Regional myocardial asynchrony, characterized by regional wall motion abnormalities (RWMA) commonly occur; however, their impact on global left ventricular (LV) performance has not been quantified. This is caused in part by difficulties in modeling RWMA as they impact on regional contraction relative to total LV contraction. A major problem with modeling RWMA reflects uncertainties in determining regional end-systole in heterogeneously contracting myocardium and assessing their impact on global LV performance. Previously, Fourier analysis was used to quantitate regional myocardial dysfunction (1,2). By using this analysis, a temporal Fourier transform is applied to the time-activity curves of various digitized ventriculograms, and the phase and amplitude information is used to describe regional wall motion. Unfortunately, this method is limited because it is computationally complex, fails to define regional contraction relative to global ventricular ejection, fails to combine temporal and spatial dysfunction as a single index, and is difficult to apply at bedside (3). Other measures of myocardial dysfunction have been either insensitive to regional dysfunction or limited by the “semiquantitative” nature of their analyses using subjective visual imaging techniques (4).
RWMA are common in patients during normal (5–7) and abnormal (8–10) cardiac physiology. RWMA are monitored intraoperatively to detect regional myocardial ischemia (11–13). If an easy to use, quantitative measure of regional myocardial dysfunction could be developed, it would minimize subjective bias in the diagnosis of myocardial ischemia (4,14,15) and might aid in the evaluation of treatments and titration of therapies used to restore regional myocardial function.
We reasoned that decreases in LV ejection can be produced not only by decreased regional stroke volume (SV), but also by asynchronously contracting regions (16). We hypothesized that the impact of RWMA on global LV ejection could be quantified by analysis of the phase relationship among regions of asynchronously contracting myocardium relative to global LV contraction. Such regional phase angle analysis may permit measurement of effective regional SVs (that portion of the regional SV in phase with and contributing to the total LV SV). Accordingly, we developed and tested models for detecting and quantitating RWMA in the heterogeneously contracting LV. To quantify regional asynchrony, we measured the regional phase angle of contraction, defined as that point during the cardiac cycle where regional volume was minimal relative to minimal total LV volume. We divided the cardiac cycle into 360° and defined delayed regional contraction relative to either the R wave of the electrocardiogram (ECG) or the minimal total (global) LV volume. To assess this methodology, we measured effective regional SVs in a canine preparation with stable but reversible RWMA induced by the subselective coronary arterial bolus infusion of esmolol.
After approval of our Animal Care and Use Committee, we studied eight mongrel dogs (24.6 ± 0.5 kg, mean ± SEM). Anesthesia was induced with IV morphine sulfate (0.5 mg/kg) and sodium pentobarbital (30 mg/kg) and was maintained with a continuous infusion of sodium pentobarbital (1.0 mg · kg−1 · hr−1) with intermittent boluses if needed for light anesthesia and a maintenance infusion of 0.9% NaCl at 100 mL/hr. All animals had their trachea intubated, and their lungs were ventilated with 100% oxygen. Blood gas tensions were measured before and after the experimental protocol and more frequently if hemodynamic instability developed. Acid-base status was adjusted with intermittent boluses of bicarbonate solution, as needed, to maintain arterial blood pH between 7.35 and 7.45, and the ventilator was adjusted to maintain arterial blood PCO2 between 35 and 45 mm Hg. Neuromuscular blockade was established with IV boluses of pancuronium (1.0 mg IV as needed). Body temperature was maintained at 36° to 38°C by using a thermostatically controlled heating blanket.
A fluid-filled arterial catheter with multiple side holes was inserted into the thoracic aorta via the left femoral artery to measure arterial pressure. A double-lumen, 12F catheter was inserted into the left external jugular vein to administer IV fluids. A 7.5F, balloon-tipped pulmonary artery catheter (List #5328, Model #P7110-EP8-H, 9510 animal model; Baxter-Edwards, Santa Ana, CA) was introduced through the right external jugular vein. To measure LV volume on a continuous basis, a 6F, 11-pole, multi-electrode, dual-excitation conductance catheter (Webster Laboratories, Irvine, CA) was inserted through the aortic valve and into the LV via the right internal carotid artery. Positioning of the conductance catheter was verified by both fluoroscopy and repeated inspection of the regional volume signals with respect to time.
