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Background: Intermittent dobutamine infusions (IDI) combined with oral amiodarone improve the survival of patients with end-stage congestive heart failure (CHF). The purpose of the present study was to evaluate whether the response to long-term treatment with IDI+amiodarone is different in patients with ischemic heart disease (IHD) versus idiopathic dilated cardiomyopathy (IDC). Methods: The prospective study population consisted of 21 patients with IHD (the IHD Group) and 16 patients with IDC (the IDC Group) who presented with decompensated CHIF despite optimal medical therapy, and were successfully weaned from an initial 72-h infusion of dobutamine. They were placed on a regimen of oral amiodarone, 400 mg/day and weekly IDI, 10 mu g/kg/min, for 8 h. Results: There were no differences in baseline clinical and hemodynamic characteristics between the 2 groups. The probability of 2-year survival was 44% in the IDC Group versus 5% in the IHD Group (long-rank, P=0.004). Patients with IDC had a 77% relative risk reduction in death from all causes compared to patients with IHD (odd ratio 0.27, 95% confidence interval 0.13 to 0.70, P=0.007). In contrast, no underlying disease-related difference in outcomes was observed in a retrospectively analyzed historical comparison Group of 29 patients with end stage CHIF treated by standard methods. Conclusions: Patients with end stage CHF due to IDC derived a greater survival benefit from IDI and oral amiodarone than patients with IHD. (c) 2005 Elsevier Ireland Ltd. All rights reserved.

Background: Anemia is common in patients with congestive heart failure (CHF), although its etiology and pathophysiology remain largely unexplained. The purpose of this study was to examine the prognostic significance of a low hematocrit (Hct) in patients with CHF and the possible role of angiotensin-converting enzyme inhibition in anemia development. Methods: Hct was measured at the time of enrollment of 160 patients with CHF, mean age 56 12 years, in New York Heart Association (NYHA) functional class 2.6 +/- 0.7 and with left ventricular ejection fraction of 20 +/- 9%. They were randomized to standard (mean: 17.9 +/- 4.3 mg/day) or high (mean: 42 +/- 19.3 mg/day) doses of enalapril. The follow-up duration was 2 years. Cox regression models were used to identify prognostic factors, and correlations among individual variables were tested. Results: Mean baseline Hct was 42.7 +/- 5%. In multivariate analyses, low Hct (p = 0.036), older age (p = 0.022) and low systolic blood pressure (p = 0.032) were independent predictors of death within 2 years. A correlation was found between baseline Hct and NYHA class (Spearman’s correlation coefficient: -0.183, p = 0.008). A significant decrease in Hct from 43.2 +/- 4.9% at baseline to 40.7 +/- 4.4% at 2 years was observed in the group treated with high doses of enalapril (p < 0.001). Conclusions: Low baseline Hct predicted poor 2-year prognosis in patients with CHF. Enalapril administered in high doses increased the incidence of anemia in this population. The underlying pathophysiologic mechanism and effects of maintaining a normal Hct on clinical outcomes remain to be determined.

A 32-year-old man with severe congestive heart failure due to idiopathic cardionnyopathy developed ventricutar tachycardia followed by etectromechanical dissociation. High doses of conventional inotropic medications failed to restore haemodynamics. The additional infusion of levosimendan in conjunction with external chest compressions for 2.5h restored haemodynamics, followed by complete recovery, including normal neurological function. The anti-stunning properties of levosimendan probably attenuated post-ischaemic myocardial dysfunction and helped to restore normal cardiac output. (c) 2005 Elsevier Ireland Ltd. All rights reserved.

Background: The aim of this study was to evaluate the long-term effect of combined intermittent dobutamine infusions (IDI) and oral amiodarone on reverse left ventricular (LV) remodeling and hemodynamics of patients with idiopathic dilated cardiomyopathy (IDC) and end-stage congestive heart failure (CHF). Methods: This non-randomized, prospective, clinical trial included sixteen consecutive patients suffering from dyspnea for a mean of 76 43 months, who presented with acute cardiac decompensation and were weaned from dobutamine therapy after an initial 72-h infusion. They were then placed on a regimen of oral amiodarone, 400 mg/day and weekly IDI, 10 mu g/kg/min, for 8 h. The long-term clinical outcomes and the effects of treatment on reverse LV remodeling (echocardiographic parameters) and hemodynamics were evaluated at 3, 6, and 12 months of follow up. Results: A significant degree of reverse LV remodeling, hemodynamic improvements, and survivals > 1.5 years were observed in 9 of the 16 patients (56%). In addition, 5 patients (31% of entire cohort) were weaned from IDI after a mean of 61 41 weeks, and 4 remained clinically stable for 116 66 weeks thereafter. At 12 months of follow-up, LV end-diastolic and end-systolic volume indices had decreased from 231 +/- 91 to 206 +/- 80 ml/m(2) (P=0.002) and from 137 +/- 65 to 110 +/- 50ml/m(2) (p= 0.003), respectively, right atrial pressure from 16 +/- 6 to 5.6 +/- 4 mm Hg, (P=0.031), and pulmonary capillary wedge pressure from 29 +/- 4 to 16 +/- 5.4 min Hg, P=0.000, while LV ejection fraction had increased from 22 +/- 6% to 27.3 +/- 8% (P = 0.006). Conclusions: In end-stage CHF due to IDC, long-term treatment with IDI and oral amiodarone caused reverse LV remodeling, and allowed permanent and successful weaning from IDI in 1/4 of patients. (c) 2005 Elsevier Ireland Ltd. All rights reserved.

