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1Heart Failure Research Group, Guidant Corporation, St. Paul, Minnesota 55112; and 2Department of Cardiology, University Hospital, Otto-von-Guericke Universität, Magdeburg, D-39120, Germany
Submitted 5 February 2003 ; accepted in final form 13 August 2003
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ABSTRACT |
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 TOP ABSTRACT MATERIALS AND METHODSRESULTSDISCUSSIONDISCLOSURESREFERENCES |
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III, QRS duration 120 ms) were tested. Contractile function was measured by left ventricular maximum first derivative of pressure over time (dP/dtmax). Biventricular mechanical asynchrony was quantified by the normalized pressure-pressure (NPP) loop area formed by the cross-plot of right and left intraventricular pressure curves from each cardiac cycle. Any ventricular pacing increased dP/dtmax if it decreased baseline NPP loop area and almost always worsened dP/dtmax and asynchrony when baseline NPP loop area <0.3. The quantitative relationship between dP/dtmax and NPP loop area change depended on ventricular pacing site and timing relative to intrinsic activation. For similar NPP loop decreases, dP/dtmax increased 16% more with left and biventricular pacing compared with right ventricular pacing. In conclusion, right, left, or biventricular pacing can improve contractile function only in patients having sufficient baseline biventricular asynchrony. However, biventricular resynchronization is only one of the improvement mechanisms.
resynchronization; heart failure; pressure-pressure loop; intraventricular conduction delay; developed pressure over time
Many questions remain about the validity and completeness of the resynchronization theory. It has been proposed that resynchronization is indicated by shortening of the QRS duration with biventricular pacing, because positive clinical outcome was predicted by QRS shortening in some studies (2, 17), but QRS shortening is neither necessary nor sufficient to predict hemodynamic improvement (13, 24) or outcome (3) in other studies. In particular, LV pacing increases systolic function as effectively as biventricular pacing while usually increasing the QRS duration. Experimental studies in normal canine hearts show that LV pacing preexcites the lateral wall and creates a contraction delay on the right side associated with reduced LV function (23, 24) analogous to the well-known negative hemodynamic effects of right ventricular (RV) pacing in patients with normal ventricular conduction (4, 9, 25). Paradoxically, univentricular left or right pacing can increase contractile function in heart failure patients with intraventricular conduction delay (6, 13). Several nonresynchronization mechanisms have been proposed that might resolve some of these apparent contradictions, including preload improvement and reduction of mitral regurgitation after restoring a more normal atrioventricular (AV) sequence (5, 11).
To test the biventricular resynchronization theory, we measured global biventricular mechanical asynchrony by quantifying the synchrony of left and right intraventricular pressure changes during the whole cardiac cycle in severe heart failure patients with primarily LV conduction delay and assessed the relationship between LV hemodynamic function and biventricular asynchrony at baseline and during atrial-synchronous univentricular and biventricular pacing.
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MATERIALS AND METHODS |
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TOPABSTRACTMATERIALS AND METHODSRESULTSDISCUSSIONDISCLOSURESREFERENCES |
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Data collection. The acute data collection protocol for the PATH-CHF study has been described in detail previously (6). Briefly, each patient was paced in atrial-synchronous ventricular pacing mode at the RV apex (RV pacing), LV freewall (LV pacing), or at both right and left sites simultaneously (biventricular pacing) with five preset AV delays (evenly spaced between 0 and the intrinsic AV interval–30 ms). Each chamber and AV delay pacing combination was randomly repeated five times in a 5 paced beat/15 nonpaced beat episode. Throughout the acute test, high-fidelity pressure recordings (Millar catheters) and intracardiac electrogram recordings from the RV and LV electrodes were stored on tape and later digitized for off-line analysis. The maximum first derivative of LV pressure (LV dP/dtmax) was calculated to provide an index of LV contractile function (14).
