Pericardial Constraint Research Articles

Pericardiotomy as a novel treatment for heart failure with preserved ejection fraction.

The pericardium plays an important role in modulating cardiac performance and hemodynamics in patients with heart failure with preserved ejection fraction (HFpEF). Pericardial constraint increases filling pressures in patients with HFpEF, particularly those with the obesity phenotype, atrial myopathy, right ventricular dysfunction, and tricuspid regurgitation. Preclinical and early stage clinical studies indicate that pericardiotomy may become a novel treatment for HFpEF. This review summarizes and discusses the pathophysiology of pericardial restraint and the possibility of pericardiotomy in HFpEF.

Epicardial adipose tissue and pericardial constraint in heart failure with preserved ejection fraction.

Obesity and epicardial adiposity play a role in the pathophysiology of heart failure with preserved ejection fraction (HFpEF), and both are associated with increased filling pressures and reduced exercise capacity. The haemodynamic basis for these observations remains inaccurately defined. We hypothesize that an abundance of epicardial adipose tissue (EAT) within the pericardial sac is associated with haemodynamic signs of pericardial constraint. HFpEF patients who underwent invasive heart catheterization with simultaneous echocardiography were included. Right atrial pressure (RAP), right ventricular end-diastolic pressure, and pulmonary capillary wedge pressure (PCWP) were invasively measured. The presence of a square root sign on the right ventricular pressure waveform and the RAP/PCWP ratio (surrogate parameters for pericardial constraint) were investigated. EAT thickness alongside the right ventricle was measured on echocardiography. Sixty-four patients were studied, with a mean age of 73±10years, 64% women, and a mean body mass index (BMI) of 28.6±5.4kg/m2. In total, 47 patients (73%) had a square root sign. The presence of a square root sign was associated with higher BMI (29.3 vs. 26.7kg/m2, P=0.02), higher EAT (4.0 vs. 3.4mm, P=0.03), and higher RAP (9 vs. 6mmHg, P=0.04). Women had more EAT than men (4.1 vs. 3.5mm, P=0.04), despite a comparable BMI. Women with a square root sign had significantly higher EAT (4.3 vs. 3.3mm, P=0.02), a higher mean RAP (9 vs. 5mmHg, P=0.02), and a higher RAP/PCWP ratio (0.52 vs. 0.26, P=0.002). In men, such associations were not seen, although there was no significant interaction between men and women (P>0.05 for all analyses). Obesity and epicardial adiposity are associated with haemodynamic signs of pericardial constraint in patients with HFpEF. The pathophysiological and therapeutic implications of this finding need further study.

Ventricular systolic dysfunction with and without altered myocardial contractility: Clinical value of echocardiography for diagnosis and therapeutic decision-making

The inability of one of the two or both ventricles to contract normally and expel sufficient blood to meet the functional demands of the body results from a complex interplay between intrinsic abnormalities and extracardiac factors that limit ventricular pump function and is a major cause for heart failure (HF).Even if impaired myocardial contractile function was the primary cause for ventricular dysfunction, with the progression of systolic dysfunction, additionally developed diastolic dysfunction can also contribute to the severity of HF. Although at the first sight, the diagnosis of systolic HF appears quite easy because it is usually defined by reduction of the ejection fraction (EF), in reality this issue is far more complex because ventricular pumping performance depends not only on myocardial contractility, but also largely on loading conditions (preload and afterload), being also influenced by valvular function, ventricular interdependence, pericardial constraint, synchrony of ventricular contrac-tion and heart rhythm. Conventional echocardiography (ECHO) combined with new imaging techniques such as tissue Doppler and tissue tracking can detect early subclinical alteration of ventricular systolic function. However, no single ECHO parameter reveals alone the whole picture of systolic dysfunction. Multiparametric ECHO evaluation and the use of integrative approaches using ECHO-parameter combinations which include also the ventricular loading conditions appeared particularly useful especially for differentiation between primary (myocardial damage-induced) and secondary (hemodynamic overload-induced) systolic dysfunction.This review summarizes the available evidence on the usefulness and limitations of comprehensive evaluation of LV and RV systolic function by using all the currently available ECHO techniques.

