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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The rest and exercise hemodynamic-inotropic response to administration of the beta-blocker pindolol was evaluated in 10 patients with congestive cardiomyopathy to determine whether the intrinsic sympathomimetic activity (ISA) of this agent may preserve ventricular function in the setting of beta-blockade. A significant (p less than .05) rise in systemic and pulmonary vascular resistance and a decline in stroke volume and cardiac index was observed after a single 10 mg dose. The change in cardiac index was negatively correlated with free drug concentration (r = -.59, p less than .01); the change in pulmonary and systemic vascular resistance showed a positive correlation with plasma concentration (r = .67, r = .57, respectively; all p less than .05). The response to exercise reflected a predominant beta-blocking effect, with a significant decrease in peak heart rate and cardiac index and an increase in pulmonary vascular resistance. There were no significant changes in variables of right or left ventricular inotropy after administration of the drug. The mean baseline plasma norepinephrine concentration for the population was 609 +/- 172 pg/ml (normal = 196 +/- 7 pg/ml) and was markedly elevated in two patients (931 and 2053 pg/ml) who developed severe pindolol-induced hypotension. Renin increased markedly in these two patients, but decreased in each of the remaining eight patients. These data indicate that although inotropy is not adversely affected by pindolol, increased afterload, which appears to be mediated by peripheral beta-blockade, results in a reduction in ventricular performance.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hemodynamic-inotropic response to beta-blocker with intrinsic sympathomimetic activity in patients with congestive cardiomyopathy. 353 53

In a number of cardiac conditions (acute myocardial infarction, chronic left ventricular aneurysm, dilated cardiomyopathy, infective endocarditis and atrial fibrillation in the absence of valvular disease), the risk of embolism gives cause for concern. Although anticoagulation with warfarin (Coumadin)-derivatives has been shown to be effective in some of these situations, there is no evidence regarding the role of antiplatelet agents. The common factor in the thromboembolic potential of acute myocardial infarction, chronic left ventricular aneurysm and dilated cardiomyopathy is mural thrombus. This can be detected by two-dimensional echocardiography and indium-111 platelet scintigraphy. Although of value in elucidating the natural history of mural thrombus, in most cases, management is not substantially aided by these investigations. In patients with extensive myocardial infarction, particularly anterior infarction, moderate intensity anticoagulation started soon after hospital admission reduces the rate of embolism. After 8 to 12 weeks, embolic risk is low so that anticoagulants can usually be discontinued. Patients with chronic left ventricular aneurysm have a low incidence of embolism; anticoagulation is, therefore, inappropriate. Dilated cardiomyopathy is associated with a high risk of embolism; moderate intensity anticoagulation may be advisable in many such cases. Little information is available regarding the incidence of thromboembolism or the role of antithrombotic therapy in the patient with a diffusely dilated left ventricle due to ischemic heart disease. In native valve infective endocarditis, the risk of hemorrhage is high, and the efficacy of conventional anticoagulants unclear; thus, anticoagulation should not be instituted for the cardiac condition as such. However, in prosthetic valve endocarditis, the risk of embolism seems to be very high, and anticoagulant therapy should be continued, but with great care because there is a substantial risk of cerebral hemorrhage. Atrial fibrillation in patients with valvular heart disease is dealt with in a previous review. Patients with nonvalvular atrial fibrillation are at varying risk of embolism, depending on the etiology of the arrhythmia; trials of antithrombotic therapy are needed for the various subsets of patients. In most elderly patients, the etiology is not known, and their stroke risk is high. The risk of embolism in younger patients with idiopathic atrial fibrillation is so low as to make any antithrombotic therapy unnecessary.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Thrombosis and embolism from cardiac chambers and infected valves. 353 72

