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Biomedical subjects

P L Thompson

Publications and source records attributed to P L Thompson.

At least 37 records · Page 2Linked to original sources

Angiotensin-converting enzyme gene polymorphism and carotid wall thickening in a community population.

The insertion/deletion (I/D) polymorphism of the angiotensin-converting enzyme (ACE) gene has been associated with an increased risk of coronary heart disease, but whether it is a risk factor for underlying atherosclerosis remains unclear. Therefore, we examined to see whether the ACE gene deletion polymorphism was associated with carotid wall thickening and atherosclerotic plaque formation in a large randomly selected community population. A total of 1111 subjects, aged 27 to 77 years, with an equal male:female ratio and equal numbers in each age decile, were randomly selected from the Perth community population. Mean common carotid intima-medial wall thickness (IMT) and focal plaque formation were assessed by high-resolution B-mode ultrasound. The ACE gene I/D polymorphism was detected by PCR. The distribution of the ACE genotypes conformed to the Hardy-Weinberg equilibrium (DD, 31.0%; ID, 48.4%; and II, 20.6%). The D allele was strongly correlated in a codominant fashion with plasma ACE activity (r(s)=0.53, P<0.0001), and accounted for 33% of the total variance in circulating ACE activity. No significant differences among the ACE genotypes were found with respect to age, sex, and conventional risk variables, including a history of hypertension and vascular disease. The average mean IMT and prevalence of increased IMT and focal plaque were not significantly different among genotypes in the overall population or in the subset (n=852) who were conventionally low risk by Framingham coronary heart disease risk score. Logistic regression analysis selected age, systolic blood pressure, pack-years of smoking, LDL cholesterol level, waist/hip ratio, and history of hypertension, but not the D allele, as multivariate predictors of increased IMT and carotid plaque formation. We conclude that, although the ACE I/D polymorphism is strongly related to ACE activity, it is not a risk predictor of carotid wall thickening or focal plaque formation when examined in a large randomly selected community population.

Adult↗

The primary angioplasty vs thrombolysis debate.

Early and complete coronary reperfusion can improve survival in myocardial infarction. Primary angioplasty can achieve TIMI grade 3 flow (complete restoration) in over 90% of cases. In comparison thrombolysis can achieve TIMI grade 3 flow in only just over 50%. Comparative trials have shown superior rates of death and reinfarction with a low haemorrhagic risk with PTCA compared with thrombolysis. Early clinical trials showed a clear superiority of primary angioplasty over thrombolysis but larger trials with larger number of endpoints have shown less impressive superiority. Wider application in community studies has not shown the benefits promised in the earlier studies, possibly due to dilution of experience. The impact of newer stent regimens vs nonnewer thrombolytic and antithrombotic regimens can only be determined by further clinical trials.

Angioplasty, Balloon, Coronary↗

Cardiology.

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Angiotensin-Converting Enzyme Inhibitors↗

Follow-up care after acute myocardial infarction.

OBJECTIVE: To examine the medical care received by patients following discharge from hospital after acute myocardial infarction (AMI). SETTING AND DESIGN: Community-based cross-sectional survey. PATIENTS: 2836 consecutive patients aged 25-64 years living in the Perth Statistical Division who were admitted to hospital with AMI during 1984-1988. After one reminder the response rate was 71%. RESULTS: Half of all respondents were in full-time employment at the time of their AMI. At follow-up this had fallen to a third. Over 80% of patients visited a cardiologist after AMI, with half remaining under consultant care to the time of survey. However, one in five patients reported no follow-up care at the time of survey. Seventy-three per cent of patients reported undergoing at least one exercise stress test after AMI, with 61% undergoing angiography, 16% angioplasty and 24% coronary bypass surgery. Large proportions of the patients accurately reported being prescribed beta-blockers and antiplatelet agents. The pattern of prescribing at discharge corresponded closely with the use of cardioactive agents at the time of survey and with drugs reported to have been taken continuously since discharge to the time of survey. CONCLUSIONS: These data suggest that follow-up care after AMI is both comprehensive and widespread. Such care may have contributed significantly to the overall decline in mortality from ischaemic heart disease.

Adrenergic beta-Antagonists↗

Changing patterns of medical treatment in acute myocardial infarction. Observations from the Perth MONICA Project 1984-1990.

TYPE OF STUDY: Descriptive study of trends in the drug therapy for acute myocardial infarction. SETTING: Population-based register of acute coronary events compiled for the years 1984 to 1990 in the course of the Perth MONICA project. CASES: 5294 cases meeting clinical criteria for acute myocardial infarction. RESULTS: Striking changes were seen in the use of aspirin before admission to hospital (from 4% to 18%). During the stay in hospital the use of beta-blockers increased steadily from 52% to 76%, while the use of aspirin increased 3.5-fold from 25% to 88% and the use of streptokinase increased 13.5-fold from 2.4% to 32.4%. The proportion of patients prescribed beta-blockers on discharge from hospital increased from 46% to 65% and that for aspirin rose from 16% to 83%. There were also major relative increases in the use of lipid-lowering agents and declines in the use of antiarrhythmic drugs. CONCLUSION: These trends in the pharmacological management of myocardial infarction mirror the emerging evidence from clinical trials, although the increases in the use of certain types of drugs antedated publication of the results of major randomised studies. The changes in therapy would partly explain observed improvements in case fatality and may have contributed to the decline in coronary mortality observed in the Perth community.

