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Biomedical subjects

M Sturm

Publications and source records attributed to M Sturm.

At least 37 records · Page 2Linked to original sources
PubMed1997

Angiographically undetected plaque in the left main coronary artery. Findings of intravascular ultrasound imaging.

The absence of angiographic findings despite significant coronary artery disease has been previously described. Possible explanations for the limitation of plaque detection by angiography include compensatory vessel enlargement in face of intracoronary plaque formation, the lack of reference segments in diffuse atherosclerosis as well as technical limitations. Intracoronary ultrasound (ICUS) imaging provides the possibility of direct plaque visualization. We studied angiographically normal left main coronary arteries (LMCA) in 72 patients prior to diagnostic angiography or therapeutic interventions using ICUS (30 MHz). ICUS images were continuously recorded and recalled from memory for morphometric analysis. Lumen area, plaque area and the total vessel area were determined by computer software. ICUS imaging revealed atherosclerotic plaque in 55 of the 72 patients with angiographically normal LMCA (76%). The average plaque area stenosis was 22 +/- 12% (range 3-44%). Total vessel area showed a significant direct correlation with plaque area, indicating compensation of coronary plaque formation. The average percent change in plaque area (difference between maximal and minimal plaque area within the LMCA) was 11 +/- 19%, indicating a diffuse pattern. Measurement of change in lumen area (difference between maximal and minimal lumen area within the LMCA) revealed an average value of 6 +/- 7%. Lumen area of the LMCA was 15.9 +/- 3.2 mm2 in patients with and 17.2 +/- 1.9 mm2 without atherosclerotic plaque (n.s.). Thus, the lack of angiographic changes despite advanced plaque formation in the LMCA could be explained by compensatory vessel enlargement and by diffuse distribution of plaque in the vessel; true lumen narrowings overlooked by angiography seem not to account for the failure of angiography to detect plaque.

Aged↗
PubMed1997

Acute effects of celiprolol on angiographically normal and stenotic coronary arteries.

Unselective and beta 1-selective beta-blockers may induce vasoconstriction of normal and stenotic epicardial coronary arteries. To analyze the influence of the "vasodilatory" beta-blocker celiprolol on coronary vasomotility, 0.4 mg celiprolol/kg were intravenously infused over 4 minutes in 13 patients with coronary artery disease. Coronary angiograms were taken before (control) and at 4, 6, 8, 10, 15, and 20 minutes after the onset of infusion and 4 minutes after final sublingual administration of 0.4 mg nitroglycerin. Quantitative analysis of cinefilms demonstrated no significant diameter changes in angiographically normal coronary segments and stenoses. The vasodilatory capacity of normal segments (18 +/- 12%; p < 0.001) and stenoses (17 +/- 14%; p < 0.01) was proven by nitroglycerin. Systolic blood pressure, heart rate, and pulmonary wedge pressure revealed no significant changes with celiprolol. Thus, celiprolol exerts no vasoconstricting effects on angiographically normal and stenotic coronary arteries.

Adrenergic beta-Antagonists↗
PubMed1996

Familial defective apolipoprotein B-100 (FDB): effect of simvastatin therapy on LDL-receptor binding.

Heterozygotes for familial defective apolipoprotein B-100 (FDB) have two populations of low density lipoprotein (LDL), one bearing normal apolipoprotein B-100 (apo B) and the other bearing defective apo B which exhibits a much lower affinity for the LDL-receptor. If HMGCoA reductase inhibitors such as simvastatin lowered LDL mainly by up-regulating LDL-receptor mediated clearance, they should decrease the overall binding affinity of LDL from an FDB heterozygote by selectively decreasing LDL bearing normal apo B. We compared how LDL from FDB heterozygotes competed with normal 125I-labelled LDL for binding to LDL-receptors while on and off therapy with simvastatin. The LDL of FDB heterozygotes had 40% (n = 10) the affinity of normal LDL (n = 12) for the LDL receptor on cultured fibroblasts, and 55% (n = 6) of normal LDL (n = 6) for that on HepG2 cells. Treatment of FDB subjects with simvastatin (n = 10) decreased serum LDL by 22% but had no effect on its binding affinity for LDL receptors, indicative of lowering of LDL containing both normal and defective apo B. This is consistent with the major LDL lowering effect being associated with decreased synthesis of LDL, rather than enhanced LDL-receptor clearance.

