Vascular delay and intermittent stimulation: keys to successful latissimus dorsi muscle stimulation.

BACKGROUND: The goal of this study was to obtain physiologically significant increases in peak left ventricular (LV) systolic pressure and stroke volume with latissimus dorsi muscle (LDM) stimulation in cardiomyoplasty (CMP). We hypothesized that preserving LDM integrity by vascular delay and intermittent stimulation would significantly increase LDM cardiac assistance. METHODS: In 4 control dogs and 12 dogs that had undergone a vascular delay (VD) procedure, LV dysfunction was induced by intracoronary microsphere injections. Cardiomyoplasty surgery was performed 14 days later, followed by progressive LDM conditioning. In the control dogs and in 6 of the VD dogs, the LDM was stimulated 24 hours per day (VD plus constant stimulation [CS]). In the other 6 VD dogs, LDMs were stimulated on a daily schedule of 10 hours on and 14 hours off (VD plus interrupted stimulation [IS]). Latissimus dorsi muscle stimulated beats were compared with nonstimulated beats 9 weeks later. RESULTS: In the control dogs, LDM stimulation had minimal effects. In VD + CS and VD + IS, LDM stimulation increased peak LV pressure, stroke volume, stroke work, and stroke power (p < 0.05). However, these changes were greater in the VD + IS group, in which LDM stimulation increased peak aortic pressure by 17.6 +/- 1.7 mm Hg, peak LV pressure by 19.7 +/- 1.1 mm Hg, peak positive LV dp/dt by 398 +/- 144 mm Hg per second, stroke volume by 5.1 +/- 0.7 mL, stroke work by 10.9 +/- 0.9 gm.m, and stroke power by 122.7 +/- 11.6 gm.m per second (p < 0.05 compared with VD + CS). Quantitative morphometric analysis showed minimal LDM degeneration in the VD + IS group (7.5% +/- 1.1%), and VD + CS group (10.5% +/- 4.5%) compared with the control group (29.5% +/- 4.5%, p < 0.05). CONCLUSIONS: VD and IS considerably increased the LV assistance with LDM stimulation. Further studies of this combined approach to CMP should be planned.

Two step cardiomyoplasty with vascular delay: effect of stimulation of latissimus dorsi muscle on diastolic function.

A common concern in cardiomyoplasty is whether latissimus dorsi muscle (LDM) stimulation impairs diastolic function. This study determined the time course of left ventricular (LV) contraction and relaxation and their relationship to the diastolic function. Ten mongrel dogs underwent vascular delay of the left latissimus dorsi muscle 2 weeks before cardiomyoplasty. Fourteen to 18 days later, the effects of LDM stimulation were evaluated. Our study demonstrated that LDM stimulation significantly increased peak LV systolic pressure (131.3 +/- 7.5 to 152.0 +/- 7.5* mm Hg), +dP/dt (1585 +/- 151 to 2088 +/- 176 x mm Hg/s), stroke volume (10.8 +/- 1.5 to 13.8 +/- 1.9* ml), stroke work (17.2 +/- 2.7 to 25.6 +/- 3.8* gm x m), and peak aortic flow (4751 +/- 698 to 6712 +/- 926* ml/min), and significantly decreased the pre-ejection time (113.9 +/- 12.6 to 92.3 +/- 7.8* ms) and total systolic time (366.0 +/- 26.9 to 333.6 +/- 21.3* ms) (*p < 0.05). As for diastolic function, LDM stimulation decreased -dP/dt (-1462 +/- 116 to -1781 +/-116* mm Hg/s) and tau (64.0 +/- 6.1 to 52.1 +/- 2.9* ms). The diastolic filling time (Tdf) was significantly longer (177.9 +/- 17.6 to 213.7 +/- 18.7* ms) during the beat immediately after LDM stimulation. These changes reflected an overall stronger contraction and faster relaxation. Our results imply that with vascular delay, stimulation of LDM not only assists systolic function but also improves diastolic function in cardiomyoplasty.

