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Stefan Kluge, Hans Jörg Baumann, Jan Regelsberger, Uwe Kehler, Jan Gliemroth, Barbara Koziej, Hans Klose and Andreas Meyer

Object

Ventriculoatrial (VA) shunts inserted for the treatment of hydrocephalus are known to be a risk factor for pulmonary hypertension. The aim of this study was to evaluate the incidence of pulmonary hypertension among adult patients with VA shunts.

Methods

All patients who had received a VA shunt at one of two institutions between 1985 and 2000 were invited for a cardiopulmonary evaluation. The investigation included a thorough history taking, clinical examination, echocardiography, and pulmonary function testing including diffusing capacity of the lung for carbon monoxide (DLCO). Pulmonary hypertension was defined as systolic pulmonary artery pressure > 35 mm Hg at rest.

Results

The study group consisted of 86 patients, of whom 38 (44%) could be examined. The patients' mean age was 47.1 ± 18.4 years; the median interval between shunt insertion and cardiopulmonary evaluation was 15 years (range 5–20 years). Of the 38 patients, 20 (53%) had Doppler velocity profiles of tricuspid regurgitation that were adequate for the estimation of pulmonary artery systolic pressure. Doppler-defined pulmonary hypertension was observed in 3 patients (8%), 2 of whom underwent right heart catheterization. Chronic thromboembolic pulmonary hypertension was confirmed in both patients, and medical therapy, including anticoagulation, was started. The VA shunt was removed in both cases and replaced with a different type of device. Pulmonary function tests revealed a restrictive pattern in 15% and typical obstructive findings in 9% of patients. In 30% of patients the DLCO was less than 80% of predicted, and blood gas analysis showed hypoxemia in 6% of patients. No significant differences in pulmonary function tests were noted between the patients with and without echocardiographic evidence of pulmonary hypertension. However, patients with pulmonary hypertension had significantly lower DLCO values.

Conclusions

The authors detected pulmonary hypertension by using Doppler echocardiography in a significant proportion of patients with VA shunts. It is therefore recommended that practitioners perform regular echocardiography and pulmonary function tests, including single-breath DLCO in these patients to screen for pulmonary hypertension to prevent hazardous late cardiopulmonary complications.

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Peter Vajkoczy, Bernhard Meyer, Stefan Weidauer, Andreas Raabe, Claudius Thome, Florian Ringel, Volker Breu, Peter Schmiedek and the other Study Participants

Objective

The goal of this study was to investigate the safety and tolerability of the novel endothelin A (ETA) receptor antagonist clazosentan in patients with subarachnoid hemorrhage (SAH) and its potential to reduce the incidence and severity of cerebral vasospasm following surgical clipping of the aneurysm.

Methods

This Phase IIa multicenter study had two parts: a double-blind, randomized Part A (some patients given clazosentan [0.2 mg/kg/hr] and others given placebo), in which statistical inference was performed, and an open-label Part B (patients with established vasospasm given clazosentan [0.4 mg/kg/hr for 12 hours followed by 0.2 mg/kg/hr]) for exploratory purposes only. Primary end points were the incidence and severity of angiographic vasospasm on Day 8 after SAH and the safety and tolerability of the drug.

Thirty-four patients (Hunt and Hess Grades III and IV and Fisher Grade ≥3) were recruited and 32 (15 in the clazosentan group and 17 in the placebo group) were retained in the intent-to-treat population; 19 patients entered Part B. In Part A, treatment with clazosentan resulted in a reduced incidence of angiographically evident cerebral vasospasm (40% compared with 88% of patients, p = 0.008). In addition, the severity of vasospasm was reduced in the clazosentan group (p = 0.012). In Part B of the study, in 50% of assessable patients who were initially treated with placebo reversal of vasospasm was observed following the initiation of clazosentan therapy. The incidence of new infarctions was 15% in the clazosentan group and 44% in the placebo group (p = 0.130). There was no adverse event pattern indicating a specific organ toxicity of clazosentan.

Conclusions

This study indicates that clazosentan reduces the frequency and severity of cerebral vasospasm following severe aneurysmal SAH with the incidence and severity of adverse events comparable to that of placebo.

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Oral Presentations

2010 AANS Annual Meeting Philadelphia, Pennsylvania May 1–5, 2010