A thoracotomy was performed through the left fourth intercostal space and a pericardotomy was performed over the anterior surface of the heart. To administer intracoronary esmolol, a 22-gauge, 1.25-in. IV catheter was placed into the left anterior descending (LAD) coronary artery. The catheter was heparin-locked to prevent thrombus formation, and care was taken to prevent air embolism. Two independent pairs of piezoelectric dimension crystals (Triton, San Diego, CA) were introduced into two different coronary artery perfusion zones. Both pairs of crystals were aligned parallel with the horizontal hoop fibers of the LV. The crystals were inserted by using rubber bumpers to a depth of 1.0 to 1.5 mm. The crystals of each pair were positioned 1 cm apart. To document regional dysfunction, one pair of crystals was positioned in the LAD coronary arterial perfusion zone distal to the insertion of the 22-gauge catheter (near the left ventricular apex). To document function of normal myocardium, a second pair of control crystals was inserted in the perfusion zone of the left circumflex coronary artery.
A 5F, high-fidelity pressure transducer (Millar Micro-tip catheter model SPC-350; Millar, Houston, TX) was inserted 2 cm through an apical puncture in the LV to record LV pressure. Immediately before termination of the experiment, 2 mL of 1% crystal violet dye was injected into the LAD coronary artery catheter to document the size of the perfusion zone. The dog was then killed, while still under general anesthesia, by using an IV injection of 10 mL of saturated KCl, and the heart was removed to document the position of the conductance catheter in the LV. The dyed area (LAD coronary artery perfusion zone) was dissected out and weighed postmortem. The remaining LV myocardium was dissected free and weighed.
Esmolol-Induced Regional Dysfunction
Nine milligrams of esmolol (10 mg/mL) was administered by bolus infusion for 3 s through the LAD catheter to produce transient pharmacological regional dysfunction, as confirmed in real time by observation of the associated regional pressure-dimension loop. After approximately 30 s, the bolus infusion of esmolol induced stable regional dysfunction lasting for at least 6 min. This dosage of esmolol was chosen because it induced selective regional myocardial paresis without measurable changes in either global cardiac function (heart rate or remote myocardial paresis) or systemic hemodynamic status (mean arterial pressure).
Regional myocardial function was compared both before (baseline), 3 to 5 min after the bolus infusion of esmolol (esmolol), and 20 min after the esmolol infusion (recovery). An example of the raw regional and global LV volume signals during baseline, esmolol, and recovery steps of the protocol are shown in Figure 1.
We recorded the following experimental variables: arterial blood pressure, LV pressure, LV dP/dt, intercrystal dimensions for the piezoelectric crystals, total and regional LV conductance (volume), and lead II of the ECG. All data were recorded on an eight-channel physiologic recorder (Gould, Cleveland, OH). Additionally, all data were digitized and recorded on magnetic disc for subsequent analysis as described below.
Signals from the two pairs of sonomicrometer dimension crystals were processed simultaneously on two synchronized channels using a four-channel sonomicrometer (model 120; Triton). dP/dt was derived from the LV pressure signal by using a differentiator (Gould) with a 100-Hz high-cutoff and a 1-V/s slope. Signals were collected and processed with a conductance catheter data processor and signal conditioner (5DF; Leycom Sigma, Leyden, Netherlands). A four-electrode calibration chamber was used to determine blood conductivity (α value). Intermittent cardiac outputs were determined in triplicate using a 10-mL iced 0.9% saline bolus thermodilution technique (model 9520 cardiac output computer; Baxter-Edwards) as a guide to cross-reference the conductance catheter-derived stroke volume measures. The signal acquisition and analysis system consisted of an Apollo DN4000 Unix workstation (Hewlett-Packard, Palo Alto, CA) and a SignifiCAT® (Buffalo, NY) RTS-132 A/D subsystem. Regional myocardial function was recorded and analyzed as described below.
Calibration of the Conductance Catheter
The conductance catheter method for measuring ventricular volume has been described and validated previously (17,18). Briefly, a 20-kHz, constant-amplitude current of 30 μA RMS is passed between the electrodes of the distal and proximal extremes of the catheter in a dual-field format. An electrical field is generated within the ventricular cavity in which equipotential planes may be defined between each of the intervening electrodes at right angles to the long axis of the catheter. The volume of blood measured between any two sensing electrodes can be considered to be a disc with boundaries defined by the endothelial surfaces through to the electrodes. The change in conductance sensed during ventricular contraction in any one of these discs is caused by a change in resistance in the cross-sectional area of the disc. The sum of all such discs within a chamber reflects total chamber volume. Parallel conductance artifact was determined using the saline dilution method (19) of using 5 mL of 10 N saline injected into the right atrium.
