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At least 19 recordsLinked to original sources

PubMed1992

Dyslipidaemias, insulin resistance and atherosclerosis.

Recent studies have demonstrated that insulin resistance, a proportionate decrease in insulin action at all insulin concentrations, is associated with clustering of many cardiovascular risk factors, particularly hyperlipidaemias. Already epidemiological studies have indicated that high insulin levels are related to low high-density lipoprotein (HDL) cholesterol and high total and very-low-density lipoprotein (VLDL) triglyceride levels. Recent studies based on the direct quantification of insulin resistance by the euglycaemic clamp method have verified these findings. In contrast, insulin resistance seems not to be associated with high low-density lipoprotein (LDL) cholesterol. Abnormalities in HDL and VLDL levels may contribute to accelerated atherosclerosis, but there is evidence that insulin resistance is also directly associated with asymptomatic atherosclerosis. Thus, prevention of atherosclerosis should not be targeted only to the lowering of LDL cholesterol, but also to the reduction of the degree of insulin resistance either with diet, weight reduction, regular exercise or drug therapy.

Arteriosclerosis↗

PubMed1992

Evidence for gene-environmental interactions in Utah families with hypertension, dyslipidaemia and early coronary heart disease.

1. Among 45,258 Utah families surveyed, about 4% have a strong aggregation of early coronary disease. In detailed clinical evaluation, about 21% of such high risk coronary families were found to have familial dyslipidaemic hypertension (FDH) and about 3% were found to have heterozygous familial hypercholesterolaemia (hFH). 2. Common and potentially modifiable environmental factors seem to play an important role in these high risk families. Non-genetic obesity promotes the expression of FDH. A high fat diet promotes the expression of FH. Cigarette smoking promotes earlier death in all coronary prone families. 3. Practical approaches are suggested for helping coronary prone pedigrees by applying our understanding of genetic and environmental factors that promote earlier coronary disease onset.

Adult↗

PubMed1992

Effect of diuretics on the plasma lipid profile.

Hypertension, dyslipidaemia, glucose intolerance (associated with insulin resistance and compensatory hyperinsulinaemia) and other abnormalities are complementary coronary risk factors which often occur in association. A familial trait for essential hypertension seems to coexist commonly with defects in carbohydrate and lipoprotein metabolism which can be detected before the appearance of hypertension. Diabetes mellitus as well as obesity promotes the development of hypertension and dyslipidaemia. Moreover, certain drugs used for antihypertensive therapy can further modify lipoprotein and glucose metabolism. Thiazides in high dosage and loop-diuretics can increase serum low-density-lipoprotein cholesterol (LDL-C) and/or very-LDL-C and the total C/high-density lipoprotein cholesterol (HDL-C) ratio, while HDL-C is largely unchanged; triglycerides (Tg) are also often elevated. Premenopausal women may be protected from this side effect. Whether diuretic-induced dyslipidaemia is dose-dependent and low thiazide doses (i.e. hydrochlorothiazide < or = 12.5 mg daily) are less active, awaits clarification. The diuretic-antihypertensive agent, indapamide, given at a dose of 2.5 mg.day-1, seems to exert no relevant effect on serum lipoprotein or glucose metabolism. The potassium-sparing diuretic, spironolactone, also may be largely neutral with regard to lipids. Moreover, potassium sparing diuretics may possibly counteract, at least in part, a dyslipidaemic influence of potassium-loosing diuretics in medium dose. Drug-induced dyslipidaemia, as well as glucose intolerance, represent potentially adverse influences. In the hypertensive population, effective blood pressure control with traditional drug therapy based on thiazide-type diuretics in high dosage led to a distinct decrease in cerebrovascular morbidity and mortality, but a lesser decrease in coronary events.(ABSTRACT TRUNCATED AT 250 WORDS)

Diuretics↗

PubMed1978

[Results and prospects of therapy of type IV dyslipidemia with chenic acid].

Administration of 500 mg/day chenodeoxycholic acid for 60 days in a series of 44 patients with type IV dyslipidaemia led to gradual normalisation of triglycerides by the end of the treatment. Falls were greater in subjects with initially higher values, but were independent of age, sex, weight and type of diet. Further falls were obtained by repeating the treatment in some cases when prebetalipoproteins rose again. Decreases were already evident by the 5th day (about 24%) and could be obtained with only 4 mg/Kg/day. The rapid effect of the acid and its specific action on prebetalipoproteins were demonstrated by examination of lipid curves after a glyco-lipid load with and without pretreatment with chenic acid. Encouragement of the shunt of triacylglycerols towards the phosphoglycerides during hepatic synthesis of triglycerides is put forward as the most likely mechanism of action in endogenous hyper-triglyceridaemia. The chemical composition of bile is interfered with, which may explain why cholesterol lithiasis is significantly more common in type IV dyslipidaemia than in other forms and in controls, as shown by statistical analysis.

