Decrease In Left Ventricular Compliance Research Articles

Detection of a diastolic heart sound in children and young adults using high-frame-rate echocardiography

Abstract Funding Acknowledgements Type of funding sources: Private grant(s) and/or Sponsorship. Main funding source(s): Colin"s Kids, Inc. PO Box 93 Hopewell, NJ 08525 Introduction The auscultatory finding of a fourth heart sound (S4) is clinically associated with a pathologic decrease in left ventricular compliance, but may be seen in healthy children by phonocardiography. High-frame-rate difference imaging (HFRDI) has demonstrated several propagating myocardial phenomena in the left ventricular (LV) lateral wall throughout the cardiac cycle, including during diastole. We hypothesize that these visualized wave phenomena correlate with physiologic and pathologic heart sounds. Purpose Using HFRDI, we sought to define the characteristics of a LV lateral wall late diastolic wave in healthy children and young adults. Methods HFRDI was obtained from the apical 4-chamber view with synchronized electrocardiogram (ECG) on the T5 system (Phased Array Research Scanner) acquiring images for this study between 587 and 1174 frames per second (depending on participant imaging characteristics). In addition, tissue Doppler images were acquired with synchronized ECG and phonocardiography (PCG) on a commercial ultrasound machine (Figure 1). Timing events were measured from the QRS onset on the ECG tracing. An S4 wave correlate was defined by meeting the following criteria: 1) occurring after the P wave on ECG; 2) at or after the onset of a’ on TDI; 3) occurring during the PCG S4; and 4) occurring prior to the S1 wave complex. The timing of the S4 wave in HFRDI was measured from the onset of QRS to the first appearance of the wave, and the wave velocity was calculated by measuring the length of the lateral wall and counting temporally calibrated image frames while the wave was visible. Results Nine healthy volunteers completed the imaging protocol with a median age of 20 years (range 6 – 22 years). A single, distinct late diastolic HFRDI wave was seen in all participants propagating from apex to base of the lateral LV free wall. This wave met the defined criteria to be a visual correlate of S4 in all participants. Measurements of correlated events are presented in Table 1. S4 propagating velocity was 2.96 ± 1.8 m/sec and occurred 25 ± 18 msec prior to the QRS onset. There is a strong positive correlation between age and S4 velocity [r(7) = 0.76, p = 0.019]. Conclusion The S4 heart sound can be reliably visualized by high frame rate imaging and has similar characteristics in healthy children and young adults. Further definition of normal and abnormal S4 wave characteristics may lead to a novel tool in defining LV diastolic function. Abstract Table 1 Abstract Figure 1

Low-Gradient Severe Mitral Stenosis: Hemodynamic Profiles, Clinical Characteristics, and Outcomes.

BackgroundOptimal management of patients with severe mitral stenosis (MS) and low transmitral gradient is incompletely understood.Methods and ResultsWe examined 101 consecutive patients with severe rheumatic MS (mitral valve area ≤1.5 cm2) who underwent balloon valvuloplasty. Low gradient was defined as mean transmitral gradient <10 mm Hg and low flow as stroke volume index ≤35 mL/m2 by echocardiography. Symptoms and mortality data were collected. Systolic, diastolic, and arterial function were characterized by measuring left ventricular (LV) end‐systolic elastance, LV stiffness constant (β), diastolic capacitance (predicted LV end‐diastolic volume at a common LV filling pressure of 30 mm Hg), and effective arterial elastance. Low gradient (<10 mm Hg) was present in 55 patients, including low flow/low gradient in 11 and normal flow/low gradient in 44 patients, and high gradient was present in 46 patients. Participants with low‐flow/low‐gradient (LG) MS were older with higher rates of atrial fibrillation (64%) and subvalvular thickening, higher afterload, and decreased LV compliance with lower ejection fraction (57±10% versus 65±4% versus 63±6%, P=0.002) but similar end‐systolic elastance compared with patients with normal‐flow/LG and high‐gradient MS. The normal‐flow/LG group had larger mitral valve area and lower left atrial pressure by catheterization, as well as favorable long‐term outcomes compared with the low‐flow/LG and high‐gradient MS group. A total of 40% of patients with LG MS had no symptomatic benefit from valvuloplasty compared with 18% of patients with high‐gradient MS (P=0.02).ConclusionsPresence of low gradient in patients with severe MS was associated with lesser symptomatic benefit from valvuloplasty. In the subset with low stroke volume index, this may be related to independent ventricular‐vascular uncoupling, decreased LV compliance, and high prevalence of atrial fibrillation in addition to intrinsic MS.

