Low-intensity anticoagulation with warfarin prevented cerebral infarction in patients with nonrheumatic atrial fibrillation without producing an excess risk of major hemorrhage. This benefit extended to patients over 70 years of age.

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It has been shown that the antiarrhythmic and toxic effects of lidocaine may be in part dependent on its two active metabolites, monoethylglycylxylidide (MEGX) and glycylxylidide (GX). Presently available gas liquid chromatographic analytic methods require long and tedious steps or sophisticated equipment such as gas liquid chromatography-mass spectrometry. The assay method reported here with the use of high-performance liquid chromatography is rapid and allows accurate, precise determination of lidocaine, MEGX, and GX in biologic fluids. On the 3 patients studied extensively with the use of this assay, one patient had MEGX concentrations almost twice those of lidocaine. At 83% lidocaine potency, the contribution of MEGX in this patient was about 1.5 times that of lidocaine. The second patient studied on two consecutive days had a 20% increase in serum lidocaine concentration and an equivalent decrease in MEGX concentration on the second day. In the third patient lidocaine was stopped with a resulting half-life of 3.8 hr, which is consistent with previously reported values for patients on long-term lidocaine infusion. Urinary excretion of lidocaine and its metabolites is in agreement with previous work. These data suggest that much information still remains to be learned about the active metabolites of lidocaine as well as of lidocaine.

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SUMMARYSystolic time intervals (STI) and serum digoxin concentrations (SDC) were measured in eight patients with compensated atherosclerotic and/or hypertensive heart disease who received oral digoxin 0.25 mg/day or 0.5 mg/day for alternate two-week periods without a loading dose. Control data were obtained both before and after the four weeks of treatment. After 13 days treatment with digoxin, 0.5 mg/day, there was a significant decrease in total electromechanical systole corrected for heart rate (QS2i), pre-ejection period (PEP), pre-ejection period corrected for heart rate (PEP,) Methods Eight patients, all in normal sinus rhythm, with compensated atherosclerotic and/or hypertensive heart disease were studied. Four patients were male and four patients were female. Ages ranged from 35 years to 68 years. Five patients were receiving maintenance doses of digoxin, orally, at the time of selection for the study. Digoxin was discontinued at least two weeks prior to the first control observation. In all patients, SDC at the time of the first control observation was less than 0.4 ng/ml. Diuretics, antihypertensive agents, and sedatives were continued in unchanged doses. Patients taking diuretics received supplemental oral potassium chloride. The purpose of the study was fully explained to each patient and written informed consent was obtained.The initial evaluation of each patient included determinations of blood urea nitrogen, serum creatinine, sodium, potassium, chloride, carbon dioxide combining power, calcium, carotene, and thyroxine. The results of these studies were all within the normal range. Chest X-rays and 12-lead electrocardiograms were compatible with the clinical diagnoses.Two sets of control observations (Cl and C2) were obtained two weeks before starting digoxin. Four of the patients then received digoxin 0.25 mg/day for two weeks

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Two hundred consecutive catheterized patients with unstable angina pectoris were reviewed to find clinical and noninvasive indicators of left main coronary artery disease (greater than or equal to 50% lesion). Thirty-five patients (17.5% of total) had left main coronary artery disease. There were no differences between patients with and without left main coronary artery disease in age, sex, results of resting electrocardiogram, congestive heart failure, dyspnea during pain, duration of longest pain, arrhythmias, response to medical therapy, or other risk factors. Crescendo angina pectoris (worsening of pre-existing angina), transient ST-segment depression with pain, simultaneous anterior and inferior ST changes during pain, and fluoroscopic calcification of the left main coronary artery were all significantly more common in patients with left main coronary artery disease. However, low sensitivity or low predictive value, or both, limit the usefulness of these clinical predictors. Left main coronary artery disease cannot be reliably predicted in patients with unstable angina pectoris before coronary arteriography.

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