Pulmonary resection in the management of metastases from gestational choriocarcinoma.

Case histories of five patients with pulmonary metastases from choriocarcinoma resistant to multidrug chemotherapy are presented. Thoracotomy was performed in all cases. All tumor was removed in three patients with no other site of active disease, and these patients are surviving with no evidence of recurrent disease. In one patient, the lesion could not be completely excised because of involvement of contiguous structures, and she died of progressive disease. A second patient, with liver metastases at the time of thoracotomy, also died of progressive disease. The indications for performing thoracotomy in the management of pulmonary metastases of choriocarcinoma are discussed.

Dynamic cardiomyoplasty acutely impairs left ventricular diastolic function.

In patients with congestive heart failure, medical treatment has a high rate of mortality and morbidity, and transplantation is limited by the availability of donor hearts. Dynamic cardiomyoplasty is being investigated as surgical therapy to improve left ventricular function in these patients. To evaluate the early postoperative effects of this procedure on left ventricular diastolic function, we studied seven dogs through the use of sonomicrometry and micromanometry in a canine model of dynamic cardiomyoplasty. Left ventricular diastolic parameters were determined before wrapping the latissimus dorsi muscle (baseline), after latissimus dorsi muscle wrap but without stimulation, and with synchronous left ventricular contraction-latissimus dorsi muscle stimulation. End-diastolic pressure was increased in both conditions after latissimus dorsi muscle wrap (without stimulation, 5 +/- 1; with stimulation, 6 +/- 2 mm Hg; p < 0.05) compared with baseline (3 +/- 2 mm Hg). The peak rate of diastolic pressure decay was greater at baseline (1560 +/- 370 mm Hg/sec) than after latissimus dorsi muscle wrap, both without (1260 +/- 330 mm Hg/sec, p < 0.01) and with (1120 +/- 420 mm Hg/sec, p < 0.01) stimulation. The constant of pressure decay was prolonged both without (53 +/- 10 seconds, p < 0.05) and with (62 +/- 11 seconds, p < 0.01) latissimus dorsi muscle stimulation compared with the baseline (38 +/- 5 seconds). Compared with baseline (0.2 +/- 0.2 cm-2), the constant of passive chamber stiffness increased after the latissimus dorsi muscle was wrapped around the heart (1.6 +/- 0.7 cm-2, p < 0.05) and with stimulation (2.1 +/- 1.0 cm-2, p < 0.01). The maximal diastolic filling rate (baseline, 18.1 +/- 6.7; without stimulation, 16.6 +/- 8.9; with stimulation, 16.6 +/- 4.1 cm2/sec, not significant) and end-diastolic short-axis area (baseline, 7.3 +/- 2.3; without stimulation, 7.4 +/- 2.1; with stimulation, 7.5 +/- 2.3 cm2, not significant) were similar among the three conditions. The latissimus dorsi muscle wrap prolonged relaxation and increased left ventricular passive stiffness. Synchronous latissimus dorsi muscle stimulation with left ventricular contraction did not improve diastolic function in this model. The results suggest that in the early postoperative period, dynamic cardiomyoplasty impairs diastolic function.

Diastolic ventricular properties in patients during coronary revascularization. Intermittent ischemic arrest versus cardioplegia.

Left ventricular diastolic properties were examined in 24 patients undergoing coronary revascularization with either 32 degrees C intermittent ischemic arrest (IA) or 4 degrees C potassium cardioplegia (CP) for myocardial protection. The ages, numbers of grafts, and preoperative cardiac function were similar for the two groups of patients. For compliance data, hearts were filled passively during bypass perfusion to diastolic pressures between 0 and 20 mm Hg by clamping the left ventricular vent. Simultaneously, minor axis dimensions were measured with 8 mm epicardial ultrasonic crystals. End-diastolic lengths (EDL), normalized to a Lagrangian strain definition (epsilon), were compared at each pressure (P) by the nonlinear regression equation, P = alpha(e beta epsilon-1). Both elastic constants, alpha and beta, as well as linear regression slopes (k) of pressure-strain data were compared as indices of ventricular stiffness. Prior to determinations, the EDL at 0 mm Hg transmural pressure was defined as l0. At each filling pressure, a leftward shift in the compliance curve developed following IA but not CP. Moreover, shifts in alpha, beta, and k constants occurred with IA alone, l0 did not change in either group. Therefore, stiffening did not occur when CP was used for protection, despite ischemic durations twice those of IA (31 versus 15 minutes). These data confirm CP to be a superior method of cardiac protection during coronary bypass grafting and show diastolic ventricular properties to be a sensitive indicator of subclinical ischemic injury.