The conductance catheter generated continuous regional volume with respect to time for each of four LV regions. Regional volume signals were then summed to derive total LV volume. Regional and total LV maximal and minimal volumes were determined as the averaged value for four consecutive cardiac cycles. Regional minimal and maximal volumes were defined as regional end-systole and end-diastole, respectively. The sonomicrometer signals generated similar continuous signals of length dimension with respect to time. Electrical systole was defined arbitrarily to occur at the R wave of the ECG.
To measure alterations in the phase of regional contraction independent of heart rate, we divided the cardiac cycle into 360° and defined global end-systole (minimal total volume) as 0°. Regional end-systolic phase angle (α) was defined as the relative distance, measured in degrees, that the regional minimal volume differs from global end-systole. Arbitrarily, regional phase delays were defined as positive values and phase advances as negative values. Additionally, regional end-systole and end-diastole were also defined relative to the R wave of the ECG that was designated 0°. We adopted a model of LV contraction that assumed that ejection approximates a sine wave and that the relative contribution of regional ejection to total LV ejection should equal the product of the maximal regional SV and the cosine of the phase angle α. If the region contracts synchronously with the total LV, then α = 0°, cosine α = 1, and all of the regional SV contributes to LV ejection. If the contracting region reaches its minimal volume either before or after total LV end-systole, then a proportion of its contraction equal to 1-cosine of this phase shift will not contribute to total LV ejection.
Because heart rate may change among treatments, we further characterized regional myocardial contraction independent of phase angle, by determining the systolic time interval of regional systole. The systolic time interval measures the duration of regional end-systole in ms from the R wave of the preceding QRS. We studied this measure because it reflects the effect of both phase delay and heart rate on regional contraction.
To quantify the contribution of regional SV to total LV ejection, we determined regional ejection by three different methods. Maximal SV was defined as the difference of the maximal and minimal regional volume (or segmental length) for each cardiac cycle independent of the phase of regional contraction. Observed effective SV was measured for each region using maximums and minimums of the total LV volume as gated markers of the time when regional contraction would contribute to total LV ejection. If regional systole is not synchronous with global systole, then part of the ejection of some regions may occur either before or after total end-ejection. Accordingly, not all of the regional SV may contribute to total LV SV. Finally, calculated effective SV was defined according to our model as the product of regional cosine α and the regional maximal SV as described above.
Stroke work was calculated as the area within the pressure-volume relation of the respective region or total volume signal and stroke force as the area within the pressure-length loops for the piezoelectric crystal data.
Phase shifts, maximal SVs, effective SVs, and end-diastolic volumes were compared among regions to the total SV and between experimental treatments by using repeated measures analysis of variance (20). Post hoc analysis was conducted with Tukey’s method when appropriate. All data were reported as mean ± SEM. Differences associated with a P value < 0.05 were considered significant.
Esmolol bolus infusion affected the apical regional myocardium, averaging 23% of the total LV mass (perfused zone 29.8 ± 2.63 g; left ventricle 127.9 ± 13.5 g). Intracoronary infusion of esmolol reduced mean arterial pressure (101.5 ± 3.5 to 94.2 ± 2.8 mm Hg) and LV systolic pressure (118.1 ± 2.8 to 109 ± 2.6 mm Hg) relative to both baseline and recovery values (P < 0.05). Intracoronary esmolol increased LV end-diastolic pressure (7.9 ± 0.9 to 10.4 ± 1.2 mm Hg) and increased minimal dP/dt (−2209 ± 88 to −1938 ± 105 mm Hg/s) (P < 0.05). Maximal dP/dt decreased during intracoronary esmolol (1804 ± 113 to 1584 ± 123 mm Hg/s) from baseline (P = 0.06) and increased in the recovery period (1584 ± 123 to 1855 ± 128 mm Hg/s) (P < 0.05). Heart rate was unchanged by esmolol bolus (132.6 ± 6.1 to 134.7 ± 3.9 bpm) but increased (132.6 ± 6.1 to 148.0 ± 3.6 bpm) (P < 0.05) in the recovery period. No other differences were seen between baseline and recovery values.
