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Am J Physiol Heart Circ Physiol 292: H158-H164, 2007. First published August 18, 2006; doi:10.1152/ajpheart.00406.2006
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Reduction in postsystolic wall thickening during late preconditioning

Xavier Monnet,1 Laurence Lucats,1,2,3 Patrice Colin,1 Geneviève Derumeaux,5 Jean-Luc Dubois-Rande,1,2,3,4 Luc Hittinger,1,2,3,4 Bijan Ghaleh,1,2,3,4 and Alain Berdeaux1,2,3,4

1Institut National de la Santé et de la Recherche Médicale, U-660, Créteil; 2Faculté de Médecine, Laboratoire de Pharmacologie, Université Paris XII, Créteil; 3Ecole Nationale Vétérinaire d'Alfort, Maisons-Alfort; 4Assistance Publique-Hôpitaux de Paris, Groupe Hospitalier Henri Mondor, Fédération de Cardiologie, Créteil; and 5Institut National de la Santé et de la Recherche Médicale E0226, Lyon University Hospital, Lyon, France

Submitted 20 April 2006 ; accepted in final form 7 August 2006


   ABSTRACT
TOP
 ABSTRACT
METHODS
 RESULTS
 DISCUSSION
 GRANTS
 REFERENCES
 
Brief coronary artery occlusion (CAO) and reperfusion induce myocardial stunning and late preconditioning. Postsystolic wall thickening (PSWT) also develops with CAO and reperfusion. However, the time course of PSWT during stunning and the regional function pattern of the preconditioned myocardium remain unknown. The goal of this study was to investigate the evolution of PSWT during myocardial stunning and its modifications during late preconditioning. Dogs were chronically instrumented to measure (sonomicrometry) systolic wall thickening (SWT), PSWT, total wall thickening (TWT = SWT + PSWT), and maximal rate of thickening (dWT/dtmax). Two 10-min CAO (circumflex artery) were performed 24 h apart (day 0 and day 1, n = 7). At day 0, CAO decreased SWT and increased PSWT. During the first hours of the subsequent stunning, evolution of PSWT was symmetrical to that of SWT. At day 1, baseline SWT was similar to day 0, but PSWT was reduced (–66%), while dWT/dtmax and SWT/TWT ratio increased (+48 and +14%, respectively). After CAO at day 1, stunning was reduced, indicating late preconditioning. Simultaneously vs. day 0, PSWT was significantly reduced, and dWT/dtmax as well as SWT/TWT ratio were increased, i.e., a greater part of TWT was devoted to ejection. Similar decrease in PSWT was observed with a nonischemic preconditioning stimulus (rapid ventricular pacing, n = 4). In conclusion, a major contractile adaptation occurs during late preconditioning, i.e., the rate of wall thickening is enhanced and PWST is almost abolished. These phenotype adaptations represent potential approaches for characterizing stunning and late preconditioning with repetitive ischemia in humans.

regional function; myocardial dysfunction

POSTSYSTOLIC THICKENING IS the part of myocardial contraction that occurs beyond the closure of the aortic valve (5, 16, 29) and is a marker of left ventricular (LV) asynchrony (10), which has been extensively described during experimental and clinical myocardial ischemia (5, 29). However, the mechanisms involved in this phenomenon remain presently unclear and depend on the level of wall thickening (26) and ischemic substrate (28, 32, 33). Whether it is a passive and/or an active mechanism (5) and whether it is a marker of myocardial viability (5, 12, 29) are still debated. Postsystolic thickening has also been reported during myocardial stunning (6, 9, 11, 23) and has been shown to result from both a reduced contractile velocity and an inhomogeneity in the LV contraction (11). However, the overall time course of postsystolic thickening during myocardial stunning has never been fully described. In addition, it is interesting to consider that the time course of postsystolic thickening can also be modified with repetitive ischemia, i.e., the reduction in the duration and severity of myocardial stunning that occurs 24 h after a first brief ischemic episode during late preconditioning (7, 25, 27). Despite intensive investigations, the regional function pattern and phenotype of the preconditioned myocardium have not been described yet, especially regarding postsystolic wall thickening.

