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Ann Thorac Surg 2001;71:284-289
© 2001 The Society of Thoracic Surgeons
a Division of Cardiothoracic Surgery, Case Western Reserve University School of Medicine, Cleveland, Ohio, USA
Accepted for publication June 3, 2000.
Address reprint requests to Dr Cmolik, Division of Cardiothoracic Surgery, Case Western Reserve University School of Medicine, 11100 Euclid Ave, Cleveland, OH 44106-5011
e-mail: blc3{at}po.cwru.edu
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Abstract |
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Methods. In dogs (n = 6, 20 to 25 kg), the left latissimus dorsi muscle was isolated, wrapped around the descending thoracic aorta, and conditioned by chronic electrical stimulation. Heart failure was induced by rapid ventricular pacing. In a terminal study, left ventricular and aortic pressures, and blood flow in the left anterior descending coronary artery and descending aorta were measured. The endocardial-viability ratio was calculated.
Results. Aortomyoplasty increased mean diastolic aortic pressure (70 ± 5 to 75 ± 5 mm Hg, p < 0.05) and reduced peak left ventricular pressure (86 ± 4 to 84 ± 4 mm Hg, p < 0.05), leading to a 16% increase in endocardial-viability ratio (1.29 ± 0.05 to 1.49 ± 0.05, p < 0.05). Coronary blood flow was increased by 15% (8.2 ± 1.5 to 9.4 ± 1.6 mL/min, p < 0.05). During muscle contraction, 2.7 ± 0.5 mL was ejected from the wrapped aortic segment.
Conclusions. These data demonstrate that aortomyoplasty provides successful diastolic counterpulsation after muscle conditioning and heart failure.
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Introduction |
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TopAbstractIntroductionMaterial and methodsResultsCommentAcknowledgmentsReferences |
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Aortomyoplasty may be applied to a class of patients who may or may not be transplant candidates but who are not ill enough to require a left ventricular (LV) assist device or total artificial heart implantation. The group of patients considered likely to benefit from aortomyoplasty are those in moderate to early-severe heart failure (New York Heart Association class III to early class IV) for whom maximal medical therapy has been insufficient.
Aortomyoplasty may also represent an option for patients with intractable angina who cannot be revascularized by conventional techniques. The IABP is used clinically for these patients in the acute setting as a bridge to either percutaneous transluminal coronary angioplasty or coronary artery bypass grafting. Therefore, based on the same principle, aortomyoplasty should provide a chronic treatment for coronary artery disease not amenable to other therapies. As these patients are now considered candidates for therapy with transmyocardial laser revascularization, increased coronary artery blood flow by aortic counterpulsation may benefit these patients as well.
This study was designed to correlate the effects of aortomyoplasty on pressure/time indices of counterpulsation to direct measurements of coronary blood flow in a model of moderate heart failure. Results demonstrate that counterpulsation by aortomyoplasty augments indices of counterpulsation and that these correlate with increases in coronary blood flow.
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Material and methods |
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TopAbstractIntroductionMaterial and methodsResultsCommentAcknowledgmentsReferences |
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Surgical aortomyoplasty
Six mongrel dogs weighing 20 to 25 kg were used in this study. The dogs were premedicated with Buprenex (buprenorphine, 0.3 mg, subcutaneously) and anesthesia was induced using thiopental sodium (25 mg/kg, intravenously). The dogs were intubated and anesthesia maintained with Halothane (1% to 1.5%). Limb-lead electrocardiogram (ECG) was monitored. Intravenous antibiotic was administered before incision (cefazolin 1,000 mg). The animals were then placed in the left thoracotomy position.
The left latissimus dorsi muscle (LDM) was harvested through a longitudinal incision beginning in the axilla of the animal and extending to the midthorax. The muscle was mobilized, with suture ligation of the distal intercostal arterial blood supply. Care was taken to preserve the thoracodorsal neurovascular bundle. Intramuscular pacing electrodes were then placed near the thoracodorsal nerve and the stimulation threshold was determined. A 6-cm portion of the third rib was resected, and the left pleura was entered. The LDM and affixed electrodes were transposed into the left chest through the bed of the resected rib. A left thoracotomy was performed through the fifth intercostal space, and the descending thoracic aorta was exposed from the level of the subclavian artery to just above the diaphragm. One to four pairs of intercostal arteries were ligated beginning at the level of the left subclavian artery.
The muscle was wrapped circumferentially around the descending thoracic aorta in a counterclockwise direction (Fig 1). The proximal-to-mid region of well-vascularized LDM was used to cover the aorta. Excess distal muscle was then excised. Mattress sutures of 2-0 polypropylene suture (Prolene; Ethicon, Somerville, NJ) were used to secure the muscle to itself.
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Muscle stimulation was performed with a custom-designed single-channel stimulator [1] worn externally in a jacket. Beginning at the end of the second postoperative week, the muscle was stimulated with a 2-Hz twitch to convert it to a fatigue-resistant phenotype [2–4].
