Comparison of an implanted abdominal aortic counterpulsation device with the intraaortic balloon pump in a heart failure model.

The abdominal aortic counterpulsation device is a round pumping chamber with a valveless opening which is implanted retroperitoneally on the abdominal aorta. The Utah driver is connected to the device through an air conduit and is synchronized on the electrocardiographic signal to provide diastolic aortic augmentation. For comparison an intraaortic balloon was also driven by the Utah driver system. The abdominal aortic counterpulsation device (stroke volume = 30, 40 and 60 ml) and the intraaortic balloon pump (balloon volume = 20 ml) were tested in dogs with acute left ventricular failure. The abdominal aortic counterpulsation device was also tested in normal animals. In acute left ventricular failure the abdominal aortic counterpulsation device at a stroke volume of 30, 40 or 60 ml decreased left ventricular end-diastolic pressure by an average of 28.56 (p less than 0.001), 39.56 (p less than 0.001) and 44.14% (p less than 0.005), respectively; aortic end-diastolic pressure by 24.11 (p less than 0.001), 26.67 (p less than 0.001) and 19.57% (p less than 0.01); and aortic systolic pressure by 18.56 (p less than 0.002), 26.0 (p less than 0.001) and 22.43% (p less than 0.005). It increased cardiac index by 27.58 (p less than 0.02), 35.59 (p less than 0.005) and 43.42% (p less than 0.001) and it provided peak aortic diastolic augmentation of 64.5 (p less than 0.001), 69.78 (p less than 0.001) and 74.43% (p less than 0.001), respectively, above the control aortic end-diastolic pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Recainam, a potent new antiarrhythmic agent: effects on complex ventricular arrhythmias.

The antiarrhythmic efficacy and safety of intravenous recainam, a newly synthesized compound displaying potent class I antiarrhythmic activity, were tested in 10 hospitalized patients with frequent (greater than 30/h) complex ventricular ectopic beats. There were seven men and three women of average age 57 years (range 21 to 74); five had ischemic heart disease, three had cardiomyopathy and two had valvular heart disease. Recainam was given as a 3.0 mg/kg per 40 min loading infusion followed by a 0.9 mg/kg per h maintenance infusion over a 24 hour observation period. Arrhythmia response was assessed both in the short term (comparing 2 hours before and 1 hour after drug loading) and in the long term (comparing 48 hours before drug loading and 23 hours of maintenance infusion). The median frequency of total premature ventricular complexes decreased in the short term by 99.6% (from 392.5 to 1.5/h, p less than 0.005) and in the long term by 99.7% (from 435 to 1.3/h, p less than 0.01). Repetitive beats were suppressed by a median of 100% both in the short term (p less than 0.006) and during 24 hour infusion (from 80.9 to 0/h, p less than 0.003). More than 90% suppression of repetitive beats occurred in all 10 patients (100%) and more than 90% suppression of total arrhythmias occurred in 9 patients (90%) during the maintenance period. Electrocardiographic PR and QRS intervals increased by 19% (p less than 0.001) and 24% (p less than 0.003), respectively, during therapy, but the JTc interval decreased (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Outcome of patients with congestive heart failure treated with standard versus high doses of enalapril: a multicenter study. High Enalapril Dose Study Group.

