Ballistocardiographic indicators of prognosis in ischemic heart disease.

Bimonthly recordings of ultra-low-frequency acceleration ballistocardiograms overa 2 to 7 year period in 73 patients with ischemic heart disease and 50 matched control subjects within the framework of a clinical follow-up were subjected to measurement of IJ amplitude (reflecting force of contraction), IJ velocity (reflecting contractility), and IJ velocity variation coefficient. These repeated measurements were correlated with 24-hour vanillylmandelic acid (VMA) excretion in the urine, arthythemia incidence, heart rate, and clinical outcome in each subject. Moth-to-month variability of the IJ velocity was highly significantly correlated with 24-hour VMA excretionas well as with the likelihood of subsequent myocardial infartion or sudden death. Data on 24 of the patients with ischemic heart disease were available during a two-year period prior to their death from documented myocardial infarction or presumed fatal arrhythmia without a fresh infarction at autopsy. Their records were compared with those made during the same time period on individually matched control subjects and on patients with documented ischemic heart disease who survived the period of study. The mean force of cardiac contraction (IJ amplitude) was consistently lower in the group destined todie early than in the other two groups during the first 18 months. During the 6 monthsprior to death, however, their tracings show a relatively increased force of cardiac contraction and an increased product of force x pulse rate (referred to as the "drive index"), as well as an increase in the incidence of cardiac arrhythmias. None of these late increases was observed during comparable periods of time among surviving patients orcontrol subjuects.     

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A study of potential cholinergic mechanisms involved in the central control of body temperature in golden hamsters.

The intrahypothalamic injection of 0·003 and 0·006 μmol of carbamylcholine chloride (CCh) was found to elicit a dose-dependent increase in rectal temperature in unanaesthetized, normothermic golden hamsters. In agreement with a proposed depolarization block in heat gain pathways, the similar administration of 0·01 μmol of this cholinergic agonist produced a significant hypothermic response. In the case of hyperthermia, thermogenesis appeared to be initiated mainly by shivering with a possible lesser contribution from an increase in cardiac rate. Heat conservation in this instance was indicated by the occurrence of peripheral vasoconstriction. Heat loss and the resultant hypothermia elicited by the highest CCh dose was primarily achieved by peripheral vasodilation. In addition, a possible decrease in thermogenesis was indicated by a reduction in cardiac rate. However, this dose of agonist also produced marked behavioural agitation and struggling which led to a substantial increase in electromyographic activity. The effects of both 0·006 and 0·01 μmol of CCh were abolished by the prior central administration of atropine, whereas similar pretreatment with phentolamine and methysergide failed to alter either CCh response.