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Recent experiments with heavy ions and planned experiments with ultraintense lasers require nonperturbative solutions to quantum field theory for predicting and interpreting the results. To propel this theoretical direction, we solve the nonperturbative problem of an electron in a strong transverse confining potential using Hamiltonian light-front quantum field theory. We evaluate both the invariant mass spectra and the anomalous magnetic moment of the lowest state for this two-scale system. The weak external field limit of the anomalous magnetic moment agrees with the result of QED perturbation theory within the anticipated accuracy.

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We estimate the two-photon exchange contribution to elastic electron-proton scattering at large momentum transfer through the scattering off a parton in the proton. We relate the two-photon exchange amplitude to the generalized parton distributions which appear in hard exclusive processes. We find that when taking the polarization transfer determinations of the form factors as input, adding in the 2-photon correction does reproduce the Rosenbluth cross sections.

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We performed percutaneous balloon angioplasties in five patients who had congenital coarctation of the aorta (six procedures) and in five patients who had congenital valval pulmonic stenosis. In the patients with coarctation, the systolic BP difference across the coarctation decreased an average of 39 mm Hg (range, 32 to 44 mm Hg) and the mean BP difference decreased an average of 21 mm Hg (range, 19 to 27 mm Hg). The diameter of the coarcted area increased an average of 5 mm (range, 3 to 8 mm). In the patients with valval pulmonic stenosis, the systolic BP difference across the pulmonary valve decreased an average of 17 mm Hg (range, 0 to 20 mm Hg) in the resting state and decreased an average of 33 mm Hg (range, 19 to 56 mm Hg) in a state of isoproterenol hydrochloride-induced stress. This form of therapy offers an alternative to surgery in selected patients.

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Two patients with committed dual unipolar AV sequential pacing systems are presented in whom atrial capture was unable to be demonstrated on the surface electrocardiogram. The bedside examination is proposed as a means of identifying the presence or absence of atrial capture with subsequent confirmation by M-mode echocardiographs and jugular venous pulse tracings. Mode, rate, and output programmability may aid in the evaluation of these pacing systems. Intentional reduction of the ventricular output to subthreshold levels in pacemakers capable of this degree of programmability will permit the rapid bedside confirmation of atrial capture without the need for expensive and time-consuming noninvasive tests.

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The effect of isometric upper extremity exercise on pacemaker function was evaluated in 27 patients who remained pacemaker-dependent during testing. Inhibition was demonstrated in eight (31 percent) of which five were symptomatic. Based on design of the sensing amplifier and return to an all-metal housing in the unipolar lithium pulse generators, myopotential inhibition is being recognized as one cause of symptomatic pacemaker inhibition that is more common than generally appreciated. A method of evaluation and management options for symptomatic patients are discussed. Routine testing of all patients should be performed at the time of a regular office evaluation. If one model pulse generator appears to be particularly prone to myopotential inhibition, this knowledge should be considered in the choice of future pacing systems.

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The effects of verapamil were assessed in 26 patients with stable exertional angina pectoris in a double-blind, placebo-controlled, randomized crossover protocol using serial treadmill tests. Verapamil, 480 mg/day, reduced anginal frequency from 5.6 +/- 7.3 to 2.2 +/- 3.9 attacks per week (p less than 0.001) and nitroglycerin consumption from 3.4 +/- 4.9 to 1.2 +/- 2.5 tablets per week (p less than 0.05) compared with placebo. Treadmill time increased from 6.4 +/- 2.1 minutes during the placebo phase to 7.5 +/- 1.8 minutes during the verapamil phase (p less than 0.001). Verapamil's beneficial effect appeared to be related, in part, to a 10% reduction of the rate-pressure product at rest (p less than 0.05) and a 12% reduction during submaximal exercise (p less than 0.001). Verapamil also caused less marked ST-segment depressions at peak exercise (p less than 0.05) at a similar rate-pressure product, suggesting a favorable redistribution of coronary blood flow to the ischemic zone. Side effects from verapamil were minimal, consisting mainly of constipation (six patients). Verapamil appears to be a safe and effective drug for treating angina of effort.

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A 35-year-old man with class 2 angina pectoris was enlisted in a serial exercise test protocol to evaluate oral verapamil therapy for angina pectoris. During both the single-blind open dose titration phase and the double-blind phase, short salvoes of ventricular tachycardia (VT) were followed by angina and ischemic ST segment depression during exercise with placebo. With verapamil therapy, no ventricular ectopy was noted during exercise, and the patient exercised longer before angina or ischemic ECG changes developed. Twenty-four hour ECG monitoring revealed multiform ventricular premature depolarizations and three-beat salvoes of VT with placebo and no ventricular ectopy whatsoever with verapamil. Verapamil's antiarrhythmic effect may be secondary to its anti-ischemic action, or, by inhibiting slow channel conduction (with its propensity for enhanced automaticity and reentry) induced by ischemia and the sympathetic response to exercise, exerts a primary antiarrhythmic action.

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Electrolyte abnormalities cause fatal cardiac arrhythmias in patients with diabetic ketoacidosis. A patient is reported with electrocardiogram (ECG) abnormalities characteristic of toxic hyperkalemia and hypocalcemia. The ECG abnormalities were noted during the first hour after arriving at the hospital. The laboratory values confirming the electrolyte abnormalities were not available for more than 1 h after the ECG indicated the danger of myocardial toxicity. During the initial 2 h of therapy the patient was urinating and not in shock. ECG monitoring of this patient prevented the routine administration of intravenous potassium, which was potentially lethal. The clinical importance of electrolyte levels in the management of diabetic ketoacidosis is the prevention of cardiac arrhythmias. ECG monitoring should be a minimal standard in the management of diabetic ketoacidosis.

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