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Biomedical subjects

P L Thompson

Publications and source records attributed to P L Thompson.

At least 55 records · Page 3Linked to original sources
PubMed1988

Prognostic significance of an early rise to peak creatine kinase after acute myocardial infarction.

Because an early rise to peak creatine kinase (CK) is regarded as a noninvasive marker of early coronary reperfusion, the short- and long-term significance of this phenomenon was studied. In a series of consecutive patients admitted between 1974 and 1976 with acute myocardial infarction (AMI), 2 hourly CK estimations were performed. Complete CK curves were obtained in 102 patients, all of whom have been followed for 10 years. Without reference to their clinical course or follow-up, patients were divided into those with CK curves peaking less than or equal to 15 hours (mean 11 hours; n = 41) and those with curves peaking greater than 15 hours (mean 21 hours; n = 61). There were no differences in age, Norris index, location of AMI or past history of coronary artery disease between the groups; however, the mean peak CK was higher in the late peak group (p less than 0.05) and there were more non-Q-wave infarcts in the early peak group (p less than 0.01). In the first 9 months of follow-up there were fewer cardiac deaths in the early peak group (5 vs 13%), but this difference was not significant, and at 12 months the survival curves crossed. At 10 years, survival was 42% in the early peak group and 65% in the late peak group (p less than 0.05). Cox regression analysis showed that early peaking of the CK curve was an independent marker for cardiac death overall (relative risk 2.3, p less than 0.02). In 1-year survivors the relative risk increased to 3.8 (p less than 0.008).(ABSTRACT TRUNCATED AT 250 WORDS)

Clinical Enzyme Tests↗
PubMed1987

Differences in left ventricular function between anterior and inferior myocardial infarction of equivalent enzymatic size.

The reasons for the poorer prognosis of anterior versus inferior myocardial infarction of equivalent enzymatic size remain uncertain. We investigated whether there are differences in left ventricular function between patients with anterior and inferior infarctions of equivalent enzymatic size to account for their differing outcomes. Clinical, serum enzyme, and electrocardiographic data were prospectively recorded in a consecutive series of patients less than 70 years of age with their first myocardial infarction. At 29 +/- 6 days following infarction, ejection fraction and left ventricular wall motion were assessed by gated heart scintigraphy and functional capacity by treadmill exercise testing in 19 patients with anterior and in 23 patients with inferior myocardial infarction. Peak creatine kinase and QRS scores were used to estimate total infarct size and left ventricular infarct size respectively. The anterior infarcts were of similar size to the inferior infarcts as determined by peak creatine kinase (1444 [mean] +/- 1161 [SD] U/L versus 1484 [mean] +/- 1182 [SD] U/L, respectively, P = 0.91) and peak aspartate transaminases (174 +/- 112 U/L versus 164 +/- 102 U/L, P = 0.78). The anterior myocardial infarct group had a greater percentage of the left ventricle infarcted on QRS scoring than the inferior infarct group (25.9 +/- 14.4% versus 11.1 +/- 6.0% respectively, P = 0.0004), lower global left ventricular ejection fraction (45.8 +/- 16% versus 54.6 +/- 9.2%, P = 0.04) and greater left ventricular regional wall abnormality. A significant negative correlation existed between left ventricular ejection fraction and peak creatine kinase for both groups, but was more marked with anterior infarction (r = -0.78, P less than 0.01) compared with inferior infarction (r = -0.49, P less than 0.05). Exercise-induced ST segment elevation was more frequent in the anterior than the inferior infarct group (59% versus 18%, P less than 0.02). However, both infarct locations had similar exercise tolerance, exercise-induced angina and ST segment depression. Despite equivalence of infarct size of the two infarct locations on enzyme testing, anterior infarction was associated with greater abnormality of left ventricular function with lower resting global left ventricular ejection fraction; greater resting left ventricular regional wall abnormality and greater exercise-induced ST segment elevation. These differences probably contribute to the poorer prognosis of patients with anterior infarction compared to those with inferior infarction of equivalent enzymatic size, given the previously well-documented prognostic importance of left ventricular function.

