Stent impact on the geometry of the carotid bifurcation and the course of the internal carotid artery.

A measurement system is proposed to evaluate reconstructive effects of carotid stents on the geometry of the carotid bifurcation and the course of the internal carotid artery. To describe deviations of the stenotic internal carotid artery (ICA) from the extended axis of the common carotid artery (CCA) the CCA-ICA angle is measured between the CCA midaxis and the midaxis of the stenotic ICA segment. Maximal extensions of ICA tortuosities perpendicular to the course of the CCA axis are defined as ICA offset. The measurements were applied to DSA images of 224 carotid stenoses to evaluate variation and correlation between the two parameters. Comparative pre- and post-stent evaluation was performed in two series of 55 and 31 carotid stenoses treated with Wallstents and in a historic control group of 35 stenoses treated with Strecker stents. Straight course of the ICA was associated with low angle and low offset values, whereas tortuous course of the ICA showed larger angle and offset. A moderate linear correlation between the two parameters was found. Corresponding to a straightening of the stented segment, Wallstents reduced mean angle and offset values significantly. In five cases of the second series of Wallstents, transferrals of curves above the distal stent end associated with kinks were observed, and offset remained constant or increased. Strecker stent implantation caused no significant changes of bifurcational geometry. The proposed parameters corresponded to visual aspects of ICA tortuosity and detected reconstructive effects of self-expanding Wallstents on the ICA course. The measurement system may provide a basis for geometric evaluation of different stent types or implantation concepts with the aim: to optimize anatomic recanalization results in tortuous high angle-high offset bifurcations.

Review of medical prevention of vasospasm after aneurysmal subarachnoid hemorrhage: a problem of neurointensive care.

Cerebral vasospasm remains a devastating medical complication of aneurysmal subarachnoid hemorrhage (SAH). It is associated with high morbidity and mortality rates, even after the aneurysm has been secured surgically or radiologically. A great deal of experimental and clinical research has been conducted in an effort to find ways to prevent this complication. The literature includes extensive coverage of in vivo animal model studies of SAH and vasospasm. These experimental studies have contributed to tremendous advances in the understanding of the mechanisms leading to cerebral vasospasm. Most of the experimental settings, however, have demonstrated varying levels of ability to predict accurately what occurs in human SAH. Therefore, although animal models have been developed to test new therapies, most of the treatment effects have been shown to be less compelling when trials have been conducted in clinical settings. The interpretation of current literature is complicated further by the imprecise estimation of the incidence of cerebral vasospasm, which is due to various degrees of clinical expression, ranging from the absence of symptoms in the presence of increased blood flow velocities at transcranial Doppler or vessel diameter reduction at angiography to neurological manifestations of severe ischemic deficits. In addition, a change over time in the incidence pattern of human SAH and vasospasm, possibly related to improved surgical techniques and overall patient management, may have occurred. This topic review collects the relevant literature on clinical trials investigating prophylactic therapies for cerebral vasospasm in patients with aneurysmal SAH and emphasizes the need for large clinical trials to confirm the results derived from clinical experience. In addition, it points out some experimental therapies that may hold promise in future clinical trials to prevent the occurrence of vasospasm.

Intravenous amiodarone or magnesium sulphate is not cost-beneficial prophylaxis for atrial fibrillation after coronary artery bypass surgery.

Our aims were to examine whether the administration of amiodarone or magnesium sulphate after coronary artery bypass graft surgery (CABG) could reduce the occurrence of atrial fibrillation, and to identify the risk factors associated with atrial fibrillation after CABG. Patients scheduled for elective CABG (n = 155) were allocated randomly, in a controlled double-blind study, to receive immediately after surgery a 72-h infusion of amiodarone (900 mg per 24 h), magnesium (4 g per 24 h) or placebo (0.9% NaCl; 50 ml per 24 h) intravenously. A 72-h Holter ECG was recorded concomitantly. The primary end-point was the prevention of atrial fibrillation; its onset was considered as prophylactic failure. An interim safety analysis was performed in 147 patients. The cumulative occurrence of atrial fibrillation was 27% in the placebo group, 14% in the amiodarone group (P = 0.14) and 23% in the magnesium group (P = 0.82). Although amiodarone delayed the onset of the first tachyarrhythmic episode (P = 0.02), it was associated with the need for longer periods of vasoactive drug infusion and invasive monitoring and a longer stay in the intensive care unit. Variables associated with the onset of atrial fibrillation were older age (odds ratio 1.9) and a plasma magnesium concentration at 24 h of less than 0.95 mmol litre-1 (odds ratio 6.7). Postoperative administration of amiodarone reduced the occurrence of atrial fibrillation after elective CABG surgery, but was associated with a longer duration of cardiovascular instability and longer need for intensive care; magnesium prophylaxis had no effect. Advanced age and a low plasma magnesium concentration are risk factors for postoperative atrial fibrillation.

Hemodynamic effects of synchronized high-frequency jet ventilation compared with low-frequency intermittent positive-pressure ventilation after myocardial revascularization.

BACKGROUND: The purpose of this prospective study was to examine the effect on cardiac performance of selective increases in airway pressure at specific points of the cardiac cycle using synchronized high-frequency jet ventilation (sync-HFJV) delivered concomitantly with each single heart beat compared with controlled mechanical ventilation in 20 hemodynamically stable, deeply sedated patients immediately after coronary artery bypass graft. METHODS: Five 30-min sequential ventilation periods were used interspersing controlled mechanical ventilation with sync-HFJV twice to control for time and sequencing effects. Sync-HFJV was applied using a driving pressure, which generated a tidal volume resulting in gas exchanges close to those obtained on controlled mechanical ventilation and associated with the maximal mixed venous oxygen saturation. Hemodynamic variables including cardiac output, mixed venous oxygen saturation and vascular pressures were recorded at the end of each ventilation period. RESULTS: The authors found that in 20 patients, hemodynamic changes induced by controlled mechanical ventilation and by sync-HFJV were similar. Cardiac index did not change (mean +/- SD for controlled mechanical ventilation: 2.6 +/- 0.7 l x min(-1) x m(-2); for sync-HFJV: 2.7 +/- 0.7 l x min(-1) x m(-2); P value not significant). This observation persisted after stratification according to baseline left-ventricular contractility, as estimated by ejection fraction. CONCLUSIONS: The authors conclude that after coronary artery bypass graft, if gas-exchange values are maintained within normal range, sync-HFJV does not result in more favorable hemodynamic support than controlled mechanical ventilation. These findings contrast with the beneficial effects of sync-HFJV, resulting in marked hypocapnia, on cardiac performance observed in patients with terminal left-ventricular failure.