Chronic Volume Overload Research Articles

Regional heterogeneity of mural mechanics in left ventricular hypertrophy from chronic volume overload

Regional heterogeneity of mural mechanics in left ventricular hypertrophy from chronic volume overload

Effect of Right Ventricular Volume Overload on Left Ventricular Diastolic Function in Patients With Atrial Septal Defect

This study was undertaken to investigate the effect of chronic right ventricular (RV) volume overload on left ventricular (LV) diastolic function. Twelve patients with atrial septal defect and 7 age-matched normal controls were examined. Patients with atrial septal defect were divided into 2 groups based on their Qp/Qs values (ASD1:Qp/Qs < or = 3, n = 7; ASD2:Qp/Qs > 3, n = 5). The LV volume curve and its first derivative were derived by a frame-by-frame analysis of the left ventriculogram. The peak filling rate was defined by the peak positive first derivative of the LV volume curve. We measured the time constant, isovolumetric relaxation time, stiffness constant and compliance at LV end-diastole. The time constant was significantly prolonged in the ASD2 group compared with the controls, and the isovolumetric relaxation time in both atrial septal defect groups was also prolonged compared with the controls. The peak filling rate, which was normalized by end-diastolic volume, was lower in the ASD2 group than in the controls. Although the stiffness constant and the compliance at LV end-diastole in the controls were not significantly different from those in the atrial septal defect group, an upward and leftward displacement of the left ventricular pressure-volume curve was observed in patients with atrial septal defect. Moreover, a significant correlation (r = 0.78, p < 0.01) was observed between the time constant and RV end-diastolic pressure. Thus, these results suggest that chronic RV volume overload affects left ventricular diastolic function.

Bidirectional cavopulmonary shunt in patients with multiple risk factors

Twenty-five patients in whom a modified Fontan operation was deferred because of multiple risk factors underwent a bidirectional cavopulmonary shunt. Two or more of the following risk factors were present in all: age less than 1 year, severe pulmonary artery distortion, impaired left ventricular function, subaortic obstruction, anomalous systemic-pulmonary venous connection, atrioventricular valve incompetence, and increased mean pulmonary artery pressure. Additional procedures included take-down of systemic-pulmonary artery shunt, atrial septectomy, pulmonary artery reconstruction, bulboventricular foramen enlargement, and atrioventricular valve repair. There were three hospital deaths (12%). Mean follow-up is 21 months. There was no late mortality. Mean oxygen saturation increased from 71% to 83%. Results obtained from pulmonary artery reconstruction, enlargement of bulboventricular foramen, and atrioventricular valve repair were satisfactory for the patients in whom these risk factors were present preoperatively. Ventricular function also improved in the survivors in whom it was previously deteriorated, this being related to the suppression of the sources of ventricular volume overload. In this risk group of patients for a modified Fontan operation, a bidirectional cavopulmonary shunt provided adequate palliation at reasonable low risk. Early bidirectional cavopulmonary shunt would minimize complications originating from systemic-pulmonary shunts such as pulmonary artery distortion and the potential harm of chronic ventricular volume overload.

Increased ACE and chymase-like activity in cardiac tissue of dogs with chronic mitral regurgitation.