Prognostic Importance of Pathophysiologic Markers in Patients With Heart Failure and Preserved Ejection Fraction

Heart failure with preserved ejection fraction (HFpEF) is a heterogeneous syndrome associated with multiple pathophysiologic abnormalities, including left ventricular (LV) diastolic dysfunction, longitudinal LV systolic dysfunction, abnormal ventricular-arterial coupling, pulmonary hypertension, and right ventricular (RV) remodeling/dysfunction. However, the relative prognostic significance of each of these pathophysiologic abnormalities in HFpEF is unknown. We prospectively studied 419 patients with HFpEF using echocardiography and sphygmomanometry to assess HFpEF pathophysiologic markers. Cox proportional hazards analyses were used to determine the associations between pathophysiologic markers and outcomes. Mean age was 65±12 years; 62% were women; 39% were black; comorbidities were common; and study participants met published criteria for HFpEF. RV abnormalities were frequent: 28% had abnormal tricuspid annular plane systolic excursion, 15% had reduced RV fractional area change, and 34% had RV hypertrophy. During a median follow-up time of 18 months, 102 (24%) were hospitalized for HF and 175 (42%) experienced the composite end point of cardiovascular hospitalization or death. Decreased LV compliance, measured as reduced LV end-diastolic volume at an idealized LV end-diastolic pressure of 20 mm Hg (EDV20), and RV remodeling, as indicated by increased RV wall thickness, were the 2 pathophysiologic markers most predictive of worse outcomes: adjusted hazard ratio per 1 SD decrease in EDV20=1.39 (95% confidence interval [CI], 1.10-1.75; P=0.006), and hazard ratio per 1 SD increase in RV wall thickness=1.37 (95% CI, 1.16-1.61; P<0.001). These associations persisted after additional adjustment for markers of HF severity. By contrast, markers of LV relaxation, longitudinal LV systolic dysfunction, and ventricular-arterial coupling were not significantly associated with adverse outcomes. In patients with HFpEF, reduced LV compliance and RV remodeling are the strongest pathophysiologic predictors of adverse outcomes.

Mid-diastolic mitral flow vectors in complete atrioventricular block.

An 81-year-old man who was treated for prostate cancer was referred to our department because of bradycardia. He had a 1-month history of shortness of breath. A 12-lead electrocardiogram (ECG) showed complete atrioventricular (AV) block. His blood pressure was 165/78 mmHg and pulse rate was 38 beats/ min. Results of blood sampling were normal. A transthoracic echocardiogram revealed normal left ventricular (LV) wall thickness (interventricular septal thickness, 8 mm; LV posterior wall thickness, 8 mm) and normal LV systolic function (LV end-diastolic dimension, 39 mm; LV end-systolic dimension, 22 mm; LV ejection fraction, 76 %). A color-coded 2-dimensional echocardiogram showed no significant valvular disease. During mid-diastole, mitral forward and regurgitant flows were intermittently observed (Fig. 1). Color-coded M-mode echocardiography also showed intermittent mitral forward and regurgitant flows (Fig. 2). Simultaneous ECG recording indicated a relationship between the timing of the P wave and the T wave and the direction of mid-diastolic flow. Middiastolic mitral inflow was observed when the P wave was on the T wave, while diastolic mitral regurgitation (MR) was observed when the P wave emerged after the T wave (Figs. 1, 2). After treatment of complete AV block by pacemaker implantation, neither type of mitral flow was observed. Mid-diastolic mitral forward flow can be observed in some patients with advanced LV diastolic dysfunction. In these cases, mid-diastolic flow may be a result of interruption of early diastolic mitral inflow (E wave) by transient elevation of LV pressure [1, 2]. In the present case of complete AV block, mid-diastolic forward flow was observed when the P wave overlapped with the T wave. It is probable that mid-diastolic flow in this case might be a result of E wave interruption by transient fall of left atrial (LA) pressure by atrial relaxation. Diastolic MR is observed when the AV pressure gradient is reversed because the mitral valve does not close firmly during diastole. In complete AV block, diastolic MR can be observed when atrial relaxation occurs during ventricular diastole [3]. Moreover, decreased LV compliance [4] and early diastolic LV hyperinflation [5] may also play a part. In this patient with complete AV block, the timing of atrial relaxation might have played a decisive role in the mid-diastolic mitral inflow velocity and diastolic MR.

