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The Romano-Ward syndrome is a familial disorder inherited as an autosomal dominant trait, the gene of which has been linked to the HLA locus on chromosome 6 or the Harvey-ras oncogene on chromosome 11. The genetic linkage, left and right ventricular function, and the integrity of the baroreflex were studied in subjects from two unrelated families with this condition. Neither family showed genetic linkage to either the HLA locus or to the Harvey-ras gene. Blood pool tomography was used to assess left and right ventricular function: left ventricular wall motion abnormalities were seen only in one family; the degree of dysfunction was related to the presence of symptoms. Minor disturbances of right ventricular function were seen in some subjects from both families, but did not correlate to the presence nor to the severity of symptoms. Using 14 frequencies of cyclical neck suction, the frequency response of the carotid baroreceptor heart-rate reflex was studied. One family had essentially a normal baroreflex. However, all members of the other family had similarly abnormal responses: a higher sensitivity at high and low suction frequencies, suggesting abnormalities of parasympathetic and sympathetic tone respectively. The Romano-Ward syndrome is a heterogeneous disorder: differences in genetic linkage (compared with historical controls), left ventricular function, and baroreflex sensitivity have been demonstrated.

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No description available.

Reperfusion of the isolated rat heart following 10 min of coronary artery ligation under constant flow conditions results in the development of arrhythmias - premature ventricular contractions (PVCs), ventricular tachycardia (VT) and ventricular fibrillation (VF). Increasing concentrations of magnesium (0 - 4.8 mM) and/or potassium (2.5 - 10.0 mM) attenuate, while calcium (0.6 - 2.4 mM) exacerbates these arrhythmias. The protective effects of magnesium and potassium were additive. Magnesium reduced heart rate, perfusion pressure and developed tension. Potassium reduced perfusion pressure and increased developed tension. These haemodynamic effects contributed to the antiarrhythmic action of magnesium but did not completely account for its antiarrhythmic action. Calcium increased developed tension and heart rate and reduced perfusion pressure. Post-ligation administration of magnesium and potassium also protected against reperfusion arrhythmias. These results demonstrate that reperfusion arrhythmias are significantly affected by the ionic environments of the heart. Superoxide dismutase (5 - 20 Um1-1 ), glutathione (10 -5 - 10-3M), ascorbic acid (10-4 -5 x 10-4 M) and histidine (5 x 10-3 M) when given before coronary artery ligation attenuated the development of reperfusion arrhythmias. Mannitol (2 x 10-2 M) and catalase (100 - 300 Uml-1) did not have any significant effect on reperfusion arrhythmias when given alone but they did potentiate the effect of superoxide dismutase. Glutathione and a combination of superoxide dismutase, catalase and mannitol also reduced the incidence of reperfusion induced ventricular fibrillation when given just before reperfusion. Ferrous ion exacerbated the severity of reperfusion arrhythmias. Mannitol (2 x 10-2 M), catalase (100 uml-1) and histidine (5 x 10-3 M) when given before coronary ligation or just before reperfusion prevented the effect of ferrous ion while superoxide dismutase did not, indicating that the presence of ferrous ion is important for the production of hydroxyl radicals. Pretreatment with 6- OHDA attenuated the incidence of reperfusion arrhythmias but pre-ligation administration of allopurinol had no effect on reperfusion arrhythmias. By perfusing hearts with ferricytochrome C it was possible to show an increased reduction of ferricytochrome C during the first minute of reperfusion which could be prevented by the addition of superoxide dismutase and 6-OHDA treatment. These results provide evidence that oxygen free radicals are produced and may be important in the genesis of reperfusion induced arrhythmias in the isolated rat heart. Adenosine (10-6 M), verapamil (10 -8 - 10-7 M), ZK 36374 (10-10 - 10 -9 M) and sodium nitroprusside (10-6 -10-9 M) attenuate the incidence of reperfusion arrhythmias which may be via a coronary steal effect. Agents which affect arachidonic acid metabolism yielded conflicting results which may reflect nonspecific mechanisms other than inhibition of arachidonic acid metabolism. Glutathione and a mixture of superoxide dismutase, catalase and mannitol when given before coronary ligation and just before reperfusion reduced the increase in 86 rubidium efflux rate constant shown on reperfusion. The effect of glutathione on 86 rubidium efflux may be at least in part due to its vasodilator effect. Superoxide generation by xanthine/xanthine oxidase system increased the rate of efflux of 86 rubidium. A mixture of superoxide dismutase, catalase and mannitol also reduced the transient increase in the rate of release of 3H-noradrenaline shown to be produced on reperfusion after 10 min of ischaemia in the isolated rat heart.