OBJECTIVES: We sought to prospectively and randomly compare survival with clinical and hemodynamic variables in patients with congestive heart failure (CHF) treated with standard versus high doses of enalapril. BACKGROUND: Angiotensin-converting enzyme (ACE) inhibitors produce hemodynamic and symptomatic benefits in patients with CHF, but there is still controversy about the optimal dose in this clinical setting. METHODS: Two hundred and forty-eight patients with advanced CHF (age 56.3+/-12 years) were randomized to receive a maximal tolerated dose of enalapril, up to 20 mg/day in group 1 (mean dose achieved 17.9+/-4.3 mg/day, n = 122) and 60 mg/day in group 2 (mean dose achieved 42+/-19.3 mg/day, n = 126). RESULTS: At enrollment, patients in group 1 were in New York Heart Association (NYHA) functional class 2.6+/-0.7 and had a mean systolic blood pressure (SBP) of 117+/-18 mm Hg, a mean heart rate (HR) of 85+/-16 beats/min and a left ventricular ejection fraction (LVEF) of 20.0+/-9.8%. In group 2, patients were in NYHA class 2.6+/-0.7; their SBP was 118+/-17 mm Hg, HR 83+/-15 beats/min and LVEF 18.8+/-8.1%. There were no significant differences in these characteristics between the two groups of patients at enrollment. After 12 months of follow-up, 22 (18%) of 122 patients in group 1 and 23 (18%) of 126 patients in group 2 had died (p = 0.995, with 80% power of the study to detect a delta difference of 13%). The NYHA class was the same (1.9+/-0.7) in both groups; SBP was 111+/-16 and 111+/-17 mm Hg, HR 77+/-12 and 79+/-13 beats/min and LVEF 31+/-19% and 30+/-12% in groups 1 and 2, respectively. These differences were not statistically significant. The study had a power of 80% to detect (p = 0.05) the following changes: 13% in death rate, 0.25 units in NYHA class, 6 mm Hg in SBP, 5 beats/min in HR and 6% in LVEF. CONCLUSIONS: No significant differences were found in survival and clinical and hemodynamic variables between patients receiving standard and those receiving high doses of enalapril.

Effects of amiodarone on refractory ventricular fibrillation in acute myocardial infarction: experimental study.

OBJECTIVES: The aim of this study was to evaluate the efficacy of a single dose of intravenous amiodarone in facilitating defibrillation of ventricular fibrillation refractory to lidocaine and epinephrine plus direct current countershocks in experimental acute myocardial infarction. BACKGROUND: Amiodarone has been hailed as the most effective single antiarrhythmic drug for the treatment of ventricular arrhythmias. However, intravenous amiodarone has only sporadically been used in the defibrillation of ventricular fibrillation in acute myocardial infarction. METHODS: Acute myocardial infarction was induced in 60 dogs by ligation of the proximal left anterior descending coronary artery for 2 h. Animals that developed spontaneous ventricular fibrillation were treated with lidocaine and epinephrine plus five direct-current countershocks. Dogs with ventricular fibrillation refractory to this regimen were randomized to further treatment with additional intravenous administration of epinephrine and bolus lidocaine plus < or = 15 direct-current countershocks (group I) or administration of amiodarone, 10 mg/kg body weight intravenously, followed by defibrillation with direct-current counter-shock (group II). RESULTS: Sixteen (27%) of the 60 dogs in which the protocol was attempted developed spontaneous ventricular fibrillation 21 min after ligation and were included in the study. Lidocaine and epinephrine plus five direct-current countershocks succeeded in converting ventricular fibrillation in one dog (6%). The other 15 dogs were randomized to group I (8 dogs) or group II (7 dogs). Defibrillation was achieved in one of the eight dogs in group I and in six of the seven dogs in group II (p < 0.005). CONCLUSIONS: In an experimental model of acute ischemia, intravenous amiodarone (10 mg/kg) influences positively the response to defibrillation of ventricular fibrillation refractory to lidocaine and epinephrine plus direct current countershocks.

Reversible symmetric polyneuropathy with paraplegia after heart transplantation.

BACKGROUND: Neurotoxicity is a well-recognized side effect of cyclosporine therapy in transplant recipients. Cyclosporine can cause a wide range of adverse effects on both the central and peripheral nervous systems. METHODS: We present a case history of symmetric polyneuropathy with flaccid paraplegia, a rare neurological complication of cyclosporine administration. RESULTS: Blood levels of the drug above the therapeutic range accompanied the neurological manifestations. The syndrome subsided fully with dose reduction. Patients' symptoms were attributed to axonal degeneration of the peripheral nerves, according to electromyography findings. CONCLUSIONS: Cyclosporine neurotoxicity should always be considered in patients with neurological complications following transplantation. The case presented in this article illustrates an additional potential mechanism of this adverse effect, namely, axonal degeneration of the peripheral nerves, causing symmetric polyneuropathy.

Evolution of late potential parameters in thrombolyzed acute myocardial infarction might predict patency of the infarct-related artery.