Vascular delay of the latissimus dorsi provides an early hemodynamic benefit in dynamic cardiomyoplasty.

OBJECTIVES: Dynamic cardiomyoplasty (CMP) as a surgical treatment for chronic heart failure improves functional class status for most patients. However, significant hemodynamic improvement with latissimus dorsi muscle (LDM) stimulation has not been consistent. The current protocols do not allow early LDM stimulation after CMP surgery. We hypothesized that vascular delay of LDM would increase myocardial assistance after CMP and allow early (48-h) LDM stimulation after CMP. METHODS: Mongrel dogs (n = 24) were divided in four groups: 1) controls (n = 6), single-stage CMP; 2) Group ES (n = 6), single-stage CMP with early LDM stimulation beginning 48 h, postoperatively; 3) Group VD (n = 6), vascular delay of the LDM followed by CMP without early LDM stimulation, and 4) Group VDES (n = 6), vascular delay of LDM (14-18 days), followed by CMP with early stimulation (48 h postoperatively). Two weeks after CMP, global cardiac dysfunction was induced by injecting microspheres into the left coronary artery. LDM-assisted (S) beats were compared with nonstimulated beats (NS) by measuring aortic pressure (AoP), LV pressure, aortic flow, and by calculating first derivative of LV contraction (+/-dP/dt), stroke volume (SV), and stroke work (SW). RESULTS: In ES, LDM stimulation had no effect on the hemodynamic parameters. In the other groups, LDM stimulation significantly (p < 0.05) increased AoP, LVP, dP/dt, SV, and SW. However, these increases were much larger in VD and VDES. In VD, LDM stimulation increased peak AoP by 21.5+/-3.8 mm Hg, LVP by 22.1+/-4.1 mm Hg, dP/dt by 512+/-163 mm Hg/sec, SV by 10.4+/-2.3 mL, and SW by 22.1+/-5.4 g/m(-1). Similarly, in VDES, LDM stimulation increased peak AoP by 24.1+/-4.7 mm Hg, LVP by 26.2+/-4.3 mm Hg, dP/dt by 619+/-47 mm Hg/sec, SV by 6.5+/-0.7 mL, and SW by 16.7+/-4.1 g/m(-1). CONCLUSIONS: In dogs with global LV dysfunction, CMP after vascular delay resulted in a significant improvement in hemodynamic function measured 2 weeks after surgery. This improvement was not provided by single-stage CMP with or without early stimulation. Vascular delay of the LDM before surgery may play an important role for early benefit after CMP, shorten the overall muscle training period, as well as increase hemodynamic response to LDM stimulation.

Preconditioning of the latissimus dorsi muscle in cardiomyoplasty: vascular delay or chronic electrical stimulation.

OBJECTIVES: In standard single stage cardiomyoplasty (CMP), the latissimus dorsi muscle (LDM) is not preconditioned prior to surgery. We hypothesized that latissimus dorsi preconditioning by vascular delay or by chronic electrical stimulation would result in an improved LV hemodynamic function early (14 days) after CMP. METHODS: Mongrel dogs had preconditioning of the latissimus dorsi by a vascular delay procedure followed by CMP 14-18 days later (group I VD). Dogs in group II underwent 4 weeks of chronic stimulation (CS) of the latissimus dorsi (2 V/30 Hz, six bursts/min) followed by CMP. The latissimus dorsi muscle was fully stimulated from 48 h after cardiomyoplasty in both groups (2 V/30 Hz, three bursts/min). Two weeks after myoplasty, injecting 2.0-3.0 x 10(5) 90 microm latex microspheres in the left main coronary artery induced global cardiac dysfunction. Hemodynamic function was then evaluated for latissimus dorsi muscle assisted (S) beats and non-stimulated beats (NS) in each group by measuring peak systolic aortic pressure (AOP), left ventricular pressure (LVP) and end diastolic pressure (LVEDP), and by calculating maximum and minimum dP/dt. RESULTS: Dogs with vascular delay of the latissimus dorsi showed a marked increase for all hemodynamic indices (AOP: 23.9+/-2.5%, LVP: 23.5+/-2.2%, max dP/dt: 49.4+/-3.3%) for LDM assisted (S) beats compared to non-stimulated beats (P < 0.001). Animals with chronic electrical training did not demonstrate a significant increase in any hemodynamic parameter with LDM stimulation. CONCLUSION: Preconditioning the LDM may play an important role in providing early cardiac assistance in CMP. Preconditioning the LDM with vascular delay resulted in improving performance of the LDM with consistent increases in LV hemodynamics. This was not observed after preconditioning with chronic electrical stimulation. Vascular delay of the latissimus dorsi can significantly improve muscle performance in CMP and could provide hemodynamic assistance early after surgery.

