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Ann Thorac Surg 1999;67:1022-1029
© 1999 The Society of Thoracic Surgeons


Original Articles

Dynamic abdominal and thoracic aortomyoplasty in heart failure: assessment of counterpulsation

Edmundo I. Cabrera Fischer, MDa, Alejandra I. Christen, MDa, Eduardo de Forteza, EEnga, Marcelo R. Risk, EEnga

a Basic Sciences Research Institute, Favaloro University, Buenos Aires, Argentina

Accepted for publication September 21, 1998.

Address reprint requests to Dr Cabrera Fischer, Basic Sciences Research Institute, Favaloro University, Solís 453, (1078) Buenos Aires, Argentina
e-mail: fischer{at}favaloro.edu.ar


    Abstract
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 References
 
Background. Aortic counterpulsation, either biologic or mechanical, is a useful technique to support circulation during left ventricular dysfunction.

Methods. In this study we used an induced cardiac failure model in acute open chest sheep to compare hemodynamic improvements between thoracic and abdominal aortic counterpulsation. This was achieved with left latissimus dorsi and left hemidiaphragm muscle flaps.

Results. Thoracic and abdominal aortic counterpulsation in heart failure resulted in a significant improvement of hemodynamic parameters. Subendocardial viability index, defined as diastolic pressure-time index to systolic tension-time index, in thoracic and abdominal aortomyoplasty showed significant improvement (p < 0.05) when cardiac assistance was performed by electrical stimulation of each muscle flap. A new counterpulsation index derived from diastolic and systolic areas beneath the aortic pressure curve was tested, obtaining a correlation coefficient with the subendocardial viability index of 0.758 (p < 0.001). Values of subendocardial viability index and counterpulsation index showed minimal variability.

Conclusions. Treatment of experimentally induced cardiac failure with dynamic abdominal aortic counterpulsation allows an effective hemodynamic improvement in open chest sheep. Furthermore, this diastolic arterial pressure augmentation could be evaluated through a new counterpulsation index derived from diastolic and systolic areas beneath the aortic pressure curve.


    Introduction
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 References
 
Arterial counterpulsation has been used for treating severe right and left [13] or short-term and long-term [46] ventricular dysfunction in those patients with refractory heart failure. Indeed, arterial counterpulsation using intraaortic balloon pump has been widely used during the last 20 years in acute left ventricular failure cases [5]. Hemodynamic benefits of pulmonary artery counterpulsation for right ventricular failure have also been reported [3, 4, 7]. External counterpulsation is a noninvasive alternative to intraaortic balloon pump; this circulatory assistance has clinically demonstrated improvement in hemodynamic parameters of heart failure and chronic angina [8, 9]. Furthermore, long-term counterpulsation has successfully been applied in humans through dynamic aortomyoplasty to reverse severe heart failure [10, 11].

Dynamic aortomyoplasty is an attractive alternative for treating severe heart failure because of the noncardiac character of this technique. It has been performed in both ascending and descending thoracic aortas, and no hemodynamic differences have been reported between them. Possibly, a dynamic myoplasty in the upper third of the abdominal aorta could also assist the circulatory insufficiency, resulting in a treatment as efficient as thoracic counterpulsation.

The subendocardial viability index (diastolic pressure-time index to systolic tension-time index [DPTI/TTI]), described by Buckberg and colleagues [12], is usually used to evaluate aortic counterpulsation, either biologic or mechanical, to measure diastolic augmentation [12, 13]. This assessment can only be performed in experimental animals, and no clinical application of this invasive index has been reported. A noninvasive index for measuring the extent of diastolic augmentation should be provided to obtain an accurate assessment of the hemodynamic benefits of both intraaortic balloon pump in acute cardiac failure and dynamic aortomyoplasty in ambulatory patients. Such a noninvasive index could allow evaluations of diastolic augmentation variability.

Thus, in the present study we performed (1) a comparative study of thoracic versus abdominal aortic counterpulsation obtained with latissimus dorsi and diaphragm muscle flaps, respectively, in an animal model of heart failure; (2) an analysis of the ability of a new index to indicate diastolic augmentation changes during experimental counterpulsation; and (3) an evaluation of record-to-record repeatability for this new index.


