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Biomedical subjects

H Schulte

Publications and source records attributed to H Schulte.

At least 19 recordsLinked to original sources
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

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↗
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↗
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↗
PubMed1996

A missense mutation (Thr-6Pro) in the lysosomal acid lipase (LAL) gene is present with a high frequency in three different ethnic populations: impact on serum lipoprotein concentrations.

A frequent missense mutation (Thr-6Pro) found in the prepeptide of the lysosomal acid lipase (LAL) gene was analyzed in a cohort of 1003 randomly selected samples from Germany, Japan and Sardinia (Italy). Using the mutagenically separated polymerase chain reaction (MS-PCR), allele frequencies of 0.269, 0.238 and 0.245 were determined in the three populations, respectively. Statistical analysis showed a lack of association with a dyslipidemic phenotype in all three groups. Additionally, in a subgroup of 126 German individuals no association was observed between genotype and LAL activity. We conclude that this mutation appears to be a frequent LAL gene polymorphism causing no impaired function of the enzyme and no measurable dyslipidemia in the general population.

Base Sequence↗
PubMed1996

High-density lipoprotein cholesterol as a predictor of coronary heart disease risk. The PROCAM experience and pathophysiological implications for reverse cholesterol transport.

The incidence of coronary heart disease (CHD) was assessed via the Prospective Cardiovascular Münster (PROCAM) study in 19,698 volunteer subjects aged between 16 and 65 years. An adequate incidence of atherosclerotic CHD was only found in male subjects greater than 40 years of age. The analysis and subsequent 6 year follow-up period was, therefore, confined to 4559 male participants aged 40-64 years. In the follow-up period, 186 study participants developed atherosclerotic CHD (134 definite non-fatal myocardial infarctions (MIs) and 52 definite atherosclerotic CHD deaths including 21 sudden cardiac deaths and 31 fatal MIs). Univariate analysis revealed a significant association between the incidence of atherosclerotic CHD and high-density lipoprotein cholesterol (P < 0.001), which remained after adjustment for other risk factors.

Adolescent↗
PubMed1996

Synthesis and release of phosphatidylcholine by isolated porcine gastric mucous cells in primary culture.

Phosphatidylcholine (PC) is the major phospholipid of the hydrophobic gastric mucosal barrier and is chiefly released from mucous cells into the gastric mucus. Whereas the mucosa contains highly unsaturated PC, gastric mucus predominantly contains palmitoyl-oleoyl-PC and palmitoyl-linoleoyl-PC, indicating a selective release of these PC species into the gastric lumen. In order to understand gastric PC metabolism, we investigated synthesis and release of PC in cultivated porcine gastric mucous cells, using dual labelling with [methyl-3H]-choline and [1-14C]-palmitate, in the presence of 12-O-tetradecanoylphorbol-13-acetate (TPA), indomethacin and prostaglandin E2 (PGE2). Linear incorporation of [methyl-3H]-choline and [1-14C]-palmitate into PC was achieved for at least 8h. In contrast to type II pneumocytes TPA increased PC synthesis in gastric mucous cells but not its release. Indomethacin did not influence PC synthesis, but it decreased the release of newly synthesized PC. PGE2 antagonized the effect of indomethacin on PC release. We conclude that PC release by isolated porcine gastric mucous cells is regulated in a manner different from type II pneumocytes. PC release is impaired by indomethacin and this impairment is restored by PGE2.

Animals↗
PubMed1996

Ethinylestradiol 20 versus 30 micrograms combined with 150 micrograms desogestrel: a large comparative study of the effects of two low-dose oral contraceptives on the hemostatic system.

In a 6-month, randomized, double-blind study the effects of two combined oral contraceptives containing 150 micrograms desogestrel and either 20 or 30 micrograms ethinylestradiol on hemostatic parameters were investigated in 1633 healthy women. Compared with baseline, the 30 micrograms ethinylestradiol formulation increased prothrombin fragment 1 + 2 (+72.2%), D-dimer (+42.4%) and protein C activity (+6.1%), whereas antithrombin-III activity (-6.3%) and protein S activity (-19.7%) were decreased. The use of the 20 micrograms ethinylestradiol formulation was associated with the same pattern of changes, but with lower magnitude (F1+2 + 61.1%, D-dimer +36.0%, antithrombin III -5.3%, protein C +4.6% and protein S-16.0%). The changes from baseline were significantly smaller in the 20 micrograms ethinylestradiol group for D-dimer, antithrombin III and protein S than in the 30 micrograms ethinylestradiol group (p = 0.019, p = 0.038 and p = 0.001, respectively). One woman with a combined deficiency of proteins C and S developed deep venous thrombosis while using the 20 micrograms ethinylestradiol formulation. Use of both formulations was associated with a shift of the coagulation-fibrinolysis balance to an enhanced fibrin-generating and fibrin-degradating activity. The less-pronounced effect on hemostasis with the 20 micrograms ethinylestradiol preparation is reassuring with regard to thromboembolic risk in general. However, women with coagulation inhibitor deficiency should be advised not to use oral contraceptives.

Adolescent↗
PubMed1996

Elevated low-density lipoprotein-cholesterol in women with polycystic ovary syndrome.

