Improving heart failure care by using a telemedicine system.

Heart failure constitutes the most frequent and expensive hospital discharge diagnosis in the United States, costing annually over $10 billion. Optimal care requires an understanding of their illness, participating in clinical decisions, and frequent communication. Current surveillance is labor intensive and expensive. Follow-up is often inadequate, incomplete, and inconsistent. To address these problems, we developed an Internet-based telemedicine system, consisting of a secure server and database. Patients send or receive data to or from their care provider via the Internet. The system optimizes function and minimizes cost (all hardware is off the shelf and FDA approved). This paper describes our initial experience with this system. We are currently using this telemedicine system in a prospective, randomized clinical trial, comparing Class III or IV heart failure patients with standard care versus standard care plus telemedicine.

Can latissimus dorsi muscle stimulation benefit heart during training period after vascular delay?

We hypothesized that a two-stage vascular delay procedure followed by 5 weeks of conditioning of the latissimus dorsi muscle (LDM) could benefit the heart during the training period and greatly increase cardiac assistance when examined with maximum potential. In mongrel dogs (n = 10), left ventricle (LV) dysfunction was induced by intracoronary injections of latex microspheres [90 +/- 2 micro diameter]. Vascular delay of the LDM was performed in one group (n = 6), whereas the other group (control, n = 4) did not undergo vascular delay. After 2 weeks, CMP was performed in all animals followed by LDM conditioning. After 5 weeks of muscle training, we examined left ventricular function at 20 Hz-4 volts, 33 Hz-4 volts, and 50 Hz-10 volts stimulation by assessing peak aortic pressure (AoP), left ventricular pressure (LVP), maximum LV +dP/dt, stroke volume (SV), stroke work (SW), stroke power (SP), and aortic flow. LDM assisted beats were compared with nonstimulated beats. LDM stimulation caused significant increases in pressure and flow in the vascular delay group. At 20 Hz-4 volts, absolute increases were LVP (10.2 +/- 0.6) mm Hg, AoP (9.8 +/- 1.7) mm Hg, SV (1.8 +/- 0.4) ml, SW (5.3 +/- 1.0) gm x m, SP (40.8 +/- 12.7) gm x m/sec, max LV dP/dt (104.8 +/- 53.2) mm Hg/sec, and peak aortic flow (0.9 +/- 0.3) L/min. At 33 Hz-4 volts, the absolute increases were LVP (13.6 +/- 1.3) mm Hg, AoP (12.1 +/- 2.4) mm Hg, SV (2.7 +/- 0.7) ml, SW (7.4 +/- 1.4) gm x m, SP (72.7 +/- 16.5) gm x m/sec, max LV dP/dt (294 +/- 19) mm Hg/sec, and peak aortic flow (1.8 +/- 0.5) L/min. At 50 Hz-10 volts, the absolute increases were LVP (17.7 +/- 0.7) mm Hg, AoP (21.1 +/- 1.9) mm Hg, SV (6.0 +/- 1.1) ml, SW (14.6 +/- 2.2) gm.m, SP (128.2 +/- 15.3) gm x m/sec, max LV dP/dt (352 +/- 62) mm Hg/sec, and peak aortic flow (3.3 +/- 0.4) l/min (p < 0.05). The percentage increases were significantly larger in the vascular delay group compared with controls at 50 Hz-10 volts LDM stimulation. By using a two-stage vascular delay procedure, LDM stimulation can provide meaningful cardiac assistance during training periods. Furthermore, brief periods of maximal potential benefit (demand cardiomyoplasty) can be achieved during the training period.

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.

Chemoreflexes: an experimental study.