Effects of phenylephrine on transmural distribution of myocardial blood flow in regions supplied by normal and collateral arteries during cardiopulmonary bypass.

Cardiopulmonary bypass is frequently accompanied by decreased peripheral vascular resistance with resultant hypotension that is unresponsive to increased flow rates. Alpha adrenergic agonists are routinely used to increase peripheral vascular resistance and augment blood pressure. In this study, the effects of the alpha adrenergic stimulant phenylephrine on blood flow distribution during cardiopulmonary bypass in myocardium supplied by normal and collateral arteries were studied in eight mongrel dogs. Microsphere determinations of blood flow were made following augmentation of perfusion pressure with phenylephrine and were compared with intraoperative normotensive and hypotensive control levels. With systemic flow rates held constant, phenylephrine was infused in doses adequate to raise perfusion pressure to normotensive levels following hypotension. In the normal region (NR), blood flow was returned to normotensive control levels with flow favoring the subendocardium. In the region supplied by collateral vessels (CR), however, phenylephrine infusion failed to return flow to the normotensive control level in the subendocardial layer, and the flow imbalance present during hypotension was not corrected. An analogue model of the calculable resistances in the CR is presented, which indicates that phenylephrine increased resistance in the collateral vessels. Associated with this inflow restriction is decreased resistance or vasodilatation of the intramyocardial vessels supplied by collateral coronary arteries.

Hemangioma of the right ventricle causing outflow tract obstruction.

A 3 1/2-year-old child had a murmur of pulmonary stenosis. Echocardiography and cardiac catheterization revealed a pulmonary infundibular obstruction. Magnetic resonance imaging of the heart demonstrated a mass in the interventricular septum. The mass was successfully resected and a pathologic diagnosis of capillary hemangioma was made. Only two previous cases of hemangioma causing right ventricular outflow obstruction have been reported; both of these cases involved adults. This case represents the first report of a hemangioma causing right ventricular outflow tract obstruction in a child. An exploratory operation with resection is the treatment of choice.

Effects of dynamic cardiomyoplasty on indices of left ventricular systolic and diastolic function in a canine model of chronic heart failure.

The effects of cardiomyoplasty were evaluated with multiple-gated equilibrium radionuclide angiocardiography and catheterization in a canine model of chronic heart failure. Doxorubicin was administered to 12 dogs at a dose of 1 mg/kg/wk intravenously for 10 weeks. Left ventricular ejection fraction was reduced from a mean of 53.6% +/- 3.4% to 33.5% +/- 2.3% preoperatively. Two dogs died of presumed arrhythmia during this period. Cardiomyoplasty with the left latissimus dorsi muscle was performed on 10 dogs. The muscle was wrapped around both the left and right ventricles. Five dogs died of infection or arrhythmia after the operation. Postoperatively the muscle remained unstimulated for 2 weeks to allow adhesion to the heart. After this period, the latissimus dorsi muscle was conditioned by a progressive stimulation protocol. After the muscle was conditioned, multiple-gated equilibrium radionuclide angiocardiography studies showed that left ventricular global ejection fraction was 18.4% +/- 7.2% at 0 volts (nonstimulation), 26.2% +/- 3.7% at 5-volt stimulation (p less than 0.05), and 31.0% +/- 5.4% at 10-volt stimulation (p less than 0.05). Regional ejection fractions in low lateral, apical, and low septal regions at 5 volts and 10 volts were higher than those at 0 volts (p less than 0.05). Regional wall motion (percent radial shortening) of the low lateral region was higher than that during nonstimulation (p less than 0.05). Peak emptying rate was 2.07 +/- 0.95 end-diastolic counts per second at 0-volt, 3.10 +/- 0.67 at 5-volt, and 3.34 +/- 0.89 at 10-volt stimulation (p less than 0.05). Peak filling rate was 1.81 +/- 0.52 end-diastolic counts per second at 0-volt, 2.67 +/- 1.18 at 5-volt, and 3.11 +/- 0.65 at 10-volt stimulation (p less than 0.05). Cardiac catheterization data showed a nonsignificant increase in left ventricular rate of pressure rise with increasing voltage (1302 +/- 355 mm Hg/sec at 0 volts, 1450 +/- 413 mm Hg/sec at 5 volts, and 1568 +/- 455 mm Hg/sec at 10 volts). Left ventricular systolic pressures were unchanged. End-diastolic pressures decreased (11.2 +/- 1.48 mm Hg at 0 volts, 10.4 +/- 2.30 mm Hg at 5 volts, and 9.6 +/- 1.52 at 10 volts; p less than 0.05). These data show that cardiomyoplasty can improve indices of systolic and diastolic function in a canine model of chronic heart failure.

