/E'. Systolic right ventricular to atrial pressure gradients (RVPGs) were measured in order to estimate pulmonary artery pressures. At 490 m, E/A decreased similarly with exercise in HAPE-S and control subjects (HAPE-S, 1.5 +/- 0.3 to 1.3 +/- 0.3; control, 1.7 +/- 0.4 to 1.3 +/- 0.3; p = 0.12 between groups) [mean +/- SD], whereas RVPG increased significantly more in HAPE-S subjects (20 +/- 5 to 43 +/- 9 mm Hg vs 18 +/- 3 to 28 +/- 3 mm Hg, p < 0.001). Changes in RVPG levels during exercise did not correlate with changes in E/A (p > 0.1). From 490 to 4,559 m, no correlations between changes in RVPG and changes in E/A or atrial reversal (both p > 0.1) were observed. Neither of the groups showed an increase in E/E' from 490 to 4,559 m. Increased pulmonary artery pressure associated with exercise and acute exposure to 4,559 m appears not to cause LV diastolic dysfunction in healthy subjects. Therefore, ventricular interaction seems not to be of hemodynamic relevance in this setting.

Echocardiographic evaluation of hemodynamic parameters

Hemodynamic assessment is a constant and common task in critically ill and injured patients. Correct interpretation of this data is vital to implement the appropriate intervention, if any. It can be difficult to properly interpret derived and measured data from a pulmonary artery catheter for optimal care of these difficult patients. Catheter use remains controversial because some researchers believe there is no clear benefit to the mortality rate. This conundrum will never be settled without a prospective blinded study. However, echocardiography is a vital and reliable monitoring tool to interrogate pressures, ventricular function, ventricular volumes, ventricular interactions, and diastolic compliance. In some institutions, it is used to construct a pressure/volume curve to measure contractility, which is load-dependent. Echocardiography easily can measure intracardiac pressures accurately but in a static fashion, which is one of its major benefits.

Rechtsherzinsuffizienz und Cor pulmonale

Whereas the right ventricle tolerates volume loads without any substantial increase of the pressure in the pulmonary circulation by recruiting capacitance vessels and capillaries, it possesses only small contractile reserves and reacts unadapted with right ventricular dysfunction. Its size and pressure load are relevant factors for prognosis of all forms of pulmonary hypertension, in particular if linked to left-sided heart failure. Differentiation of pulmonary hypertension according to the Venice classification is highly important. Right-sided ventricular heart failure worsens left ventricular hemodynamics due to reduced ejection fraction and in addition due to direct diastolic ventricular interaction in which left ventricular diastolic dysfunction increases even though the left ventricular systolic function is still intact. Right ventricular ejection fraction <40% is an important predictor of prognosis after myocardial infarction or chronic stages of left ventricular heart failure. The most important noninvasive diagnostic method is transthoracic echocardiography with determination of the Tei index and Doppler echocardiographic estimation of pulmonary artery pressure. Chronic obstructive pulmonary disease is the most frequent cause of cor pulmonale. While long-term oxygen therapy in patients with COPD and cor pulmonale and for example the administration of endothelin receptor antagonists in patients with idiopathic pulmonary hypertension is beneficial, the therapeutic use of drugs effective for left-sided heart failure is very limited in patients with right ventricular dysfunction.

Diastolic ventricular interactions in endurance-trained athletes during orthostatic stress

Enhanced left-ventricular (LV) compliance is a common adaptation to endurance training. This adaptation may have differential effects under conditions of altered venous return. The purpose of this investigation was to assess the effect of cardiac (un)loading on right ventricular (RV) cavity dimensions and LV volumes in endurance-trained athletes and normally active males. Eight endurance-trained (Vo(2max), 65.4 +/- 5.7 ml.kg(-1).min(-1)) and eight normally active (Vo(2max), 45.1 +/- 6.0 ml.kg(-1).min(-1)) males underwent assessments of the following: 1) Vo(2max), 2) orthostatic tolerance, and 3) cardiac responses to lower-body positive (0-60 mmHg) and negative (0 to -80 mmHg) pressures with echocardiography. In response to negative pressures, echocardiographic analysis revealed a similar decrease in RV end-diastolic cavity area in both groups (e.g., at -80 mmHg: normals, 21.4%; athletes, 20.8%) but a greater decrease in LV end-diastolic volume in endurance-trained athletes (e.g., at -80 mmHg: normals, 32.3%; athletes, 44.4%; P < 0.05). Endurance-trained athletes also had significantly greater decreases in LV stroke volume during lower-body negative pressure. During positive pressures, endurance-trained athletes showed larger increases in LV end-diastolic volume (e.g., at +60 mmHg; normals, 14.1%; athletes, 26.8%) and LV stroke volume, despite similar responses in RV end-diastolic cavity area (e.g., at +60 mmHg: normals, 18.2%; athletes, 24.2%; P < 0.05). This investigation revealed that in response to cardiac (un)loading similar changes in RV cavity area occur in endurance-trained and normally active individuals despite a differential response in the left ventricle. These differences may be the result of alterations in RV influence on the left ventricle and/or intrinsic ventricular compliance.