Adrenergic beta-Antagonists↗

The benefits of beta-blockade at the time of myocardial infarction.

Data from the World Health Organization Monitoring Trends and Determinants in Cardiovascular Disease (WHO MONICA) project, collected in Perth, are described. Patients taking a beta-blocker at the time of onset of myocardial infarction are a high-risk group, but univariate analysis of the data showed that the overall survival of patients on beta-blockers at 28 days was the same as for those not taking beta-blockers. A multiple logistic regression model analysis showed that the patients treated with beta-blockers had a survival advantage at 28 days, with a relative risk of death of 0.5. The mechanism of benefit is unclear. It does not appear to be an anti-arrhythmic effect, because beta-blockers did not affect survival in the first 24 h following a myocardial infarction, nor did they affect ventricular fibrillation. The effect may be due to a reduction in myocardial necrosis. Furthermore, an analysis of the incidence of coronary disease and type of drugs prescribed in Perth has indicated that beta-blockers may be contributing to a decrease in mortality due to coronary events.

Adrenergic beta-Antagonists↗

A randomized comparison of intravenous heparin with oral aspirin and dipyridamole 24 hours after recombinant tissue-type plasminogen activator for acute myocardial infarction. National Heart Foundation of Australia Coronary Thrombolysis Group.

BACKGROUND: This study addressed the need for heparin administration to be continued for more than 24 hours after coronary thrombolysis with recombinant tissue-type plasminogen activator (rt-PA). METHODS AND RESULTS: A total of 241 patients with acute myocardial infarction were treated with 100 mg rt-PA and a bolus of 5,000 units i.v. heparin followed by 1,000 units/hr i.v. heparin for 24 hours. At 24 hours, 202 patients were randomized to continue intravenous heparin therapy (n = 99) in full dosage or to discontinue heparin therapy and begin an oral antiplatelet regimen of aspirin (300 mg/day) and dipyridamole (300 mg/day) (n = 103). On prospective recording, there were no differences in the pattern of chest pain, reinfarction, or bleeding complications. Coronary angiography on cardiac catheterization at 7-10 days showed no differences in patency of the infarct-related artery. The proportion of patients with total occlusion (TIMI grade 0-1) of the infarct-related artery was 18.9% in the heparin group and 19.8% in the aspirin and dipyridamole group. In the patients with an incompletely occluded infarct-related artery, the lumen was reduced by 69 +/- 2% of normal in the heparin group and 67 +/- 2% in the aspirin and dipyridamole group. Left ventricular function assessed on cardiac catheterization and radionuclide study at day 2 and at 1 month showed no differences between the two groups. Left ventricular ejection fraction on radionuclide ventriculography at 1 month was 52.4 +/- 1.2% in the heparin group and 51.9 +/- 1.2% in the aspirin and dipyridamole group. CONCLUSIONS: We conclude that heparin therapy can be discontinued 24 hours after rt-PA therapy and replaced with an oral antiplatelet regimen without any adverse effects on chest pain, reinfarction, coronary patency, or left ventricular function.

Administration, Oral↗

Reduced risk of death at 28 days in patients taking a beta blocker before admission to hospital with myocardial infarction.

OBJECTIVE: To see whether patients taking an oral beta blocker at the time of admission to hospital with myocardial infarction have a reduced risk of death at 28 days. DESIGN: Retrospective analysis of data collected on patients admitted over four years. SETTING: Community based study. PATIENTS: 2430 Consecutive patients living in the Perth statistical division admitted to hospital with myocardial infarction during 1984-7. MAIN OUTCOME MEASURE: Survival at 28 days among patients taking a beta blocker at onset of myocardial infarction. RESULTS: Patients were grouped into those who were and were not taking a beta blocker at the time of admission. Though patients taking a beta blocker were older and more likely to have a history of myocardial infarction, angina, or hypertension, the overall mortality at 28 days was similar in the two groups. A logistic regression model used to adjust for factors predictive of cardiac death at 28 days confirmed that patients taking a beta blocker at the time of admission had a significantly reduced risk of death (relative risk 0.50; 95% confidence interval 0.34 to 0.76). Though the incidence of fatal ventricular fibrillation was similar in the two groups, mean peak creatine kinase activity was significantly lower in the beta blocker group. CONCLUSIONS: These data support the value of long term use of beta blockers in patients at risk of myocardial infarction. They suggest that patients taking these agents before admission to hospital with myocardial infarction have a significant survival advantage at 28 days, which may be due to a reduction in infarct size.

Adrenergic beta-Antagonists↗