The current study was designed to test the hypothesis that intracardiac angiotensin-converting enzyme (ACE) activity, chymase-like activity, and angiotensin (ANG) peptide levels are increased and are positively related to wall stress estimates in response to the chronic low pressure volume overload of mitral regurgitation produced by percutaneous chordal rupture in the dog. Chronic mitral regurgitation (MR) resulted in an increase in left ventricular (LV) end-diastolic volume [59 +/- 11 (SD) to 103 +/- 32 ml, P < 0.001], LV mass (96 +/- 17 to 114 +/- 23 g, P < 0.001), and a decrease in the LV mass-to-end-diastolic volume ratio (1.64 +/- 0.22 to 1.16 +/- 0.23 g/ml, P < 0.001) measured by magnetic resonance imaging. In vitro studies of heart tissue extracts demonstrated that the majority of ANG II-forming activity was from chymase-like activity rather than from ACE activity in five normal (83.5 +/- 7.5 vs. 6.04 +/- 5.2%) and seven MR hearts (86 +/- 3.9 vs. 2.6 +/- 1.7%). ACE activity (1.22 +/- 0.22 vs. 3.55 +/- 0.62 mU/g, P < 0.05) and chymase-like activity (9.42 +/- 4.64 vs. 20.60 +/- 8.41 nmol.g-1.min-1, P < 0.05) were increased in MR compared with normal hearts. ACE activity correlated with the LV mass-to-volume ratio (r = -0.93, P < 0.001) and LV diastolic wall stress ( r = 0.71, P < 0.05); however, chymase-like activity did not correlate with any hemodynamic parameter. ANG II levels were significantly higher in the midwall of the left ventricle in MR hearts than in normal controls (85 +/- 39 vs. 27 +/- 16 pg/g, P < 0.01). Our results demonstrate a positive correlation between LV diastolic wall stress and increased ACE activity with increased ANG II stores, suggesting that mechanical wall stress activated intracardiac ACE. Although chymase accounted for most ANG II formation in vitro in extracts of both normal and MR dog hearts, the significance of this enzyme in vivo remains unclear.

Regulation of blood volume—implications for cardiovascular pathophysiology in sleep apnoea

Volume homeostasis plays an important role in the regulation of the cardiovascular system and maintenance of haemodynamics. The heart-kidney axis represents the central part of the volume regulating system: the heart senses changes in the volume status and influences renal function via neural and humoral pathways in order to compensate for disturbances in volume homeostasis and prevent under- or overfilling of the heart. An undisturbed circadian rhythmicity of volume homeostasis, renal function and secretory pattern of volume regulating hormones may be of physiological importance. Disturbances in volume regulation are involved in the pathogenesis of cardiovascular diseases, e.g. arterial hypertension and heart failure. Nocturia in sleep apnoea (suggesting heart failure) may be explained by changes in volume-regulating hormones indicating hypervolaemia of the central part of the cardiovascular system ('central hypervolaemia') caused by exaggerated venous return during repetitive Müller manoeuvres. Treatment of sleep apnoea abolishes nocturia and restores normal circadian rhythm of volume homeostasis and secretion of volume-regulating hormones. Chronic cardiac volume overload during sleep may be implicated in the pathogenesis of cardiovascular sequelae in sleep apnoea: cardiac hypertrophy and heart failure. Central hypervolaemia during sleep can cause long-term disturbances in blood pressure control by different mechanisms and may be in part responsible for the development of daytime hypertension in sleep apnoea. In summary, volume homeostasis is controlled by a complex interaction of heart and kidney. Disturbances may reflect cardiovascular diseases or may even be the cause. In sleep apnoea disturbances in volume regulation may be important for the development of cardiovascular sequelae.

794–4 Compensated Pulmonic Insufficiency: Is the Right Ventricular Response to Exercise Normal?

Chronic right ventricular (RV) volume overload due to pulmonic insufficiency (PI) can unpredictably lead to irreversible RV failure. We sought to assess the effect of chronic volume overload on RV exercise response. 10 patients (2 male, 8 female, mean age 24 yrs) with compensated moderate to severe PI due to surgically corrected Tetralogy of Fallot or pulmonic stenosis and 7 controls (4 male, 3 female, mean age 29 yrs) were studied on a symptom limited stationary cycle progressive ramp protocol with measurement of VO 2 and respiratory quotient. Stress echocardiography was performed at rest and during exercise (mid = RQ 0.85, 100% = peak). RV function was described as end diastolic RV area (RVEDA), end diastolic RV/LV area ratio (RV/LV) and percent systolic RV area change (%RVAΔ), the latter a reflection of RV ejection fraction. patients (P) controls (c) rest mid 100% rest mid 100% RVEDA * 28.5 26.4 24.7 19.2 16.1 13.8 RV/LV ** 0.98 0.95 0.97 0.56 0.53 0.49 %RVAΔ † 0.37 0.36 0.34 0.34 0.41 0.43 By ANOVA P vs C * P &lt; 0.005 ** p &lt; 0001 Although there was no significant difference in percent systolic RV area change at rest, in patients RV systolic function declined during exercise as compared with an increase in controls, †p &lt; 0.001. Cardiac index, HR, and BP did not significantly differ between patients and controls. VO 2 max was reduced in patients with PI (23.0 vs 38.8 ml/kg/min, p &lt; 0.001), but was not predicted by any resting echocardiographic variable. However, in controls larger RVEDA was associated with a greater exercise capacity. The change in RV systolic performance during exercise was associated with resting RVEDA, RV/LV and %RVAΔ, p &lt; 0.005. Patients with compensated significant PI have an abnormal RV response to exercise demonstrable by stress echocardiography. This may have implications for the timing of pulmonic valve replacement.

