Changes In Ventricular Compliance Research Articles

Modulating Cardiac Hemodynamics Using Tunable Soft Robotic Sleeves in a Porcine Model of HFpEF Physiology for Device Testing Applications

AbstractHeart failure with preserved ejection fraction (HFpEF) is a major challenge in cardiovascular medicine, accounting for ≈50% of all cases of heart failure. Despite the ongoing efforts, no medical device has yet received FDA approval. This is largely due to the lack of an in vivo model of the HFpEF hemodynamics, resulting in the inability to evaluate device effectiveness in vivo prior to clinical trials. Here, the development of a highly tunable porcine model of HFpEF hemodynamics is described using implantable soft robotic sleeves, where controlled actuation of a left ventricular and an aortic sleeve can recapitulate changes in ventricular compliance and afterload associated with a broad spectrum of HFpEF hemodynamic phenotypes. The feasibility of the proposed model in preclinical testing is demonstrated by evaluating the hemodynamic response of the model post‐implantation of an interatrial shunt device, which is found to be consistent with findings from in silico studies and clinical trials. This work overcomes limitations of prior HFpEF models, such as low hemodynamic accuracy, high costs, and long development phases. The versatile and adjustable platform introduced can transform HFpEF device development, aiming to enhance the lives of the 32 million people affected globally.

The Relationship between Left Ventricular Function Indices in Tissue Doppler Imaging and Exaggerated Blood Pressure Response During the Exercise Stress Test

Background: Studies have indicated that exaggerated hypertension during activity and stress can be a good predictor of the incidence of hypertension. This study tries to evaluate left ventricular (LV) function by tissue Doppler to assess early changes in ventricular compliance before the onset of Hypertension (HTN) in patients with exaggerated blood pressure response during the exercise test. Materials and Methods: In this case-control study, 40 patients without a history of hypertension with systolic blood pressure less than 140/90 which referred for exercise test, were included. The exercise test was performed for all patients. Patients who had exaggerated blood pressure during the stress test were considered as cases and the controls with normal blood pressure responses. Then standard echocardiography and Tissue Doppler imaging performed and indices of LV systolic and diastolic were recorded. Results: The LV mass in cases and controls were 174.9±50.78 and 152.9±33.59, respectively (P=0.114), and LV mass index in cases and controls were 127.4±13.5 and 79.8±15.75, respectively (P=0.023). Moreover, the LV Myocardial Performance Index were 0.68±0.11 and 0.48±0.06 in cases and controls, respectively (P<0.001). The heart rate, E/A, EE, E Velocity and S velocity were measuremented. Except E/A (P=0.009), there was no significant difference between the other variables measured between the cases and controls (P>0.05). Conclusion: The results of this study showed that using 2D conventional echocardiography as a noninvasive method if performed in prestigious centers can evaluate systolic and diastolic function Tissue Doppler parameters very well in the early stages of heart disease caused by HTN. [GMJ.2020;9:e1323]

The Relationship between Left Ventricular Function Indices in Tissue Doppler Imaging and Exaggerated Blood Pressure Response During the Exercise Stress Test.

Background: Studies have indicated that exaggerated hypertension during activity and stress can be a good predictor of the incidence of hypertension. This study tries to evaluate left ventricular (LV) function by tissue Doppler to assess early changes in ventricular compliance before the onset of Hypertension (HTN) in patients with exaggerated blood pressure response during the exercise test. Materials and Methods: In this case-control study, 40 patients without a history of hypertension with systolic blood pressure less than 140/90 which referred for exercise test, were included. The exercise test was performed for all patients. Patients who had exaggerated blood pressure during the stress test were considered as cases and the controls with normal blood pressure responses. Then standard echocardiography and Tissue Doppler imaging performed and indices of LV systolic and diastolic were recorded. Results: The LV mass in cases and controls were 174.9±50.78 and 152.9±33.59, respectively (P=0.114), and LV mass index in cases and controls were 127.4±13.5 and 79.8±15.75, respectively (P=0.023). Moreover, the LV Myocardial Performance Index were 0.68±0.11 and 0.48±0.06 in cases and controls, respectively (P<0.001). The heart rate, E/A, EE, E Velocity and S velocity were measuremented. Except E/A (P=0.009), there was no significant difference between the other variables measured between the cases and controls (P>0.05). Conclusion: The results of this study showed that using 2D conventional echocardiography as a noninvasive method if performed in prestigious centers can evaluate systolic and diastolic function Tissue Doppler parameters very well in the early stages of heart disease caused by HTN.