HYPOTHESIS: Transmyocardial laser revascularization (TMLR) will not denervate the heart, because it does not destroy all of the afferents. This study was designed to determine if stimulation of cardiac sympathetic and vagal afferents from an area of the left ventricle treated with TMLR could evoke reflex effects, and thus whether TMLR would denervate the heart. METHODS: The effect of TMLR on reflexes evoked by chemically stimulating cardiac afferents was examined in 9 dogs. Bradykinin and capsaicin were applied topically or injected into the left anterior descending coronary artery before and after TMLR and after bilateral vagotomy and sympathectomy. Aortic (AoP) and left ventricular pressures (LVP) and electrocardiography were monitored. The first derivatives of LVP (dP/dt) were calculated. RESULTS: Topical bradykinin elicited variable hemodynamic responses. Topical capsaicin evoked pressor responses, increasing mean (+/- SEM) AoP (105+/-9 to 115+/-9 mm Hg; P<.001) and positive dP/dt (+dP/dt) (1032+/-81 to 1159+/-10 mm Hg/s; P<.01) before TMLR. Intracoronary capsaicin evoked a depressor response before TMLR. Pressor responses remained intact after TMLR with increases in mean AoP and +dP/dt (115+/-6 to 128+/-5 mm Hg and 1039+/-98 to 1136+/-100 mm Hg/s, respectively; P<.01). Depressor responses also remained intact after TMLR (91+/-10 vs 101+/-11 mm Hg [P<.02], and 865+/-104 vs 931+/-104 mm Hg/s [P<.05], respectively). Hemodynamic responses were diminished after bilateral vagotomy and abolished after bilateral sympathectomy. CONCLUSION: Since activation of cardiac afferent nerves and reflex responses remained intact after TMLR, but changed after vagotomy or sympathectomy, TMLR does not denervate the heart sufficiently to be the cause of improved angina after TMLR.

Evaluation of stimulation parameters on aortomyoplasty, using Latissimus Dorsi muscle in a goat model: an acute study.

OBJECTIVE: Dynamic aortomyoplasty using Latissimus Dorsi muscle (LDM) has been shown to improve myocardial function. However, systematic examination of the effects of stimulation parameters on aortic wrap function has not been done. Thus, the present study measures the direct effect of stimulation voltage, pulse train duration, frequency of the pulses, and the duration of the stimulation delay from R wave on the aortic wrap function. METHODS: In eight female goats, the left LDM was wrapped around the descending aorta. The muscle was then subjected to electrical stimulation, altering frequency of stimulation pulses (16.6, 20, 25, 33 and 50 Hz), amplitude (2, 4, 6, 8 and 10 V), and number of pulses (2, 4, 6, 8 and 10 pulses) in a train stimulation. Left ventricular, aortic pressure, and pressure generated by LDM on aorta (wrap pressure) was measured. The changes in hemodynamic parameters mentioned above were calculated and compared for different stimulation parameters during unassisted and assisted cardiac cycles. RESULTS: Aortomyoplasty counterpulsation using LDM provided significant improvement in wrap pressure (78 mmHg +/- 2), aortic diastolic pressure, and changes in aortic diastolic pressure from 2 to 4 V (P < 0.05). Further increase in amplitude did not make any significant improvements of the above mentioned parameters. Significant augmentation of wrap pressure (82 mmHg +/- 2), aortic diastolic pressure (79 mmHg +/- 3) and changes in aortic diastolic pressure (12 mmHg +/- 1) occurred at 6 pulses (P < 0.05). Other changes in number of pulses did not show any significant improvements. Significant improvement of wrap pressure (80 mmHg +/- 2), aortic diastolic pressure (73 mmHg +/- 3) and changes in aortic diastolic pressure (12 mmHg +/- 1) was observed with a frequency of 33 Hz. To examine a wide range of delays from the onset of the QRS complex to LDM stimulation, stimulation was delivered randomly. The exact delay was determined from the ECG signal and superimposed LDM stimulation pulses. CONCLUSIONS: In this study we present a new measurement, wrap pressure. We also present that in aortomyoplasty using LDM, the most significant improvement in wrap pressure, aortic diastolic pressure and changes in aortic diastolic pressure occurs when the stimulation consists of an amplitude of 4 V, a frequency of 33 Hz and a train stimulation of 6 pulses.

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.

Estimation of oxygen delivery in newborns with a univentricular circulation.

