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Biomedical subjects

J Kaliman

Publications and source records attributed to J Kaliman.

At least 37 records · Page 2Linked to original sources
PubMed1988

[Return to work following myocardial infarct].

The aim of this retrospective study involving 471 patients was to investigate the percentage of patients who returned to work after acute myocardial infarction. In the group of 350 patients who did not undergo subsequent aortocoronary bypass operation 70% returned to work, whereby half of these patients started work again within 6 months after infarction. A significantly higher number of patients who were enrolled in a cardiac rehabilitation programme returned to work as compared with patients not participating in such a programme (72% vs. 59%, respectively; p less than 0.04). There was, however, no difference between these 2 groups with respect to either the time point of resumption of work after myocardial infarction or the duration of employment between infarction and eventual retirement. Of the 121 patients who underwent an aortocoronary bypass operation, only 38% returned to work (p less than 0.001 vs. patients without bypass surgery).

Coronary Artery Bypass↗
PubMed1988

Comparable effect of prostaglandin E1 in decreasing in vivo platelet deposition on human lesion sites after intravenous and intraarterial application.

It had been claimed that prostaglandin E1 is degraded during first lung passage to a major extent. Clinical results, however, as well as various platelet function tests and coagulation parameters revealed no apparent difference after i.v. and i.a. infusion. Thus, we examined the question what the quantitative difference between i.v. and i.a. PGE1-application would be upon in-vivo platelet function assessed by platelet uptake over active lesion sites as well as platelet half-life monitoring after autologous 111-In-oxine platelet labelling. In patients suffering from peripheral vascular disease stage II according to Fontaine PGE1 was able to decrease platelet uptake after i.v. and i.a. therapy to a comparable extent; similarily, a significant prolongation in platelet half-life was noted, again revealing no difference. As the decrease in platelet uptake is assumed to be predominantly a vascular effect, it is hypothetized that more stable derivatives of PGE1 are active, counterbalancing a lower biological activity with a longer half-life.

Alprostadil↗
PubMed1988

Diminished platelet residence time on active human atherosclerotic lesions in-vivo--evidence for an optimal dose of aspirin?

Although aspirin is an old drug, its optimal dose for the treatment of human atherosclerosis has not been finally proven. Various in-vitro and ex-vivo platelet function tests revealed a dose range from 1 to 3000 mg as being optimal. It was thus the goal to examine its in-vivo efficacy in human suffering from peripheral vascular disease in 7 different doses ranging from 1 mg to 1000 mg a day. All these patients have been treated for 3 months. Platelet half-life and platelet uptake ratio show an in part significant improvement being most pronounced at the daily doses of 20 and 1000 mg respectively. No change occurs in the placebo treated controls. These findings indicate, that 20 or 1000 mg aspirin taken daily per os, are superior to the other doses examined concerning the in-vivo platelet function (as measured by platelet half-life) and rendering the arterial surface less thrombogenic (as reflected by platelet uptake ratio-measurements).

Administration, Oral↗
PubMed1988

Epoprostenol in patients with Raynaud's disease.

Prostaglandin metabolism and the clinical effect of epoprostenol (prostacyclin, PGI2) infusions were studied in thirteen patients with Raynaud's disease. Epoprostenol was infused at 5 ng/kg/min for six hours daily for two consecutive five day periods, separated by a two day interval. No beneficial effects either during or after infusion could be detected in terms of frequency of severity of attacks or on skin temperature measurement. Raynaud's patients had significantly lower serum thromboxane B2 levels than normal controls though plasma levels of thromboxane B2, 6-oxo-PGF1 and the bicyclic metabolite of PGE2 did not differ between the two groups. Platelets from Raynaud's patients had a significantly lower conversion rate of arachidonic acid into thromboxane B2 and HHT and a significantly higher rate of HETE production than platelets from controls.

6-Ketoprostaglandin F1 alpha↗
PubMed1988

Survival rate and causes of death in patients with pacemakers: dependence on symptoms leading to pacemaker implantation.