    Material and methods
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 References
 
Surgical procedure
Twenty-one adult Corriedale sheep weighing 25 to 35 kg were chosen at the beginning of this study, aged between 48 and 72 months. General anesthesia was induced with thiopental sodium (20 mg/kg, intravenously), followed by intubation and maintenance of anesthesia with 2.5% enflurane delivered through a Bain tube connected to a Bird Mark 8 ventilator (Bird Corp, Palm Springs, CA).

In all sheep a left lateral thoracic skin incision was performed to facilitate dissection of the left latissimus dorsi muscle. The muscle was derived from its insertion on the lateral side of the last four ribs and thoracolumbar fascia, and was mobilized proximally as a pedicled flap. Pacing electrodes manufactured in our laboratory were implanted into the proximal part of the left latissimus dorsi muscle flap, which was brought into the chest through a left lateral thoracotomy in the fourth intercostal space. Special care was taken to preserve the neurovascular bundle. After this procedure an aortomyoplasty was performed, wrapping the left latissimus dorsi muscle flap around the upper third of the ascending thoracic aorta in a counterclockwise fashion. Then, a long left lateral incision exposed the diaphragm. The diaphragm was divided, and dissection of the left hemidiaphragm from its peripheral attachments was performed. The blood supply and the left phrenic nerve were preserved. Pacing electrodes manufactured in our laboratory were implanted into the muscle mass where the phrenic branches enter the diaphragm. The left hemidiaphragm was wrapped around the upper third of the abdominal aorta in a clockwise fashion (Fig 1).



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Fig 1. Ascending and descending abdominal aorta wrapped with left latissimus dorsi and left hemidiaphragm muscle flaps, respectively.

 
All electrodes from both myoplasties were coupled to a pulse generator, which was manufactured in our laboratory. It was capable of generating a stimulation burst of voltage pulses synchronized with the R wave of the electrocardiogram, with the following characteristics: pulse amplitude, 0.3 to 8.5 V, pulse width, 50 to 999 µs; synchronization delay, 9 to 999 ms; burst rate, 30 to 1,000 Hz; and 1 to 40 pulses per burst. The pulse generator was built around a 68HC11 microcontroller (Motorola Corp, USA), allowing us to control the generator parameters by a PC through its RS-232 port, using a Visual Basic for Windows program written for this purpose (Fig 2).



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Fig 2. Block diagram showing a surface electrocardiogram (EKG), aortic pressure (AoP), and left ventricular pressure (LVP) signals connected through Gould amplifiers to a pulse generator, built around a 68HC11 microcontroller and programmed using an Ansi-C-compatible C language compiler, and connected to a PC computer with an A/D converter. The generator parameters were controlled by the PC through its RS-232 port. Synchronization (Sync) of both muscle flap stimulations was achieved by processing surface electrocardiogram signals and reached the experimental setup through two-channel amplifiers.

 
Left latissimus dorsi and left hemidiaphragm muscle flaps were alternatively stimulated, using a heart to muscle contraction ratio of 1:1 and 1:2, and trains of 6 pulses with a burst rate of 32 Hz. Synchronization of the stimulation of both muscles with cardiac rhythm was achieved by processing a ventricular electrogram signal. To obtain an accurate synchronization with the cardiac rhythm, the 68HC11-based pulse generator was programmed using an Ansi-C-compatible C language compiler (Fig 3).



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Fig 3. Example of the effect of the left latissimus dorsi muscle flap stimulation recorded in a sheep. (A) Electrical stimuli (*) obtained with standardized pulse trains and a ratio of 1:1 with the surface electrocardiogram signal (EKG, mV). (B) Corresponding aortic pressure signal (mm Hg) showing a notorious diastolic augmentation (*) during thoracic aortic counterpulsation.

