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Biomedical subjects

J Emmerich

Publications and source records attributed to J Emmerich.

At least 145 records · Page 8Linked to original sources
PubMed1992

[Is regression of atherosclerosis possible?].

Experimental studies have shown the regression of atherosclerosis in animals given a cholesterol-rich diet and then given a normal diet or hypolipidemic therapy. Despite favourable results of clinical trials of primary prevention modifying the lipid profile, the concept of atherosclerosis regression in man remains very controversial. The methodological approach is difficult: this is based on angiographic data and requires strict standardisation of angiographic views and reliable quantitative techniques of analysis which are available with image processing. Several methodologically acceptable clinical coronary studies have shown not only stabilisation but also regression of atherosclerotic lesions with reductions of about 25% in total cholesterol levels and of about 40% in LDL cholesterol levels. These reductions were obtained either by drugs as in CLAS (Cholesterol Lowering Atherosclerosis Study), FATS (Familial Atherosclerosis Treatment Study) and SCOR (Specialized Center of Research Intervention Trial), by profound modifications in dietary habits as in the Lifestyle Heart Trial, or by surgery (ileo-caecal bypass) as in POSCH (Program On the Surgical Control of the Hyperlipidemias). On the other hand, trials with non-lipid lowering drugs such as the calcium antagonists (INTACT, MHIS) have not shown significant regression of existing atherosclerotic lesions but only a decrease on the number of new lesions. The clinical benefits of these regression studies are difficult to demonstrate given the limited period of observation, relatively small population numbers and the fact that in some cases the subjects were asymptomatic. The decrease in the number of cardiovascular events therefore seems relatively modest and concerns essentially subjects who were symptomatic initially. The clinical repercussion of studies of prevention involving a single lipid factor is probably partially due to the reduction in progression and anatomical regression of the atherosclerotic plaque.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1992

[Optimal serum cholesterol and efficacy of methods for lowering cholesterolemia].

Analysis of epidemiological studies enables definition of the optimal serum cholesterol level between 2 and 2.2 g/l (5.2 and 5.7 mmol/l). Higher levels are associated with an exponential risk of coronary artery disease: lower levels should be interpreted with caution because of the J-shaped curve of global mortality reported in several trials. In primary prevention, therapeutic trials have clearly shown that a significant reduction in the number of coronary event may be obtained by lowering the serum cholesterol (15 for every 1,000 patients treated). In trials performed to date this benefit has not resulted in any gain in global mortality. In secondary prevention, the benefits of lowering serum cholesterol on the incidence of coronary disease seems identical in terms of relative risk to that observed in primary prevention. Nevertheless, the benefits in terms of absolute risk are much higher because of the high incidence of coronary mortality in a patient population with a previous coronary event. Thus, for 1,000 patients treated, there are 50 less cardiac events and this is reflected in a reduction of global mortality of about 20 for every 1,000 patients treated.

Cholesterol↗
PubMed1992

[Should men aged 20 to 30 years with hypercholesterolemia be managed in the same way as older men?].

Serum cholesterol intervention studies have been mainly performed in middle-aged men. Is the extrapolation of these results to men aged 20 to 30 years justified? Atherosclerosis is a process which continues throughout life. It is clear that increased serum cholesterol levels are associated with a higher coronary risk. In addition, serum cholesterol levels increase with age up to 60 years old. Do young men obtain the same benefits from medical intervention as older men? Therapeutic trials have been performed in middle-aged men. The increase in life expectancy associated with a 6.7% lowering of the serum cholesterol by life-long dietary restrictions would only be 4 months in 20 year old subjects at high risk (hypertension, smokers, low HDL cholesterol). With a 20% reduction in serum cholesterol, the gain would be 12 months. There is no reason for not extrapolating acquired data in the over 30s to 20 to 30 year old subjects. Due to the fact that young subjects are exposed to the risk for longer periods, it is advisable to treat their hypercholesterolaemia even more seriously than that of older patients.

Adult↗
PubMed1992

[Should hypercholesterolemic women be treated?].

There have been few studies designed to evaluate the problem of hypercholesterolaemia in women despite the fact that, like men, cardiovascular disease is their main cause of death. Serum cholesterol is a risk factor in women, but the increased risk appears at much higher values of serum cholesterol than observed in men. In women, low HDL-cholesterol seems to be the best predictive factor for the occurrence of a coronary event, especially if the triglycerides are raised. The absence of therapeutic data on the treatment of hypercholesterolaemia in women underlines the need for a specific trial to assess the effects of lipid-lowering drugs in this population. The cardiovascular benefits of hormone substitute therapy at the menopause have been reported in several studies and a large scale randomised trial is under way to confirm these results. The benefit of hypercholesterolaemic therapy in women with mild hypercholesterolaemia has not been proved. When the serum cholesterol level is over 3 g/l (7.77 mmol/l), early treatment is advisable.

