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

The following hemodynamic parameters were measured at rest and 1, 2, 4, 6, 8, 12 and 24 hours after 100 mg of ISDNSR p.o. in 10 patients with dilated cardiomyopathy (NYHA class III-IV): mean pulmonary artery, pulmonary capillary wedge (PCW) and arterial pressures (AP), and cardiac output (thermodilution). Plasma levels of ISDN were determined by capillary gas chromatography at the same intervals and correlated with the hemodynamic changes. PCW fell from 24 +/- 1.5 (SE) to 18 +/- 1.8 mm Hg after 1 hour (p less than 0.05) and after 2 hours to 16.9 +/- 1.6 mm Hg. This change was sustained for 8 hours. At 12 hours PCW had increased again to 21 +/- 1.5 mm Hg and at 24 hours to 22 mm Hg. AP dropped from 89 +/- 5 to 81 +/- 4 mm Hg at 1 hour (p less than 0.2) and remained 80-84 mm Hg for 8 hours. It returned to baseline levels at 12 hours. Heart rate, cardiac index, systemic vascular resistance, stroke index and left ventricular work index did not change significantly during the observation period. Plasma levels of ISDN remained between 3 and 12 ng/ml for 16 hours. Thus, ISDNSR is an effective long-acting nitrate preparation which reduces preload for 8-12 hours. After this interval, nitrate tolerance starts to develop.
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PMID:[Hemodynamic effects of a new long-acting isosorbide dinitrate]. 408 1

Semantic difficulties arise when hypertrophic obstructive cardiomyopathy is seen without obstruction and with congestive failure, and also when congestive cardiomyopathy is seen with gross hypertrophy but without heart failure. Retention of a small left ventricular cavity and a normal ejection fraction characterizes hypertrophic cardiomyopathy at all stages of the disorder. Congestive cardiomyopathy is recognized by the presence of a dilated left ventricular cavity and reduced ejection fraction regardless of the amount of hypertrophy and the presence or not of heart failure. Longevity in congestive cardiomyopathy seems to be promoted when hypertrophy is great relative to the amount of pump failure as measured by increase in cavity size. Conversely, death in hypertrophic cardiomyopathy is most likely when hypertrophy is greatest at a time when outflow tract obstruction has been replaced by inflow restriction caused by diminishing ventricular distensibility. Hypertrophy is thus beneficial and compensatory in congestive cardiomyopathy, whereas it may be the primary disorder and eventual cause of death in hypertrophic cardiomyopathy. Reasons are given for believing that hypertension may have been the original cause of left ventricular dilatation in some case of congestive cardiomyopathy in which loss of stroke output thenceforward is followed by normotension. Development of severe hypertension in these patients after recovery from a prolonged period of left ventricular failure with normotension lends weight to this hypothesis. No fault has been found in the large or small coronary arteries in either hypertrophic cardiomyopathy or congestive cardiomyopathy when they have been examined in life by selective coronary angiography, or by histological methods in biopsy or post-mortem material. Coronary blood supply may be a limiting factor in the compensatory hypertrophy of congestive cardiomyopathy, and the ability to hypertrophy may explain the better prognosis of some patients. In hypertrophic cardiomyopathy excessive metabolic demand may not be met, and inadequacy of blood flow may contribute both to sudden death and to progressive replacement fibrosis in this disease. Histochemical and ultrastructural methods have failed to show any fundamental differences between hypertrophic cardiomyopathy and congestive cardiomyopathy, whereas conventional histology permits recognition of hypertrophic cardiomyopathy and distinction both from congestive cardiomyopathy and from ;normal' secondary hypertrophy in organic aortic stenosis.
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PMID:Ventricular hypertrophy in cardiomyopathy. 425 44

In the first study of combined chemotherapy and radiation therapy for small cell lung cancer by the Southwest Oncology Group, 17 patients survived more than five years after treatment was initiated (4.6 percent). Late relapse, or a second primary malignancy three to six years after diagnosis, accounted for death in five of these patients. Late recurrences involved the chest, bone, and liver; none occurred in the central nervous system. Disease-free survival continues in 10 patients (6 percent of those with limited disease and 1 percent of those with extensive-stage diseases) at a minimal follow-up in excess of six years. One definite case of chronic treatment-related toxicity occurred: congestive cardiomyopathy after 450 mg/m2 of doxorubicin, successfully managed with digitalis and diuretics. One severe neurologic problem (orthostatic hypotension with preterminal dementia) and two less severe neurologic complications (occasional falling episodes without documented cause and cerebrovascular accident) may be treatment-related. Progressive pulmonary disability, post-herpetic pain syndromes, organic brain syndrome, and hematologic abnormalities have not been observed to date. Nitrosourea administration and/or co-administration of a nitrosourea or methotrexate during the induction phase of treatment with radiotherapy to the brain may account for the higher incidence of complications observed by others in long-term survivors.
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PMID:Long-term survival and toxicity in small cell lung cancer. Southwest Oncology Group study. 608 60