Rapid-pacing heart failure
Rapid ventricular pacing was initiated during the fourth postoperative week. The single-channel muscle stimulator was replaced with a multichannel version for the purposes of simultaneous rapid-ventricular pacing and muscle stimulation [1]. The cardiac channel was set to 240 beats per minute, with a stimulus amplitude twice the threshold, and a pulse width of 2 ms. Muscle conditioning was maintained at 120 twitches per minute (2 Hz). Each animal was monitored daily for clinical signs of heart failure. Echocardiography was performed at base line then at weekly intervals to document chamber dilation during the rapid-pacing period.
Hemodynamic study
Rapid ventricular pacing was terminated after 3 weeks and the dogs were then prepared for a nonsurvival terminal study. Anesthesia was induced with thiopental sodium (25 mg/kg, intravenously) and maintained with inhaled halothane (1.0% to 1.5%). A median sternotomy was performed. Solid-state pressure transducers (Millar, Inc, Houston, TX) were positioned in the left ventricle through a stab wound at the apex, and in the ascending aorta through the right carotid artery, to measure LV and aortic pressures (Fig 1). Doppler ultrasonic flow probes were positioned on the proximal left anterior descending (LAD) coronary artery, as well as on the descending thoracic aorta just distal to the left subclavian artery, and at the level of the middescending thoracic aorta. In this way, flow probes were positioned both proximal and distal to the wrapped aortic segment.
A bench-top version of the computer-controlled stimulator [1] triggered a Grass stimulator (S8800, Grass Instruments, Quincy, MA) to provide stimulus isolation (SIU5, Grass Instruments) and elicit muscle contraction. A physiologic recorder (Gould Inc, Cleveland, OH) provided ECG triggering. The flow, pressure, and stimulus signals were sampled at 500 Hz and stored to hard disk.
The pacer was turned off for the duration of the data collection. With the heart in sinus rhythm, the R-wave delay was adjusted so that the increase in aortic pressure due to muscle contraction coincided with the dicrotic notch. Stimulus train duration was then varied, and the best train was identified. Each pulse was 210 µs in duration with an intraburst stimulus frequency of 30 Hz. Signals were recorded for 15 seconds during held end-expiration. Muscles were stimulated on alternate diastoles (1:2 mode) for this investigation.
Data analysis
From stored data files, stimulated and unstimulated beats were identified and analyzed. Mean diastolic aortic pressure was calculated as the mean aortic pressure during the time when aortic pressure exceeded LV pressure. Endocardial-viability ratio (EVR) was calculated as the aortic diastolic pressure-time integral divided by the LV systolic tension-time index (TTI) (Fig 2). The TTI, the area under the LV systolic pressure curve, is correlated with myocardial oxygen requirements, and was found to be a reliable measurement of total LV work [5, 6]. Diastolic pressure-time integral—the integral of aortic pressure minus LV pressure during diastole—is related to myocardial blood flow and may be used as an index of oxygen availability to the myocardium. Thus, the EVR can be used to estimate the oxygen supply/demand ratio of the heart [7].
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) were calculated from measurements of LV pressure. Left ventricular end-diastolic pressure was LV pressure when dP/dt equaled 10% of peak +dP/dt. Peak +dP/dt was the maximum of the time derivative of LV pressure. Peak -dP/dt was the minimum time derivative of LV pressure. Tau (), the constant of isovolumic pressure relaxation, was calculated as the negative reciprocal of the slope of the plot of the natural logarithm of LV pressure versus time from maximum negative dP/dt (maximum rate of decrease of LV pressure) to 5 mm Hg above the LV end-diastolic pressure. The blood volume ejected from the wrapped aortic segment, wrap stroke volume, was calculated as the algebraic summation of the proximal and distal aortic flows measured after the onset of stimulation. Coronary minute-flow in the LAD coronary artery was calculated by integrating the coronary flow signal over each cardiac cycle and multiplying by heart rate.
Data are presented as the mean ± SEM; stimulated and unstimulated beats were compared by paired t tests. When the data failed normality, they were compared by a Wilcoxon signed rank test. For this study, peak LV pressure failed normality. A probability value less than 0.05 was considered statistically significant.
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Results |
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TopAbstractIntroductionMaterial and methodsResultsCommentAcknowledgmentsReferences |
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Sample data taken during aortic counterpulsation when the muscle was stimulated following every second R-wave (1:2 mode) are shown in Figure 3. The optimum R-wave delay and train duration ranged from 34% to 58% and 53% to 75% of the R-R interval, respectively. The top panel shows LV and aortic pressures, together with the ECG. The closely spaced spikes on the ECG are the muscle stimulation pulses. During counterpulsation, aortic diastolic pressure was increased and peak LV pressure in the ensuing cardiac systole was decreased. The second panel shows that coronary blood flow increased during stimulation (first and third beats). In the third panel, aortic blood flow proximal and distal to the muscle-wrapped region shows that, during muscle stimulation, proximal flow was negative (flow was directed toward the heart) and distal flow became more positive (flow was directed toward the viscera). The bottom panel shows the difference of the proximal and distal flow signals—net flow out of (positive), or into (negative) the wrapped segment. During muscle contraction, there was flow out of the wrapped segment; during muscle relaxation, net inflow occurred.
