Biomedical subjects

H Schulte

Publications and source records attributed to H Schulte.

At least 55 records · Page 3Linked to original sources

PubMed1998

Genetic and biochemical screening for endocrine disease.

The development of biochemical and genetic screening tests for inherited endocrine diseases has dramatically changed our approach to surgical patients with endocrine tumors. Among more than 1800 patients with endocrine tumors and a possible inherited disease operated on between 1986 and 1997, there were 6.1% to 7.3% who were found to have a familial disease associated with familial medullary thyroid cancer, (MTC), multiple endocrine neoplasia type IIa (MEN-IIa), MEN-IIb, or MEN-I. Genetic testing for the RET proto-oncogene is therefore recommended for all patients with MTC, and testing for the MEN-I gene is recommended in patients with suspected MEN-I and in specific clinical subgroups with an increased probability of endocrine tumor heredity. Early treatment based on early diagnosis by genetic testing appears to improve survival and to decrease morbidity in these patients.

Biomarkers↗

PubMed1998

Basal growth hormone levels in women are positively correlated with high-density lipoprotein cholesterol and apolipoprotein A-I independently of insulin-like growth factor 1 or insulin.

Previous studies in growth hormone (GH)-deficient or acromegalic patients yielded contradictory results on the effect of GH on lipoprotein metabolism. In a cross-sectional study, we analyzed the relationships between unstimulated GH, insulin-like growth factor 1 (IGF1), insulin, and lipoprotein metabolism in 44 non-obese young women. On univariate analysis, basal serum levels of GH correlated positively with triglycerides, high-density lipoprotein (HDL) cholesterol, apolipoprotein A-I (apoA-I) and apoA-II and negatively with lipoprotein lipase (LPL) activity. These associations remained significant on multivariate analyses that, in addition to GH, took into account the effects of insulin or C-peptide, as well as the effects of total, protein-bound, or free IGF1. In most cases, the relationships of these lipid parameters with insulin/C-peptide and IGF1 and its free or protein-bound subfractions were opposite of those with GH and not significant. Thus, GH appears to regulate the metabolism of HDL and triglycerides independently of IGF1 and insulin.

Adult↗

PubMed1998

Smoking, lipoproteins and coronary heart disease risk. Data from the Münster Heart Study (PROCAM).

AIMS: The mechanism of the increase in coronary heart disease risk associated with smoking is unclear, but may partly be due to smoking-related changes in intermediate risk factors such as lipid levels, fibrinogen and blood pressure. We therefore examined the distribution of these variables among smokers and non-smokers in the Münster Heart Study. METHODS: 20696 men, aged 41.7+/-2.7 years (mean +/- SD) and 10212 women, aged 37.0+/-2.6 years, were enrolled between 1978 and 1995. Thirty-two percent of women and 36% of men smoked. Compared to non-smokers, mean levels of low density lipoprotein cholesterol, total cholesterol, triglycerides and fibrinogen were increased, respectively, by 1.4%, 0.9%, 15% and 12.1% in male and by 2.0%, 5.5%, 12% and 3.4% in female smokers. Mean high density lipoprotein cholesterol levels, body mass index and blood pressure were reduced, respectively, by 6.4%, 3.8%, and 2% in male, and by 6.7% 1.2% and 2% in female smokers. In the subgroup of 4639 men aged 40 to 65 with 8 years of follow-up, the coronary event rate (definite myocardial infarction, sudden cardiac death) in cigarette smokers was more than twice that of non-smokers with otherwise identical risk factors. CONCLUSION: In the Münster Heart Study, smoking was associated with adverse changes in lipids (of greater magnitude in women), and fibrinogen (of greater magnitude in men). However, these changes explained only a small part of the smoking-related increase in coronary heart disease risk.

Adult↗

PubMed1998

Plasminogen activator inhibitor-1 4G/5G-polymorphism and factor V Q506 mutation are not associated with myocardial infarction in young men.