The objective was to predict the patency grade of an infarct-related artery by identifying the time course of the changes of the late potential parameters before, during, and shortly after thrombolysis. The study population consisted of 51 patients with acute myocardial infarction (AMI) who received thrombolytic therapy within 3.2 +/- 1.3 hours from the onset of symptoms. Multiple signal-averaged electrocardiograms (SAECGs) were recorded before, during, and shortly after thrombolysis. A total of 489 single-averaged electrocardiographic tracings were evaluated. Late potentials were defined as: QRS duration > 114 ms, low amplitude signals (LASs) > 38 ms, and root mean square (RMS) < 20 microV. Late potentials were found in 37% of patients (21 before and 16 during the first 2 hours of thrombolysis), disappeared in all of patients within 89 +/- 75 minutes (range 25 to 350) but reappeared and persisted in 12% of patients, all with an occluded artery (grade 0). The late potential parameters (QRS, LAS, RMS) showed a gradual improvement which occurred earlier (2 vs 4 hours) and was more marked (0.01 vs 0.05) in cases with a patent artery. This improvement expressed by the late potential parameter index (LnQRS + LnLAS - LnRMS) predicts the patent artery with a sensitivity of 0.94 and specificity of 0.79. The improvement of late potential parameters jointly with close to normal initial values or the late potential parameter index and its changes constituted a satisfactory prediction of the patency grade. Thus, the signal-averaged electrocardiographic technique is capable of predicting the early success or failure of thrombolytic therapy.

Correlation and stability of heart rate and ventricular ectopy variability in patients with congestive heart failure.

The stability of indexes of heart rate variability and their possible association with spontaneous variability of ventricular ectopy was examined in 13 patients with advanced congestive heart failure over 14 consecutive days of 24-hour ambulatory electrocardiographic recording. It was found that time and frequency domain measures of heart rate variability are stable over time and are inversely correlated with spontaneous variability of ventricular ectopy.

Efficacy of recainam, a new antiarrhythmic drug, for control of ventricular arrhythmias.

The antiarrhythmic efficacy and safety of oral recainam hydrochloride, a newly synthesized compound, were assessed during a 2-part study of 12 patients with frequent (at least 30/hour) ventricular premature complexes (VPCs). During the initial dose-ranging phase, 11 patients with qualifying arrhythmias (median VPC frequency 575/hour, range 37 to 1,494) received incremental oral doses of 100, 300 and 500 mg of recainam given every 8 hours, each for 3 days. Efficacy was assessed on the last day of each dose. The 300-mg/day dose of recainam was generally ineffective; the 900-mg/day dose was partially effective (58% median VPC reduction, p = 0.03); and the 1,500-mg/day dose was very effective (79% reduction, p less than 0.003). Median reductions in repetitive beats (beats in couplets and runs) for the 3 doses were 18% (difference not significant), 94% (p less than 0.01), and 98% (p less than 0.004), respectively. Recainam provided individual efficacy (at least 70% VPCs or at least 90% repetitive beat suppression, or both) in 7 (64%) of the patients taking 900 mg/day and in 8 (73%) taking 1,500 mg/day. Minimum steady-state plasma concentrations were higher in responders (1.8 +/- 0.5 microgram/ml) than in nonresponders (1.0 +/- 0.5 microgram/ml) (p less than 0.05). The electrocardiographic response to recainam (1,500 mg/day) included increases in PR (by 22%, p less than 0.003) and QRS (by 14%, p less than 0.002) intervals and a small decrease in JTc duration (by 9%, p less than 0.04). Radionuclide ejection fraction did not change. Noncardiac adverse reactions were minimal.(ABSTRACT TRUNCATED AT 250 WORDS)

Indium-111 monoclonal antimyosin cardiac scintigraphy in men with idiopathic dilated cardiomyopathy.

