UMLS:C0038454 - FACTA Search

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By definition, the pulmonary "venous" system consists of the pulmonary veins and the left atrium. The stiffness of the pulmonary "venous" (P'V') system and the left ventricle (LV) at the end of the slow filling period (at the point of pre-a) were estimated sequentially in a total of 26 patients, divided into a control group and mitral stenosis (MS), angina pectoris (AP), hypertrophic cardiomyopathy (HCM) groups. The stiffness (delta P/delta V) of the P'V' system was estimated from the pulmonary artery wedge (PAW) pressure tracings and the stroke volume. The stiffness (dP/dV) of LV was obtained from the pressure-volume (P-V) relationship of LV with a model of P = beaV. The present study is aimed primarily at obtaining factual information. The stiffness of the P'V' system was 0.063 +/- 0.022 mmHg/ml (mean +/- SD) in the control group and 0.052 +/- 0.006 mmHg/ml in the HCM group (p greater than 0.1). The stiffness of LV in diastole was 0.091 +/- 0.016 mmHg/ml in the control group and 0.199 +/- 0.056 mmHg/ml in the HCM group (p less than 0.01). The ratio of the stiffness of LV in diastole to that of the P'V' system was 1.6 +/- 0.6 in the control group and 3.8 +/- 0.7 in the HCM group. The volume elastic constant (a) of the P'V' system was 0.008 +/- 0.005 ml-1 in the control group and the values of (a) occupied a range of 0.007 to 0.008 ml-1 in the remaining 3 groups of patients. The values of (a) of LV were 0.011 +/- 0.004 ml-1 in the control group and 0.022 +/- 0.007 ml-1 in the HCM group (p less than 0.01). The present study suggests that the P'V' system is usually 2 to 3 times more complaint than LV in diastole. On the other hand, the P'V' system remained compliant in spite of the decreased compliance of LV in diastole in the HCM group, maintaining the reservoir function with which pulmonary edema is prevented.
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PMID:A quantitative analysis of reservoir function of the human pulmonary "venous" system for the left ventricle. 373 56

The clinical and haemodynamic significance of the subaortic pressure gradient in patients with muscular (hypertrophic) subaortic stenosis (hypertrophic obstructive cardiomyopathy) has long been debated. In this report we summarize the evidence which indicates that true obstruction to left ventricular outflow exists in these patients. Rapid left ventricular ejection, through an outflow tract narrowed by ventricular septal hypertrophy, results in Venturi forces causing systolic anterior motion of the anterior (or posterior) mitral leaflets. Mitral leaflet-septal contact results in obstruction to outflow and the accompanying mitral regurgitation. The time of onset of mitral leaflet-septal contact determines the magnitude of the pressure gradient and the severity of the mitral regurgitation, as well as the degree of prolongation of left ventricular ejection time and the percentage of left ventricular stroke volume that is ejected in the presence of an obstructive pressure gradient. Early and prolonged mitral leaflet-septal contact results in a large pressure gradient, significant mitral regurgitation, as well as dramatic prolongation of the ejection time and a large percentage of left ventricular stroke volume being obstructed. Late and short mitral leaflet-septal contact results in little haemodynamic perturbation. Hypertrophic cardiomyopathy patients with obstructive pressure gradients are significantly more symptomatic than those without. Thus the obstructive pressure gradients in hypertrophic cardiomyopathy are of clinical as well as haemodynamic significance. To deny the existence of obstruction to outflow in patients with muscular subaortic stenosis is to deny these patients appropriate medical and surgical therapy.
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PMID:Muscular (hypertrophic) subaortic stenosis (hypertrophic obstructive cardiomyopathy): the evidence for true obstruction to left ventricular outflow. 377 88