Several recent studies have reported contradicting results concerning the relevance of the plasminogen activator inhibitor-1 (PAI-1) 4G/5G-polymorphism for myocardial infarction. In addition, the common factor V Q506 (FV:Q506) mutation is frequently discussed as a risk factor for arterial thrombosis, but evidence is rare. In order to further highlight the role of both polymorphisms in myocardial infarction, we investigated 241 young male myocardial infarction patients (< or = 45 years-of-age) aged 38.6+/-4.4 years (mean+/-SD) for the presence of both genotypes. The control group consisted of 179 healthy men aged 47.1+/-6.4 years (mean+/-SD) of the same ethnic background as the patients. Neither the distribution of the PAI-1 4G/5G-polymorphism nor the prevalence of the FV: Q506 mutation was significantly different between young patients and controls (4G/4G-genotype: chi2=2.08, NS; odds ratio 1.36, 95% confidence interval 0.89-2.06; FV:Q506 mutation: chi2=0.33, NS; odds ratio 1.33, 95% confidence interval 0.64-2.78). Moreover, the PAI-1 4G/5G-distribution did not differ significantly between patients and controls in subgroups by tertiles of triglyceride levels. In conclusion, in the present study neither homozygosity for the 4G allele of the PAI-1 4G/5G-polymorphism nor the FV:Q506 mutation led to an increased risk of myocardial infarction in young men.

Adult↗

PubMed1998

Hemostasis in normotensive and hypertensive men: results of the PROCAM study. The prospective cardiovascular Münster study.

BACKGROUND: The greater than normal cardiovascular risk of hypertensive patients could be partly due to an impairment of hemostatic balance found in such individuals. OBJECTIVE: To examine the relationship between hemostatic variables and blood pressures in 1950 apparently healthy male participants in the prospective cardiovascular Münster study aged 40-65 years. METHODS: Blood pressure and other variables were determined, including fibrinogen level, coagulation factor VII clotting activity, protein C level, antithrombin III level, plasminogen activator inhibitor-1 level, euglobulin fibrinolytic activity, and von Willebrand factor level. RESULTS: Age-adjusted mean values of coagulation factor VII clotting activity, plasminogen activator inhibitor-1 level, antithrombin III level, and protein C level in hypertensives and borderline hypertensives were significantly higher than those in normotensive men (e.g. for hypertensive versus normotensive men, coagulation factor VII clotting factor activity 111.5 versus 106.1%, plasminogen activator inhibitor-1 level 5.05 versus 3.22 arbitrary units/ml, and protein C level 111.1 versus 107.0%, P < 0.05-0.01). For most of the hemostatic variables we found positive bivariate correlations to blood pressure (P < or = 0.05). Exceptions were von Willebrand factor level (no correlation to blood pressure), and euglobulin fibrinolytic activity (a negative correlation to systolic blood pressure and no correlation to diastolic blood pressure). Significance persisted in the multiple logistic regression analysis with the exception of the relationships between systolic and diastolic blood pressures and fibrinogen level as well as euglobin fibrinolytic activity after adjustment for age. After adjustment for age and body mass index significance for relationships between systolic blood pressure and coagulation factor VII clotting activity as well as protein C level was also lost. CONCLUSIONS: We conclude that the greater than normal cardiovascular risk of hypertensive patients is partly due to an imbalance in hemostasis.

Adult↗

PubMed1998

Relationship between plasma viscosity and the severity of coronary heart disease.

Several studies have indicated that plasma viscosity contributes to cardiovascular risk in men. So far, a significant relationship between plasma viscosity and the severity of coronary heart disease has not been found. Thus, the present study is the first to report on the relationship of plasma viscosity and the severity of coronary heart disease. In a collective of 1142 male myocardial infarction patients, plasma viscosity and additional laboratory parameters were determined. Atherosclerotic changes were quantified by coronary angiography. Patients were divided into groups without any, and with one to three stenosed vessels. We found a positive relationship between plasma viscosity and the severity of coronary heart disease, even after adjusting groups for age, fibrinogen, and use of diuretics. Mean plasma viscosity ranged from 1.141+/-0.035 mPa s in patients without stenosed vessels to 1.162+/-0.044 mPa s in patients who had three coronary vessels with stenoses >50%. Differences between the groups were significant (P<0.001 to 0.05), with two exceptions: differences between patients without any and with one stenosed vessel, as well as between patients with one and two stenosed vessels, did not reach the significance level. On the whole, we can give further support to the hypothesis that cardiovascular risk factors and coronary heart disease may be linked by plasma viscosity.