Adult↗

PubMed1978

[Blood lipid disorders and chronic pancreatitis. 4 cases].

The literature dealing with the debated and not yet completely settled question of the causal relationship between dyslipidaemia and acute and chronic diseases of the pancreas is reviewed. Four personal cases of chronic pancreatitis associated with dyslipidaemia are presented and their possible pathogenetic relationships are discussed.

Adult↗

PubMed1977

[Renal control of acid-base equilibrium during dyslipidemia].

Possible correlations between lipid metabolism and hydroelectrolytic and acid base balances were studied in pathological conditions. For this purpose 24 patients with essential dyslipidaemia without renal or hepatic disease, and 47 patients with varying disease conditions, 25 with profound alterations in the lipid balance, 22 with plasmatic lipid fractions completely normal, were studied. In cases of essential hyperlipidaemia, alongside the profound changes in the lipid complement, no significant alterations in plasma pH were observed; by contrast other cases frequently showed an upset acid base balance with or without changes in the lipid picture. Urinary determinations suggested different conclusions. The most important aspect was the observation in most cases of essential dyslipidaemia and in certain cases of secondary dyslipaemia, of paradoxical aciduria, namely aciduria of much greater extent than might have been expected on the basis of plasma pH value.

Acid-Base Equilibrium↗

PubMed2026

Effects of Short-Term Energy Limitation at Different Levels With Normal Protein Intake on Hepatic Lipid Metabolism and the Gut Microbiota in Overweight/Obese Mice.

This study investigated the sex-specific effects of graded short-term energy limitation (EL) with normal protein intake on hepatic lipid metabolism and the gut microbiota in overweight/obese mice. Mice were allocated to a normal control (NC) group, a high-fat diet model (MC) group, and groups receiving 20%, 30% or 40% EL (n = 8 per group). All mice underwent blood biochemistry, liver biochemistry, histological, liver metabolomic, and fecal microbiota community genomic analyses. Relative to the NC group, both male and female MC mice developed varying degrees of insulin resistance, dyslipidaemia, and sex hormone dysregulation. However, disrupted hepatic lipid metabolism was detected solely in male mice, in association with changes in key lipid-metabolizing enzymes and metabolites; female mice showed only disturbed total cholesterol (TC) metabolism, which was linked to alterations in the cholesterol synthesis rate-limiting enzyme HMGCR. With normal protein intake, 20%, 30%, and 40% EL reduced hepatic triglyceride and TC synthesis in overweight/obese male mice by suppressing the expression of the key lipogenic enzyme DGAT and the activities of ACC and HMGCR (p < 0.05). An effect on the lipolytic enzymes CPT1 and CYP7A1 was detected only at 30% EL (p < 0.05), and hepatic metabolite profiles varied with the degree of EL. In female mice, only 40% EL significantly decreased TC synthesis by inhibiting both HMGCR expression and enzymatic activity (p < 0.05). Furthermore, irrespective of sex, short-term EL (all levels) with normal protein intake reduced the gut Firmicutes/Bacteroidetes ratio in overweight/obese mice (p < 0.05). In conclusion, graded short-term EL with adequate protein intake exerts differential effects on hepatic lipid metabolism and the gut microbiota in overweight/obese mice, with pronounced sex-specific differences.

energy limitation↗

PubMed2025

GWAS of CRP response to statins further supports the role of APOE in statin response: A GIST consortium study.

