The relation between left ventricular wall stress shortening and preload changes in ventilated patients

In reply Sir: With regard to our study on the left ventricular stress-shortening relationship [1], Dr Kolev suggests a formula for calculating left ventricular end-systolic wall stress (ESWS) that appears to be different from the one that we used in our study. He also makes a comment on various methods for the determination of left ventricular ejection time (LVET). The original formula for ESWS derives from experimental work by Sandler and Dodge [2]. With the introduction of M-mode echocardiography into clinical practice, this formula was adapted by Grossman [3] and Reichek [4] for uni-dimensional measurements of cardiac structures. Recalculation of the formula for a two-dimensional approach using cardiac cross-sectional areas rather than diameters yields the formula (1,33 × SAP × ESA)/(ESTA-ESA), with SAP = systolic arterial pressure, ESA = end-systolic area, and (ESTA-ESA) represents the cross-sectional myocardial area. The formula was validated in several studies [5,6] and used in the same format in our investigation [1]. It has the advantage that 2D-echo area measurements for estimating myocardial mass and ventricular cavity provide spatial information and errors in measurement are not potentiated by calculation. In contrast, with the formula proposed by Kolev, uni-dimensional instead of 2D-measurements are considered, and small errors e.g. in the measurement of left ventricular end-systolic wall thickness (h) will be magnified by multiplication. A major disadvantage of 2D-echocardiography is that it does not allow for exact timing of cardiac events due to the low frame of real-time echographic or video images. This leads to inaccuracy in the measurement of systolic time intervals, e.g. LVET, and I thank Dr Kolev for his comment. Any error in LVET determination potentially increases the confidence limits of the relation between wall stress and fibre shortening and adds to the scatter of the stress-velocity data. Inaccuracy may increase with rising heart rate, as 2D-echo timing of end-systole and end-diastole becomes less precise, while heart-rate correction of circumferential fibre shortening may compensate for it to some extent. In our study, the inaccuracy in LVET may explain the only moderate correlation of the stress-velocity data in our patient groups, but the method was sufficient to establish a significant linear stress-velocity relation that responded to changes in myocardial contractility. The sensitivity of this approach to clinically relevant changes in myocardial contractility is unclear, as we stressed in the discussion, and amongst others may be limited by LVET determination. C. A. GREIM Klinik für Anaesthesiologie der Universität Würzburg, Würzburg, Germany