BACKGROUND: The management of neonates with complex congenital anomalies depends on careful interpretation of arterial blood gas values. Improved interpretation of these oxygen parameters may allow clinicians to avoid unexpected cardiovascular events. This study examined whether systemic oxygen delivery (DO2) can be maximized by the use of indices derived from oxygen saturation measurements in neonates with hypoplastic left heart syndrome. METHODS AND RESULTS: For the single-ventricle heart with both circulations in parallel, we used a previously developed computer simulation to obtain DO2 as a function of systemic arterial (SaO2) and venous (SvO2) oxygen saturation, arteriovenous oxygen difference (Sa-vO2), or pulmonary-to-systemic flow ratio (Qp/Qs). We also examined the oxygen excess factor, SaO2/Sa-vO2 (Omega). We found that (1) slight increases in SaO2 may be associated with large decreases in DO2. (2) Low values for SvO2 indicate low values for DO2. (3) Curves for Sa-vO2 and Qp/Qs are redundant in the data provided. (Qp/Qs, however, provides these data in more physiologically relevant terms.) (4) High values for Qp/Qs (>4) are associated with low DO2. (5) Estimating Qp/Qs from oxygen saturation measurements may result in errors when pulmonary venous oxygen saturation is not available. (6) Maximizing DO2 is extremely difficult using SaO2, SvO2, and Qp/Qs. (7) A linear relationship exists between Omega and DO2, and this linear relationship is not altered by changes in cardiac output. CONCLUSIONS: Patients with low SvO2 values require attention. Ideally, after reducing Qp/Qs to <1.5, Omega might be a better index to guide further therapy and maximize DO2. Interventions that increased Omega would be considered beneficial, whereas interventions that decreased Omega would be considered detrimental.

Effects of positive pressure ventilation and inspired oxygen on pulmonary vascular resistance and tissue oxygen delivery in neonatal pigs.

Management of pulmonary vascular resistance in neonates with congenital heart disease is important for stabilization before and after surgical interventions. Thus, we determined which combination of positive end-expiratory pressure ventilation and fraction of oxygen in the inspired air increases pulmonary vascular resistance without compromising delivery of oxygen to the tissue. Eight piglets were anesthetized, intubated and ventilated. Pulmonary flow and pulmonary arterial and left atrial pressures were monitored continuously. At all levels of inspired oxygen (1.00, 0.21 and 0.15), ventilation at a pressure of 15 cm of water increased pulmonary vascular resistance. At all levels of positive pressure ventilation, a fraction of 0.15 of inspired oxygen increased pulmonary vascular resistance. The combination of a ventilatory pressure of 15 cm of water and inspired oxygen of 1.00, or ventilatory pressure at 5 cm of water and oxygen delivery of 0.15, produced similar changes in pulmonary vascular resistance (19.1 +/- 2.8 vs. 20.0 +/- 3.8 mmHg/(L/min)) and cardiac output (0.78 +/- 0.07 vs. 0.93 +/- 0.10 L/min) but, the higher level of positive pressure plus 1.00 inspired oxygen gave a significantly higher arterial oxygen saturation (0.99 +/- 0.03 vs. 0.72 +/- 0.19%) and delivery of oxygen to the tissues (13.7 +/- 2.9 vs. 7.4 +/- 1.5 ml O2/min, p < 0.05). Thus, both high positive pressure ventilation and hypoxia increase pulmonary vascular resistance. Only high pressure ventilation plus high concentrations of inspired oxygen, however, increased pulmonary vascular resistance without compromising delivery of oxygen, suggesting that this combination is a superior means of increasing pulmonary vascular resistance.

Theoretical optimization of pulmonary-to-systemic flow ratio after a bidirectional cavopulmonary anastomosis.

