Joseph P. Hart

Echocardiographic analysis of ventricular geometry and function during repair of congenital septal defects

BACKGROUND This study investigated changes in left ventricular (LV) geometry and systolic function after corrective surgery for atrial (ASD) and ventricular septal defects (VSD). METHODS Transesophageal LV short-axis echocardiograms were recorded before and after operative repair of ASD (n = 11) and VSD (n = 7). Preload was measured using LV end-diastolic area indexed for body surface area. Measurements of septal-freewall (D1) and anterior-posterior (D2) endocardial diameters were used to assess LV symmetry from D1/D2. Systolic indices included stroke area, area ejection fraction, and fractional shortening. RESULTS Preload, stroke area, area ejection fraction, and fractional shortening of D1 increased after ASD repair but decreased after VSD repair (p < 0.05). End-diastolic symmetry increased after ASD closure and decreased after VSD closure (p < 0.05). Increases in stroke area and ejection fraction after ASD correction primarily reflected increased shortening of D1. A positive correlation was found overall between percent change in end-diastolic area (EDA) and percent change in area ejection fraction (r(2) = 0.80, p < 0.0001, n = 18). CONCLUSIONS Preload was the primary determinant of changes in LV function in this series of ASD and VSD repairs. Intraoperative changes in position of the interventricular septum affected systolic and diastolic LV symmetry and septal free wall shortening. Additional studies are needed to define changes in afterload and contractility as well as diastolic compliance and systolic mechanics.

Coronary perfusate composition influences diastolic properties, myocardial water content, and histologic characteristics of the rat left ventricle

BACKGROUND Recent studies found that edema, histology, and left ventricular diastolic compliance exhibit quantitative relationships in rats. Edema due to low osmolarity coronary perfusates increases myocardial water content and histologic edema score and decreases left ventricular filling. The present study examined effects of perfusate osmolarity and chemical composition on rat hearts. METHODS Arrested American Cancer Institute (ACI) rat hearts (4 degrees C) were perfused with different cardioplegia solutions, including Plegisol (289 mOsm/L), dilute Plegisol (172 mOsm/L), Stanford solution (409 mOsm/L), and University of Wisconsin solution (315 mOsm/L). Controls had blood perfusion (310 mOsm/L). Postmortem left ventricular pressure-volume curves and myocardial water content were measured. After glutaraldehyde or formalin fixation, dehydration, and paraffin embedding, edema was graded subjectively. RESULTS Myocardial water content reflected perfusate osmolarity, being lowest in Stanford and University of Wisconsin solutions (p<0.05 versus other groups) and highest in dilute Plegisol (p<0.05). Left ventricular filling volumes were smallest in dilute Plegisol and Plegisol (p<0.05). Osmolarity was not a major determinant of myocardial edema grade, which was highest with University of Wisconsin solution and dilute Plegisol (p<0.05 versus other groups). CONCLUSIONS Perfusate osmolarity determined myocardial water content and left ventricular filling volume. However, perfusate chemical composition influenced the histologic appearance of edema. Pathologic grading of edema can be influenced by factors other than osmolarity alone.

Validation of left ventricular end-diastolic volume from stroke volume and ejection fraction.

The present study examines an innovative approach to measurement of left ventricular (LV) end-diastolic volume (LVEDV). Measurement of LVEDV is fundamental to the assessment of intraoperative systolic and diastolic LV function. We compared steady state LVEDV values obtained from stroke volume (SV) and ejection fraction (EF) with echocardiographic and postmortem LVEDV measurements. Five anesthetized pigs (40–45 kg) underwent median sternotomy and pericardiotomy. A transit time ultrasonic flow probe was placed on the ascending aorta to provide cardiac output. A micromanometer provided LV end-diastolic pressure. LV short axis cross sectional echocardiograms and electrocardiograms were also obtained. LV end-diastolic area (LVEDA) and end-systolic area (LVESA) were measured to obtain EF. LVEDVsv/ef was calculated from cardiac output, heart rate, and EF. LVEDVecho was determined using a three-plane echocardiography model. Postmortem (LVEDVpmlvv) volumes were also measured. LVEDVsv/ef correlated well with volumes obtained by echocardiography (r2 = 0.92) and postmortem (r2 = 0.73) measurements. Values of p < 0.05 indicated significant linearity of LVEDA-LVEDVsv/ef (r2 =0.93), LVEDA-LVEDVecho (r2 = 0.96), and LVEDA-LVEDVpmlvv (r2 = 0.81) relationships. Determination of LVEDV from SV and EF is valid and may facilitate real-time determination of LV mechanics

Aortic regurgitation in the heterotopic rat heart transplant: effect on ventricular remodeling and diastolic function