Acute Unloading Effects of Sildenafil Enhance Right Ventricular–Pulmonary Artery Coupling in Heart Failure

BackgroundPhosphodiesterase-5A inhibitors (PDE5i) are sometimes used in patients with advanced heart failure with reduced ejection fraction before heart transplant or left ventricular assist device implantation to decrease right ventricular (RV) afterload and mitigate the risk of right heart failure. Conflicting evidence exists regarding the impact of these drugs on RV contractility. The aim of this study was to explore the acute effects of PDE5i on ventricular–vascular coupling and load-independent RV contractility. MethodsTwenty-two patients underwent right heart catheterization and gated equilibrium blood pool single photon emission computed tomography, before and after 20 mg intravenous sildenafil. Single photon emission computed tomography and right heart catheterization-derived data were used to calculate RV loading and contractility. ResultsPDE5i induced a decrease in the right atrial pressure (–43%), pulmonary artery (PA) mean pressure (–26%), and PA wedge pressure (PAWP; –23%), with favorable reductions in pulmonary vascular resistance (–41%) and PA elastance (–40%), and increased cardiac output (+13%) (all P < 0.01). The RV ejection fraction increased with sildenafil (+20%), with no change of RV contractility (P = 0.74), indicating that the improvement in the RV ejection fraction was related to enhanced RV–PA coupling (r = 0.59, P = 0.004) by a decrease in the ventricular load. RV diastolic compliance increased with sildenafil. The decrease in the PAWP correlated with RV end-diastolic volume decrease; no relationship was observed with the change in LV transmural pressure, suggesting decreased pericardial constraint. ConclusionsAcute PDE5i administration has profound RV afterload-reducing effects, improves the RVEF, decreases RV volumes, and decreases the PAWP, predominantly through relief of pericardial constraint, without effects on RV chamber contractility. These findings support further study of PDE5i in protection of RV function in advanced heart failure with reduced ejection fraction who are at risk of RV failure.

Altered Hemodynamics and End-Organ Damage in Heart Failure: Impact on the Lung and Kidney.

Heart failure is characterized by pathologic hemodynamic derangements, including elevated cardiac filling pressures ("backward" failure), which may or may not coexist with reduced cardiac output ("forward" failure). Even when normal during unstressed conditions such as rest, hemodynamics classically become abnormal during stressors such as exercise in patients with heart failure. This has important upstream and downstream effects on multiple organ systems, particularly with respect to the lungs and kidneys. Hemodynamic abnormalities in heart failure are affected by processes that extend well beyond the cardiac myocyte, including important roles for pericardial constraint, ventricular interaction, and altered venous capacity. Hemodynamic perturbations have widespread effects across multiple heart failure phenotypes, ranging from reduced to preserved ejection fraction, acute to chronic disease, and cardiogenic shock to preserved perfusion states. In the lung, hemodynamic derangements lead to the development of abnormalities in ventilatory control and efficiency, pulmonary congestion, capillary stress failure, and eventually pulmonary vascular disease. In the kidney, hemodynamic perturbations lead to sodium and water retention and worsening renal function. Improved understanding of the mechanisms by which altered hemodynamics in heart failure affect the lungs and kidneys is needed in order to design novel strategies to improve clinical outcomes.

Diastolic Ventricular Interaction in Heart Failure With Preserved Ejection Fraction.

BackgroundExercise‐induced pulmonary hypertension is common in heart failure with preserved ejection fraction (HFpEF). We hypothesized that this could result in pericardial constraint and diastolic ventricular interaction in some patients during exercise.Methods and ResultsContrast stress echocardiography was performed in 30 HFpEF patients, 17 hypertensive controls, and 17 normotensive controls (healthy). Cardiac volumes, and normalized radius of curvature (NRC) of the interventricular septum at end‐diastole and end‐systole, were measured at rest and peak‐exercise, and compared between the groups. The septum was circular at rest in all 3 groups at end‐diastole. At peak‐exercise, end‐systolic NRC increased to 1.47±0.05 (P<0.001) in HFpEF patients, confirming development of pulmonary hypertension. End‐diastolic NRC also increased to 1.54±0.07 (P<0.001) in HFpEF patients, indicating septal flattening, and this correlated significantly with end‐systolic NRC (ρ=0.51, P=0.007). In hypertensive controls and healthy controls, peak‐exercise end‐systolic NRC increased, but this was significantly less than observed in HFpEF patients (HFpEF, P=0.02 versus hypertensive controls; P<0.001 versus healthy). There were also small, non‐significant increases in end‐diastolic NRC in both groups (hypertensive controls, +0.17±0.05, P=0.38; healthy, +0.06±0.03, P=0.93). In HFpEF patients, peak‐exercise end‐diastolic NRC also negatively correlated (r=−0.40, P<0.05) with the change in left ventricular end‐diastolic volume with exercise (ie, the Frank‐Starling mechanism), and a trend was noted towards a negative correlation with change in stroke volume (r=−0.36, P=0.08).ConclusionsExercise pulmonary hypertension causes substantial diastolic ventricular interaction on exercise in some patients with HFpEF, and this restriction to left ventricular filling by the right ventricle exacerbates the pre‐existing impaired Frank‐Starling response in these patients.