A univentricle with parallel pulmonary and systemic circulations is inherently inefficient because mixing of pulmonary and systemic venous return occurs. Thus a cavopulmonary anastomosis is used as a staged palliative procedure to reduce volume overload in patients with cyanotic congenital heart disease. On the basis of oxygen uptake and consumption, an equation was derived that related cardiac output, pulmonary venous oxygen saturation, upper body oxygen consumption, and superior-to-inferior vena caval blood flow ratio (QSVC/QIVC) to oxygen delivery. The primary findings were as follows. 1) As QSVC/QIVC increases, total body oxygen delivery and arterial and superior vena caval oxygen saturations increase. 2) As QSVC/QIVC increases, lower body oxygen delivery and inferior vena caval oxygen saturation initially increase, then peak, and then decrease. 3) As the percentage of lower body oxygen consumption increases, oxygen delivery and saturation decrease. 4) A cavopulmonary anastomosis decreases the required cardiac output for a given oxygen delivery. Thus we concluded that a high systemic arterial oxygen saturation after cavopulmonary anastomosis requires a high percentage of upper body oxygen consumption and a high QSVC/QIVC and that the cavopulmonary anastomosis reduces the volume load on the single ventricle.

Ventricular interdependence: significant left ventricular contributions to right ventricular systolic function.

This article reviews diastolic and systolic ventricular interaction, and clinical pathophysiological conditions involving ventricular interaction. Diastolic ventricular interdependence is present on a moment-to-moment, beat-to-beat basis, and the interactions are large enough to be of physiological and pathophysiological importance. Although always present, ventricular interdependence is most apparent with sudden postural and respiratory changes in ventricular volume. Left ventricular function significantly affects right ventricular systolic function. Experimental studies have shown that about 20% to 40% of the right ventricular systolic pressure and volume outflow result from left ventricular contraction. This dependency of the right ventricle on the left ventricle helps to explain the right ventricular response to volume overload, pressure overload, and myocardial ischemia. The septum and its position are not the sole mechanism for ventricular interdependence. Ventricular interdependence causes overall ventricular deformation, and is probably best explained by the balance of forces at the interventricular sulcus, the material properties, and cardiac dimensions.

Can indices of left ventricular function be applied to the right ventricle?

This article compares conventional indices of contractile function in the right and left ventricles. The low operating pressures and left ventricles. The low operating pressures and complex geometry complicate evaluation of right ventricular function. However, when the characteristics of its vascular load are taken into account, the complex right ventricular chamber has pump properties that are similar to the high pressure left ventricular chamber.

A versatile microprocessor-based multichannel stimulator for skeletal muscle cardiac assist.

A versatile, microprocessor-based stimulator for skeletal muscle cardiac assist (SMCA) has been designed, constructed, and used in several studies. The stimulator uses multiple bipolar electrodes to deliver arbitrarily specified electrical stimulus sequences to three nerve branches of the latissimus dorsi muscle. The electrodes are electrically isolated to effect regional stimulation of the muscle. The width, amplitude, and interpulse interval of each pulse in the stimulus sequence are independently variable, and the three channels are independently programmable, allowing a wide variety of stimulus patterns. Battery powered units have been used in studies for up to one year. In this paper, the stimulator and sample applications in SMCA are described.

Overcoming right ventricular failure with left ventricular assist devices.

BACKGROUND: Right ventricular failure can lead to circulatory collapse while on left ventricular assist device support. By shunting blood from the femoral vein to the left ventricular assist device, cardiac output can be increased, but arterial oxygen saturation will decrease. METHODS: To determine the effects on O2 delivery, a model was developed on the basis of O2 uptake in the lungs and whole body O2 consumption. An equation was derived that related cardiac output, pulmonary venous O2 saturation, O2 consumption, and the ratio of shunt-to-systemic blood flow to systemic O2 delivery. RESULTS: When total cardiac output increases, the shunt will increase systemic O2 delivery while decreasing arterial O2 saturation and leaving systemic venous O2 saturation unaltered. When total output does not increase, the shunt will decrease systemic O2 delivery, arterial O2 saturation, and systemic venous O2 saturation. CONCLUSIONS: The analysis suggests that measuring systemic venous oxygen saturation may be a useful way to monitor patient safety. A decrease in systemic venous O2 saturation when creating the shunt implies an inadequate increase in cardiac output.

