Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033036 (APC)
 10,214 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sixty-six consecutive patients without left ventricular volume overload, significant arrhythmia or significant pericardial effusion were examined by M-mode echocardiography immediately before diagnostic left- and right-heart catheterization. Using various echocardiographic measurements, left ventricular stroke volume (SV) was calculated according to eight different echocardiographic formulas (SVE) that have been proposed previously. At catheterization SV was also determined by thermodilution (SVT) and by single-plane left ventricular cineangiography in the right anterior oblique projection (SVA). When comparing SVE with SVT, the four formulas developed to calculate mitral or aortic flow failed (r = 0.10 to 0.54). As expected, poor correlations (r = 0.22 to 0.47) were also found when formulas used to calculate ventricular volumes from the ventricular diameter or SV from the change in diameter (left ventricular formulas) were used in coronary patients with grossly asymmetrical ventricular contraction patterns. When the use of the left ventricular formulas was confined to patients with symmetrical or almost symmetrical contraction, two formulas yielded favorable correlations of r = 0.84, SEE = 12.7 ml and r = 0.86, SEE = 12.2 ml, respectively. These correlations were comparable to the correlation between our two invasive reference techniques (r = 0.81; SEE = 12.2 ml). The comparison between SVE and SVA confirmed the results of the thermodilution study, though the correlations were generally weaker. We conclude that the formula of Teichholz et al., which was the best of all tested formulas, may be used to obtain a clinically useful estimate of SV in patients in whom symmetrical or almost symmetrical left ventricular contraction can be anticipated.
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PMID:Comparative value of eight M-mode echocardiographic formulas for determining left ventricular stroke volume. A correlative study with thermodilution and left ventricular single-plane cineangiography. 49 56

The purpose of this study was to determine whether segment lengths measured from the right ventricular inflow and outflow tract regions of the right ventricle would accurately reflect true volume changes of the right ventricle and to determine the response of the right ventricle to afterload increases induced by both constricting the pulmonary artery (PAC) and embolizing the pulmonary circulation with glass beads (GBE). Three excised hearts were instrumented with segment-length crystals attached to the inflow and outflow tract regions, and saline was instilled into a balloon implanted inside the right ventricular cavity. The experiments showed a high correlation (r greater than or equal to 0.90 in all cases) between static segment lengths and volume instilled. In open chest, open pericardial canine experiments, vena caval occlusion reduced end-diastolic segments lengths and right ventricular systolic pressure consistent with a reduction in right ventricular end-diastolic volume. In a separate group of animals, volume loading with dextran increased inflow and outflow end-diastolic segment lengths and increased cardiac output. In two further groups of animals, one of which was pretreated intravenously with propranolol (Inderal), both forms of pressure overload increased end-diastolic lengths in both regions. However, GBE increased right ventricular stroke work compared with PAC. We conclude that end-diastolic segment lengths reflect true volume changes of the right ventricle. Furthermore, during acute pressure overload, the right ventricle dilates to compensate for the afterload change. However, ventricular function is better maintained after GBE.
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PMID:Pressure segment length analysis of right ventricular function: influence of loading conditions. 201 15

During the period January 1982 till June 1988, 536 patients underwent 577 carotid thrombendartectomies in the Department of Vascular Surgery RK in the University Hospital in Copenhagen. Preoperatively, 270 patients (47%) had experienced transient ischaemic attacks (TIA), 247 (43%) had experienced stroke (APC) and 19 (3%) had non-focal symptoms while 41 (7%) had asymptomatic stenoses. Postoperatively, 17 (2.9%) patients developed TIA, 22 (3.8%) developed slight neurological symptoms and 40 (7%) had more severe neurological complications and six of these (1%) died. None of the patients died from other causes during the first month. The frequency of complications had no relationship to the preoperative focal symptoms, but in patients with non-focal symptoms this was 37%. The degree of stenosis of the contralateral internal carotid artery (ICA) was correlated positively with the occurrence of severe neurological complications which were observed in 5% without contralateral ICA changes, in 7% with stenoses and in 20% with contralateral ICA occlusion. Patients with cerebral infarction developed complications significantly more frequently (20%) than patients with normal CT scans. The risk was also found to be increased in cases with a high pressure gradient across the stenosis and low pressure peripherally in the occluded artery (stump pressure). Follow-up examination of the 73 patients with complications on average 39 months after operation revealed that 37 patients (6.4%) had severe neurological symptoms resulting either from the operation or subsequent APC; seven patients required complete nursing care (1.2%) and 17 patients died during the period of observation. On follow-up examination, 15 patients had been occupationally active for at least 1.5 years.
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PMID:[Neurologic complications in connection with the surgical treatment of 577 cases of carotid artery stenosis]. 232 34