Normalized pressure-pressure loop area calculation. Intraventricular pressure changes are a consequence of the integrated chamber mechanics during the cardiac cycle. Asynchrony of the RV and LV mechanics (i.e., biventricular mechanical asynchrony) thus results in relative differences in the timing and rate of pressure changes in the two ventricles (i.e., phase differences). We quantified biventricular mechanical asynchrony from a Lissajous phase plot (16) of the right and left intraventricular pressures. The digitally sampled intraventricular RV and LV pressure values that were simultaneously recorded during one complete cardiac cycle (defined as the interval between adjacent atrial sense markers) were plotted in two dimensions [LV pressure (LVP) values on the x-axis and RV pressure (RVP) values on the y-axis] to create a pressure-pressure loop (PP loop), as shown in Fig. 1. In this method, if the two pressure curves are in phase (i.e., covary) during systole and diastole, the PP loop is narrow with small area; otherwise the PP loop has a large area and a clockwise rotation (dextrorotatory) when the right systolic and diastolic pressure changes precede the left or counterclockwise rotation (levorotatory) when the left systolic and diastolic pressure changes precede the right. Thus the PP loop area is a combined measure of biventricular systolic and diastolic mechanical asynchrony. By normalization, we quantified the biventricular synchrony relationships independent of right and left pressure magnitudes, which were variable among beats and patients. The PP loop interior area was calculated for each recorded cycle and normalized PP (NPP loop area) by the maximum possible loop area (a rectangle) for that cycle, as follows (Fig. 1B): NPP loop area = PP loop area/[(LVPmax – LVPmin) x (RVPmax – RVPmin)], where LVPmax and LVPmin are the maximum and minimum LVP, respectively, and RVPmax and RVPmin are the maximum and minimum RVP, respectively. The NPP loop area ranges between 0 and 1, with larger values indicating more asynchrony between the RV and LV pressure curves.
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Statistical analysis. Both LV dP/dtmax and NPP-loop area were computed for each cardiac cycle. Baseline values for each patient were calculated by averaging all normal sinus beats during the acute protocol. Paced values were calculated by averaging all the beats paced with the same pacing chamber and AV delay. Differences and percent changes of paced values from baseline values were calculated using a local baseline method (6), whereby the average value of the last four paced beats in a pacing episode are compared with the average value of the six nonpaced beats immediately preceding the pacing episode, and the differences (or percent changes) for all episodes with the same pacing chamber and AV delay are averaged. Results for different pacing chambers and AV delays were compared by paired t-test. Data from different patient groups were compared by unpaired t-test. The relationship between changes in NPP loop area and LV dP/dtmax was tested by univariate linear regression analysis and ANOVA was used to compare regressions. A P < 0.05 was considered statistically significant. Values in the text are reported as means ± SD.
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RESULTS |
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TOPABSTRACTMATERIALS AND METHODSRESULTSDISCUSSIONDISCLOSURESREFERENCES |
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Hemodynamic response to pacing. The hemodynamic response to pacing in the PATH-CHF patients has been classified previously into type I (predominately positive) and type II (predominately negative) (6). A type I response was defined as a positive mean response over a range of short to long AV pacing delays for either LV dP/dtmax or aortic pulse pressure and a type II response was zero or negative for both LV dP/dtmax and aortic pulse pressure. Of the 30 PATH-CHF patients analyzed here, 25 had type I and 5 had type II LV dP/dtmax and aortic pulse pressure responses for the best pacing chamber. Similar to previously reported results (6), most patients with baseline QRS duration >150 ms had a type I response, whereas most patients with a shorter QRS had a type II response (Fig. 2). A QRS threshold of 150 ms had a response type prediction accuracy of 87% (88% sensitivity and 80% specificity). With the use of a previously reported prediction method combining a QRS threshold of 155 ms and baseline LV dP/dtmax threshold of 700 mmHg/s (22), prediction accuracy was 83% (80% sensitivity and 100% specificity). The best pacing chamber was LV in 20 patients, biventricular in eight patients, and RV in two patients. On average, RV pacing increased LV dP/dtmax by 8% and aortic pulse pressure by 5%, whereas both LV and biventricular pacing increased LV dP/dtmax and pulse pressure by more than twice as much at the best AV delay (Table 1).