Adult↗
PubMed1996

Standardization of coronary vasomotor tone with intracoronary nitroglycerin.

Maximal, reproducible, and thus "standardized" dilation of epicardial coronary arteries can be easily achieved with intracoronary bolus administration of 0.1 mg nitroglycerin without considerable decrease in blood pressure. The addition of other nitrocompounds or calcium antagonists cannot increase coronary dilation after nitroglycerin, but may be hampered by adverse effects.

Blood Pressure↗
PubMed1996

Comparison of different quantitative coronary analysis systems: ARTREK, CAAS, and CMS.

It has been known that the first generation quantitative coronary analysis systems overestimate small vessel sizes. In the 2nd generation the contour detection algorithms, e.g., of the new Cardiovascular Measurement System (CMS), were modified to correct for the limited resolution of the X-ray imaging chain. This study validated and compared the CMS with the well-known Coronary Angiography Analysis System (CAAS) and the vessel tracking program ARTREK in a phantom study and a clinical study. In addition, the influence of different acquisition media (cinefilm vs. digitally acquired angiograms) on the accuracy of quantitative analysis was examined. The phantom study comprised 19 stenotic or non-stenotic glass tubes with a diameter range from 0.54 mm to 4.9 mm. In the clinical study the mean diameters of 322 coronary segments were analysed and the results of the systems were compared among each other. The results of the phantom study were presented in terms of the mean difference (accuracy) between true and measured values. In the phantom study the overall accuracy of the CMS was -6 microns (ARTREK: 85 microns; CAAS: 35 microns) with an overestimation of small vessels of only -11 microns (ARTREK: 97 microns: CAAS: 51 microns). The clinical study showed that the CMS corrected the usually occurring overestimation of small coronary arteries and that the influence on the accuracy of different acquisition media is minor. Due to the modified algorithms the new CMS is able to measure coronary diameters down to 0.5 mm accurately. Therefore, the CMS seems to provide more precise measurements in quantitative analysis of small coronary diameters than CAAS and ARTREK.

Coronary Angiography↗
PubMed1995

The metabolism of platelet-activating factor in severe and cerebral malaria.

In order to examine the effects of platelet-activating factor (PAF) in complicated Plasmodium falciparum infections, plasma concentrations of lyso-PAF, stable metabolite and principal precursor of PAF, were measured in 25 Vietnamese adults with severe malaria. The concentration of PAF in the cerebrospinal fluid (CSF) was determined in a sub-group of 23 comatose patients and, together with that of lyso-PAF, in the plasma of 20 patients on recovery of consciousness. The concentration of lyso-PAF in the plasma was depressed on admission to hospital (median [range]; 21 [8-143] vs. 293 [215-410] ng/ml in 10 controls; P < 0.001). There was, however, no change in plasma activity of acetylhydrolase which converts PAF to lyso-PAF (P > 0.01 vs. controls) while simultaneous reduction in the concentration of lipoproteins associated with lyso-PAF were less than those of lyso-PAF per se in the plasma. The plasma concentration of lyso-PAF on admission was associated with parasitaemia and the concentration of serum triglycerides (rs = -0.42, P = 0.04 in each case), the latter being consistent with hepatic effects of PAF reported in previous studies. CSF concentrations of PAF on admission were low (2.3 [0.5-7.7] vs. 0.9 [0-2.5] ng/ml after recovery, P < 0.01) compared with values reported previously in bacterial meningitis. Plasma concentrations of lyso-PAF after recovery lay between admission and control values. While increased availability of PAF may reflect parasite burden and may modulate liver-mediated metabolic disturbances such as hypoglycaemia and lactic acidosis, the role of PAF in cerebral malaria is uncertain.

Adult↗
PubMed1994

[Follow-up of vena cava filters with color Doppler ultrasound].