The hemodynamic effects of a new cardioselective beta agonist, prenalterol, were evaluated in 12 patients with moderate or severe impairment of left ventricular function due to coronary heart disease or primary cardiomyopathy. In doses up to 7 mg the drug led to a substantial increase of left ventricular pressure rise (+55%) and mean circumferential fiber shortening (+59%) and a decrease of left ventricular end-diastolic pressure (-52%), mean pulmonary artery pressure (-24%) and pulmonary vascular resistance (-37%) indicating augmented myocardial contractility and reduced left ventricular preload. Cardiac output was increased only in 4 of 12 patients, heart rate, left ventricular systolic and mean right atrial pressures and the pressure-rate product as an index for myocardial oxygen demand remained essentially unchanged. The same is true for stroke index, stroke work index, total peripheral resistance, left ventricular end-diastolic and end-systolic volume and ejection fraction. The positive inotropic effect was achieved with good tolerance and without arrhythmogenic or other side effects. Prenalterol may be especially useful in patients with low sympathetic activity and hypotension. In patients with diffuse congestive cardiomyopathy, high sympathetic activity, pronounced peripheral vasoconstriction and normal blood pressure, vasodilator therapy alone or in combination with prenalterol should be considered.
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PMID:Hemodynamic assessment of prenalterol: a cardioselective beta agonist in patients with imparied left ventricular function. 612 57

In 12 patients with severe congestive heart failure due to ischaemic heart disease (n = 6) and due to congestive cardiomyopathy (n = 6) the haemodynamic effects of a new beta 1-agonist, prenalterol, were studied. Left ventricular (LV) function was studied before and 20 min after infusion of 12 mg prenalterol. Heart rate was kept constant by atrial pacing at a rate of 100 min-1 unless intrinsic heart rate exceeded it. As a sign of positive inotropic support, prenalterol enhanced peak rate of LV pressure development (dP/dt) from 1160 +/- 100 mm Hg/s to 1590 +/- 190 mm Hg/s (p less than 0.005). In the mean LV end-diastolic and end-systolic volume determined by cineventriculography and two-dimensional echocardiography decreased. LV stroke work index measured with both methods increased with 4 ml/m and 5 ml/m, respectively (p less than 0.02). LV ejection fraction was improved by 6% and 8% (p less than 0.005). Increase of peak fall of left ventricular pressure (dP/dt) (1050 +/- 60 mm Hg/s to 1270 +/- 100 mm Hg/s, p less than 0.005) and shortening of time constant (T) of pressure fall from 64.5 +/- 5.0 ms to 44.5 +/- 6.0 ms (p less than 0.005) demonstrated the improved LV relaxation. Analysis of LV volume and myocardial compliance revealed decrease of left ventricular stiffness. Thus, LV filling pressure was reduced from 22.1 +/- 4 mm Hg to 14 +/- 3.5 mm Hg (p less than 0.001). Pressure volume analysis showed a significant increase of LV power and work, as well as a slight decrease of wall stress. Our study could demonstrate, even in patients with severe heart failure, a sustained positive inotropic effect of prenalterol leading to an improved left ventricular contractility, relaxation and compliance. LV power and work was enhanced. The increase of oxygen demand seemed to be counterbalanced by an improved perfusion of particularly subendocardial layers indicated by an increased transmyocardial pressure gradient.
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PMID:Haemodynamic effects of prenalterol in patients with severe congestive heart failure--NYHA III-IV. 612 87

Experimental pharmacology indicates that prenalterol is a selective beta 1-adrenoceptor activator. In 5 normal individuals, 15 minutes after the drug (infused at a dose of 15 micrograms/kg over 5 min) the following circulatory changes were seen: a) increase of cardiac index (+31%), heart rate, stroke index, systolic aortic pressure, left and right ventricular mean rate of ejection and mean rate of the pressure rise in either ventricle during the pre-ejection phase; b) reduction of systemic vascular resistance (-18%), appearance, built-up and disappearance times in the left ventricular dye dilution curves. Pulmonary systolic, diastolic and wedge pressures and vascular resistance did not vary consistently. The circulatory effects persisted almost unchanged 30 minutes after the infusion. In a group of 5 patients with heart failure due to primary congestive cardiomyopathy, refractory to conventional therapy, the haemodynamic response to prenalterol (infused at a dose of 30 micrograms/kg over 5 min) was qualitatively similar to that of normal subjects in 3 cases. In 2 other patients cardiac performance deteriorated. The reasons for this paradoxical effect were not identified. These preliminary results suggest that prenalterol is a potent selective inotropic agent in man, that may assist in the therapeutic management of refractory heart failure due to congestive cardiomyopathy. However, careful haemodynamic monitoring is advisable for its use in this dysfunction until broader clinical experience can be accumulated.
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PMID:Circulatory response to prenalterol in normal subjects and in patients with primary congestive cardiomyopathy. 612 92