Patients With Obesity Exhibit a Plateau Pattern of the Right Ventricular Waveform.

BackgroundVentricular waveforms are characterized by a dip-and-plateau pattern during diastole owing to an abrupt termination of ventricular filling because of pericardial constraint under conditions such as constrictive pericarditis (CP). However, constrictive hemodynamics is not specifically caused by CP. Therefore, this study aimed to evaluate whether patients with obesity exhibited constrictive hemodynamics.MethodsOverall, 60 consecutive Japanese patients (mean age, 69.5 years; 45% women) who underwent right heart catheterization at the Japan Community Healthcare Organization Osaka Hospital from July 2016 to September 2018 were examined. Two-dimensional echocardiography was used to measure the epicardial adipose tissue (EAT) in the standard parasternal long-axis view during end-diastole. Because patients who underwent open-heart surgery were highly likely to have CP, they were excluded.ResultsAmong the 60 patients, 11 (18%) exhibited a plateau pattern of the right ventricular waveform and had a mean EAT value of 4.2 mm, which was significantly higher than that of patients without such a pattern (2.1 mm, P < 0.001). Similarly, the mean body mass index (BMI) values were significantly higher in patients with a plateau pattern than in those without it (27.2 vs. 21.8 kg/m2, P < 0.001). EAT was significantly correlated with the BMI (r = 0.72, P < 0.001). In patients with a plateau pattern, the triglyceride (TG) and low-density lipoprotein cholesterol (LDL-C) levels were significantly higher (TG: 150 vs. 100 mg/dL, LDL-C: 121 vs. 95 mg/dL, P < 0.05) and the left atrial diameter (52.8 vs. 44.7 mm, P < 0.01) and left atrial volume index (58.7 vs. 47.6 mL/m2, P < 0.05) were significantly greater than those in the patients without it. The EAT was also significantly correlated with the TG level (r = 0.37, P < 0.01).ConclusionsObese patients may present with constrictive hemodynamics, suggesting left ventricular diastolic dysfunction. EAT was significantly correlated with metabolic syndrome components, namely obesity and TG levels.

One-dimensional haemodynamic modeling and wave dynamics in the entire adult circulation.

One-dimensional (1D) modeling is a powerful tool for studying haemodynamics; however, a comprehensive 1D model representing the entire cardiovascular system is lacking. We present a model that accounts for wave propagation in anatomically realistic systemic (including coronary and cerebral) arterial/venous networks, pulmonary arterial/venous networks and portal veins. A lumped parameter (0D) heart model represents cardiac function via a time-varying elastance and source resistance, and accounts for mechanical interactions between heart chambers mediated via pericardial constraint, the atrioventricular septum and atrioventricular plane motion. A non-linear windkessel-like 0D model represents microvascular beds, while specialized 0D models are employed for the hepatic and coronary beds. Model-derived pressure and flow waveforms throughout the circulation are shown to reproduce the characteristic features of published human waveforms. Moreover, wave intensity profiles closely resemble available in vivo profiles. Forward and backward wave intensity is quantified and compared along major arteriovenous paths, providing insights into wave dynamics in all of the major physiological networks. Interactions between cardiac function/mechanics and vascular waves are investigated. The model will be an important resource for studying the mechanics underlying pressure/flow waveforms throughout the circulation, along with global interactions between the heart and vessels under normal and pathological conditions.