Chronic heart failure is a clinical syndrome associated with an ominous long-term prognosis and major economic consequences for Western societies. In recent years, considerable progress has been made in the pharmacological management of heart failure, and several treatments have been confirmed to confer survival and symptomatic benefits. However, pharmaceuticals remain underutilised, and the combination of several different drugs present challenges for their optimal prescription, requiring a thorough knowledge of potential side effects and complex interactions. This article reviews in detail the evidence pertaining to the out-patient pharmacological management of chronic heart failure, and offers recommendations on the use of various drugs in complex clinical conditions, or in areas of ongoing controversy.

The aim of this study was to examine whether pulsatility by intraaortic balloon counterpulsation (IABP) is an important adjunct to the treatment of profound cardiogenic shock (CS) with a widely used, nonpulsatile centrifugal pump (CP). In each of 18 anesthetized, open chest pigs, the outflow cannula of the CP was inserted in the aortic arch through the right external carotid artery, and the inflow cannula of the CP was placed in the left atrium. A 40 cc IABP was subsequently placed in the descending aorta through the left external carotid artery. CS was induced by occlusion of coronary arteries and the infusion of propranolol and crystalloid fluid. Mean aortic pressure, pulse pressure, aortic end diastolic pressure, left ventricular end diastolic pressure, right atrial pressure, and heart rate were monitored. Cardiac output and left anterior descending artery flow were measured with a transit time ultrasound flowmeter. During profound CS, life sustaining hemodynamics were maintained only with the support of the assist devices. Hemodynamic support with the CP was associated with a nearly nonpulsatile flow and a pulse pressure of 7 +/- 4 mm Hg, which increased to 33 +/- 10 mm Hg (p = 0.000) after combining the CP with the IABP. Compared with the hemodynamic support offered by the CP alone, addition of the IABP increased mean aortic pressure from 40 +/- 15 to 50 +/- 16 mm Hg (p = 0.000), cardiac output from 810 +/- 194 to 1,200 +/- 234 ml/min (p = 0.003), and left anterior descending artery flow from 26 10 to 39 14 ml/min (p = 0.001). In profound CS, mechanical support provided by a continuous flow CP is enhanced by the added pulsatility of the IABP.

Autonomic nervous system dysfunction is common in congestive heart failure (CHF) and is believed to predispose patients to an increased risk of death. This study aimed to assess the prognostic significance of heart rate variability (HRV) measurements in conjunction with scintigraphic imaging using metaiodobenzylguanidine (MIBG) labeled with iodine-123 (I-123-MIBG), which detects abnormalities in autonomic nervous activity, in patients with stable CHF during optimal medical treatment. The study population included 52 patients (56 +/- 12 years of age) with a mean left ventricular ejection fraction of 31 +/- 12%. All underwent I-123-MIBG scanning and 24-hour ambulatory electrocardiographic monitoring for the analysis of HRV on entrance into the study. The heart/mediastinum MIBG uptake ratio was calculated. HRV analysis included the assessment of time- and frequency-domain variables. During the 2-year follow-up, 14 patients (27%) died. MIBG uptake at I hour was less (1.39 +/- 0.10) in nonsurvivors than in survivors (1.50 +/- 0.16; p = 0.013). In univariate Cox regression analysis, MIBG uptake was a significant prognostic factor (p = 0.038, hazard ratio [HR] 0.017, 95% confidence interval [CI] 0.00 to 0.79). Time- and frequency-domain variables were similar in survivors and nonsurvivors. However, high-frequency power was associated with an increased risk for sudden death (HR 0.310, 95% CI 0.101 to 0.954, p = 0.041) but not with all-cause mortality. In conclusion, cardiac I-123-MIBG imaging identifies patients with CHF at high risk of dying and may be a more reliable predictor of overall mortality than HRV. (c) 2005 Elsevier Inc. All rights reserved.