The survival rate of 2256 patients with pacemakers was analyzed. Patients paced for Adams-Stokes equivalents (e.g. dizziness) showed a significantly better survival rate than did patients with pacemakers implanted for Adam-Stokes attacks or heart failure (P less than 0.0001). The estimated survival of the latter two groups did not differ significantly. Of the deceased patients who had received a pacemaker for the treatment of heart failure, 54% died due to this condition despite pacemaker implantation. The relative percentage of cases of sudden death after pacemaker implantation was high in the groups with Adams-Stokes attacks (12%) and Adams-Stokes equivalents (13%). In patients paced for Adams-Stokes attacks, sudden death occurred more frequently in the first year after pacemaker implantation (P less than 0.015) than during the following years. Therefore, increased efforts should be made to monitor patients carefully after pacemaker implantation to enable prompt detection of malignant tachyarrhythmias, probably the cause of sudden death in a substantial number of patients with pacemakers.

Adams-Stokes Syndrome↗
PubMed1988

Rate dependent depression of subsidiary ventricular impulse formation--cause of Stokes-Adams attacks in a patient with rate modulated pacing.

Following His bundle ablation and implantation of a rate adaptive pacemaker (Vitatron TX 911) a 52-year-old gentleman experienced several presyncopal attacks while driving a car. On examination pectoralis muscle contraction caused temporary pacemaker inhibition. Incremental overdrive stimulation demonstrated progressive depression idioventricular automaticity and was associated with similar symptoms following overdrive at high pacing rates. Following appropriate pacemaker programming the patient remained symptom free.

Adams-Stokes Syndrome↗
PubMed1988

Subsidiary pacemaker function in complete heart block after His-bundle ablation.

To investigate the electrophysiological properties of ventricular impulse formation after His-bundle ablation in 11 patients, incremental ventricular overdrive stimulation studies were performed. The studies, which were spread over a follow-up period of up to 601 days, were carried out invasively with temporary leads as well as noninvasively with the implanted pacemakers and chest wall inhibition. The overdrive pacing rate was increased in steps of 10 beats/min, and the pacing duration was 2 minutes at each level. Ten out of 11 patients had a reliable ventricular escape rhythm; in the remaining patient, consistently no subsidiary pacemaker function was observed up to 10 seconds. In 83% of the studies, incremental ventricular overdrive stimulation caused progressive suppression of ventricular impulse formation with exponential increase in ventricular recovery time and progressive postrecovery subsidiary pacemaker depression. In the remaining 17%, ventricular recovery time showed a heterogeneous response to overdrive stimulation--as possible cause alterations in the sympathetic tone and limitations attributable to the method used are discussed. The results of this study demonstrate a rate-dependent overdrive suppression of subsidiary ventricular pacemaker tissue. This can be of clinical importance in patients with complete heart block and rate-adaptive pacemakers because sudden pacemaker failure or temporary pacemaker inhibition at high stimulation rates may cause Stokes-Adams attacks not reproducible at lower pacing rates.

Aged↗
PubMed1988

In vivo modulation of platelet deposition on human atherosclerotic lesions by various antiaggregatory prostaglandins.

The influence of intravenous infusions of various prostaglandins on in vivo platelet function was studied after labelling of autologous platelets with 100 mu ci 111 indium-oxinesulfate in patients with peripheral vascular disease stage II according to FONTAINE. PGI2 (5 ng/kg/min) provoked a significant decrease of platelet deposition and a prolongation in platelet half-life time (74 +/- 6 vs 68 +/- 5 hours). PGE1 (25 ng/kg/min) failed to influence platelet deposition, but prolonged significantly platelet half-life time (82 +/- 6 vs 76 +/- 8 hours). CG 4203 (25 ng/kg/min) decreased significantly platelet deposition and prolonged significantly platelet half-life time (73 +/- 10 vs 67 +/- 11 hours). Iloprost (1 and 2 ng/kg/min) reduced significantly platelet deposition without dose relation. Half-life time was increased significantly after therapy compared to placebo (1 ng: 76 +/- 7 vs 69 +/- 7; 2 ng: 73 +/- 9 vs 67 +/- 9 hours).

Aged↗
PubMed1987

Exercise testing after surgical repair of coarctation of the aorta.