 
Hemodynamic measurements
Aortic and left ventricular pressures were measured by using two catheters introduced through the left femoral artery and the left atrium appendage, respectively. The tip of the aortic catheter was positioned in the descending aorta between thoracic and abdominal aortomyoplasties, preserving the same distance for the two procedures. All catheters were 8F in size. The cardiac output was measured using a Swan-Ganz catheter placed in the pulmonary trunk through the right femoral vein, and the thermodilution signal was processed with an Edwards (Edwards Lab, Santa Ana, CA) Model 9520A cardiac output computer. All cardiac output measurements were obtained after 60 seconds of 1:1 skeletal muscle stimulation. All animals were given heparin (300 U/kg). Pressure signals were registered on millimeter-marked paper on a Gould multichannel recorder (Model 2600 S; Gould, Inc, Cleveland, OH) with Statham transducers and Gould 4600 series preamplifiers. On-line data acquisition of the electrocardiogram and pressure signals was obtained with a Keithley DAS802 (Keithley Corp, USA) data acquisition board, driven by a Visual Basic for Windows (Microsoft Corp, Seattle, WA) specially written program. The recording parameters were 150 Hz sampling frequency, three acquisition channels, synchronizing signal taken from the pulse generator, and 800 samples per acquisition.

In all animals, blood pressures and cardiac output were measured before and after cardiac failure induced by a high dose of propranolol hydrochloride (3 mg/kg intravenously), and before and after muscle flap electrical stimulation. Thus, in this single cohort of 21 sheep, each animal was studied in control (before and after dynamic counterpulsation) and after induced heart failure (also before and after dynamic counterpulsation). Alternative muscle flap stimulations were randomly performed, and in this protocol no simultaneous stimulation of both muscles was pursued.

In this experimental preparation the muscle stimulation parameters were synchronization delay using the R wave of a surface electrocardiogram, pulse amplitude, pulse width, burst rate, and burst duration. All of them could be modified according to the characteristics of the hemodynamic parameters in both myoplasties to avoid competition with the natural systole. Therefore, the stimulation characteristics were synchronization delay, adjusted to provide optimal diastolic aortic pressure augmentation; pulse amplitude, 8 V; pulse width, 210 µs; burst rate, 32 Hz; and 6 pulses per burst.

The parameters described above are approximate values, because changes in heart rate permanently obliged to perform arrangements in both surgical procedures (Fig 2).

Because we used untrained latissimus dorsi muscle flaps, muscle fatigue and ischemia because of repetitive contractions would appear approximately 5 minutes after the beginning of stimulation [14]. Consequently, we performed latissimus dorsi muscle flap stimulations for periods shorter than 3 minutes. The first derivative of the left ventricular pressure (dP/dt) was monitored in all cases to determine propranolol effects.

After each experimental session all animals were euthanized with an overdose of thiopental sodium. All animals received humane care in compliance with the "Guide for the Care and Use of Laboratory Animals" published by the National Institutes of Health (NIH publication 85-23, revised 1985).

Calculations and statistical treatment
Cardiac output and mean pressures were used to obtain systemic vascular resistance values and cardiac index. The extent of the diastolic aortic augmentation was measured by the subendocardial viability index (DPTI/TTI) [12, 13], and by a new counterpulsation index derived from the diastolic and systolic areas beneath the aortic pressure curve, respectively (DABAC/SABAC). Values of left ventricular dP/dt were used to determine the systolic and diastolic areas taken into account in the calculation of the subendocardial viability index. The DPTI/TTI and DABAC/SABAC indexes were calculated through a program specifically developed in C++ language. This program was used on an IBM PC-compatible computer.

A correlation coefficient was calculated between DPTI/TTI and DABAC/SABAC indexes to estimate the degree of association between these two sets of data. Furthermore, these indexes were submitted to the ordinary least squares regression analysis, to describe the relationship between them. Statistical significance of regression analysis was assessed with the two-tailed Student’s t test. Normality of the distribution of data and measurement of asymmetry were obtained through average, median, mode, and kurtosis calculations.

The percent coefficient of variation was calculated to evaluate the variability in DPTI/TTI and DABAC/SABAC values. In 4 sheep, two measurements were performed at 15 and 30 minutes after the first experimental record, in the same experimental session, to perform this variability study. Hemodynamic results were subjected to a repeated measures one-way analysis of variance and Newman-Keuls test to determine differences between assisted and unassisted values.