Background: Acute myocardial ischemia and the mode of ventricular fibrillation (VF) induction influence the ventricular defibrillation threshold (DFT). Methods: Ventricular effective refractory period (ERP), ventricular fibrillation threshold (VFT), and DFT were measured under nonischemic conditions (control) in 26 pigs weighing 25-35 kg. Myocardial ischemia was then induced by occlusion of the mid left anterior descending coronary artery, and measurements of ERP and VFT were repeated after 2 minutes of Occlusion. The coronary artery ligation was released immediately after the onset of VF and DFT was measured. Results: LV ERP was unchanged by ischemia (199 +/- 19 ms at control vs. 200 22 Ins under ischemic conditions, P=0.799), whereas VFT was significantly lower during coronary Occlusion (10.7 +/- 15.4 mA vs. 37.7 +/- 13 mA, P = 0.000). Brief myocardial ischemia caused a significant increase in DFT (13.5 +/- 12.6 J after coronary occlusion vs. 6.8 +/- 6.8 J at control, P = 0.023). The duration of coronary occlusion was not Correlated with the amounts of energy required to defibrillate (P = 0.526). Conclusions: This experimental study shows that transient myocardial ischemia markedly increases the DFT suggesting that specific defibrillation algorithms should be designed for recipients of implantable defibrillators at risk of myocardial ischemia.

Thirty-six consecutive patients in New York Heart Association functional class IV, who were resistant to 24-hour continuous dobutamine infusion, were treated with continuous infusions of dobutamine 10 mu g/kg/min for >= 48 hours (group I, In = 18), followed by weekly intermittent 8-hour infusions or more often if needed. In group II (n = 18), after the initial 24-hour infusion of dobutamine, a 24-hour levosimendan infusion was added followed by biweekly 24-hour infusions. The addition of intermittent levosimendan infusions prolonged the survival of patients with advanced heart failure refractory to intermittent dobutamine infusions (45-day survival rates were 6% and 61% in groups I and II, respectively; p = 0.0002, log-rank test). (c) 2005 by Excerpta Medica Inc.

Introduction: The effects of myocardial ischaemia preconditioning in pigs on the vulnerability to ventricular fibrillation during subsequent ischaemic events are controversial. This study examined the time course of changes in ventricular fibrillation (VFT) and defibrillation (DFT) thresholds during transient myocardial ischaemia after a 45 min preconditioning period. Methods and results: In five open-chest pigs, VFT was measured after 3 min of regional myocardial ischaemia, at time 0, 2, 15, 30, 60 and 90 min (Control group). In seven other pigs (Test group), VFT was measured before (time 0) and 2, 15, 30, 60 and 90 min after ischaemic preconditioning by three consecutive 5 min periods of regional coronary occlusion, followed by 10 min of reperfusion. DFT was measured by increasing the stored energy systematically until successful defibrillation. Ischaemic preconditioning caused no significant change in the effective refractory period (ERP), VFT or DFT over the 90 min of the experiments. In the Control group, ERP remained stable for 30 min, though was significantly lower at 90 min (178 +/- 28 ms) than at baseline (204 +/- 32 ms, P = 0.007). VFT and DFF remained unchanged throughout the experiments, and no difference was observed in ERP, VFT and DFT between the two groups at any time during the experiment. Conclusion: No changes were observed in the refractory duration, ventricular vulnerability or defibrillation energy requirements up to 90 min after ventricular ischaemic preconditioning in the pig. (c) 2004 Elsevier Ireland Ltd. All rights reserved.

Study objectives: To examine the effects of long-term intermittent dobutamine infusion, combined with oral amiodarone in patients with congestive heart failure (CHF) refractory to standard medical treatment. Design: Prospective, randomized, double-blind, placebo-controlled clinical trial. Setting: Inpatient and outpatient heart failure clinic in a university teaching hospital. Patients and interventions: Thirty patients with end-stage CHF refractory to standard medical treatment who could be weaned from dobutamine therapy after a first 72-h infusion were randomized in a double-blind manner to receive IV infusions of placebo (group 1; 14 patients) vs dobutamine in a dose of 10 mug/kg/min (group 2; 16 patients) for 8 h every 14 days. All patients received standard medical therapy and also were treated with oral amiodarone, 400 mg/d, which was started at least 2 weeks before randomization. Measurements and results: Kaplan-Meier survival analysis showed a 60% reduction in the risk of death from any cause in the group treated with the combination of dobutamine and amiodarone, compared with the group treated with placebo and amiodarone (hazard ratio, 0.403; 95% confidence interval, 0.164 to 0.992; p = 0.048). The 1-year and 2-year survival rates were 69% and 44%, respectively, in the dobutamine-treated group, vs 28% and 21%, respectively, in the placebo-treated group (p < 0.05 for both comparisons). Median survival times were 574 and 144 days, respectively, for groups 2 and 1. At 6 months, the New York Heart Association functional class was significantly improved in the patients who survived from both groups. Conclusions: Long-term intermittent dobutamine infusion combined with amiodarone added to the conventional drugs improved the survival of patients with advanced CHF that was refractory to conventional treatment.