After repair of coarctation, exercise testing was performed in 20 patients with an isolated coarctation (group I) and in 26 with additional congenital cardiac malformations (group II). Ages at time of operation were significantly different in both groups (7.9 +/- 6.0 years in group I; 4.6 +/- 3.8 years in group II; p less than or equal to 0.01). Simultaneous blood pressures were obtained from upper and lower limbs at rest and after exercise. There was no significant difference regarding the systolic blood pressures at rest (122.5 +/- 15.6 mmHg in group I versus 119 +/- 15.8 mmHg in group II). Seven (14%) of the patients were hypertensive; five of them had blood pressure gradients between arms and legs of 15-45 mmHg. But the gradients at rest were found to be significantly different in both groups (9.0 +/- 10.5 mmHg in group I; 18.5 +/- 16.1 mmHg in group II; p less than or equal to 0.05). Six patients, all in group II, had gradients greater than or equal to 30 mmHg at rest. After exercise there were no significant differences in systolic blood pressure and gradients in both groups. Values for blood pressures and gradients at rest and after exercise showed a positive correlation (blood pressure r = 0.76, p less than or equal to 0.001; gradient r = 0.44, p less than or equal to 0.01). Thus exercise testing can provide valuable information about blood pressure and gradient changes during physical activity, but angiography is required to reveal restenosis or residual stenosis.

Adolescent↗
PubMed1987

Prostaglandin I2 during radiolabelling improves recovery, but does not change platelet half-life and platelet uptake over active human lesion sites.

The fact that prostacyclin is able to preserve platelets in-vitro stimulated the question whether platelets being treated in presence of prostacyclin might behave different after reinjection in human. We therefore studied the effect of synthetic PG12 in-vitro, being added immediately after blood sampling. It is demonstrated that the presence of prostacyclin does not change the labelling efficiency and in-vitro viability beside the alterations induced by this compound itself, however, it results in a significantly improved recovery. Furthermore, the platelet half-life in the patients as well as the deposition of the radiolabelled platelets on active human atherosclerotic lesions does not seem to be affected. Thus, the addition of PGI2-improves cellular viability during the preparation without negatively interfering with the in-vitro and in-vivo results later on. Thus, the use of PGI2 can be strongly recommended.

Aged↗
PubMed1987

Prostaglandin I2 reduces activation of human arterial smooth muscle cells in-vivo.

Patients suffering from peripheral vascular disease have been "ultima ratio"-treated with PGI2 at a rate of 5 ng/kg/min for 6 hours a day and 5 consecutive days i.v. 20 of them underwent surgery thereafter as therapy was not sufficient. A histological examination and quantification of vascular tissue revealed that the number of activated smooth muscle cells was significantly lower in treated patients vascular segments than in untreated ones in all the different age groups. A comparable suppression was found in the intima and the media as well. It is thus concluded, that PGI2 inhibits smooth muscle cell proliferation most probably by inhibiting PDGF-release from the platelets and stimulation of smooth muscle cell cAMP. To achieve a more beneficial PGI2-effect at the vascular level, a prolonged PGI2-therapy looks rather promising.

Arteries↗
PubMed1987

Prostacyclin synthesis stimulating plasma factor in patients with peripheral vascular disease.

Human plasma contains a factor capable of stimulating vascular prostacyclin generation even in atherosclerotic vessels with minimal in-vitro capacity for PGI2-synthesis. The activity of this prostacyclin stimulating plasma factor (PSPF) has been reported to be elevated in renal failure and hepatic coma. We are not aware of any data as to whether this PSPF plays a role in maintaining hemostatic balance in patients with peripheral vascular lesions. Therefore, we examined 62 patients with peripheral vascular disease (PVD). This study group was subdivided into normo- and hyperlipemic subjects, patients with and without maturity onset diabetes, and plasma beta-thromboglobulin levels higher and lower than 50 ng/ml. 10 healthy sex and age matched persons served as controls. Vascular prostacyclin formation was studied in vitro after incubation of the patients' plasma and a buffer control with various tissue samples (human femoral artery, rat abdominal and thoracic aorta of healthy and of streptozotocin induced diabetic animals, swine endothelial layer and remaining tissue (media and adventitia) and cultured endothelial (EC) and smooth muscle cells (SMC) of minipig arota. In addition, 6-oxo-PFG1 alpha formation by cultured EC and SMC (minipig aorta source) after incubation with tris HCl-buffer or plasma were estimated by means of specific radioimmunoassays. In general, tissue samples and cells incubated in plasma exhibit a marked increase of in-vitro PGI2-formation as compared to buffer. No difference could be found between PSPF of CHD-patients and healthy controls. Similar findings were obtained using incubated vascular tissue and cultured cells by means of the bioassay and specific RIA, respectively. These findings indicate that the PSPF does not seem to be of any clinical relevance in hemostatic regulation in patients with advanced atherosclerosis.

Adult↗