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 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The acute hemodynamic effects of captopril were evaluated at cardiac catheterization in 16 children (age, 0.3-18 years) with cardiomyopathy. Twelve children had congestive cardiomyopathy, whereas four had restrictive cardiomyopathy. Hemodynamic measurements were obtained 30 and 60 minutes after the oral administration of captopril (0.5 mg/kg). Blood pressures were measured in the aorta, pulmonary artery, right atrium, and pulmonary capillary wedge position; cardiac outputs were measured by the thermodilution technique. Hemodynamic data could not be obtained after the administration of captopril in one child with congestive cardiomyopathy because of an immediate, severe hypotensive response. In 11 of 12 children with congestive cardiomyopathy, cardiac index increased by 22%, from 2.3 to 2.8 l/min/m2 (p less than 0.05), and stroke volume increased by 22%, from 23 to 28 ml/m2 (p less than 0.05). Systemic vascular resistance decreased from 32 to 21 units.m2 (p less than 0.01), but the mean aortic pressure did not change significantly. In contrast, four children with restrictive cardiomyopathy had no change in cardiac output after captopril, but there was a trend toward significant arterial hypotension (mean aortic pressure decreased from 78 to 59 mm Hg). Thus, captopril acutely reduced systemic vascular resistance and increased both cardiac output and stroke volume in children with congestive cardiomyopathy. In children with restrictive cardiomyopathy, however, captopril did not affect cardiac output, but it did decrease aortic pressure. These data indicate that captopril may benefit children with a congestive cardiomyopathy but that captopril probably should not be used in children with restrictive disease.
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PMID:Acute hemodynamic effects of captopril in children with a congestive or restrictive cardiomyopathy. 199 88

The benzimidazol analogue BM14.478 is a phosphodiesterase inhibitor with both vasodilator and positive inotropic properties. Hemodynamic parameters and plasma hormone levels of 8 patients (1 female, 7 male) with chronic congestive heart failure NYHA Classes II-IV (1 patient with coronary artery disease, 7 patients with primary dilated cardiomyopathy) were assessed before and until 6 h after the intravenous application of 1.0 mg BM14.478. There was a significant decrease of mean pulmonary artery pressure (28 +/- 11 vs. 23 +/- 11 mmHg; p less than 0.05), mean right atrial pressure (8.6 +/- 5.2 vs. 5.0 +/- 4.7 mmHg; p less than 0.02), and systemic vascular resistance (1651 +/- 484 vs. 1206 +/- 252 dynes.s.cm-5; p less than 0.05) as early as 10 min after injection of BM14.478. Pulmonary vascular resistance also was reduced (128 +/- 86 vs. 61 +/- 39 dynes.s.cm-5, 30 min after injection; p less than 0.02). Simultaneously there was a significant increase of cardiac index (2.3 +/- 0.7 vs. 3.1 +/- 0.8 l.min-1.m-2, 10 min after injection; p less than 0.02), and stroke volume index (28.8 +/- 11.7 vs. 33.9 +/- 8.5 ml.min-1.m-2; 30 min after injection; p less than 0.05). Although mean heart rate did not change significantly, some patients reacted with a transient increase. There was also a slight but insignificant increase of the double product. No serious side effects were observed. The hemodynamic improvement was followed by a delayed reduction of plasma levels of epinephrine (51 +/- 20 vs. 41 +/- 21 pg/ml; p less than 0.02; 30 min after injection) and atrial natriuretic peptide (229 +/- 283 vs. 121 +/- 168 pg/ml; p less than 0.05; 1 h after injection). Mean levels of plasma norepinephrine, however, did not change significantly and individual responses showed large variations, which could not be predicted by the behavior of the hemodynamic parameters. Three of eight patients (2 of these with elevated baseline filling pressures) even showed a marked increase of plasma norepinephrine levels after BM14.478. Response of plasma renin activity and plasma vasopressin levels to BM14.478 also was heterogeneous. According to the results of this study, acute administration of the phosphodiesterase inhibitor BM14.478 has an immediate beneficial hemodynamic effect in patients with severe congestive heart failure by reducing both preload and afterload, and by increasing cardiac index and stroke volume. However, this improvement of hemodynamic parameters is not necessarily accompanied by a favorable short-term response of plasma hormones, and therefore does not allow any conclusions on survival of these patients.
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PMID:Hemodynamic and neuroendocrine response to acute administration of the phosphodiesterase inhibitor BM14.478 in patients with congestive heart failure. 204 89

