[Isolated left anterior descending coronary artery disease. Clinical and angiographic studies of 70 cases].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to J Marco.
Explore the source record for details and available documents.
Repeated continuous ambulatory electrocardiography by Holter monitoring was performed after early mobilisation post-myocardial infarction in 100 patients, without ventricular extrasystoles on classical ECG. Frequent ventricular arrhythmias were recorded in 58 p. 100 cases, unrelated to the localisation of the infarct. The observation of ventricular arrhythmias in the Coronary Care Unit (CCU) was not related to the occurrence of VEs during Holter monitoring. On the other hand, VEs were less frequent (38 p. 100 compared to 68 p. 100) in patients taking amiodarone or betablockers on transfer from the CCU. The reduced activity of patients during Holter monitoring minimises the frequency of arrhythmias, and 10 p. 100 patients were observed to have VEs only after exercise tolerance testing. These VEs seem to be a bad prognostic factor; the 9 patients who died in this series all presented VEs on ambulatory monitoring (7) or during exercise tolerance testing (2). However the number of patients with triple vessel disease was greater in the group with VEs on ambulatory monitoring (57 p. 100 compared with 13 p. 100). It is difficult to assess the precise role of the VEs amongst the other risk factors of sudden death. This is not a randomised study, but it would appear that long=term amiodarone or betablockers therapy may influence the medium-term prognosis.
The action of orciprenaline, tolazoline, propanolol and inpea on platelet aggregation induced by ADP epinephrine and norepinephrine was studied in vitro in human platelet-rich plasma. Orciprenaline did not significantly affect aggregation induced by ADP. Tolazoline inhibits the aggregation induced by epinephrine and norepinephrine more intensely than the beta-blockers. Inpea blocks the platelet aggregation induced by epinephrine and norepinephrine to a greater extent than propanolol at similar concentrations. The beta-blockers inhibit platelet aggregation non-specifically.
The aim of this study based on a series of 200 patients, was to define the outcome and the prognostic factors of patients presenting with unstable angina, according to Bertolazi's criteria [3] and at least one stenosis greater than 80% on a proximal segment of a main coronary trunc, and to determine which factors should eventually be taken into consideration in the discussion of surgical indications. 70 out of 200 patients (35%) were turned down for direct revascularisation surgery because of an ejection fraction less than 0,35 and/or a poor arterial run off. Coronary arteriography showed 30% patients with a menacing stenosis (greater than 80%) on all three vessels, 36% on two vessels and 22% on a single vessel. The distribution and the extent of the lesions was about the same as in the operated patients. 20% patients had an ejection fraction less than 0,35, 24% between 0,34 and 0,50, and 56% greater than 0,50. At patient, the follow up period ranges from 22 to 66 months (average 32 months). In this group, the hospital mortality was 2,9%, the secondary cardiac deaths 16% and the global mortality 19% compared to 12,6% for the operated patients in the same period. The incidence of secondary non-fatal infarction was low (9%). 52% of survivors have persistent angina, 39% severe (Class II or III). Two prognostic factors were detected from this study: the type of angina: the intermediary syndrome had a bad prognosis, 38,5% mortality compared to 13% for aggravated chronic angina; and the ventriculography: patients with ejection fractions less than 0,35 had 64% mortality compared to 7,3% for those with ejection fractions greater than 0,40. The number of menacing lesions, the extent of the lesions of the artery involved did not affect the prognosis when severe abnormalities of left ventricular function were absent.