Blood Viscosity↗

PubMed1998

Incidence and risk factors for stroke in an occupational cohort: the PROCAM Study. Prospective Cardiovascular Muenster Study.

BACKGROUND AND PURPOSE: The purpose of this study was to assess the incidence of stroke and the magnitude of classic stroke risk factors in an occupational cohort of white-collar and blue-collar workers. METHODS: We studied a prospective cohort of 12 866 male employees, aged 30 to 65 years, in 52 companies in northwestern Germany, with an average follow-up of 7.2 years. Participants were free of self-reported stroke, transient ischemic attack, and myocardial infarction at baseline. Physical examination, blood tests, and a face-to-face interview to assess presence of various risk factors were performed at the workplace. Follow-up was done by standardized mailed questionnaire. Main outcome measure was first stroke occurrence. RESULTS: Overall stroke incidence was 42.4 per 100000 person-years, increasing from 10.1 per 100000 person-years in the age category 30 to 39 years to 33.6, 80.6, and 159.2 per 100000 person-years in the age categories 40 to 49, 50 to 59, and 60 years and older, respectively. After adjustment for potential confounders, the relative risks of total stroke associated with systolic blood pressure < or = 120, 121 to 140, and > or = 141 mm Hg were 1.00 (reference), 2.99 (95% confidence interval, 0.85 to 10.49), and 5.56 (1.56 to 19.88). The risks associated with smoking status of never/past, < or = 20 cigarettes per day, and >20 cigarettes per day) were 1.00 (reference), 1.65 (0.62 to 4.42), and 3.56 (1.78 to 7.15), respectively. A history of hypertension at baseline (yes versus no) was independently associated with a relative risk of 2.37 (1.20 to 4.71) for total stroke and a history of diabetes mellitus (yes versus no) with a risk of 2.21 (1.00 to 4.87). A comparison of risk factor levels with a general population study revealed only small differences. CONCLUSIONS: This occupational cohort had a 2-fold lower stroke incidence than that observed in cohorts of the general population. In the absence of a strong healthy-worker effect, moderate differences in behavioral risk factors and a higher treatment rate for hypertension contribute to the explanation of this favorable stroke incidence.

Adolescent↗

PubMed1998

The Münster Heart Study (PROCAM). Results of follow-up at 8 years.

The Münster Heart Study (PROCAM) was initiated in 1979 in order to examine cardiovascular risk factors, cardiovascular events including myocardial infarction and stroke, and mortality in people at work. Examination at entry comprised a standardized case history, measurement of blood pressure and anthropometric data, a resting electrocardiogram, and measurement of more than 20 laboratory parameters in a fasting blood sample. The prevalence data in this report are based upon a single examination of 17,437 men aged 40.4 +/- 11.3 years (mean +/- SD) and 8065 women aged 35.7 +/- 12.1 years, which took place between 1979 and 1991. Severe hypercholesterolaemia (> 300 mg.dl-1) was seen in 5% of men and 8% of women aged 45 to 64 years. In men, the prevalence of hypertriglyceridaemia (> 200 mg.dl-1) rose from 5% at age 20 to 20% at age 45 and remained constant thereafter; in women the prevalence of hypertriglyceridaemia increased linearly from 2% at age 20 to 7% at age 60. The LDL/HDL ratio was higher in men than in women at all age groups; in the age group 45 to 64 years, LDL/HDL ratios > 5 were approximately twice as common in men. Lipoprotein(a) levels were distributed in a highly skewed fashion. In men, a slight rise in the geometric mean lipoprotein(a) concentration occurred with age, whereas in women a dramatic increase was seen after age 40. Using multivariate analysis by the multiple logistic function method, total cholesterol, HDL cholesterol, LDL cholesterol and log-transformed triglycerides showed a significant (P < 0.001) age-adjusted correlation with the presence of major coronary events. A risk algorithm has been developed for men aged 40 to 65 years which takes into account the independent risk factors of HDL cholesterol, LDL cholesterol, triglycerides, fibrinogen, age, systolic blood pressure, cigarette smoking, presence of diabetes mellitus and family history of myocardial infarction and angina pectoris. This algorithm can be used in clinical practice to calculate the 8-year risk of an individual suffering a myocardial infarction.

