Publications
429 results found
Thompson GR, 1992, Progression and regression of coronary artery disease, Current Opinion in Lipidology, Vol: 3, Pages: 263-267, ISSN: 0957-9672
The probability that coronary atherosclerotic lesions will progress increases with their severity and is accentuated further by concomitant hyperlipidaemia. Effective lipid-lowering therapy often arrests or induces regression of such lesions, as has been shown in seven randomized angiographic studies. In three of these trials significant reductions in cardiovascular events were observed, suggestive of plaque stabilization in treated patients.
Thompson GR, Wilson P, 1992, Coronary risk factors and their assessment, ISBN: 9781870026819
Thompson GR, 1991, Lipid-lowering drugs: focus on HMG-CoA reductase inhibitors. Introduction., Atherosclerosis, Vol: 91 Suppl, Pages: S1-S2, ISSN: 0021-9150
, 1991, Dietary reduction of serum cholesterol concentration., BMJ, Vol: 303, Pages: 1331-1333, ISSN: 0959-8138
THOMPSON GR, 1991, DIETARY REDUCTION OF SERUM-CHOLESTEROL CONCENTRATION, BRITISH MEDICAL JOURNAL, Vol: 303, Pages: 1332-1332, ISSN: 0959-8138
MAHER VMG, GALLAGHER JJ, THOMPSON GR, et al., 1991, RESPONSE TO CHOLESTEROL-LOWERING DRUGS IN FAMILIAL DEFECTIVE APOLIPOPROTEIN-B-100, ATHEROSCLEROSIS, Vol: 91, Pages: 73-76, ISSN: 0021-9150
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- Citations: 23
, 1991, Risk of fatal coronary heart disease in familial hypercholesterolaemia. Scientific Steering Committee on behalf of the Simon Broome Register Group., BMJ, Vol: 303, Pages: 893-896, ISSN: 0959-8138
OBJECTIVES: (a) To determine the excess mortality from all causes and from coronary heart disease in patients with familial hypercholesterolaemia; (b) to examine how useful various criteria for selective measurement of cholesterol concentration in cardiovascular screening programmes are in identifying these patients. DESIGN: Prospective cohort study. SETTING: Eleven hospital outpatient lipid clinics in the United Kingdom. PATIENTS: 282 men and 244 women aged 20-74 with heterozygous familial hypercholesterolaemia. MAIN OUTCOME MEASURE: Standardised mortality ratio, all adults in England and Wales being taken as standard (standardised mortality ratio = 100 for standard population). RESULTS: The cohort was followed up for 2234 person years during 1980-9. Fifteen of the 24 deaths were due to coronary heart disease, giving a standardised mortality ratio of 386 (95% confidence interval 210 to 639). The excess mortality from this cause was highest at age 20-39 (standardised mortality ratio 9686; 3670 to 21,800) and decreased significantly with age. The standardised mortality ratio for all causes was 183 (117 to 273) and also was highest at age 20-39 (standardised mortality ratio 902; 329 to 1950). There was no significant difference between men and women. Criteria for measurement of cholesterol concentration in cardiovascular screening programmes (family history, presence of myocardial infarction, angina, stroke, corneal arcus, xanthelasma, obesity, hypertension, diabetes, or any of these) were present in 78% of patients. CONCLUSIONS: Familial hypercholesterolaemia is associated with a substantial excess mortality from coronary heart disease in young adults but may not be associated with a substantial excess mortality in older patients. Criteria for selective measurement of cholesterol concentration in cardiovascular screening programmes identify about three quarters of patients with the clinically overt condition.