Acute Left Ventricular Dynamic Effects of Primary Percutaneous Coronary Intervention: From Occlusion to Reperfusion

We studied the left ventricular (LV) dynamic effects of primary percutaneous coronary intervention (PCI) for ST-segment elevation myocardial infarction (STEMI) by directly obtaining pressure-volume (PV) loops during the procedure. An acute myocardial infarction causes a decrease in LV compliance. The instantaneous effects of primary PCI on LV compliance are unknown. We studied 15 consecutive patients (10 males, ages 59 +/- 12 years), who presented with their first acute anterior STEMI within 6 h after onset of symptoms, and in whom coronary angiography revealed an occluded left anterior descending coronary artery. Before performing primary PCI, we inserted a pressure-conductance catheter in the LV to continuously obtain PV loops. Immediately after successful reperfusion, significant improvements were observed in LV diastolic function, as indicated by an increased end-diastolic compliance with a 6.0 +/- 2.8 mm Hg (p < 0.0001) downward shift of the compliance curve. There was a decrease in end-diastolic pressure of 24 +/- 18% (p = 0.0002), in stiffness of 27 +/- 18% (p = 0.0003), and in wall stress of 20 +/- 24% (p = 0.004). Systolic function mainly showed an immediate improvement in apical contractility from 40 +/- 17% to 54 +/- 15% (p = 0.01). Primary PCI in anterior STEMI patients causes an immediate improvement in diastolic function, assessed by online PV loop measurements.

Diastolic dysfunction: A link between hypertension and heart failure

Diastolic heart failure is characterized by the symptoms and signs of heart failure, a preserved ejection fraction and abnormal left ventricular (LV) diastolic function caused by a decreased LV compliance and relaxation. The signs and symptoms of diastolic heart failure are indistinguishable from those of heart failure related to systolic dysfunction; therefore, the diagnosis of diastolic heart failure is often one of exclusion. The majority of patients with heart failure and preserved ejection fraction have a history of hypertension. Hypertension induces a compensatory thickening of the ventricular wall in an attempt to normalize wall stress, which results in LV concentric hypertrophy, which in turn decreases LV compliance and LV diastolic filling. There is an abnormal accumulation of fibrillar collagen accompanying the hypertension-induced LV hypertrophy, which is also associated with decreased compliance and LV diastolic dysfunction. There are no specific guidelines for treating diastolic heart failure, but pharmacological treatment should be directed at normalizing blood pressure, promoting regression of LV hypertrophy, preventing tachycardia and treating symptoms of congestion. Preventive strategies directed toward an early and aggressive blood pressure control are likely to offer the greatest promise for reducing the incidence of diastolic heart failure.

Physiology of the Third Heart Sound: Novel Insights from Tissue Doppler Imaging

The third heart sound (S(3)) is thought to be caused by the abrupt deceleration of left ventricular (LV) inflow during early diastole, increased LV filling pressures, and decreased LV compliance. We sought to determine whether the ratio of early mitral inflow velocity to diastolic velocity of the mitral annulus (E/E') could confirm the proposed mechanism of the S(3). A total of 90 subjects underwent phonocardiography, echocardiography, tissue Doppler imaging, and left-sided heart catheterization. Phonocardiography detected an S(3) in 21 patients (23%). Subjects with an S(3) had lower ejection fraction (P = .0006) and increased E deceleration rate (P < .0001), E/E' (P < .0001) and filling pressures (P < .0001). The phonocardiographic S(3) confidence score correlated with E/E' (r = 0.46; P < .0001) and E deceleration rate (r = 0.43, P = .0001). Of the echocardiographic variables, only E/E' was independently associated with the S(3) confidence score (P = .009), independently of invasively determined LV filling pressures (P = .001). The most important determinants of the pathologic S(3) are an increased deceleration rate of early mitral inflow, elevated LV filling pressures, and abnormal compliance of the myocardium as measured by tissue Doppler imaging.