Accordingly, the purposes of this study were 1) to investigate the respective time course of systolic (SWT) and postsystolic wall thickenings (PSWT) that occurs after a brief ischemia and 2) to determine whether the relative contribution of these two parameters to total wall thickening in the stunned myocardium is altered by late preconditioning. For these purposes, we used a model of chronically instrumented conscious dogs that enables us to perform two brief episodes of coronary artery occlusion (CAO) 24 h apart (7). Both SWT and PSWT were measured by sonomicrometry.


   METHODS
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 ABSTRACT
 METHODS
RESULTS
 DISCUSSION
 GRANTS
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The animal instrumentation and the ensuing experiments were conducted in accordance with the official regulations of the French Ministry of Agriculture.

Surgical preparation. As previously described (19), a left thoracotomy was performed in 11 dogs under anesthesia (pentobarbitone sodium, 30 mg/kg iv). Filled fluid catheters were implanted in the descending thoracic aorta and the left atria. A solid-state micromanometer (Konigsberg Instruments) was introduced into the LV through the apex. A Transonic flow probe and a pneumatic occluder were implanted around the circumflex coronary artery. Two pairs of ultrasonic crystals were placed within the distribution of the circumflex coronary artery (ischemic zone) and of the left anterior descending coronary artery (nonischemic zone) for LV wall thickening measurement. One crystal was implanted in the endocardium, and the other was sutured to the epicardium, independently from the muscle fiber's orientation. Finally, in four dogs, bipolar electrodes were sewn on the epicardial surface of the right ventricle for subsequent electrical pacing. All catheters and wires were exteriorized between the scapulae. Cefazolin (1 g iv) and gentamycin (40 mg iv) were administered before and during the first week after surgery. Peri- and postoperative analgesia were provided with morphine.

Experimental protocol. Three weeks after instrumentation (day 0), seven dogs were installed to lie quietly on a table in the conscious state. After baseline measurements, a 10-min occlusion of the left circumflex coronary artery (CAO) was performed using the occluder. Twenty-four hours later (day 1), the 10-min CAO was repeated. All hemodynamic and wall thickness parameters were recorded and calculated during CAO and during the 6 h of the subsequent reperfusion period.

To investigate whether changes in regional function observed at day 1 were independent from residual myocardial stunning, late preconditioning was induced in four additional dogs with a nonischemic stimulus, i.e., rapid ventricular pacing (240 beats/min during 40 min) (17). Dogs underwent 2 days of experiments: on day 0, the animals underwent the late preconditioning stimulus, i.e., rapid ventricular pacing, and, on day 1, i.e., 24 h later, a 10-min CAO was performed. The time course of myocardial stunning was compared with another sequence performed 1 wk apart when dogs were only subjected to a 10-min CAO without preliminary rapid ventricular pacing.

Hemodynamic measurements. Data were recorded and analyzed using the data-acquisition software Notocord-HEM 3.3. Aortic and left atrial pressures were measured with Statham P23ID strain-gauge transducers and were used to cross-calibrate the Konigsberg gauge. LV pressure was measured using the Konigsberg gauge, and LV pressure first derivative (LV dP/dt) was computed from the LV pressure signal. Circumflex coronary artery blood flow was measured with a Transonic transit-time flowmeter to assess proper CAO.

Measurements of regional systolic function. End-diastolic and end-systolic wall thicknesses were measured with an ultrasonic transit-time dimension gauge. End-diastolic time was defined at the initiation of the upstroke of LV pressure tracing and end-systolic time 20 ms before the negative peak of LV dP/dt (Fig. 1) (29).


Figure 1
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  		Fig. 1. Left: typical waveform representing the evolution of myocardial wall thickness during a single beat recorded from a stunned posterior wall: systolic wall thickening (SWT) was defined as the difference between end-diastolic and end-systolic wall thicknesses; maximal wall thickness was defined as the maximal distance between crystals measured after end systole; left ventricular (LV) postsystolic wall thickening (PSWT) was defined as the maximal minus end-systolic wall thicknesses. Right: representative recordings of aortic and LV pressures, LV pressure first derivative (LV dP/dt), and LV posterior wall thickness measured at baseline and during myocardial stunning. dWT/dtmax, maximal systolic rate of wall thickening.