Statins are first-line treatments in the primary and secondary prevention of cardiovascular disease. Clinical studies show statins act independently of lipid-lowering mechanisms to decrease C-reactive protein (CRP), an inflammation marker. We aim to elucidate genetic loci associated with CRP statin response. CRP statin response is the change in log-CRP between off-treatment and on-treatment measurements. Cohort-level Genome-Wide Association Studies (GWAS) of CRP response were performed using 1000 Genomes imputed data, testing ∼10 million common genetic variants. GWAS meta-analysis combined results from seven cohorts and clinical trials totalling 14,070 statin-treated individuals of European ancestry within the GIST consortium. Secondary analyses included statin-by-placebo interaction analyses, and lookups in African ancestry cohorts. Our GWAS identified two genome-wide significant (P < 5e-8) loci: APOE and HNF1A for CRP statin response corrected for baseline CRP. The missense lead variant rs429358 at APOE, contributing to the APOE-E4 haplotype, is a risk locus for dyslipidaemia, Alzheimer's and coronary artery disease (CAD). The HNF1A locus is associated with diabetes, cholesterol levels, and CAD. Both loci are also associated with baseline CRP levels, and neither locus achieved a significant (P < 0.05) result from the statin v. placebo interaction meta-analysis using randomized clinical trial data. However, the interaction result (P-int=0.09) for APOE was suggestive and possibly underpowered. The APOE-E4 signal may therefore be associated with both CRP and LDL-cholesterol statin response. Combined with suggestions in the literature that APOE also leads to differential statin benefit in Alzheimer's, the APOE locus warrants further investigation for potential genetic effects on healthcare with statin treatment.

Humans↗

PubMed2026

Omics Profiling of Patients with Obstructive Sleep Apnoea Reveals Risks of Diabetes Mellitus and Cardiovascular Diseases.

Obstructive sleep apnoea (OSA) constitutes a multisystemic disorder often associated with cardiovascular and metabolic disorders. Thus, far, the underlying pathophysiological processes are not fully understood. In total, 142 plasma samples were acquired: 50 from controls (CON), 45 from mild/moderate OSA (M-OSA) patients, and 47 from severe OSA (S-OSA) patients. Proteomic and metabolic signatures significantly differed among S-OSA, M-OSA, and CON samples. A novel plasma biomarker panel including two proteins (ACTR2 and ENO1) and three metabolites (2-aminobicyclo[2 2·1], heptane-2-carboxylic acid, 1-O-[2r-hydroxy-hexadecyl]-sn-glycerol, and 1-pentadecene) was developed to identify S-OSA (AUC: 1.000) and distinguish severe cases from nonsevere cases (AUC: 0.813). An independent cohort was used to validate the model by distinguishing S-OSA samples from M-OSA (AUC: 0.729) and CON (AUC: 0.990) samples. Glycolysis pathway activation was identified as a characteristic of OSA; it may contribute to diabetes mellitus onset in OSA patients. Dyslipidaemia, foamy macrophage formation, platelet activation, and actin cytoskeleton might collectively play a key role in vascular damage in OSA patients, contributing to the development of atherosclerosis. These findings reveal molecular bases for OSA-related cardiometabolic complications and provide new diagnostic biomarkers for OSA and the identification of severe cases.

Humans↗

PubMed1992

The Apo A, B, a of coronary risk: back to kindergarten.

Approximately 1% of the population have a dominantly inherited lipid disorder predisposing to premature vascular disease. Apolipoproteins (Apo) B, and A1, the carrier proteins for the atherogenic low density lipoprotein (LDL) and the protective high density lipoprotein (HDL) cholesterol respectively are markers for these disorders, as is Apo(a), the unique carrier protein for lipoprotein(a). We assessed changes in these apolipoproteins during the first 12 years of life, aiming to detect young families with inherited dyslipidaemia and implement early prevention. Among 1032 consecutively born babies in whom levels were measured within their first week and at a mean age of 8.5 months, the Apo B/A1 ratio and Apo(a) both tracked closely (p < 0.01 and < 0.0001). High B/A1 ratios (> 95 percentile) identified two families with familial hypercholesterolaemia, and infants with high Apo B identified two families with hyperapolipoprotein B. Apo(a) levels increased twofold between the first week and 8.5 months and were highly correlated (r = 0.73, p < 0.0001). Levels at 8.5 months were not different from parental values and were closely correlated with them. We then assessed school children aged eight to 12 years. In a pilot study (n = 1400) we have established normal apolipoprotein values and distribution patterns and defined the 95th percentile for each. This study is continuing and parents of children with high levels are being recalled (with their children) for lipid measurements. Our findings indicate that our approach is feasible and has wide acceptance, and that measuring Apo B/A1 and Apo(a) in childhood identifies families at increased cardiovascular risk. We have yet to assess the efficacy of our family-based coronary prevention programme.

Apolipoproteins A↗

PubMed1992

Risk factors for peripheral vascular disease in hypertensive subjects with type 2 diabetes mellitus.