The renin-angiotensin system and volume overload-induced changes in cardiac collagen and elastin.

Besides cardiac load, the renin-angiotensin system (RAS) and aldosterone may regulate collagen accumulation during maturation or hypertrophic growth. The effect of cardiac volume overload on both left ventricular (LV) and right ventricular (RV) collagen and elastin and the possible role of the RAS in such changes have not yet been assessed. In the present study we assessed (1) the effects of 4 to 10 weeks of volume overload by an aortocaval shunt or minoxidil on LV and RV collagen and elastin and (2) the potential of the angiotensin-converting enzyme inhibitor enalapril and the angiotensin II receptor blocker losartan to prevent and regress volume overload-induced changes in cardiac collagen and elastin. Cardiac volume overload by aortocaval shunt or minoxidil treatment decreased LV collagen accumulation as compared with control rats. In contrast, RV collagen accumulation was potentiated during the initial weeks but not during chronic aortocaval shunt. Enalapril and losartan prevented the relative decreases in LV collagen content and concentration induced by a shunt. Losartan also reversed the decrease in LV collagen content by aortocaval shunt. Neither blocker significantly affected the enhanced RV collagen accumulation during the initial weeks of shunt, but both blockers further potentiated RV collagen accumulation during chronic volume overload. Aortocaval shunt for 4 weeks but not 10 weeks enhanced LV and RV elastin accumulation. This initial increase in LV and RV elastin content was blocked by both enalapril and losartan. Cardiac volume overload, even when accompanied by increased plasma renin activity, decreases LV collagen accumulation, suggesting that in contrast to the stimulatory effect of systolic wall stress, increased diastolic wall stress inhibits collagen accumulation. In support of this concept, enalapril and losartan decreased LV preload and maintained LV collagen accumulation. In contrast to LV collagen, RV collagen accumulation was potentiated during the initial weeks of volume overload, possibly related to acute RV pressure overload shortly after aortocaval shunt and its decrease with chronic shunt. Enalapril and losartan had minimal effect on the enhanced RV collagen during the initial weeks of aortocaval shunt but potentiated RV collagen during chronic shunt, possibly by decreasing RV diastolic pressures. Altogether, these data suggest that during cardiac volume overload, the RAS affects cardiac collagen primarily by its hemodynamic effects. The RAS, however, may potentiate RV and LV elastin accumulation during the initial weeks of volume overload since both enalapril and losartan block this increase.

Chronic Volume Overload

Chronic Volume Overload Get access European Heart Journal, Volume 15, Issue suppl_4, September 1990, Pages 466–467, https://doi.org/10.1093/eurheartj/15.suppl_4.466 Published: 12 September 1994

14 Changes in beta-adrenergic receptors during left ventricular hypertrophy caused by chronic pressure or volume overload

14 Changes in beta-adrenergic receptors during left ventricular hypertrophy caused by chronic pressure or volume overload

Anesthesia for noncardiac surgery in infants with hypoplastic left heart syndrome following hemi-fontan operation

