Each year 1.5 million patients are admitted to coronary-care units (CCUs) for suspected acute ischemic heart disease; for half of these, the diagnosis is ultimately "ruled out." In this study, conducted in the emergency rooms of six New England hospitals ranging in type from urban teaching centers to rural nonteaching hospitals, we sought to develop a diagnostic aid to help emergency room physicians reduce the number of their CCU admissions of patients without acute cardiac ischemia. From data on 2801 patients, we developed a predictive instrument for use in a hand-held programmable calculator, which requires only 20 seconds to compute a patient's probability of having acute cardiac ischemia. In a prospective trial that included 2320 patients in the six hospitals, physicians' diagnostic specificity for acute ischemia increased when the probability value determined by the instrument was made available to them. Rates of false-positive diagnosis decreased without any increase in rates of false-negative diagnosis. Among study patients with a final diagnosis of "not acute ischemia," the number of CCU admissions decreased 30 per cent, without any increase in missed diagnoses of ischemia. The proportion of CCU admissions that represented patients without acute ischemia dropped from 44 to 33 per cent. Widespread use of this predictive instrument could reduce the number of CCU admissions in this country by more than 250,000 per year.

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A B S T R A C T Cardiovascular actions of insulin were studied by intravenous infusions of insulin (4 and 8 mU/kg per min) in normal conscious dogs. This resulted in increases in cardiac output, heart rate, and left ventricular derivative of pressure with respect to time (dP/dt) and dP/dt/P, as blood glucose was reduced. The inotropic and chronotropic effects of insulin were not related to hypoglycemia, as they persisted even when blood glucose was restored to control values or when it was prevented from falling by a simultaneous infusion of glucose. These cardiac effects were accompanied by increases in plasma catecholamines, and were abolished by propranolol pretreatment. Both plasma epinephrine and norepinephrine increased during insulin hypoglycemia, but only norepinephrine increased during insulin infusion when euglycemia was maintained.Mean arterial blood pressure did not change significantly during insulin hypoglycemia, but rose if euglycemia was maintained, probably due to the selective increase in norepinephrine in the latter condition. A pressor response also occurred in propranolol-pretreated dogs during insulin hypoglycemia, but was abolished when the animals also had been pretreated Insulin infusion increased left ventricular work and myocardial blood flow in dogs with and without hypoglycemia. Myocardial blood flow, however, did not change significantly during insulin infusion in dogs pretreated with propranolol. As propranolol also diminished the inotropic response, it appears that the increase in myocardial blood flow caused by insulin in the normal dog is causally related to the increased myocardial metabolic demand.Insulin also produced vasomotor effects on other vascular beds. In skeletal muscle, blood flow was increased under all study conditions, except during insulin hypoglycemia after propranolol-pretreatment when unopposed alpha-mediated vasoconstriction was present. The persistent increase in flow during both alpha and beta adrenergic blockade suggests that insulin has a direct dilator effect on skeletal muscle vasculature. In the adrenal gland, flow was increased except during euglycemia, when no rise in plasma epinephrine was observed, suggesting coupling between adrenal flow and catecholamine release. In the splanchnic bed, flow was decreased during euglycemia, when plasma norepinephrine rose, and during beta adrenergic blockade with propranolol, when unopposed alpha-mediated vasoconstriction also predominated. A similar pattern was found in the kidney, except that renal blood flow also fell after combined alpha and beta adrenergic blockade. The results show that the vasomotor effects on regional flows are mediated both via adrenergic mechanisms, and in the case of skeletal muscle and kidney, via mechanisms unrelated to sympathetic stimulation.

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We evaluated the diagnostic accuracy of exercise-induced ST-segment depression in detecting coronary-artery disease by applying the likelihood-ratio formulation of Bayes's theorem to stress-test data, which were partitioned into half-millimeter ranges of depression. The graphic relation between the predictive value of a given test result and the pretest risk of disease in the test subjects was obtained for each of these half-millimeter intervals. This method reveals that the predictive value of testing depends on the degree of ST-segment depression, and that the pretest risk of coronary-artery disease is an important determinant of the predictive value of any test result in the individual patient. These findings suggest that the use of the terms "positive" and "negative" are inappropriate to describe most stress-test results. Instead, the results should be interpreted in terms of a continuum of risk based on the extent of ST-segment depression.

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