Characteristics of conduction of premature impulses during acute myocardial ischemia and reperfusion: a comparison of epicardial and endocardial activation.
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Acute Disease↗
Biomedical subjects
T Peter
Publications and source records attributed to T Peter.
Intracoronary thrombolysis in evolving myocardial infarction.
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Coronary Circulation↗
Noninvasive identification of a high risk subset of patients with acute inferior myocardial infarction.
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Adult↗
Indications for antiarrhythmic therapy as prophylaxis against sudden death.
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Angina Pectoris↗
Regional 99m technetium diphosphonate uptake in experimental dog heart infarct: relation to duration and severity of ischaemia.
Regional uptake of 99mTechnetium diphosphonate was compared with regional myocardial blood flow 6, 12 and 24 h after the onset of myocardial infarction in dogs, and with regional creatine kinase depletion 24 h after the onset. Uptake of the imaging agent increased from 6 to 24 h, but no consistent relationship could be demonstrated between regional myocardial blood flow and regional uptake of the diphosphonate nor between uptake and regional creatine kinase depletion at the centre or border of the infarct. In addition, inappropriately high levels of 99m Technetium uptake could be demonstrated in the epicardial layer of the normal tissue surrounding the infarct. We conclude that diphosphonate uptake is not quantitatively related to the severity of ischaemia, and that use of this substance for imaging may over-estimate myocardial infarct size.
Animals↗
Hemodynamic and cardiometabolic effects of infrarenal aortic and common iliac artery declamping in man--an approach to optimal volume loading.
Nineteen patients undergoing abdominal aortic aneurysm surgery were randomly assigned to two groups and investigated to elucidate the mechanisms of declamping hypotension. The control group of nine patients was kept at an average mean pulmonary artery occlusion pressure (MPAOP) of 11 mmHg (1.46 kPa) before declamping. The other group was volume loaded to a MPAOP of 16 mmHg (2.13 kPa) shortly before declamping. Following declamping there was a significantly greater decrease in mean arterial pressure in the control group, with the same reduction of MPAOP in both groups. In parallel, cardiac and stroke volume indices decreased in the control patients, but remained unchanged in the volume-loaded patients. In the control group there was a reduction in myocardial substrate utilization which was not seen in the volume-loaded patients. No signs of myocardial ischemia could be demonstrated in any of the groups. The results indicate that mismatching between intravascular volume and blood volume is the main cause of infrarenal aortic or common iliac artery declamping hypotension. Volume loading before declamping to a slightly elevated MPAOP can effectively prevent hypotension, while a normal MPAOP does not guarantee a stable hemodynamic situation after declamping.
Aged↗
Acute myocardial infarction in women. The influence of age on complications and mortality.
The prognostic implications of a past history of ischaemic heart disease, site of infarction, ectopic ventricular dysrhythmias (ventricular premature beats (VPB) more than one in 10 sinus beats, and/or ventricular tachycardia (VT), ventricular fibrillation (VF), atrioventricular blocks (AVB), bundle branch blocks (BBB)) and the occurrence of electrical and/or mechanical complications during stay in the Coronary Care Unit (CCU) were analysed in 154 women with definte (WHO Class 1) acute myocardial infarction, admitted sequentially to the CCU over a four-year period. The prognosis in these women was then compared with the prognosis in a group which represented the general male population in the CCU and an age-matched group of men. The results showed that the long-term prognosis in women with acute myocardial infarction is remarkably similar to age-matched groups of men.
Acute Disease↗
The effect of glucose-insulin-potassium on experimental myocardial infarction in the dog.
The effect of glucose-insulin-potassium (GIK) infusions was studied in 45 dogs after left anterior descending coronary artery ligation. GIK caused a modest increase in lactate concentration in small veins draining the infarct but did not affect glucose uptake. No effect on creatine kinase activity in the infarct was seen from GIK, although there was a slight increase in blood flow to the centre of the infarct. We concluded that GIK did not reduce infarct size in this experimental model.
Animals↗
Effect on survival after myocardial infarction of long-term treatment with phenytoin.
A prospective, randomised, open trial was performed in 150 patients to test for any beneficial effects on 2-year mortality of long-term antiarrhythmic therapy with phenytoin in patients with acute myocardial infarction. Patients were stratified according to age, sex, past history of myocardial infarction, and the presence of absence of electrical or mechanical complications in the course of acute infarction. They were then randomised to treatment or control groups (74 v. 76). The former received phenytoin in doses aimed at maintaining plasma phenytoin levels between 40 and 80 mumol/litre. All patients entered the study before discharge from the coronary care ward. Plasma phenytoin levels were in the therapeutic range in between 51 and 75 per cent of subjects at any follow up visit. There were 19 withdrawals from the treatment group, 10 of which were the result of side effects. There were 5 withdrawals from the control group. According to the original intention to treat, there were 18 deaths at 2 years in the treatment group and 14 deaths in the control group. There was no reduction in the incidence of instantaneous or sudden deaths. Deaths on treatment were not associated with a low phenytoin plasma level. Phenytoin treatment showed no beneficial effects on mortality and was associated with a high incidence of side effects.
Adult↗
Failure of high doses of propranolol to reduce experimental myocardial ischemic damage.