Aged↗
PubMed1986

Anterior ST segment depression in inferior myocardial infarction: effect on complications and long-term survival.

The effect of anterior ST segment depression in inferior myocardial infarction on early complications and long-term prognosis was studied. A modification of the Minnesota Code was used for grading the extent of ST segment depression in leads V2 to V4 on the first hospital electrocardiogram. In 267 patients with acute inferior myocardial infarction, 107 had isoelectric anterior ST segments, 84 had minor (less than or equal to 0.5 mm) depression, and 76 had major (greater than 0.5 mm) depression. Patients with anterior ST segment depression had higher serum enzyme levels, higher Norris coronary prognostic indices, and more frequent cardiac failure during the acute stages, but similar 28 day case fatality rate (11.1%) compared with patients without anterior ST segment depression (12.6%). In the subsequent four years total cardiac death rates were not significantly different and the pattern of survival was not influenced, but there was a higher fatal re-infarction rate in patients with major anterior ST segment depression. Thus, anterior ST segment depression in inferior myocardial infarction was associated with more severe infarction in the early phase but was not a reliable marker of high risk after recovery. Selection of patients for further investigation should not be based on this observation alone.

Actuarial Analysis↗
PubMed1986

Prognostic significance of electrocardiographic site of infarction after correction for enzymatic size of infarction.

To assess whether the site of myocardial infarction is an independent prognostic indicator, the outcome of patients with anterior myocardial infarction was compared with that of patients with inferior infarction. A consecutive series of patients who had suffered their first myocardial infarction was analyzed (398 with anterior and 391 with inferior infarction). Patients with anterior myocardial infarction had a higher 1 year mortality than those with inferior infarction (18.3% vs 10.5%, p = .002). When patients were matched for infarct size determined by peak creatine kinase (CK) level expressed as a multiple of the upper limit of normal, those with anterior myocardial infarction tended to have a higher 1 year mortality than those with inferior infarction for all subgroups of peak CK. Early mortality (day 1 to 28 after myocardial infarction) was greater in the anterior than in the inferior myocardial infarction group (10% vs 6.4%, p = .03); this was most significant when peak CK was greater than four times normal (12.4% vs 7.0%, p = .04). Late mortality was also higher in the anterior (8.4% vs 4.1%, p = .04) than the inferior infarction group and this was most significant when peak CK was less than two times normal (15.2% vs 0%, p = .02) or greater than eight times normal (10.6% vs 4.1%, p = .04). Multivariate analysis with proportional-hazards regression confirmed the prognostic significance of location of infarction independent of peak CK level. Thus, infarct location was found to be a predictor of prognosis that is independent of infarct size based on peak CK levels.

Actuarial Analysis↗
PubMed1985

Prognostic significance of left ventricular ejection fraction after acute myocardial infarction. A bedside radionuclide study.

The prognostic significance of left ventricular ejection fraction measurements obtained at the bedside was assessed in 171 patients as soon as possible after acute myocardial infarction. Ejection fraction was measured with a radionuclide first pass portable probe method within a mean of 24 hours of the onset of major symptoms. The results were related prospectively to the subsequent incidence of ventricular fibrillation in hospital, and to hospital and postdischarge deaths in a mean follow up period of 15 (range 9-21) months. All eight episodes of primary ventricular fibrillation, all 12 deaths due to pump failure in hospital, and also 12 out of 13 postdischarge deaths occurred in that minority of 81 patients whose initial postinfarction left ventricular ejection fraction was less than 0.35. Multivariate correlation with clinical, enzymatic, and electrocardiographic indicators of myocardial infarction showed that the prognostic significance of these indicators could largely be explained by their association with low left ventricular ejection fractions. Left ventricular ejection fraction measured within the initial 24 hours after acute myocardial infarction predicts prognosis throughout the subsequent year.