Phase Angles and Systolic Time Intervals
Esmolol was associated with increased heterogeneity of the phase angles of regional contraction (Table 1). Apical and papillary regional phase angles increased 10% to 16% relative to baseline (P < 0.05), whereas apical piezoelectric crystals displayed a 27% increase in the phase angle (P < 0.05). At the same time, the total LV phase angle relative to baseline using the R wave as 0° was unaffected by esmolol. Also unaffected were the phase angles for the uninvolved chordal and basal regional volume signals and uninvolved basal region piezoelectric crystals.
Esmolol increased apical and papillary mean regional systolic time intervals (P < 0.05), but did not change systolic time intervals in the uninvolved basal regions. The systolic time interval of the apical piezoelectric crystals also increased 25% (P < 0.05), whereas the basal region piezoelectric crystals systolic interval decreased insignificantly (4%, P = not significant). The systolic time interval for total LV volume remained unchanged from baseline to esmolol, but decreased 12% (an average 31 ms earlier) (P < 0.05) between esmolol and recovery associated with an increased heart rate.
Regional SV and Shortening
Estimates of regional SV varied among regions according to the method used to define regional end-systole and end-diastole (Table 1): regional maximal SVs were greater than regional observed effective SVs. Regional SV decreased in apical regions by 3% to 33%, depending on the method used to identify systole and diastole. At the same time, esmolol increased regional SV in uninvolved chordal and basal regions, with the latter increasing by 13% to 28%, depending on the measurement method.
Esmolol induced no significant change in any regional maximal SV (Table 1). When regional SVs were measured as effective SV, apical SV decreased and uninvolved chordal and basal SV increased (P < 0.05). Effective SV returned toward baseline values in the apical region during recovery. Both directly measured effective regional SV and calculated effective regional SV (Table 2) (calculated as the product of maximal SV and cosine α) for the apical region correlated well with each other (r = 0.98, P < 0.01, Fig. 2). Regional sonomicrometer signals correlated with their corresponding regional SV and similarly reached significance only when global SV or regional pressure-volume loops were used as gated markers of end-systole and end-diastole. Total LV SV increased (21% to 30%, P = not significant) during esmolol, but these changes did not reach significance with any of the methods used to determine end-systole and end-diastole.
Apical RWMA are shown in greater detail, for one representative dog in Figure 3. Not only is apical regional end-diastolic volume increased by esmolol but the rate of volume decrease during ejection is slower than either baseline or recovery and the region continues to eject after the remainder of the ventricle has begun relaxation. Recall that the time to total LV end-systole was not altered by esmolol. An alternative method of displaying these same data is shown as a polar plot (Fig. 4). In this presentation, esmolol is seen to not only increase the regional end-diastolic volume (circumference) relative to baseline and recovery, but also to rotate the end-systolic nadir or systolic hilus clockwise to approximately 280°. Analysis of uninvolved regions did not reveal any similar changes as seen in Figures 3 and 4.
Esmolol decreased apical regional stroke work (219 ± 33 to 170 ± 24 mm Hg/mL, P < 0.05) by using apical regional volume and reduced apical regional stroke force (132 ± 21 to 52 ± 13 mm Hg/mm, P < 0.05) when apical piezoelectric crystal segmental length was used. In all other regions, stroke work increased but did not reach statistical significance (P = not significant). Esmolol did not alter global LV stroke work.
This study demonstrates that effective regional SV and phase angle analyses are sensitive measures of regional LV dysfunction in an esmolol-induced model of RWMA. Furthermore, measures of regional or global LV contraction (such as maximal SV) that do not take into account such phase shifts may be insensitive. Finally, as previously described in patients with coronary artery disease (21), regional stroke work also appears to be a sensitive measure of regional dysfunction. In a contrasting study, regional maximal amplitude analysis was found to be more sensitive than regional phase angle analysis (22). These different conclusions reflect inconsistencies in the definitions of regional systole used by various authors. When only regional systole is gated by markers of total LV systole, regional amplitude changes can be detected as decreased regional amplitude. When regional maximal amplitude is measured, however, as in our study and that of Leighton et al. (23), then RWMA are not detected. Conceptually, this difference is important because, if regional dysfunction is associated with delayed shortening, it might be better characterized by phase angle analysis than with ungated regional amplitude analysis.
Application of phase angle analysis to assess regional myocardial function was previously described (24) using data from regional sonomicrometer thickness crystals in dogs by applying a temporal Fourier transform. Unfortunately, the data were not analyzed relative to markers of total LV systole. The phase shift between unaffected and affected regions, however, correlated strongly with regional thickening.
