The electrophysiologic properties of hydroxyzine hydrochloride in the normal and digitalis-toxic heart

Abstract

The Electrophysiologic Properties of Hydroxyzine Hydrochloride in the Normal and Digitalis-Toxic Heart GUSTAVUS A. BOBB and ANTHONY N. DAMATO, MD Staten Island, New York In 20 dogs the effects of hydroxyzine hydrochloride on ventricular automaticity, expressed as ventricular escape time, intraventricular conduction and atrioventricular conduction, were investigated both in vivo and in vitro in the digitalis-toxic and normal heart’. Digitalis toxicity (stable ventricular tachycardia) was produced by a constant infusion of ouabain. Wit.h the use of His bundle electrograms, A-V conduction was measured from P wave to His bundle (H) spike, intraventricular conduction from H to end of QRS. Hydroxyzine hydrochloride (10 to 20 mg/kg intravenously) consistently converted the ventricular tachycardia to sinus rhythm within 2 minutes. This effect appeared at lower doses (5 to 10 mg/kg) when the vagi were cut. A-V conduction was prolonged (-t-610/,) ; intravent,ricular conduction showed no change. In vagotomized dogs A-V conduct,ion was prolonged ( + 11 y0 ) ; intraventricular conduction was unaffected; ventricular escape time returned to normal. These effects of hydroxyzine seemed to be mediated in part via the vagus. Cardiac action potentials were recorded from isolated perfused canine Purkinje fibers. Hydroxyzine HCl (10-b ml) consistently decreased phase 4 depolarization induced by ouabain or anoxia while prolonging the effective refractory period. These findings demonstrate that the antiarrhythmic effect of hydroxyzine HCl is probably mediated through direct action on t,he heart and through its known neural effects. Evaluation of Pulmonary Arterial End-Diastolic Pressure as an Estimate of Left Ventricular End-Diastolic Pressure in Patients with Acute and Chronic Alterations in Left Ventricular Performance RICHARD J. BOUCHARD, MD/JAMES H. GAULT, MD and JOHN ROSS, Jr., MD, FACC La Jolla, California It has been suggested that the pulmonary arterial end-diastolic pressure (PAEDP) may accurately reflect the level of left ventricular end-diastolic pressure (LVEDP) and therefore be useful in the continuous monitoring of LVEDP in acutely ill patients. Accordingly, pulmohary arterial pressure was recorded with a catheter tip micromanometer (SF-l) simultaneously with left ventricular pressure in 11 patients who had normal left ventricular function, and in 170 patients with myocardial disease and elevated LVEDP (range 14 to 38 mm Hg, average 23). In patients with normal left ventricular function, the LVEDP and PAEDP were equal (range 5 to 12 mm Hg, average 8). In contrast, in patients with impaired left ventricular function, the LVEDP was consistently higher than PAEDP, exceeding the latter by 2 to 18 mm Hg (average 10) ; in 12 of these 17 patients, the PAEDP was less than 12 mm Hg, the upper limit of normal for the LVEDP. Furthermore, when LVEDP was increased acut.ely by pharmacologic means by 6 to 14 mm Hg (average increase 10 mm Hg) in 4 patients (3 with initially normal LVEDP), PAEDP remained unchanged or increased only slightly (less than 3 mm Hg) . The left ventricular diastolic pressure before atrial contraction correlated more closely with LVEDP (maximal difference less than 5 mm Hg) . These data indicate that pulmonary art,erial end-diastolic pressure does not provide an accurate estimate of left ventricular end-diastolic pressure in patients with chronic left ventricular disease, and in addition often fails to reflect acute increment.s in left ventricular end-diastolic pressure. The Lipid Clinic Concept HENRY BUCHWALD, MD, PhD, FACC/RICHARD B. MOORE, MD DONALD B. HUNNINGHAKE, MD and RICHARD L. VARCO, MD, PhD Minneapolis, Minnesota The complications of atherosclerotic cardiovascular disease account for the largest mortality and morbidity rate in our population, and this problem has been demonstrated to be positively correlated with the hyperlipidemias. We, therefore, believe that a medical center consultation and treatment facility specifically concerned with this problem fulfills an important community need. Our experienae with such a medical-surgical group approach at the University of Minnesota, utilizing both inpatient and outpatient facilities, has led to the conviction that hyperlipidemia should be treated, even in patients with no present indication of atherosclerotic disease. The Fredrickson type I abnormality can be managed by dietary fat restriction alone. The patient with type II may benefit from a low cholesterol, low saturated fat diet; patients with types III and IV usually show a fair response to this diet plus additional carbohydrate restriction and weight loss if obese. Clofibrate (Atromid-w) is of distinct value in the treatment of many patient,s with types III and IV; however, our experience with this drug in the patient with type II has demon66 The Amorlcan Journal of CARDlOLOaY