The Relationship between Left Ventricular Function Indices in Tissue Doppler Imaging and Exaggerated Blood Pressure Response During the Exercise Stress Test

Background: Studies have indicated that exaggerated hypertension during activity and stress can be a good predictor of the incidence of hypertension. This study tries to evaluate left ventricular (LV) function by tissue Doppler to assess early changes in ventricular compliance before the onset of Hypertension (HTN) in patients with exaggerated blood pressure response during the exercise test. Materials and Methods: In this case-control study, 40 patients without a history of hypertension with systolic blood pressure less than 140/90 which referred for exercise test, were included. The exercise test was performed for all patients. Patients who had exaggerated blood pressure during the stress test were considered as cases and the controls with normal blood pressure responses. Then standard echocardiography and Tissue Doppler imaging performed and indices of LV systolic and diastolic were recorded. Results: The LV mass in cases and controls were 174.9±50.78 and 152.9±33.59, respectively (P=0.114), and LV mass index in cases and controls were 127.4±13.5 and 79.8±15.75, respectively (P=0.023). Moreover, the LV Myocardial Performance Index were 0.68±0.11 and 0.48±0.06 in cases and controls, respectively (P&lt;0.001). The heart rate, E/A, EE, E Velocity and S velocity were measuremented. Except E/A (P=0.009), there was no significant difference between the other variables measured between the cases and controls (P&gt;0.05). Conclusion: The results of this study showed that using 2D conventional echocardiography as a noninvasive method if performed in prestigious centers can evaluate systolic and diastolic function Tissue Doppler parameters very well in the early stages of heart disease caused by HTN. [GMJ.2020;9:e1323]

Abstract 16866: Depressed Biventricular Outputs in Fetuses of Diabetic Mothers When Standardized to Estimated Fetal Weight

Background: Although the results of maternal diabetes on the newborn heart are well described, in-utero cardiovascular effects of maternal diabetes and obesity are not as well understood. Hypothesis: Echocardiographically derived measures of right and left heart flow volumes in fetuses of diabetic mothers (FDM) and fetuses of obese mothers (FOM) differ from those of normal fetuses. Methods: We prospectively enrolled 264 normal fetuses, 30 FDM and 49 FOM for prenatal research echocardiography. Estimated fetal weight (EFW) based norms for aortic and pulmonary valve velocity time integrals (AVVTI, PVVTI), right and left ventricular outflow tract diameters (LVOTD, RVOTD), aortic and pulmonary valve stroke volume (AVSV, PVSV), and cardiac output (LVCO, RVCO) were derived from the 264 control group fetuses using nonlinear regression to a Gompertz growth function. Z values for each parameter were determined, then analyzed using a non-paired two-tailed t-test to compare the three groups. Results: The mean ± SD EFW (g) for normal fetuses, FDM and FOM were 1610 ± 1201, 964 ± 694 and 1075 ± 1013; respective mean gestational ages (weeks) were 28.1±1.3, 25.3± 5, and 25 ± 6.6. The table shows mean Z value comparisons of VTI, OTD, SV and CO for the RV and LV in the three groups. Conclusions: FDM have significantly lower right and left heart stroke volumes and outputs than other fetuses matched for size, while FOM did not have demonstrable right or left heart stroke volume or cardiac output changes relative to normal fetuses. Similar to their relationship with gestational age, normal right and left ventricular stroke volumes and outputs follow a non-linear correlation with estimated fetal weight. Flow volumes in macrosomic fetuses may be better normalized to EFW rather than to gestational age. Reduced placental blood flow and ventricular compliance changes may be contributing to depressed biventricular cardiac output in FDM.

