Ståle Barvik
Stavanger University Hospital
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Resuscitation | 2010
Alf Inge Larsen; Åshild S. Hjørnevik; Vernon Bonarjee; Ståle Barvik; Tor Melberg; Dennis Winston T. Nilsen
Patients with pulseless electrical activity or refractory ventricular fibrillation have a very bad prognosis. Coronary angiography and angioplasty may be required to restore an effective circulation, but this must be performed whilst chest compressions are continued. The LUCAS chest compression device is suitable for this purpose. So far there are no reports on the effect of this device on coronary circulation in humans. We monitored the coronary perfusion pressure assessed invasively as the difference between the diastolic pressures at the coronary ostium and right atrium, and compared these pressures with coronary flow graded using the TIMI scale in 6 patients. In 4 out of 6 we found a satisfactory coronary artery perfusion pressure and TIMI grade 3 flow (normal) on coronary angiography. Two of these patients survived the first 24h. Two patients did not have a satisfactory perfusion pressure and adequate flow rate was not seen.
Journal of the American College of Cardiology | 1991
Kenneth Dickstein; Ståle Barvik; Torbjørn Aarsland
Forty-one men with documented myocardial infarction greater than 6 months previously were randomized to long-term (48 weeks) therapy with placebo or enalapril on a double-blind basis. All patients were receiving concurrent therapy with digitalis and a diuretic drug for symptomatic heart failure (functional class II or III). The mean age was 64 +/- 7.3 years and no patient suffered from exertional chest pain. Patients underwent maximal cardiopulmonary exertional chest pain. Patients underwent maximal cardiopulmonary exercise testing to exhaustion on an ergometer cycle nine times over the course of 48 weeks. Gas exchange data were collected on a breath by breath basis with use of a continuous ramp protocol. In the placebo group (n = 21), the mean (+/- SD) peak oxygen consumption (VO2) at baseline was 18.8 +/- 5.2 versus 18.5 +/- 5.5 ml/kg per min at 48 weeks (-1.4%, p = NS). In the enalapril group (n = 20), the corresponding values were 18.1 +/- 3.1 versus 18.3 +/- 2.6 ml/kg per min (+2.8%, p = NS). The mean VO2 at the anaerobic threshold for the placebo group at baseline study was 13.1 +/- 3.5 versus 12.8 +/- 2.1 ml/kg per min at 48 weeks (-2.2%, p = NS). The corresponding values for the enalapril group were 11.8 +/- 2.3 versus 11.8 +/- 2.4 ml/kg per min (+1.4%, p = NS). The mean total exercise duration in the placebo group at baseline study was 589 +/- 153 versus 620 +/- 181 s at 48 weeks (+5.4%, p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)
International Journal of Cardiology | 1990
Torbjørn Omland; Ståle Barvik; A. Aakvaag; Torbjørn Aarsland; Kenneth Dickstein
The response in terms of production of atrial natriuretic factor to maximal cardiopulmonary exercise was investigated in 13 patients with mild heart failure (New York Heart Association function class II) secondary to previous myocardial infarction. Exercise induced a rapid and gradually increasing production of atrial natriuretic factor. The concentration at the termination of the test was statistically higher than at rest (64.5 +/- 9.7 versus 119.4 +/- 18.3 pmol/l. P = 0.001). Resting levels of the natriuretic factor correlated well to levels at peak exercise (r = 0.797, P = 0.001). The increase in concentration from rest to peak exercise (atrial natriuretic factor delta) was inversely correlated to the peak consumption of oxygen (r = -0.584, P = 0.036), indicating that the response to exercise is not attenuated in the patients with most marked functional impairment. The relationship between resting levels of atrial natriuretic factor and peak consumption of oxygen did not reach statistical significance (r = -0.421, P = 0.152), but a significant inverse relationship was observed between concentration at peak exercise and peak consumption of oxygen (r = -0.671, P = 0.012). Levels of atrial natriuretic factor during peak exercise are related to functional impairment in mild heart failure and may discriminate between the functional capacity of patients belonging in the same class of clinical function.
American Journal of Cardiology | 1993
Kenneth Dickstein; Torbjørn Aarsland; Helle Svanes; Ståle Barvik
Abstract Assessment of submaximal cardiopulmonary exercise performance is clinically relevant in the evaluation of functional capacity.1 Although peak results are readily determined, commonly employed methods for estimation of the onset of anaerobiosis are subjective, highly dependent on the ventilatory response and require expertise to interpret.2 We compared the reproducibility of oxygen consumption (O2) at the anaerobic threshold determined by regression analysis of carbon dioxide elimination (CO2) as a function of O2, with the O2 at a respiratory exchange ratio (R) ( CO 2 2 ) = 1.