This study examined the prognostic value and the evolution of the heart-to-lung ratio of monoclonal antimyosin antibody (MAA) uptake in patients with a diagnosis of idiopathic dilated cardiomyopathy (IDC). Uptake of indium-111-labeled MAA occurs when the myocytes become irreversibly damaged. The study included 29 men with IDC followed up for 3 years. The diagnosis was verified by endomyocardial biopsy in all patients. Patients who survived beyond 1 year were restudied. Baseline heart-to-lung ratio of MAA was 1.74+/-0.22. Multivariate Cox regression analysis revealed that MAA and New York Heart Association class were independent predictors of late mortality, with a hazard ratio of 4.4 (95% confidence interval 1.1 to 17.9, p = 0.036) and 7.5 (95% confidence interval 2.0 to 28.4, p = 0.003), respectively, when heart-to-lung ratio of MAA uptake was > 1.74 and New York Heart Association class was >11. When these patients were divided into those with chronic IDC (group I [n = 19]) and those with subacute IDC (group II [n = 10]), baseline heart-to-lung ratio was 1.7+/-0.2 and 1.86+/-0.25, respectively (p = NS). In the surviving patients, on restudy, the heart-to-lung ratio of MAA uptake was unchanged in group I (1.64+/-0.20, p = NS), but had decreased to the level of group I (1.66+/-0.21 [p = 0.008]) in group II. Thus, men with IDC and a high heart-to-lung ratio of MAA uptake have a worse long-term prognosis than patients with a lower ratio. The heart-to-lung ratio of MAA decreases comparably over time in subacute IDC and remains stable in chronic IDC.

Relation of dispersion of QRS and QT in patients with advanced congestive heart failure to cardiac and sudden death mortality.

This study examined the usefulness of 01 and QRS dispersion in the prognosis of patients with advanced congestive heart failure (CHF). One hundred four patients in New York Heart Association functional classes II to IV, with a left ventricular ejection fraction of <35%, and untreated with antiarrhythmic drugs, were followed prospectively. QRS and QT dispersion were defined as the maximum difference in QRS and QT interval duration, respectively, measured on all leads of standard 12-lead electrocardiograms. The end points of the study were non-sudden and sudden cardiac mortality. During an average follow-up of 20 months, there were 13 non-sudden and 10 sudden deaths. The average QRS duration was significantly longer in nonsurvivors than in survivors (125 ¿ 34 vs 113 ¿ 34 ms, respectively, p <0.04). Similar results were obtained with 01 dispersion (95 ¿ 48 ms vs 78 ¿ 31 ms, respectively, p <0.03) and QRS dispersion (54 ¿ 17 ms vs 46 16 ms, respectively, p <0.02). Furthermore, patients who died suddenly had significantly greater QRS dispersion than patients who survived (56 ¿ 13 vs 46 ¿ 16 ms, respectively, p <0.02). In a multivariate analysis, QT and QRS dispersion were both independent predictors of non-sudden cardiac death (p = 0.01 and p = 0.001, respectively), and QRS dispersion was also an independent predictor of sudden cardiac death (p = 0.04). Death rate in patients with 01 dispersion >90 ms was 2.8-fold higher than those with 01 dispersion 90 ms (95% confidence intervals [CI] 1.2 to 6.4). Similarly, the death rate in patients with QRS dispersion >46 ms was 3.9-fold higher than in those with QRS dispersion 46 ms (95% Cl 1.6 to 9.5). These findings suggest that QT and QRS dispersion are useful predictors of mortality in patients with advanced CHF. ¿2000 by Excerpta Medica, Inc.

Effect of acute allograft rejection on exercise hemodynamics in patients who have undergone cardiac transplantation.

The effect of acute allograft rejection on exercise hemodynamics was evaluated in 8 consecutive cardiac allograft recipients (group 1) when the right ventricular endomyocardial biopsy showed evidence of allograft rejection (R), and when no evidence of rejection (NR) was present. A separate group of 10 cardiac transplant recipients (group 2) with no evidence of rejection on biopsy done at the end of the first and second year post-transplantation served as controls. The exercise hemodynamics were abnormal in both groups in both studies with a moderate increase of the pulmonary artery wedge pressure to a mean of 17.2 (NR) and 19.4 mm Hg (R) in group 1 (p = not significant [NS]) and 20.1 and 21.2 mm Hg in group 2 (p = NS), a mild increase of the mean right atrial pressure to a mean of 10 mm Hg (NR) and 10 mm Hg (R) in group 1 (p = NS), 11.9 mm Hg and 12.5 mm Hg in group 2 (p = NS), and a moderate increase of the arteriovenous oxygen content difference to a mean of 8.5 (NR) and 8.4 vol percent (R) in group 1 and 8.3 and 8.0 vol percent in group 2. No significant difference was observed between the two studies of the same group in any of the hemodynamic parameters except for the heart rate in group 1 (from 91 +/- 16 to 97 +/- 16 beats/min [p < 0.05] with and without evidence of allograft rejection, respectively). In conclusion, heart transplant recipients do not usually manifest further exercise hemodynamic deterioration during mild to moderate rejection.