S TAGE I PALLIATION (Norwood operation) for neonates with hypoplastic left heart syndrome (HLHS) enables survival to allow these children to ultimately be managed in the same fashion as other patients with univentricular cardiac malformations.’ This operation consists of (1) atria1 septectomy, (2) creation of a “neoaorta” that associates the proximal main pulmonary artery with the aortic arch providing unobstructed blood flow from the right ventricle to the systemic circulation, and (3) placement of a systemic to pulmonary artery shunt. On completion of stage I, both the pulmonary and systemic circulations continue to be supplied from the single ventricle in a parallel fashion. This physiology will ultimately result in morbidity due to chronic ventricular volume overload and to chronic hypoxemia. The ultimate goals are to eliminate the excess volume work and to achieve a systemic arterial oxygen saturation that enables normal growth and development without inducing polycythemia. The Fontan procedure satisfies these objectives by creating a series circulation that requires the singleventricle to pump fully saturated blood only to the systemic circulation as the systemic venous return passes directly through the pulmonary vascular bed.2 When Fontan’s operation was undertaken 12 to 18 months after stage I, a high operative mortality (16% to 40%) occurred.3-5 In many, death was attributed to an abrupt change in ventricular geometry when the volume load imposed on the ventricle returned to normal. Echocardiograms obtained postoperatively when compared with the preoperative study showed a small, thick-walled ventricular cavity with a low diastolic volume. Although systolic shortening appeared normal the ventricular compliance was diminished. The anatomic and physiologic consequences of this sudden reduction in the ventricular volume load are diminishing end-diastolic volume with an apparent increase in wall thickness because the muscle mass does not change as rapidly, and impaired diastolic function of the ventricle leading to increased end-diastolic pressure. The resulting increase in pulmonary venous pressure impedes pulmonary blood flow thereby decreasing systemic output. Retrospective analysis of the data available preoperatively proved insufficient to predict those children who would develop a physiologically important reduction of ventricular compliance associated with rapid contraction of cnddiastolic volume following Fontan’s operation.

Measurement of left ventricular volume in normal and volume-overloaded canine hearts

Serial studies of adaptation to aortic regurgitation (AR) were undertaken to determine whether sonomicrometry and echocardiography could be combined to measure changes in left ventricular (LV) cavitary volume (Vlv) and wall mass using the geometric formula [Vlv = K pi b2 alpha--wall volume], where K is a constant depending on the geometric model and a and be are epicardial major- and minor-axis diameters, respectively. Postmortem studies were performed in six normal dogs and in nine with AR; ultrasonic ventricular dimensions were measured as Vlv was varied with an intracavitary balloon. Three models were tested: 1) ellipsoid (model I; K = 1/6), 2) cylinder-ellipsoid (model II; K = 5/24), and 3) cylinder (model III; K = 1/4). The slope of the relationship between calculated Vlv and balloon volume varied between models (I, 0.71 +/- 0.11; II, 0.89 +/- 0.14; III, 1.07 +/- 0.17), and empiric determination of K to produce a slope of 1.0 resulted in a value of 0.26 +/- 0.04, not significantly different from the cylindrical model. Serial measurements of LV dimensions in 10 chronically instrumented conscious dogs revealed no significant change in end-diastolic or end-ejection LV shape after up to 16 wk of AR. Sonomicrometry and echocardiography can be integrated using a cylindrical geometric model to accurately estimate changes in end-diastolic or end-ejection Vlv during chronic volume overload.

Left ventricular remodeling in chronic aortic regurgitation.

Left ventricular (LV) shape in chronic volume overload due to aortic regurgitation is commonly described as rounder than in normal subjects. This statement derives from observations of qualitative nature or based on the measure of eccentricity index. We analyzed LV shape and function in 16 normal subjects (N) and in 24 patients with chronic pure aortic regurgitation (AR), without coronary artery disease or associated mitral regurgitation. LV cavity geometry was quantitatively evaluated from end-diastolic and end-systolic outlines obtained in 30 degrees RAO angiographic projection, by calculating: 1. the eccentricity and circularity indexes, 2. the regional curvature at 90 equidistant points using a windowed Fourier series approximation of contours, in which the number of harmonics and filter-window were locally chosen in order to minimize the reconstruction errors and to maximize the smoothness of the curve, 3. by measuring the length of the anterior and posterior hemi-perimeter of LV outlines and 4. by performing a Fourier analysis of LV contours. Neither eccentricity nor circularity indexes were adequate to differentiate shape abnormalities, whereas Fourier geometric analysis indicated abnormalities of shape in AR. Regional curvature showed that diastolic outline of AR had a greater curvature of the anterobasal, anterolateral and inferoapical regions and a lower curvature of the anteroapical one. Systolic outline showed a greater curvature of the inferoapical region and a lower curvature of the anteroapical one.(ABSTRACT TRUNCATED AT 250 WORDS)