Acute haemodynamic effects of molsidomine, antianginal drug with vasodilator properties, were evaluated in 12 male patients with chronic congestive heart failure in New York Heart Association functional class 3 or 4 (mean age 56 +/- 7 years; ischemic heart disease in 8 cases, dilated cardiomyopathy in 3 cases, heart disease of combined aetiology in 1 case). After sublingual molsidomine (4 mg: 6 cases; 8 mg: 6 cases) the following haemodynamic changes were observed: mean right atrial pressure - 35% (p less than 0.01), left ventricular filling pressure -30% (p less than 0.01), total pulmonary resistance -33% (p less than 0.01), pulmonary arteriolar resistance -32% (p less than 0.01), cardiac index -6% (p less than 0.05), stroke volume index -12% (p less than 0.05), stroke work index +18% (p less than 0.01), heart rate -6% (p less than 0.01), double product -10% (p less than 0.01) (Fig. 3). Peak haemodynamic effect was reached between 30 and 90 minutes, lasting till 180 minutes. Molsidomine acutely reduced preload, did not show side effects and was well tolerated. These results suggest that molsidomine might be used in the treatment of chronic congestive heart failure, especially if characterized by an increased right and left ventricular filling pressure.
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PMID:[Hemodynamic effects of molsidomine in chronic congestive heart failure]. 375 13

To assess the hemodynamic effects of digoxin (0.01 mg/kg) on congestive heart failure, we evaluated 19 patients with decreased contraction force of left ventricle (old myocardial infarction n = 9, and dilated cardiomyopathy n = 10, group 1) and 8 patients with mechanical impaired left ventricular filing (mitral stenosis n = 8, group 2). In groups 1 and 2, heart rate and pulmonary capillary pressure significantly decreased (p less than 0.05). In group 1, stroke volume increased, but not significantly. In group 2, stroke volume increased significantly (p less than 0.05). There were no significant changes in blood pressure and systemic vascular resistance in either group. We divided group 1 into two groups (group 1A: cardiac index increased more than 15%, group 1B: cardiac index increased less than 15%). In group 1A, cardiac index and % fractional shortening before digoxin administration were lower than in group 1B (1.97 + 0.27 vs 2.80 + 0.481/min/m2, p less than 0.001, and 10.9 + 8.0 vs. 19.5 +11.9%, p less than 0.05, respectively). These data suggested that digoxin exerted a positive inotropic effect with decreased pulmonary capillary pressure but cardiac index did not always increase in congestive heart failure.
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PMID:Hemodynamic effects of digoxin on congestive heart failure. 377 33

We evaluated the acute hemodynamic responses to hydralazine during cardiac catheterization in 13 infants with idiopathic dilated cardiomyopathy. Ages ranged from 2 to 13 months (6.7 +/- 4.0 months, mean +/- SD). Each infant had congestive heart failure and angiographic evidence of markedly depressed left ventricular ejection fraction (0.24 +/- 0.11; normal = 0.58-0.78) with left ventricular dilation (left ventricular end-diastolic volume = 349 +/- 125% of normal). Hydralazine (0.5 to 1.0 mg/kg administered intravenously) acutely decreased systemic arteriolar resistance from 21.1 +/- 3.3 to 12.0 +/- 2.7 U/m2 (p less than 0.001). This 41 +/- 14% decrease in systemic resistance was accompanied by a 45 +/- 16% increase in cardiac index (3.24 +/- 0.53 to 4.71 +/- 0.99 L/min/m2; p less than 0.001). Mean arterial blood pressure declined from 70 +/- 8 to 60 +/- 11 mm Hg (p less than 0.001). Hydralazine also increased heart rate (122 +/- 19 to 138 +/- 18 bpm; p less than 0.001), but this increase did not account entirely for the change in cardiac index as evidenced by a rise in stroke volume index (26.9 +/- 4.9 to 34.5 +/- 7.5 ml/beat/m2; p less than 0.001). Pulmonary arteriolar resistance and pulmonary capillary wedge pressure fell slightly in response to hydralazine. Subsequently, oral hydralazine was included in the treatment regimen of 10 infants followed for 3 to 38 months (mean = 15 months). Of these, eight demonstrated sustained clinical improvement. We conclude that hydralazine may be a beneficial adjunct to the management of congestive heart failure in young infants with a dilated cardiomyopathy.
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PMID:Hemodynamic effects of hydralazine in infants with idiopathic dilated cardiomyopathy and congestive heart failure. 379 28