Dissociation Between Structural and Functional Changes in Arterial Stiffness After High Intensity Endurance Training in Sedentary Middle-Aged Adults

Increased arterial stiffness resulting from sedentary aging has been implicated as a marker for atherosclerosis, as well as a strong predictor for future cardiovascular disease. Arterial stiffness also increases afterload and may restrain exercise-induced increases in cardiac output. In sedentary seniors aged > 65 yrs, we have demonstrated that there is little structural plasticity of either the heart or large blood vessels despite a year of training, though stroke volume may nevertheless increase by functional (probably endothelial) mechanisms. Whether initiating training earlier in life may be better able to alter arterial structure is unknown. PURPOSE: To investigate the effect of a progressive, high-intensity endurance exercise program in improving central pulse wave velocity (cPWV) and peak cardiac output (Qc) in middle-aged adults. METHODS: 41 sedentary, healthy middle-aged adults (19 males; 52 ± 5 yrs) were recruited and randomized to one of two study groups, Exercise (EX; n=21) or non-exercise Control (CON; n=20); EX completed a 9-month progressive phase of a 24-month exercise prescription. At baseline and month 10 of training, all subjects underwent cPWV analysis [SphygmoCor tonometry] and maximal exercise testing, in which VO2max [Douglas Bags] and peak Qc [C2H2 rebreathing] were measured during incremental treadmill exercise. RESULTS: CON participants had no change in cPWV (719 ± 122 to 754 ± 117cm/s, p=0.148) or peak Qc (14.35 ± 3.75 to 14.95 ± 3.73L/min, p=0.228). EX also had no change in cPWV (716 ± 136 to 716 ± 94cm/s, p=1.000), yet increased peak Qc substantially (14.77 ± 3.06 to 16.05 ± 3.29L/min, p=0.016) entirely due to an increased peak SV (86.6 ± 20.1 to 93.5 ± 20.3mL, p=0.02). There was a modest association between cPWV change and peak Qc change in EX (R2=0.2194, p=0.032), but none in CON. CONCLUSION: 9 months of progressive, high-intensity training improved peak Qc without a measureable change in arterial stiffness. Thus, training allowed an augmented exercise stroke volume, due either to changes in ventricular compliance or v-a coupling, without evidence of meaningful changes in arterial structure. Whether such training can prevent (if not reverse) age-associated deterioration in arterial stiffness remains to be determined.

Contribution of Doppler atrioventricular flow waves to ventricular filling in the human fetus.

The normal fetal flow velocity profile across the atrioventricular valves is characterized by an early peak (E), which is related to preload and to active ventricular muscle relaxation, and a higher late peak (A), which is caused by the atrial contraction and also influenced by ventricular compliance. The purpose of this study was to determine how these two elements of ventricular filling change during gestation in both ventricles. A total of 485 normal fetuses from 17 weeks to term were examined by Doppler echocardiography. We measured E and A peak velocities and E/A ratio for both mitral and tricuspid valves. Simple regression analysis was applied to assess possible correlation between Doppler variables and gestational age. Moreover, E and A peak velocities were compared using paired Student's t-test. With the advance of gestation a significant linear increase in the E wave and E/A ratio was found for both mitral and tricuspid valves. The A wave shows little change throughout pregnancy. We found significantly higher Doppler velocities for the tricuspid valve than for the mitral valve. The relationship between the E/A ratios for the two valves and gestational age diverge slightly, with higher values for the mitral E/A ratio. This study shows that the A wave velocity remains constant throughout gestation, suggesting little or no change in ventricular compliance. The E wave is mainly responsible for the change in E/A ratio for both atrioventricular valves during gestation. These findings suggest progressive enhancement of relaxation and elastic recoil, an increase in preload, or both, throughout gestation, rather than a change in myocardial compliance as an explanation for the observed increase in the E/A ratio.

Real-time intraoperative monitoring of myocardial ischemia in noncardiac surgery.

Real-time intraoperative monitoring of myocardial ischemia in noncardiac surgery.

Starling resistor effects on pulmonary artery occlusion pressure in endotoxin shock provide inaccuracies in left ventricular compliance assessments.