Acute cardiac remodeling in short term acute afterload increase - the effect of pericardial constraint

Aim: As acute short-lived increase in afterload may be a contributory mechanism to sudden death, we studied an acute 30% systolic pressure increase (SBPI) in a closed chest, closed pericardium porcine model, closed pericardium being essential to the model clinical applicability. Methods: 7 pigs were studied. All had an acute 5 beat 30% SBPI induced by a non-occlusive mid-descending aortic balloon inflation and release. Each challenge was continuously monitored for changes in cardiac morphology and function by cardiac ultrasound (2D, Doppler and Doppler Myocardial Imaging) and changes were correlated with pressure data from 3 Millar catheters (LV/Ao; LA; RV/RA). Continuous 12 lead ECG and intracardiac electrograms were also recorded. Results: Balloon inflation caused an acute diastolic pressure increase in all cavities (except pulmonary artery) with early diastolic preceding late changes and a corresponding systolic increase in LV, LA and RA pressures. Acute LV dilatation resulted in pericardial flattening (which is a visualization of the effects of pericardial constraint), a septal shift towards the RV and a decrease in RV size with a 30% reduction in LVEF % (Figure 1a). During inflation, pericardial excursion flattened >40% in basal, mid and apical LV segments, mostly mid wall (from 3.4 ±1.4 mm to 1.6 ±0.7 mm,

Acute cardiac remodeling in short term acute afterload increase – the effect of pericardial constraint

Aim: As acute short-lived increase in afterload may be a contributory mechanism to sudden death, we studied an acute 30% systolic pressure increase (SBPI) in a closed chest, closed pericardium porcine model, closed pericardium being essential to the model clinical applicability. Methods: 7 pigs were studied. All had an acute 5 beat 30% SBPI induced by a non-occlusive mid-descending aortic balloon inflation and release. Each challenge was continuously monitored for changes in cardiac morphology and function by cardiac ultrasound (2D, Doppler and Doppler Myocardial Imaging) and changes were correlated with pressure data from 3 Millar catheters (LV/Ao; LA; RV/RA). Continuous 12 lead ECG and intracardiac electrograms were also recorded. Results: Balloon inflation caused an acute diastolic pressure increase in all cavities (except pulmonary artery) with early diastolic preceding late changes and a corresponding systolic increase in LV, LA and RA pressures. Acute LV dilatation resulted in pericardial flattening (which is a visualization of the effects of pericardial constraint), a septal shift towards the RV and a decrease in RV size with a 30% reduction in LVEF % (Figure 1a). During inflation, pericardial excursion flattened >40% in basal, mid and apical LV segments, mostly mid wall (from 3.4 ±1.4 mm to 1.6 ±0.7 mm,

Index of biventricular interdependence calculated using cardiac MRI: a proof of concept study in patients with and without constrictive pericarditis

We sought to propose a magnetic resonance (MR) imaging-derived index of biventricular interdependence as a diagnostic parameter to distinguish patients with surgically-confirmed pericardial constriction from those without. Free-breathing real time MR pulse sequences of seventeen subjects with surgically proven constrictive pericarditis and thirty-five patients referred for clinically-indicated cardiac MR examinations but without documented constriction were analyzed using a novel index of biventricular interdependence. Cross-sectional biventricular areas at end diastole using the epicardial surface were traced at the mid left ventricular level at end-inspiration and end-expiration and an index of biventricular interdependence, defined as the ratio of (biventricular end-diastolic area at end-inspiration)/(biventricular end-diastolic area at end-expiration) was calculated for each subject. The mean index for both groups was calculated and results were statistically compared. The index of biventricular interdependence approximated unity (mean index 1.03 ± 0.03 SD) in patients with surgically confirmed pericardial constriction, indicating similar biventricular area at end-inspiration and end-expiration, and was significantly lower than in individuals without constrictive pericarditis (mean index 1.28 ± 0.10 SD; p < 0.0001). The MR-derived index of biventricular interdependence was significantly different between subjects with surgically-confirmed pericardial constriction and subjects where pericardial constraint was not suspected and may serve as a useful metric in the hemodynamic assessment of patients with a potential diagnosis of constrictive pericarditis.

