The cardiac function during haemodialysis has been studied using a non-invasive method in a prospective investigation of 7 elderly patients, all of whom had an enlarged heart on the chest X-ray and in all of whom experience had shown that a fall in blood pressure developed during haemodialysis. The cardiac output was determined by impedance cardiography and showed no significant changes during dialysis. A significant rise was observed in the heart rate and this was found to reach a maximum during the periods in which the blood pressure was lowest. Left ventricular function was evaluated from the systolic time intervals, PEP/LVET (PEP = pre-ejection period and LVET = left ventricular ejection time) and the noninvasive contraction index BP diastolic/PEP. The electromechanical systole (QS2), LVET and the non-invasive contraction index all decreased significantly during dialysis, while PEP and PEP/LVET were significantly increased. All the changes were most pronounced at the time when the blood pressure was lowest. It is concluded from the investigation that the cause of the fall in blood pressure during haemodialysis of elderly patients with impaired cardiac function may be ascribed to transient reduction in left ventricular performance.
Twelve of 56 patients with chronic renal failure, all treated with frusemide (Lasix®) in daily doses of 0.5–2 g, developed bullae in areas exposed to light. In most cases the bullae developed during summer months and disappeared later in the year whether the frusemide treatment was continued or not. In two patients the eruption reappeared when treatment was resumed. Disturbance of the porphyrin metabolism was not found, neither could a change in the frusemide metabolism be demonstrated. Tissue typing and blood groups showed no difference from the average population. It is concluded that the condition presumably is a photo reaction due to the frusemide treatment but it cannot be said whether it is allergic or toxic.
The PARAGON Investigators* Background-Unstable angina and non-Q-wave myocardial infarction involve coronary arterial plaque rupture, platelet activation, and thrombus formation. This study tested the benefit of different doses of lamifiban (a platelet IIb/IIIa antagonist) alone and in combination with heparin in patients with these conditions to select the most promising lamifiban regimen for subsequent evaluation. Methods and Results-At 273 hospitals in 20 countries, 2282 patients were randomly assigned to lamifiban (2ϫ2 factorial design: low-dose [1 g/min] with and without heparin versus high-dose [5 g/min] with and without heparin) or to standard therapy (placebo and heparin). All patients received aspirin. The composite primary end point of death or nonfatal myocardial infarction at 30 days occurred in 11.7% of those receiving standard therapy, 10.6% receiving low-dose lamifiban, and 12.0% receiving high-dose lamifiban (Pϭ0.668). By 6 months, this composite was lowest for those assigned to low-dose lamifiban (Pϭ0.027) and intermediate for those assigned to high-dose lamifiban (Pϭ0.450) compared with control (13.7%, 16.4%, and 17.9%, respectively). Compared with control, the combination of high-dose lamifiban and heparin resulted in more intermediate or major bleeding (12.1% versus 5.5%; Pϭ0.002) and a similar rate of ischemic events. Conversely, low-dose lamifiban and heparin yielded similar bleeding rates as in the control group but fewer ischemic events at 6 months (12.6% versus 17.9%; Pϭ0.025). Conclusions-In unstable angina and non-Q-wave infarction, platelet IIb/IIIa antagonism with lamifiban reduces adverse ischemic events at 6 months beyond that of aspirin and heparin therapy. The role of conjunctive heparin remains uncertain but appears more favorable with low-dose IIb/IIIa antagonism. Larger-scale study is needed to more reliably estimate these effects. (Circulation. 1998;97:2386-2395.)
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