The purpose of this study is to assess the right atrial and ventricular function by radionuclide ventriculography using continuous infusion of 81mKr in normal subjects and in patients with heart disease. 1) Reproducibility of RVEF measurement by continuous infusion of 81mKr was good (interobserver; gamma = 0.97, p less than 0.001, n = 20: intraobserver; gamma = 0.97, p less than 0.001, n = 20). This method had a excellent correlation with RVEF of 99mTc first-pass technique (gamma = 0.92, p less than 0.001, n = 20). 2) RVEF was measured in 10 normal volunteers, 76 patients with myocardial infarction (OMI), 20 patients with dilated cardiomyopathy (DCM), 5 patients with arrhythmogenic right ventricular dysplasia (ARVD) and 5 patients with primary pulmonary hypertension (PPH). In OMI and DCM, their RVEF was lower than that of normal volunteers and, in ARVD and PPH, lower than that of OMI and DCM. There was a significant inverse correlation between RVEF, mean pulmonary artery pressure and right ventricular end-diastolic volume index. 3) The effect of the location of right coronary artery (RCA) lesions on RVEF during exercise was also evaluated. Ten normal volunteers and 27 patients with OMI were studied at rest and during exercise. The patients with OMI were divided into two groups: those without proximal RCA lesions (non RCA group, n = 12) and those with proximal RCA lesions (RCA group, n = 15). Although there were no significant increases of RVEF during exercise in both group, the percent change in RVEF was less in RCA group than in non RCA group. These findings suggested that proximal RCA stenosis is a major determinant of exercise RVEF. 4) To assess the right atrial function, right atrial volume curve was measured in 10 normal volunteers, 32 patients with OMI and 4 patients with PPH. The curve was clearly divided into 4 phase; filling phase (312 +/- 40 msec), early ejection phase (276 +/- 53 msec), plateau an index of right atrial reservoir function, was 0.41 +/- 0.05 and Contractile Volume/Stroke Volume (Contr. V/SV), as an index of right atrial pump function, was 0.23 +/- 0.05 in normal volunteers. In OMI and PPH, atrial reservoir function decreased and atrial pump function increased. It was concluded that radionuclide ventriculography using continuous infusion of 81mKr was useful to assess the right heart function.
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PMID:[Assessment of right atrial and ventricular function by radionuclide ventriculography using continuous infusion of 81mKr]. 206 Sep 2

Dynamic cardiomyoplasty has been reported in the treatment of severe myocardial failure. In this investigation significant improvement of left ventricular function with dynamic cardiomyoplasty was demonstrated in patients with dilated cardiomyopathy or Chagas' disease for more than 1 year of follow-up. Thirteen patients with advanced heart failure who were in New York Heart Association class III or IV were operated on. There were no operative deaths. Patients were followed up for a mean of 11.5 months, and two patients died during the late follow-up period. Five of nine patients observed long term are in New York Heart Association class I, three in class II, and one in class III. At 3 months of follow-up, Doppler echocardiography demonstrated that left ventricular segmental wall shortening increased from 11.4% +/- 2.3% to 16.4% +/- 3.9% (p less than 0.01), and left ventricular stroke volume from 23.9 +/- 5.7 to 34.4 +/- 10 ml (p less than 0.01). Radioisotopic left ventricular ejection fraction improved from 20.9% +/- 3.3% to 25.4% +/- 7.7% (p = 0.06), and its better increases occurred in patients with lesser left ventricular end-diastolic dimensions. Cardiac catheterization showed that left ventricular stroke work index increased from 14.6 +/- 3.8 to 23.7 +/- 6.7 gm.m/m2 (p less than 0.01), whereas pulmonary wedge pressure decreased from 24.8 +/- 3.7 to 17.2 +/- 5.8 mm Hg (p less than 0.01). At 6 and 12 months of follow-up, all the preceding values remained essentially unchanged. Thus cardiomyoplasty improves left ventricular function and may halt the steady evolution of severe cardiomyopathies.
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PMID:Left ventricular function changes after cardiomyoplasty in patients with dilated cardiomyopathy. 207 11