Assessment of left ventricular preload and left ventricular compliance changes in septic shock using pulmonary artery occlusion pressure (PAOP) presumes that this pressure accurately reflects left heart filling pressure. We tested the hypothesis that Starling resistor forces render PAOP inaccurate as an index of left heart filling pressure, resulting in misleading assessments of left ventricular compliance changes. Prospective, randomized, controlled study. Large-animal research laboratory at a university. Fourteen anesthetized domestic pigs weighing 20 to 25 kg. Pulmonary artery flotation catheters and systemic arterial catheters were placed via right cervical vessels. The left atrium was directly catheterized for left atrial pressure measurements. Left ventricular end-diastolic diameter was measured using sonomicrometry. Other measured or calculated variables were mean arterial pressure, mean pulmonary arterial pressure, PAOP, pulmonary capillary pressure, and pulmonary arterial and venous resistances. Pigs received endotoxin (0.5 mg/kg i.v. over 30 mins), or an equivalent volume of saline. At t = 60 mins, pigs were resuscitated with lactated Ringer's solution (40 mL/kg over 30 mins). Measurements were taken before and after endotoxin administration, and immediately and 30 mins after lactated Ringer's solution administration. Data were analyzed by two-way analysis of variance (p < or = .05). PAOP, mean pulmonary arterial pressure, and pulmonary capillary pressure increased after endotoxin infusion, while left atrial pressure and left ventricular end-diastolic diameter decreased. Left atrial pressure and left ventricular end-diastolic diameter returned to baseline immediately after lactated Ringer's solution administration, while PAOP remained increased. Pulmonary arterial resistance and pulmonary venous resistance increased after endotoxin administration, with pulmonary venous resistance showing the greater percent increase. Pulmonary venous resistance decreased transiently immediately after lactated Ringer's solution administration. These changes were not observed in the control group. Accordingly, comparisons of PAOP vs. left ventricular end-diastolic diameter, and left atrial pressure vs. left ventricular end-diastolic diameter yielded divergent results. The dissociation between PAOP and left atrial pressure, while left ventricular and -diastolic diameter (preload volume) decreased, and changes in pulmonary venous resistance, are strong evidence for Starling resistor forces (venocompression) rather than active venoconstriction. These data indicate that PAOP overestimates left atrial pressure during endotoxin shock, making it an inaccurate index of left ventricular preload. This overestimation can cause misleading assessments of left ventricular compliance.

Passive ventricular mechanics in tight-skin mice

Although changes in the extracellular matrix have been associated with changes in ventricular compliance in certain diseased states, this relationship has not been entirely established. Accordingly, we studied passive ventricular mechanics in the tight-skin (TSk) mouse, a mutant strain known to have increased cardiac collagen. In the arrested left ventricle, we determined the pressure-volume relationship and the stress-free state, as defined by the "opening angle" of an equatorial ring with a radial cut. The results showed the mean opening angle in the TSk mouse to be smaller than that in phenotypic negative controls (7 +/- 6 vs. 21 +/- 9 degrees), and there was no statistical difference in the pressure-volume curves. Histological quantification of the transmural collagen showed a uniform increase of collagen area fraction across the wall in TSk mouse, and a significantly thicker superficial epicardial collagen layer (4.68 +/- 0.87 vs. 3.34 +/- 0.76 micron). Thus, although there appears to be a decrease of residual stress in the TSk mouse heart, which may be related to the thicker epicardial collagen layer, the combination of increased myocardial collagen and the change in stress-free state did not seem to affect the passive pressure-volume relationship of the left ventricle.

Numerical modeling of ventricular filling.