Cardiomyoplasty: hemodynamic benefit to normal and depressed canine left ventricular function.

This study examined the effects of cardiomyoplasty with vascular delay on canine normal and depressed left ventricular (LV) function. To improve viability of the latissimus dorsi muscle (LDM), vascular delay was performed 2 weeks before cardiomyoplasty in 10 mongrel dogs. Two weeks after cardiomyoplasty, LV function was evaluated by simultaneously measuring LV and aortic pressure, and aortic flow. The LDM was stimulated at a ratio of 1:4-1:7 synchronously with ventricular systole. Microspheres (90 mu) were sequentially injected into the left coronary artery to depress LV function. Data were acquired and analyzed on a beat to beat basis. Results were as follows: LDM stimulation significantly augmented LV systolic pressure (LVSP) from 138 +/- 2 to 161 +/- 2* mmHg, the peak rate of change of LV pressure (+dP/dt) from 1888 +/- 46 to 2584 +/- 43* mmHg/sec, aortic systolic pressure (AoSP) from 140 +/- 2 to 159 +/- 2* mmHg, stroke volume (SV) from 11.2 +/- 0.3 to 13.3 +/- 0.3* ml, stroke work (SW) from 19 +/- 1 to 26 +/- 1* gm.m, peak aortic flow (P Qa) from 5542 +/- 142 to 7190 +/- 161* ml/min, and decreased -dP/dt from -1683 +/- 31 to -1689 +/- 49* mmHg/sec (* = p < 0.05). Microsphere injections depressed LV function, but did not affect the magnitude of the net changes between stimulated and nonstimulated beats. However, the percent changes significantly increased. Preconditioning of LDM with vascular delay augments cardiac function in LDM assisted beats. This improved performance was present in both normal as well as depressed LV function groups. Thus, investigations of cardiomyoplasty may not necessarily require a model of severe myocardial dysfunction. Vascular delay offers an important preconditioning method of LDM to augment cardiac function in cardiomyoplasty.

Variable effects of cardiomyoplasty on left ventricular function.

Cardiomyoplasty (CMP) has been considered as a possible treatment for patients with heart failure. Symptomatic improvements occur almost uniformly among survivors with CMP, but changes in left peak ventricular systolic pressure (PVSP) and stroke volume vary in patients. This study examined whether there is variability present shortly after cardiomyoplasty surgery. Cardiomyoplasty was performed in 11 mongrel dogs with normal ventricular function. Nine to twelve days after CMP, left ventricular (LV) function was evaluated by simultaneously measuring LV volume (conductance catheter) and pressure (Millar catheter). The latissimus dorsi muscle (LDM) was stimulated synchronously with ventricular systole in a ratio of 1:4 to 1:7 to avoid muscle fatigue. Data were analyzed on a beat by beat basis. The PVSP, and maximum dP/dt (+dP/dt) increased, but the absolute value of minimum dP/dt (-dP/dt) decreased in stimulated beats in 7 dogs while 4 dogs did not respond. The net changes in stimulated beats versus nonstimulated beats of PVSP were 6.1 +/- 1.8 mm Hg (4.3%), of stroke work was 4.5 +/- 1.9 gm x m (29.5%), of +dP/dt was 185 +/- 47 mm Hg/s (8%), and of -dP/dt was 168 +/- 43 mm Hg/s (7.8%) (p < 0.05) for all these net changes in the responding group while these variations were not significant in the nonresponding group. From the results of our study, active LDM assist improves left ventricular systolic function, occurring in only 7 of 11 experiments. This improvement is inconsistent and varied individually. The integrity of the LDM, tightness of wrapping, and adhesions might contribute to the variability which is present early after surgery and before the LDM is converted into a fatigue resistance muscle.