 
SWT was defined as the difference between end-diastolic and end-systolic wall thicknesses, i.e., the wall thickening (expressed in mm) that occurs during the ejection period. The total deficit of SWT during the 6 h of the recovery period (arbitrary units) was calculated by measuring the area between the SWT vs. time line and baseline (100% line) (4).

Maximal wall thickness was defined as the maximal distance between crystals, irrespective of the time point in the cardiac cycle. PSWT was defined as the maximal minus end-systolic wall thicknesses, i.e., the wall thickening that occurs after the ejection period. Total wall thickening was calculated as the sum of SWT and PSWT.

Rate of wall thickening (dWT/dt) was computed from the wall thickness signal, and the maximal value of dWT/dt was measured during systole (dWT/dtmax).

Measurements of regional myocardial blood flows. Regional myocardial blood flows were measured by the fluorescent microspheres technique, as previously reported (20). Microspheres labeled with fluorescent dyes (FluoSpheres, Triton System, San Diego, CA) were injected via the left atrial catheter. Arterial blood reference samples were withdrawn (7.5 ml/min during 2 min). At termination of the study, the heart was excised, and LV was cut into three to four slices and further divided into subendocardium, midmyocardium, and subepicardium layers. Samples were then processed to extract the fluorescence, and blood flows (expressed as milliliter per minute per gram of myocardium) were calculated. Mean transmural flow was calculated as the combined flow of all three layers.

Regional work index. The regional myocardial work index was computed on three consecutive beats as the area of the LV pressure-wall thickness loop.

Statistical analysis. Data are reported as means ± SE. Analysis was performed using a two-way ANOVA for repeated measures and by checking for interactions. The F-test was used to test the significance of analysis of variance. When needed, pairwise comparisons between day 0 and day 1 were performed using a paired two-sided Student’s t-test with Bonferroni correction. Significance was accepted at P < 0.05.


   RESULTS
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DISCUSSION
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Hemodynamics. As shown in Table 1, heart rate, mean arterial pressure, LV pressure, and LV dP/dtmax were not significantly different at baseline and during CAO and reperfusion between day 0 and day 1. Regional myocardial blood flows measured were similar during CAO between day 0 and day 1 (0.11 ± 0.06 and 0.09 ± 0.05 ml·min–1·g–1, respectively) (n = 4).


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  		Table 1. Hemodynamics

 
SWT. In the ischemic zone (Table 2), SWT was not significantly different at baseline between day 0 and day 1 (2.9 ± 0.3 and 2.8 ± 0.3 mm, respectively) but was dramatically and similarly reduced during ischemia in both sequences (–103 ± 6 and –108 ± 5% at days 0 and 1, respectively). During reperfusion, ischemic SWT remained initially depressed and progressively returned to its corresponding baseline value, indicating myocardial stunning. As illustrated in Fig. 2, values of SWT measured during the first 6 h of reperfusion at day 1 were significantly greater compared with day 0. The deficit of wall thickening over the 6 h of recovery was reduced at day 1 compared with day 0 (60 ± 20 vs. 136 ± 27 units, respectively, P < 0.05), demonstrating late preconditioning.


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  		Table 2. Regional function

 

Figure 2
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  		Fig. 2. Percent change from baseline of SWT measured during coronary artery occlusion (CAO) and reperfusion at days 0 and 1. Inset: deficit of wall thickening calculated at days 0 and 1. The duration and severity of myocardial stunning were reduced at day 1 vs. day 0, indicating late preconditioning. *P < 0.05 vs. day 0.

 
In the nonischemic zone (Table 2) at day 0, SWT increased up to 3.0 ± 0.3 mm during CAO but returned to its baseline value (2.7 ± 0.3 mm) immediately after relief of the occlusion and remained unchanged throughout reperfusion. There were no significant differences in nonischemic SWT between days 0 and 1 (Table 2).