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.

What in-vitro method should surgeons use to evaluate the clinical behavior of arterial bypass conduits.

UNLABELLED: Surgeons have traditionally relied on ring preparations to predict how arterial bypass conduits will behave in the postoperative circulation. OBJECTIVE: This study compared pharmacologic [norepinephrine (NE) challenge] and physiologic [arterial preload] responses of gastroepiploic (GEA) and internal thoracic (ITA) arteries in a standard static ring preparation and a dynamic perfusion system. METHODS: Six GEAs (1.0-1.5 mm dia.) and six ITAs (1.5-2.0 mm dia.) 11 cm long were harvested from adult pigs and mounted on a computer controlled perfusion system. Inflow pressure was set at 80 mmHg and outflow resistance was adjusted to simulate high (80-90 ml/min) and low (15-20 ml/min) flow demands. NE response (10(-9)-10(-5) M) was measured under low flow conditions and at high flow conditions when distal arterial pressure (load) was reduced. NE response (10(-9)-10(-5) M) was also evaluated in arterial rings (ITA N = 6, GEA N = 6) with tensions adjusted to simulate the loads occurring at low flow (80 mmHg) and high flow (60 mmHg) situations. RESULTS: In the static ring preparation, NE response [ED50] was similar for both GEA and ITA and was not affected by load. The dynamic preparation demonstrated that the GEAs were significantly more responsive to NE than the ITAs [ED50 high flow ITA 6.1 +/- 0.3**, GEA 7.2 +/- 0.3***; *P < 0.05 versus baseline, **P < 0.05 versus low flow values, ***P < 0.05 versus ITA]. Furthermore, in the dynamic preparation, NE response was profoundly affected by reduced load which occurs under high flow conditions [7.18 +/- 0.3 versus 6.1 +/- 0.3 under high flow and 5.8 +/- 0.1 versus no response under low flow conditions]. CONCLUSION: Static ring preparations do not discern differences between ITA and GEA susceptibility to spasm and fail to detect the effect of load. The dynamic preparation demonstrated significant differences between the GEA and ITA potential to spasm which is consistent with widespread clinical experience. Furthermore a dynamic preparation is highly sensitive to reduced load which occurs under high flow conditions. Although it is more demanding, the dynamic preparation provides superior information to the surgeon in predicting the behavior of arterial bypass grafts.

Variable-frequency train stimulation of canine latissimus dorsi muscle during shortening contractions.

In cardiomyoplasty, the latissimus dorsi muscle (LDM) is wrapped around the heart ventricles and electrically activated with a constant-frequency train (CFT). This study tested the hypotheses that increased mechanical performance from the LDM could be achieved by activating the muscle with variable-frequency trains (VFTs) of shorter duration or containing fewer stimulus pulses than the CFT now used. The mechanical performance of the canine LDM (n = 7) during shortening contractions was measured while the muscle was stimulated with 5- and 6-pulse CFTs (of duration 132 and 165 ms, respectively) and 5- and 6-pulse VFTs (of duration 104 and 143 ms, respectively) that were designed to take advantage of the catchlike property of skeletal muscle. Measurements were made from fresh and fatigued muscles. For the fresh muscles, the VFTs elicited significantly greater peak power than did the 6-pulse CFT. When the muscles were fatigued, VFT stimulation significantly improved both the peak and mean power produced compared with stimulation by CFTs. These results show that stimulation of the LDM with shorter duration VFTs is potentially useful for application in cardiomyoplasty.

Preventing gastroepiploic artery spasm: papaverine vs calcium channel blockade.