In 49 patients, colour-coded Duplex sonography was performed after implantation of a Greenfield caval filter. A plain film radiograph of the abdomen was taken additionally. The examination could be assessed free of artifacts in the longitudinal and transverse section in a total of 41 patients (84%). The procedure facilitates not only a diagnosis of thrombotic changes in the vena cava but can also display the topographical position of the filter and the venous flow. Caval thrombosis was verified in 5 patients. In 7 cases there was a decentral position of the filter apex with tilting. The penetration of filter struts through the vein wall eluded sonographic diagnosis as did morphological changes to the filter (e.g. filter fracture). In combination with the plain film radiograph, colour-coded Duplex sonography can replace cavography or computed tomography in the investigation of position and venous flow.

Adult↗
PubMed1994

[Cava filter for prevention of lung embolism: is implantation still justified?].

During a period of 11 years operative placement of a Greenfield vena caval filter was planned in 132 patients. The clinical records of these patients were reviewed retrospectively. Main indications for filter placement were pulmonary embolism in patients with deep venous thrombosis in spite of anticoagulation therapy (45%) and patients with contraindications for anticoagulation (40%). Insertion was successful in 117 patients with a failure rate of 14.6% (21 of 143 procedures). Follow-up data were obtained of all 117 patients with inserted filter (6 of them with 2 filters). Physical examination was performed in 67 of 74 patients alive after a mean postoperative period of 57 months (median: 52.5/range: 1-128). In addition, plain abdominal X-ray was available of all patients. CT scans of the abdomen or venacavography studies were obtained in 60 patients. Major complications as recurrent pulmonary embolism (8%), caval thrombosis (13%), penetrations of struts through the caval wall (33%), tilting of filters (25%), migration (5%) and filter fracture (two cases) were observed. In conclusion, indication should be restricted to certain cases with failure of surgical intervention or drug therapy (thrombectomy, lysis, anticoagulation).

Adult↗
PubMed1993

Platelet-activating factor and lipid metabolism in acute malaria.

Platelet-activating factor (PAF) contributes to a range of pathophysiological responses in severe illness. To examine PAF metabolism in acute malaria, venous blood was drawn from 10 untreated adults with falciparum malaria, from 8 with untreated vivax malaria, and from 10 controls. Plasma lyso-PAF, produced from PAF through the enzyme acetylhydrolase (AH), was bioassayed, after acetylation to PAF, by platelet [14C]-serotonin release. AH activity was measured by hydrolysis of [3H]-acetyl-PAF. Amounts of plasma lyso-PAF were lower in falciparum (median [range] 24 [9-221] ng/ml) and vivax (35 [7-236] ng/ml) infected patients than in controls (399 [212-504] ng/ml; P < 0.01), and correlated significantly with serum total and HDL-cholesterol (P < 0.001). Plasma AH activities were similar in the control, falciparum and vivax malaria groups. These data suggest that in malaria plasma lyso-PAF values fall together with other blood lipids, but independently of changes in AH activity. This may reflect a generalised decrease in lipid and phospholipid synthesis. However, the reduction of plasma lyso-PAF concentrations in our patients was much greater than that of serum lipoproteins. This is consistent with conversion of lyso-PAF to PAF or with increased PAF-receptor interactions. These two possibilities would have pathophysiological implications.

Acute Disease↗
PubMed1991

The lyso-precursor of platelet-activating factor (lyso-PAF) in ischaemic myocardium.

While it has been postulated that lyso-PAF and PAF might contribute to structural and functional damage in myocardial ischaemia, there has been no clear evidence for the accumulation of these bioactive compounds in ischaemic myocardium. In open chest, anaesthetised dogs, the proximal left anterior descending coronary artery was ligated and myocardial samples from the central ischaemic and normal areas assayed for lyso-PAF, free arachidonic acid and PLA2 activity. Ischaemic myocardium contained 50 +/- 29% (SD) more lyso-PAF than non-ischaemic myocardium after 20 min ischemia (P less than 0.002; N = 8) and 53 +/- 39% more after 60 min (P less than 0.01; N = 8) but there was no difference after 10 min (N = 8). Free arachidonic acid significantly increased in ischaemic myocardium after 60 min (122 +/- 136%; P less than 0.05) while no increase in PLA2 activity was found in-vitro. Since lyso-phospholipids themselves damage cell membranes and, additionally, lyso-PAF is the precursor of PAF which has potent effects on platelets, leukocytes and small vessels, the increase in lyso-PAF in ischaemic myocardium could contribute to myocardial damage.