Values reported are expressed as mean ± SD. Computed pressure values were the mean of five consecutive cardiac cycles; cardiac output, systemic vascular resistance, cardiac index, DPTI/TTI, and DABAC/SABAC values were the mean of three consecutive determinations. A 95% confidence limit was chosen as indicator of statistical significance (p < 0.05).


    Results
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 References
 
From the 21 sheep initially operated on, 2 animals were discarded because of technical problems during the recording. No animal deaths occurred during the course of any surgical procedure or experimental session, and no aortic regurgitation was observed. No cardiac arrythmias or significant blood pressure variations were found during the skeletal muscle placements or while electromyostimulation was performed before heart failure induction. After heart failure induction, sheep 13 died and 7 animals showed arrhythmias that enabled the beginning of electromyostimulation. Aortic counterpulsation monitored on the oscilloscope always showed a high degree of diastolic pressure augmentation, as high as systolic pressure, both in thoracic and abdominal aorta assistance, as shown in Figure 4.



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Fig 4. (A) Diastolic left ventricular pressure changes (*, mm Hg) induced by latissimus dorsi muscle flap stimulation. (B) Diastolic thoracic aortic pressure augmentation (*, mm Hg) synchronous with left ventricular pressure changes (*). (C) Later, in the same animal, abdominal aortic counterpulsation determined a notable diastolic augmentation (*, mm Hg).

 
In the control group, thoracic aortomyoplasty counterpulsation (n = 19) resulted in a significant increase (p < 0.05) of cardiac output (1.47 ± 0.17 to 1.64 ± 0.15 L/min) and cardiac index (0.050 ± 0.007 to 0.056 ± 0.007 L · min-1 · kg-1). Abdominal aortomyoplasty counterpulsation (n = 19) resulted in a significant increase (p < 0.05) of cardiac output (1.47 ± 0.18 to 1.58 ± 0.15 L/min) and cardiac index (0.050 ± 0.007 to 0.054 ± 0.007 L · min-1 · kg-1). The increases in cardiac output and cardiac index were significantly higher (p < 0.05) in thoracic aortomyoplasty counterpulsation than in abdominal aortomyoplasty counterpulsation (Table 1).


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Table 1. Hemodynamic Variables in Control Group (N = 19)a

 
In the induced cardiac failure group, thoracic aortomyoplasty counterpulsation (n = 11) resulted in a significant increase (p < 0.05) of mean aortic pressure (64.40 ± 14.35 to 71.20 ± 14.20 mm Hg), cardiac output (0.85 ± 0.06 to 0.98 ± 0.08 L/min), and cardiac index (0.029 ± 0.004 to 0.034 ± 0.005 L · min-1 · kg-1). It also resulted in a significant decrease in end-diastolic left ventricular pressure (15.60 ± 2.88 to 13.10 ± 2.42 mm Hg) and systemic vascular resistance (77.12 ± 16.75 to 71.39 ± 13.73 mm Hg · min · L-1). Abdominal aortomyoplasty counterpulsation (n = 11) resulted in a significant increase (p < 0.05) of mean aortic pressure (62.10 ± 12.43 to 67.00 ± 10.79 mm Hg), cardiac output (0.85 ± 0.06 to 0.96 ± 0.08 L/min), and cardiac index (0.029 ± 0.004 to 0.033 ± 0.004 L · min-1 · kg-1). It also resulted in a significant decrease (p < 0.05) in end-diastolic left ventricular pressure (16.00 ± 2.91 to 13.80 ± 2.44 mm Hg) and systemic vascular resistance (74.36 ± 14.06 to 69.12 ± 14.12 mm Hg · min · L-1). The increases in mean aortic pressure and cardiac index were significantly higher (p < 0.05) in thoracic aortomyoplasty counterpulsation than in abdominal aortomyoplasty counterpulsation (Table 2).