PSWT. At day 0, PSWT dramatically increased by 115% from baseline during CAO (from 0.67 ± 0.09 to 1.44 ± 0.13 mm) (Fig. 3, Table 2). After reperfusion, PSWT still increased during the first 10 min and then progressively decreased. Indeed, PSWT not only returned to its corresponding baseline value, but, interestingly, at day 1, baseline PSWT was reduced by 66% compared with its corresponding value at day 0 (0.23 ± 0.06 and 0.67 ± 0.09 mm, respectively, P < 0.05).


Figure 3
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  		Fig. 3. Time course of PSWT (expressed in mm) measured at baseline and during CAO and reperfusion at days 0 and 1. The pattern was symmetrical to that observed with SWT. At day 1, PSWT was reduced at baseline and throughout reperfusion vs. day 0. *P < 0.05 vs. day 0.

 
At day 1 (Fig. 3, Table 2), PSWT increased up to 1.58 ± 0.15 mm during CAO. This value was significantly greater than corresponding PSWT at day 0. During reperfusion, the time course of PSWT paralleled that observed at day 0, but its values remained significantly lower throughout the whole recovery period (average of –49%) compared with day 0. The area under the curve for PSWT was significantly reduced at day 1 compared with day 0 (4.7 ± 1.1 vs. 10.2 ± 1.8 mm/h).

In the nonischemic zone, PSWT values were not altered during CAO and/or reperfusion, with no differences being observed between days 0 and 1 (Table 2).

Total wall thickening. Total wall thickening, i.e., the sum of SWT and PSWT, remained unchanged throughout the reperfusion period (averaging 2.9 ± 0.1 mm) at day 0 and was similar between days 0 and 1. Importantly, as illustrated in Fig. 4, the systolic-to-total wall thickening ratios were significantly greater at day 1 vs. day 0 at baseline (0.92 ± 0.02 vs. 0.81 ± 0.03) and throughout the recovery period (e.g., at 2 h of reperfusion, 0.92 ± 0.04 vs. 0.78 ± 0.04).


Figure 4
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  		Fig. 4. Time course of the SWT-to-total wall thickening ratio measured at baseline and during CAO and reperfusion at days 0 and 1. At day 1, a greater part of total wall thickening was devoted to ejection, as demonstrated by increased ratio values at baseline and during reperfusion vs. day 0. *P < 0.05 vs. day 0.

 
dWT/dtmax. At day 0, dWT/dtmax was depressed during the post-CAO period compared with baseline and progressively tended to return to its corresponding baseline value, i.e., with a pattern similar to the evolution of SWT (Fig. 5, Table 2). At day 1, baseline dWT/dtmax was significantly increased by 30 ± 10% compared with its corresponding value at day 0. During reperfusion, the pattern of recovery was also similar to day 0, but all values were significantly higher (averaging 48 ± 5%). Interestingly, this effect was not related to differences in SWT, as the ratio of dWT/dtmax to SWT was significantly greater at baseline and during the whole recovery at day 1 vs. day 0.


Figure 5
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  		Fig. 5. Evolution of dWT/dtmax in relation to SWT measured at baseline and during CAO and reperfusion at day 0 and 24 h later (day 1). At day 1, dWT/dtmax was significantly increased at baseline and throughout recovery. Inset: evolution of the ratio between dWt/dtmax and SWT. This ratio was significantly increased at day 1 vs. day 0, demonstrating that the increases in this ratio observed at day 1 were not related to differences in SWT values between day 1 and day 0. *P < 0.05 vs. day 0.

 
Regional work index. As illustrated in Fig. 6, the regional work index was significantly reduced at day 1 compared with day 0.


Figure 6
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  		Fig. 6. Comparison of baseline values of SWT (A), PSWT (B), dWT/dtmax (C), and regional work index (D) measured at days 0 and 1. In the late preconditioned heart, although SWT was similar, PSWT and work index were significantly reduced concomitantly with an increase in dWT/dtmax. *P < 0.05 vs. day 0.