Adult↗
PubMed1984

Trends in ischemic heart disease mortality and morbidity in Perth Statistical Division.

Trends in mortality from Ischemic Heart Disease (IHD) and other principal causes of death, and in hospital admission rates for Acute Myocardial Infarction (AMI) have been studied in residents aged 35-64 years of the Perth Statistical Division for the period 1968-1982. Death rates were based on data abstracted from official statistics or computer tapes of unit death records. Hospital admission rates were derived from the computer tapes of the Western Australian Hospital Inpatient Survey, 1968-1982. Since 1968, mortality from IHD has fallen in the Perth Statistical Division in both males and females by 30% and 33%, respectively. This fall has occurred principally in deaths occurring out-of-hospital and has been accompanied by similar falls in mortality from other vascular diseases and in total mortality. Hospital admission rates for Acute Myocardial Infarction (AMI) in the Perth Statistical Division have fallen since 1971 by 17% in males and 27% in females. These findings taken together suggest that the improvement in IHD mortality in Western Australia has been due mainly to a fall in the incidence of acute manifestations of IHD (sudden death and AMI), rather than improvements in case fatality. The possible underlying mechanisms responsible for this are discussed.

Adult↗
PubMed1984

Assessment of the impact of coronary artery surgery on mortality after recovery from myocardial infarction.

Death rates over a nine year period were studied in 1,232 survivors of myocardial infarction. From 1973 to 1981, the 29 to 365 day case fatality rate in 28 day survivors dropped from 13.3% to 3.2%. This down-trend in case fatality was highly significant, averaging 14.3% in each year. After adjustment for changes in age and severity of infarction, using a prognostic score derived from the Perth Coronary Register (the PCR score), the estimated decline was still 12.2% in each year. During the nine years, the rate of coronary surgery in the post-infarction year rose from 1.5% to 12.0%. Overall, the surgically treated cases had a lower case fatality rate (1.6%) than the medically treated cases (7.7%). However, the surgical cases had a better prognosis at the time of infarction than the medical cases. When the severity of infarction (PCR score) and year of admission were considered, coronary surgery in the post-infarction year had no independent effect on outcome.

Australia↗
PubMed1983

Long-term prognosis after recovery from myocardial infarction: a nine year follow-up of the Perth Coronary Register.

Patients registered by the 1971 Perth Coronary Register as having suffered a myocardial infarction were followed up for 9 years. The Register was a community-based study that used standard methods and criteria as part of a World Health Organization collaborative investigation. Of the 1078 patients studied, 77% survived the first 24 hr and 62% the first 28 days; 0.3% were lost to follow-up. For the 666 patients alive at 28 days, the crude 1, 5, and 9 year survival rates were 88%, 67%, and 52%, respectively. The relationship between 54 variables and the survival of patients alive 28 days after myocardial infarction was examined by life-table methods and the log rank test, and then by fitting a proportional hazards model to the data. The important prognostic factors were age, sex, past history of myocardial infarction, stroke, diabetes and hypertension, tachycardia at presentation, hypotension at presentation, and the occurrence of arrhythmias as short-term complications. The most appropriate mathematical description of the joint effects of the prognostic factors was a multiplicative model with no interaction.

Adult↗
PubMed1980

Mitochondrial myopathy with cardiomyopathy, lactic acidosis and response to prednisone and thiamine.

Clinical, biochemical and pathological findings are described in a 23-year-old male with a mitochondrial myopathy who had a high-output circulatory state and cardiomyopathy which resulted in cardiac insufficiency 22 years before presentation of the skeletal myopathy. Venous lactate levels were elevated and severe lactic acidosis developed at one stage of the illness. Electron microscopy of muscle tissue showed various mitochondrial abnormalities and accumulation of neutral lipids which was confirmed histochemically and by thin-layer chromatography. Marked improvement in the myopathy occurred after commencement of prednisone and thiamine and was maintained following withdrawal of these drugs. The metabolic defect in this case has not been defined, but an abnormality in the Kreb's over-production of lactate and lipid accumulation in muscle is postulated.