The Relationship Between Left and Right Pericardial Pressures in Humans: An Intraoperative Study

Background The purpose of this study was to show the similarity between the pericardial constraint over the right and left ventricles of humans at various levels of central venous pressure (CVP) using flat Silastic balloons in the pericardial space during elective cardiac surgery. Methods Six subjects (aged 19-76 years) were instrumented with flat, liquid-containing Silastic balloons in the pericardial space during elective cardiac surgery. No subject had valvular disease or right ventricular (RV) hypertrophy. These balloons were positioned to lie over the RV and left ventricular (LV) free walls to measure RV and LV pericardial pressure (P prv and P plv, respectively). Volume loading was achieved by an intravenous infusion of 1 to 2 L of Ringer's lactate or normal saline. Depending on the patient's status during the operative procedure, the mean CVP was increased by 5-10 mm Hg from the baseline postinduction levels. RV and LV pericardial pressures were measured continuously throughout the volume loading. Results The pooled data from all subjects demonstrate that RV pericardial pressure is equal to LV pericardial pressure over central venous pressures ranging from 4 to 18 mm Hg and that the RV late-diastolic (pre–a-wave) cavitary pressure (P rv) correlates with LV pericardial pressure. Conclusions Changes in LV pericardial pressure are approximately equal to changes in RV pericardial pressure and RV late-diastolic (pre–a-wave) cavitary pressure is a good predictor of LV pericardial pressure.

Effects of pericardial constraint and ventricular interaction on left ventricular hemodynamics in the unloaded heart

Pericardial constraint and ventricular interaction influence left ventricular (LV) performance when preload is high. However, it is unclear if these constraining forces modulate LV filling when the heart is unloaded, such as during upright posture, in humans. Fifty healthy individuals underwent right heart catheterization to measure pulmonary capillary wedge (PCWP) and right atrial pressure (RAP). To evaluate the effects of pericardial constraint on hemodynamics, transmural filling pressure (LVTMP) was defined as PCWP-RAP. Beat-to-beat blood pressure (BP) waveforms were recorded, and stroke volume (SV) was derived from the Modelflow method. After measurements at -30 mmHg lower body negative pressure (LBNP), which approximates the upright position, LBNP was released, and beat-to-beat measurements were performed for 15 heartbeats. At -30 mmHg LBNP, RAP and PCWP were significantly decreased. During the first six beats of LBNP release, heart rate (HR) was unchanged, while BP increased from the fourth beat. RAP increased faster than PCWP resulting in an acute decrease in LVTMP from the fourth beat. A corresponding drop in SV by 3% was observed with no change in pulse pressure. From the 7th to 15th beats, LVTMP and SV increased steadily, followed by a decreased HR due to the baroreflex. A decreased TMP, but not PCWP, caused a transient drop in SV with no changes in HR or pulse pressure during LBNP release. These results suggest that the pericardium constrains LV filling during LBNP release, enough to cause a small but significant drop of SV, even at low cardiac filling pressure in healthy humans.

Effects of Pericardial Constraint on Left Ventricular Hemodynamics During Release of Lower Body Negative Pressure in Healthy Humans

Effects of Pericardial Constraint on Left Ventricular Hemodynamics During Release of Lower Body Negative Pressure in Healthy Humans

The Relationship of Right- and Left-Sided Filling Pressures in Patients With Heart Failure and a Preserved Ejection Fraction

Although right-sided filling pressures often mirror left-sided filling pressures in systolic heart failure, it is not known whether a similar relationship exists in heart failure with preserved ejection fraction. Eleven subjects with heart failure with preserved ejection fraction underwent right heart catheterization at rest and under loading conditions manipulated by lower body negative pressure and saline infusion. Right atrial pressure (RAP) was classified as elevated when >or=10 mm Hg and pulmonary capillary wedge pressure (PCWP) when >or=22 mm Hg. If both the RAP and the PCWP were elevated or both not elevated, they were classified as concordant; otherwise, they were classified as discordant. Correlation of RAP and PCWP was determined by a repeated measures model. Among 66 paired measurements of RAP and PCWP, 44 (67%) had a low RAP and PCWP and 8 (12%) a high RAP and PCWP, yielding a concordance rate of 79%. In a sensitivity analysis performed by varying the definition of elevated RAP (from 8 to 12 mm Hg) and PCWP (from 15 to 25 mm Hg), the mean+/-SD concordance of RAP and PCWP was 76+/-10%. The correlation coefficient of RAP and PCWP for the overall cohort was r=0.86 (P<0.0001). Right-sided filling pressures often reflect left-sided filling pressures in heart failure with preserved ejection fraction, supporting the role of estimation of jugular venous pressure to assess volume status in this condition.