The fluid dynamical and physiological assumptions underlying general mathematical modeling of ventricular filling are outlined. We then describe the use of a lumped parameter model and computer simulation to study how the early transmitral velocity profile is affected by isolated changes in ventricular compliance and relaxation, atrial pressure and compliance, and valvular morphology. We show that the transmitral velocity is fundamentally affected by two physical determinants: the transmitral pressure difference and the net compliance of the atrium and the ventricle. These physical determinants in turn are specified by the various physiologic parameters of interest. This approach has shown that peak velocity is most strongly affected by initial left atrial pressure, lowered somewhat by prolonged relaxation, low atrial and ventricular compliance, and systolic dysfunction. Peak acceleration is directly affected by atrial pressure and inversely affected by the time constant of isovolumic relaxation, with little influence of compliance, whereas the deceleration rate is almost purely given by mitral valve area divided by instantaneous atrioventricular compliance at the end of the rapid filling wave.

Myocardial oedema and ventricular function after cardioplegia with added mannitol

Myocardial oedema may contribute to the impaired myocardial performance which commonly follows open heart surgery with cardioplegia-induced cardiac arrest. The rate of oedema formation during crystalloid cardioplegia and the relation of this to changes in ventricular compliance and ventricular function following reperfusion were studied using an isolated rabbit heart preparation. Myocardial tissue water content increased during cardioplegic arrest and the water content prior to reperfusion demonstrated an inverse correlation with ventricular function after reperfusion. In further studies the effect of adding mannitol to a standard crystalloid cardioplegic solution was investigated. The preparations were divided into two groups: nine were administered a standard cardioplegic solution (Plegisol*) (control group) and a further eight were administered the same solution mixed with mannitol to adjust the osmotic pressure to 360 mOsmol.L-3 (mannitol group). The mannitol group demonstrated less increase in RV water content and superior LV dP/dtmax following reperfusion. It is concluded that mannitol enhances protection of the myocardium during cardioplegic cardiac arrest.

Poor correlation between pulmonary arterial wedge pressure and left ventricular end-diastolic volume after coronary artery bypass graft surgery.

The authors studied 12 surgical patients in the intensive care unit post coronary artery bypass graft surgery and ten nonsurgical patients in the coronary care unit with chronic heart failure to determine the usefulness of the pulmonary arterial wedge pressure as an indicator of left ventricular preload. Left ventricular end diastolic volume was derived from concomitant determination of ejection fraction (gated blood pool scintigraphy) and stroke volume (determined from thermodilution cardiac output). In the nonsurgical patients, there was a significant correlation between changes in pulmonary arterial wedge pressure and left ventricular end-diastolic volume (P less than 0.05, r = 0.57). In the 12 patients studied during the first few hours after surgery, there was a poor correlation between changes in pulmonary wedge pressure (range = 4-32 mmHg) and left ventricular end-diastolic volume (range = 25-119 ml/m2), and a poor correlation between pulmonary arterial wedge pressures and stroke work index. In contrast, there was a good correlation between left ventricular end-diastolic volume and stroke work index. The poor correlation between the pulmonary arterial wedge pressure and left ventricular end-diastolic volume was not explained by changes in systemic or pulmonary vascular resistance. The altered ventricular pressure-volume relationship may reflect acute changes in ventricular compliance in the first few hours following coronary artery bypass graft surgery. While measurement of pulmonary arterial wedge pressure remains valuable in clinical management to avoid pulmonary edema, it cannot reliably be used as an index of left ventricular preload while attempting to optimize stroke volume in patients immediately following coronary artery bypass graft surgery.

Early detection of diastolic impairment in long-standing hypertension by a noninvasive volume challenge method.

A simple, easily reproducible, noninvasive, provocative test for the assessment of early diastolic impairment in long-standing hypertension is presented. Volume challenge of the heart was produced by elevating the subject's legs to 45 degrees for 5 minutes, thus increasing the venous return to the right heart. Using gated radionuclide ventriculography and Fourier analysis, the atrial structures were delineated and time-activity curves were generated. Early diastolic emptying slope of the left atrium was used to assess left ventricular compliance changes in hypertensives. The left atrial early diastolic emptying rate was markedly reduced in 38 hypertensive patients (45.5 +/- 15.4 counts/s) when compared with 14 healthy subjects (78 +/- 16 counts/s). The legs-up procedure induced subsequent decrease in left atrial emptying rate in patients with long-standing hypertension and left ventricular hypertrophy (-27.4 +/- 11%). In patients with recent onset hypertension there was a depressed early diastolic emptying rate (55.79 +/- 10 counts/s), but a "normal" response to the legs-up procedure (an increase in left atrial emptying rate: 12.84 +/- 7%). Global ejection fraction was normal in all subjects studied, decreasing after induction of augmented venous return in long-standing hypertension. Reduction in left atrial early diastolic emptying rate, caused by the legs-up manoeuvre appears to be an early and sensitive indicator of the left ventricular diastolic impairment in essential hypertension.