Study objectives: To examine the effects of low arterial BP (ABP) during reperfusion on the extent of myocardial infarction and on coronary blood flow (CBF) in an occlusion/reperfusion experimental model. Design: Prospective, randomized animal study. Setting: University hospital. Participants: Normal pigs that were anesthetized, intubated, and mechanically ventilated. Interventions: Twenty-seven open-chest pigs underwent occlusion of the mid left anterior descending (LAD) coronary artery for I h followed by reperfusion for 2 h. During reperfusion, the animals were randomly assigned to either continuous infusion of nitroglycerin in therapeutic doses and fluid infusion at rates to maintain a mean ABP greater than or equal to 80 mm Hg (group 1, n = 13), or continuous nitroglycerin infusion at rates to maintain a mean ABP between 60 mm Hg and 75 mm Hg (group 2, n = 14). Measurements and results: The hemodynamics and the coronary ABP distal to the occlusion were recorded throughout the experiment. In addition, the LAD CBF and peak hyperemia CBF before occlusion and during reperfusion periods were measured by transit-time flowmetry. At the end of the experiment, the infareted left ventricular myocardial size was measured. There were no significant hemodynamic differences, including the distal coronary arterial pressure, between the two groups before or during the LAD artery occlusion period. During reperfusion, mean ABP was 90 +/- 3 min Hg in group 1 vs 69 +/- 3 mm Hg in group 2 (p < 0.001). In group 1, the infarcted myocardium represented 50.3 +/- 4.3% of the myocardium at risk, vs 69.4 +/- 7.2% in group 2 (p < 0.001). During reperfusion, CBF and peak hyperemia CBF were significantly higher in group 1 than in group 2. Conclusions: Low ABP during reperfusion increases the size of myocardial infarction and decreases CBF.

Experimental studies have described an increase in ventricular fibrillation threshold (VFT) by intravenous amiodarone. The aim of this study was to examine the early time course of changes in VFT and defibrillation thresholds (DFT) after an intravenous bolus of amiodarone in an experimental pig model of transient myocardial ischemia. Methods and results: VFT and relative effective ventricular refractory period (ERP) were measured in 15 anaesthetized open-chest pigs after 3 min of regional coronary ischaemia before (time 0) and 2, 15, 30, 60, and 90 min after the intravenous injection of normal saline (group A, n = 5) or amiodarone, 5 mg/kg over 15 s (group B, n = 10). DFT was measured by increasing the strength of DC shocks until defibrillation was accomplished. Amiodarone caused an increase in VFT, starting at 2 min after the infusion (11.4 +/- 8.4 mA versus 9.2 +/- 4.6 mA, P = 0.113), became significant at 15 min (13.7 +/- 6.5 mA, P = 0.009) continued to rise at 30 min (34.2 +/- 28.7 mA, P = 0.03) and reached a plateau at 60 min (50.3 +/- 37.8 mA, P = 0.008). An increase was also observed in the ERP (204 +/- 25 ms at 2 min versus 197 +/- 26 ms at baseline, P = 0.074, 211 +/- 38 ms at 15 min, P = 0.084, 212 +/- 40 ms at 30 min, P = 0.037, 220 +/- 34 ms at 60 min, P = 0.002, and 227 32 ms at 90 min, P = 0.008). No change was observed in DFT after amiodarone administration. No significant change in VFT, ERP, or DFT occurred in the control group. Conclusion: In this porcine model, the intravenous administration of amiodarone increased VFT and ERP over 60 min after the injection, without effect on DFT. (C) 2003 Elsevier Ireland Ltd. All rights reserved.

A 24-hour infusion of levosimendan was added to dobutamine in 18 patients (aged 63 +/- 9 years) hospitalized for management of decompensated New York Heart Association functional class IV heart failure refractory to a continuous 24-hour infusion of dobutamine (10 mug/kg/min) and furosemide (10 mg/hour); the primary study end point was a greater than or equal to40% increase in cardiac index and a greater than or equal to25% decrease in pulmonary capillary wedge pressure compared with pretreatment measurements. The primary end point was reached in none of the patients treated with dobutamine alone versus 7 patients (39%) treated with levosimendan and dobutamine combined (p = 0.008), whereas at 24 hours, the combined treatment was associated with a 0.76 +/- 0.78 L/min/m(2) (p = 0.001) mean increase in cardiac index and a 6.4 +/- 7.3 mm Hg (p = 0.002) mean decrease in pulmonary capillary wedge pressure compared with measurements obtained after 24 hours of dobutamine infusion alone. Symptoms were alleviated in, all patients, and all but 3 were discharged from the hospital. (C) 2004 by Excerpta Medica, Inc.