Using a human cardiovascular-respiratory model to characterize cardiac tamponade and pulsus paradoxus

BackgroundCardiac tamponade is a condition whereby fluid accumulation in the pericardial sac surrounding the heart causes elevation and equilibration of pericardial and cardiac chamber pressures, reduced cardiac output, changes in hemodynamics, partial chamber collapse, pulsus paradoxus, and arterio-venous acid-base disparity. Our large-scale model of the human cardiovascular-respiratory system (H-CRS) is employed to study mechanisms underlying cardiac tamponade and pulsus paradoxus. The model integrates hemodynamics, whole-body gas exchange, and autonomic nervous system control to simulate pressure, volume, and blood flow.MethodsWe integrate a new pericardial model into our previously developed H-CRS model based on a fit to patient pressure data. Virtual experiments are designed to simulate pericardial effusion and study mechanisms of pulsus paradoxus, focusing particularly on the role of the interventricular septum. Model differential equations programmed in C are solved using a 5th-order Runge-Kutta numerical integration scheme. MATLAB is employed for waveform analysis.ResultsThe H-CRS model simulates hemodynamic and respiratory changes associated with tamponade clinically. Our model predicts effects of effusion-generated pericardial constraint on chamber and septal mechanics, such as altered right atrial filling, delayed leftward septal motion, and prolonged left ventricular pre-ejection period, causing atrioventricular interaction and ventricular desynchronization. We demonstrate pericardial constraint to markedly accentuate normal ventricular interactions associated with respiratory effort, which we show to be the distinct mechanisms of pulsus paradoxus, namely, series and parallel ventricular interaction. Series ventricular interaction represents respiratory variation in right ventricular stroke volume carried over to the left ventricle via the pulmonary vasculature, whereas parallel interaction (via the septum and pericardium) is a result of competition for fixed filling space. We find that simulating active septal contraction is important in modeling ventricular interaction. The model predicts increased arterio-venous CO2 due to hypoperfusion, and we explore implications of respiratory pattern in tamponade.ConclusionOur modeling study of cardiac tamponade dissects the roles played by septal motion, atrioventricular and right-left ventricular interactions, pulmonary blood pooling, and the depth of respiration. The study fully describes the physiological basis of pulsus paradoxus. Our detailed analysis provides biophysically-based insights helpful for future experimental and clinical study of cardiac tamponade and related pericardial diseases.

Cardiovascular magnetic resonance in pericardial diseases.

The pericardium and pericardial diseases in particular have received, in contrast to other topics in the field of cardiology, relatively limited interest. Today, despite improved knowledge of pathophysiology of pericardial diseases and the availability of a wide spectrum of diagnostic tools, the diagnostic challenge remains. Not only the clinical presentation may be atypical, mimicking other cardiac, pulmonary or pleural diseases; in developed countries a shift for instance in the epidemiology of constrictive pericarditis has been noted. Accurate decision making is crucial taking into account the significant morbidity and mortality caused by complicated pericardial diseases, and the potential benefit of therapeutic interventions. Imaging herein has an important role, and cardiovascular magnetic resonance (CMR) is definitely one of the most versatile modalities to study the pericardium. It fuses excellent anatomic detail and tissue characterization with accurate evaluation of cardiac function and assessment of the haemodynamic consequences of pericardial constraint on cardiac filling. This review focuses on the current state of knowledge how CMR can be used to study the most common pericardial diseases.

A further analysis of why pulmonary venous pressure rises after the onset of LV dysfunction

Based on a dynamic computational model of the circulation, Burkhoff and Tyberg (Am J Physiol Heart Circ Physiol 265: H1819-H1828, 1993) concluded that the rise in pulmonary venous pressure (Pvp) with left ventricular (LV) dysfunction requires a decrease in vascular capacitance and transfer of unstressed volume to stressed volume (nu). We argue that the values they used for venous resistance (Rvs), venous compliance (Cvs), and nu were too low, and changing these values significantly changes the conclusion. We used a computational model of the circulation that was similar to theirs, but we made Rvs four times higher (0.06 versus 0.015 mmHg.s.ml(-1)), Cvs larger (110 versus 70 ml/mmHg), and nu larger (1,400 versus 750 ml); all other parameters, including those for the heart, were essentially the same. We simulated left ventricular dysfunction by decreasing end-systolic elastance (Eeslv) as they did and examined changes in cardiac output, arterial blood pressure, and Pvp. We then examined the effect of changes in Rvs, heart rate, and nu when Eeslv was depressed with and without pericardial constraint. In contrast to their findings, with our parameters the model predicts that decreasing Eeslv substantially increases Pvp. Furthermore, increasing systemic vascular resistance or decreasing Rvs or heart rate produces large increases in Pvp when Eeslv is reduced. Pericardial constraint limits the changes in Pvp. In conclusion, when Rvs and Cvs are increased, baseline nu must be higher to maintain normal cardiac output. This increased volume can shift between compartments under flow conditions and account for the increase in Pvp with decreased left ventricular function even without recruitment of unstressed volume.