MAHER VMG, GALLAGHER J, THOMPSON GR, et al., 1991, RESPONSE TO CHOLESTEROL-LOWERING THERAPY IN PATIENTS WITH FAMILIAL DEFECTIVE APOLIPOPROTEIN B-100, ATHEROSCLEROSIS, Vol: 90, Pages: 227-227, ISSN: 0021-9150
WILE D, NITHTHYANANTHAN S, TRAYNER I, et al., 1991, APOLIPOPROTEIN-E(2) ISOFORMS OF DIFFERENT MOBILITY - A NOVEL CAUSE OF TYPE-III HYPERLIPOPROTEINEMIA, ATHEROSCLEROSIS, Vol: 90, Pages: 223-223, ISSN: 0021-9150
THOMPSON GR, 1991, CHOLESTEROL LOWERING AND NONCARDIAC MORTALITY, LANCET, Vol: 338, Pages: 126-126, ISSN: 0140-6736
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- Citations: 1
Barbir M, Banner N, Thompson GR, et al., 1991, Relationship of immunosuppression and serum lipids to the development of coronary arterial disease in the transplanted heart., Int J Cardiol, Vol: 32, Pages: 51-56, ISSN: 0167-5273
Coronary arterial disease in the cardiac allograft has emerged as the most serious long term complication of cardiac transplantation. The influence of patient-related and other potential risk factors on the development of coronary arterial disease at 1 year subsequent to cardiac transplantation was examined in 207 recipients. The mean age of donors in patients with coronary arterial disease was 28.5 +/- 9.5 years, compared to 22.6 +/- 7.9 years in patients without coronary arterial disease (P less than 0.01). Eight of the 35 patients who received immunosuppression by means of prednisone and azathioprine developed coronary arterial disease compared to 5 of the 172 patients who were treated with cyclosporin and azathioprine without routine oral prednisone (P less than 0.01). The relationship of levels of serum lipids to the subsequent development of coronary arterial disease was investigated in 95 patients with angiographically normal coronary arteries one year after cardiac transplantation. The cumulative probability of coronary arterial disease in those with total cholesterol greater than 5.8 mmol/l was 9.3% at 2 years (n = 40), 24.4% at 4 years (n = 21) and 45% at 4 years (n = 9) compared with 4.3% at 2 years (n = 45), 7.4% at 3 years (n = 32) and 14% at 4 years (n = 14) in those with a total cholesterol less than 5.8 mmol/l (P less than 0.05). Similarly, the incidence of coronary arterial disease was increased in patients with serum triglyceride greater than 1.4 mmol/l (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
BARBIR M, BANNER N, THOMPSON GR, et al., 1991, RELATIONSHIP OF IMMUNOSUPPRESSION AND SERUM-LIPIDS TO THE DEVELOPMENT OF CORONARY ARTERIAL-DISEASE IN THE TRANSPLANTED HEART, INTERNATIONAL JOURNAL OF CARDIOLOGY, Vol: 32, Pages: 51-56, ISSN: 0167-5273
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- Citations: 29
SCOPPOLA A, MAHER VMG, THOMPSON GR, et al., 1991, QUANTITATION OF PLASMA MEVALONIC ACID USING GAS-CHROMATOGRAPHY ELECTRON-CAPTURE MASS-SPECTROMETRY, JOURNAL OF LIPID RESEARCH, Vol: 32, Pages: 1057-1060, ISSN: 0022-2275
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- Citations: 52
MICHISHITA I, THOMPSON GR, 1991, CHOLESTEROL FLUX IN CHOLESTEROL ESTER-LOADED MACROPHAGES IN AN INVITRO PERFUSION SYSTEM, ATHEROSCLEROSIS, Vol: 88, Pages: 203-211, ISSN: 0021-9150
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- Citations: 4
THOMPSON GR, 1991, WHAT SHOULD BE DONE ABOUT ASYMPTOMATIC HYPERCHOLESTEROLEMIA, BRITISH MEDICAL JOURNAL, Vol: 302, Pages: 605-606, ISSN: 0959-8138
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- Citations: 7
THOMPSON GR, 1991, GUIDELINES ON MANAGEMENT OF HYPERLIPEMIA, BRITISH MEDICAL JOURNAL, Vol: 302, Pages: 239-239, ISSN: 0959-8138
Thompson GR, 1991, Editorial, Current Opinion in Lipidology, Vol: 2, ISSN: 0957-9672
Laker M, Reckless J, Betteridge J, et al., 1991, Facilities for the management of patients with lipid disorders in the United Kingdom: results of the British Hyperlipidaemia Association Survey., Health Trends, Vol: 23, Pages: 147-149, ISSN: 0017-9132
A national survey was undertaken by the British Hyperlipidaemia Association to obtain data on the current clinical practice for the investigation and management of patients with hyperlipidaemia. An additional objective of the survey was to establish a United Kingdom register of lipid clinics. The results show a considerable variation in the availability of lipid clinics, and medical practitioners involved in these clinics came from a variety of specialty backgrounds. Some clinics had clearly defined policies with regard to acceptance of referrals. However, deficiencies in clinical services were identified including the lack of dietetic and laboratory support.