Changes in diastolic function during development and correction of chronic LV volume overload produced by mitral regurgitation.

Mitral regurgitation (MR) causes an augmentation in left ventricular (LV) diastolic function, increasing early diastolic filling rate and decreasing LV stiffness. Whether these changes in diastolic function persist, return to normal, or become abnormal after mitral valve replacement (MVR) is unknown. Simultaneous LV echocardiography and catheterization studies were performed in six dogs in the baseline state (baseline), 3 months after creation of MR (chronic MR), and 3 months after MVR. Chronic MR caused LV dilation (end-diastolic dimension increased from 4.5 +/- 0.1 cm in baseline to 5.8 +/- 0.1 cm in chronic MR, p < 0.05) and eccentric LV hypertrophy (LV-to-body weight ratio increased from 3.6 +/- 0.2 g/kg in baseline to 4.9 +/- 0.4 g/kg in chronic MR, p < 0.05). Chronic MR caused an increase in LV early diastolic filling rate (peak rate of increase in minor-axis dimension increased from 11 +/- 1 cm/sec in baseline to 18 +/- 1 cm/sec in chronic MR, p < 0.05), did not change the time constant of myocardial relaxation (tau was 31 +/- 4 msec in baseline and 30 +/- 2 msec in chronic MR), and caused a decrease in the modulus of regional chamber stiffness from 7.7 +/- 1.2 in baseline to 2.4 +/- 0.03 in chronic MR, p < 0.05. MVR caused the resolution of LV dilation (end-diastolic dimension returned to normal [4.8 +/- 0.2 cm]), but three months after MVR, regression of LV hypertrophy was incomplete (LV-to-body weight ratio remained elevated [4.4 +/- 0.5 g/kg]). After MVR, LV early diastolic filling rate (8 +/- 1 cm/sec), the relaxation time constant (31 +/- 2 msec), chamber stiffness (7.1 +/- 1.8), myocardial stiffness (11.2 +/- 3.1), and LV end-diastolic pressure (8 +/- 1 mm Hg) returned to normal. The enhanced diastolic function seen in chronic MR returned to normal after correction of the chronic volume overload by MVR.

Suppression of protein degradation in progressive cardiac hypertrophy of chronic aortic regurgitation.

The heart adapts to the volume overload of aortic regurgitation with dilation and hypertrophy. The development of left ventricular hypertrophy at the protein level is a dynamic process resulting from an imbalance between cardiac protein synthesis and degradation. The objective of the present study was to determine in vivo the relative contributions of cardiac protein synthesis and degradation to the progressive hypertrophy that occurs in response to chronic aortic regurgitation and to compare these with responses earlier in the course of this stress. Continuous intravenous infusions of [3H]-leucine were administered 3 days and 1 month after surgical induction of aortic regurgitation and sham operation in rabbits. Total cardiac protein and myosin heavy chain fractional synthesis rates were obtained by analysis of plasma and protein hydrolysate data using [14C]-dansyl chloride assays. Left ventricular growth rates were determined from serial echocardiographic and postmortem left ventricular weight and protein concentration measurements; protein degradation rates were determined by subtraction of growth rates from synthesis rates. In comparison with sham-operated control rabbits, protein fractional synthesis rates were increased at 3 days but not at 1 month after induction of aortic regurgitation Progressive cardiac hypertrophy occurring at 1 month was caused by a decrease in protein fractional degradation rates. An increase in protein synthesis contributes only to the early phase of hypertrophy caused by acute aortic regurgitation, whereas progressive eccentric hypertrophy in chronic volume overload is due to suppression of protein degradation.