The relationship between stroke volume (SV) measured simultaneously by impedance cardiography (SVI) and echocardiography (SVE) has been analyzed. Change in stroke volume in 6 healthy volunteers was induced by passive head-up tilting (80 degrees) and by oral administration of the sympathomimetic drug amezinium. A correlation of r = 0.83 (p much less than 0.01) was found between SVI and SVE calculated by the equation: SVE = 16.0 + (0.528 x SVI). Though stroke volume is overestimated by impedance cardiography, the method may be useful for the clinical pharmacologist interested in a simple non-invasive tool to estimate stroke volume and change in it.
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PMID:Comparison of impedance cardiography and echocardiography for measurement of stroke volume. 716 Apr 14

Stroke volume (SV) and systolic time intervals (STI) were measured automatically using impedance cardiography signals (ICG) and compared with those obtained by pulsed-wave Doppler echocardiography using the apex approach. The comparison was made in 9 healthy male subjects, mean age 24.9 +/- 12.2 years, using recordings of 10 heart cycles simultaneously obtained by the two methods. During measurements the subjects rested in the supine position. There were no differences between mean values of SV determined by the two methods as well as between mean values of ejection time (ET) (p > 0.8 and p > 0.9, respectively). The pre-ejection period (PEP) estimated by ICG was 22 ms longer than that determined by echocardiography (p < 0.001). The relationship between SV values measured by impedance cardiography (SVA) vs those calculated by echocardiography (SVE) was found to be close to the line of identity in the range of measurements. The regression equation for SV was: SVA = 0.784.SVE + 15 (r = 0.69, p < 0.001, SEE = 10.7 ml). We conclude that automatic determination of SV and ET from ICG signals provides results comparable in absolute values with those obtained by the pulsed wave Doppler ultrasonocardiography using the apex approach for subjects remaining in the supine position.
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PMID:A comparison between the automatized impedance cardiography and pulsed-wave Doppler echocardiography methods for measurements of stroke volume (SV) and systolic time intervals (STI). 824 26

APC resistance, due to a point mutation in factor V at amino acid position Arg506, has been identified as a major cause of inherited thrombophilia. Here we report the presence of the factor V Arg506-->Gln mutation in 2 Italian families. In 1 family 3 subjects heterozygous and 2 subjects homozygous for the factor V Arg506-->Gln mutation were identified. The only subject who developed a thrombotic event was a 20-yr-old girl who was found to be homozygous for the factor V Arg506-->Gln mutation. In the second family 10 subjects were identified to be heterozygous for the factor V Arg506-->Gln mutation; among them 2 developed a thrombotic event. In the same family 2 individuals were found to be homozygous for the mutation: the first had a myocardial infarction at age 25 yr and the second suffered from multiple episodes of deep venous thrombosis and had a stroke at age 24 yr. These data show that the risk of developing deep venous thrombosis for the carriers of the factor V Arg506-->Gln mutation is high in the families investigated. Furthermore our data imply that the factor V Arg506-->Gln mutation in its homozygous form may relate to myocardial infarction and stroke.
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PMID:Arterial and venous thrombosis in two Italian families with the factor V Arg506-->Gln mutation. 869 38

This study was designed to prospectively evaluate haemostatic activation in 75 children undergoing cardiac catheterisation with intermittent flush heparin (10 IU/ml saline) and to relate these data to clinical findings and inherited risk factors for thrombophilia. In addition to flush heparin in infants < 6 months of age in whom additional arterial catheterisation was performed (n = 5) or patients with thrombophilia, heparin (300-400 IU/kg/d) was administered for a further 24 h. APTT was prolonged and anti Xa activity was significantly increased at the end of catheterisation and returned to normal 24 hours later. Whereas thrombin generation (F1 + 2) showed a significant coagulation activation at the end of catheterisation, no concomitant fibrinolytic activation (D-Dimer) was observed. Four children showed resistance to APC: one of them in whom stroke had occurred before and one additional child heterozygous for APCR received further prophylactic heparin. Two neonates with APCR and flush heparin only suffered from thrombosis after catheterisation. No further thrombotic events occurred. This study indicates that low-dose flush heparin during catheterisation may prevent long-term haemostatic activation in children without thrombophilia. Whether further heparin after cardiac catheterisation in children with APCR prevents vascular insults requires a more intensive study.
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PMID:Flush heparin during cardiac catheterisation prevents long-term coagulation activation in children without APC-resistance-preliminary results. 886 15

