Closed chest myocardial biopsies: clinical uses and related problems.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to F van de Werf.
Explore the source record for details and available documents.
A patient with osteogenesis imperfecta and mitral and aortic insufficiency, who underwent valve replacement, is described. The post-operative course was complicated by mitral valve dehiscence due to extreme friability of the mitral valve annulus.
Explore the source record for details and available documents.
Coronary thrombolysis was induced by infusion of highly purified human pro-urokinase isolated from a transformed kidney cell line (ACHN) or by infusion of urokinase of urinary origin in anesthetized dogs with 1-hr-old clots in the left anterior descending coronary artery. The clots were induced with a copper coil and thrombolysis was detected by repeat coronary angiography. Intravenous infusion of pro-urokinase at a rate of 10 micrograms/kg/min for 30 min in two dogs did not induce thrombolysis, which was only obtained after 8 and 15 min of its subsequent intracoronary administration. Intravenous infusion of pro-urokinase at a rate of 20 micrograms/kg/min for 30 min in four dogs induced coronary thrombolysis within 23 +/- 2 min (mean +/- SEM). This was not associated with systemic fibrinolytic activation because the alpha 2-antiplasmin and fibrinogen levels did not decrease. Intravenous infusion of urokinase at a rate of 10 micrograms/kg/min for 30 min elicited thrombolysis in four of seven dogs within an average of 19 +/- 2 min. In the other three dogs thrombolysis was only obtained within 11 +/- 3 min of its subsequent intracoronary infusion. Administration of urokinase was associated with systemic fibrinolytic activation as evidenced by a decrease of alpha 2-antiplasmin to about 10% and of fibrinogen to 43 +/- 13% of the preinfusion value. It is concluded that intravenous infusion of pro-urokinase at a sufficiently high rate produces coronary thrombolysis without systemic fibrinolysis in dogs.
A myocardial infarction may be caused by a blunt chest trauma. The myocardium may be directly contused or a coronary artery may be occluded. The present paper describes a patient in whom no obstructive lesions of the coronary arteries were found after a posttraumatic infarction and a second patient with a posttraumatic occlusion of the left anterior descendents. The first patient had an abnormal connection between the right coronary artery and the circumflex artery, which is also thought to be posttraumatic.
Moxaprindine, a new anti-arrhythmic drug, with characteristics similar to aprindine, has been demonstrated to be highly effective in suppressing ventricular arrhythmias occurring before, during and after maximal exercise stress testing. This effect was obtained both in subjects with clinically normal hearts and in a limited number of patients with ischemic heart disease. These findings demonstrate the efficacy and safety of anti-arrhythmic treatment by drugs prolonging ventricular depolarization for ventricular arrhythmias occurring during exercise.
We have developed an open environment for quantitative analysis of left ventricular function using ultrasound images. The system is primarily intended for experimental purposes, i.e. clinical research and the evaluation of quantification algorithms. The modular design allows easy expansion with new analysis methods. The core of our system is the user-interface and image presentation. Image analysis methods are included as a set of tools available to the operator. Using this approach, the expensive, expert knowledge of the cardiologist is used more efficiently than in most delineation systems. During delineation, images of a complete heart cycle can be simultaneously displayed dynamically ('cine mode') in a separate window. This feature improves visual edge perception and enables accurate determination of the endocardium even in cases of very poor echogenicity. The resulting contour can be corrected locally by interactive modification using 'rubber banding'. After delineation of the images from different echocardiographic views, volume, ejection fraction, and regional wall motion are determined. Studies using contrast-enhanced echocardiography can be quantified by image intensity analysis in a region of interest in order to determine myocardial perfusion. We evaluated our method by quantifying echocardiographic studies from 12 healthy volunteers. We compared the results with magnetic resonance imaging and concluded that there was no significant difference in volume and ejection fraction calculated from both modalities. Moreover, the image display features and contour correction methods were greatly appreciated by the cardiologists who used the system.