Examination of epimysial leads used to stimulate the latissimus dorsi muscle.

Cardiomyoplasty is a new surgical treatment for heart failure in which the patient's latissimus dorsi muscle (LDM) is isolated, wrapped around the heart, and electrically stimulated to provide cardiac assistance. At present, long term stimulation of the LDM is achieved with intramuscular electrodes, which produce minimal nerve damage. This study examined the use of epimysial electrodes by measuring the epimysial lead characteristics during a four-week LDM training. Lead resistance started at 463 +/- 41 omega after implantation, decreased during the following week (251 +/- 16 omega), and remained less than the initial value during the last three weeks (weeks two: 282 +/- 19 omega and week four: 341 +/- 28 omega). The recruitment properties were similar to nervecuff electrodes: low threshold voltages (week one: 0.75 +/- 0.12, week two: 0.90 +/- 0.33, week four: 0.52 +/- 0.10 V) and a very steep recruitment curve with low saturation voltages. Histological examination revealed normal muscle fibers with no inflammatory response. Epimysial leads may be more convenient for most surgeons because the design does not require any free-dissection of the nerve nor guiding a needle around the nerve with the risk of perforating vessels or nerve branches. These results indicate that epimysial leads are worthy of further investigation.

The effect of interferon-gamma on rejection and neutrophil function following transplantation.

Rats were used as a model for a living heterotopic cardiac allograft organ transplant. Rats treated in this model with recombinant rat interferon-gamma (IFN-gamma) showed accelerated rejection in a dose-dependent fashion. However, rats treated with maintenance doses of cyclosporine and IFN-gamma expressed increased rejection at 20 days that had resolved completely by 45 days post-transplantation. Polymorphonuclear leukocytes (neutrophils) were isolated from the blood of rats, and their function was determined by treating the cells with f-Met-Leu-Phe (fMLP) and measuring superoxide produced. Results indicate that the neutrophils from rats treated with maintenance doses of cyclosporine and IFN-gamma still had increased IFN-gamma-modulated fMLP-induced respiratory burst and that maintenance cyclosporine therapy can inhibit the IFN-gamma-mediated accelerated rejection without compromising the antimicrobial effects of IFN-gamma treatment.

The effects of interferon-alpha/beta in a model of rat heart transplantation.

Interferons have multiple immunologic effects. One such effect is the activation of expression of cell surface antigens. Interferon alpha/beta enhance expression of class I but not class II histocompatibility antigens. Contradictory information has been published regarding the effect of interferon-alpha/beta administration in patients with kidney transplantation. In a model of rat heart transplantation we demonstrated that administration of interferon-alpha/beta accelerated rejection in a dose-dependent fashion in the absence of maintenance cyclosporine. Animals treated with maintenance cyclosporine had evidence of increased rejection at 20 days that was resolved completely at 45 days with cyclosporine alone.

Quantitative electroencephalographic monitoring during myocardial revascularization predicts postoperative disorientation and improves outcome.