 
Rapid ventricular pacing. In the four additional dogs submitted to rapid ventricular pacing, PSWT was significantly reduced at day 1 (0.38 ± 0.08 mm) compared with day 0 (0.77 ± 0.02 mm), although SWT was similar at baseline (day 0 vs. day 1: 3.0 ± 0.3 and 3.1 ± 0.4 mm, respectively). Rapid ventricular pacing did not induce myocardial stunning per se.


   DISCUSSION
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 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
GRANTS
 REFERENCES
 
Brief ischemia is well known to induce myocardial stunning and the development of an endogenous protective mechanism that confers resistance to postischemic dysfunction 24 h later, i.e., late preconditioning (7, 25, 27). To date, few if any data are yet available about the regional function and phenotype of the preconditioned myocardium, especially regarding PSWT, although numerous studies have been devoted to the investigation of the intracellular mechanisms of late preconditioning, particularly those involving the nitric oxide hypothesis (3). Indeed, a postsystolic phenomenon develops during reperfusion, but its overall time course during myocardial stunning and late preconditioning had never been fully described. In this context, the present study demonstrates that the recovery in SWT of the stunned myocardium is accompanied by a progressive and symmetrical decrease in PSWT. More importantly and for the first time to our knowledge, our results demonstrate that the PSWT almost vanishes 24 h after a brief ischemia, although SWT returns to baseline. In other words, in the late preconditioned heart, a greater part of total wall thickening is devoted to the ejection. Interestingly, a significant increase in the dWT/dtmax was simultaneously observed.

Experimental setting. The model of conscious and chronically instrumented dog used in this study is particularly suitable to investigate late preconditioning against myocardial stunning (7). First, it allows measurement of regional systolic function using a "gold standard method," i.e., sonomicrometry, without interference of anesthesia or recent surgical intervention (30). Second, the overall hemodynamic parameters are extensively investigated. Third, it allows the repetition of CAOs performed 24 h apart. Fourth, the evaluation of regional systolic function is accurate, repetitive, and reproducible. With this technique, measurements of wall thickening are always made on the same area of the LV wall, independently from the investigator, as determined by the implanted ultrasonic crystals. It should also be stressed that these results cannot be extended to other ischemic substrates, i.e., acute vs. chronic ischemia and CAO vs. stenosis (14). One potential pitfall needs, however, to be addressed. One could argue that postsytolic wall thickening might result from translation motion between the crystals. This is unlikely, as PSWT has also been described using echocardiographic measurements, either in animal models (8, 14, 18) or humans (31). Moreover, using tissue Doppler imaging, we also observed PSWT in our animal preparation, either at baseline or during stunning, thus confirming our sonomicrometric measurements (data not shown).

PSWT during ischemia. PSWT has been described to occur in the normal heart (26, 29, 31). Strain rate imaging has identified postsystolic shortening in normal human subjects as a result of a very early and fast antero-septal midwall lengthening. The mechanisms underlying the phenomenon of ischemia-induced postsystolic wall motion have been, however, extensively debated between a delayed active contraction, a late passive thickening, or an elastic recoil overshoot after bulging. During ischemia, postsystolic shortening may occur in dyskinetic segments by an entirely passive mechanism, whereas, in hypokinetic or akinetic segments, it may represent an actively contracting myocardium (26). It must be stressed that the latter study investigated myocardial ischemia but not normal or stunned myocardium. In the normal heart, PSWT was suggested to be related to the heterogeneity of repolarization toward the LV (24). Investigation of the mechanism underlying PSWT was, however, beyond the scope of our investigation. Finally, it should be acknowledged that PSWT among LV is heterogeneous. In our study, PSWT was not observed in the anterior wall, whereas it was always present in the posterior wall at baseline. This heterogeneity has already been described using MRI in humans. It has been attributed to segmental prestretch (34), or it could result from ventricular electrical asynchrony (22).

In the present study, PSWT increased during ischemia (2, 13), but, 24 h later, the amount of PSWT during CAO was greater in the preconditioned state, although the dramatic decrease in SWT was similar to that observed at day 0. Interestingly, in this context, the positive predictive value of postsystolic contraction during ischemia for subsequent recovery has been described in many studies performed both in experimental (5, 29) and clinical settings (12). However, it has been emphasized that postsystolic contraction should not be considered as an invariable marker of segment viability (28).