Measurement of global ventricular function in patients during cardiac operations using sonomicrometry.

In these studies, we evaluated the applicability of pulse-transit sonomicrometry for measuring changes in global cardiac activity in patients during cardiac operative procedures. In six patients two epicardial ultrasonic crystals (8 mm) were sutured across the left ventricular minor axis. Diastolic pressure-length data were recorded as left ventricles were filled passively to transmural pressures (P) from 0 to 20 mm Hg. Data were collected at the beginning of cardiopulmonary bypass and again 15 minutes following periods of induced global ischemia (29.8 +/- 0.8 minutes). Minor axis length data were normalized to Lagrangian strain (epsilon), and best-fit regression curves were obtained from P-epsilon by computer analysis. Nonlinear elastic constants, alpha and beta, were mathematically derived as additional curve descriptors. Decreases in ventricular compliance were demonstrated as leftward shifts in both computed and measured P-epsilon curves. Global ischemia appeared to effect a decrease in overall ventricular diastolic compliance in all patients studied (p =7E 0.01 at 5, 10, 15, 20 mm Hg). Simultaneously, no statistical change occurred in lo (62.93 +/- 2.80 mm), which represented end-diastolic length (EDL) at 0 mm Hg transmural pressure. Following coronary grafting several patients showed augmented systolic excursion when compared at similar EDL. For those analyses, shortening was compared at specific minor axis EDLs rather than filling pressures. These data indicate that experimentally developed sonomicrometry may safely provide accurate indices of systolic and diastolic ventricular properties during operations necessitating cardiopulmonary bypass. Thus various cardioplegic solutions, ischemic arrest periods, and inotropic agents may be evaluated more objectively.

Management of critical aortic stenosis in infancy.

Critical aortic valvular stenosis presents in infancy with severe congestive heart failure. Clinical assessment and electrocardiography are of value, but cardiac catheterization with angiography has been considered mandatory prior to surgical treatment. With cross-section echocardiography an accurate diagnosis of aortic stenosis and associated lesions is possible. Over the past 2 years, we have established a protocol according to which, if a clinical diagnosis of critical aortic stenosis is confirmed by cross-sectional echocardiography in the absence of major associated cardiac anomalies, infants are submitted for aortic valvotomy under inflow occlusion without invasive studies. This protocol was used in an effort to decrease the mortality rate by avoiding the preoperative stress of cardiac catheterization and angiography, as well as the hazards of cardiopulmonary bypass in the severely ill infant. Eight infants with critical aortic stenosis have been operated upon, five without prior cardiac catheterization. Ages at operation ranged from 2 days to 7 months, with six children less than 2 weeks of age. The noninvasive diagnosis was confirmed at operation in each case. There was one early postoperative death and one late death. No death has been related to the technique of inflow occlusion. A decision tree for the noninvasive assessment of suspected critical aortic stenosis based on the clinical features and echocardiographic findings is presented.

Correlation of mitochondrial function and ischemic contracture.