Myofibrillar Protein Turnover in Cardiac Hypertrophy due to Aortic Regurgitation

We recently demonstrated that total cardiac protein and myosin heavy chain fractional synthesis rates were not increased during the progressive cardiac hypertrophy that occurred 1 month following induction of aortic regurgitation. The increase in total cardiac protein and myosin heavy chain observed after 1 month of chronic volume overload was caused by a decrease in protein fractional degradation rates. The objective of the present study was to determine in vivo the relative contributions of protein synthesis and degradation of a variety of individual myofibrillar protein constituents, other than myosin heavy chain, to the left ventricular hypertrophic response to chronic aortic regurgitation. Intravenous infusions of [3H]-leucine were administered 3 days and 1 month following surgical induction of aortic regurgitation and sham operation in rabbits, and actin, myosin light chains 1 and 2, alpha-actinin and desmin fractional synthesis rates were obtained by analysis of plasma and protein hydrolysate data using [14C]-dansyl chloride assays. Individual myofibrillar protein growth rates were determined from protein concentration and serial echocardiographic and postmortem left ventricular weight measurements; protein degradation rates were determined by subtraction of growth rates from synthesis rates. Individual myofibrillar protein content increased most rapidly during the 1st week and progressively increased at a slower rate between 1 week and 1 month, in parallel with increases in left ventricular weight. In comparison with sham-operated controls, individual myofibrillar protein fractional synthesis rates were consistently increased at 3 days but not at 1 month. Progressive myocyte hypertrophy occurring at 1 month was caused by a decrease in myofibrillar protein fractional degradation rates. Increased myofibrillar protein synthesis contributed only to the early phase of myocyte hypertrophy while progressive hypertrophy in chronic aortic regurgitation was due to suppression of myofibrillar protein degradation.

Effect of mitral valve repair for mitral valve prolapse on regression of left ventricular mass

Mitral regurgitation (MR) represents a condition of chronic volume overload in which the left ventricle develops eccentric hypertrophy to accommodate a significantly increased end-diastolic left ventricular (LV) volume without significant increases in filling pressures or diastolic sarcomere length. 1,2 LV mass is significantly greater in patients with MR than in normal subjects. 2 In patients with chronic MR and moderate LV dilatation, there is regression of LV hypertrophy when the mitral valve is replaced. 1 Interpretation of changes in LV volumes and mass after valve replacement may be confounded by alterations in wall stress specifically related to disruption of the mitral apparatus and because all prosthetic valves are at least minimally obstructive. Compared with replacement, mitral valve repair may result in better preservation of LV function by retaining the tethering effect of the chordal apparatus and moderating the increase in systolic wall stress that occurs after relief of MR. 3,4 The present quantitative echocardiographic investigation examines the effect of mitral valve repair on LV mass and volume in patients with severe, isolated MR.

Decreased levels of oxygen free radical scavengers in chronic volume overload heart failure

Decreased levels of oxygen free radical scavengers in chronic volume overload heart failure

Fatty acid oxidation and mechanical performance of volume-overloaded rat hearts

Chronic volume overload was induced in 2-mo-old rats by surgical opening of the aortocaval fistula. Rats were killed 3 mo later and their hearts were atrially perfused. During the perfusions with 1.2 mM palmitate, mechanical performance of volume-overloaded hearts was significantly decreased both under conditions of a moderate work load and, mainly, after the clamp of the aortic outflow line. Respective O2 consumption rates as well as the rates of 14CO2 production from [U-14C]palmitate were decreased to the same extent. When 2.4 mM octanoate was used as the exogenous substrate, both the O2 consumption rates and the rates of CO2 production of volume-overloaded hearts became comparable to those of control hearts perfused with same substrate. Mechanical activity of volume-overloaded hearts returned to control values and remained stable during the entire perfusion period tested. Total tissue L-carnitine was decreased by approximately 30% in volume-overloaded hearts, which may suggest that palmitate oxidation has been limited at the level of carnitine-acylcarnitine translocase. However, our polarographic studies of the respiratory activity of isolated mitochondria indicated that the palmitoylcarnitine translocation proceeds normally. On the other hand, state 3 respiration of the mitochondria from volume-overloaded hearts supplemented with either palmitate or palmitate and L-carnitine was significantly lower than that of control ones. This may suggest that an alteration of the enzymes involved in long-chain fatty acid activation and/or long-chain fatty acyl transfer to L-carnitine has developed under conditions of chronic mechanical overloading of the heart.