Adult↗
PubMed1992

[Hyperlipidemia in patients over 60 years old].

The management of hyperlipidemia in individuals aged 60 or over is a serious problem, given the frequency of metabolic abnormalities in this age group. The decision to treat must take into account a number of uncertainties. Hypercholesterolemia is a risk factor in the elderly and, in general, its importance varies like the other major risk factors (hypertension and smoking): the relative risk decreases with age but this decrease in relative risk is associated with an increase in the absolute risk because the prevalence of cardiovascular disease greatly increases with age. The serum cholesterol level increases with age but the physiopathological mechanism os this increase is poorly understood (reduction in the number of LDC receptors?). In the over 70s, serum cholesterol levels decrease, probably because of a selection due to the deaths of subjects at higher risk. No therapeutic trials have been performed to evaluate the effects of lowering the serum cholesterol in the over 60s. In addition, strict application of international recommendations in this age group would result in a large number of therapeutic interventions, the value of which would be questionable. Under these conditions, practical clinical advice is based on reasoned extrapolation of epidemiological data obtained in middle-aged men. Treatment should therefore be reserved for sever forms of hyperlipidemia, taking into consideration the life expectancy of the individual.

Aged↗
PubMed1992

Molecular abnormalities responsible for thrombosis. Genetic aspects.

The association between congenital deficiencies and recurrent thrombosis strongly suggests that antithrombin III, protein C and protein S play a major role in inhibiting thrombin formation in vivo. Genetic analysis using DNA fragment amplification by polymerase chain reaction and direct gene sequencing has led to the identification of many novel mutations in qualitative and quantitative deficiencies. Elucidation of the molecular basis of these deficiencies is critical to our understanding of natural antithrombotic mechanisms. It not only provides information on the structural features governing protein function, but also permits a better classification, based on genomic abnormalities of hereditary deficiencies responsible for mild to severe phenotypes and may prove of further value to define the most pertinent plasma assays for routine diagnosis.

Antithrombin III Deficiency↗
PubMed1991

Molecular basis for antithrombin III type I deficiency: three novel mutations located in exon IV.

Antithrombin III (AT III) type I deficiencies are characterized by a 50% decrease of both immunoreactive and functional protein and carry a high risk of thrombotic complication. We have studied the molecular basis for such deficiencies by asymmetric polymerase chain reaction amplification and direct sequencing of the seven exons and of the intron-exon junction of the AT III gene. Three different mutations were observed in the exon IV: a 4-bp deletion, a 2-bp deletion, and a nucleotide insertion. Each of these mutations results in a frameshift introducing premature stop codons at positions 313, 309, and 232, respectively. These results were confirmed by dot-blot analysis with allele-specific oligonucleotide probes. Furthermore, no mutation was observed in the other six exons. The comparison of the type of mutations observed by our group in six cases of type I deficiencies and in 16 cases of type II heparin binding site variants deficiencies suggests that the former are caused by heterogeneous molecular abnormalities while the latter are caused by recurrent missense mutations.

Adult↗
PubMed1991

Molecular basis for hereditary antithrombin III quantitative deficiencies: a stop codon in exon IIIa and a frameshift in exon VI.

Antithrombin III (AT III) is an inhibitor of serine protease (serpin) comprising 432 amino acids. Quantitative AT III deficiencies are associated with a high risk of thrombotic disease. Although this risk is smaller in patients with qualitative AT III deficiencies, the molecular defects characterizing the latter have been the subject of many studies. However, in quantitative AT III deficiencies, only three mutations have been described: Pro 407 to Leu and A1a404 to Thr (both located in the C-terminal part of the AT III molecule) and also a frameshift in exon IIIa. Using the asymmetric polymerase chain reaction (PCR) and genomic DNA analysis by direct sequencing, we detected two mutations in three unrelated families: (i) a C----T transition in exon IIIa in two families, leading to the replacement of the codon corresponding to Arg 129 by a stop codon, and (ii) in the third family, insertion of an adenine in the codon corresponding to Phe 408, a highly conserved serpin amino acid. This insertion altered the reading frame and led to the appearance of a premature stop signal. Patients of all three families were heterozygous for their abnormality. These results show that asymmetric PCR and genomic DNA analysis by direct sequencing permit fast identification of the molecular basis of quantitative AT III deficiencies. It is concluded that in many cases the absence of AT III gene product probably results from point mutation, as previously observed for another serpin, alpha-1-antitrypsin.

Adolescent↗
PubMed1990

Efficacy and safety of simvastatin (alone or in association with cholestyramine). A 1-year study in 66 patients with type II hyperlipoproteinaemia.