Acidosis↗
PubMed1979

Embolism in thyrotoxic atrial fibrillation.

Of 210 patients with thyrotoxicosis, 21 (10%) had atrial fibrillation. Five of these patients (24%) had systemic emboli (which were multiple in three patients, one of whom died) and two other patients had pulmonary embolism. Embolic disease is common in thyrotoxic atrial fibrillation, and anticoagulant therapy should be considered for all patients.

Aged↗
PubMed1979

Limitation of myocardial infarct size: review of experimental basis and clinical trials.

Limitation of myocardial injury after coronary occlusion is an exciting, recently recognised, but as yet unconfirmed, possibility in the treatment of myocardial infarction. Review of the experimental basis for the concept indicates that although manipulation of the ST segment of the electrocardiogram is not sufficient proof that myocardial necrosis can be limited, more robust experimental methods have confirmed the efficacy of a variety of interventions in experimental coronary occlusion. The effect of myocardial infarct size in determining acute prognosis and complications has been confirmed in clinical studies though the importance of infarct size lessens after recovery. Reported attempts at limiting myocardial necrosis in patients with myocardial infarction have so far not been sufficiently convincing to merit universal clinical application. Results of large scale randomised trials currently underway are awaited with interest.

Animals↗
PubMed1979

Enzymatic indices of myocardial necrosis: influence on short- and long-term prognosis after myocardial infarction.

The prognostic effect of the peak level of serum creatine kinase (CK) and aspartate transaminase (AST), estimated daily for 3--5 days after acute myocardial infarction, was studied in 560 patients who survived the first day in hospital. In a subgroup of 54 patients, peak enzyme levels correlated well with the cumulated CK release (r = 0.90 with peak CK, r = 0.74 with peak AST), thus reflecting the extent of myocardial necrosis. Total mortality within a year after infarction was not significantly different in the lower three quintiles of peak serum enzyme level, but increased from 15.5% to 27.9% (p less than 0.001) when peak CK level exceeded eight times the upper limit of normal (8 X N) and form 13.1% to 34.8% (p less than 0.001) when peak AST level exceeded five time the upper limit of normal (5 X N). The effect of high enzyme levels was more marked in patients with a prior history of myocardial infarction; mortality increased from 14.7% for first infarctions to 18.2% for recurrent infarctions, with peak CK greater than 8 X N, and from 27.0% for first infarctions to 38.0% for recurrent infarctions with peak CK greater than 8 X N. Early mortality was more significantly affected (p less than 0.0001) than late mortality (p less than 0.05). In hospital survivors, late deaths from cardiac decompensation were three times (p less than 0.05) more frequent in the high enzyme group as in the low enzyme group, but the number of sudden deaths was unaffected. These findings have important implications for studies of reduction of myocardial infarct size.

Aspartate Aminotransferases↗
PubMed1978

Stroke after acute myocardial infarction: relation to infarct size.

In a consecutive series of 783 patients with acute myocardial infarction, 13 (1.7%) suffered a stroke. In all but one case the strokes occurred among the 255 patients whose peak creatine kinase (CK) concentrations fell in the upper third of the range of values (over 1160 IU/l, about eight times the upper limit of normal); the exception was a patient with a pre-existing ventricular aneurysm. The incidence of stroke in the patients with CK over 1160 IU/l was 4.7%, 24 times the incidence when peak CK was below this value (0.2%). Higher peak serum enzyme concentrations were associated with an even higher incidence of stroke. Comparison of peak enzyme concentrations with cumulated CK showed a close correlation (r = 0.90 with peak CK; r = 0.85 with peak aspartate transaminase), suggesting that the peak enzyme values reflected infarct size. Thus the risk of stroke after infarction was a function of the size of the myocardial infarct; two-thirds of the patients had negligible risk of stroke and did not need anticoagulant prophylaxis.

Adult↗