Adult↗

PubMed1998

Lipoproteins and cardiovascular risk--from genetics to CHD prevention.

Increased levels of low density lipoprotein (LDL) cholesterol and triglyceride, and low levels of high density lipoprotein (HDL) cholesterol, are associated with increased risk of coronary heart disease (CHD). Only a minor part of the variation in lipids can be explained by defects in single genes of large effect; the bulk of variation in most cases is due to the interaction of polygenes and environment. This paper describes a strategy for unravelling such complex genetic effects in the population at large. A person's risk of developing CHD is, however, not determined by levels of circulating lipids alone, but by a number of factors which contribute to his or her global risk. Based on the data of the Münster Heart Study (PROCAM), a multiple logistic function using nine independent variables for the prediction of risk has been developed. This function allows an almost 40-fold degree discrimination in risk between persons in the lowest and highest quintiles of the algorithm. Data from the Münster Heart Study and other prospective studies indicates a log-linear relationship between LDL cholesterol and CHD risk. The results of recent large scale intervention trials indicate that this relationship also holds true for LDL levels which are achieved by treatment. This indicates that the benefit achieved by cholesterol lowering is greatest at high baseline LDL cholesterol levels, and that at least for LDL cholesterol levels of > or = 80 mg. dl-1, there is no theoretical threshold below which lowering of LDL cholesterol cannot be expected to reduce CHD risk. However, at low LDL cholesterol levels the benefits of treatment may be outweighed by side-effects and by practical cost-benefit considerations. These issues are also discussed in detail in the present report.

Cholesterol↗

PubMed1998

Failure to confirm ferritin and caeruloplasmin as risk factors for the angiographic extent of coronary arteriosclerosis.

BACKGROUND: It has been suggested that iron overload, as assessed by increased serum ferritin concentration, may be a risk factor for coronary artery disease (CAD). Recent studies have reported conflicting data on the role of ferritin and other parameters of oxidative metabolism in CAD. OBJECTIVE: The aim of this study was to assess the relation between the extent of CAD and parameters of oxidation. METHODS: We studied 275 patients (208 men aged 55.1 +/- 9.6 years and 67 women aged 54.6 +/- 10.0 years) who underwent coronary angiography or percutaneous transluminal coronary angioplasty for the first time. The parameters assessed were: iron, ferritin, transferrin, copper, caeruloplasmin and lipid. Cinefilms were assessed by the use of three scores: (1) Vessel score: 0-3 points; 1 point for each of the three main coronary arteries with a stenosis >70%. (2) Stenosis score: 0-32 points; the coronary artery tree was divided into eight segments that were scored 1-4 points per segment with respect to the maximal degree of stenosis. (3) Extent score: 0-100 points; extent of diffuse coronary lesions in each segment in relation to the length of the vessel. Multiple regression analyses were used to evaluate the results. RESULTS: Total cholesterol and low-density lipoprotein cholesterol (P < 0.001) in women, low-density lipoprotein cholesterol (P < 0.05) in men, and patient age showed a significant correlation with all three scores, but none of the parameters of oxidative metabolism (iron, transferrin, ferritin, copper, caeruloplasmin) correlated significantly with any of the three scores. CONCLUSION: This study demonstrated a correlation between lipoproteins and the angiographic extent of CAD, but did not confirm a role for serum ferritin and other oxidative parameters as risk factors for the extent of CAD.