In the present study 13 patients with severe chronic heart failure were investigated by right heart catheterization at rest and during handgrip before and 6 months after treatment with captopril (mean dose 2 X 37.5 mg per day). Before initiating captopril therapy all patients were clinically stable on digitalis and diuretics. During the observation period 3 patients died suddenly. Of the remaining cases, 5 had dilated cardiomyopathy and 5 ischemic heart disease. After 6 months, resting hemodynamic measurements changed as follows: systemic vascular resistance decreased from 1594 to 1284 dyn X sec X cm-5 (p less than 0.005), left ventricular end-diastolic pressure decreased from 17 to 10 mm Hg (p less than 0.01) and stroke volume index increased from 32 to 40 ml/m2 (p less than 0.05). Before captopril, 9 patients showed no increase or even a decrease of stroke work index during isometric exercise, whereas after captopril 5 out of the 10 patients showed an increase in stroke work index. The results demonstrate that, in patients with severe chronic heart failure, long-term afterload reduction with captopril is accompanied by a significant improvement in left ventricular performance at rest. Furthermore, during isometric exercise after captopril an improvement in left ventricular function was found in 5 out of 10 patients.
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PMID:[Rest and effort hemodynamics during long-term treatment of dilated and ischemic cardiomyopathy with captopril]. 390 90

TA-064 is a new cardiotonic agent which is also effective orally, according to investigations conducted in Japan. We analyzed computer-assisted alterations of pressure-volume relationships serially and of indirect myocardial oxygen consumption (MVO2) estimations on line during TA-064 influence in 16 patients with congestive cardiomyopathy: left ventricular function was moderately decreased in seven patients (group A) and drastically decreased in nine (group B). Results showed that TA-064, 8 micrograms/kg/min intravenously, exerted positive inotropic effects in both groups and induced mean maximal delta percentage changes at about 5 minutes of infusion as follows: left ventricular stroke work index +65% and +47%; dP/dtmax +61% and 59%; left ventricular efficiency +62% and 53%; MVO2 +31% and +11% (p less than 0.05). TA-064, 20 mg by mouth induced serum levels (group A = 23.8 +/- 12ng/ml and group B = 26.4 +/- 20 ng/ml) corresponding to the effects with dosages of 1 to 2 ng/kg/min intravenously (p greater than 0.05), thus implying that significant changes in left ventricular function require higher oral dosages. We conclude that TA-064 improves left ventricular function, primarily via a contractility increase, also in group B patients without toxic side effects. On-line indirect MVO2 assessment and analysis of serial pressure-volume relationships helped to provide a more complex definition of the mechanism and efficiency of the cardiotonic agent under study.
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PMID:Analysis of the efficacy of the new cardiotonic agent TA-064. 402 18

The pattern of abnormal left ventricular diastolic filling and its specificity in coronary disease patients with severe left ventricular dysfunction has received little attention. We evaluated the left ventricular diastolic filling curve derived from gated blood pool scans in 21 normals, 61 coronary disease patients with ejection fractions less than or equal to 30%, and 51 congestive cardiomyopathy patients with ejection fraction less than or equal to 30%. The peak filling rate (PFR), peak ejection rate (PER), PFR/PER and the % stroke volume filled at 1/3 of diastole (%SV-1/3 DT) and at the end of the rapid filling period (%SV-RFP) were determined for each group. The PFR and PER were reduced in both coronary disease and congestive cardiomyopathy groups. The PFR/PER was increased in the coronary disease group (1.19 +/- 0.28) and congestive cardiomyopathy group (1.21 +/- 0.32) as compared to normals (0.93 +/- 0.20, P less than 0.001). A greater %SV-1/3 DT and %SV-RFP were noted in both coronary disease and congestive cardiomyopathy groups. Coronary disease and congestive cardiomyopathy patients with a mean pulmonary capillary pressure (PCP) greater than or equal to 18 mm Hg had a greater PFR/PER, %SV-1/3 DT, and %SV-RFP than patients with a PCP less than 18 mm Hg. An abnormal and nonspecific pattern of left ventricular diastolic filling is present in both coronary disease and congestive cardiomyopathy patients and is characterized by an increased PFR/PER, a greater %SV-1/3 DT, and a greater %SV-RFP. This pattern may be related to elevated PCPs.
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PMID:Left ventricular diastolic filling in patients with left ventricular dysfunction. 403 Jan 45