To assess the immediate haemodynamic and myocardial metabolic effects of the beta 1-agonist prenalterol, we studied by cardiac catheterisation the response to 50 and 100 micrograms/kg given intravenously in 16 patients with congestive heart failure secondary to coronary artery disease or non-ischaemic cardiomyopathy. At peak effect, cardiac index increased from 2.6 +/- 0.5 to 3.2 +/- 0.8 1/min/m2 (mean +/- SD) p less than 0.001); peak rate of left ventricular pressure development rose from 963 +/- 242 to 1355 +/- 411 mm Hg per second (p less than 0.001); left ventricular end-diastolic pressure fell from 27 +/- 6 to 13 +/- 7 mm Hg (p less than 0.001); coronary sinus blood flow increased from 120 +/- 39 to 147 +/- 55 ml/min (p less than 0.01); myocardial oxygen consumption was augmented from 12.9 +/- 3.9 to 15.7 +/- 5.8 ml/min (p less than 0.001); and heart rate increased slightly (76 +/- 12 to 86 +/- 14 beats per minute, p less than 0.05). No significant changes occurred in left ventricular systolic pressure, stroke volume index, myocardial lactate extraction rate, myocardial arteriovenous oxygen difference and no patient developed angina, ECG-changes or ventricular arrhythmias. Infusion of prenalterol effectively improved the haemodynamic function and cardiac metabolism in congestive cardiomyopathy.
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PMID:Effect of intravenous prenalterol on haemodynamics and myocardial lactate extraction in patients with left ventricular failure. 612 95

Prenalterol administration (150 micrograms/kg i.v.) exerted beneficial effects on resting and/or exercise cardiac performance in patients with congestive cardiomyopathy (n = 12) and 1 patient with hypertensive heart disease (= group I, n = 13), while the haemodynamic response in patients with severe coronary heart disease (n=3) or cor pulmonale (n = 1) was non-uniform. At rest mean right and left ventricular filling pressures decreased by 26 and 19% (p less than 0.02 and p less than 0.02), respectively, while stroke volume increased by 8% (p less than 0.05), cardiac index by 25% (p less than 0.01) and heart rate by 15% (p less than 0.005) 5 min after prenalterol administration in group I. During exercise there was no further increase in heart rate, while filling pressures decreased and cardiac index increased significantly compared to control exercise. This typical inotropic response to prenalterol was observed in fully digitalised patients. Maximal effects occurred about 15 min after i.v. administration.
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PMID:Effects of i.v. prenalterol in patients with severe cardiac failure at rest and during exercise. 612 97

We administered 150 mg of ibopamine orally to 10 patients suffering from idiopathic congestive cardiomyopathy. Hemodynamic function was evaluated by right heart catheterization and by measurement of cardiac output with the thermodilution technique. Ibopamine caused no significant change in heart rate or mean arterial pressure. Cardiac index, stroke volume index, and left ventricular work index all increased significantly by about 30%. Mean pulmonary arterial pressure decreased by about 30%, and systemic vascular resistance decreased by about 20%. The effects peaked at about 3 h and lasted 5-7 h. No side effects were noted. These findings with invasive techniques confirm those of others using noninvasive techniques, and suggest that ibopamine may be useful in the treatment of congestive heart failure.
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PMID:Hemodynamic effects of ibopamine in patients with idiopathic congestive cardiomyopathy. 618 98

Serial measurements of left ventricular short axis dimensions were made to determine reproducibility in ten normal subjects and in ten patients with congestive cardiomyopathy without asynergic wall motion, conduction abnormalities, or arrhythmias. Three echocardiograms were performed over a period of three weeks in each subject. In the congestive cardiomyopathy group, mean coefficients of variation for diastolic and systolic left ventricular dimensions (LVlDd, LVlDs) and fractional shortening (FS) were 3.5%, 4.3% and 10.3% respectively. In the normal subjects they were slightly less; LVlDd (2.2%), LVlDs (3.1%) and FS (8.0%) but the difference was not statistically significant. Coefficients of variation for calculated diastolic and systolic volumes in the normal ventricle group (Teichholz formula) were 5.0% and 7.1% respectively and for ejection fraction, stroke volume and cardiac output 5.8%, 9.8% and 11.8%. The results demonstrate that M-mode echocardiography is a reliable technique for serial quantitative studies of left ventricular dimensions in both normal subjects, and in selected patients with congestive cardiomyopathy. M-mode echocardiography may be used to assess the responses of patient groups but not of individual patients to interventions which change ventricular volume and cardiac output in subjects with normal left ventricles in whom good quality endocardial echoes are recorded.
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PMID:M-mode echocardiography: reproducibility of serial left ventricular measurements in subjects with normal ventricles and patients with congestive cardiomyopathy. 622 16


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