Adult↗

PubMed1998

The emergence of triglycerides as a significant independent risk factor in coronary artery disease.

The Prospective Cardiovascular Münster (PROCAM) study involved 4849 middle-aged men who were followed up for 8 years to record the incidence of coronary heart disease (CHD) events according to the risk factors present at study entry. The study showed that fasting levels of triglycerides were an independent risk factor for CHD events, irrespective of serum levels of high density lipoprotein cholesterol (HDL-C) or low density lipoprotein cholesterol (LDL-C). Other independent predictors of CHD included serum levels of LDL-C and HDL-C, age, systolic blood pressure, cigarette smoking, diabetes mellitus, a family history of myocardial infarction and angina pectoris, but did not include total serum cholesterol levels. Individuals with an LDL-C/HDL-C ratio > 5 had a 19.2% chance of experiencing a CHD event in the next 8 years. Furthermore, if an LDL-C/HDL-C ratio > 5 was combined with hypertriglyceridaemia (> or = 2.3 mmol. l-1), the risk of CHD increased to 26.9%. The association between hypertriglyceridaemia and CHD events may be related to the presence of atherogenic, triglyceride-rich particles in plasma, such as LDL and very low density lipoproteins. High triglyceride levels may also predispose to thrombosis. Individuals with potentially atherogenic lipid profiles should be managed initially through the introduction of lifestyle changes. However, if these fail to achieve recommended target values, lipid-lowering therapy should be considered.

Anticholesteremic Agents↗

PubMed1997

The Münster Heart Study (PROCAM): total mortality in middle-aged men is increased at low total and LDL cholesterol concentrations in smokers but not in nonsmokers.

BACKGROUND: Some large epidemiological studies have shown an increase in mortality at low levels of total and LDL cholesterol. It has been speculated that low cholesterol levels may play a causative role in this association. To investigate this question, we analyzed all deaths occurring among middle-aged men in the Münster Heart Study (PROCAM), one of the largest prospective epidemiological studies of coronary heart disease risk markers in Europe. METHODS AND RESULTS: In the Münster Heart Study, 10,856 men aged 36 to 65 years at study entry (46.8+/-7.3 years [mean+/-SD]) were followed for 4 to 14 years (7.1+/-2.4 years). During this period, 313 deaths occurred--46 from myocardial infarction, 48 from suspected or definite sudden cardiac death, 14 from cerebrovascular disease, and 10 from other diseases of the circulatory system. There were 121 deaths from cancer and 33 deaths from violent causes (injuries in 16, suicide in 14, and homicide in 3 cases). Death in 29 cases occurred from other causes and was unexplained in 12 cases. Total cholesterol, LDL cholesterol, and the LDL/HDL ratio showed a J-shaped relationship with total mortality. At high total and LDL cholesterol concentrations, increased mortality was due to increased coronary deaths. At low total and LDL cholesterol concentrations, increased mortality was seen in smokers only and was explained by an increase in smoking-related cancer deaths. CONCLUSIONS: The increase in mortality at low levels of total and LDL cholesterol among middle-aged men in the Münster Heart Study is explained by an increase in smoking-related cancer deaths among smokers.

Adult↗

PubMed1997

New and classical risk factors--the Münster heart study (PROCAM).

A total of 4,849 male participants of the prospective cardiovascular Münster Study (PROCAM), aged 40 - 65 years underwent extensive screening for cardiovascular risk factors before 1986 and were subsequently followed up for at least 8 years. During this time 189 non-fatal and 49 fatal myocardial infarctions occurred, 28 men suffered a sudden cardiac death and 169 persons died of other causes. Using multivariate statistical methods we confirmed that age, increased LDL cholesterol levels, decreased HDL cholesterol levels, high blood pressure, cigarette smoking, diabetes mellitus, angina pectoris and a positive family history are important risk factors for a myocardial infarction or cardiac death. The results of the PROCAM Study demonstrate that elevated triglycerides are an independent risk factor for an early myocardial infarction or cardiac death. Using a multiple logistic function analysis an algorithm for the assessment of the global risk was derived from the data. The observed incidence of coronary heart disease rises sharply as the global risk increases, thus permitting the use of this algorithm in clinical practice for the assessment of the individual risk of myocardial infarction. Risk factors such as lipoprotein(a) and coagulation factors may improve the predictive value of this algorithm. Furthermore it is expected that the exploration of genetic defects will strongly increase the predictive value and precise determination of individual risk.