Left ventricular cineangiograms performed at the time of diagnosis in 88 patients with hypertrophic cardiomyopathy were digitized to evaluate the relation of left ventricular function and prognosis in hypertrophic cardiomyopathy. Eleven patients died suddenly after a mean follow-up period of 7.5 +/- 7 years, 10 patients died of congestive heart failure or after cardiac surgery and 67 were alive after a mean follow-up period of 8.6 +/- 4 years. Measurements of left ventricular volume, ejection fraction, peak rate of ejection and filling and time to peak rate of ejection and filling were derived from curves of ventricular volume and its rate of change during the cardiac cycle. Patients who died suddenly had a lower peak rate of ventricular ejection (stroke volume-normalized peak ejection rate 5.41 +/- 0.69 versus 6.24 +/- 1.33 s-1; p = 0.006) and lower peak rate of ventricular filling (end-diastolic volume-normalized peak filling rate 4.02 +/- 0.94 versus 4.88 +/- 1.53 s-1; p = 0.02) and stroke volume-normalized peak filling rate (4.75 +/- 1.08 versus 5.82 +/- 1.70 s-1; p = 0.01) compared with survivors. Stepwise regression analysis revealed that sudden death was best predicted by the combination of increased end-diastolic volume, small end-systolic volume and low peak filling rate (predictive accuracy 32%, false negative 18% and false positive 28%). The addition of clinical features and hemodynamic measurements to the analysis improved predictive accuracy to 43% (false negative 18% and false positive 18%). Ambulatory electrocardiographic monitoring performed in 57 of the 88 patients 1 month to 17 years (median 8 years) after diagnosis revealed ventricular tachycardia in 14 (25%). Of these, 10 who survived had hyperkinetic systolic function at diagnosis, whereas the 4 who died suddenly had impaired systolic function (end-diastolic volume-normalized peak ejection rate 5.93 +/- 1.2 versus 4.01 +/- 1.2 s-1, respectively; p = 0.04). In hypertrophic cardiomyopathy, ventricular tachycardia is a sensitive but nonspecific marker of adults who are at risk of sudden death. Impaired systolic function may be an important determinant of which patients with ventricular tachycardia die suddenly. This study shows that indexes of ventricular function contribute to the identification of patients at particular risk of sudden death. However, the predictive power of the clinical features and hemodynamic and angiographic measurements that could be assessed was poor.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Relation of left ventricular function and prognosis in hypertrophic cardiomyopathy: an angiographic study. 403 43

The hemodynamic effects of sublingual nifedipine were examined in 36 patients with hypertrophic cardiomyopathy. Twenty-one patients were initially given 20 mg and 15 patients were given 10 mg of the drug; 30 min after this first dose 26 patients received 10 mg and one patient 20 mg as a second dose. Hemodynamic findings in patients who received different doses of the drug were similar. Peak effects included an increase in heart rate from 79 +/- 12 to 91 +/- 14 (mean +/- 1 SD) beats/min (p less than .01), and a decrease in mean blood pressure from 89 +/- 12 to 77 +/- 10 mm Hg (p less than .01). Cardiac index increased after nifedipine (2.8 +/- 0.6 to 3.3 +/- 0.8 liters/min/m2; p less than .01); stroke volume index, however, did not change (36 +/- 7 to 36 +/- 8 ml/beat/m2; NS). Peripheral vascular resistance index fell significantly from 822 +/- 261 to 610 +/- 197 dynes X sec X cm-5 (p less than .01). Overall, left ventricular outflow tract gradient (LVOTG) did not change in patients with significant (greater than or equal to 30 mm Hg) basal LVOTG (75 +/- 22 to 83 +/- 22 mm Hg; NS), but it increased significantly in those six patients in whom peripheral vascular resistance fell by 25% or more (73 +/- 28 to 99 +/- 22 mm Hg; p less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of sublingual nifedipine on hemodynamics and systolic and diastolic function in patients with hypertrophic cardiomyopathy. 404 88

The indices of systolic and earli diastolic function (relaxation and rapid filling) were established in 16 healthy subjects and 35 patients with idiopathic hypertrophic cardiomyopathy by computer analysis ("Echocomputer" RIEMT--MA, Sofia) and left ventricular and mitral valve M-type echocardiogram. In a considerable part of the partients with hypertrophic cardiomyopathy, pathological changes were established in the diastolic function of left ventricle--lengthening of iso-voluminal relaxition, reduction of velocity and increase of the dimension of left ventricular cavity, reduction of velocity and fraction of blood flow in the phase of rapid filling of left ventricle. Those changes of diastolic function are a manifestation of increased resistance, restriction of left ventricular filling that could partially explain the tendency to reduction of stroke and minute volume in some patients with hypertrophic cardiomyopathy with normal and increased indices of systolic function of left ventricle (fraction of shortening, ejection fraction, veloycity of reduction of dimension of left ventricle in the phase of ejection)? There is considerable correlation between the changes of diastolic function and those of the hypetrophic process and reduction of left ventricular cavity. The computer analysis of the echogram, enables the more detailed, fast and accurate determination of important indices of diastolic and systolic function of left ventricle, with a good repeated reproducibility.
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PMID:[Relaxation and filling of the left ventricle measured by computer analysis of the unidimensional (M-type) echocardiogram in healthy subjects and patients with hypertrophic cardiomyopathy]. 407 72

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

Changes in left ventricular systolic and diastolic function and outflow gradient were evaluated in patients with obstructive hypertrophic cardiomyopathy after intravenous acute treatment with verapamil (15 patients) and after six months of oral chronic treatment (11 patients). All patients had severe symptoms despite beta blockade, and the condition of all but two improved appreciably after chronic treatment with verapamil. Resting left ventricular outflow tract gradient decreased in six of 15 patients after intravenous verapamil, and in five of 11 patients after long term treatment, but there was no change in provocable gradients nor any correlation between changes in gradient and improvement in symptoms. Left ventricular ejection rate did not change after intravenous or oral treatment. End systolic pressure/end systolic volume index remained unchanged after oral verapamil treatment. Whereas left ventricular total stroke volume index and end diastolic volume index increased without any significant change in left ventricular end diastolic pressure, indicating improved left ventricular diastolic function. In some patients the left ventricular diastolic pressure-volume curve shifted downwards or to the right or both. These findings suggest that improvement in symptoms with verapamil in patients with obstructive hypertrophic cardiomyopathy is unlikely to be related to changes in left ventricular outflow gradient or in systolic function and may be related to improved diastolic function.
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PMID:Hypertrophic obstructive cardiomyopathy. Effects of acute and chronic verapamil treatment on left ventricular systolic and diastolic function. 653 20