Myocardial ischemia in patients with hypertrophic cardiomyopathy: contribution of inadequate vasodilator reserve and elevated left ventricular filling pressures.

To study the mechanism and hemodynamic significance of myocardial ischemia in hypertrophic cardiomyopathy, 20 patients (nine with resting left ventricular outflow tract obstruction greater than or equal to 30 mm Hg) with a history of angina pectoris and angiographically normal coronary arteries underwent a pacing study with measurement of great cardiac vein flow, lactate and oxygen content, and left ventricular filling pressure. Compared with 28 control subjects without hypertrophic cardiomyopathy, their resting coronary blood flow was higher (91 +/- 27 vs 66 +/- 17 ml/min; p less than .001) and their coronary resistance was lower (1.13 +/- 0.38 vs 1.55 +/- 0.45 mm Hg/ml/min; p less than .001). Left ventricular end-diastolic pressure (16 +/- 6 vs 11 +/- 3 mm Hg; p less than .001) and pulmonary arterial wedge pressure (13 +/- 5 vs 7 +/- 3 mm Hg; p less than .001) were significantly higher in patients with hypertrophic cardiomyopathy. During pacing, coronary flow rose in both groups, although coronary and myocardial hemodynamics differed greatly. In contrast to the linear increase in flow in control subjects up to heart rate of 150 beats/min (66 +/- 17 to 125 +/- 28 ml/min), patients with hypertrophic cardiomyopathy demonstrated an initial rise in flow to 133 +/- 31 ml/min at an intermediate heart rate of 130 beats/min. At this point, 12 of 20 patients developed their typical chest pain. With continued pacing to a heart rate of 150 beats/min, mean coronary flow fell to 114 +/- 29 ml/min (p less than .002), with 18 of 20 patients experiencing their typical chest pain and metabolic evidence of myocardial ischemia. This fall in coronary flow was associated with a substantial rise in left ventricular end-diastolic pressure (30 +/- 9 mm Hg immediately after peak pacing). In the 14 patients whose coronary flow actually fell from intermediate to peak pacing, the rise in left ventricular end-diastolic pressure in the same interval was greater than that of the six patients whose flow remained unchanged or increased (11 +/- 8 vs 2 +/- 2 mm Hg; p less than .01). In addition, despite metabolic and hemodynamic evidence of myocardial ischemia, the arteriovenous O2 difference actually narrowed at peak pacing. Thus most patients with hypertrophic cardiomyopathy achieved maximum coronary vasodilation and flow at modest increases in heart rate. Elevation in left ventricular filling pressure, probably related to ischemia-induced changes in ventricular compliance, was associated with a decline in coronary flow.(ABSTRACT TRUNCATED AT 400 WORDS)

An isolated, blood-perfused, feline heart preparation for evaluating pharmacological interventions during myocardial ischemia

A preparation is described in which feline hearts were perfused with arterial blood drawn from a blood-donor cat. Ventricular function was measured with a fluidfilled latex balloon within the left ventricle. Left ventricular developed pressure, maximum left ventricular dP/dt, ventricular compliance, and coronary blood flow changed only slightly during two hours of perfusion at a constant pressure of 75 mmHg. Water, sodium, potassium, and calcium contents, and creatine kinase activity of isolated hearts did not differ from the values obtained for intact hearts from the blood-donor cats. Isolated hearts subJected to 40 minutes of normothermic global ischemia with one hour of reperfusion exhibited significantly decreased contractility, but no change in ventricular compliance. Myocardial water and sodium contents were increased after 40 minutes of ischemia and reperfusion. Hearts subJected to 60 minutes of ischemia with reperfusion exhibited decreases in both contractility and compliance. A prolonged reactive hyperemic response was maintained throughout the hour of reperfusion. Myocardial sodium content increased more than could be accounted for by edema formation; decreases were observed in potassium content and creatine kinase activity while calcium content was increased. The applicability of this model for evaluating the effects of pharmacological interventions on myocardial ischemic injury are discussed.