Previous attempts to quantify RWMA have included angiography, regional radionucleotide scans, regional sonomicrometry, and two-dimensional echocardiography. All of these methods have technical difficulties (25). Echocardiography has been the most widely used technology because it is affordable and portable, displays LV function in real time, and is minimally invasive. Some of the difficulty evaluating regional cardiac dysfunction using echocardiography can be explained by subjective estimates of RWMA independent of global end-systole. Because dysfunctional myocardium often continues to contract after global end-systole, the extent of regional dysfunction can be systematically underestimated.
Clinically, the application of conductance catheter technology, although feasible, reflects a highly invasive procedure and may not be widely applicable. However, we recently demonstrated (26) that echocardiographic techniques can be used to quantify regional SV in a similar fashion. The phase shift of regional shortening can be quantified by reference to total LV ejection. Because the calculated effective SV can be derived from our model as the product of total regional SV and the cosine of this phase shift (Fig. 4), this measure should be definable at the bedside. Thus, using tissue Doppler echocardiography, the clinical application of these concepts may be possible using surrogate markers of regional volume and global end-systole, such as echocardiographic measures of LV area and the dicrotic notch, respectively.
Parallel conductance artifact in conductance catheter signals may produce uncertainty in determining absolute volumes. We corrected for this by using the hypertonic saline calibration method and by the dual-field method of determining conductance (27), as we previously validated when we compared sonomicrometer crystals, echocardiographic area, and aortic flow probe data. 1 Furthermore, relative volume changes are accurate despite potential parallel conduction artifacts (18,29), and finally, our piezoelectric crystal data support our regional volume data and have none of these limitations. Previous investigators used piezoelectric crystals to study regional myocardial dysfunction (30) in vivo. Although accurate, crystals may estimate ventricular volumes poorly because they measure only a single dimension. Conductance catheters have been used to study regional myocardial function (31,32). Thus, the use of both piezoelectric crystal and conductance catheter-defined measures of contraction minimizes the limitations of each method.
Our analysis of RWMA assumed that the only asynchrony during contraction occurred among a series of stacked discs of myocardium arranged along the long axis of the LV. Thus, our phase angle analysis compared regional volume changes among these regions. As the ultrasonic crystal data demonstrate, segmental regions of the myocardium directly altered by esmolol infusion become profoundly dysfunctional and are less well represented by larger regional volume measures. Clearly, further refinements of regional wall motion analysis with respect to global systole will require simultaneous analysis of much smaller regions of the myocardium, both along and across the ventricular walls. However, this study serves to define a methodology for measuring asynchrony among regions of the myocardium and to demonstrate its relevance in quantifying regional contraction asynchrony and the importance that RWMAs have in reducing the overall effectiveness of ventricular systolic function.
β-adrenergic blocking drugs, such as esmolol, may induce systemic negative chronotropic effects on heart rate in addition to regional dysfunction. The regional phase shifts we observed could have been caused by systemic chronotropic effects rather than by regional dysfunction per se. This is unlikely, however, because neither heart rate nor regional systolic time intervals in control regions were affected by intracoronary esmolol administration. It can be argued that esmolol failed to induce sufficient LV dysfunction to be measured. This also seems unlikely, however, because intracoronary esmolol decreased mean arterial pressure and maximal LV dP/dt and increased end-diastolic pressure. Esmolol also affected an average 23% of the total LV mass, corresponding to a small- or medium-sized myocardial infarction in humans (33).
Finally, esmolol-induced regional dyskinesis is an artificial model of regional myocardial paresis and may not model accurately regional contraction abnormalities seen during regional myocardial ischemia, stunning, or fibrosis. However, delayed myocardial shortening and postsystolic shortening seen in our model are characteristics of regional myocardial ischemia. Furthermore, we chose this model as a method to validate this form of analysis because it induced reliable and reversible regional myocardial contractile impairment allowing us to examine phase angle shifts among regions during paresis and after recovery without confounding postischemic mechanical changes. Additional analysis needs to be done using similar models but with the regional dysfunction induced by ischemia. However, the mathematical treatment of this analysis should be identical for any contractile state characterized by asynchrony of contraction within the heart.
The authors thank John Melick and Brian Ondulick for outstanding technical assistance and John Lutz for computerized analysis of the conductance catheter and piezoelectric crystal data. The authors are indebted to Masao Takata for contributing the mathematical notation used to describe phase angle interactions and for his several excellent critiques of this work.
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