Using a Human Cardiopulmonary Model to Study and Predict Normal and Diseased Ventricular Mechanics, Septal Interaction, and Atrio-Ventricular Blood Flow Patterns

We upgraded our human cardiopulmonary (CP) model with additional data that enables it to more accurately simulate normal physiology. We then tested its ability to explain human disease by changing two parameter values that decrease ventricular compliance, and found that it could predict many of the hemodynamic, gas exchange, and autonomic abnormalities found in patients with left ventricular diastolic dysfunction (LVDD). The newly incorporated information includes high-fidelity pressure tracings simultaneously recorded from the RV and LV of a normal human in a cardiac catheterization laboratory, Doppler echocardiographic inlet flow velocity patterns, measures of right and left ventricular impedance, and atrial volumes. The revised cardiovascular section details the hemodynamics of a normal subject to the extent that it can now explain the effects of septal compliance on ventricular interaction, the differences in left and right ventricular pressure development, and venous blood gas mixing in the right atrium. The model can isolate the highly interrelated features of normal and abnormal physiology, and simultaneously demonstrate their interaction in a manner that would be very difficult or impossible using an intact organism. It may therefore help physicians and scientists understand, diagnose, and improve their treatment of complicated cardiovascular and pulmonary diseases. It could also simulate the hemodynamic and respiratory effects of ventricular and pulmonary assist devices, and thus help with their development.

Cardiovascular magnetic resonance for pericardial disease

Diseases of the pericardium are an uncommon but important group of diseases in cardiology with several different pathologies. The current mainstay of cardiac imaging, echocardiography has some limitations in visualizing pericardial and mediastinal disease. Recent improvement in cardiac MRI allows new insight into imaging the pericardium and the pericardial space. This article describes different pathologies, including pericardial constriction, masses and congenital absence of the pericardium. CMR protocols and techniques are discussed including the use of different sequences, along with the use of contrast media and real time imaging for ventricular:ventricular interaction. The role of CMR is placed in context with other imaging modalities.

Ventricular-Arterial and Ventricular-Ventricular Interactions and Their Relevance to Diastolic Filling

Chronic heart failure is a common clinical problem, and, until recently, attention has focused predominantly on those patients with reduced left ventricular (LV) systolic function, as evidenced by a reduced LV ejection fraction. However, nearly half of all patients thought clinically to have heart failure have a "preserved" LV ejection fraction, variously defined as greater than 40% to 45% ("heart failure with normal ejection fraction" syndrome). The interaction of the heart with the systemic vasculature, termed ventricular-arterial coupling, is a key determinant of cardiovascular performance. The capacity of the body to augment cardiac output, regulate systemic blood pressure, and respond appropriately to elevations in heart rate and preload depends on both the properties of the heart and the properties of the vasculature into which the heart ejects blood. Although the marked increase of arterial and cardiac stiffness with aging can maintain ventricular-vascular coupling within a normal range, it does have detrimental effects on hemodynamic stability and cardiac reserve. Patients with heart failure with normal ejection fraction have been shown to have both arterial and ventricular stiffening, resulting in enhanced pressure-load dependence and sensitivity of blood pressure to circulating volume and diuretics. There is also indirect evidence to suggest that on exercise, increased external constraint to LV filling (as a result of diastolic ventricular interaction and pericardial constraint) may contribute to impaired use of the Starling mechanism in this group of patients.