A 72-year-old man developed a sudden weakness in his left hand on October 5, 1991. He was admitted two weeks thereafter. Physical examination revealed minimal weakness, and clumsiness of the fingers on his left hand. Exaggerated tendon reflexes and spasticity were also noted only on his left upper limb. He had neither dementia nor psychiatric symptoms. Subsequently he developed weakness in his left leg on November 17. Within 12 days he developed left facial weakness, and myoclonic movements on the left side. By December 2, he developed spastic tetraparesis with bilateral facial palsy, and generalized myoclonic jerks. A few days after that he started to show decorticate posture. From December 16, his mental status deteriorated rapidly, and he became mute, and uncooperative within a week. His clinical course can be summarized as stepwise progression similar to a cerebrovascular accident. Electroencephalography was normal on admission, but periodic synchronous discharge developed in January 1992. Brain CT that showed only mild brain atrophy at first was considered to be compatible with his age, changed to have severe brain atrophy in March 1992. He died of pneumonia on May 24, 1992 after eight months of progressive clinical course. Autopsy was done. The brain weighed 930 grams. Macroscopically there was prominent cortical atrophy. Microscopic examination revealed severe spongy state throughout the cerebral cortex. Typical spongiform changes were confined to the hippocampus. The cerebral white matter appeared to be normal. In the cerebellar cortex, the granular cell layer disappeared and Purkinje's cells were reduced in number. Kuru plaques were not seen. The cerebellar white matter, dentate nucleus, and brainstem seemed to be normal. The spinal cord was not examined. There were no pathological changes to indicate cerebrovascular accident, except for a lacuna in the right basal ganglion and a small angionecrosis in the pons. Western blotting test using Anti-APC (amyloid plaque core) antibody was positive. Neuropathological changes of the present case were consistent with those of CJD. However, the sudden onset of monoparesis without dementia or ataxia is rare as the initial symptom of this disease. The subsequent clinical course with stepwise progression of hemiplegia, which was mimicking a progressive stroke, was also rare for CJD. In comparison to typical case of CJD, this case had a different clinical onset as acute monoparesis. We can find such cases of CJD presenting as stroke in 5.6% in the previous English literatures.
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PMID:[A case of Creutzfeldt-Jakob disease (CJD) started with monoparesis of the left arm]. 904 57

Hyperhomocysteinemia is a condition which, in the absence of kidney disease, indicates a disrupted sulfur amino acid metabolism, either because of vitamin (folate, B12 and B6) deficiency or a genetic defect. Epidemiological evidence suggests that mild hyperhomocysteinemia is associated with increased risk of arteriosclerotic disease and stroke. The relationship between hyperhomocysteinemia and thrombosis has been investigated in 10 studies involving a total of 1200 patients and 1200 controls. Eight of these studies demonstrated positive association with odds ratios that ranged from 2 to 13. This association was enhanced by including a methionine loading test. There is some evidence which suggests that hyperhomocysteinemia and APC resistance have a synergistic effect on the onset of thrombotic disease. Studies on the mechanism that underlies the relationship between thrombosis and hyperhomocysteinemia used non-physiologically high levels of homocysteine, rendering the data doubtful as to their patho-physiological relevance.
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PMID:Hyperhomocysteinemia and thrombosis: acquired conditions. 919 9

Two families with type I plasminogen deficiency and APC resistance are reported. The proposita of family A suffered from ischemic stroke when taking estrogen-progesterone-containing oral contraceptive. Several hemostatic challenges in the past (ovariectomy, appendectomy, and two pregnancies) were without thrombosis. Plasminogen activity and antigen (60 and 58%, normal range 72-136 and 69-135%, respectively) were reduced, and an increased APC resistance (APC-SR= 1.55; normal range 1.8-3.00) associated with G --> A change at 1,691 nucleotide position in exon 10 of FV gene (FV Leiden) was observed. The asymptomatic son had isolated plasminogen deficiency (activity 57% and antigen 60%) whereas the asymptomatic daughter had isolated APC resistance (APC-SR = 1.61) and FV Leiden mutation. The proposita of family B, referred for superficial thrombophlebitis, had low plasminogen levels (activity 55% and antigen 53%) and APC resistance (APC-SR = 1.5) whereas the asymptomatic mother and the brother had isolated APC resistance (APC-SR = 1.62 and 1.8, respectively) and the asymptomatic father isolated plasminogen deficiency (activity 61% and antigen 62%). These data suggest that the combination of plasminogen deficiency and APC resistance probably does not significantly increase the risk of venous thrombosis. However, larger experience with additional cases is needed to definitely assess the magnitude of thrombotic risk in these families.
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PMID:Low risk of venous thrombosis in two families with combined type I plasminogen deficiency and factor V R506Q mutation. 954 82


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