Right Ventricular Function in Cardiovascular Disease, Part II

Right ventricular (RV) function may be impaired in pulmonary hypertension (PH), congenital heart disease (CHD), and coronary artery disease and in patients with left-sided heart failure (HF) or valvular heart disease. In recent years, many studies have demonstrated the prognostic value of RV function in cardiovascular disease. In the past, however, the importance of RV function has been underestimated. This perception originated from studies on open-pericardium dog models and from the observation that patients may survive without a functional subpulmonary RV (Fontan procedure). In the 1940s, studies using open-pericardium dog models showed that cauterization of the RV lateral wall did not result in a decrease in cardiac output or an increase in systemic venous pressure.1–3 As was later demonstrated, the open-pericardium model did not take into account the complex nature of ventricular interaction. In 1982, Goldstein and colleagues2 showed that RV myocardial infarction (RVMI) in a closed-chest dog model led to significant hemodynamic compromise. These findings were further supported by clinical studies demonstrating an increased risk of death, arrhythmia, and shock in patients with RVMI.4 The study of the RV is a relatively young field. In 2006, the National Heart, Lung, and Blood Institute identified RV physiology as a priority in cardiovascular research.5 The goal of this review is to present a clinical perspective on RV physiology and pathobiology. In the first article of the series, the anatomy, physiology, embryology, and assessment of the RV were discussed. In this second part, we discuss the pathophysiology, clinical importance, and management of RV failure. RV failure is a complex clinical syndrome that can result from any structural or functional cardiovascular disorder that impairs the ability of the RV to fill or to eject blood. The cardinal clinical manifestations of RV failure are (1) fluid retention, which may lead …

Disparate Patterns of Left Ventricular Mechanics Differentiate Constrictive Pericarditis From Restrictive Cardiomyopathy

The purpose of this study was to compare the longitudinal, circumferential, and radial mechanics of the left ventricle (LV) in patients with constrictive pericarditis (CP) and restrictive cardiomyopathy (RCM). Diastolic dysfunction in CP is related to epicardial tethering and pericardial constraint, whereas in RCM it is predominantly characterized by subendocardial dysfunction. Assessment of variations in longitudinal and circumferential deformation of LV might be useful to distinguish these 2 conditions. Longitudinal, radial, and circumferential mechanics of the LV were quantified by 2-dimensional speckle tracking of B-mode cardiac ultrasound images in 26 patients with CP, 19 patients with RCM, and 21 control subjects. In comparison with control subjects, patients with CP had significantly reduced circumferential strain (base; -16 +/- 6% vs. -9 +/- 6%; p < 0.016), torsion (3 +/- 1 degrees /cm vs. 1 +/- 1 degrees /cm; p < 0.016), and early diastolic apical untwisting velocities (E(r); 116 +/- 62 degrees /s vs. -36 +/- 50 degrees /s; p < 0.016), whereas longitudinal strains, displacement, and early diastolic velocities at the LV base (E(m)) were similar to control subjects. In contrast, patients with RCM showed significantly reduced longitudinal displacement (base; 14.7 +/- 2.5 cm vs. 9.8 +/- 2.8 cm; p < 0.016) and E(m) (-8.7 +/- 1.3 cm/s vs. -4.4 +/- 1.1 cm/s; p < 0.016), whereas circumferential strain and E(r) were similar to those of control subjects. For differentiation of CP from RCM, the area under the curve was significantly higher for E(m) in comparison with E(r) (0.97 vs. 0.76, respectively; p = 0.01). After pericardiectomy, there was a significant decrease in longitudinal early diastolic LV basal myocardial velocities (7.4 cm/s vs. 6.8 cm/s; p = 0.023). Circumferential strain, torsion, and E(r), however, remained unchanged. Deformation of the LV is constrained in the circumferential direction in CP and in the longitudinal direction in RCM. Subsequent early diastolic recoil of LV is also attenuated in each of the 2 directions, respectively, uniquely differentiating the abnormal diastolic restoration mechanics of the LV seen in CP and RCM.