Intra-aortic ballon pump for relief of aortic regurgitation. Experimental study.

Backflow from the aorta to the left ventricle during diastole in aortic regurgitation can be reduced by expanding, during diastole, a small air balloon positioned in the ascending aorta downstream to the regurgitant valve. A spherical catheter-mounted balloon, acting as a prosthetic aortic valve for the correction of acute aortic regurgitation, was tested in 12 dogs. This "valve" was actively inflated and deflated by means of a common intra-aortic balloon pumping system (Datascope). A significant increase of end-diastolic pressure in the descending aorta, from 51.72 +/- 1.72 to 70.35 +/- 1.92 mm Hg (mean +/- standard error, p less than 0.001), was obtained, without a significant pressure gradient across the "valve". The "valve" prevented the backward flow of the descending aorta by up to 100%, so that there was a mean increase in t-e effective forward flow of 12.61 +/- 5.27% (mean +/- standard error, p less than 0.05). Coronary arterial flow changes varied during the application of the "valve." They depended directly on the changes of the diastolic component of the flow velocity wave, and this relationship was significant (x2 = 33.04, p less than 0.0001). Contractility indices were not significantly affected during the function of the "valve." It is suggested that the spherical "valve" mounted on a catheter may easily be inserted without thoracotomy for a temporary satisfactory correction of the aortic regurgitation.

Effect of protracted dobutamine infusion on survival of patients in cardiogenic shock treated with intraaortic balloon pumping.

UNLABELLED: The survival of subjects with postmyocardial infarction cardiogenic shock treated with intra-aortic balloon pumping (IABP) differs significantly among various reports. Differences in the criteria for IABP application and in the timing of its initiation have been considered as the main reasons for variations in survival. This study examines whether the way patients in cardiogenic shock are treated prior to IABP may affect their survival. Fifty-five patients in severe postmyocardial infarction cardiogenic shock were classified into three groups according to the rate of dobutamine infusion prior to IABP: the "nondobutamine" (group A, n = 31), the "high-dose dobutamine" (8 to 20 micrograms.kg-1.min-1, group B, n = 17), and the "low-dose dobutamine" (up to 7 micrograms.kg-1.min-1, group C, n = 7). All subjects seen from 1978 to 1983 were recruited for group A, from 1986 to 1990 for group B, and in years 1984, 1985, and 1991 for group C, without using any other classification criteria. It was shown a posteriori that the three groups did not differ in the features of the subjects, in the severity of shock, and in the time length between onset of shock and pumping initiation. None of the 17 subjects of group B could survive under pumping, while 10 of the 31 subjects in group A and 4 of the 7 subjects in group C were weaned off pumping. CONCLUSIONS: A protracted, high-dose pre-IABP administration of dobutamine may adversely affect the survival of patients with postmyocardial infarction cardiogenic shock.

Long-term intermittent dobutamine infusion combined with oral amiodarone improves the survival of patients with severe congestive heart failure.

STUDY OBJECTIVE: To evaluate the effects of long-term intermittent dobutamine infusion (IDI) with concomitant administration of low-dose amiodarone in patients with congestive heart failure (CHF) refractory to standard medical treatment. DESIGN: Prospective, interventional clinical trial. SETTING: Inpatient and outpatient heart failure clinic in a university teaching hospital. PATIENTS AND INTERVENTIONS: Twenty-two patients with CHF refractory to standard treatment who could be weaned from dobutamine therapy after an initial 72-h infusion were included in this study. The first 11 patients (group 1) were treated with IDI, 10 micromin, as needed (mean, once every 16 days, lasting for 12 to 48 h); the next 11 patients (group 2) received oral amiodarone, 400 mg/d, and IDI, 10 microg/kg/min, for 8 h every 7 days. MEASUREMENT AND RESULTS: There were no differences in baseline clinical, hemodynamic, and five biochemical characteristics between the two groups. The left ventricular ejection fraction was 13.5 +/- 4.5% in group 1 vs 15.5 +/- 4.9% in group 2 (mean +/- SD; p = 0.451); mean pulmonary capillary wedge pressure was 31.3 +/- 4.4 mm Hg vs 29.4 +/- 3.3 mm Hg (p = 0.316); serum creatinine was 1.9 +/- 0.4 mg/dL vs 1.6 +/- 0.5 mg/dL (p = 0.19); and serum Na was 139.6 +/- 6.2 mEq/L vs 138.4 +/- 3.1 mEq/L (p = 0.569). At 12 months of follow-up, 1 of 11 patients (9%) was alive in group 1 vs 6 of 11 patients (55%) in group 2 (p = 0.011). Furthermore, in group 2, the functional status improved significantly within the first 3 months of treatment, from New York Heart Association functional class IV to 2.63 +/- 0.5 (p = 0.0001). CONCLUSION: Long-term IDI in conjunction with amiodarone, added to conventional drugs, improved clinical status and survival of patients with severe CHF.