Adult↗

PubMed1997

Basal growth hormone levels are positively correlated with high-density lipoprotein cholesterol levels in women.

Previous studies in patients with either a deficiency or an excess of growth hormone (GH) yielded contradictory results on the regulation of lipoprotein metabolism by GH. In a cross-sectional study of 563 male and 126 female participants of the Prospective Cardiovascular Münster (PROCAM) Study, we determined biometric and demographic data, serum levels of total cholesterol, triglycerides, high-density lipoprotein (HDL) cholesterol, low-density lipoprotein (LDL) cholesterol, apolipoprotein (apo)A-I, A-II, and B, and unstimulated GH levels. The median of basal GH levels was higher in women than in men. Moreover, 44.2% of men but only 8.7% of women had basal GH levels less than the detection limit of 0.05 microgram/L. The relationship between basal GH and lipoprotein metabolism was investigated by univariate and multivariate regression analysis of data from 315 men and 126 women with detectable basal GH levels. In men, GH correlated positively with HDL cholesterol and negatively with body mass index (BMI), age, and triglycerides. After multivariate analysis, the correlation with triglycerides remained independent of age and BMI. Among women, GH correlated positively with the use of hormonal contraception, HDL cholesterol, apoA-I, and apoA-II, and negatively with BMI, age, menopause, triglycerides, and apoB. With multivariate analysis, the positive correlations of GH with HDL cholesterol and apoA-I in women were independent of age. BMI, menopause, and oral contraception. We conclude that GH contributes to the regulation of HDL cholesterol levels. Moreover, in women the well-known effects of exogenous estrogen or estrogen loss on HDL metabolism may be partially mediated via GH.

Adult↗

PubMed1997

Afferent large fiber polyneuropathy predicts the development of postherpetic neuralgia.

Acute zoster infection may be followed by a chronic pain syndrome, i.e., postherpetic neuralgia (PHN). Besides older age, the intensity of pain and neuronal damage within the acutely affected body region are regarded as predictors or risk factors for PHN. As an alternative approach an underlying peripheral polyneuropathy may be considered as potential co-factor. Is a preexisting generalized impairment of certain fiber classes important in initiating chronic pain states after subsequent localized nerve lesion due to zoster infection? Neurophysiological tests of different efferent and afferent small and large fiber systems were performed prospectively at unaffected body regions in patients with acute herpes zoster. Patients that were still in pain 6 months later (PHN, n = 17) and pain free patients (non-PHN, n = 17) were compared regarding the results obtained during the acute phase. Both groups were age matched. Nociceptive C-fiber function was assessed at the forearm by quantitative measurement of the axon reflex vasodilatation and flare induced by histamine iontophoresis. Mechanosensitive A beta-fibers were tested at all extremities by quantitative vibrametry. Parasympathetic small fiber function was studied by heart rate variability tests. No clinically manifest polyneuropathy was present. However, in PHN risk patients considerably higher vibration detection thresholds in hands and feet were detected compared with non-PHN patients. Pathologic test results of vibration sense at the lower extremity predicted PHN with a sensitivity of 70%. Nociceptive C-fiber and parasympathetic fiber function demonstrated no significant differences in both groups. Acute zoster pain was slightly more intense in the PHN group. We concluded that (i) a mild generalized impairment of afferent A beta-fiber function (A beta-polyneuropathy) seems to be an important co-factor in the development of PHN and (ii) impairment of vibration sense, i.e., impairment of afferent A beta-fiber function, may be used as a predictor of PHN.

Acute Disease↗

PubMed1997

Coagulation factor VII and the risk of coronary heart disease in healthy men.

