Patient Acceptance of Noninvasive and Invasive Coronary Angiography

BACKGROUND: Noninvasive angiography using multislice computed tomography (MSCT) is superior to magnetic resonance imaging (MRI) for detection of coronary stenoses. We compared patient acceptance of these two noninvasive diagnostic tests and invasive conventional coronary angiography (Angio). METHODS AND FINDINGS: A total of 111 consecutive patients with suspected coronary artery disease underwent MSCT, MRI, and Angio. Subsequently, patient acceptance of the three tests was evaluated with questionnaires in all patients. The main acceptance variables were preparation and information prior to the test, degree of concern, comfort, degree of helplessness, pain (on visual analog scales), willingness to undergo the test again, and overall satisfaction. Preparation for each test was not rated significantly differently, whereas patients were significantly more concerned about Angio than the two noninvasive tests (p<0.001). No pain during MSCT, MRI, and Angio as assessed on visual analog scales (0 to 100) was reported by 99, 93, and 31 patients, respectively. Among the 82 patients who felt pain during at least one procedure, both CT (0.9±4.5) and MRI (5.2±16.6) were significantly less painful than Angio (24.6±23.4, both p<0.001). MSCT was considered significantly more comfortable (1.49±0.64) than MRI (1.75±0.81, p<0.001). In both the no-revascularization (55 patients) and the revascularization group (56 patients), the majority of the patients (73 and 71%) would prefer MSCT to MRI and Angio for future imaging of the coronary arteries. None of the patients indicated to be unwilling to undergo MSCT again. The major advantages patients attributed to MSCT were its fast, uncomplicated, noninvasive, and painless nature. CONCLUSIONS: Noninvasive coronary angiography with MSCT is considered more comfortable than MRI and both MSCT and MRI are less painful than Angio. Patient preference for MSCT might tip the scales in favor of this test provided that the diagnostic accuracy of MSCT can be shown to be high enough for clinical application

Controlled prospective randomised trial on the effects on pulmonary haemodynamics of the ambulatory long term use of nitric oxide and oxygen in patients with severe COPD

Background: Pulmonary hypertension is a frequent complication of severe chronic obstructive pulmonary disease (COPD) and a major cause of morbidity and mortality in this condition. Based on the improved survival of these patients due to long term oxygen therapy and the potent and selective pulmonary vasodilation by inhaled nitric oxide, the safety and effectiveness of the combined inhalation of these two gases over a 3 month period was assessed. Methods: Forty patients with secondary pulmonary hypertension due to COPD were randomly assigned to receive either oxygen alone or "pulsed" inhalation of nitric oxide with oxygen over a period of 3 months. "Pulsed" inhalation of nitric oxide was used to reduce pulmonary ventilation-perfusion mismatch and formation of toxic reaction products of nitric oxide and oxygen. Results: Compared with oxygen alone, the combined inhalation of nitric oxide and oxygen caused a significant decrease in mean (SE) pulmonary artery pressure (from 27.6 (4.4) mm Hg to 20.6 (4.9) mm Hg, p<0.001) and pulmonary vascular resistance index (from 569.7 (208.1) to 351.3 (159.9) dyne•s(-1)•cm(-5)•m(-2), p<0.001) without decreasing arterial oxygenation. Cardiac output increased by 0.5 litres (from 5.6 (1.3) l/min to 6.1 (1.0) l/min, p=0.025). Systemic haemodynamics and left heart function remained unchanged during this period and no increase in toxic reaction products of nitric oxide was observed. Conclusions: This is the first controlled trial indicating that the "pulsed" inhalation of nitric oxide together with oxygen may be safely and effectively used for the long term treatment of severe COPD

Treatment with epoprostenol reverts nitric oxide non-responsiveness in patients with primary pulmonary hypertension

OBJECTIVE—To assess whether long term treatment with epoprostenol might restore primary non-responsiveness to nitric oxide (NO) in patients with primary pulmonary hypertension.
METHODS—Seven patients with primary pulmonary hypertension receiving intravenous epoprostenol continuously because of failure of NO to influence pulmonary haemodynamics during initial testing were followed over a period of 13-29 months. Afterwards, acute vascular reactivity towards NO was tested again during right heart catheterisation.
RESULTS—Administration of NO after continuous epoprostenol treatment for a mean period of 18 months improved arterial oxygen saturation (p < 0.01) and cardiac index (p < 0.05), and decreased mean pulmonary artery pressure (p < 0.01) and total pulmonary vascular resistance (p < 0.01) in patients previously unresponsive to NO.
CONCLUSIONS—Long term treatment with epoprostenol reverts initial refractoriness to NO in patients with primary pulmonary hypertension. Thus the addition of NO to epoprostenol treatment might cause further improvement in the course of the disease.


Keywords: primary pulmonary hypertension; epoprostenol; vascular reactivit

Dexamethasone inhibits endotoxin-induced coagulopathy in human lungs

Background: Activation of local and systemic coagulation is a common finding in patients with pneumonia. There is evidence that glucocorticoids have procoagulant activity in the circulation, particularly in the context of inflammation. The effects of glucocorticoids on local pulmonary coagulation have not yet been investigated. Objective: To use a human model of lung inflammation based on the local instillation of endotoxin in order to investigate whether glucocorticoids alter pulmonary coagulation. Methods: Twenty-four healthy volunteers were randomized to receive either dexamethasone or placebo in a double-blind trial. Endotoxin was instilled via bronchoscope into right or left lung segments, followed by saline into the contralateral site. Six hours later, a bilateral bronchoalveolar lavage (BAL) was performed and coagulation parameters were measured. Results: Endotoxin induced activation of coagulation in the bronchoalveolar compartment: the level of prothrombin fragment 1 + 2 (F1 + 2) was increased three-fold (248 pmol L-1, 95% confidence interval [CI] 43-454 versus 743 pmol L-1, 95% CI 437-1050) and the level of thrombin-antithrombin complex (TATc) was increased by similar to 50% (31 mu g L-1 , 95% CI 18-45 versus 49 mu g L-1, 95% CI 36-61) as compared with saline-challenged segments. Dexamethasone reduced F1 + 2 (284 pmol L-1, 95% CI 34-534) and TATc (9 mu g L-1, 95% CI 0.7-17) levels almost to those measured in BAL fluid from the saline-instilled segments in the placebo group. Dexamethasone even profoundly reduced F1 + 2 levels (80%) in saline-instilled lung segments (50 pmol L-1, 95% CI 12-87). In contrast, dexamethasone had no effect on systemic F1 + 2 levels. Conclusions: Dexamethasone inhibits endotoxin-induced coagulopathy in lungs. This trial is the first to provide insights into the effects of glucocorticoids on pulmonary coagulation in response to endotoxin.F 5404-B21(VLID)311287