The aim of this study was to document the effects of enoximone in congestive cardiac failure. The haemodynamic data (aortic pressure, pulmonary pressures, left ventricular pressure, cardiac output, isovolumic contractility index: Vmax) and left ventricular kinetics of 20 patients with dilated cardiomyopathy (11 ischemic and 9 idiopathic in Stages III or IV of the NYHA Classification before recompensation) were recorded under basal conditions, after 30 minutes infusion of dobutamine (10 micrograms/kg/mn) and after 3 hours infusion of enoximone (total dose: 3.6 mg/kg). The two drugs had an equivalent inotropic effect: ejection fraction + 4 +/- 22% with dobutamine and + 16 +/- 39% with enoximone; Vmax increased from 1.53 +/- 0.5 c/sec to 2.49 +/- 0.8 c/sec with dobutamine and to 1.82 +/- 0.5 c/sec with enoximone. Enoximone induced a greater degree of vasodilation (systemic resistances - 14 +/- 21% with dobutamine and - 21 +/- 27% with enoximone) and a more pronounced fall in ventricular filling pressures (- 35 +/- 42% with dobutamine and - 58 +/- 24% with enoximone). Enoximone was less effective than dobutamine in increasing cardiac output (+ 46 +/- 42% with dobutamine and 16 +/- 33% with enoximone) and stroke volume (+ 23 +/- 47% with dobutamine and + 2 +/- 41% with enoximone). This difference in efficacy may be explained by the major reduction in ventricular preload which enoximone induced after that observed with dobutamine. "Responders" (12 patients) had basal cardiac outputs of less than 2.3 l/mn/m2; the peripheral vasodilatation caused by enoximone was greater. Finally, the reduction in left ventricular end diastolic pressure and the increase in Vmax were significantly less in the 11 patients with ischemic cardiomyopathy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Enoximone, vasodilator and/or inotropic agent in congestive cardiac insufficiency? Hemodynamic and ventriculographic study of 20 cases]. 214 34

The adenosine diphosphate (ADP)-adenosine triphosphate (ATP) carrier of the inner mitochondrial membrane is identified as an autoantigen in myocarditis and dilated cardiomyopathy. Sera of patients with these diseases contain autoantibodies to the ADP-ATP carrier capable of inhibiting nucleotide transport in vitro. Recently, an antibody-related infringement of energy metabolism was shown in intact perfused hearts isolated from guinea pigs immunized with the ADP-ATP carrier. A decreased cytosolic-mitochondrial difference of the phosphorylation potential of ATP was measured that originated from a reduction in mitochondrial-cytosolic nucleotide transport. Nonimmunized animals did not show these changes in energy metabolism, despite being in a comparable metabolic state and performing equal external heart work. To establish whether antibodies to the ADP-ATP carrier can also alter cardiac function, hemodynamic parameters of isolated hearts of guinea pigs that were preimmunized with the carrier protein were measured. Cardiac metabolism was stimulated by exposing the hearts to a high calcium concentration in conjunction with a maximum elevation of the afterload. Mean aortic pressure, stroke volume, stroke work, and external heart work were found to be lowered significantly (p less than 0.005). The external heart work of the immunized hearts reached only about 20% of the level performed by control hearts. Myocardial oxygen consumption was lowered 2.5-fold, whereas the extent of lactate production was found to be more than doubled. These results show a diminished cardiac performance of hearts from animals immunized with the ADP-ATP carrier. Our findings demonstrate that autoimmunity to the ADP-ATP carrier may contribute to the pathophysiology of dilated cardiomyopathy as a subsequent stage of myocarditis by causing an autoantibody-mediated reduction in cardiac function on the basis of an imbalance between energy delivery and demand.
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PMID:Antibodies to ADP-ATP carrier--an autoantigen in myocarditis and dilated cardiomyopathy--impair cardiac function. 215 73

Twenty patients (5 females, 15 males) with severe heart failure (NYHA IV), due to coronary artery disease in 14, and congestive cardiomyopathy in 6, received an intravenous bolus of the calcium blocker nisoldipine 0.2 mg followed by a continuous infusion of 0.2 micrograms.kg-1.min-1. Haemodynamic measurements were performed at baseline and after 30 min. The mean arterial pressure fell from 91 to 73 mmHg, pulmonary capillary wedge pressure from 31 to 26 mm Hg and systemic vascular resistance from 1695 to 1040 dyn.s.cm-5. The cardiac index (2.2 to 2.71.min-1.m-2, and stroke volume index (25 to 33 ml.m-2) were markedly increased. There was no reflex tachycardia as the heart rate dropped from 92 to 85 beats.min-1. Plasma renin activity and norepinephrine concentration did not change significantly. The findings indicate that nisoldipine acts as a strong vasodilator and that it has a beneficial acute haemodynamic effect in patients with severe left heart failure irrespective of its aetiology.
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PMID:Acute haemodynamic and neurohumoral effects of intravenous nisoldipine in patients with severe congestive heart failure. 218 40