Myocardial creatine phosphokinase (CPK) activity and myocardial blood flow (MFB, 15 +/- mu microspheres) were measured at 24 hours after ligation of the left anterior descending coronary artery in nine untreated anesthetized dogs, in eight dogs pretreated with intravenous propranolol 5 mg/kg and in eight which had both pretreatment as well as infusion of propranolol (1.25 mg/kg/hour) after occlusion. Loss of CPK activity from the border and center zones of the myocardial infarct was similar in extent in dogs which had pretreatment but no infusion of propranolol as it was in the control group. Loss of CPK from the center zone was greater (P less than 0.005) in dogs receiving pretreatment followed by constant infusion of the drug. Propranolol had no significant effect on collateral blood flow to the border or center zone of the infarct. In separate experiments, there was no important difference in hemodynamic measurements, except a slower heart rate (P less than 0.01), when pretreated dogs were compared with control dogs up to 2 hours after coronary ligation. We conclude that propranolol given in this dose does not influence nyocardial damage, on the basis of regional myocardial blood flow or tissue CPK depletion values at 24 hr after coronary occlusion.
Animals↗
Reduction of enzyme levels by propranolol after acute myocardial infarction.
The effect of propranolol (0.1 mg/kg intravenously followed by 320 mg given over 27 hour orally) on serum levels of creatine kinase enzyme was studied in a randomized trial involving 95 patients seen within 12 hours of onset of symptoms of uncomplicated myocardial infarction. In 15 patients who were treated with propranolol within 4 hours of onset, and who eventually developed pathological Q waves, peak measured enzyme levels were 27% (P less than 0.0125) lower than in 19 control patients who were also seen within 4 hours of the onset but had no specific treatment. Total calculated enzyme appearance was also lower in the treated patients (reduced 25%, P less than 0.05) as was the calculated rate of the appearance (33%, P less than 0.005). No significant difference was found for treated compared with control patients entering the trial more than 4 hours after the onset of chest pain. This evidence suggests that propranolol may reduce the size of uncomplicated infarctions if it is given intravenously within 4 hours of the onset.
Acute Disease↗
[Postnatal development , up to age 3 of intrauterine immature infants].
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Child Development↗
Membrane structure and drug actions.
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Cell Membrane↗
Wenckebach phenomenon in the exit area from a transvenous pacing electrode.
An unusual type of exist block from a transvenous pacing electrode was recorded in a 63-year-old man with an acute inferior infarct and cardiogenic shock. The pacemaker artefact to QRS interval increased gradually till there was loss of capture. A gradual change from I:I pacing rhythm to 4:3 and 3:2 Wenckebach cycles was recorded. This was followed by a fixed 2:I pacemaker artefact to QRS block.
Electrocardiography↗
Inhibition of demand pacemakers caused by potentials associated with inspiration.
A 69-year-old man with a permanent demand pacemaker and a unipolar electrode system had intermittent failure of pacing during deep inspiration. Pacing was not interrupted when the unit was switched to fixed rate mode by an external magnet. Thus, the problem was not caused by a change in electrode position or to a loose connexion. The likely cause was inhibition by non-cardiac potentials, possibly myopotentials associated with respiration.
Aged↗
Enzyme release after myocardial infarction: comparison of serial serum alpha-hydroxybutyrate dehydrogenase with creatine phosphokinase levels.
Serial measurements on serum creatine phosphokinase (CPK) and alpha-hydroxybutyrate dehydrogenase (HBD) activity were made in 17 patients with acute myocardial infarction. Activities of both enzymes were measured 4-hourly from less than 12 h after the onset of chest pain until CPK activity had returned to near-normal levels. Blood was then sampled twice daily for a further 4--6 days in order to follow the decline in HBD activity. Degradation rates (KD) were calculated for both enzymes, and individual figures for KD were used in order to estimate the total cumulative release of each enzyme. We found a significant correlation between the duration (r = 0.66, P less than 0.01) and magnitude (r = 0.67, P less than 0.01) of release of the 2 enzymes, comparing different patients with one another. Duration od HBD release was 11 h greater than the duration of CPK release in 9 of the 17 patients who were suffering from cardiac failure (t = 0.01, P less than 0.02). Degradation rate (KD) for HBD was on average about one quarter of that for CPK, but there was no significant correlation between KD for the 2 enzymes. KD did not appear to be reduced in patients with cardiac failure. We conclude that the release patterns of CPK and HBD after myocardial infarction are similar, and this strengthens the case for acceptance of total enzyme release as a valid index of myocardial infarct size.
Adult↗
Establishment of the Melbourne mobile intensive care service.
As the majority of deaths after infarction occur in the first hour, a mobile intensive care ambulance service has been instituted in Melbourne to enable adequate care and early monitoring facilities. Initially the service was manned by doctors and ambulance officers, but currently each ambulance is manned by two specially trained officers. Over a 27-month period 52 patients have been resuscitated from ventricular fibrillation or ventricular standstill. Half of the patients had sustained a definite acute myocardial infarction and another 16 had probable but not proven myocardial infarction. Of the 52 patients, 31 survived to leave hospital and all patients known to be alive are leading active and useful lives. In spite of an initial fear that medical treatment might be overused or misused by the officers, this has not been the case, and only about 13% of patients have received drugs from the officers. This paper deals with the setting up, staffing and training of the ambulance service and reviews its results.
Adult↗
The floppy mitral valve syndrome--a review of fourteen patients requiring valve surgery.
The correlation of clinical features with the operative findings in 14 patients with a floppy mitral valve is discussed. The clinical course is typified by rapidly progressive disability. An abrupt deterioration was present in five of our subjects and this may be due to rupture of chordae tendinea or stretching of the valve apparatus. The redundancy of the anterior cusp in 13 of our series may explain the absence of mid systolic clicks in all except one patient. The diagnosis of prolapse can be difficult to make prior to surgery because the prolapsed cusp may be masked by the regurgitant contrast medium. Hypokinesis and prominent inflow sacculation of the left ventricular inflow tract suggest an associated myocardial abnormality. Calcium was present in one valve and thus mitral valve calcification does not exclude the possibility of a floppy valve in patients with mitral regurgitation.
Adolescent↗