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Table 2. Hemodynamic Variables in Cardiac Failure Group (N = 11)a

 
Hemodynamic evaluation of aortic diastolic pressure changes with the DPTI/TTI index, during thoracic aortic counterpulsation before propranolol administration, showed a significant increase compared with unassisted values (0.619 ± 0.174 to 0.733 ± 0.192; p < 0.05), as seen in Table 3 and Figure 5. Aortic diastolic pressure changes, evaluated through the DPTI/TTI index during abdominal aortic counterpulsation stimulating the left hemidiaphragm before propranolol administration, showed a significant increase compared with unassisted values (0.594 ± 0.169 to 0.673 ± 0.198; p < 0.05), as can be seen in Table 3. Values of the DPTI/TTI index obtained with the left latissimus dorsi muscle flap stimulation (thoracic counterpulsation) were significantly higher (p < 0.05) than values of the DPTI/TTI index observed with left hemidiaphragm stimulation (abdominal counterpulsation).


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Table 3. Subendocardial Viability Index (DPTI/TTI) in Aortomyoplasty

 


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Fig 5. (A) Effect of latissimus dorsi muscle flap stimulation in cardiac failure. The electrical stimuli (*) obtained with standardized pulse trains and a ratio of 1:1 with the EKG (mV) determined diastolic pressure changes (*, mm Hg), both in the left ventricular (B) and aortic (C) pressures.

 
In the induced cardiac failure group, only 1 animal (sheep 6) showed DPTI/TTI values outside the expected range values (1.49 to 1.78 for unassisted and assisted values before propranolol administration and 2.10 to 2.27 for unassisted and assisted values after propranolol administration), which led to a large standard deviation for the DPTI/TTI ratio. It was decided to leave out these extreme values from the analysis of variance for repeated measures. Thus, mean and standard deviation of the DPTI/TTI index values (n = 10) were reduced in thoracic counterpulsation (0.701 ± 0.312 to 0.622 ± 0.180 for nonstimulated values and 0.829 ± 0.379 to 0.734 ± 0.221 for stimulated values), and in abdominal counterpulsation (0.744 ± 0.496 to 0.608 ± 0.220 for nonstimulated values and 0.881 ± 0.561 to 0.742 ± 0.337 for stimulated values) (Table 3).

Results of the analysis of variance and application of the Newman-Keuls test showed that in the induced cardiac failure group, the aortic diastolic pressure changes, as evaluated through the DPTI/TTI index during thoracic aortic counterpulsation by stimulating latissimus dorsi muscle flap, showed a significant increase compared with unassisted values (0.622 ± 0.180 to 0.734 ± 0.221; p < 0.05), as shown in Table 3. Similarly, aortic diastolic pressure changes in cardiac failure, evaluated through the DPTI/TTI index during abdominal aortic counterpulsation by stimulation of the left hemidiaphragm, showed a significant increase compared with unassisted values (0.608 ± 0.220 to 0.742 ± 0.337; p < 0.05), as seen in Table 3. No significant differences were observed between increases in DPTI/TTI obtained with thoracic counterpulsation and DPTI/TTI obtained with abdominal counterpulsation in the cardiac failure group.

The ability of the new index of diastolic augmentation was first analyzed using 33 randomized experimental records. Values of DABAC/SABAC and DPTI/TTI indexes were obtained in each cardiac cycle. Values of DABAC/SABAC (1.028 ± 0.198 and 1.152 ± 0.224, for nonassisted and assisted cardiac cycles, respectively) were similar to DPTI/TTI values (1.008 ± 0.319 and 1.117 ± 0.352, for nonassisted and assisted cardiac cycles, respectively). A close association between DPTI/TTI and DABAC/SABAC was shown by (1) a high correlation coefficient (r = 0.759; p < 0.001); (2) an ordinary least squares regression analysis showing a slope for the linear relationship equal to 0.854 (p < 0.001); and (3) a two-tailed t test of the regression relationship showing a slope value not significantly different from 1 (0.854) and an intercept value near zero (0.027), also with no significant difference (Fig 6).



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Fig 6. Plot of diastolic augmentation values obtained by the subendocardial viability index (DPTI/TTI) and the new index derived from the diastolic and systolic areas beneath the aortic pressure curve (DABAC/SABAC) recordings. Data are shown as percentages of diastolic augmentation of 33 measurements in 8 animals before and after abdominal and thoracic counterpulsation. Numbers at the right of the panel refer to the correlation coefficient (r), the regression coefficient (b), and the intercept (a) of the linear regression between the DPTI/TTI and DABAC/SABAC indexes.