A valveless high stroke volume counterpulsation device restores hemodynamics in patients with congestive heart failure and intractable cardiogenic shock awaiting heart transplantation.

The paraaortic counterpulsation device is a round pumping chamber with one valveless opening 20 mm in diameter and a 100 ml stroke volume. The paraaortic counterpulsation device was implanted on the ascending aorta of three male patients with intractable cardiogenic shock. Patients were assisted for 4 hours and 8 and 54 days, respectively; the first patient died as a result of nonresponding peripheral vasodilation and the other two died of septic shock. The two patients who were assisted for 8 and 54 days were conscious and able to function in a limited manner during the mechanical assistance. Discontinuation of the mechanical support for a few seconds was followed by low systolic arterial pressure (30 to 60 mm Hg) and syncopal episodes. Biochemical tests and autopsy results in these patients showed no evidence of blood cell destruction, thrombus formation, brain infarction, or other distal emboli. In conclusion, satisfactory hemodynamic effects, excellent biocompatibility, and simplicity of the implantation procedure in these patients encourage the use of the paraaortic counterpulsation device as a bridge to heart transplantation.

Redistribution of amiodarone in heart transplant recipients treated with the drug before operation.

Seven heart transplant recipients (six men and one woman) treated with oral amiodarone 194 +/- 100 mg/day before operation for a period of 30 +/- 48.5 months were studied. The myocardial concentrations of amiodarone in the transplanted heart peaked in the second posttransplantation week (87.6 +/- 80.7 microg/g myocardial tissue) and remained detectable in the twelfth week (10.2 +/- 8.4 microg/g myocardial tissue). The ratio of myocardial/plasma concentrations peaked at the end of the sixth posttransplantation week. In conclusion, amiodarone accumulated rapidly in the transplanted myocardium of heart transplant recipients treated with the drug before operation and remained detectable for at least 3 months.

Mechanical ventilation in conjunction with the intra-aortic balloon pump improves the outcome of patients in profound cardiogenic shock.

OBJECTIVE: To examine the effects of mechanical ventilation with positive end-expiratory pressure (PEEP), in conjunction with the intra-aortic balloon pump (IABP), on the outcome of patients in profound cardiogenic shock. PATIENTS: Twenty-eight consecutive patients presenting with myocardial infarction complicated by cardiogenic shock refractory to medical therapy, including dobutamine, dopamine and fluid administration. Eighteen patients were assisted by the IABP alone (IABP group), and ten patients by the IABP plus controlled mechanical ventilation with PEEP set at 10 cmH(2)O (IABP + CMV group). RESULTS: Weaning from mechanical assistance was accomplished in 8 out of 18 patients in the IABP group versus 9 out of 10 patients in the IABP + CMV group (p = 0.04). Ultimately, 5 of 18 patients in the IABP group were discharged from the hospital versus 8 of 10 patients in the IABP + CMV group (p = 0. 01). CONCLUSION: Mechanical ventilation with PEEP at 10 cmH(2)O supplements the IABP and may improve the survival rates of patients suffering from cardiogenic shock.

The disposition of recainam hydrochloride during and after intravenous loading and maintenance infusion in cardiac patients.