Acetylation↗
PubMed1991

Release of platelet activating factor by the isolated kidney is not linked to the production of prostaglandins.

In many isolated tissues, including glomerular mesangial cells and endothelial cells, the synthesis of platelet activating factor (PAF) occurs by remodeling the phospholipids so that the production of PAF results in the release of arachidonic acid with subsequent production of cyclooxygenase or lipoxygenase products. In some tissues, including the renal medulla, another pathway for PAF biosynthesis (the de novo pathway) has been found in which the production of PAF is not linked to the production of arachidonic acid products. We tested the hypothesis that the remodeling pathway was active in the release of PAF into renal venous effluent of the isolated kidney. Isolated rat kidneys perfused at constant flow with albumin-containing buffer were stimulated to produce prostaglandin by an infusion of angiotensin II or bradykinin. Some kidneys were also challenged with the calcium ionophore A23187. Perfusate was collected for bioassay of PAF and radioimmunoassay of prostaglandin (PG) E2; urine was collected for PAF bioassay. Angiotensin II (10(-9) to 10(-8) M) increased renal vascular resistance, and bradykinin (10(-8) to 10(-7) M) and A23187 (3 x 10(-6) M) reduced renal vascular resistance. PGE2 production was increased significantly by bradykinin and angiotensin II but not by A23187. Only A23187 increased the release of PAF into the perfusate. Urine PAF was not changed by any of the stimuli. These data indicate that the release of PGE2 by the isolated, perfused rat kidney can be dissociated from the release of PAF. The findings support the suggestion that PAF released by the kidney into the renal venous effluent is not produced by remodeling the lipids that are the source of renally released prostaglandins.

Angiotensin II↗
PubMed1990

[Measurement of the power of artificial intraocular lenses].

Fifty five anterior chamber artificial lenses of the Hellgrebe model 2(35) and Fiodorov's (20) were verified from the angle of the power quoted by the producer. The measurement of the length of the frontal power were performed by means of a measurer 70 (Carl Zeiss, Jena, GDR) and by a specially designed plastic cuvette suitable for sterilization. The mean deviation amounted -1.42 dptr. for the Hellgrebe's 2 lens and 0.23 dptr. for Fiodorov's lens. The Hellgrebe type 2 lenses do not answer the international quality norms of tolerance +/- 0.25 dptr.

Anterior Chamber↗
PubMed1989

Plasma levels of the lyso-derivative of platelet-activating factor are related to age.

1. The effect of age on the plasma level of the lyso-derivative of platelet-activating factor (lyso-PAF) was studied in 72 normal subjects, (32 females, 40 males) aged 12-64 years. Lyso-PAF was acetylated in vitro to PAF which was measured by bioassay using 5-[14C]hydroxytryptamine-labelled rabbit platelets. 2. Under 40 years there were similar direct relations between plasma lyso-PAF and age in both sexes (linear regression; males, P less than 0.001; females, P less than 0.002), the level approximately doubling from the adolescent level around 100 ng/ml. However, in the later years the levels fell, the fall seeming to commence earlier in females, so that between 40 and 65 years the level was greater in males [169 +/- 47 (SD) vs 120 +/- 30 ng/ml; P less than 0.01]. 3. The increase in plasma lyso-PAF up to middle-age may be related to the reported increase in prostanoid production with age, since these platelet and vasoactive compounds can have a common origin in membrane phospholipid. This would be consistent with increasing phospholipase A2 activity and decreasing stability of cell membranes with age, but the later fall in lyso-PAF is then unexplained; the lesser values in females than males in the more advanced years could be related to females' generally lesser vascular disease. However, knowledge of the biological roles and metabolism of PAF is still very limited and the real significance of the findings remains to be determined.

Adolescent↗
PubMed1989

Whole blood aggregation, thromboxane release and the lyso derivative of platelet activating factor in myocardial infarction and unstable angina.