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Baseline biventricular pressure synchrony. Baseline NPP loop area ranged from 0.03 to 0.66 and was bimodally distributed, with two groups separated by a threshold of 0.3 (Fig. 3). The 22 patients with NPP loop areas >0.3 were designated as group 1 and the 8 patients <0.3 as group 2. Typical examples of baseline PP loops from group 1 and group 2 patients are compared in Fig. 4, A and B. All group 1 PP loops were large and dextrorotatory resulting from a right-to-left ventricular contraction sequence. All group 2 PP loops were small because RV and LV pressure curves started and ended together. As shown in Table 2, group 1 and group 2 patients did not differ in baseline NYHA class, Minnesota Living with Heart Failure Questionnaire score, 6-min walk distance, peak O2 consumption on maximum exercise test, or LV ejection fraction (20 ± 5% vs. 22 ± 9%). However, consistent with differences previously reported between type I and II patients (6), the group 1 and group 2 patients differed in average baseline QRS duration and baseline LV dP/dtmax and differed significantly in the magnitude of LV dP/dtmax response to pacing and the AV delay required for best response (Table 1). All group 1 patient responses were type I, and 5 of 8 group 2 patient responses were type II (Fig. 3), resulting in a response type prediction accuracy of 90% (88% sensitivity and 100% specificity) for baseline NPP loop area. Baseline NPP loop area was positively correlated with the mean (R2 = 0.42, P < 0.001) and maximum (R2 = 0.35, P < 0.001) LV dP/dtmax response for the best pacing chamber in each individual. In group 1 patients, the peak LV dP/dtmax response with RV pacing was significantly less than with LV and biventricular pacing (P < 0.001), and the 7.6% larger peak response (1.8 percentage points) with LV pacing compared with biventricular pacing was also significant (P = 0.011).
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Clinical effects of pacing. The positive short- and long-term clinical outcomes of the PATH-CHF patients have been reported previously (8). Table 2 compares clinical changes of the group 1 and group 2 patients after the first month of continuous pacing in the PATH-CHF study. Each patient was randomized to either biventricular pacing or the best univentricular pacing determined by preimplant hemodynamic testing. As shown in Table 2, for all patients combined (group 1 + group 2), all clinical measures significantly improved compared with baseline, similar to results reported for the whole PATH-CHF population (8). The group 1 patients had significant improvements in all clinical measures except the rate of O2 consumption at anaerobic threshold, whereas group 2 patient changes were significant only for NYHA classification reduction. The mean changes in LV dP/dtmax and aortic pulse pressure with the chronically programmed pacing mode were significantly larger for group 1 than group 2 patients (Table 2). The 6-min walk distance after 1 mo of pacing was significantly longer in group 1 than group 2 patients.
Effect of pacing on biventricular pressure synchrony. The PP loop area decreased when group 1 patients were paced and increased when group 2 patients were paced (Fig. 4, C and D). This is quantified in Table 1, which presents average changes in NPP loop area resulting from RV, LV, and biventricular pacing at a short AV delay that minimized fusion with intrinsic conduction. The average paced NPP loop areas were very similar for group 1 and group 2 patients, although the change from baseline was a decrease for group 1 and an increase for group 2, regardless of whether pacing RV, LV, or biventricular. For example, biventricular pacing had an average NPP loop area of 0.14 for both group 1 and group 2, but this represented a decrease from baseline of –0.39 for group 1 and an increase from baseline of 0.06 for group 2. LV pacing created the largest increase in NPP loop area over baseline (0.28) in group 2 patients. This was because LV pacing at short AV delays created reversed (levorotatory) loops due to a left-to-right ventricular contraction sequence in all group 2 patients, as well as in 16 (73%) group 1 patients (Fig. 4, C and D).