Cascade model of ventricular-arterial coupling and arterial-cardiac baroreflex function for cardiovascular variability in humans

Cardiovascular variability reflects autonomic regulation of blood pressure (BP) and heart rate (HR). However, systolic BP (SBP) variability also may be induced by fluctuations in stroke volume through left ventricular end-diastolic pressure (LVEDP) variability via dynamic ventricular-arterial coupling during respiration. We hypothesized that dynamic ventricular-arterial coupling is modulated by changes in left ventricular compliance associated with altered preload and that a cascade control mechanism of ventricular-arterial coupling with arterial-cardiac baroreflex function contributes to the genesis of cardiovascular variability at the respiratory frequency. Seven healthy young subjects underwent 6-min recordings of beat-by-beat LVEDP, SBP, and HR in the supine position with controlled respiration at 0.2 Hz during hyper- and hypovolemia. Spectral and transfer function analysis of these variables was conducted between 0.18 and 0.22 Hz. Dynamic ventricular-arterial coupling gain (Gain LVEDP-SBP) was smaller by 25% (P = 0.009) during hypervolemia than during hypovolemia, whereas arterial-cardiac baroreflex function gain (Gain SBP-HR) was similar. As predicted from a cascade model, a linear relationship between Gain LVEDP-HR and LVEDP-SBP times Gain SBP-HR was identified (R(2) = 0.93, P < 0.001). Gain LVEDP-HR was smaller by 40% (P = 0.04) during hypervolemia than during hypovolemia, leading to a reduction in spectral power of HR variability by 45% (P = 0.08). We conclude that dynamic ventricular-arterial coupling gain is reduced during hypervolemia because of a decrease in left ventricular compliance. A cascade model of ventricular-arterial coupling with the arterial-cardiac baroreflex contributes to the genesis of cardiovascular variability at the respiratory frequency.

Familial Hypertrophic Cardiomyopathy With Triphasic Transmitral Flow Velocity

We describe a family in which five members had hypertrophic cardiomyopathy (HCM) with a similar distribution of left ventricular (LV) hypertrophy and LV filling pattern. All five family members had myocardial hypertrophy localized between the anterior LV wall and ventricular septum, in addition to having a triphasic transmitral flow (TMF) velocity pattern with a mid-diastolic wave. The HCM patients with this TMF velocity pattern exhibit decreased LV compliance and delayed LV relaxation, suggesting that the features of diastolic failure may be specific. Thus, these findings may provide an important clue to elucidating the relationship between the pathophysiology and mode of inheritance in patients with HCM.

Role of Diastole in Left Ventricular Function, II: Diagnosis and Treatment

Left ventricular diastolic dysfunction plays an important role in congestive heart failure. Although once thought to be lower, the mortality of diastolic heart failure may be as high as that of systolic heart failure. Diastolic heart failure is a clinical syndrome characterized by signs and symptoms of heart failure with preserved ejection fraction (0.50) and abnormal diastolic function. One of the earliest indications of diastolic heart failure is exercise intolerance followed by fatigue and, possibly, chest pain. Other clinical signs may include distended neck veins, atrial arrhythmias, and the presence of third and fourth heart sounds. Diastolic dysfunction is difficult to differentiate from systolic dysfunction on the basis of history, physical examination, and electrocardiographic and chest radiographic findings. Therefore, objective diagnostic testing with cardiac catheterization, Doppler echocardiography, and possibly measurement of serum levels of B-type natriuretic peptide is often required. Three stages of diastolic dysfunction are recognized. Stage I is characterized by reduced left ventricular filling in early diastole with normal left ventricular and left atrial pressures and normal compliance. Stage II or pseudonormalization is characterized by a normal Doppler echocardiographic transmitral flow pattern because of an opposing increase in left atrial pressures. This normalization pattern is a concern because marked diastolic dysfunction can easily be missed. Stage III, the final, most severe stage, is characterized by severe restrictive diastolic filling with a marked decrease in left ventricular compliance. Pharmacological therapy is tailored to the cause and type of diastolic dysfunction.

Left ventricular pressure-volume relationship in a murine model of congestive heart failure due to acute viral myocarditis