To investigate the pathophysiology of intracoronary thrombus formation we measured whole blood aggregation in response to ADP, platelet activating factor (PAF) and collagen, along with thromboxane B2 (TXB2) production during collagen induced aggregation, plasma TXB2 and plasma levels of lyso-PAF, in 38 subjects with and without ischaemic heart disease (12 with acute myocardial infarction, 9 with prolonged ischaemic chest pain without infarction and 17 normals). Lyso-PAF was measured, after in vitro acetylation to active PAF, by bioassay using 14C-serotonin labelled rabbit platelets. TXB2 was measured by radioimmunoassay. Plasma TXB2 was elevated at presentation only in patients with myocardial infarction (p less than 0.01). While impedance aggregation was similar in the three groups, aggregation to collagen resulted in greater release of TXB2 in subjects with myocardial infarction (p less than 0.01), an abnormality persisting 2-4 months later. Plasma lyso-PAF levels were significantly depressed throughout the first week in subjects with infarction (p less than 0.002), but after 2 to 4 months the level was greater than in normal subjects (p less than 0.001), changes presently unexplained. It is possible that the disorder of platelet function preceded and predisposed to coronary thrombosis. The findings strengthen the grounds for aspirin therapy in acute myocardial infarction.

Adenosine Diphosphate↗
PubMed1988

Time dependence of whole blood aggregation in response to platelet activating factor (PAF).

The aggregation/adhesion response to platelet activating factor (PAF) was studied in diluted whole blood by impedance aggregometry. The extent of aggregation varied directly with the interval between blood sampling and aggregation measurement over the first 30 minutes from sampling, then remained stable for the next 60 minutes of observation. This is an effect opposite to that described for aggregation to PAF in platelet rich plasma which, however, cannot be studied soon after sampling. Time dependence of aggregation is important and comparative measurements should be made during the period of stable aggregability.

Humans↗
PubMed1987

Whole blood platelet aggregation is not affected by cigarette smoking but is sex-related.

1. In normal subjects, 18-49 years old, the effects of the smoking habit (greater than 10 cigarettes/day) and the act of smoking two cigarettes over 10 min were studied on whole blood platelet aggregation (in vitro impedance method). 2. Acute smoking (n = 10) did not affect platelet aggregation to ADP, collagen or to platelet activating factor (PAF) nor thromboxane B2 production during aggregation. There was no difference between smokers (n = 13) and non-smokers (n = 10). However, aggregation to all aggregants was greater in females (n = 11) than males (n = 12) (ADP and collagen, P less than 0.001; PAF, P less than 0.01; ANOVA). 3. Although others have obtained diverse results studying platelet-rich plasma, the absence of an effect of cigarette smoking on whole blood platelet aggregation is consistent with many of those observations. Greater in vitro aggregability in females than males is consistent with the few studies of platelet-rich plasma. It seems unlikely that the role of cigarette smoking as a risk factor for ischaemic heart disease is related to a direct effect on platelet aggregability.

Adenosine Diphosphate↗
PubMed1981

Characterisation of viral RNA in cells infected with the murine coronavirus JHM.

The murine coronavirus JHM induces in Sac(-) cells seven major and two minor RNA species. These RNAs are polyadenylated and single stranded. Their sizes were estimated by electrophoresis in agarose gels containing methylmercury hydroxide. The mol. wts. for the major species are 6.67 x 10(6) for RNA of genome size, 3.42 x 10(6) for RNA 2, 2.76 x 10(6) for RNA 3, 1.35 x 10(6) for RNA 4, 1.19 x 10(6) for RNA 5, 0.93 x 10(6) for RNA 6 and 0.62 x 10(6) for RNA 7. The minor species have a size of 4.7 x 10(6) (RNA a) and 1.5 x 10(6) (RNA b). No essential difference in the number and proportion of each RNA species was found between total cytoplasmic RNA, polyadenylated cytoplasmic RNA and RNA extracted from pelleted polysomes, nor was any difference found during the infection cycle. The major RNA species are likely to be subgenomic mRNAs.

Animals↗