The LV dP/dtmax increased when pacing group 1 patients and decreased when pacing group 2 patients, which was opposite to changes in NPP loop area. This is shown in Fig. 5, which compares the average changes in LV dP/dtmax and NPP loop area when pacing RV, LV, or biventricular at five different AV delays (normalized to each individual's intrinsic AV delay) in group 1 and group 2 patients. For group 1 patients (Fig. 5A), each type of pacing at any AV delay decreased the NPP loop area and increased the LV dP/dtmax, whereas the pattern was opposite for group 2 patients (Fig. 5B). Focusing on group 1, the NPP loop area decreased linearly with increasing LV dP/dtmax as the AV pacing delay was shortened from near the intrinsic AV interval (a long AV delay) to 
50% of the intrinsic interval (a middle AV delay) (Fig. 5A). This relationship was quantified by correlating the NPP loop area and LV dP/dtmax changes normalized by the largest NPP loop area decrease and LV dP/dtmax increase, respectively, in this AV delay range for each group 1 patient. As shown in Fig. 6, decreases in NPP loop area were strongly correlated with increases in LV dP/dtmax with RV (R2 = 0.63), LV (R2 = 0.74), and biventricular (R2 = 0.77) pacing. The linear regression slopes for these correlations were similar for RV, LV, and biventricular pacing, but the offsets for biventricular (19%) and LV (21%) pacing were significantly larger (P < 0.001) than for RV pacing (4.3%). Thus the LV dP/dtmax increased nearly the same amount for a given decrease in NPP loop area with LV and biventricular pacing, whereas it increased 16% less for the same NPP loop area decrease with RV pacing.
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When pacing between the middle and shortest AV delays in group 1 patients (Fig. 5A), the average LV dP/dtmax declined slightly from its peak value, whereas the NPP loop area continued to decrease to an average minimum of 0.29 ± 0.14 at an average AV delay of 29 ± 46 ms with RV pacing and to a minimum of 0.14 ± 0.11 at an AV delay of 21 ± 40 ms with biventricular pacing. With LV pacing, the loops passed through a near-zero minimum area of 0.10 ± 0.06 at an AV delay of 64 ± 52 ms and reversed from dextrorotatory to levorotatory at shorter AV delays (Fig. 5A). With LV pacing, the peak increase in LV dP/dtmax occurred when the NPP loops were still dextrorotatory in 18 group 1 patients (82%) at an AV delay 26 ± 46 ms longer than the AV delay corresponding to the minimum NPP loop area (P = 0.014).
All group 2 patients decreased LV dP/dtmax as AV delays were shortened from intrinsic with each type of pacing (Fig. 5B). Correspondingly, the NPP loop area increased as AV delays were shortened, but the magnitude of NPP loop area increases did not correlate to the magnitude of decreases in LV dP/dtmax. Specifically, the largest increases in NPP loop area occurred with LV pacing, although the largest decreases in LV dP/dtmax occurred with RV pacing. Also NPP loop area increased only slightly with biventricular pacing, although LV dP/dtmax decreased to a similar degree with either biventricular or LV pacing.
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DISCUSSION |
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TOPABSTRACTMATERIALS AND METHODSRESULTSDISCUSSIONDISCLOSURESREFERENCES |
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Role of baseline biventricular asynchrony. All the patients had a QRS duration >120 ms but exhibited a wide variation of biventricular asynchrony, as measured by baseline NPP loop area. The effect of pacing on contractile function depended on the magnitude of baseline biventricular asynchrony. Pacing was ineffective or even decreased LV dP/dtmax in patients having little or no asynchrony (group 2). A baseline NPP loop area greater than 0.3 (group 1) was necessary for univentricular or biventricular pacing to significantly increase LV dP/dtmax. It is unlikely that these differences are due to pacing having different direct effects in the two types of patients, because with maximal preexcitation (at the shortest AV delays), the paced NPP loop areas were of similar magnitude in all patients, regardless of whether LV dP/dtmax was improved. Rather, it appears that baseline biventricular asynchrony is a necessary condition for pacing to increase LV dP/dtmax. The magnitude of LV dP/dtmax increase with pacing was directly proportional to the decrease in biventricular asynchrony. Pacing that did not decrease asynchrony did not increase LV dP/dtmax. These results support the theory that biventricular resynchronization is an important mechanism by which pacing improves contractile function. With maximal preexcitation, pacing resulted in a biventricular asynchrony index of 0.14–0.27, depending on the pacing chamber. This degree of possible resynchronization is consistent with the baseline NPP loop area threshold of 0.3 that was empirically observed to separate patients by whether pacing is likely to improve (>0.3) or not improve (<0.3) contractile function.