OBJECTIVES Use of the heterotopic rat cardiac isograft model is limited by ventricular atrophy attributable to the left ventricles non-working state. Previous studies indicate that increased left ventricular pressure-volume work minimizes atrophy. We used a simpler approach to increase ventricular work, imposing aortic regurgitation on the transplant. We hypothesized that this would prevent atrophy and preserve left ventricular compliance. METHODS We analyzed heterotopic transplants with aortic valvotomy and without aortic valvotomy (controls). Recipient native hearts served as separate controls. After 15 to 25 days, we measured cardiac wet weight, dry weight, and water content of all groups and measured echocardiographic left ventricular wall thickness and end-diastolic and end-systolic diameters in both transplant groups. Left ventricular volume infusions yielded pressure-volume data that we analyzed using regression methods. RESULTS Aortic regurgitant transplants weighed more than control transplants (dry weight, 0.109 +/- 0.013 g vs 0.097 +/- 0.016 g; p = 0.020, 2-way analysis of variance), but all transplants weighed less than native hearts weighed (p = 0.001). Control transplants were less compliant than regurgitant transplants (p = 0.002), but the latter were similar to their own native hearts (p = 0.34). Wall thickness decreased in regurgitant vs control transplants (p = 0.020, Students t-test), but end-diastolic and end-systolic diameters increased (p < or = 0.001). CONCLUSIONS Aortic regurgitation in heterotopic transplants improves left ventricular compliance through chamber dilatation without preventing atrophy. Moderate acute aortic regurgitation affects ventricular remodeling more than it stimulates myocardial hypertrophy. Smaller end-diastolic diameter, greater wall thickness, and myocardial edema may explain decreased compliance in non-working transplants.

Experimental transplantationAortic regurgitation in the heterotopic rat heart transplant: effect on ventricular remodeling and diastolic function☆

OBJECTIVES Use of the heterotopic rat cardiac isograft model is limited by ventricular atrophy attributable to the left ventricles non-working state. Previous studies indicate that increased left ventricular pressure-volume work minimizes atrophy. We used a simpler approach to increase ventricular work, imposing aortic regurgitation on the transplant. We hypothesized that this would prevent atrophy and preserve left ventricular compliance. METHODS We analyzed heterotopic transplants with aortic valvotomy and without aortic valvotomy (controls). Recipient native hearts served as separate controls. After 15 to 25 days, we measured cardiac wet weight, dry weight, and water content of all groups and measured echocardiographic left ventricular wall thickness and end-diastolic and end-systolic diameters in both transplant groups. Left ventricular volume infusions yielded pressure-volume data that we analyzed using regression methods. RESULTS Aortic regurgitant transplants weighed more than control transplants (dry weight, 0.109 +/- 0.013 g vs 0.097 +/- 0.016 g; p = 0.020, 2-way analysis of variance), but all transplants weighed less than native hearts weighed (p = 0.001). Control transplants were less compliant than regurgitant transplants (p = 0.002), but the latter were similar to their own native hearts (p = 0.34). Wall thickness decreased in regurgitant vs control transplants (p = 0.020, Students t-test), but end-diastolic and end-systolic diameters increased (p < or = 0.001). CONCLUSIONS Aortic regurgitation in heterotopic transplants improves left ventricular compliance through chamber dilatation without preventing atrophy. Moderate acute aortic regurgitation affects ventricular remodeling more than it stimulates myocardial hypertrophy. Smaller end-diastolic diameter, greater wall thickness, and myocardial edema may explain decreased compliance in non-working transplants.

Conductance artifacts in a novel in vitro model of ventriculothoracic electrical coupling.

The utility of open chest conductance (COND) ventriculography is limited by artifacts altering the relationship between COND and left ventricular (LV) volume. Pressure-COND loops often lean to the left during LV volume reduction by caval occlusion. Time varying alterations in the pericardial-LV contact area affect electrical coupling in the open chest during the cardiac cycle, producing COND artifacts. In this study, an open-mediastinum model was constructed. Components represented the LV, blood, pericardium, and thoracic contents. Varying ventriculothoracic coupling was simulated by changing the volume of pericardial saline (0, 30, 60 ml). Raw dual field COND was repeatedly (n = 20) compared with volumes of normal saline from 60 to 120 ml at 5 ml intervals. Groups were compared by linear regression and repeated measures ANOVA. Artifacts significantly (p < 0.01) altered parallel COND, indicated by the y-intercept, with the exception of 0 versus 30 ml. The slope constant also changed significantly, with the exception of 30 versus 60 ml. These results suggest that variable pericardial-LV contact can cause time varying artifacts in COND in the open chest. Therefore, posterior insulation may reduce artifacts in COND ventriculography and should be tested for this effect.

Intraoperative Echocardiography: Interpretation of Changes in Left Ventricular Wall Thickness

Quantitative two-dimensional echocardiography (Q2-DE) may be used to detect intraoperative changes in left ventricular (LV) mass (M) and wall thickness (h). Potential causes of change in h include physiological redistribution of myocardium, myocardial edema, reactive hyperemia, and intramyocardial hemorrhage. Changes in h, in the absence of changes in LV shape and volume, generally indicate increased LVM. When changes in h are accompanied by changes in shape or volume, changes in LVM can only be detected by mathematical modeling, unless the direction of the observed changes is opposite that expected with physiological redistribution. Histological observations essential to understanding current mathematical models are presented and related to the inherent solid geometry. Technical considerations in determination of LV mass by Q2-DE are discussed. New procedures that alter LV volume and geometry, such as the Batista operation, defy modeling by conventional methods. Modeling techniques that allow an experimental approach to understanding LVM and h under such conditions are presented.