Background: Exercise capacity, assessed by cardiopulmonary exercise treadmill testing (CPET), does not return to normal following heart transplantation. This study evaluated the ventilatory response to exercise and the kinetics of oxygen (O-2) recovery in heart transplant recipients (HTR) compared to healthy volunteers (HV) and heart failure patients. Methods: Eighteen patients with end-stage heart failure (ESHF), 12 with mild heart failure (MHF) matched for peak oxygen consumption (Vo(2)) with the HTR, 12 HTR and 12 HV underwent CPET for measurements of peak Vo(2), Vo(2) at anaerobic threshold (AT), first-degree slope of Vo(2) decline during early recovery (Vo(2)/t-slope), time required for a 50% fall from peak Vo(2) (T-1/2 of Vo(2)) and the slopes of VE/Vco(2) and VE/Vo(2). Results: The MHF and HTR groups had similar ventilatory responses to exercise and O-2 recovery kinetics. Peak Vo(2) (18.5 +/- 5.7 vs 9.4 +/- 0.9 ml/kg/min, p < 0.001), AT (3.8 +/- 4.8 vs 6.7 +/- 1.8 ml/kg/min, p < 0.001) and Vo(2)/t-slope (0.6 +/- 0.2 vs 0.3 +/- 0.2 liter/min/min, p = 0.055) were higher in the HTR than in the ESHF group. In contrast, HTR had lower VE/Vco(2)-slope (31.4 +/- 3.8 vs 9.2 +/- 9.9, p = 0.015) and T-1/2 Vo(2) (1.5 +/- 0.3 vs 2.4 +/- 1.1 minute, p = 0.014) than the ESHF group. Compared to HV, HTR had lower Vo(2) peak (18.5 +/- 5.7 vs 28.4 +/- 6.9 ml/kg/min, p < 0.001), AT (3.8 +/- 4.8 vs 19.8 +/- 4.5 ml/kg/min, p = 0.04), Vo(2)/t-Slope (0.6 +/- 0.2 vs 1.0 +/- 0.4 liter/min/min, p = 0.005) and steeper VE/Vco(2) slope (31.4 +/- 3.8 vs 23.6 +/- 2.7, p = 0.062). Heart rate deceleration during recovery was significantly slower in HTR than in all other groups. Conclusions: Exercise intolerance and delayed O-2 recovery kinetics were only partially reversed after heart transplantation. This finding suggests that some of the pathophysiologic mechanisms of heart failure persist after heart transplantation.

Objectives:. To evaluate the effect of bone marrowpluripotent stem cell mobilization with granulocyte-monocyte colony stimulating factor (GMCSF) on infarct size and left ventricular function, in the setting of acute myocardial infarction, with a protocol easily applicable in clinical practice. Methods:. Ten pigs underwent left thoracotomy and left anterior descending coronary artery occlusion for 1 h, followed by reperfusion. After 50 min of arterial occlusion, the animals were randomly divided between treatment with placebo (Group 1) and subcutaneous GM-CSF (Group 2). The thoracotomy was closed and the animals recovered. In Group 2, GM-CSF, 20 mug/kg, was administered daily, 5 days/week, for 3 weeks. Echocardiograms were obtained at 5 and 28 days after acute myocardial infarction. At 30 days, infarct size, expressed as a percentage of the whole left ventricular mass, was measured. Results:. The white blood cell count increased from 13000 +/- 3338/mul to 28700 +/- 4916/mul (p = 0.001) in the GM-CSF-treated group. Infarct size was 7.8 +/- 6.1% in Group 1 vs 7.5 +/- 7.7% in Group 2 (ns). Similarly, no significant difference was observed between the 2 study groups in any of the echocardiographic measurements made at 28 days. Conclusions:. Subcutaneous GMCSF administered during the early post acute myocardial infarction period neither decreased infarct size nor improved left ventricular function. Other protocols for mobilization of stem cells and their concentration in the injured area should be developed to combine efficacy and clinical applicability.

A 44-year-old man presented with symptoms and signs of cardiac tamponade. Cytologic examination of the pericardial fluid was negative for malignancy and no manifestations of primary tumor were detected. Two weeks after pericardiocentesis the patient developed constrictive pericarditis. An emergency exploratory thoracotomy revealed a thick, fibrotic pericardium firmly adherent to the underlying myocardium. Histologic examination of the pericardium showed the presence of an adenocarcinoma, suspected to be a metastatic dissemination from a primary pulmonary source. The lymphatic spread of the tumor to the heart may explain the early development of pericardial effusion without malignant cells and the later development of pericardial and epicardial thickening. Cardiac tamponade of unknown origin should prompt a search for metastatic carcinoma, including in presence of a negative cytology.

