[Chronic intravascular hemolysis following mitral valve replacement with Björk-Shiley, Lillehei-Kaster, and Starr-Edwards prosthesis].
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Biomedical subjects
Publications and source records attributed to F Loogen.
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Postoperative hemodynamic studies were conducted at rest and during exercise in 24 patients who, in addition to mitral and/or aortic valve surgery, had De Vega's tricuspid anuloplasty. To determine the degree of tricuspid insufficiency (TI), right atrial pressure (PRA) tracings, biplane right ventricular cineangiograms, and ultrasonic Doppler flow patterns were obtained. 20 patients had postoperative by a mild to moderate TI, but after operation the TI had improved by one or more degrees in 14 cases. In addition, a mild to moderate tricuspid stenosis with pressure gradients from 2.0 to 7.8 mm Hg were found in 12 patients. There was no significant change in mean right atrial pressure (PRA) with 8.0 +/- 4.5 mm Hg preoperatively and 7.5 +/- 3.5 mmHg postoperatively at rest. During exercise PRA rose to 17.0 +/- 6.5 mmHg. This pressure increase is in part due to the persistent elevation of left atrial and pulmonary artery pressure, in part to the TI and the tricuspid stenosis. De Vega's anuloplasty does not answer the tricuspid challenge, since the results are unpredictable.
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In 61 patients sinus node function was tested by programmed (sinoatrial conduction time, SACT) and overdrive atrial pacing (sinus node recovery time, SRT). In the control group (N = 20), mean sinus cycle length was 773 +/- 140.2 msec, mean absolute SRT 1044 +/- 215.8 msec [corrected SRT (CSRT) 270 +/- 112.5 msec; mean +/- SD] and calculated SACT was 82 +/-19.2 msec. The upper limit of normal SACT was defined as 120 msec. In 41 patients with sinus node dysfunction, mean age (55 +/- 14.7 years), mean spontaneous cycle length during the study (1094 +/- 248.0 msec), the lowest heart rate observed (42 +/- 7.5 beats/min), maximal SRT (2110 +/- 1269.1 msec), maximal CSRT (1016 +/- 1182.8 msec), and calculated SACT (126 +/- 47.3 msec) were significantly longer than in the control group. Abnormalities of sinus node function, as evidenced by the degree of spontaneous bradycardia, SRT and calculated SACT were more frequent in patients with bradycardia-tachycardia syndrome or spontaneous sinoatrial block than in those exhibiting isolated sinus bradycardia. We conclude 1) that in patients with sinus node dysfunction both sinus node automaticity and sinoatrial conduction may be abnormal, and 2) that overdrive and programmed premature atrial stimulation can separate patients with sinus node dysfunction according to their clinical presentation.
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The results of long term oral therapy of cardiac arrhythmias in 43 patients successfully treated with propafenone are reported. The patients were treated for periods ranging between 1 month and 34 months with a mean of 13.4 months. The administered dose varied between 150 mg tds and 300 mg qds with an average daily dose of between 600 and 750 mg. The doses were decided on a body-weight basis with range of 6 to 17 mg/kg and an average of 12 mg/kg. Altogether 30 patients were successfully treated over a long period, sometimes in combination with other antiarrhythmic agents, particularly beta-blockers. 2 patients did not appear after some first controls. In 7 patients the drug was not effective, even when used in combination with others. 4 patients stopped the treatment due to side-effects. Further 18 patients complained temporarily of gastrointestinal and cerebral side-effects. Some Ecg changes were noted, particularly A-V conduction delays and spreading of the QRS-complex. We suggest that the clinically most important parameters for monitoring an antiarrhythmic regimen of propafenone are the patients's own history and Ecg-examination noting the PQ interval and particularly the width of the QRS-complex and long-term monitoring.
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Ventricular arrhythmias represent a common precursor of ventricular fibrillation in acute myocardial infarction in man. Frequent ventricular ectopic beats (greater than 5/min), multifocal ectopic beats, ventricular bigeminy, ventricular salvoes, ventricular tachycardia, and the R-on-T phenomenon have been considered as warning arrhythmias. However, recent studies have given rise to some doubt concerning the value of warning arrhythmias as predictors of ventricular fibrillation. In many a case there is no warning arrhythmia prior to ventricular fibrillation or these arrhythmias do not fulfill the criteria of warning arrhythmias. In other cases the warning arrhythmias develop so briefly before ventricular fibrillation that no prophylactic measure can be instituted. Warning arrhythmias may occur at equal frequency in patients with and without consecutive ventricular fibrillation. This also applies to the R-on-T phenomenon as a warning arrhythmia and as the initiating mechanism of ventricular fibrillation. In nearly half the cases ventricular fibrillation is initiated by a late ventricular ectopic beat. In view of these data of the literature, the so-called warning arrhythmias seem to have lost their predictive value. They represent a common phenomenon in acute myocardial infarction in man. However, ventricular fibrillation may also occur without any prior ventricular arrhythmias, above all during the first day of acute myocardial infarction. The frequency of ventricular fibrillation decreases in the course of infarction. Therefore the time during acute myocardial infarction may be a better guide whether to institute prophylactic antiarrhythmic therapy than the occurrence of ventricular arrhythmias. To date, the beneficial effect of prophylactic administration of lidocaine has remained controversial though a recent double-blind study has strongly suggested that lidocaine is able to prevent ventricular fibrillation. If these results should be confirmed by others, this would ask for routine administration of lidocaine in each case with acute myocardial infarction during the first day.
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