Hypertrophic cardiomyopathy is characterised by hyperkinetic left ventricular function, but the effect of an outflow tract gradient on the haemodynamics of ejection remains controversial. To determine the functional importance of left ventricular gradients in hypertrophic cardiomyopathy technetium-99m gated equilibrium radionuclide angiography was performed in 18 normal subjects and 57 patients, 26 with and 31 without left ventricular gradients. Time activity curves were generated from list mode data, and the proportion of stroke volume ejected during various phases of systole was computed. The proportion of stroke volume ejected during the initial third, the initial 50%, and the initial 80% of systole was greater in patients with hypertrophic cardiomyopathy than in normal subjects but was identical in patients with and without left ventricular gradients. The duration of systole was similar in the three groups. These findings favour the interpretation that a left ventricular gradient does not represent true obstruction and are consistent with previous observations that clinical features and prognostic indicators do not relate to gradients in this disease.
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PMID:Relation between left ventricular gradient and relative stroke volume ejected in early and late systole in hypertrophic cardiomyopathy. Assessment with radionuclide cineangiography. 654 20

Electrocardiogram gated cardiac computed tomography (CT) was performed to evaluate the usefulness in the measurement of left ventricular volume and left ventricular wall thickness in 25 patients; five with angina pectoris, five with old myocardial infarction, eight with hypertrophic cardiomyopathy, four with dilated cardiomyopathy, and three healthy men. The left ventricular volume was calculated as the sum of the volume of each slice, which was area times thickness of the slice. The left ventricular wall thickness was measured in reconstructed short-axis view at the level of the mitral valve and papillary muscle. The left ventricular volume and left ventricular wall thickness determined by CT were compared with that by left ventriculography (LVG), and that by two-dimensional echocardiography (2 DE), respectively. The following results were obtained. There were good relationships between left ventricular volume, end-diastolic volume, end-systolic volume, ejection fraction by CT and those by LVG, but left ventricular volume by CT was smaller by about 20% than that by LVG. In the measurement of stroke volume, no relationship was recognized between CT and LVG. Concerning the measurement of left ventricular wall thickness, more available figures were obtained by CT than by 2 DE, particularly at the apical region, lateral wall, and posterior wall. In the other segments of the left ventricle, CT was also more suitable for the measurement of the wall thickness. Interventricular septal thickness was correlated between reconstructed short-axis view of CT (Y) and transverse view of CT (X), and the equations Y = 0.66X + 2.13 (r = 0.79) at the mitral valve level, and Y = 0.56X + 3.00 (r = 0.81) at the papillary muscle level were obtained. Therefore, reconstructed short-axis view should be used for the measurement of the left ventricular wall thickness not to overestimate the thickness.
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PMID:[Usefulness of ECG gated cardiac computed tomography in measurement of left ventricular volume and wall thickness]. 654 27

In the study of cardiac abnormalities responsible for the development of cerebral embolism two-dimensional echocardiography was performed on 350 patients with ischemic cerebrovascular disease. The results were compared with those obtained from 350 controls without any history of stroke. Atrial fibrillation was detected on ECG in 115 cases (33%) of the patients and in 35 cases (10%) of the controls (p less than 0.001). The structural cardiac diseases observed in stroke patients were: rheumatic heart disease (RHD) in 37, congestive cardiomyopathy (CCM) in 7, hypertrophic cardiomyopathy (HCM) in 19, mitral annulus calcification (MAC) in 29, mitral valve prolapse (MVP) in 9, and myocardial infarction (MyI) in 10 patients. Controls were found to have these lesions in 11, 2, 3, 12, 4 and 9 patients respectively. RHD (p less than 0.001), HCM (p less than 0.01) and MAC (p less than 0.01) were significantly more frequent in patients with ischemic cerebrovascular disease, but not MyI, CCM or MVP. Intracardiac thrombi were diagnosed in 29 cases of patients and in 4 cases of controls (p less than 0.001). Our data suggested that nonrheumatic heart diseases such as MAC and HCM could also be considered as causes of embolic stroke. The reasons for the variable frequencies of cardiac abnormalities reported in the literature for stroke patients are discussed.
Stroke
PMID:Cardiac abnormalities in ischemic cerebrovascular disease studied by two-dimensional echocardiography. 665 29

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