Pericardial adaptation in severe chronic pulmonary hypertension. An intraoperative transesophageal echocardiographic study.

The pericardium both limits cardiac distension and accentuates ventricular interdependence. Although this effect appears minimal under normal circumstances, the pericardium markedly restricts acute cardiac enlargement. Animal studies have demonstrated gradual pericardial adaptation and expansion in chronic volume overload and cardiomegaly, but the pericardial response in humans with cardiac hypertrophy and enlargement has not been examined fully. To investigate this further, 14 patients with right ventricular hypertrophy and cardiomegaly secondary to chronic pulmonary thromboembolic disease and severe pulmonary hypertension were studied during pulmonary thromboendarterectomy. Simultaneous intraoperative transesophageal Doppler echocardiography and direct biventricular hemodynamic measurements were performed at steady state immediately before and after pericardiotomy. All hemodynamic variables showed no significant change before and after pericardiotomy, including heart rate (76 +/- 16 versus 75 +/- 15 beats per minute), mean pulmonary arterial pressure (46.3 +/- 11.1 versus 45.5 +/- 11.7 mm Hg), cardiac index (1.8 +/- 0.5 versus 2.0 +/- 0.6 l/min/m2), left ventricular end-diastolic pressure (5.9 +/- 5.7 versus 7.1 +/- 5.0 mm Hg), and right ventricular end-diastolic pressure (7.9 +/- 6.6 versus 8.0 +/- 6.7 mm Hg). Similarly, there were no significant changes in all Doppler echocardiographic parameters, including right ventricular end-diastolic area (23.2 +/- 5.7 versus 22.6 +/- 5.4 cm2), left ventricular end-diastolic area (15.3 +/- 5.9 versus 15.5 +/- 4.4 cm2), the position of the interventricular septum, and the Doppler-derived mitral inflow measures of diastolic function. The pericardium appears to have little influence on the marked cardiac and septal deformations seen in patients with chronic, severe right ventricular pressure overload and cardiomegaly. This study confirms that the human pericardium is capable of adapting over time to changes in cardiac size and geometry.

Effect of aortic valve stenosis (pressure overload) and regurgitation (volume overload) on left ventricular systolic and diastolic function

In secondary hypertrophy from chronic pressure or volume overload, or both, systolic as well as diastolic abnormalities of left ventricular (LV) function have been described, but their relation has not been defined. In 58 patients with aortic valve disease (28 with aortic valve stenosis, and 30 with aortic regurgitation) and in 11 control subjects, LV biplane cineangiography was performed simultaneously with LV high-fidelity pressure measurements. LV ejection performance was assessed by ejection fraction, and diastolic function by the time constant of LV pressure decay, the early and late peak filling rates, and the constants of chamber (pressure-volume relation) and myocardial stiffness (stress-strain relation). In the entire cohort (n = 69), ejection fraction was inversely related to the time constant of LV relaxation (r = −0.58, p < 0.001) and to the constant of myocardial stiffness (r = −0.62, p < 0.001). Despite preserved systolic contractile function (as evaluated from the ejection fraction-mean systolic stress relation), abnormalities in LV diastolic function were present in 9 of 18 patients with pressure overload and 20 of 22 with volume overload. None of the 58 patients with aortic valve disease had a reduced early peak filling rate, whereas a reduction in late peak filling rate was observed in 3 with aortic stenosis, but in none with aortic regurgitation. Thus, it appears that abnormalities of relaxation and passive diastolic myocardial stiffness precede alterations in myocardial contractility. Assessment of peak filling rates is not helpful to detect diastolic dysfunction in patients with aortic valve disease.