The load dependence of the myocardial performance index in congenital heart disease has been evaluated. No significant change was found before or after surgical correction of atrial septal defect (right ventricular preload), pulmonic stenosis (right ventricular afterload), or congenitally corrected transposition of the great vessels (right ventricular preload and afterload).1Acute changes in myocardial performance index with manipulation of preload/afterload have been demonstrated in adult volunteers with healthy hearts—to Valsalva maneuver, leg lifting, and nitroglycerine administration. However, the patients in this study with previous myocardial infarction and abnormal ventricular function did not exhibit any changes in myocardial performance index.2 

Doppler tissue imaging has load dependence3,4but has been demonstrated to be more independent of preload than conventional Doppler measures of mitral inflow.5,6In addition, in patients with ventricular dysfunction, changes in preload affect Doppler tissue imaging velocities much less and correlate well with invasive measures of left ventricular diastolic pressure.6Significant increases in afterload seen in patients with aortic stenosis do decrease Doppler tissue imaging velocity.7However, no significant impact on Doppler tissue imaging velocities of increased left ventricular preload with ventricular septal defects was noted.

With regard to the loading conditions for the patients in our current study,8preload was not specifically assessed, largely because of the inability to use conventional methods to compute left ventricular end-diastolic volume, because of the irregular geometry of the functional single ventricle. Central venous pressure, a rough estimate of preload, was not changed with either of the two anesthetic levels with the two regimens we studied. In a previous study of two-ventricle patients with congenital heart disease, we demonstrated that neither fentanyl-midazolam nor sevoflurane, in doses similar to those used in the current study, had any effect on left ventricular end-diastolic volume measured by the biplane method of Simpson.9In the same previous study, neither fentanyl-midazolam nor sevoflurane changed systemic vascular resistance index, calculated echocardiographically. In the current study, we did not specifically calculate systemic vascular resistance index because the patients had a functional single ventricle, and systemic and pulmonary blood flow both occurred in the aorta of most patients, so the conventional concept of systemic vascular resistance did not apply. However, if one was to calculate a combined systemic and pulmonary vascular resistance index in the patients of our current study, by dividing the difference between mean arterial pressure and central venous pressure (assuming no change in central venous pressure from baseline) by the aortic or neoaortic outflow, there is no change in systemic and pulmonary vascular resistance index with fentanyl-midazolam but a significant decrease with sevoflurane at both anesthetic levels (table 1).

Table 1. Combined Systemic and Pulmonary Vascular Resistance Index 

Table 1. Combined Systemic and Pulmonary Vascular Resistance Index 
Table 1. Combined Systemic and Pulmonary Vascular Resistance Index 

Therefore, the changes in loading conditions induced by the anesthetic regimens for congenital heart disease can be estimated to be no change with fentanyl-midazolam and a 17% decrease in afterload with sevoflurane.

Although we agree with the caution of Drs. Poelaert and Amà to consider changes in loading conditions and other pathophysiologic factors when performing and interpreting echocardiographic studies assessing response to anesthetics, we believe our conclusions are valid for single-ventricle infants. Myocardial performance index in particular represents an appropriate method to assess myocardial function in patients with abnormal ventricular geometry, such as those with a functional single ventricle.

* Baylor College of Medicine/Texas Children's Hospital, Houston, Texas.

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