915 The second regional systolic shortening found in LV lateral wall motion is due to ventricular interaction and should not be used to infer late contraction in this wall when studying LV dysynchrony

Variations in regional systolic velocity profiles (SVP) have been widely used to assess cardiac dyssynchrony. However, regional longitudinal SVP have a non-uniform pattern. SVP in the septum (SEP) and inferior wall are similar being mono-phasic with an early systolic peak. In contrast, SVP in the anterior (ANT) and lateral (LAT) walls differ, being bi-phasic with two systolic peaks. Thus when assessing the timing of delayed contraction in the ANT and LAT walls it is important to know what each peak represents. Ventricular interaction could be responsible for the early deceleration of the first peak in ANT and LAT wall motion and could explain the bi-phasic systolic pattern. We postulated that early cessation of the first systolic motion and appearance of a second shortening motion in the LAT wall may be due either to a combination of cardiac twisting around the long axis of the heart and interaction with right ventricle (RV) contractility rather than local myocardial shortening. As regional strain rates (SR) but not velocities (VEL) reflect myocardial contractile function we investigated the relationship between regional peak systolic SR and SVP in the RV free wall, SEP and LAT wall. Methods: In 23 normals (age 45.5±2) long axis regional SVP and SR were obtained from the basal segments of RV, SEP and LAT. Time to max deceleration of the first peak was measured in the LAT and its relationship to RV peak SVP determined. In addition the time to peak VEL and SR in all walls was calculated. Results: The timing of peak SVP in the RV corresponded to the end of deceleration of the first peak in the LAT SVP (0.199±0.03 vs 0.197±0.03 s. p=NS). There was a consistent and significant difference between the time to peak systolic VEL in LAT vs RV (0.130±0.02 vs 0.199±0.03 s, p<0.001) with the SEP peak systolic VEL in an intermediate position at 0.154±0.03 s (p=NS vs RV and LAT). Systolic SR in all walls had a single peak which occurred in early systole with no significant difference between cardiac walls (0.100±0.02; 0.103±0.02; and 0.105±0.02 s in SEP, LAT and RV respectively). The second systolic peak in the LAT wall was not associated with any measurable deformation on the SR curve. Conclusions: This study showed that the early cessation of the first peak systolic VEL and second VEL peak in the LW wall is due to motion induced by RV contraction and does not represent LV contractile function. Furthermore, first rather second peak in LAT corresponds to peak systolic SR, which reflects true myocardial contraction. Therefore measurement of cardiac synchronization should not be based on SVP but rather on SR profiles.

742 Systolic septal flattening as a sign of pulmonary hypertension varies with left ventricular dysfunction: A study in ventricular interaction

742 Systolic septal flattening as a sign of pulmonary hypertension varies with left ventricular dysfunction: A study in ventricular interaction

395 Ventricular interaction in pressure and volume overloaded right ventricles

395 Ventricular interaction in pressure and volume overloaded right ventricles

264 Diastolic dysfunction in pediatric renal transplant patients

Eur J Echocardiography Abstracts Supplement, December 2006 and if there were records of the left ventricular inflow by Doppler. Restrictive pattern was defined as E/A >1.5 and E-wave deceleraration time (DTE) 150 ms being pseudonormal if there was left atrium dilation. Results: Echocardiograms of 535 patients were studied, 78% male, aged 64±14. Normal pattern was present in 84 patients (16%), 65 (12%) had abnormal relaxation, 257 (48%) had a pseudonormal pattern and 129 (24%) had restrictive filling pattern. Coronary heart disease was more prevalent in the abnormal relaxation group than in the pseudonormal group (p=0.03). Patients with a restrictive pattern had a higher probability of being hospitalized than those with normal (p=0.001) and pseudonormal patterns (p=0.006). They had higher LVEDV (p=0.0007) and LV end-systolic volume (p<0.0001), lower LV fractional shortening fraction (p<0.0001), higher right ventricle enddiastolic volume (p<0.0001) and bigger left and right atrium dimensions (p<0.0001). A multiple linear regression model (R2=0.114; p<0.0001) determined that right ventricular end-diastolic volume (p=0.0007) was the only independent predictor of DTE. Conclusions: In DCM patients a restrictive filling pattern in a common finding especially in hospitalized patients. It relates to worse LV systolic function and to findings that may traduce higher filling pressures. Right ventricle dimension was the best predictor of the low DTE that characterizes restrictive filling pattern. This finding brings the focus on the possible role of ventricular interaction as a contribution to worse filling of the left ventricle in DCM.