ObjectivesThis study, performed in a murine model of encephalomyocarditis virus myocarditis, used a new Millar 1.4F conductance-micromanometer system for the in vivo determination of the left ventricular (LV) pressure-volume relationship (PVR). BackgroundViral myocarditis is an important cause of congestive heart failure and may lead to dilated cardiomyopathy. However, the hemodynamic changes associated with its acute phase have not been analyzed in detail. MethodsFour-week-old DBA/2 mice were inoculated with EMCV (day 0). Serial hemodynamic measurements, compared with uninfected control mice were made on days 0, 1, 3, 4, 5, 7, 9, 12, and 14. ResultsOn day 1, the hearts of infected mice manifested enhanced contractile function, decreased LV compliance, and abnormal diastolic function with increased LV end-diastolic pressure (EDP). Mean stroke index, ejection fraction (EF), and cardiac index (CI) were significantly higher than in uninfected control mice (p < 0.05). Contractile function decreased from days 4 to 14. On day 7, when hemodynamic abnormalities consistent with heart failure culminated, end-diastolic volume (EDV), EDP, and EDPVR were significantly higher, and CI, EF, end-systolic pressure (ESP), and ESPVR significantly lower in the infected than in control mice. Heart rate remained comparable in both groups. Although heart failure receded between day 9 and day 14, ESPVR, ESP, and EF remained significantly depressed up to day 14, and EDV and EDP remained significantly higher. ConclusionsThese hemodynamic data provide new insights into the pathophysiology of acute viral myocarditis and may be useful in the development of therapeutic interventions.

Doppler echocardiographic assessment of left ventricular diastolic function in 74 boxer dogs with aortic stenosis

Objective To evaluate left ventricular (LV) diastolic function in boxer dogs with aortic stenosis (AS). Background LV relaxation, elastic recoil, filling and stiffness have been found to be abnormal in people with AS and were related to disease severity, clinical signs and prognosis. Methods 2-D, M-mode and Doppler echocardiography was done in 74 boxers with AS (55 with mild AS, 7 with moderate AS and 12 with severe AS) and compared with reference values from 66 normal boxers. Measurements included isovolumic relaxation time (IVRT), peak early (E) and late (A) transmitral filling velocities, mitral E wave deceleration time, peak systolic, and early and late (AR) diastolic pulmonary wenous flow velocities and related variables. In addition, left atrial (LA) function, LV dimensions and hypertrophy and LV systolic performance were assessed. Results Eight dogs (15%) with mild AS had abnormal LV diastolic function, compared with 16 dogs (84%) with moderate or severe AS. Two dogs (3%) had also systolic abnormalities. The flow pattern of delayed relaxation, pseudonormal mitral inflow and restrictive flow were found in 10, 11 and 3 dogs, respectively. IVRT and E:A were heterogeneous in dogs with moderate or severe AS, being either high, normal, or low. Peak AR velocity was significantly higher (p ≤ 0.05) in dogs with severe AS, and the A duration:AR duration ratio was significantly lower (p ≤ 0.05) in dogs with moderate and severe AS compared with the other dogs, suggesting decreased LV compliance, increased LV end-diastolic pressure, and normal or increased LA systolic function. Bivariate linear regression analysis revealed significant correlations between the severity of AS based on Doppler and LV hypertrophy (IVSd: r = 0.61, p ≤ 0.001 and LVPWd: r = 0.46, p ≤ 0.001) and AS severity and A duration: AR duration (r = -0.64, p ≤ 0.001). Conclution In most boxer dogs with moderate or severe AS, LV diastolic function is abnormal even in the presence of normal systolic performance.

An androgenic steroid decreases left ventricular compliance in rats

The effect of chronic administration of an androgenic steroid on left ventricular (LV) compliance and contractility was studied in rats. Rats received a biweekly intramuscular injection of nandrolone decanoate (5 mg/kg; steroid group) or the vehicle (control group) for 3 mo. Cardiac performance was measured in anesthetized open-chest ventilated rats. LV compliance was determined from the slope of the LV end-diastolic pressure (LVEDP) vs. LV end-diastolic (LVED) strain relation measured in the long and short axes of the LV. LV regional myocardial compliance was determined from the slope of the LVED stress vs. LVED strain relation (myocardial elastic stiffness constant). Cardiac contractility was determined from the slope of the LV end-systolic (LVES) pressure vs. LVES strain relation. Systolic performance was also assessed from the slope of the pressure-length area (PL area) or stroke work vs. LVED strain and LVEDP relations. Nandrolone decanoate decreased body weight, heart weight, and plasma testosterone concentrations but increased the heart weight-to-body weight ratio. Nandrolone decanoate decreased LV compliance (slope of LVEDP vs. LVED strain relation in long and short axes; steroid vs. control, P < 0.01). This occurred as a result of an increased regional myocardial stiffness (myocardial elastic stiffness constant; steroid vs. control, P < 0.01), which resulted in a reduced cardiac systolic performance (PL area vs. LVEDP, slope of steroid vs. control group, P < 0.005). Diastolic geometry (LV wall thickness-to-radius ratio) and cardiac contractility were unchanged with steroid administration. In conclusion, chronic administration of the androgenic steroid nandrolone decanoate decreases LV myocardial compliance and thus overall cardiac performance without altering contractility in rats.