Contractile adaptations of the late preconditioned heart. During myocardial stunning at day 0, the impairment in contractile function was characterized not only by the well-known depression of SWT but also by a concomitant increase in PSWT throughout the reperfusion period. Interestingly at day 1, PSWT was dramatically reduced vs. day 0 at baseline but also during stunning. This was associated with a significant increase in the dWT/dt at day 1 (Fig. 6), independently from the SWT value or changes in the ejection time. To ensure that these changes in regional systolic function were independent from residual myocardial stunning, late preconditioning was induced in additional animals by a nonischemic stimulus, i.e., rapid ventricular pacing (17). The results of the present study might also be biased by denervation during CAO or a greater sympathetic stimulation at day 1. This is, however, unlikely, as no change was observed in the nonischemic anterior zone, and reduction in PSWT was also observed following rapid ventricular pacing. Regional myocardial blood flows were similarly reduced during the 2 days of the protocol. In addition, absence of changes in the nonsichemic anterior wall exclude a global effect of late preconditioning. Finally, the lack of simultaneous increase in ischemic SWT and PSWT in the remote anterior zone excludes any interaction between both regions.

The present study demonstrates that, in the preconditioned heart, a greater course of thickening occurred during the ejection period, i.e., more thickening was devoted to ejection. This result suggests that the wasted oxygen due to PSWT is spared in the late preconditioned heart and, therefore, could participate in the anti-ischemic effect of late preconditioning. Interestingly, our laboratory recently reported that late preconditioning induced changes in the metabolic phenotype, i.e., myocardial oxygen consumption of the late preconditioned myocardium was reduced (21). Although not directly assessed here, all of these results suggest a major contractile adaptation associated with an improved cardiac efficiency that could contribute to the protection against myocardial ischemia and stunning. Late preconditioning not only reduces the severity and duration of myocardial stunning but also alters the overall course of myocardial wall thickening, i.e., a smaller part of contraction is wasted after the ejection. This might be the consequence of a positive inotropic-like effect, as reflected by the increase in the dWT/dt. It is unlikely related to changes in loading conditions and ventricular stretch, as we did not observe any significant changes in LV end-diastolic wall thickenesses. Although investigation of the cellular mechanisms of these contractile and metabolic adaptations was beyond the scope of our study, it is interesting to speculate that changes in calcium handling (1), e.g., modulation of the ryanodine receptor or L-type calcium channels, or due to enhanced nitric oxide production with late preconditioning might occur (3). Further studies are needed to investigate these issues.

In conclusion, our study demonstrates major changes in the course of myocardial wall thickening during repetitive stunning with late preconditioning, i.e., the dWT/dt is enhanced and PSWT is almost abolished, involving the almost entire total wall thickening to ejection. This study may have important clinical implications, particularly with the use of Doppler tissue imaging. These results suggest that both the amplitude and the temporal patterns of regional myocardial thickening have to be assessed during myocardial stunning and also during adaptation of the heart to transient ischemia. This would precisely evaluate not only the regional function of the myocardium but also the progressive changes in its contractile phenotype that could appear in the setting of chronic and repetitive ischemia (15).


   GRANTS
TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
 GRANTS
REFERENCES
 
This study was supported by grants from the Fondation de France (2001–005170 and 2003–005607) and Bonus Qualité Recherche 2003 (University Paris XI, France).


   ACKNOWLEDGMENTS
 
The authors are greatly indebted to Alain Bizé, Stéphane Bloquet, and Georges Zadigue for excellent technical assistance.


   FOOTNOTES
 

Address for reprint requests and other correspondence: A. Berdeaux, Laboratoire de Pharmacologie, INSERM U660, Faculté de Médecine de Créteil, 8, rue Général Sarrail, 94010 CRETEIL Cedex, France (e-mail: alain.berdeaux{at}creteil.inserm.fr)

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.


   REFERENCES
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 DISCUSSION
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