Coupling of a 3D Finite Element Model of Cardiac Ventricular Mechanics to Lumped Systems Models of the Systemic and Pulmonic Circulation

In this study we present a novel, robust method to couple finite element (FE) models of cardiac mechanics to systems models of the circulation (CIRC), independent of cardiac phase. For each time step through a cardiac cycle, left and right ventricular pressures were calculated using ventricular compliances from the FE and CIRC models. These pressures served as boundary conditions in the FE and CIRC models. In succeeding steps, pressures were updated to minimize cavity volume error (FE minus CIRC volume) using Newton iterations. Coupling was achieved when a predefined criterion for the volume error was satisfied. Initial conditions for the multi-scale model were obtained by replacing the FE model with a varying elastance model, which takes into account direct ventricular interactions. Applying the coupling, a novel multi-scale model of the canine cardiovascular system was developed. Global hemodynamics and regional mechanics were calculated for multiple beats in two separate simulations with a left ventricular ischemic region and pulmonary artery constriction, respectively. After the interventions, global hemodynamics changed due to direct and indirect ventricular interactions, in agreement with previously published experimental results. The coupling method allows for simulations of multiple cardiac cycles for normal and pathophysiology, encompassing levels from cell to system.

Abstract 599: RV Protection Conferred by Chronic Effects of Percutaneous Transluminal Septal Myocardial Ablation During High Level LV Unloading in Sheep

Background: Severe RV failure is common (~25%) following acute LVAD unloading. The role of IVS dysfunction in this response remains uncertain, so we studied chronic ventricular interactions with incremental LV unloading following IVS damage. Methods: Percutaneous transluminal septal myocardial ablation (PTSMA) with ethanol caused irreversible IVS damage in 6 sheep. Main septal artery catheterization was performed in 6 other sham animals, and both groups underwent hemodynamic assessment 4w later. RV volume was derived from a 3-axis ellipsoidal subtraction model using sonomicrometer dimensions. RV- ejection fraction (EF), pressure recruitable stroke work (PRSW), end-systolic elastance (Ees), 1 st derivative of maximum RV pressure (dP/dt), and Tau were derived from P/V loops during IVC occlusion and LV unloading (25/50/75/100%) using a Bio-Medicus pump. Flow-probes measured % steady-state pulmonary, aortic, and mechanical bypass flow. Results: Response to varying LV assist levels is shown in the Figure ( * =P&lt;0.05). RV- EF, PRSW and Ees decreased in shams, but remained stable in PTSMA during high level LV unloading. DP/dt decreased in shams at 75% LV unloading and trended down at 100%. In contrast, high baseline Tau after PTSMA normalized with moderate ≥50% LV assist. Conclusions: Institution of LV unloading in a chronic IVS damaged but otherwise healthy heart protects against compromised RV function, whereas sham animals respond adversely. Chronic IVS fibrosis may confer protection by limiting changes in RV chamber geometry.

Apex techniques, old and new, hold the key to estimated left ventricular end-diastolic and right ventricular systolic pressure

The clinical syndrome of heart failure is characterised by a raised venous pressure, dilated ventricular cavity, and exercise intolerance. Raised left ventricular (LV) end-diastolic pressure and high left atrial pressure suggest a poor prognosis [1, 2]. Detection of raised filling pressures are important not only in the progression of coronary artery disease and dilated cardiomyopathy, but also because recent evidence suggests that restrictive LV filling may predict non-responders [3] to the increasingly popular intervention of cardiac resynchronisation therapy. Measurements of ventricular long axis function rely on the fact that the cardiac apex is fixed with respect to the chest wall [4]. Atrio-ventricular coupling during systole and diastole is mediated by an anatomically distinct set of sub-endocardial and sub-epicardial fibres organised longitudinally from base to apex [5]. Systolic function is quantified by familiar measurements such as ejection fraction, fractional shortening or peak rate of pressure change (dp/ dt). Wiggers [6] defined diastole as the period in the cardiac cycle from the ‘‘end of aortic ejection until the onset of ventricular tension development’’. Diastole is a complex sequence involving mechanisms of restoring forces and ventricular compliance, changes in atrial and ventricular pressure, transmitral filling, ventricular interaction, and atrial mechanical activity [1]. Consequently, diastolic function has proved more elusive to quantify, accumulating a stable of surrogates indicative of left atrial (LA) pressure, left ventricular end-diastolic pressure (LVEDP), transmitral flow velocities or long axis function. Assessment is further complicated because abnormalities observed in diastole may arise during the isovolumic periods, as well as in systole. Diastolic function is far more age-dependent than systolic function because physiologically normal values in the young may indicate pathologies in the elderly [1]. Isovolumic relaxation time (from A2 [end of ejection] to mitral cusp separation on M-mode) shortens with raised left atrial pressure, but prolongs with age. Normal ranges for isovolumic relaxation time are 60 – 20 ms (M-mode) [1] or 85 – 15 ms (Doppler) [7]; values less than 40 ms indicate raised left atrial pressure, and zero isovolumic relaxation R. Chung AE M. Y. Henein (&) National Heart and Lung Institute, Department of Echocardiography, Royal Brompton Hospital, Sydney Street, SW3 6NP London, UK e-mail: m.henein@rbht.nhs.uk Int J Cardiovasc Imaging (2006) 22: 643–646 DOI 10.1007/s10554-006-9097-4