Recainam hydrochloride is a newly synthesized propylurea compound demonstrating potent antidysrhythmic effects. Recainam was administered as a loading dose of 3 mg/kg/40 minutes followed by a continuous infusion of 0.9 mg/kg/hr for 23 hours and 20 minutes to ten patients with cardiac disease and frequent PVCs (more than 30/hr). A total of 15 plasma samples were drawn over 36 hours during and after the infusion. Plasma recainam concentration was determined by high performance liquid chromatography (HPLC). The mean (+/- SD) postload and 24-hour plasma concentrations were 5.19 +/- 0.51 and 3.41 +/- 0.71 micrograms/mL, respectively. The data were best described by a two-compartment model yielding the following mean (+/- SD) pharmacokinetic parameters: lambda 1 = 2.62 +/- 0.68 hr-1, lambda 2 = 0.144 +/- 0.014 hr-1, t1/2 lambda 2 = 4.84 +/- 0.46 hr, CLT = 0.268 +/- 0.057 L/hr/kg, CLR = 0.143 +/- 0.052 L/kg/hr, CLNR = 0.125 +/- 0.041 L/hr/kg, Vdss = 1.3 +/- 0.19 L/kg, and Vd lambda 2 = 1.9 +/- 0.43 L/kg. There were no adverse reactions. Based on these data, recainam can be safely administered as a loading dose followed by a continuous infusion in patients with stable cardiac disease without significant ventricular dysfunction.

Treating severe cardiogenic shock by large counterpulsation volumes.

BACKGROUND: Intraaortic balloon pumping is known to be ineffective in severe cardiogenic shock. The efficacy of balloon volumes larger than those commonly used is examined. METHODS: In 18 dogs with severe experimental cardiogenic shock (systolic aortic pressure < 60 mm Hg, aortic flow < 45 mL.min-1.kg-1) the effect of three intraaortic balloon volumes (15, 30, and 45 mL) and a 60-mL paraaortic pump was examined. RESULTS: The 45-mL balloon covering the full length of the aorta induced the highest (+ 12.4 +/- 2.2 mL.min-1.kg-1; mean +/- standard error of the mean) and the 15-mL balloon the lowest increase in aortic flow (F = 14.6, p < 0.0001). Only the 45-mL balloon increased (p < 0.05) urine output and renal artery flow. The 60-mL paraaortic pump induced the highest (F = 10.72, p < 0.002) increase (+ 36.6 +/- 6.5 mL.min-1.kg-1) in aortic flow compared to the three balloons. An 80- to 100-mL paraaortic pump maintained the life of 3 patients in severe cardiogenic shock for 4 hours, 8 days, and 54 days, whereas a 40-mL conventional balloon was completely ineffective. CONCLUSIONS: Experimental and clinical data indicate that the effectiveness of intraaortic balloon pumping in severe cardiogenic shock may be improved by increasing the volume of the balloon (i.e., until it fully occupies the aorta).

Myocardial salvage by the use of reperfusion and intraaortic balloon pump: experimental study.

BACKGROUND: Thrombolytic therapy improves left ventricular ejection fraction and survival. The study was undertaken to evaluate the effects of intraaortic balloon pump used in conjunction with reperfusion in reducing infarct size. METHODS: Twenty-two dogs were subjected to proximal left anterior descending coronary artery occlusion. In group 1 (n = 7) occlusion lasted for 6 hours. In group 2 (n = 6) 2 hours of occlusion was followed by reperfusion. In group 3 (n = 9) after 2 hours of occlusion the dogs were assisted with the intraaortic balloon pump throughout the 4 hours of reperfusion. At the end of 6 hours the infarcted myocardium of the left ventricle was determined and expressed as percentage of the myocardium at risk. RESULTS: In group 1, the infarcted myocardium was 79.3 +/- 9.9% of the myocardium at risk, in group 2, 59.0 +/- 19.9% (p < 0.05 versus group 1), and in group 3, 37.1 +/- 16.7% (p < 0.001 versus group 1 and p < 0.05 versus group 2). Endocardial viability ratio was increased by the intraaortic balloon pump; in group 1 it was 1.02 +/- 0.14, in group 2, 1.25 +/- 0.24, and in group 3, 1.47 +/- 0.31 (p < 0.001 versus group 1 and p < 0.02 versus group 2). CONCLUSIONS: Reperfusion and intraaortic balloon pump increased salvage of the ischemic myocardium over that achieved by reperfusion alone in a canine occlusion-reperfusion model.