UNLABELLED: The gastroepiploic artery (GEA) is a highly vasoactive artery gaining wider acceptance as a conduit for coronary artery bypass surgery. A variety of agents are used to dilate the GEA prior to grafting; however, little is known about the duration of their effect in the immediate postoperative period. This study evaluated three calcium channel blockers and papaverine in preventing graft spasm. METHODS: Porcine GEA segments (10-12 cm in length) were connected to a computer-controlled perfusion system with a constant in-flow pressure and distal resistance to simulate bypass flow (80-100 ml/min). Norepinephrine (NE; 10(-9) to 10(-5) M) was given in incremental doses at baseline before the vasodilator, immediately after (0 hr), and again at 2 hr after the vasodilator. Changes in flow and ED50 were recorded. Group INT (N = 25) received papaverine (PAP), diltiazem, nifedipine (NFP), or verapamil (VPL) intraluminally, while group EXT (N = 25) received the same dilators externally. RESULTS: All arteries showed dose-dependent vasoconstriction to NE prior to treatment. Immediately after receiving the vasodilator, arteries in both groups (INT and EXT) showed initial protection against NE-induced spasm with the exception of arteries receiving NFD externally. However, at 2 hr, for group INT, only VPL and NFD prevented NE-induced graft spasm (VPL: 40.4 +/- 6.8 ml/min vs 17.9 +/- 3.3 ml/min and NFD: 27.0 +/- 6.5 ml/min vs 13.1 +/- 0.9 ml/min, P < 0.02). In group EXT, after 2 hr, only VPL- and PAP-treated grafts showed resistance to NE-induced vasospasm (VPL: 35.6 +/- 7.3 ml/min vs 15.0 +/- 6.9 ml/min and PAP: 47.4 +/- 15.1 ml/min vs 8.0 +/- 2.0 ml/min, P < 0.001). CONCLUSIONS: Papaverine, a lipophilic vasodilator, when given externally on the perivascular fat of the GEA, prevented graft spasm for up to 2 hr. In contrast, intraluminally applied papaverine did not show graft protection against NE-induced spasm. Nifedipine prevented NE-induced spasm only when given intraluminally. Verapamil proved to be the most potent and versatile vasodilator with effective graft protection of up to 2 hr whether applied externally or internally and was the preferred agent for protecting against GEA spasm.

Cardiomyoplasty. Latissimus dorsi muscle function and blood flow during isolation.

Cardiomyoplasty is a new surgical treatment for heart failure in which skeletal muscle assists the heart. However, for the first 2 weeks postoperatively, the latissimus dorsi muscle (LDM) remains unstimulated, and during the next 2 weeks, the LDM is stimulated with only one pulse every other heart beat. Thus, for the initial 4 postoperative weeks, minimal systolic assistance is provided. The present study determined if the LDM is capable of providing early assistance. Cardiomyoplasty surgery involves severing the perforating intercostal arteries to the LDM, detaching the LDM from its distal insertion, and wrapping it around the heart. At each of these steps, we measured LDM force development, shortening, and blood flow in six dogs. At control, LDM shortening, work, and power decreased during a 2 min fatigue test: fatigue indices (final/ initial value) for shortening, work, and power were 47.6 +/- 6.9%, 47.5 +/- 7.1%, and 46.9 +/- 6.6%, respectively. Blood flow increased in the proximal (P), mid (M), and distal (D) LDM during the fatigue test. After partial vascular isolation, initial shortening, work, and power decreased by 29.4%, 32.5%, and 31.7% from their respective control values. During the fatigue test, fatigue indices for shortening, work, and power were 24.7 +/- 3.3%, 19.5 +/- 4.6%, and 22.2 +/- 4.7%, respectively, all significantly (p < 0.05) less than control values. Resting blood flows were unaltered. During exercise, flow to the P increased, whereas flow did not increase in M (p < 0.05). Loss of LDM function was most apparent after mobilizing and reattaching the muscle. Initial shortening, work, and power significantly decreased (p < 0.05) by 74.1%, 76.8%, and 74.4%, from their respective control values. During a fatigue test, final values for shortening, work, and power were all near zero. Resting blood flow decreased in the M and D (p < 0.05) and, during exercise, blood flow increased only in P. Thus, LDM function was severely depressed during the isolation procedure. This functional loss is associated with inadequate blood flow responses. Therefore, preconditioning and/or revascularization is needed if the LDM is to provide cardiac assistance shortly after cardiomyoplasty surgery.