We evaluated computerized quantitative electroencephalography for the intraoperative detection of cerebral dysfunction. The quantitative electroencephalogram was recorded continuously during 96 myocardial revascularizations involving hypothermic cardiopulmonary bypass using Cerebrovascular Intraoperative MONitor (CIMON) software. CIMON relies on an adaptive statistical approach to detect subtle, but clinically relevant, changes in electroencephalographic activity indicative of cerebrocortical dysfunction. Relative (percent of total) low-frequency (1.5 to 3.5 Hz) power was chosen as the single quantitative electroencephalographic descriptor because it is an established hallmark of cortical dysfunction and is surprisingly insensitive to moderate changes in body temperature and level of opioid anesthesia. Reference values for this measure were established for each patient after anesthetic induction before sternotomy. The large sample variance often seen in low-frequency power was dramatically decreased by using log-transformed data and allowing each patient to serve as his own control. Quantitative electroencephalographic changes in standard deviation units or z-scores were determined from the individualized reference self-norm. Prolonged (greater than 5 minutes) and statistically significant (greater than 3 standard deviation) focal increases in relative low-frequency power were temperature-corrected to determine a standardized cerebrocortical dysfunction time at 37 degrees C. (CDT37). In phase I (n = 48), this objective quantitative electroencephalogram-based numeric descriptor was used to predict neuropsychologic outcome. These CDT37 greater than 5-minute episodes occurred 38 times in 19 patients. The quantitative electroencephalogram-based descriptor predicted the occurrence of such disorientation (n = 14 or 29%) with a 68% false positive rate but only an 8% false negative rate. Since these intraoperative quantitative electroencephalographic episodes were often (19/38) associated with low (less than 50 mm Hg) pump pressures, phase II (n = 48) sought to correct the quantitative electroencephalographic abnormality and prevent postoperative disorientation by appropriate increases in cerebral perfusion. Although the number of episodes of quantitative electroencephalographic abnormality was similar (n = 31) in phase II, these ischemic events disappeared after prompt elevation of perfusion pressure. The phase II disorientation rate fell significantly (p less than 0.002) to 4%. Thus statistically significant increases in low-frequency electroencephalographic relative power persisting for a temperature-corrected duration of 5 minutes or more are a reliable means of alerting the surgical/anesthesia team to the presence of cerebrocortical dysfunction and provide a rational and objective basis for corrective intervention. This form of electroencephalographic monitoring appears to offer an opportunity for the timely correction of perfusion abnormalities or the administration of cerebroprotectant compounds.

Is defibrillation testing safe?

Determination of defibrillation thresholds (DFTs) and implantable cardioverter defibrillator (ICD) testing requires repeated inductions of ventricular fibrillation (VF) and defibrillation attempts using known energy outputs. Little is known about the individual and cumulative effects of repetitive brief episodes of VF and hypoperfusion on cerebral function. The potential clinical utility of quantitative electroencephalographic (QEEG) monitoring during intraoperative ICD testing, by using processed 19-channel EEG (0.5-35 Hz bandwidth), was examined in ten anesthetized patients, five males and five females (mean age 62 +/- 10 years), who underwent ICD implantation and testing. Ischemic QEEG patterns were defined as those with a 3 standard deviation increase (P less than 0.01) in absolute delta (1.5-3.5 Hz) power persisting for greater than or equal to 2.5 minutes. The majority (80%) of the VF episodes (70) were accompanied by QEEG "slowing" (doubling of the pre-VF low frequency delta waves amplitude). All the patients (5/5) experiencing greater than 6 VF episodes showed a statistically significant increase in the low frequency amplitude. In contrast, this EEG abnormality was apparent in only one of five patients experiencing less than 6 VF episodes. These results suggest a cumulative QEEG depression associated with ICD testing. QEEG may provide an objective means for establishing an individualized upper safe limit of DFT testing and the total number of induced VF episodes.

Lateral thoracotomy for the automatic implantable defibrillator.

In 51 patients who required automatic implantable cardioverter defibrillator implantation without additional cardiac procedures, the lead system was implanted using a lateral thoracotomy approach, with complete muscle sparing in the last 24 patients. Exposure was excellent and allowed repositioning of leads for optimal defibrillation thresholds in 18 patients. Five of 19 patients who had previously undergone intrapericardial procedures required intrapericardial dissection for lead placement to provide satisfactory defibrillation thresholds. There were no intraoperative deaths or infarctions. The 30-day mortality rate of 3.9% was comparable with those in other series, and the use of muscle-sparing techniques and supplemental epidural anesthesia prevented pulmonary complications or the need for prolonged ventilatory support. We favor a muscle-sparing lateral thoracotomy incision for automatic implantable cardioverter defibrillator insertion, particularly in patients with a history of previous intrapericardial procedures.