904-53 Left Ventricular Structure and Function Eleven Years After Doxorubicin Treatment for Childhood Leukemia: Is this a Restrictive Cardiomyopathic Process?

We previously characterized the progressive abnormalities of left ventricular (LV) structure and function in 115 survivors of childhood acute lymphoblastic leukemia 6.4 years (mean) after completion of doxorubicin therapy. 65% of patients having received &gt;228 mg/m 2 of doxorubicin had either increased afterload or decreased contractility, or both. Progressive increases in afterload due to a thin LV wall appeared related to an inability to increase LV mass in response to somatic growth. Of these 115 patients, 36 have died, relapsed, or are no longer followed at our institution. 8 patients had both early and late congestive heart failure. Findings noted in patients with late heart failure included normal LV size in the setting of a mean LV fractional shortening &lt;10%, as well as frequent pulmonary hypertension, increased pulmonary resistance, and left atrial dilation. We wished to characterize the late outcome of doxorubicin cardiotoxicity by reviewing the long-term echocardiographic findings of this cohort. The remaining 79 of the original 115 patients have had echocardiographic follow-up 11.1 years (mean) after completing doxorubicin. Changes in LV structure and function adjusted for age or body surface area at 3 time points were compared: prior to doxorubicin (A), 6.4 years after doxorubicin (B), and 11.1 years after doxorubicin (C). LV fractional shortening fell from normal at A to significantly depressed at B, and remained stable but depressed at C. LV mass was normal for body surface area at A, below normal at B, and continued to become more abnormal at C (p = 0.001). LV wall thickness was normal for body surface area at A below normal at B, and continued to become more abnormal at C(p = 0.03). LV end-diastolic dimension was normal for body surface area at A and B, but during the subsequent 4.7 years, a significant fall in LV end-diastolic dimension for body surface area occurred (p = 0.03). LV afterload increased significantly from A to B, but remained elevated without further increase at C. LV contractility remained normal at all 3 times. In conclusion, the fall in LV dimension to subnormal levels with increasing follow-up, in spite of a reduced mass:volume ratio, is the pattern seen in restrictive cardiomyopathy with a loss of the capacity of the LV to dilate. Both the echocardiographic and clinical findings suggest that the moderate to long term course of children treated with boluses of doxorubicin may follow the clinical findings of a restrictive cardiomyopathic process with decreased LV compliance and a small thin-walled LV.

VENTRICULAR FUNCTION DURING LIVER REPERFUSION IN HEPATIC TRANSPLANTATION

Postreperfusion syndrome (PRS) is the most dramatic and acute hemodynamic alteration that occurs in OLT. Our aim was to determine heart function by hemodynamic monitoring and transesophageal echocardiography during PRS. We studied 24 nonconsecutive patients allocated to 2 groups: group A (n = 8), patients with PRS, and group B (n = 16), patients without PRS. Usual hemodynamic data were obtained simultaneously with transesophageal echocardiography recording of the left ventricular imaging in 4 different stages: after induction of anesthesia, 5 min before the end of the anhepatic phase, between 2 and 5 min after reperfusion, and 5 min after graft reperfusion. The hemodynamic and echocardiographic findings during reperfusion were (group A vs. group B patients): mean arterial pressure, 50.0 +/- 15.2 vs. 74.7 +/- 13.9 mmHg (P < 0.01); pulmonary capillary wedge pressure, 12.7 +/- 6.1 vs. 13.9 +/- 5.7 mmHg (NS); left ventricular ejection fraction, 79.6 +/- 9.3 vs. 83.4 +/- 9.4% (NS); left ventricular end diastolic volume index, 35.5 +/- 12.7 vs. 54.7 +/- 21.3 ml/m2 (P < 0.05); and stroke volume index, 27.9 +/- 8.9 vs. 45.5 +/- 15.9 ml/m2 (P < 0.01). There was a mild decrease in left ventricular compliance in group A. We found no alteration in left ventricular function that can justify PRS. The hemodynamic changes during PRS seemed to be caused by an insufficient increase in preload after unclamping.