Right ventricular hypertrophy causes impairment of left ventricular diastolic function in the rat

Right ventricular (RV) pressure overload causes right ventricular hypertrophy in several types of pulmonary and congenital heart diseases. The associated cardiac dysfunction has generally been attributed to alterations in RV function. However, due to global neurohormonal adaptations and mechanical ventricular interaction left ventricular (LV) function could be affected as well.Therefore,LV function, RV function and their interaction were studied in rats with monocrotaline (MCT)-induced RV hypertrophy and control rats. MCT (30 mg/kg) was used to induce pulmonary hypertension, which resulted, after 28 days, in marked RV hypertrophy (RV-weight: control 220 +/- 15,MCT 437 +/- 34mg,p < 0.05). In Langendorff-perfused hearts with balloons inserted in both the LV and the RV, the diastolic pressure-volume relations showed increased stiffness, and relaxation was prolonged in the LV and RV in the MCT group compared to controls. In the MCT group, developed pressures were increased only in the RV. An increase of LV volume increased RV diastolic pressure to a similar extent in both groups. However, an increase in RV volume did not affect LV diastolic pressure in controls, but significantly increased LV diastolic pressure in the MCT group. LV and RV developed pressure-volume relations were not affected. Calculated circumferential end-diastolic wall stresses (sigma) were larger in the MCT group (LV-sigma: 0.55 +/- 0.02, RV-sigma: 1.94 +/- 0.30 kN/m(2), both p< 0.05 to control) compared to controls (LV-sigma: 0.34 +/- 0.06,RV-sigma: 1.23 +/- 0.46 kN/m2). In the MCT group, collagen content was increased in the LV, septum and RV compared to controls. In conclusion, structural changes of the RV and LV result in depressed LV diastolic function during RV hypertrophy.

The Incidence of Right Ventricular Dysfunction Is Similar in Pulsatile and Continuous-Flow Left Ventricular Assist Devices

Introduction: Continuous-flow left ventricular assist devices (LVADs) augment cardiac output without the degree of left ventricular decompression and septal shift seen with pulsatile LVADs. Rotor speed is adjusted based on hemodynamic, echocardiographic and clinical data to optimize output and ventricular interaction. For these reasons, we theorized that the incidence of right ventricular dysfunction (RVD) may be reduced in patients implanted with continuous-flow LVADs. Methods: We retrospectively compared the incidence of RVD in patients implanted with pulsatile (Thoratec, Novacor or Heartmate XVE) and continuous-flow (Jarvik, Ventrassist or Heartmate II) LVADs.

Diastolic ventricular interaction: from physiology to clinical practice

The ventricles share a common septum and, therefore, the filling of one influences the compliance of the other. This phenomenon is known as direct diastolic ventricular interaction. The interaction is noticeably increased when the force exerted by the surrounding pericardium is raised, which is termed pericardial constraint. In healthy individuals, pericardial constraint is minor in the resting state. When right ventricular volume-to-pressure ratio acutely increases, however, such as during exercise, massive pulmonary embolism, or right ventricular infarction, notable diastolic ventricular interaction occurs. In this setting, the measured left ventricular intracavitary diastolic pressure overestimates the true left ventricular filling pressure, because the effect of external forces must be subtracted. Although growth of the pericardium can be a feature of chronic cardiac enlargement, here we review the evidence of the importance of diastolic ventricular interaction in certain acute and chronic disease processes, including heart failure.

AB45-3: Echocardiographic analysis of right ventricular electromechanical interaction identifies patients with tetralogy of Fallot potentially suitable for cardiac resynchronisation therapy

AB45-3: Echocardiographic analysis of right ventricular electromechanical interaction identifies patients with tetralogy of Fallot potentially suitable for cardiac resynchronisation therapy