Structural and functional changes in the mitochondrium have been described following timed cardiac ischemia. However, mitochondrial abnormalities associated with acute muscular dysfunction have not been well defined. In the present investigation, the isolated rat heart subjected to global ischemia was used to determine the relationship between the biochemical parameters of high-energy phosphate content and mitochondrial function and the physiological event of ischemic contracture. High-energy phosphate content and mitochondrial structure and function were determined under control conditions, at the initiation of ischemic contracture, at the completion of ischemic contracture, and 20 minutes after completion of contracture. Contracture initiation and completion were associated with the anticipated depletion of high-energy phosphate content. Also demonstrated were specific degrees of structural and functional deterioration of the mitochondria associated with specific degrees of contracture. In addition to its prior applications, this model seems well suited for investigation of the interdependence of high-energy phosphate levels, ischemic contracture, and mitochondrial function as affected by specific protective interventions designed to limit ischemic injury.

Metabolic deterioration during global ischemia as a function of time in the intact normal dog heart.

High-energy phosphate content and mitochondrial function were analyzed at the initiation and completion of ischemic contracture in dog hearts exposed to normothermic ischemia while on cardiopulmonary bypass. Contracture initiation and completion were detected by a balloon catheter placed within the left ventricle. In seven dogs, inner and outer layers of the myocardium were assayed for adenosine triphosphate (ATP) and creatine phosphate (CP). ATP and CP content in these two layers were compared prior to ischemia and at contracture initiation and completion. Inner layer ATP levels were 23.88 +/- 0.73 (mean +/- SM) mu moles/gm dry weight prior to ischemia, 5.14 +/- 0.49 at initiation, and 0.73 +/- 0.2 at completion. Inner layer CP content was 41.29 +/- 0.87 prior to ischemia, 3.49 +/- 0.34 at initiation, and 4.06 +/- 0.48 at completion. Mitochondrial respiratory control indices (RCI) were assayed in a second group of seven dogs prior to ischemia, at contracture initiation, and at contracture completion and were, respectively, 11.5 +/- 1.18, 3.1 +/- 0.43 and 1.76 +/- 0.29 (alpha ketoglutarate as substrate). Despite the specific degrees of metabolic deterioration associated with the events of contracture, ischemic time required to develop contracture initiation and completion was variable, ranging from 29.5 to 72 minutes for initiation and 60.25 to 101 minutes for completion. A third group of five dogs had biopsy specimens taken for ATP at fixed ischemic time intervals, and at 45 minutes of ischemia they were found to have greater ranges in ATP values than the ranges associated with contracture initiation. In contrast to ischemic time, the physiological events of ischemic contracture are reliable predictors of the degree of metabolic injury in the intact dog heart exposed to normothermic ischemic arrest during cardiopulmonary bypass.

Improved tolerance to ischemia in hypertrophied myocardium by preischemic enhancement of adenosine triphosphate.

In prior studies from this laboratory to determine the mechanisms whereby hypertrophied myocardium is more sensitive to ischemic injury than normal myocardium, it was demonstrated that hypertrophied rat hearts have lower basal high-energy phosphate levels and develop ischemic contracture sooner than normal myocardium. The purposes of this study were (1) to determine if the decrease in myocardial adenosine triphosphate (ATP) was associated with the increased rate of ischemic contracture and (2) to determine if arrest and perfusion of hypertrophied myocardium prior to the ischemic interval would allow recovery of high-energy phosphate stores and improve tolerance to ischemia. ATP levels were measured in isolated normal and hypertrophied rat hearts during (1) control nonworking Langendorff perfusion, (2)2 minutes of potassium chloride-arrested perfusion (30 mEq/L), or (3) 15 minutes of potassium chloride-arrested perfusion (30 mEq/L). Both groups were then made globally ischemic (37 degrees C) and the time to ischemic contracture recorded. Hypertrophied hearts were produced by permanent banding of the ascending aorta and confirmed by left ventricular (mg) body weight (gm) ratios (normal, 1.95 wet, p less than 0.05). After 2 minutes of mechanical arrest the time to ischemic contracture was increased 75% +/- 10% in normal and 44% +/- 4% in hypertrophied hearts. After 15 minutes of mechanical arrest with perfusion, hypertrophied myocardium re-established normal ATP levels and increased its time to ischemic contracture by 130% +/- 7%. These studies suggest that during potassium chloride arrest, additional preischemic metabolic recovery is possible by hypertrophied myocardium and leads to increased tolerance to ischemia beyond that accomplished by cessation of mechanical activity alone. This effect is seen only to a minor degree in normal myocardium.