A prospective randomized study was performed in 46 consecutive patients with refractory congestive heart failure (CHF) due to idiopathic dilated cardiomyopathy to compare the hemodynamic responses to 48-hour infusions of amrinone and dobutamine. Both drugs substantially reduced pulmonary arterial wedge pressure, right atrial pressure and systemic vascular resistance and increased cardiac index. Amrinone caused a greater decrease in right atrial pressure than dobutamine (p less than 0.02) and had a positive chronotropic effect not observed with dobutamine (p less than 0.01). The increase in heart rate produced by amrinone correlated inversely with the changes in right atrial and pulmonary arterial wedge pressures, suggesting a baroreceptor response to reduced preload. Dobutamine produced a larger increase in stroke volume index than amrinone (p less than 0.01). Ninety-one percent of patients receiving amrinone and only 65% receiving dobutamine had reduction of greater than or equal to 30% in pulmonary arterial wedge pressure (p less than 0.05). Cardiac index increased greater than or equal to 30% in similar numbers of patients given amrinone (74%) and dobutamine (65%). Negative fluid balance was recorded in all patients receiving amrinone and in 78% of patients receiving dobutamine (p less than 0.05). Target hemodynamic criteria were achieved in 83% of patients receiving 10 micrograms/kg/min of amrinone. The effective maintenance dose of dobutamine was extremely variable. No clinically important adverse effects were observed with either drug regimen. Both amrinone and dobutamine are effective and safe agents for short-term parenteral therapy of patients with dilated cardiomyopathy in severe CHF that is unresponsive to oral medication.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of intravenous amrinone and dobutamine in congestive heart failure due to idiopathic dilated cardiomyopathy. 222 Jun 38

To assess the left ventricular (LV) global and regional (anterior, apical, inferior) diastolic filling dynamics in compensated dilated cardiomyopathy (DCM), we measured left ventricular pressure and instantaneous volume from angiography in 7 normal controls (CTL) and 6 DCM patients with sinus rhythm. Global and regional peak filling rate (PER), time constant of LV pressure decline (T; Weiss's method) and LV chamber stiffness (k; Gaasch's method) were calculated. In DCM, left ventricular end-diastolic volume (ml/m2) was larger than in CTL (137 +/- 29 vs. 74 +/- 6, p less than 0.001), and stroke index (ml/m2) was not different from CTL (46 +/- 14 vs. 46 +/- 8, NS), indicating a compensated state of LV. Mitral valve opening pressure (mmHg) tended to increase in DCM compared with CTL (12 +/- 6 vs. 8 +/- 4). Global PFR (ml/sec/m2) (CTL = 216 +/- 47 vs. DCM = 201 +/- 36) and k (CTL = 0.044 +/- 0.023 vs. DCM = 0.029 +/- 0.016) were not different between 2 groups. However, T (msec) was markedly prolonged in DCM compared with CTL (61 +/- 10 vs. 35 +/- 5, p less than 0.001). In CTL, regional PFR (1/sec) showed almost the same values in each region, but in DCM, apical region showed higher PFR than in other regions. Thus, early diastolic filling might play an important role in maintaining the total transmitral flow in DCM despite severe impairment of LV relaxation. This compensation could be related mainly to accelerated regional lengthening of the LV apical region.
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PMID:Global and regional diastolic filling dynamics in compensated dilated cardiomyopathy. 223 17

Using both transthoracic and transesophageal echocardiography we studied 13 consecutive patients with recent CT-proven ischemic stroke in which a carotid arteries high-resolution ultrasound study failed to detect thrombosis or other relevant atherosclerotic lesions in the pertinent arteries. The mean age was 53 years (range: 36-65). Two patients exhibited clinical signs of cardiac disease at physical examination i.e. absolute arrhythmia, mitral stenosis. Conventional transthoracic echocardiography allowed the detection of potential cardiac sources of emboli in 2/13 patients (15.4%): mitral stenosis in one patient and dilated cardiomyopathy in another. Transesophageal echocardiography was successfully performed without general sedation in all patients. Potential cardiac sources of emboli could be identified in 12/13 patients (92%). Left atrial thrombi were found in 3 patients: in two of them they were associated with rheumatic alterations of mitral valve leaflets; in the third patient a small thrombus was located inside a normal-sized, poorly contracting left atrial appendage. Left atrial appendage could be clearly visualized in all patients. A myxoid degeneration of a prolapsing mitral leaflet was found in 3 patients and an interatrial septum aneurysm in 2. Furthermore, at color-flow Doppler and contrast transesophageal echocardiography, 7 patients (54%) showed patency of the foramen ovale. In 5 of these patients paradoxical right to left shunting after cough or Valsalva manoeuvre could be evidenced. With reference to 11/13 patients with no clinical signs of cardiac disease at physical examination, subclinical potential cardiac sources of emboli could be detected at conventional transthoracic echocardiography in 1 and at transesophageal echocardiography in 10 patients (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Transesophageal echocardiography in the definition of intracardiac sources of emboli in patients with recent ischemic stroke. 227 17


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