The mechanism by which hydralazine improves cardiac function in patients with heart failure is not well characterized. Hydralazine may improve left ventricular (LV) function by decreasing afterloading wall stress or by increasing myocardial contractility. The effect of intravenous hydralazine was assessed in 8 patients with severe idiopathic dilated cardiomyopathy. Hydralazine increased stroke volume index (from 24 +/- 8 to 40 +/- 9 ml/m2, p less than 0.01) and decreased systemic vascular resistance from 1,603 +/- 619 to 810 +/- 317 dynes s cm-5, p less than 0.01) and peak LV wall stress (from 476 +/- 118 to 410 +/- 68 kdynes/cm2, p = 0.02). Two groups were defined by normal or high LV wall stress. Patients with high LV stress had higher LV end-diastolic pressure (38 +/- 12 vs 17 +/- 8 mm Hg, p less than 0.01), LV end-diastolic volume index (184 +/- 24 vs 149 +/- 7 ml/m2, p less than 0.01) and systemic vascular resistance (1,423 +/- 686 vs 846 +/- 293 dynes s cm-5, p = 0.01). Hydralazine decreased stress more in these patients (-101 +/- 57 vs -6 +/- 9 kdynes/cm2, p = 0.02), LV end-diastolic pressure (-12 +/- 7 vs 2 +/- 2 mm Hg, p = 0.02), systolic pressure (-15 +/- 13 vs 3 +/- 4 mm Hg, p = 0.03) and systemic vascular resistance (-1,053 +/- 247 vs -363 +/- 83 dynes s cm-5, p less than 0.01) than in patients with normal LV stress. Decreased LV stress was caused by decreased systolic and diastolic pressures and/or volumes. Late systolic pressure-volume relations in patients with normal LV stress suggested increased myocardial contractility, but this was not confirmed by LV dP/dt. Hydralazine improves LV function in patients with dilated cardiomyopathy by reducing elevated LV wall stress, with little inotropic effect.
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PMID:Effects of hydralazine on pressure-volume and stress-volume relations in congestive heart failure secondary to idiopathic dilated cardiomyopathy. 405 Jul 8

The purpose of this study is to evaluate four methods of determining left ventricular stroke volume (SV) from aortic valve (AV) and aortic root (AR) M-mode echocardiogram (Table I, formulas 1-4); secondly, to study relations between echocardiographic aortic variables and SV. We studied 20 patients (Pts) in our Coronary Unit, 14 men and 6 women; their ages ranged from 38 to 76 (mean 53.4) years. Seventeen Pts had acute myocardial infarction; two Pts had previous myocardial infarction and heart failure; one Pt had dilated cardiomyopathy and heart failure. Three out of the twenty Pts, had mitral insufficiency (Table II, clinical and hemodynamic data). Patients were studied with high quality M-mode echocardiography. Immediately after the examination repeated measurements of cardiac output by thermodilution technique (TD) were carried out, and values of SV calculated (SV-TD). Twenty-five complete procedures were accomplished. The formulas were applied to every patient's echocardiographic data, and results (SV-ECHO) compared with SV-TD (Table III). Echocardiographic variables, whether single or multiple (terms), were also studied with regard to their relation with SV-TD (Table IV). Mean +/- SD value of SV-TD of the study group was 60.3 +/- 24.7 ml; range 22.7 to 108 ml. Mean +/- SD values of SV-ECHO were as follows: Yeh's formula, based on squared mean AV opening and LVET, 56 +/- 22.6 (ml), r = 0.8278, SEE 12.98; Jacobs' formula, based on aortic box planimetry, 68 +/- 32.5 (ml), r = 0.7129, SEE 23.31.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Methods of determination of stroke volume from M-mode echocardiogram of the aortic valve and aortic root. A comparative evaluation]. 406 79


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