Possible factors predisposing to peripheral vascular disease (PVD) in hypertensive subjects with Type 2 diabetes mellitus were studied. Details of age, sex, duration of diabetes, blood pressure, and smoking habit were recorded in 180 subjects of either White, West Indian Black or Asian ethnic origin. Glycosylated haemoglobin, fasting serum total cholesterol, total high density lipoprotein (HDL), HDL2, low density lipoprotein (LDL-cholesterol), and triglycerides were measured in all subjects. Peripheral vascular disease was defined as an ankle/brachial systolic pressure < 1.0 as measured by the Doppler technique. Multivariate analysis was performed and the following factors were identified as being strongly associated with the presence of PVD with a statistical significance of p < 0.001; LDL-cholesterol, total HDL-cholesterol, age, male sex, diet or oral hypoglycaemic therapy, diastolic blood pressure, and of p < 0.003; systolic blood pressure. When blood pressure was excluded from the analysis the other factors retained their predictive value. We conclude that hypertension and dyslipidaemia are important risk factors for peripheral vascular disease in Type 2 diabetes mellitus.

Blood Pressure↗

PubMed1992

Multiple metabolic syndrome: aspects of genetic epidemiology and molecular genetics.

Epidemiological studies have documented the association between cardiovascular disease and high blood pressure, dyslipidaemia, impaired glucose tolerance, non-insulin-dependent diabetes mellitus (NIDDM), and central obesity. In fact, several of these abnormalities, often all of them, can be identified in the very same individuals, constituting the entity of the multiple metabolic syndrome. Furthermore, many of these abnormalities seem to run in families. These findings raise important questions about the genetic epidemiology of the disease and about the molecular genetic background of the most likely common nominator of this syndrome, namely insulin resistance. Therapeutic actions must also be carefully considered to avoid the encouragement of some abnormalities while treating others.

Apolipoproteins E↗

PubMed1975

[Etiology of Paget's disease of bone].

The etiology of Paget's disease is just as doubtful in 1975 as it was in 1876 when Sir James Paget described the disease. The authors analyse the etiology on the basis of 100 personal cases and the literature. Although there are undoubtedly familial cases of the disease, investigation of the leucocyte grouping of 46 patients with Paget's disease did not reveal any correlation between occurrence of the disease and the HL-A antigens. Various pathological associations have been reported in the literature and were also found in this series. These associations were at the limits of coincidence (inflammatory rheumatism, diffuse chondrocalcinosis, multiple myeloma...). Metabolic changes (hyperuricaemia, hyperglycaemia, dyslipidaemia) did not appear to be more frequent than in control patients. Involvement of elastic tissue and the presence of pseudocrystalline inclusions in the osteoclasts constitute interesting points for discussion.

Adult↗

PubMed1975

[Medical treatment of obliterating peripheral arteriopathies, especially arteriosclerosis].

The efficacy of medical treatment of peripheral obliterating arteriopathies on an aetiopathogenetic basis in the light of diabetes and atherosclerosis is discussed. The pros and cons of management with vasoactive drugs exercising a dilatatory action of choice on the metarterioles and the arteriolocapillary sphincters are summarised, together with the possibilities offered by such drugs. A example of the short-term effects of chorionic gonadotrophin in atherosclerotic forms is presented. Such effects include the improvement of arteriolocapillary flow and the correction of dyslipidaemia. It is suggested that chorionic gonadotrophin can be successfully associated in consecutive courses with vasoactive drugs and anticoagulants to obtain long-term success, even in cases treated for ten years.

Arteriosclerosis Obliterans↗

PubMed1975

[Gout, hyperuricemia and femur head osteonecrosis (FHON)].