Effect of RV pacing. In patients with large baseline asynchrony, even RV apical pacing was able to decrease NPP loop area and increase LV dP/dtmax. Because RV pacing in normal hearts creates biventricular asynchrony (25), RV pacing in hearts with baseline LV delay must spread preexcitation to the left ventricle quickly enough to advance LV contraction relative to RV contraction. However, resynchronizing with LV and biventricular pacing provides more hemodynamic benefit than with RV pacing. For similar magnitudes of improved NPP-loop area, LV dP/dtmax improved 16% more with biventricular and LV pacing compared with RV pacing. This indicates the choice of pacing site affects LV dP/dtmax by means that are not detected by the NPP loop area method and thus may be due to some mechanism in addition to global biventricular resynchronization. One possibility is that different pacing sites create different spatiotemporal activation sequences that cause different LV regional contraction patterns and contraction effectiveness. Prinzen et al. (23) observed asymmetrical effects of RV and LV pacing on ventricular workload in normal canine hearts leading to speculation that RV pacing may activate a disproportionately larger extent of muscle more quickly than LV pacing, creating a larger loss of effective muscle mass. Alternatively, RV pacing creates a right-to-left contraction sequence that generates small or reversed transseptal pressure gradients associated with abnormal septal wall motion that are not generated by LV pacing (19) and that are associated with reduced LV contraction effectiveness (12). A third mechanism is possible in the presence of asymmetrical conduction disorder. For instance, in LBBB, most of the left ventricle will be activated slowly and gradually through intramyocardial conduction (28), although intrafasicular conduction may be partially preserved in the right ventricle, perhaps contributing to interventricular septal activation. In this situation, LV pacing also spreads activation by intramyocardial conduction so the rate of LV activation may not be changed appreciably with pacing, but the contraction will be advanced to synchronize with the intrinsic RV and septal contraction. On the other hand, while RV pacing may advance LV contraction, it also will replace any preserved intrafasicular activation of the apex and septum with slower intramyocardial activation, which could reduce LV contractile function (30).
Comparison of LV and biventricular pacing. For similar reasons, we might expect the combination of RV and LV pacing to be less effective than LV pacing for improving contractile function. In fact, it has been reported consistently that LV pacing results in a slightly larger improvement in systolic function than biventricular pacing in atrial-synchronous modes (6, 10, 13). We also observed a small but statistically larger LV dP/dtmax increase with LV pacing in group 1 patients, along with evidence that atrial-synchronized LV pacing can provide better biventricular resynchronization than biventricular pacing. LV pacing consistently could advance the LV contraction to start before the RV contraction, whereas biventricular pacing typically could not. The peak increase in LV dP/dtmax with LV pacing occurs at an average AV delay of 90 ms, which is 26 ms longer than the AV delay at which the NPP loop area passes through a minimum and LV contraction begins to precede RV contraction. Therefore, the optimal resynchronization to increase LV contractile function with LV pacing occurs with a fusion of intrinsic RV activation and paced LV activation. The peak LV dP/dtmax increase with biventricular pacing occurs at shorter AV delays (75 ms), perhaps because the minimum NPP loop area occurs at shorter delays (20 ms). Thus atrial-synchronized biventricular pacing may have two disadvantages in patients with intact AV conduction: 1) biventricular asynchrony is minimized at shorter AV delays that are associated with reduced preload, and 2) the simultaneous RV pacing may substitute slower intramyocardial conduction for preserved intrafasicular conduction in regions contributing to LV contractile function. Clinically, these disadvantages are likely minor because the hemodynamic differences with biventricular pacing are small. Biventricular pacing may have advantages over LV pacing for biventricular resynchronization of patients with heart block or atrial tachyarrhythmia, when intrinsic activation is absent or irregular so fusion is not an option.
Contractile function decreases. When biventricular pacing patients with large baseline asynchrony (group 1) at short AV delays, the LV dP/dtmax declined from the peak improvement at a middle AV delay, likely because preload is reduced at the shorter AV delays, which has been demonstrated in a similar patient cohort (5). On the other hand, the NPP-loop area continued to decrease from its value at a middle AV delay with biventricular pacing at the shorter AV delays, indicating a further improvement in biventricular synchrony at the shorter AV delays that would be expected to further improve LV dP/dtmax. Because the opposite was observed, preload effects may dominate the change in LV dP/dtmax at the short AV delays, perhaps because once the left ventricle is fully recruited by pacing, further changing biventricular synchrony may not have an appreciable effect on LV contractile function.