Numerous investigations have demonstrated the role of thrombus formation in the pathogenesis of coronary heart disease (CHD). A tendency to thrombosis may also be indicated by elevated levels of coagulation factor VII clotting activity (FVIIc). Significant associations of FVIIc with increased coronary risk, however, have been found only in the Northwick Park Heart Study. Here we present the results of the 8-year follow-up of FVIIc measurements in 2780 healthy men of the Prospective Cardiovascular Münster study. In the study population (age at entry, 49.3 +/- 6.1 years, mean +/- SD), 130 CHD events occurred during follow-up. FVIIc was significantly higher in subjects with coronary events than in those without (112.4 +/- 20.1% vs 108.7 +/- 21.4%, P = .023). Compared with individuals without coronary events, FVIIc was not significantly higher in men with nonfatal events (111.7 +/- 20.4%; P = .196, n = 93), but there was a tendency toward higher FVIIc activity in subjects with fatal events (114.6 +/- 19.5%; P = .076, n = 37). In the multiple logistic regression analysis, we did not find FVIIc to be an independent risk factor for CHD, and the significance of FVIIc disappeared after total cholesterol, LDL-cholesterol, and triglycerides were taken into account. The increase in the number of CHD events through higher levels of FVIIc was more pronounced in the presence of additional cardiovascular risk factors: smoking; myocardial infarction events in family; angina pectoris; high levels of fibrinogen, total cholesterol, LDL cholesterol, and triglycerides; and a low level of HDL cholesterol. We conclude that FVIIc is a risk factor for CHD, especially in the presence of additional risk factors, and must be taken into account when assessing cardiovascular risk in men.

Adult↗

PubMed1997

Lipoproteins and cardiovascular risk-from genetics to CHD prevention.

Dyslipidemia is said to be present when lipid or lipoprotein levels lie within a range which is known from epidemiological studies to be associated with secondary complications, in particular atherosclerosis of the coronary arteries, or when a lipid or lipoprotein grossly deviates from the norm as in abetalipoproteinemia, hypobetalipoproteinemia or the HDL deficiency syndromes. In most cases, dyslipidemia is due not to a single genetic or environmental factor, but to a combination of the effects of several genes of small effect (polygenes) and environment. In other cases, however, dyslipidemia is caused by a mutation in a single gene of large effect. In such cases, the extent and nature of the phenotype depends primarily on the identity of the gene involved, but is also modulated to an important degree by the nature of the mutation and the genetic and environmental background against which this mutation occurs. In addition, many cases of hyperlipidemia are secondary to other disorders such as hypothyroidism or renal dysfunction. Such disorders may also unmask or exacerbate a genetic lipoprotein disorder. Examples of the latter are the unmasking of type III hyperlipidemia by diabetes mellitus or the exacerbation of familial hypercholesterolemia by hypothyroidism.

Clinical Trials as Topic↗

PubMed1996

Hypertriglyceridemia and elevated lipoprotein(a) are risk factors for major coronary events in middle-aged men.

Cardiovascular risk factors were analyzed in 4,849 male participants, aged 40 to 65 years, in an 8-year follow-up of the Münster Heart Study (Prospective Cardiovascular Münster Study; PROCAM). One hundred eighty-one definite nonfatal myocardial infarctions, 49 fatal myocardial infarctions, and 28 sudden cardiac deaths were observed. Multiple logistic function analysis confirmed that age, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, systolic blood pressure, cigarette smoking, diabetes mellitus, angina pectoris, and family history of myocardial infarction were important cardiovascular risk factors. Interestingly, this analysis revealed a significant and independent association between serum levels of triglycerides and the incidence of major coronary events. The relation between lipoprotein(a) [Lp(a)] levels and the occurrence of major coronary events was analyzed in a subgroup of 878 men. Thirty-three probands with major coronary events had significantly higher geometric mean levels of Lp(a) than 828 men who did not experience major coronary events (0.09 vs 0.05 g/L; p <0.011). Thus, in addition to established risk for factors, serum levels of triglycerides and Lp(a) are sensitive indicators of increased risk major coronary events.

Adult↗