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Institute for Surgical Research and Department of Cardiology, Rikshospitalet University Hospital, Oslo, Norway
Submitted 10 September 2004 ; accepted in final form 30 December 2004
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ABSTRACT |
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sonomicrometry; pressure-strain loop
The aim of this study was to investigate if SDE can be used to construct LV pressure-strain loops and if the area of the pressure-strain loop can be used as an index of regional myocardial work (RMW). As a reference method, we used pressure-segment length loops that were constructed from pressure and implanted sonomicrometric crystals.
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METHODS |
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Pressure Measurements
A 5-Fr micromanometer-tipped catheter (model MPC-500, Millar Instruments; Houston, TX) was positioned in the LV through a carotid artery. Via the appendage, a 5-Fr micromanometer and a fluid-filled catheter were placed in the left atrium. All pressure transducers were calibrated with a mercury manometer. The pressures were zero referenced against the fluid-filled left atrial catheter. Pressure and ECG data were processed via preamplifiers and were digitized at 200 Hz for further analysis on a personal computer workstation.
Sonomicrometry
One pair of ultrasonic crystals was implanted in the inner half of the anterior LV wall near the apex and aligned parallel with the LV long axis (Fig. 1). The crystals were connected to a sonomicrometer (Sonometrics; London, Ontario, Canada), and the crystal data were digitized at 200 Hz for further analysis on a personal computer workstation.
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The method has previously been described in detail (18). Using a Vivid FiVe (GE Vingmed Ultrasound; Horten, Norway) scanner with a 3.5-MHz phased array transducer, we recorded tissue Doppler images from an apical view with a frame rate of 132 frames/s. Pulse repetition frequency was adjusted to avoid aliasing.
Calculations
Pressure-derived variables. We calculated LV peak systolic pressure, LV end-diastolic pressure, and the time derivative of LV pressure (dP/dt). The peak R wave of the ECG was used for defining end diastole, and end systole was defined 20 ms before peak negative LV dP/dt.
Sonomicrometry-derived variables.
By calculating the instantaneous length as a percentage of end-diastolic length, we obtained strain throughout the cardiac cycle, and on this trace we measured peak negative systolic strain (%
L). During ischemia, there was systolic lengthening, and we report peak positive strain.
%L was defined as
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L was defined as
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Tissue Doppler echocardiography.
Longitudinal shortening by SDE, evaluated as segmental strain, was calculated offline. Strain rate (SR) color-coded images were generated from tissue Doppler images by calculating the velocity differences at positions 8 mm apart. From the SR data, segmental strain [e = (L – L0)/L0] (where Lo is the initial length and L is the instantaneous length) was estimated as e = exp(
SRdt) – 1 (5, 18). For the purpose of this study, strain measurements were done only in the myocardial segment in which we had ultrasonic crystals. Peak systolic strains were calculated in percentage of end-diastolic dimensions. By definition, shortening strains were represented by negative values and lengthening strains by positive values.
Pressure-strain loops. Strain by sonomicrometry, strain by Doppler echocardiography, and LV pressures were exported to Matlab version 6.0 (Mathworks). The drift often seen in strain curves from SDE was adjusted for by forcing the strain at the end of the cardiac cycle to zero. This was done by assuming that the original strain curve drifted equally much during each time step of the cardiac cycle. Finally, the strain by SDE was interpolated at 200 Hz equally to the sampling frequency of LV pressure and strain by sonomicrometry. The strain and pressure curves were then transformed to CVSOFT (Odessa Computers; Calgary, Ontario, Canada) for further analysis. Pressure-strain loops were constructed, and RMW was calculated as the loop area. The strain values used in the calculation of loop area were expressed as fractional strains. The unit of the RMW index was converted from mmHg to kJ/m3 (1 mmHg = 133.4 N/m2 = 0.1334 kJ/m3).
By convention, the loop area was assigned a positive sign (i.e., active work) when the pressure-strain coordinates rotated counterclockwise and a negative sign when the rotation was clockwise.
Experimental Protocol
In six dogs after baseline recordings, we increased stroke volume by flushing 500 to 1,000 ml saline into a central vein to increase LV end-diastolic pressure by 
10 mmHg. After the return of end-diastolic pressure to baseline values, the LAD was occluded, and recordings were performed 1 min after the onset of occlusion. One baseline recording and one recording during short-term ischemia were not analyzed because of poor quality of the sonomicrometry trace. In four additional dogs, we induced long-term ischemia by occluding the LAD for 180 min.
In each experiment, we confirmed the location of the ultrasonic crystals within the ischemic zone by demonstrating systolic segmental lengthening during LAD occlusion.
Because of interference between sonomicrometry and Doppler echocardiography, we first recorded pressures, ECG, and echocardiographic data during 10 s and then pressures, ECG, and sonomicrometry during the subsequent 10 s. Data were recorded with the respirator off.
Statistics
Data are presented as mean ± SE. Differences between groups were analyzed with the Friedman test for related data. Paired data were analyzed with Student's t-test. The RMW values obtained by the two different methods (sonomicrometry and SDE) were compared by regression analysis using a least-squares method. For all statistical comparisons, P < 0.05 was considered significant.
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RESULTS |
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DISCUSSION |
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Stress Versus Pressure
Measurement of RMW requires simultaneous measurement of regional wall stress (force) and dimension, and regional work equals the product of developed stress and change in dimension or, more accurately, the integral of the stress-dimension loop. Regional myocardial wall stress equals force per unit cross-sectional area and can be calculated from measurements of LV transmural pressure, wall thickness, and local radius of curvature. The measurement of all these variables requires complex methodologies, and one needs to make a number of assumptions regarding local geometry. At present, there are no reliable clinical methods to measure regional ventricular wall stress directly.