Effects of crystalloid, blood, and University of Wisconsin perfusates on weight, water content, and left ventricular compliance in an edema-prone, isolated porcine heart model

Coronary perfusion with blood and cardioplegic solutions was examined in isolated, arrested, hypothermic porcine hearts. Myocardial water content, heart weight, and left ventricular diastolic pressure-volume curves were measured before and after coronary perfusion. Statistics were based on exponential curve fitting to pressure-volume data and analysis of variance. Thirty-two pig hearts were divided into five experimental groups and a control group; after control measurements, each experimental group underwent three successive coronary perfusions with 1 L of unmodified blood or a solution of controlled osmolarity, 150 mOsm/L (diluted Plegisol solution), 280 mOsm/L (Plegisol solution and albumin), 334 mOsm/L (University of Wisconsin solution), or 380 mOsm/L (Stanford solution). After each perfusion, measurements were repeated. All experiments were completed within 90 minutes. The first perfusion was delayed 20 minutes after excision of the heart to allow for instrumentation. Each experimental group demonstrated a statistically significant increase in heart weight and myocardial water content and a significant decrease in left ventricular compliance after perfusion. Changes were less pronounced with blood than crystalloids. Edema effects were minimized but not prevented by hyperosmolarity. University of Wisconsin solution appeared unique in minimizing progressive edema after the first perfusion. Over the 81 perfusions studied, changes in left ventricular compliance were linearly related to heart weight and water content. We conclude that in this model, in which edema sensitivity is increased by delayed perfusion and venous occlusion, edema is minimized but not eliminated by whole blood and University of Wisconsin solution. The model appears useful in assessing properties of cardioplegia vehicles intended for use in the injured myocardium.

Left ventricular dysfunction in early E. coli endotoxemia: effects of naloxone

Although the opiate receptor antagonist naloxone (NAL) has been reported to improve in vivo systolic performance of the heart in different circulatory shock syndromes, the influence of this drug on intrinsic cardiac mechanical function during hypodynamic circulatory states is unknown. The present study was designed to determine the effects of in vivo NAL on contraction-relaxation properties of isovolumic left ventricular (LV) preparations isolated from guinea pigs 4 h after induction of gram-negative endotoxemia. Animals were given a 1 mg/kg ip injection of Escherichia coli endotoxin and immediately treated intravenously with either NAL (4 mg/kg iv bolus plus 4 mg.kg-1.h-1 infusion) or an equivalent volume of saline. Endotoxin produced significant reduction of LV contractile function in coronary-perfused hearts, a response unaffected by NAL therapy. For example, LV systolic pressure at approximately 10 mmHg end-diastolic pressure averaged 78 +/- 3 and 82 +/- 6 mmHg in hearts from saline and NAL control animals, respectively, but only 41 +/- 2 and 40 +/- 2 mmHg in endotoxin and endotoxin plus NAL groups, respectively. LV end-diastolic pressure-volume relationships in endotoxin hearts were shifted upward and to the left of controls in the direction of decreased diastolic compliance (P less than 0.05). Importantly, in vivo NAL prevented the endotoxin-induced decrease in LV compliance of the isolated heart preparations (P less than 0.05). Thus intrinsic cardiac complications of early (4 h) nonhypotensive endotoxemia included decreased diastolic compliance as well as diminished contractility of the left ventricle. Only the diastolic compliance changes were NAL responsive and therefore may involve endogenous opioid systems in their pathophysiological expression.

Doppler echocardiography in cardiac tamponade: Exaggerated respiratory variation in transvalvular blood flow velocity integrals

Pulsed Doppler echocardiography has been used previously to demonstrate marked changes in transvalvular blood flow velocities during cardiac tamponade in laboratory animals and a small number of patients. To further assess the respiratory changes in transvalvular blood flow during tamponade, pulsed Doppler tracings of flow velocity profiles across all four cardiac valves were recorded during inspiration and expiration in 13 patients during cardiac tamponade, in 6 of the 13 patients after relief of tamponade by pericardiocentesis and in 8 normal control subjects. Flow velocity integrals were calculated for each valve during inspiration and expiration.In the setting of cardiac tamponade, inspiration caused an 85 ± 46% increase in the flow velocity integral across the pulmonary valve, an 81 ± 34% increase across the tricuspid valve, a 33 ± 13% decrease across the aortic valve and a 35 ± 8% decrease across the mitral valve. These phasic respiratory changes were markedly reduced after relief of tamponade (p < 0.05 compared with tamponade) and were observed to only a minimal extent in the normal individuals (p < 0.01 compared with tamponade). The exaggerated respiratory variations in transvalvular flow velocity integrals suggest that Doppler evaluation may be a valuable tool in the diagnosis of cardiac tamponade.Transmitral Doppler indexes of left ventricular filling during cardiac tamponade revealed that inspiration caused a shift to increased filling during late diastole, with a greater contribution of atrial systole to total left ventricular filling. These Doppler indexes did not vary significantly with respiration in the group studied after relief of tamponade or in the control group. The change in these indexes during inspiration in cardiac tamponade is consistent with an inspiratory decrease in left ventricular compliance.