Characteristics of chronic left ventricular hypertrophy induced by subcoronary valvular aortic stenosis. I. Myocardial blood flow and metabolism.

Using a canine model of subcoronary valvular aortic stenosis, we determined myocardial blood flow, high-energy phosphate content, and mitochondrial function in eight hearts with chronic left ventricular hypertrophy. Fourteen normal hearts were used for control data. Myocardial blood flow was determined by injection of tracer microspheres. During cardiopulmonary bypass, left ventricular transmural biopsy specimens were taken for metabolic analyses. Subepicardial and subendocardial content of adenosine triphosphate (ATP) and creatine phosphate (CP) were assayed. Respiratory control indices for isolated mitochondria were measured by use of NAD-linked and FAD-linked substrates. Endocardial blood flow, subendocardial high-energy phosphate content, and respiratory control indices for NAD-linked substrate in the hearts with chronic left ventricular hypertrophy were significantly lower than the normal values. These data provide insight into the metabolic and myocardial blood flow abnormalities occurring in cardiac hypertrophy and provide a framework for understanding the altered response of hypertrophied hearts to ischemia.

Characteristics of chronic left ventricular hypertrophy induced by subcoronary valvular aortic stenosis. II. Response to ischemia.

The increased susceptibility of hearts with chronic left ventricular hypertrophy (CLVH) to damage during ischemia has been suggested but not documented. The purpose of this study was to isolate ischemic events in hearts with CLVH from reperfusion events. Using physiological and biochemical parameters, we compared the rate and extent of myocardial injury during ischemic contracture between eight canine hearts with CLVH induced by subcoronary valvular aortic stenosis and 14 normal canine hearts. Preischemic myocardial blood flow was determined by injection of tracer microspheres. During cardiopulmonary bypass, each heart was instrumented with a left ventricular balloon and made globally ischemic. At control, contracture initiation, and contracture completion left ventricular transmural biopsy specimens were assayed for subepicardial and subendocardial adenosine triphosphate (ATP) and creatine phosphate (CP). Mitochondrial respiratory control indices for NAD-linked and FAD-linked substrates were measured. Preischemic endocardial blood flow in hearts with CLVH was significantly lower than in normal hearts. At control, subendocardial ATP and CP and the respiratory control index for NAD-linked substrate were significantly lower in hearts with CLVH than in normal hearts. Hearts with CLVH reached contracture initiation significantly sooner than normal hearts. All hearts demonstrated significant decreases in high-energy phosphate content and mitochondrial function during ischemia. Reperfusion injury notwithstanding, we concluded that hearts wih CLVH are more susceptible to ischemic injury than are normal hearts, perhaps related to lower endocardial blood flow, lower subendocardial high-energy phosphate stores, and depressed mitochondrial function prior to ischemia.

Response of hypertrophied myocardium to ischemia: correlation with biochemical and physiological parameters.

The increased susceptibility of hypertrophied hearts to ischemic injury during cardiac operations has long been recognized. Although the imbalances in oxygen supply and demand which may occur with hypertrophy during hypotension, ventricular fibrillation, or reperfusion have been extensively studied, the biochemical response of hypertrophied myocardium to ischemia has not been fully elucidated. In the present investigation, rat hearts in which hypertrophy was induced by chronic pressure overload were used to examine the relationship of the physiological parameter, ischemic contracture, to high-energy phosphate content and mitochondrial function during global ischemia. Hypertrophied hearts developed ischemic contracture after significantly shorter duration of ischemia than did normal hearts (5.8 +/- 0.3 minutes versus 10.1 +/- 0.7 minutes). High-energy phosphate content was lower in hypertrophied hearts at control and at ischemic contracture initiation and completion than in normal hearts, whereas mitochondrial function was consistently greater in the hypertrophy group. This investigation demonstrates that the hypertrophied myocardium, independent of flow-related events, is more vulnerable to ischemic injury than normal myocardium and suggests that the increased susceptibility may result from lower high-energy phosphate stores present at the onset of ischemia. The results emphasize the need for rapid cardiac arrest with the induction of ischemia in hypertrophied myocardium and suggest the potential for increasing myocardial high-energy phosphate content in the hypertrophied ventricle by interventions such as arrested perfusion with substrate containing oxygenated cardioplegic solutions prior to the onset of planned ischemia.