 
A variability study of hemodynamic parameters and DPTI/TTI and DABAC/SABAC indexes is presented in Table 4. The values shown are the coefficients of variation of each parameter obtained by averaging the values of three experimental measurements in 4 control sheep with thoracic assisted and unassisted protocols. Heart rate, mean aortic and systolic left ventricular pressures, and systemic vascular resistance presented coefficients of variation less than 5%, whereas cardiac output, cardiac index, and DPTI/TTI and DABAC/SABAC indexes showed coefficients of variation less than 10%. End-diastolic left ventricular pressure was the only parameter that showed a coefficient of variation less than 15%. The analysis of the record-to-record repeatability for all the parameters showed no statistical differences between records 1, 2, and 3 (Table 4).


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Table 4. Coefficients of Variationa

 
In 11 records of the control group and in 7 records of the cardiac failure group, we observed, only during muscle stimulation, pressure signal changes at the beginning of the diastolic period, both in thoracic (14 records) and abdominal (4 records) counterpulsation. As can be seen in Figures 4 and 5, changes in the diastolic left ventricular pressure curve were synchronous with skeletal muscle stimulation.


    Comment
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 References
 
Heart failure refractory to drug treatment is a syndrome that requires left ventricular assistance to preserve hemodynamic parameters [7, 15]. Mechanical circulatory assistance systems have been used as alternative treatments to provide recovery support in those patients suffering from severe and refractory cardiac failure [16]. However, these methods are used for short-term or intermediate-term treatment. Refractory heart failure is a major public health problem, because many patients cannot benefit from cardiac transplantation because organs need to come from healthy bodies, and fewer young people are dying in accidents; in addition, immunosuppression and scarcity of organ donors restrict this option [17]. Xenotransplantation is an attractive prospect, but unfortunately it carries the risk of viruses jumping the species barrier. Finally, at present, to the best of our knowledge, the total artificial heart is not yet a valid alternative. Because none of the available treatments of severe heart failure could be expected to benefit a large number of patients in the near future, new alternative techniques should be developed [18, 19].

Aortic counterpulsation is a well-known technique, clinically introduced in 1968 by Kantrowitz [20]. Human application with intraaortic balloon pump results in beneficial hemodynamic effects, such as reduced myocardial oxygen consumption, enhanced coronary perfusion, and increased cardiac output. However, balloon counterpulsation can only be used for short- or intermediate-term circulatory assistance. It is important to point out that the first aortic counterpulsation was experimentally performed through electrical stimulation of the left hemidiaphragm wrapped around the distal thoracic aorta. Muscle stimulation synchronized with the electrocardiogram resulted in a significant rise in diastolic aortic pressure [21].

In the last decade, dynamic thoracic aortomyoplasty has been introduced as a new surgical technique to treat patients with severe heart failure [10]. This is an attractive alternative because of the noncardiac involvement of this surgical technique. Ascending and descending dynamic aortomyoplasty have demonstrated hemodynamic benefits comparable with those achieved with an intraaortic balloon pump. Consequently, arterial counterpulsation obtained through upper abdominal aortic wrapping with a skeletal muscle would be highly desirable because a nonthoracic surgical procedure would allow future procedures without mediastinal, heart, or lung scars. Besides, a noninvasive method that allows hemodynamic assessment is the key to evaluate this chronic dynamic counterpulsation.

In this study we used an animal model of pharmacologically induced heart failure, which was previously developed to mimic as closely as possible human impairment of cardiac function [22]. Aortic counterpulsation was obtained with the left latissimus dorsi and left hemidiaphragm muscles. Because these skeletal muscles were not trained in this short-term experimental animal model, muscle fatigue and ischemia would occur approximately 5 minutes after induction of stimulation. Therefore, we performed the latissimus dorsi muscle flap stimulation for periods shorter than 3 minutes. As previously reported, fatigue-resistant muscular fibers are the consequence of an electrical stimulation program of 8 weeks. It is understood that we used untrained skeletal muscles in this short-term animal preparation only for technical reasons, and it is not an alternative for trained muscles [14].