Background: Recent progress has been made in the understanding of the cellular and molecular mechanisms of growth hormone action and of its effects on cardiac tissue. The aim of this study was to measure growth hormone concentrations, along with various other hormones, in patients with stable chronic congestive heart failure due to idiopathic dilated cardiomyopathy. Methods: The study included 23 ambulatory men, 51.2+/-9.3 years of age, on standard medical therapy for heart failure due to idiopathic dilated cardiomyopathy. All patients underwent clinical and laboratory evaluations, including echocardiogram, radionuclide ventriculography, right heart catheterization, coronary angiography, and right ventricular endomyocardial biopsy. Serum or plasma concentrations of growth, thyroid, sex and adrenal hormones were measured in all patients and compared with those found in 20 age-matched healthy men. Results: Growth hormone, insulin-like growth factor 1, and free testosterone values in patients with idiopathic dilated cardiomyopathy and heart failure were 0.37+/-0.2 ng/ml, 123.7+/-50 ng/ml and 48.6+/-23.8 pmol/l, respectively, versus 0.5+/-0.4 ng/ml (P

The purpose of this study was to compare the hemodynamic effectiveness of a 30-ml stroke volume paraaortic counterpulsation device (PACD), presenting the advantages of ease of implantation and driving by a standard intraaortic balloon pump (IABP) console (Datascope 96, Datascope Corp., Montvale, NJ, USA) to that of a 40-ml IABP, in the setting of experimental heart failure. In an acute heart failure model, the IABP was placed in the descending aorta and the PACD in the ascending aorta of eight pigs. Both devices were driven by the same system, and hemodynamic measurements were obtained with and without mechanical assistance. The two pumps significantly reduced the systolic and end-diastolic aortic pressures, but the PACD reduced the latter more effectively (42.6 +/- 18.1% vs 11.0 +/- 9.9%,p = 0.0001). Both pumps provided significant aortic diastolic augmentation, but the counterpulsation wave of the PACD was significantly greater (augmentation of 44.8 +/- 22.2% vs 37.6 +/- 15.6%, p = 0.031). Both lowered the end-diastolic left ventricular pressure with a trend toward PACD superiority (24.2 +/- 13.7% vs 19.7 +/- 13.5%,p = 0.064). It is concluded that the PACD, even with smaller stroke volume, is more effective than the IABP. The simplicity of its implantation, together with the ability of the standard IABP consoles to control its function, make it a promising device for mechanical assistance of the failing heart.

Primary graft dysfunction is a major cause of morbidity and mortality early after cardiac transplantation. We present here a case of unspecific graft dysfunction in a 47-year-old female recipient of a heart transplant that could not be attributed to the unusual causes of this disorder. The patient manifested symptoms and signs of heart failure early postoperatively, and echocardiography together with right heart catheterization confirmed the diagnosis. There was no body size mismatch, graft preservation was optimal, pulmonary vascular resistance preoperatively was normal, and rejection episodes could not explain her deterioration. Standard medical therapy for heart failure was initiated, and the patient’s symptoms improved, although graft dysfunction persisted for a period of 1.5 years. Afterward, a gradual spontaneous improvement occurred, resulting in complete recovery of graft function at six years postoperatively. In addition to the case presented, potential contributing factors to this syndrome, together with appropriate treatment options, are discussed.

Objectives -This study was performed to examine the safety of reducing the long-term doses of furosemide administered to patients with congestive heart failure (CHIF) stabilized on a standard medical treatment. Methods and results - Twenty-nine patients with advanced CHIF were treated with enalapril, digoxin, nitrates, and furosemide, as needed to alleviate their symptoms, and remained clinically stable for at least 3 months on those doses. Subsequently, the daily dose of furosemide was reduced to 1/3 of the previous dose, while the concomitant therapy was unchanged. All patients underwent a thorough clinical evaluation and right-heart catheterization before and 2 months after the furosemide dose reduction. After the treatment optimization the NYHA functional class decreased from 2.3+/-0.6 to 1.4+/-0.6 (p=0.000), and the left ventricular ejection fraction increased from 22+/-10% to 32+/-13%, (p=0.000). Clinical and haemodynamic evaluation before and after 2 months of treatment with lower furosemide doses showed that 24 of the 29 patients (83%) remained in a stable NYHA functional class and maintained a stable haemodynamic status. In the remaining 5 patients (17%), mean NYHA functional class increased from 1.8+/-0.4 to 2.4+/-0.6 (p=0.07),accompanied by a significant increase of the right and left ventricular filling pressures from 4.2+/-2.7 to 9.0+/-3.0 mm Hg, p=0.018 and from 8.6+/-3.0 to 19.8+/-3.6 mm Hg, p=0.017, respectively. These 5 patients returned to a stable clinical status upon resumption of the prior doses of furosemide. Conclusions - Most patients with chronic CHF who were clinically stabilized on high doses of furosemide remained stable on a maintenance dose equal to one-third of the dose needed for their stabilization. Patients unable to tolerate the dose reduction regained their previous clinical status following the resumption of the prior diuretic doses.