Segmental diastolic properties as an indicator of global ventricular compliance changes

Segmental diastolic properties as an indicator of global ventricular compliance changes

Early sequential changes in left ventricular dimensions and filling pressure in patients after myocardial infarction

Early consecutive changes in pulmonary arterial end-diastolic pressure (PAEDP) and echocardlographic left ventricular dimensions were measured in 14 patients within the first 8 days after acute myocardial infarction. Left ventricular volumes were estimated from echocardiographic left ventricular dimensions. Left ventricular compliance was assessed by three formulas, ΔV ΔP , ΔV/ESV/ΔP and LVID d PAEDP , where AV = echocardiographic stroke volume, ΔP = a derived left ventricular diastolic pressure change from the lowest level of early diastolic to the end-diastolic pressure, ESV = left ventricular end-systolic volume, and LVID d = echocardiographic left ventricular end-diastolic dimension. To compare pressure, dimension and compliance values, linear relations were assumed between values for left ventricular end-diastolic volume, end-systolic volume, pulmonary arterial end-diastolic pressure and the day after infarction. The estimated third day values for the variables obtained from these linear relations were used so that each patient's values would contribute equal weight to the statistical analysis. The estimated third day compliance values from each formula correlated highly with one another ( r = 0.69 − 0.82). Neither ΔV ΔP nor ΔV/ESV/ΔP had a significant correlation with LVID d. Echocardiographic end-diastolic volume correlated with both end-systolic volume ( r = 0.89) and echocardiographic stroke volume ( r = 0.62) but not with pulmonary arterial end-diastolic pressure. When the first and last measurements for each patient are used, large changes in pulmonary arterial end-diastolic pressure associated with no or small alterations in echocardiographic left ventricular end-diastolic dimension in 12 patients imply acute changes in ventricular compliance. Sequential compliance values ( ΔV ΔP ) increased in seven survivors and decreased in one. ΔV ΔP decreased in the five patients who died or had electrocardiographic evidence of extension of infarction. Early sequential changes in filling pressure, echocardiographic dimensions, and left ventricular compliance had a close correlation with the clinical course of the patients in our series and these data may assist in the management of patients with hemodynamic instability after acute myocardial infarction.

Early consecutive left ventricular compliance changes after acute myocardial infarction

Early consecutive left ventricular compliance changes after acute myocardial infarction

Effect of coronary artery disease and acute myocardial infarction on left ventricular compliance in man.

The evaluation of left ventricular (LV) compliance by use of the pressure-volume (P-V) relationship encounters several serious difficulties. Since the P-V relationship is curvilinear, it is difficult to quantitate. Furthermore, alterations of resting heart size and geometry also produce marked changes in the P-V curve. The first derivative of the P-V relationship, however, is a precisely linear function expressed by the formula dP/dV = aP+b. The slope of this linear function, a, termed the passive elastic modulus, has been shown to be independent of initial volume and primarily and predominantly determined by changes in the stiffness of the myocardium. Myocardial wall stiffness was evaluated in three groups of subjects during LV catheterization. In 13 normal subjects a = 0.005; in 13 with coronary artery disease a = 0.011; and in 12 with acute infarction a = 0.045. The differences in stiffness among the groups were highly significant ( P &lt; 0.005). It was concluded that a measurable change in ventricular compliance occurs with the development of coronary artery disease and that a further increase in wall stiffness occurs with the development of acute infarction. The magnitude of increase in LV wall stiffness correlated directly with immediate prognosis: 87% of those subjects with a ΔP/ΔV greater than 0.5 mm Hg/cc died of power failure during the acute stage of their illness. These alterations in compliance may invalidate certain traditional concepts of LV function and heart failure.