As shown in Results, dynamic diastolic thoracic and abdominal counterpulsations, obtained with latissimus dorsi muscle flap and left hemidiaphragm synchronized with the cardiac cycle for short periods of time, are capable of restoring hemodynamic parameters in our short-term animal model of cardiac failure. Our results indicate that hemodynamic improvements owing to abdominal counterpulsation in a short-term animal model of cardiac failure are very close to those obtained with thoracic counterpulsation (Table 2; Fig 3).

Counterpulsation has been described as the mechanical removal of blood during systole and the subsequent reinfusion in diastole. Because no left ventricular intervention is directly performed, it was a surprise to observe left ventricular diastolic pressure changes, such as those observed in Figures 4 and 5, which were synchronized with skeletal muscle stimulation. The presence of these left ventricular pressure changes during abdominal counterpulsation suggests an intraarterial origin, such as aortic pressure changes caused by muscle contraction. To the best of our knowledge, the load-dependent left ventricular relaxation depends on systolic interventions [23].

The left hemidiaphragm used in these experiments had a good tolerance in short-term preparations, with pulmonary function artificially supplied. Perhaps the left hemidiaphragm may be impractical from a clinical standpoint because of its anatomic and physiologic roles; in a long-term animal model or in humans, it would be more suitable to select one of the following muscles previously used, either the rectus abdominis or the internal oblique.

Arterial counterpulsation is usually measured by the subendocardial viability index (DPTI/TTI), reported by Buckberg and colleagues in 1972 [12]. The extent of diastolic augmentation measured by this index represents the balance between myocardial oxygen supply and demand. Unfortunately, a left ventricular pressure measurement is required to calculate this index, and such an invasive technique is inadequate to be implemented in ambulatory patients who undergo dynamic aortomyoplasty or external counterpulsation. Evaluation of aortic counterpulsation through an index derived from a noninvasive aortic pressure wave is an attractive idea, because no cardiac catheterization is required. Consequently, in our experimental protocol, we used the DABAC/SABAC index, which only uses aortic pressure waves for assessing diastolic augmentation. In our animal model, we observed a high correlation coefficient between both indexes, and the regression analysis demonstrated that the relationship between them was significant.

The stability of the diastolic augmentation is very important for the longitudinal evaluation of a single subject. With this purpose, we used the coefficient of variation to quantify such variability. Our results showed that in our animal model of acute heart failure both the DPTI/TTI index and the DABAC/SABAC index had a coefficient of variation less than 10% and hemodynamic parameters had a coefficient of variation between less than 5% and less than 15%. Thus it could be assumed that the DABAC/SABAC values remained constant as long as the animal preparation was not altered. The close similarity between the DPTI/TTI and DABAC/SABAC index behaviors was also observed with the record-to-record repeatability, which showed no differences in the repeated measures analysis of variance.

The final goal of the alternative counterpulsation index (DABAC/SABAC), which takes into account only the aortic pressure wave, is the noninvasive evaluation of diastolic augmentation in arterial assistance. In ambulatory patients, the arterial pressure change assessment during long-term counterpulsation could be obtained through noninvasive techniques [24]. Usually, two devices for clinical monitoring of arterial pressure waves are used (2300 Finapres, Ohmeda, CO; or Portapres Model-2, TNO-TPD Biomedical Instrumentation, Amsterdam, the Netherlands).

In conclusion, treatment of experimentally induced cardiac failure with abdominal aortomyoplasty resulted in an effective improvement of hemodynamic parameters in open chest sheep. It is important to point out that the results obtained in this study correspond to a short-term animal model of heart failure. More experiments are necessary to demonstrate the feasibility of this technique in long-term experimental studies. The original method to evaluate diastolic augmentation in aortic counterpulsation described in this study is a simple technique that allows an adequate follow-up in ambulatory patients. This new approach of diastolic pressure augmentation assessment could be used noninvasively in those patients who undergo dynamic aortomyoplasty, intraaortic balloon pump, or external counterpulsation to determine its clinical relevance.


    References
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 References
 

  1. Kantrowitz A., Kantrowitz A. Experimental augmentation of coronary flow by retardation of the arterial pressure pulse. Surgery 1953;34:678-687.[Medline]
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