The LV dP/dtmax almost always decreased from baseline with any pacing in patients with small baseline asynchrony (group 2), even with biventricular pacing, which only slightly increased the NPP loop area. On the other hand, LV pacing dramatically increased the NPP loop area from baseline while LV dP/dtmax decreased no more than with biventricular pacing. These results suggest that NPP-loop area changes are not sufficient to explain worsened contractile function. Nor is preload a likely explanation, since decreases in contractile function occurred even at the middle to long AV delays when preload is actually improved (5). We propose that in heart failure patients without baseline biventricular asynchrony, all pacing may reduce contractile function by replacing intrafascicular conduction with slow intramyocardial conduction, similar to the effects of pacing in normal hearts (24, 28, 29).
Limitations. An important limitation of the NPP loop area method is that it only measures the global effect of contraction, which prevents it from providing any information about the regional wall motion effects that may have created the phase differences between the RV and LV pressures. For example, by itself, this measure cannot separate a delayed septal contraction from a delayed RV contraction because septal contraction is responsible for a large percentage of the total RVP increase. Furthermore, by assessing the phase difference between RVP and LVP throughout the whole cardiac cycle, the NPP loop area does not provide any information about the relative importance of systolic versus diastolic phase differences. Tissue Doppler imaging and other techniques that measure intraventricular mechanical asynchrony are able to examine the local phenomena that may be responsible for the phase differences detected by the NPP loop area. For instance, they have shown that LBBB is associated with significant left intraventricular regional contraction delays, such as lateral wall contraction after aortic valve closure (26). Such intraventricular asynchrony undoubtedly contributes to a phase shift between RV and LV pressure changes, which would appear as an increase in the NPP loop area, and which when corrected by pacing, would appear as a decrease in NPP loop area. Thus, with this metric, we cannot exclude the possibility that biventricular resynchronization occurs simultaneously with intraventricular (regional) resynchronization nor determine which might be the root mechanism for contractile function improvement with pacing. Another limitation to note is that the chronic clinical impact of biventricular asynchrony and resynchronization may differ from the acute hemodynamic effects reported here, although short-term clinical benefit with cardiac resynchronization therapy is associated with improved intraventricular mechanical synchrony (26, 32) and is more evident among patients exhibiting larger baseline electrical asynchrony (7) and more evident for group 1 than group 2 patients after 1 mo of pacing.
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DISCLOSURES |
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TOPABSTRACTMATERIALS AND METHODSRESULTSDISCUSSIONDISCLOSURESREFERENCES |
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In addition to Y.Yu, A. Kramer, J. Spinelli, J. Ding, W. Hoersch, and A. Auricchio, the other PATH-CHF investigators were Drs. C. Huth, H. Klein, M. Kloss, S. Grund, T. Welte, and M. Bischoff, RN (University Hospital, Magdeburg, Germany); Drs. C. Stellbrink, F. Schöndube, B. Diem, O. Breithardt, and P. Hanrath (University Hospital, Aachen, Germany); Drs. S. Sack and U. Wolfhard (University Hospital, Essen, Germany); Drs. M. Block, D. Böcker, B. Lamp, R. Gradaus, and D. Hammel (University Hospital, Münster, Germany); Drs. P. Mortensen and A. Pedersen (University Hospital, Skejky Sygehus, Aarhus, Denmark); Drs. J. Vogt, O. Krahnefeld, and K. Minami (Heart Center North-Rhine Westphalia, Ruhr-University Bochum, Bad Oeynhausen, Germany); and Drs. P. Bakker and H. Kirkels (University Hospital, Utrecht, The Netherlands).
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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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TOPABSTRACTMATERIALS AND METHODSRESULTSDISCUSSIONDISCLOSURESREFERENCES |
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, Patients with type I; 
, patients with type II hemodynamic response.
), and both (
) chambers at five different AV delays in 22 group 1 patients (A) and 8 group 2 patients (B). Data points are means ± SE. AV delays are normalized by the intrinsic AV interval (AVI) of each patient. See text for description.