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Biomedical subjects

P Kirstein

Publications and source records attributed to P Kirstein.

10 recordsLinked to original sources
PubMed1999

A randomized controlled clinical trial comparing ventricular fibrillation detection time between two transvenous defibrillator models. The Acute Ventak AV investigator group.

The Ventak AV is an implantable cardioverter defibrillator with dual chamber pacing capability. Features include detection and treatment of ventricular arrhythmias, detection of atrial arrhythmias, as well as dual chamber pacing. The objective of the investigation was to verify the efficacy of the Ventak AV in detecting ventricular fibrillation in the presence of dual chamber pacing. Thirty-three patients, who were to receive an implantable defibrillator were randomized (1:1) in a paired comparison study to the Ventak AV (study device) and the Ventak Mini (control) during defibrillation threshold testing. In order to create a "worst case scenario" for sensing of ventricular fibrillation, pacing was performed at high lower rate limit values (Ventak AV DDD pacing at 150/min, Ventak Mini at VVI 100/min). Ventricularfibrillation was induced and the randomized device was allowed to detect and treat the arrhythmia. This test was repeated for each patient using the alternate device in a randomized order, such that all patients were tested with both devices. The mean ventricular fibrillation detection time for the Ventak AV was 2.0+/-0.11 seconds and for the control device the detection time was 1.8+/-0.11 seconds (P = 0.26). Appropriate tachyarrhythmia therapy decision was documented in all episodes for both devices. The study patient population demonstrated equivalent ventricular fibrillation detection time between the Ventak AV and the Ventak Mini. The Ventak AV demonstrated effectiveness in detecting ventricular fibrillation in the presence of high rate dual chamber pacing.

Adult↗
PubMed1990

Effects of nicotinic acid on serum cholesterol concentrations of high density lipoprotein subfractions HDL2 and HDL3 in hyperlipoproteinaemia.

Nicotinic acid was given in a 4-g daily dose for 6 weeks to 41 weight-stable patients of mean age (+/- SD) 52 +/- 9 years, with type IIa, type IIb or type IV hyperlipoproteinaemia (HLP), in order to study its effects on serum cholesterol concentrations of high density lipoprotein (HDL) subfractions HDL2 and HDL3. The triglyceride and cholesterol levels of serum very low density (VLDL) and low density (LDL) lipoproteins decreased during treatment (P less than 0.001). Serum HDL and HDL2 cholesterol levels increased by 37% and 135%, respectively. These changes were positively correlated (r = 0.93; P less than 0.001). There was no significant change in mean serum HDL3 cholesterol concentration. A negative correlation existed between changes in HDL3 and HDL2 cholesterol levels (r = -0.54; P less than 0.001). Multiple stepwise linear regression analyses revealed that the initial HDL3 cholesterol predicted more than 30% of the increase in HDL2 cholesterol. Changes in the concentrations of HDL2 and HDL3 cholesterol after 6 weeks of drug treatment were not related to the type of HLP, neither were these effects of nicotinic acid correlated with changes in VLDL or LDL lipid levels. The concept has previously been proposed, on the basis of in vitro data, that HDL2 is formed from HDL3 particles in the blood. Our results suggest that, in man, this reaction is stimulated in vivo by prolonged nicotinic acid therapy.

Adult↗
PubMed1984

Relationship between lipoproteins including HDL subfractions and the intravenous fat tolerance test.

There is a positive relationship between the HDL cholesterol concentration and the fractional removal rate k2 of intravenously administered Intralipid, the intravenous fat tolerance test (IVFTT). This relationship was analysed in 22 female and 20 male healthy normolipoproteinaemic volunteers with regard to HDL subfractions. A positive correlation between the IVFTT k2 value and HDL cholesterol (r = 0.40, P less than 0.05) was confirmed. The k2-HDL2 cholesterol relationship was strong and positive (r = 0.56, P less than 0.001), whereas the correlation between HDL3 cholesterol and k2 was negative (r = -0.37, P less than 0.05). These findings extend other observations indicating that HDL2 seems to be the HDL fraction, directly associated with removal of TG-rich particles from the circulation.

Adult↗
PubMed1984

Lipoprotein abnormalities in patients with early primary biliary cirrhosis.