Continuous arteriovenous hemofiltration in the critically ill patient.

Continuous arteriovenous hemofiltration (CAVH) is a simple extracorporeal treatment for fluid overload, electrolyte imbalances, and removal of uremic toxins. The CAVH technique can be initiated rapidly and allows effective fluid removal without compromising cardiovascular status. This article describes two illustrative cases where CAVH was used to treat fluid overload accompanying in one case cardiogenic shock and in the other case septic shock. CAVH may have contributed to the removal of sepsis-related vasodilators as well as excess fluid. This therapy is an attractive alternative to hemodialysis in the critical care setting and may be the treatment of choice in hemodynamically unstable patients.

Emergency aortocoronary bypass after failed angioplasty.

One thousand two hundred fourteen percutaneous transluminal coronary angioplasties were performed over a 38-month period. Sixty patients required immediate emergency coronary artery bypass grafting after angioplasty failure; 7 of these had evidence of acute myocardial infarction before angioplasty and were excluded from the study. Of the 53 patients remaining, 27 (51%) had electrocardiographic and enzyme evidence of postoperative myocardial infarction. Two patients died (4%), and 10 had postoperative complications (19%). No statistical significance was noted comparing age, sex, incidence of prior myocardial infarction or myocardial dysfunction, time for revascularization, or average number of grafts completed in those with single-vessel (n = 21) versus multiple-vessel (n = 32) coronary artery disease. Postoperatively, those with multiple-vessel disease required intraaortic balloon pump support (p = 0.06) and antiarrhythmic medications more frequently than single-vessel patients (p less than 0.01) and had a higher complication rate (p less than 0.05). Although not reaching statistical significance, the data also suggest a higher death and postoperative myocardial infarction rate in patients with multiple-vessel disease. Emergency coronary artery bypass grafting after failed percutaneous transluminal coronary angioplasty carries a higher morbidity and mortality than elective coronary artery bypass grafting, particularly for patients with multiple-vessel coronary artery disease.

Repetitive intraoperative mapping and cryotherapy improve the results of endocardial resection for ventricular tachycardia.

Patients with recurrent ventricular tachycardia or a history of a sudden cardiac death episode and ventricular tachycardia inducible in the electrophysiology laboratory have a high incidence of recurrence and a high mortality despite medical therapy. Map-guided endocardial resection has improved treatment results, but is associated with a 10-30% failure rate. In our initial experience with endocardial resection (Group I) we incurred a 30% treatment failure rate. In the present study we have found the addition of sequential intraoperative mapping and routine use of cryotherapy (Group II) improved our results of ventricular tachycardia control without significant additional morbidity or mortality.

Extended use of bilateral internal mammary arteries for coronary artery disease.

The internal mammary artery is the conduit of choice for coronary artery revascularization. Wide angulation between the left anterior descending coronary artery and obtuse marginal branches and the diseased segments of the coronary arteries can prevent optimal positioning of the left internal mammary artery for sequential anastomoses for revascularization. We describe a technique using a segment of the left internal mammary artery as a free graft sewn in an end-to-side fashion to the in situ left internal mammary artery. This approach has technical and physiological advantages over previously described techniques.

Management of extensive right ventricular injury or rupture.

Most penetrating right ventricular injuries require simple suture repair, but more extensive injury or rupture of the right ventricle may not be amenable to this method. We have developed an approach to the problem and a technique for repair. Compression of the area with early institution of cardiopulmonary bypass will result in decompression of the right ventricle and preservation of perfusion, preventing profound hypotension. Coverage with an onlay autologous tissue patch provides hemostatic control of the defect without compromising ventricular function. Reinforcement with omentum or muscle flap can give additional protection when risk of infection is present. Application of these principles can be lifesaving and insure good cardiac function despite massive injury to the right ventricular myocardium.