Controlled Reperfusion Following Regional Ischemia

The ability to reverse acute coronary occlusion with fibrinolytic agents and percutaneous transluminal angioplasty has increased interest in the revascularization of ischemic myocardium. This study defines changes in global ventricular function, mass, and compliance during acute coronary occlusion and following reperfusion with blood in the beating and arrested heart. In 17 dogs on cardiopulmonary bypass, the proximal left anterior descending coronary artery was occluded for 45 minutes. In 12 dogs, flow was reestablished by releasing the coronary snare in the beating heart. In the other 5 dogs, the snare was released during a continuous 10-minute infusion of blood potassium cardioplegia in the arrested heart. Coronary occlusion resulted in significant decreases in stroke work index and left ventricular (LV) mass, but compliance was unchanged. Reperfusion in the beating heart increased LV mass compared with the values measured before ischemia (104 ± 5 versus 95 ± 5 gm; p < 0.05) and decreased LV compliance (39 ± 4 versus 53 ± 4 ml at LV end-diastolic pressure of 8 mm Hg; p < 0.05). In contrast, with blood cardioplegia-based reperfusion in the arrested heart, LV mass and LV compliance remained unchanged from control values. We conclude that revascularization of acutely ischemic myocardium in the beating heart further impairs LV function by increasing LV mass and decreasing compliance. This damage can be avoided by reperfusion with blood cardioplegia in the arrested heart.

Assisted Ventilation in Patients with Preexisting Cardiopulmonary Disease: The Effect on Systemic Oxygen Consumption, Oxygen Transport, and Tissue Perfusion Variables

We have evaluated systemic oxygen consumption (VO2), systemic oxygen transport, and tissue perfusion variables in 30 patients with preexisting cardiac and underlying pulmonary disease during continuous positive-pressure ventilation and positive end-expiratory pressure [PEEP], during intermittent mandatory ventilation (IMV and PEEP), and during spontaneous ventilation (continuous positive airway pressure [CPAP]), with end-expiratory pressure held constant during all ventilatory modes. Using radionuclide angiography together with invasive determinations of pressure and flow, we also measured left and right ventricular ejection fractions and calculated the end-systolic (ESVI) and end-diastolic (EDVI) volume indices of both ventricles. We found that oxygen transport was significantly greater during CPAP (583 +/- 172 ml/min/M2)(mean +/- SD) than during either IMV and PEEP (543 +/- 151 ml/min/sq; p less than 0.01) or CPPV and PEEP (526 +/- 159 ml/min/M2; p less than 0.01); however, we found no significant change in systemic VO2 with conversion from CPPV and PEEP to CPAP. The increase in oxygen transport was related to a greater cardiac index and, more specifically, to a higher heart rate during CPAP (CPAP, 106 +/- 16 beats per minute; CPPV and PEEP, 97 +/- 14 beats per minute) (p less than 0.01). Enhanced oxygen transport during CPAP was also associated with an increase in mixed venous oxygenation and a decrease in arterial lactate. Although neither the mean left ventricular EDVI nor ESVI changed from CPPV and PEEP to CPAP, the mean pulmonary capillary wedge pressure increased (CPPV and PEEP, 12 +/- 5 mm Hg; CPAP, 14 +/- 7 mm Hg) (p less than 0.01), suggesting the possibility of a decrease in left ventricular compliance with the spontaneous ventilatory mode. This study suggests that in the absence of ventilatory failure, spontaneous ventilation provides for better systemic oxygen transport and overall tissue perfusion than either controlled ventilation or IMV; however, this benefit of enhanced oxygen delivery with spontaneous ventilation may potentially be offset by a decrease in left ventricular compliance.