, 1990, Lipoprotein (a) and coronary heart disease in patients with familial hypercholesterolemia., N Engl J Med, Vol: 323, Pages: 1773-1774, ISSN: 0028-4793
SEED M, BOERWINKLE E, THOMPSON GR, et al., 1990, LIPOPROTEIN(A) AND CORONARY HEART-DISEASE IN PATIENTS WITH FAMILIAL HYPERCHOLESTEROLEMIA - REPLY, NEW ENGLAND JOURNAL OF MEDICINE, Vol: 323, Pages: 1774-1774, ISSN: 0028-4793
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- Citations: 1
Thompson GR, 1990, Management of hyperlipidaemia, Journal of the Institute of Medicine, Vol: 12, Pages: 269-278, ISSN: 0259-0972
THOMPSON GR, 1990, HYPERLIPIDEMIA AND THE PROGRESSION OF DISEASE IN THE CORONARY CIRCULATION, CURRENT OPINION IN CARDIOLOGY, Vol: 5, Pages: 753-757, ISSN: 0268-4705
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- Citations: 1
KEHELY A, BARBIR M, TAMUGUR E, et al., 1990, HIGH PREVALENCE OF RAISED LEVELS OF LP(A) AND APO-B AFTER CARDIAC TRANSPLANTATION, ATHEROSCLEROSIS, Vol: 85, Pages: 97-97, ISSN: 0021-9150
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- Citations: 2
MAHER VMG, TRAINER PJ, ANDERSON JV, et al., 1990, MECHANISM OF ORTHO,PARA'-DDD-INDUCED HYPERCHOLESTEROL-ANEMIA IN PATIENTS WITH CUSHINGS-DISEASE, ATHEROSCLEROSIS, Vol: 85, Pages: 93-93, ISSN: 0021-9150
THOMPSON GR, 1990, PRIMARY HYPERLIPEMIA, BRITISH MEDICAL BULLETIN, Vol: 46, Pages: 986-1004, ISSN: 0007-1420
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- Citations: 18
Thompson GR, 1990, Primary hyperlipidaemia., Br Med Bull, Vol: 46, Pages: 986-1004, ISSN: 0007-1420
It is estimated that over 60% of the variability in serum lipids is genetically determined, most of this variation being due to polygenic influences. Interaction between the latter and environmental factors is probably the commonest cause of hyperlipidaemia in the general population. Familial forms of hyperlipidaemia are usually more clearly defined, especially those which have a monogenic or dominant pattern of inheritance, but are less common. This type of disorder, exemplified by familial hypercholesterolaemia, is expressed independently of environmental influences. In contrast, in familial type III hyperlipoproteinaemia inheritance of the underlying gene defect is often insufficient to produce hyperlipidaemia unless additional environmental or genetic influences coexist. Rarely, hyperlipidaemia is recessively inherited, as in familial deficiency of lipoprotein lipase and of apolipoprotein CII. Primary hyperlipidaemias characterized by severe hypertriglyceridaemia predispose to acute pancreatitis whereas those disorders characterized by hypercholesterolaemia, apart from hyper alpha lipoproteinaemia, are associated with an increased risk of premature vascular disease.
SEED M, HOPPICHLER F, REAVELEY D, et al., 1990, RELATION OF SERUM LIPOPROTEIN(A) CONCENTRATION AND APOLIPOPROTEIN(A) PHENOTYPE TO CORONARY HEART-DISEASE IN PATIENTS WITH FAMILIAL HYPERCHOLESTEROLEMIA, NEW ENGLAND JOURNAL OF MEDICINE, Vol: 322, Pages: 1494-1499, ISSN: 0028-4793
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- Citations: 574
MAHER VMG, THOMPSON GR, 1990, HMG COA REDUCTASE INHIBITORS AS LIPID-LOWERING AGENTS - 5 YEARS EXPERIENCE WITH LOVASTATIN AND AN APPRAISAL OF SIMVASTATIN AND PRAVASTATIN, QUARTERLY JOURNAL OF MEDICINE, Vol: 74, Pages: 165-175, ISSN: 0033-5622
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- Citations: 37
Maher VMG, Thompson GR, 1990, Analysis of evidence from cholesterol-lowering and regression trials, Pages: 199-203, ISSN: 0267-5323
Since 1980 five major trials of lipid-lowering therapy in the prevention of CHD have given a positive result. Three have been trials of primary prevention, two of secondary intervention. Significant decreases in CHD occured in all five but decreases in total mortality were observed only in the two secondary prevention trials. The average reduction in CHD in these five trials was 29%, which was associated with mean decreases in total cholesterol and triglyceride of 12% and 19% respectively; in two trials there was a mean increase in HDL cholesterol of 7%. Thus, relatively small changes in serum lipids achieved by diet or drug can reduce the combined morbidity and mortality of those with pre-existing CHD. Statistical analysis of these and various other diet and drug trials indicates that for every 1% decrease in serum cholesterol there is a 2% reduction in CHD risk. Until recently angiographic evidence of regression of human atherosclerosis was very limited but it is now apparent that effective lipid-lowering therapy favourably influences atheromatous lesions. Moderate reductions of LDL cholesterol and modest increases in the HDL:LDL ratio by treatment were associated with a significant reduction in the percentage of coronary lesions which progressed, whereas more marked changes in these variable resulted in a significant increase in lesions which regressed. The recent introduction of HMG CoA reductase inhibitors especially when used in conjuction with other forms of lipid-lowering therapy, provides a more effective means of reducing LDL levels than has been available previously; several regression trials which involve these drugs are now in progress.
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