PubMed Health⌕ Search

Biomedical subjects

Peter Betz

Publications and source records attributed to Peter Betz.

5 recordsLinked to original sources

Evaluation of the effect of oral verapamil on clinical outcome and angiographic restenosis after percutaneous coronary intervention: the randomized, double-blind, placebo-controlled, multicenter Verapamil Slow-Release for Prevention of Cardiovascular Events After Angioplasty (VESPA) Trial.

OBJECTIVES: We investigated the effect of oral verapamil on clinical outcome and angiographic restenosis after percutaneous coronary intervention (PCI). BACKGROUND: Thus far, there is no established systemic pharmacologic approach for the prevention of restenosis after PCIs. Five small studies reported encouraging results for calcium channel blockers. METHODS: Our randomized double-blind trial included 700 consecutive patients with successful PCI of a native coronary artery. Patients received the calcium channel blocker verapamil, 240 mg twice daily for six months, or placebo. Primary clinical end point was the composite rate of death, myocardial infarction, and target vessel revascularization (TVR) during one-year follow-up; the angiographic end point was late lumen loss at the six-month follow-up angiography. RESULTS: We obtained complete clinical follow-up in 95% of the patients, and scheduled angiography was performed in 94%. The proportion of patients treated with stents was 83%. The primary clinical end point was reached in 67 (19.3%) patients on verapamil and in 103 (29.3%) patients on placebo (relative risk [RR] 0.66 [95% confidence interval (CI) 0.48 to 0.89]; p = 0.002). This difference between the groups was driven by TVR (17.5% with verapamil vs. 26.2% with placebo; RR 0.67 [95% CI 0.49 to 0.93]; p = 0.006). Late lumen loss was 0.74 +/- 0.70 mm with verapamil and 0.81 +/- 0.75 mm with placebo (p = 0.11). Compared with placebo, verapamil reduced the rate of restenosis > or =75% (7.8% vs. 13.7%; RR 0.57 [95% CI 0.35 to 0.92]; p = 0.014). CONCLUSIONS: Verapamil compared with placebo improves long-term clinical outcome after PCI of native coronary arteries by reducing the need for TVR. This was caused by a reduction in the rate of high-grade restenosis.

Administration, Oral↗

Influence of lung fixation technique on the state of alveolar expansion-a histomorphometrical study.

Lungs removed at necropsy normally collapse due to the loss of negative pleural pressure leading to a quite unnatural appearance of both gross and histological specimens. In order to demonstrate the influence of post-mortem lung retraction on the degree of alveolar expansion, a histomorphometrical analysis was performed in lungs from a 9-month-old healthy infant. Tissue specimens from the right lung were obtained at autopsy and routinely fixed after retraction ('routinely fixed lung'), whereas the left lung was fixed in situ before opening the thoracic cage ('in situ fixed lung'). The size of the alveoli as well as the thickness of the alveolar walls were measured using an automatic image processing and analysis system (Leica QWIN) in both lungs. The mean alveolar size was 8.7 x 10(3) microm(2) in the routinely fixed lung (alveoli, n=1.1576) and 10.9 x 10(3) microm(2) in the in situ fixed lung (alveoli, n = 841). In contrast, the diameter of the alveolar walls showed no significant difference in both lungs. The average thickness of the alveolar walls was 7.9 microm (measuring sites, n = 1.190) in the routinely fixed lung and 8.1 microm in the in situ fixed lung (measuring sites, n = 1.027), respectively. The results provide evidence of significantly reduced aeration in the retracted and routinely fixed lung which could be of special forensic interest in cases of suspicious infanticide, stillbirth or infant death by drowning or suffocation.

Forensic Medicine↗

Clostridium fallax associated with sudden death in a 16-year-old boy.

Clostridial myonecrosis or gas gangrene occurs most frequently in contaminated wounds following trauma or surgery. It is caused by a wide variety of Clostridium species, the most common being Clostridium perfringens. Spontaneous, non-traumatic clostridial myonecrosis is uncommon and is usually associated with gastrointestinal and haematological malignancy, diabetes mellitus and peripheral vascular disease. The case of a previously healthy 16-year-old boy with acute onset of gastrointestinal symptoms, who died of bacterial sepsis without apparent preceding trauma, is presented here. Clostridium fallax was identified as the most probable causative agent. As far as is known, this is the first report of fatal sepsis in humans due to C. fallax, which has been described only rarely as a cause of gas oedema in animals.

Adolescent↗

Lethal cyanide inhalation with post-mortem trans-cutaneous cyanide diffusion.

A 27-year-old worker in a metal processing factory was found dead in a basin, sitting in a solution containing potassium dicyano argentate, potassium cyanide, master batch and brightener 'Elfit 73'. The worker was wearing an acid-resisting overall, rubber boots and a simple dust respirator. While the cyanide concentration in the stomach contents was only 0.05 microg/ml, it was 7.7 microg/g in the lung tissue, 6.3 microg/ml in the heart blood and 31 microg/ml in the femoral vein blood. The different concentrations suggest an initial lethal inhalation of cyanide and an extensive post-mortem diffusion of cyanide through primarily non-injured skin of buttocks and legs. The possibility of a post-mortem cyanide diffusion bars from concluding a vital sign from a high cyanide concentration in a blood sample of one single body site.

Adult↗

The course of MIB-1 expression by cerebral macrophages following human brain injury.

The course of MIB-1 expression by brain macrophages adjacent to cortical contusions has been immunohistochemically investigated during the first 30 weeks after human brain injury, in order to provide data for a forensic wound age estimation. A positive nuclear staining for MIB-1 could be observed earliest after a postinfliction interval of 3 days and regularly in cases with a survival time between 7 and 14 days, whereas in uninjured brain tissue (control group) no cellular MIB-1 reactivity was visible.

Journal Article↗