Background: This study examined the evolution of the heart to lung (H/L) ratio of monoclonal antimyosin antibody (MAA) uptake in patients with suspected acute myocarditis (AM) and its time-dependent diagnostic value in conjunction with echocardiographic findings. Methods: The study included 20 patients with a short history (1.55) associated with an LVEDdless than or equal to62 mm was diagnostic of AM with a sensitivity of 67%, a specificity of 63% and a positive predictive value of 65%. Upon restudy, the H/L ratio of MAA uptake was significantly decreased in both groups, reaching almost identical levels. No difference was found in the LVEDd between the two groups. The positivity of cardiac antimyosin scintigraphy in conjunction with an LVEDdless than or equal to62 mm had a sensitivity of 45% and a specificity of 88% for the diagnosis of myocarditis. Conclusions: In patients with suspected AM a positive antimyosin scintigraphy accompanied by a non-dilated left ventricle is highly suggestive of AM, both at the early phase and 1 year after disease onset. (C) 2003 Elsevier Ireland Ltd. All rights reserved.

The clinical and hemodynamic effects of amiodarone were examined in patients with severe congestive heart failure who were unable to tolerate metoprolol therapy. Amiodarone improved left ventricular ejection fraction and stabilized their clinical and hemodynamic condition to a level comparable with metoprolol.

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.

Purpose: Atrial fibrillation (AF) is a fairly common complication of acute myocardial infarction (AMI). The aim of this study was to examine the safety and efficacy of intravenous amiodarone in converting AF associated with AMI. Methods: Seventy patients with AMI complicated with AF were prospectively divided into 3 groups: a) In group D (n=26), 0.75 mg digoxin was administered intravenously and thereafter as needed, b) In group AM (n= 16), 300 mg of amiodarone was infused over 2 hours followed by 44 mg/hour for up to 60 hours or until sinus rhythm was restored, c) In group D +AM (n=28), 0.75 mg of digoxin was administered (as in group D) for the initial 2 hours followed by amiodarone infusion as in group AM. Results: Sinus rhythm was restored: a) by the end of the 2nd hour in 9/26 patients from group D, 4/16 from group AM, and 10/28 from group D + AM (p = NS), b) by the end of the 96th hour, in 18/26 patients from group D, and in all patients from group AM and groupd D +AM. The corresponding duration of AF was 51 +/- 34 hours, 17 +/- 15 hours and 9 +/- 13 hours, respectively (F = 15.4, p < 0.001). AF recurred in 9/26, 5/16 and 1/28 patients of groups D, AM and D + AM, respectively (p = 0.026). The required dosage of amiodarone was lower in the D + AM group than in the AM group (603 +/- 563 mg versus 1058 +/- 680 mg, p = 0.037). Conclusions: Intravenous amiodarone was well tolerated in patients with AMI complicated by AF and was effective in decreasing the duration of AF. However, the combination of amiodarone and digoxin was superior to antiodarone alone in restoring sinus rhythm faster, maintaining sinus rhythm longer, and allowing the use of a lower cumulative amount of amiodarone.

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 mug/kg/min, as needed (mean, once every 16 days, lasting for 12 to 48 h); the next 11 patients (group 2) received oral amiodarone, 480 mg/d, and IDI, 10 mug/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,vith amiodarone, added to conventional drugs, improved clinical status and survival of patients with severe CHF.

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 SEP 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; SEP 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 SEP, 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. (C) 2000 by the American College of Cardiology.

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 st 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 >II. 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 tp = 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), bur had decreased to the level of group 1 (1.66 +/- 0.2 1 [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 ct lower ratio. The heart-to-lung ratio of MAA decreases comparably over time in subacute IDC and remains stable in chronic IDC. (C) 2000 by Excerpta Medica, Inc.

This study examined the usefulness of QT 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 election fraction of 90 ms was 2.8-fold higher than those with QT dispersion less than or equal to 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 less than or equal to 46 ms (95% CI 1.6 to 9.5). These findings suggest that QT and QRS dispersion are useful predictors of mortality in patients with advanced CHF. (C) 2000 by Excerpta Medica, Inc.

The case is presented of an elderly woman with normal left ventricular (LV) systolic function and VVI pacing complicated by severe congestive heart failure. The symptoms and findings of congestive heart failure became refractory to medical treatment and resolved with the upgrade of the VVI to a DDD system. Right heart catheterization during VVI pacing showed increased mean pulmonary capillary wedge and right atrial pressures both being normalized under DDD pacing. This case report illustrates the need to consider permanent physiological pacing in elderly patients, even in presence of normal LV systolic function, to ensure AV synchrony when the atrium can be paced, since diastolic LV dysfunction is quite common in these subjects.

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.