The authors report on 14 cases of osteonecrosis of the femoral head (ONFH) in patients suffering from gout. The cases of association were discovered over a period of 10 years among 232 patients with ONFH and 651 with gout. The necrosis had no particular characteristics except that there was a clear preponderence in males and a slight tendency to be bilateral; it occurred, perhaps, at a slightly earlier age. The patients with gout did not show any special clinical features ; the gout always preceded the necrosis, on average by 7 1/2 years. There was no obvious history of painful crises in the hip that could be attributed to the acute gout, except in one case. The excess of urate was detected by the baseline level of uricaemia (91 mg/litre on average), by the frequency of tophus (4 out of 14), and by the frequency of urinary lithiasis (2 out of 14), and did not appear to be any greater in the patients with gout and ONFH than it was in the whole of the population of gout patients. In those patients in whom it was estimated, the lipid analysis showed most frequently an increase in total lipids, in triglyceridaemia, and in cholesterolaemia. In the 5 patients in whom the investigations were sufficiently detailed, the dyslipidaemia was of Frederickson type II + IV (mixed hyperlipidaemia according to de Gennes' classification). Different physiopathological hypotheses are discussed by the authors, notably those concerned with micro-particulate fatty emboli (lipomicrons), which may obstruct, among others, the terminal arteries of the femoral head. Of the 6 patients for whom it was possible to obtain information, for an average period of 10 years since the onset of the necrosis, 2 had presented with untreated hyperlipidaemia and a severe general vascular illness (myocardial infarction in one case and regressive hemiplegia in the other). These findings lead to the conclusion that correction of the hyperlipidaemia by diet is indispensable to ensure the long-term survival of these patients.

Adrenal Cortex Hormones↗

PubMed1992

[Place of the right gastro-epiploic artery in coronary revascularization by exclusive arterial grafts].

From March 1990 to July 1991, 35 patients underwent coronary artery bypass grafts using the right gastro-epiploic artery (GEA). Twenty-nine patients had exclusively arterial grafts using a combination of GEA and internal mammary artery (IMA) in situ. The selection criteria for this group of 29 patients included a life expectancy exceeding ten years to avoid the need for reoperation due to deterioration of the grafts. This group consisted of 27 men and two women under the age of 70 years (mean age: 58 years, range: 36 to 70), 11 patients (38%) were under the age of 50 years and 15 (52%) were under the age of 60 years. Cardiac status was relatively well preserved. The mean ejection fraction was 58% (range: 25-70%). Fourteen patients (48%) had had a preoperative myocardial infarction. Fifty-five p. cent were smokers, 41% suffered from HT and 31% had a dyslipidaemia. Six patients (20%) had respiratory failure, 6 others (20%) were severely overweight and 2 patients were diabetic. According to the NYHA classification, 14 patients (48%) were stage IV, 9 patients (31%) were stage III and 6 patients (20%) were stage II. The mean number of bypass grafts per patient was 2.8 and 8 sequential bypass grafts (27%) were performed. The GEA was used in 29 cases, the left IMA was used in 28 cases, the right IMA was used in 13 cases and the epigastric artery was used as a free graft in 3 cases. Associated lesions included a resected left ventricular aneurysm. No associated valve procedures were performed.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1992

Magnesium and blood pressure. II. Clinical studies.

Magnesium deficit may be considered as a cardiovascular risk because of its aetiopathogenic role in the genesis of atherogenous dyslipidaemias and the so-called "idiopathic" mitral valve prolapse. It does not, however, constitute a major antihypertensive factor, though it may sometimes be an accessory co-factor. Plasma magnesium is generally normal in untreated hypertensive patients and normotension is the rule during magnesium deficit. An inverse relationship between magnesium and renin in the plasma of hypertensives has not been confirmed. In practice, plasma magnesium seems to be related to the evolution of the disease. An inverse correlation between blood pressure and erythrocyte total and free magnesium levels has been observed in diverse selected populations but no adjustment has been made in these studies for important covariables. A weak positive association between blood pressure and erythrocyte free magnesium was lost in a multivariate regression analysis. As a rule there is no difference between erythrocyte, leucocyte, and lymphocyte magnesium in hypertensives and controls. More often no relation between urinary magnesium and blood pressure is observed. Daily urine magnesium may be increased with increased excretion of urine adrenaline. Epidemiological data on dietary magnesium, particularly in drinking water, should be carefully scrutinized: these studies do not establish a major role for magnesium as an antihypertensive factor but confirm the importance of magnesium deficit as a nephrocardiovascular risk factor and sometimes gives support for a role of magnesium as an antihypertensive cofactor. The use of magnesium-depleting drugs in hypertensive patients may induce magnesium depletion which must be palliated.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure↗

PubMed1975

[Acute coronary thrombosis in a 28 year-old woman].

A 28-year-old woman, with no previous cardiovascular history, was hospitalized for myocardial infarction complicated by bifascicular block followed by complete atrio-ventricular block with a regressive course. A coronary arteriography performed on the 10th day demonstrated a thrombosis of the anterior interventricular artery, the rest of the coronary network being normal. The influence of a dyslipidaemia and the taking of oral contraceptives was discussed as an aetiology.

Acute Disease↗