Latissimus dorsi dynamic cardiomyoplasty of the right ventricle. Potential for use as a partial myocardial substitute.

Full-thickness right ventricular latissimus dorsi dynamic cardiomyoplasty with the Medtronic Cardiomyostimulator (Medtronic, Inc., Minneapolis, Minn.) was performed in a chronic canine model. In one group (n = 2) the latissimus dorsi was electrically preconditioned before cardiomyoplasty. In a second group (n = 3) cardiomyoplasty was performed and the muscle was progressively stimulated, with conditioning accomplished while the latissimus dorsi was functioning on the ventricle. The contribution of the stimulated latissimus dorsi to global ventricular function was assessed, and the effects of varying muscle stimulation parameters on latissimus dorsi function and hemodynamics were examined. Right ventricular systolic pressure increased 8%, from 23.2 +/- 0.95 to 25.1 +/- 1.5 mm Hg. The rate of pressure rise increased 37% from 226 +/- 13 to 309 +/- 12 mm Hg/sec. Right ventricular ejection fraction was measured in two dogs and increased 29% with latissimus dorsi stimulation, from 51.5% +/- 13.5% to 66.5% +/- 14.5%. Although the sample size was small, there was no difference observed between the preconditioned and nonpreconditioned groups. Right ventricular systolic pressure, rate of pressure rise, and percent latissimus dorsi fiber shortening increased as voltage and burst frequency of the muscle stimulus increased, whereas increasing the burst duration had little effect in two dogs so studied. Latissimus dorsi dynamic cardiomyoplasty can function as a partial myocardial replacement in a chronic canine model, apparently without preconditioning of the muscle. The degree of cardiac assist obtained with cardiomyoplasty appears to be influenced by the voltage and frequency of the stimulus applied to the muscle. Although it is unclear whether these results can be extrapolated to the left ventricle, this technique may find application in the treatment of ventricular aneurysm or ventricular tumor.

Effect of B-15,000 (Iopamidol), a new nonionic contrast agent, on cardiac function of the isolated rat heart.

The isolated rat heart model was used to examine the effect of a new nonionic contrast agent, B-15,000 (Iopamidol), on cardiac function. Comparative studies were performed with Amipaque, Renografin 60, Renografin 76, and Vascoray. The three ionic contrast agents had significantly greater detrimental effects on cardiac function than either nonionic agent. The results support the continued evaluation of the nonionic agents for use in coronary angiography.

Perioperative assessment of segmental left ventricular function in man. Effects of nitroprusside after bypass operations.

Direct on-line assessment of postoperative ventricular function has not been possible. We assessed the feasibility of using pulse-transit sonomicrometry to measure regional function in man postoperatively. Ultrasonic transducers (3 mm in diameter) were implanted along the minor axis of the left ventricle at midwall depth into a region supplied by a bypass graft. All wires were tunneled subcutaneously. Pressures, ECG, and regional dimensions were monitored in eight patients continuously, and at 48 to 72 hours postoperatively, the effects of sodium nitroprusside were assessed. The transducers were withdrawn with no complications. Nitroprusside was associated with an increase in systolic shortening from 1.60 +/- 0.19 to 1.92 +/- 0.25 mm and rate of shortening from 12.13 +/- 1.85 to 15.34 +/- 2.38 mm/s at constant end-diastolic lengths. Using this technique for recording regional dimensions, nitroprusside therapy augmented function at a constant preload.

Postoperative left ventricular contractility in the cardiac surgical patient: an evaluation of the force-interval relationship.