The effects and safety of simvastatin, an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, were investigated alone or in association with cholestyramine in 66 patients with hypercholesterolaemia, in a 1-year study. In type IIa hypercholesterolaemia (41 patients), the association was more effective than simvastatin used alone in lowering total cholesterol (37% vs 29%) and LDL-cholesterol (45% vs 37%). In type IIb hypercholesterolaemia (23 patients), the association simvastatin-cholestyramine did not appear more effective than simvastatin used alone. The decrease of apoprotein B was parallel to the LDL-cholesterol decrease. Apoprotein A1 did not change significantly. The long-term safety of simvastatin was good. No lens opacity was noted. The most serious side-effect in our study was myolysis which occurred in two patients with a marked increase in creatine phosphokinase.

Adult↗
PubMed1989

Diagnosis of coronary aneurysms in siblings: treatment with a new surgical procedure.

We report the cases of two brothers who simultaneously developed myocardial infarction, and in whom we found coronary artery aneurysms at echocardiography. In one case a new surgical procedure was performed. The aneurysm was bypassed by an aorto-coronary vein graft and the coronary ostium of the related coronary artery was closed. Thus, perfusion of the dependent vessels of the aneurysm was maintained, and the risk of distal embolism was prevented. The aetiologies of coronary artery aneurysms are discussed. In our patients the aneurysms were probably congenital, but we cannot exclude the possibility of previously undiagnosed Kawasaki's disease.

Adult↗
PubMed1988

[Effects of simvastatin on plasma lipids, lipoproteins and apoproteins (A1 and B). 24 cases of major primary hypercholesterolemia].

We studied the effects of simvastatin (MK 733), a new competitive inhibitor of HMG CoA reductase, alone and in combination with a bile acid sequestrant, cholestyramine, on serum levels of lipoproteins and apoproteins A1 and B, in 24 patients with familial hypercholesterolemia. After simvastatin treatment (40 mg/day) alone for 12 weeks, serum total and low density lipoprotein cholesterol decreased by 31 and 36 percent respectively. With the addition of cholestyramine, there was a 41 per cent total decrease in serum cholesterol from the control value and a 50 percent decrease in low density lipoprotein cholesterol. After cholestyramine treatment alone for 12 weeks, serum total and low density lipoprotein cholesterol decreased by 20 percent and 29 percent respectively. With the addition of simvastatin (20 mg per day), there was a 32 percent total decrease in serum cholesterol from the control value and a 43 percent decrease in low density lipoprotein cholesterol. High density lipoprotein cholesterol remained unchanged. No major adverse effect was observed. If long term safety can be confirmed, the simvastatin-cholestyramine regimen may prove useful in heterozygous familial hypercholesterolemia.

Adult↗
PubMed1988

[Changes in serum lipids and lipoproteins in 3 cases of heterozygous familial hypercholesterolemia treated by LDL apheresis on dextran sulfate-cellulose columns].

Three patients with heterozygote type IIa hyperlipoproteinemia were treated by specific LDL apheresis with a dextran sulfate-cellulose column every two weeks. Each apheresis resulted in a fall in total cholesterolemia of about 50 p. 100 with a parallel fall in apoprotein B. The average drop of 15 p. 100 in HDL-cholesterol appeared to be due to the hemodilution induced at the end of apheresis. After two months, cholesterol and apoprotein B concentrations before removal were 15 p. 100 lower than baseline values. Treatment was well tolerated. These findings appear encouraging for the treatment of heterozygote forms of familial hyperlipoproteinemia resistant to chemotherapy.

Adult↗
PubMedDate not supplied

Follow-up electron beam CT for the management of early phase Takayasu arteritis.

PURPOSE: The purpose of this work was to assess typical findings of Takayasu arteritis on serial CT examinations following therapy. METHOD: Serial CT studies were performed on 16 patients with early phase Takayasu arteritis. Mural or luminal changes of the aorta on successive CT scans were compared with clinical data. RESULTS: Vascular lesions progressed during follow-up in 6 of 16 patients. In one patient, progression of lesions was symptomatic. In the other five of six patients with worsening lesions, vascular progression occurred without new clinical symptoms and was first identified on CT scans. One of these five had dilatation of the ascending aorta and required aortic repair. Four others had progression of stenotic vascular lesions leading to changes in medical treatment only or in combination with either surgery or angioplasty. For two of them, CT examinations showed decreased mural lesions after changes in medical treatment. CONCLUSION: CT examinations performed in treated patients with Takayasu arteritis demonstrate either regression, stabilization, or progression of vascular lesions. Serial CT examinations may thus be useful for evaluating response to treatment.

Adult↗