In twelve females with early forms of primary biliary cirrhosis (PBC) serum lipoproteins, the intravenous fat tolerance test ( IVFTT ) and the lecithin: cholesterol acyl transferase (LCAT) rate were determined and compared to healthy controls. The cholestatic LDL (LP-X) test was negative in all cases. PBC patients had lower very low density lipoprotein TG concentrations than controls and had levels of (high-density lipoprotein) HDL-TG, -cholesterol and -phospholipids that were about 50% higher than in controls. In PBC the HDL2-cholesterol concentration was double but the HDL3-cholesterol concentration was 60% of control values (P less than 0.001 for both). The LCAT rate and the IVFTT value did not differ between the groups. A typical finding on agarose gel electrophoresis was the appearance of a slow-moving alpha-band. Several interpretations of these results are possible. In PBC the hepatic lipase activity may be impaired leading to a shift of the HDL2/HDL3 relation. The transport of HDL2 to the liver lipase site may also be affected and HDL3 production reduced due to malabsorption in the intestine.

Adult↗
PubMed1981

Determination of the cholesterol content of high density lipoprotein subfractions HDL2 and HDL3, without contamination of Lp(a), in human plasma.

A method for the determination of the cholesterol content of human plasma high density lipoprotein (HDL) subfractions HDL2 and HDL3 is presented. The method is based on one preparative ultracentrifugal spin at density 1.125 to obtain HDL3 and heparin/manganese precipitation to obtain total HDL. From this spin in a fixed angle rotor at density 1.125 HDL3 is obtained as a bottom fraction in which cholesterol is determined. The total HDL cholesterol concentration is determined in the supernatant of the heparin/manganese precipitation of VLDL-free serum. HDL2 cholesterol is calculated as the difference between total HDL and HDL3 cholesterol. One of the advantages of this method is that falsely high HDL2 cholesterol levels due to incorporation of LP(a) containing B-protein in the HDL2 fraction is avoided. Some validation of the 1.125-spin is given. Results are presented from small samples of normal of both sexes as well as men with different kinds of hyperlipoproteinaemia.

Cholesterol↗
PubMed1981

Changes in high density lipoprotein subfractions and other lipoproteins by exercise.

Seventeen previously sedentary men (aged 30-45) were exercised approximately twice weekly over a 10-week period during which time there was a significant fall in low density lipoprotein cholesterol, but total high density lipoprotein (HDL) did not change. The subfraction HDL2 showed an initial fall at two weeks of training with a subsequent rise above the baseline by 10 weeks. HDL3 cholesterol tended to change in an opposite direction to HDL2 thus accounting for no significant change in total HDL cholesterol. Smoking or drinking habits did not change throughout the study. As body weights did not change significantly through the study, energy intake must have increased with probable increased very low density lipoprotein (VLDL) production. Loss of apoprotein C-peptides from HDL2 associated with activation of lipoprotein lipase, and clearance of VLDL, could have caused redistribution of C-apoproteins between HDL3 leading to the changes seen, with the establishment of a new equilibrium with continued training by 10 weeks.

Adult↗
PubMed1980

Antiaggregatory, physiological and clinical effects of ticlopidine in subjects with peripheral atherosclerosis.

Twelve patients with varying degrees of peripheral atherosclerotic disease were given an antiaggregatory drug, ticlopidine [5-(6-chlorobenzyl)-4,5,6,7-tetrahydrothieno-(3,2-C)-pyridine HCl] in a single blind trial for one or four months and the effects on platelet aggregation, blood coagulation, marcro- and micro-circulation and walking distance were studied. Two patients were excluded; one because of nausea attributable to the drug, one because of lack of co-operation. No statistically significant changes in circulation parameters or walking distance were noted. No changes were observed in APT-time, thrombine- and Reptilase-clotting time, platelet counts, concentrations of fibrinogen and fibrinopeptide A in plasma or serum antithrombin activity. The mean concentration of fibrinopeptide A was slightly increased in all patients. ADP-induced aggregation was inhibited in all patients. Aggregation induced by arachidonic acid was partially inhibited but not abolished in all patients. Prostaglandin G2-induced aggregation was not altered by ticlopidine but collagen-induced aggregation was inhibited. Ticlopidine, in contrast to acetyl-salicylic acid, inhibits the primary aggregation but also seems to interfere with the release action. Treatment of larger patient groups for longer periods are necessary to determine the clinical usefulness of ticlopidine.

Adenosine Diphosphate↗