Although most asymptomatic patients with the Wolff-Parkinson-White syndrome have a good prognosis, some die suddenly. Electrophysiological testing may identify patients at possible risk of sudden death. The mechanism of sudden death in these patients is believed to result from ventricular fibrillation due to atrial fibrillation with rapid anterograde conduction over the accessory pathway. Consequently, we performed electrophysiological studies in 40 asymptomatic patients with the Wolff-Parkinson-White syndrome. Certain electrophysiological properties clearly identified these patients: (1) in most patients sustained reciprocating tachycardia could not be induced and this explains the absence of symptoms of regular fast palpitations; (2) the incidence of inducible sustained atrial tachyarrhythmias (30%), of short RR intervals between pre-excited beats (20%) and of risk of sudden death (12.5%) was similar to the incidence in symptomatic patients with the Wolff-Parkinson-White syndrome and reciprocating tachycardia. Because of the ease with which transoesophageal study can be performed we think that the asymptomatic Wolff-Parkinson-White syndrome should be systematically evaluated so as to reassure patients with the benign form that they can lead a normal life and take part in sport and secondly to define the real prognosis of the patients whose characteristics suggests a risk of sudden death.
In addition to their effects on blood pressure, antihypertensive agents may produce additional effects on blood rheology and arterial compliance abnormalities which may play a role in target-organ damage. However, these effects may depend only on the specific pharmacological properties of certain antihypertensive agents, and may be partly unrelated to blood pressure lowering action. We compared the effects of nitrendipine 20 mg once daily to hydrochlorothiazide 25 mg once daily in 33 mildly to moderately hypertensive and otherwise healthy patients, in a double blind parallel group trial. Blood rheology (blood fibrinogen and protein concentrations, hematocrit, plasma viscosity and whole blood viscosity at shear rates 0.2 to 128 s-1, erythrocyte deformability and aggregation) and radial artery diameter and compliance (Nius I + Finapres) were measured at baseline and after 2 months of treatment. Both drugs produced similar blood pressure lowering. Blood viscosity increased for all shear rates in the hydrochlorothiazide group and decreased in the nitrendipine treated group. Erythrocyte deformability increased in the nitrendipine but not in the thiazide group. Radial artery diameter and compliance were not different between the two groups but there was a trend towards an increase in cross-sectional compliance in the hydrochlorothiazide group and towards a decrease in the nitrendipine group. Our data show that, in mildly hypertensive patients, blood pressure control by nitrendipine produced more favourable effects on relevant rheological variables than hydrochlorothiazide. Radial artery compliance changes tended to be altered also in opposite directions by the two agents. The significance and the clinical relevance of these effects may require further investigations.
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