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Comment |
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TopAbstractIntroductionMaterial and methodsResultsCommentAcknowledgmentsReferences |
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The effects of chronic aortomyoplasty have been studied in animals with normal hearts [8–11], in pharmacologically induced acute LV dysfunction [12–14], in hearts made acutely ischemic by coronary artery ligation [15, 16], and in one case, chronic heart failure [11, 17]. In the normal heart, aortomyoplasty increased EVR [8, 9, 11, 13], mean diastolic aortic pressure [11], cardiac output, and stroke volume [15]. After induction of acute LV dysfunction, EVR [8, 12–14] and mean diastolic aortic pressure [13–16] were increased by aortomyoplasty. Cardiac output was increased [12–14] and afterload was reduced—as suggested by a decrease in LV end-diastolic pressure [13, 14]. Reversal of paradoxical wall motion during counterpulsation—in a region of the heart made ischemic by coronary artery ligation—has also been observed [16]. Until this time, the demonstration of increased coronary flow with aortomyoplasty has depended on indirect measurements, such as increased mean diastolic aortic pressure or EVR. In the only other study measuring coronary blood flow during aortomyoplasty, muscle stimulation did not affect LAD coronary artery blood flow following induction of ischemia by partial occlusion of the LAD [15]. This work, however, directly demonstrates increased coronary blood flow with aortomyoplasty.
Greater volume ejection might be accomplished if a greater length of aorta could be wrapped. This study used a circumferential muscle wrap and, at the time of the original operation, we noted that about 10-cm of aorta was covered by the muscle. At the terminal study, muscle coverage of the aorta had decreased to 6 to 8 cm. We hypothesize this decrease in coverage was due to cephalad motion of the muscle wrap during the early postoperative period before muscle-to-aorta adhesion had occurred. At autopsy, no coarctation from the muscle wrap and no trauma to the intima of the aorta were noted. Perhaps if the distal portion of the muscle had been secured to the rib cage, more complete coverage might have been maintained, and the resulting volume of blood ejected from the wrapped segment might have increased.
The IABP reduces LV afterload by balloon deflation timed to the onset of cardiac systole. Analogously, muscle relaxation determines afterload reduction during aortomyoplasty. In setting the timing of balloon deflation during the IABP procedure, a presystolic dip in aortic pressure is used as a guide. Unlike the IABP procedure, however, there was no presystolic dip in aortic pressure during aortomyoplasty. Nevertheless, a decrease in peak LV systolic pressure following muscle relaxation was observed uniformly (Table 1)—suggesting reduction in LV afterload. The lack of a presystolic dip is consistent with recent studies with real timing suggesting relaxation during isovolumic contraction maximally offloads the left ventricle and optimizes ventriculoarterial coupling [18].
One other laboratory has studied aortomyoplasty in a chronic heart failure model [11, 17] in which descending aortomyoplasty was performed in dogs with heart failure induced by rapid ventricular pacing. Aortomyoplasty reduced peak LV pressure, end-diastolic pressure, and LV stroke work; EVR and maximum systolic elastance were both significantly increased. These results suggest that intrinsic myocardial function improves and that afterload is reduced with aortomyoplasty. The underlying etiology for improved load-independent function was not elucidated. As coronary flow was not measured, one cannot say whether improved intrinsic myocardial function was secondary to increased coronary blood flow, or due to other factors.
The effects of aortomyoplasty likely depend on the heart failure model used as well as the severity of heart failure. Some studies reported no effect of aortomyoplasty in normal hearts, then demonstrated an effect after induction of acute LV dysfunction [12, 13]. The study reported here and that of Lazzara and colleagues [11, 17] used the rapid-pacing heart failure model. Whether a 15% increase in coronary blood flow together with only a slight decrease in LV peak systolic pressure (Table 1) in the rapid-pacing model of (primarily) dilated cardiomyopathy will improve cardiac function is unclear. Lazzara and colleagues showed a small decrease in LV end-diastolic volume during counterpulsation by aortomyoplasty. The study reported here did not measure LV volume. Although ischemia has been included among the pathologies associated with the rapid-pacing heart failure model [19], another useful model in which to test the effects of aortomyoplasty is the coronary microembolization model of ischemic heart failure [20]. Because aortomyoplasty increases coronary blood flow, it may be effective in treating ischemic heart failure.
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Acknowledgments |
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TopAbstractIntroductionMaterial and methodsResultsCommentAcknowledgmentsReferences |
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References |
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TopAbstractIntroductionMaterial and methodsResultsCommentAcknowledgmentsReferences |
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This article has been cited by other articles:
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  N. Hedayati, J. T. Sherwood, S. J. Schomisch, J. L. Carino, and B. L. Cmolik Circulatory benefits of diastolic counterpulsation in an ischemic heart failure model after aortomyoplasty J. Thorac. Cardiovasc. Surg., June 1, 2002; 123(6): 1067 - 1073. [Abstract] [Full Text] [PDF]
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