In the present study, we used LV intracavitary pressure as a substitute for regional wall stress. Skulstad et al. (16) compared LV pressure-segment length loops to stress-segment length loops in a model similar to that used in the present study. Their interpretations regarding active and passive contributions to regional segmental shortening were qualitatively similar for the two approaches, supporting that the pressure-strain loop reflects regional work. These findings are consistent with the study of Goto et al. (4), which assessed RMW in an experimental model from wall tension-area loops and demonstrated that this measure of regional work was valid also during regional myocardial ischemia.
Although the area of the pressure-strain loop is an index rather than a direct measure of regional work, it has the advantage of being relatively simple to obtain during cardiac catheterization in a clinical setting.
Nakano et al. (12) introduced an alternative clinical method for calculating regional stress-strain loops from the relationship between mean wall stress and the natural logarithm of the reciprocal of wall thickness. In patients with ischemic myocardium, they found that the area of the ischemic loops were reduced (11).
Potential Applications of Pressure-Strain Analysis
In the present study, the orientation of the pressure-strain loop was used to differentiate between actively contracting and passive myocardium. A hallmark of actively contracting myocardium is that the segment shortens during systole when LV pressure is rising, whereas passive myocardium lengthens when pressure is rising. Furthermore, passive myocardium shortens during isovolumic relaxation when LV pressure is falling. This implies that an active pressure-strain loop rotates counterclockwise. On the other hand, an entirely passive myocardial segment moves essentially up and down along the same curve or, rather, in a clockwise fashion due to slight hysteresis caused by viscoelastic forces. This implies that the direction of rotation of the pressure-strain loop provides information regarding active and passive contributions to regional myocardial deformation and motion. Because the demonstration of active contraction implies viable myocardium, the pressure-strain loop might have potential as a method to differentiate between viable and nonviable myocardium.
In the present study, ischemia resulted in severe myocardial dysfunction with passive systolic lengthening of the segment. Although systolic lengthening implies that the myocardium behaves as a net passive structure, it does not rule out active contributions. The direction of rotation of the loop needs to be taken into account to differentiate between active and passive segments. This principle was demonstrated during short-term ischemia (Fig. 2), which caused the myocardial segment to lengthen during early systole while the pressure-segment length loop rotated counterclockwise, indicating some degree of active contraction. However, during long-term ischemia, the pressure-strain loop (Fig. 3) rotated clockwise and therefore was entirely passive. In a clinical context in patients with coronary artery disease, it is possible that a similar loop analysis may serve as a method to identify viable myocardium. This, however, remains to be determined in clinical studies.
The pressure-strain loop analysis may give us insight into how different therapeutic principles modify myocardial function and how interventions like ventricular pacing changes regional work at the pacing site (13).
Regional contractility calculated as the slope of the end-systolic pressure-segment length relationship (6, 9) has been proposed as a measure of regional myocardial function. Krams et al. (6) reported in an animal study reduction of regional elastance in stunned myocardium. Elastance would be a more direct measure of regional contractility than present methods and, importantly, is expected to be less load dependent. With further refinement of the SDE method, it may be feasible to measure multiple strain loops and LV pressure continuously and thereby calculate regional elastance.
Because the pressure-strain analysis requires invasive pressure, its potential role would be to serve as a supplementary modality during LV catheterization. In principle, however, it may be possible to estimate LV systolic pressure from noninvasive arterial pressure and to estimate regional work as the product of systolic pressure and peak systolic strain. This approach would have several limitations but would have the advantage of being entirely noninvasive.
Limitations
An important limitation of the SDE method is the marked angle dependency (18). Correct orientation of the ultrasound beam relative to the myocardial wall is critical for the application of this imaging modality. The strain curve by Doppler echocardiography was not obtained simultaneously with strain by sonomicrometry and LV pressure. However, the recordings were performed within 20 s with the respirator off, during a stable hemodynamic situation.
The use of LV pressure as a substitute for LV wall stress may lead to errors in ventricles with marked changes in local geometry. However, as demonstrated by others (4, 16), during acute ischemia this does not seem to be a major problem. Another limitation is related to the tendency of strain estimates by SDE to drift throughout one cardiac cycle, and the algorithm that was used to compensate for drifting may introduce errors. However, the most important application of this method would not be the absolute calculated area but relative changes of one region during different interventions and to determine the orientation of the loop as counterclockwise or clockwise.
A fundamental limitation of pressure-strain loops as an approach to define anatomic extension of ischemic dysfunction is related to tethering. Segmental shortening may be markedly impaired in nonischemic myocardium immediately adjacent to the ischemic region, and therefore the size of the ischemic region may be overestimated (8).
In conclusion, an estimate of RMW can be obtained by SDE in combination with LV pressure. The method can discriminate between active and passive segments by taking into account the orientation of the loops. This approach should be tested clinically and could represent a new method for the assessment of myocardial tissue viability during invasive studies.
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GRANTS |
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
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This article has been cited by other articles:
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  B. Bijnens, P. Claus, F. Weidemann, J. Strotmann, and G. R. Sutherland Investigating Cardiac Function Using Motion and Deformation Analysis in the Setting of Coronary Artery Disease Circulation, November 20, 2007; 116(21): 2453 - 2464. [Full Text] [PDF]
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, End diastole; 
, end systole. During volume loading, the area of the loops increases, indicating that more work is performed by the segments. With ischemia, the area of the loops decreases. Rotation of the ischemic loops is still counterclockwise, indicating that work is performed by the ischemic segment.