Intravenous amiodarone has been found useful in the emergent management of life-threating arrhythmias. Experimental studies have shown that its electrophysiologic effects are proportional to its myocardial concentration. However, early after its intravenous administration, the extent of the concentration of amiodarone in the human myocardium, the site of its action, is not well known. This study was performed to measure the myocardial concentration of amiodarone shortly after rapid intravenous injection. Amiodarone, 150 mg, was injected over 15 seconds intravenously into 9 patients, 52 +/- 9 years of age, weighing between 65 and 98 kg (mean = 81 +/- 15.6). All patients suffered from idiopathic dilated cardiomyopathy, were in NYHA functional class II, and the mean left ventricular ejection fraction was 21 +/- 6%. Right ventricular endomyocardial biopsy, required for the establishment of the diagnosis, was performed 2-5 minutes after drug administration for measurements of its myocardial concentration. Plasma concentrations of amiodarone were also measured at 2, 5, 10, and 60 minutes, and measurements of right heart hemodynamics were made 2 and 10 minutes after the injection. At 2.5 +/- 1.2 minutes after amiodarone administration, the mean myocardial concentration was 95.7 +/- 67.4 mu g/g (range, 16-175), and the myocardial/plasma amiodarone ratio was 5.05 +/- 5.01. Heart rate increased from 82 +/- 17 to 90 +/- 13 beats/min (P < 0.05), and systolic blood pressure decreased from 132 +/- 19 to 118 +/- 17 mmHg (P < 0.03). The extent of myocardial fibrosis was 5.13 +/- 6.55% (range, 0.3-17.5%). Intravenous amiodarone (150 mg) accumulates rapidly in the human myocardial. This pharmacokinetic characteristic probably explains its acute efficacy in the treatment of life-threatening arrhythmias.

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.

Two patients with total occlusion of the left main coronary artery and well preserved left ventricular function are reported. Twenty one similar cases have been reported in the world literature. All the patients had angina pectoris. Twenty one of the 23 patients (including our cases) underwent coronary artery bypass graft surgery while the other two received medical treatment. All are alive for a follow-up period of 0.4-67 months. It is concluded that in patients with chronic total occlusion of the left main coronary artery and well preserved left ventricular function, collateral flow is always extensive but insufficient to prevent angina. Functional status is greatly improved by surgery, although survival is excellent in both treated and non-treated surgically patients. (C) 1997 Elsevier Science Ireland Ltd.

During the last decades a number of left ventricular assist devices has been used especially for patients resistant to pharmacologic treatment and to intraaortic balloon pump (IABP) support for left ventricular failure. A high stroke volume para-aortic counterpulsation device (PACD) has been developed utilizing the principle of the diastolic counterpulsation technique. In this study the hemodynamic effects of the valveless PACD were compared to those of the centrifugal blood pump (CBP) in nine dogs in acute experimental cardiogenic shock Hemodynamic measurements were obtained at baseline with both devices off, PACD an and CBP off, or PACD off and CBP on. There was no difference in mean aortic pressure between PACD on (60.0 +/- 11.5 mmHg) and CBP on (69.0 +/- 26.8 mmHg). Similarly, there was no difference in left ventricular end-diastolic pressure with the PACD on (11.9 +/- 5.4 mmHg) versus the CBP on (9.9 +/- 5.2 mmHg) or the cardiac index with the PACD on (84 +/- 36 ml/kg/min) versus the CBP on (77 +/- 36 ml/kg/min). However, the left ventricular systolic pressure (55.0 +/- 19.0 with PACD versus 73.0 +/- 26.0 with CBP, p < 0.001), the tension time index (712 +/- 381 versus 1333 +/- 694, p < 0.01), and the double product (5629 +/- 2574 versus 7440 +/- 3294, p < 0.01) were significantly lower during assistance with the PACD than with the CBP. It was concluded that PACD is at least as effective as CBP for restoring hemodynamic status during acute experimental cardiogenic shock Moreover, the PACD unloads the left ventricle more effectively than CBP, making it suitable for left ventricular mechanical support in cases with reversible myocardial damage.

The objective was to predict the potency 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 mu V, 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 potency grade. Thus, the signal-averaged electrocardiographic technique is capable of predicting the early success or failure of thrombolytic therapy. (C) 1997 by Excerpta Medica, Inc.

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.

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.

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 posttransplantation 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 IR) 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

Background The reason for the delay in onset of the electrophysiological effects and antiarrhythmic efficacy of amiodarone is not clear. The relation between the development of the electrophysiological effects of amiodarone and its myocardial concentration is unknown. We therefore examined the time course of development of electrophysiological effects during intracoronary infusion of amiodarone and related these changes to myocardial concentrations. Methods and Results Amiodarone (0.139 mg/min) or normal saline was infused for 10 hours into the proximal left anterior descending coronary artery of 24 open-chest dogs. Nineteen animals received intracoronary amiodarone and 5 received normal saline (control group). Ten of the 19 that received amiodarone underwent electrophysiological study (amio-EPS group). Sixteen of the 19, including 7 from the amino-EPS group, underwent pharmacological study (PS group). In the amio-EPS group during pacing at a cycle length of 300 ms, changes in conduction velocities in drug-exposed myocardium referenced to nonexposed myocardium at 1 hour of infusion were -3.7% in the longitudinal direction (P=NS) and -7.2% in the transverse direction (P