Thrombosis Journal | 2010
Trygve Brügger-Andersen; Leif Bostad; Dagny Ann Sandnes; Alf Inge Larsen; Vernon Bonarjee; Ståle Barvik; Tor Melberg; Dennis W.T. Nilsen
BackgroundThe expression of pregnancy-associated plasma protein A (PAPP-A) was identified by immunohistochemistry (IHC) in culprit atherothrombotic plaque specimens harvested from patients admitted with ST-segment elevation myocardial infarction (STEMI).MethodsThe atherothrombotic samples were collected from a consecutive cohort consisting of 20 individuals admitted with STEMI to Stavanger University Hospital, Norway, from 2005-2006, presenting angiographically with an acute thrombotic occlusion of a coronary artery characterized by TIMI flow 0. The atherothrombotic plaques were obtained by aspiration thrombectomy during percutaneous coronary intervention within 12 hours from the onset of symptoms and prepared for IHC analysis.ResultsIn the IHC analysis staining for PAPP-A occurred in the extracellular matrix of the plaques and no evidence of staining for PAPP-A was found in the thrombi.ConclusionOur results indicate that in vivo PAPP-A is strongly expressed in atherothrombotic plaques harvested from patients admitted with STEMI, as documented by IHC.Trial [email protected]
Pacing and Clinical Electrophysiology | 1993
Arne M. Abrahamsen; Ståle Barvik; Torbjørn Aarsland; Kenneth Dickstein
A minute ventilation sensing rate responsive pacemaker was implanted in 15 patients (8 males and 7 females)with bradycardia. The mean age was 72.8 ± 8.7 years. The single chamber system measures transthoracic impedance between the tip electrode of a standard bipolar lead and the pulse generator case. In the adaptive mode the pulse generator calculates a rate responsive factor or slope during maximal exercise but /unctions as in the VVI mode. The patients exercised maximally on an upright cycle ergometer with the pacemaker programmed to VVI mode, adaptive mode, and rate responsive mode. Exercise and gas exchange data were collected continuously and analyzed using an automated breath‐by‐breath system. The slope, heort rate, and ventilation were measured every 20 seconds. Heart rate in pacemaker dependent patients correlated well to minute ventilation (correlation coefficient ranging from 0.72–0.95, P < 0.0001). This study demonstrates that minute ventilation is a good metabolic sensor in rate responsive pacing.
American Journal of Cardiology | 1992
Ståle Barvik; Kenneth Dickstein; Torbjørn Aarsland; Harald Vik-Mo
The effect of the nonselective beta blocker timolol on maximal cardiopulmonary exercise performance was evaluated in 28 men with previous myocardial infarction without effort angina (mean age 63 +/- 8 years). Patients were randomized to placebo or timolol (10 mg twice daily) for 4 weeks and then crossed over to the alternative therapy in a double-blind manner. At the completion of each treatment period, patients underwent symptom-limited maximal cardiopulmonary exercise on a cycle ergometer. Exercise time, heart rate, oxygen consumption (VO2), oxygen (O2) pulse and respiratory exchange ratio were measured at peak exercise and at a submaximal exercise level defined at a respiratory exchange ratio of 1.00. Timolol treatment reduced peak heart rate from 153 +/- 11 to 102 +/- 14 beats/min (-33%, p less than 0.001). Exercise time decreased from 680 +/- 91 to 633 +/- 78 seconds (-7%, p less than 0.001). Peak VO2 decreased from 25.3 +/- 4.7 to 21.4 +/- 3.5 ml/min/kg (-15%, p less than 0.001). O2 pulse increased from 12.9 +/- 1.9 to 16.7 +/- 2.3 ml/beat (+29%, p less than 0.001). Peak respiratory exchange ratio did not change significantly, indicating comparable effort. At submaximal exercise, defined at a respiratory exchange ratio of 1.00, there was no difference in exercise time between placebo and timolol. Heart rate decreased with timolol compared with placebo, from 126 +/- 16 beats/min by 31% (p less than 0.001), VO2 decreased from 18.5 +/- 4.3 ml/min/kg by 10% (p less than 0.001), O2 pulse increased from 11.5 +/- 2.0 ml/beat by 30% (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
American Heart Journal | 2006
Tor Melberg; Dennis W.T. Nilsen; Alf-Inge Larsen; Ståle Barvik; Vernon Bonarjee; Karel K.-J. Kuiper; Jan Erik Nordrehaug
International Journal of Cardiology | 2006
Dennis W.T. Nilsen; Tor Melberg; Alf-Inge Larsen; Ståle Barvik; Vernon Bonarjee
International Journal of Cardiology | 2008
Alf Inge Larsen; Tor Melberg; Vernon Bonarjee; Ståle Barvik; Dennis W.T. Nilsen