The force-interval relationship--the dependence of cardiac contractility on the rate and pattern of stimulation--was evaluated for its potential use in monitoring patients in the period immediately following heart surgery. Six patients were studied for three days after coronary artery bypass grafting. The monitoring instrumentation used during operation included a catheter-tip micromanometer introduced into the left ventricle, a pair of ultrasonic transducers placed on the left ventricular (LV) epicardium to monitor minor-axis dimension, pacing electrodes placed on the right atrium, and systemic arterial and venous catheters. During the experiments, heart rate was controlled by atrial pacing. After every twentieth systole (the control systole), a pause in the heart rate was introduced during which an extrasystole (SE) and a postextrasystole (SPES) were elicited at test intervals tE and tPES, respectively. The intervals between the control systole and test systoles SE and SPES were experimentally manipulated. When the test intervals were increased, the peak first derivative of LV pressure (Pmax) of SE and of SPES increased monophasically. To eliminate the effects of LV end-diastolic volume, we used only SPES and control systoles with the same LV end-diastolic dimension in construction of PES ratio curves (Pmax of SPES/Pmax of the control systole, as a function of tPES). The PES ratio rose monophasically with an increase in tPES; these curves were well fitted by an exponential relationship. The PES ratio exceeded unity at long tPES intervals. This ratio, denoting postextrasystolic potentiation, was inversely dependent on tE. The patients experienced no complications.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of cardiomyoplasty on biventricular function in canine chronic heart failure.

Dynamic cardiomyoplasty, the use of skeletal muscle to assist the heart, is a new therapy for the treatment of heart failure. However, the effects of cardiomyoplasty on biventricular function and the synchrony of ventricular contraction are not fully known. We assessed the efficacy of latissimus dorsi muscle (LDM) dynamic cardiomyoplasty in a chronic model of biventricular failure. Five dogs received doxorubicin (1 mg.kg-1.wk-1) for up to 12 weeks to induce heart failure and then underwent a biventricular cardiomyoplasty. After operation, the muscle was progressively stimulated according to an established protocol. When training was complete (10 weeks), radionuclide ventriculographic and catheterization data were obtained. Peak left ventricular (LV) systolic pressure and its first derivative were unchanged, whereas LV end-diastolic pressure decreased slightly with LDM assistance (11.0 +/- 1.6 to 9.6 +/- 1.5 mm Hg; p < 0.05). Right ventricular (RV) systolic pressure increased significantly with LDM assistance from 21 +/- 2 to 26 +/- 3 mm Hg (p < 0.05), whereas its first derivative and RV end-diastolic pressure were unchanged. Dynamic cardiomyoplasty significantly improved LV ejection fraction from 0.18 +/- 0.07 without LDM assistance to 0.31 +/- 0.05 with LDM assistance (p < 0.05); similarly RV ejection fraction increased from 0.32 +/- 0.07 to 0.45 +/- 0.06 with LDM assistance (p < 0.05). The temporal sequence of LV wall motion was assessed by phase analysis of the radionuclide ventriculograms. With skeletal muscle assistance, standard deviation ("spread") decreased from 31.6 +/- 17.4 to 20.0 +/- 15.4 degrees (p < 0.06), whereas skewness ("symmetry") was unchanged. Dynamic cardiomyoplasty improved both LV and RV ejection fractions without increasing diastolic pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Myocardial blood flow and oxygen consumption in the empty-beating, fibrillating, and potassium-arrested hypertrophied canine heart.

Myocardial oxygen consumption and blood flow distribution were examined in severely hypertrophied canine hearts in the empty-beating, fibrillating, and pharmacologically arrested states. Hypertrophy was produced using a subcoronary valvular aortic stenosis model that mimics the clinical situation of aortic valvular stenosis. Oxygen content of the total coronary sinus collection was compared with a large volume arterial sample using a Lex-O2-Con-TL analyzer, which had been validated by the Van Slyke-Neill method. Transmural blood flow was measured in each state using microspheres, and perfusion pressure was maintained at 80 mm Hg. Oxygen consumption in the empty-beating hypertrophied heart was found to be the same as that previously reported for normal hearts. Blood flow was evenly distributed in the empty-beating heart, with an endocardial/epicardial ratio of 0.99 +/- 0.15 (SEM) milliliters per minute per gram of left ventricular weight. Oxygen consumption failed to increase significantly with fibrillation; however, blood flow distribution favored the subepicardium, suggesting that oxygen consumption determinations in the fibrillating hypertrophied heart may not accurately reflect metabolic demand. Basal oxygen consumption of the hypertrophied heart as determined by the potassium-arrested, blood-perfused model was the same as that previously described for normal hearts. Blood flow during potassium arrest favored the subendocardium (endocardial/epicardial ratio = 1.14 +/- 0.27 ml/min/gm LV weight).