The effect of the amphetamine in coughing by trachial excitation and the delay of respiration by laryngial excitation is studied in experimental investigations in dogs, a very significant decrease of the two responses is produced in the dosis of 1 mg/kg.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
In this work we have evaluated the effects of blood sugar changes on human pancreatic polypeptide (hPP) secretion in young, healthy subjects. Mean fasting hPP level was 74 +/- 5 (SEM) pg/ml (n = 53). Insulin-induced as well as tolbutamide-induced hypoglycemia clearly provoked hPP secretion (peaks: 1201 +/- 370 pg/ml, P = 0.03, and 520 +/- 112 pg/ml, P = 0.005, respectively). In contrast, the induction of hyperglycemia by intravenous glucose infusion (0.6 g/min) elicited a significant depression of circulating hPP (37-49% of basal values); discontinuing the infusion resulted in an increase of hPP concentrations (peak: 519 +/- 141 pg/ml, P = 0.018), which coincided with the decline of blood sugar to sub-baseline levels. Glucose as an intravenous bolus (0.33 g/kg) also induced a fall in plasma hPP. Glucose ingestion (1.75 g/kg) was followed by a small and short lived elevation of hPP (154 +/- 34 pg/ml at 15 min, P = 0.04) and by a marked rise during the late hypoglycemic phase of the test (538 +/- 168 pg/ml at 120 min, P = 0.028). Finally, after intravenous arginine, a delayed increase of hPP values was observed, occurring subsequently to the plasma glucose drop. The foregoing data indicate that experimental fluctuations in glycemia inversely affect hPP secretion. Nevertheless, this relationship does not necessarily mean that hPP should be directly implicated in glucose homeostasis.
Hypoglycemia is known to stimulate human pancreatic polypeptide (hPP) secretion. To explore further the relationship between glucose availability and hPP release, we have examined the effect of tissue glucopenia induced by 2-deoxy-D-glucose (2-DG) on hPP plasma levels in normal subjects. As this glucose analogue activates the autonomic nervous system, we have also studied the influence of prior atropinization upon the hPP response to 2-DG. Moreover, we have tested the effects of iv epinephrine and norepinephrine on plasma hPP concentrations. Circulating glucagon was also measured. After the iv infusion of 2-DG (50 mg/kg), plasma hPP increased steeply from a fasting value of 104 +/- 24 pg/ml (SEM) to a peak of 2175 +/- 639 pg/ml at 45 min (P less than 0.01) and remained significantly elevated throughout the test. In contrast, prior injection of atropine (1 mg iv) lowered basal hPP levels and reduced conspicuously the hPP response to 2-DG. Epinephrine administration (6 micrograms/min for 60 min) did not significantly modify plasma hPP concentrations. However, 2 h after epinephrine withdrawal, circulating hPP showed a brisk elevation coinciding with the decline of glycemia to subbaseline values. During norepinephrine infusion (6 micrograms/min for 60 min), only a minor and transient increase of plasma hPP was found. Plasma glucagon rose significantly after 2-DG infusion, but this response was virtually absent in the atropine experiment. Whereas the well known glucagon tropic activity of epinephrine was evidenced, norepinephrine failed to exert an obvious effect on glucagonemia. Our data demonstrate that 2-DG induces a powerful stimulation of hPP secretion in normal subjects and suggest that this action is mediated in part, if not entirely, by the parasympathetic nervous system. On the other hand, a major role of the sympathoadrenal system in response of hPP to 2-DG or to hypoglycemia does not seem probable. Finally, the hyperglucagonemic effect of 2-DG seems also to be dependent on cholinergic transmission.
Explore the source record for details and available documents.
Three years after radiotherapy to the mediastinum for Hodgkin's disease, a 28 year old female presented with incapacititating angina. The presence of severe disease in the proximal arteries on coronary arteriography, with obliteration of the anterior descending artery and, of the right coronary artery, together with an unstable collateral circulation, constituted an indication for a double aorto-coronary bypass graft. A review of the literature suggests that early development of atherosclerosis may be produced by the synergistic action of radiotherapy and lipid disorders. Fifteen similar cases have been described, eight of them in patients of less than 40 years of age; three were discovered at post-mortem examination in patients aged under 21.
The case reported concerns a symptomatic transitory sinus node abnormality in a 75 years old woman treated with Lithium Carbonate (750 mg/d) for a manic-depressive psychosis. This patient, admitted to the hospital for bradycardia and repeated episodes of syncope was shown to present sinus pauses greater than 3 seconds. Lithium therapy was discontinued. 72 hours later electrophysiologic studies, performed to evaluate sinus node function, were normal. It is therefore the author's opinion that in patients receiving Lithium therapy who present syncope, dizziness, or bradycardia a sinus node abnormality of iatrogenic origin must be considered. The importance of this diagnosis is in the rapid reversibility of the sinus node dysfunction with discontinuation of therapy.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.