Previous studies have indicated that women with the polycystic ovary syndrome (PCOS) are affected by hypertriglyceridemia and low high-density lipoprotein-cholesterol (HDL-C) level. However, most of these studies did not control for confounding factors such as body mass index (BMI) or differences in ethnicity. Therefore, we compared the lipid data for 26 women with PCOS with those for 1428 female control participants of the Prospective Cardiovascular Münster (PRO-CAM) study who did not use hormonal contraceptives and were of similar age. Data were adjusted for age, BMI and ethnicity. Women with PCOS had higher total cholesterol (5.55 +/- 1.24 vs. 4.99 +/- 0.88 mmol/l, p < 0.05) and low-density lipoprotein-cholesterol (LDL-C) levels (3.61 +/- 1.19 vs. 3.08 +/- 0.82 mmol/l, p < 0.05) than the control subjects. Compared with the women in the control population, those with PCOS more frequently had triglyceride levels exceeding 2.3 mmol/l (11.5 vs. 1.6%, p < 0.001), LDL-C levels exceeding 4.2 mmol/l (30.8 vs. 12.1, p < 0.01), and HDL-C levels below 1.2 mmol/l (46.2 vs. 15.3%, p < 0.001). We conclude that dyslipidemia is found more frequently in women with PCOS, independently of the excess weight that is often found in this patient group.

Adult↗
PubMed1996

Hemostatic variables in the prediction of coronary risk: results of the 8 year follow-up of healthy men in the Münster Heart Study (PROCAM). Prospective Cardiovascular Münster Study.

Myocardial infarction is usually due to the acute formation of an occlusive thrombus within the coronary arteries, in most cases against a background of pre-existing coronary atherosclerosis. Both of these factors may be promoted by a procoagulant state of the hemostatic system. Plasma fibrinogen, factor VIIc, blood pressure, and lipid parameters were measured in 2,781 healthy men aged 40-65 in the Münster Heart Study (formerly known as the PROCAM Study). After 8 years of follow-up 130 coronary events (15 sudden cardiac deaths, 22 fatal myocardial infarctions, and 93 nonfatal myocardial infarctions) were observed. Plasma fibrinogen concentration and factor VIIc activity were significantly greater among men who suffered a coronary event. The mean plasma fibrinogen level of the event group exceeded that of the non-event group by 0.32 g/l [2.59 +/- 0.58 vs. 2.91 +/- 0.58 (mean +/- SD) respectively, P < 0.001]. The incidence of coronary events among men within the upper tertile of fibrinogen concentration was three times higher than among men within the lower tertile. Plasma factor VIIc activity was 112.4 +/- 20.1% in the event group and 108.7 +/- 21.4% in the non-event group (P < 0.05). Among men in the upper tertile of factor VIIc activity, the incidence of coronary events was 1.6 times that of men in the lower tertile. When fibrinogen and low density lipoprotein (LDL) concentration were considered together, there was a graded and dramatic eightfold increase in 8 year risk from 17 per 1,000 of population among men with both fibrinogen and LDL cholesterol in the lower tertiles to 130 per 1,000 in men with both of these parameters in the upper tertile. In men with LDL cholesterol in the lowest tertile, increasing fibrinogen levels did not increase the risk of a coronary event. The coagulation variables, fibrinogen concentration, and factor VIIc activity thus markedly improve our ability to predict coronary risk.

Adult↗
PubMed1995

Impact of polymorphisms in the alpha- and beta-fibrinogen gene on plasma fibrinogen concentrations of coronary heart disease patients.

Despite many investigations in a variety of experimental settings, uncertainty remains concerning the size of the genetic contribution to plasma fibrinogen levels. We used the polymerase chain reaction to amplify the polymorphic sites for the restriction enzymes TaqI in the alpha-fibrinogen gene and HaeIII, HindIII and BclI in the beta-fibrinogen gene. Three hundred and eighty-four male coronary heart disease patients were investigated. Two alleles for each enzyme (+ or - designating, respectively, the presence or absence of the cutting site) were detected. The HaeIII and HindIII cutting sites were in complete linkage disequilibrium. A small but significant increase in fibrinogen level was associated with the rare cutting sites of HaeIII/HindIII, BclI and TaqI. At all polymorphic sites homozygosity for the frequent alleles was associated with about 0.20 g/l lower plasma fibrinogen concentrations than heterozygosity at the respective sites (p < 0.05). The frequencies and natures of the rare alleles were as follows: TaqI (+) 0.28, HaeIII/HindIII (-) 0.22 and BclI (+) 0.17. Mean fibrinogen levels in patients heterozygous for each of the four polymorphisms were 0.47 g/l greater than in subjects homozygous for the frequent allele at each cutting site (HaeIII/HindIII + -, TaqI + -, BclI + -: fibrinogen level 3.58 g/l (n = 32); HaeIII/HindIII + +, TaqI - -, BclI - -: fibrinogen level 3.11 g/l (n = 99), p = 0.003). Each polymorphism accounted for between 0.5 and 1.4% of the overall variance in fibrinogen concentration. Together, the polymorphisms in HaeIII, HindIII and TaqI explained 5.8% of overall variance, a proportion equivalent to that explained by age, smoking and body mass index (5.5%).(ABSTRACT TRUNCATED AT 250 WORDS)

Alleles↗
PubMed1995

Molecular analysis at the Harvey Ras-1 gene in patients with long QT syndrome.

Patients with long QT syndrome (LQTS; MIM 1921500) frequently suffer from syncope and are threatened by sudden cardiac death due to ventricular arrhythmias, typically of the torsade de pointes type. Initial progress in revealing the molecular basis of the disease was made by the observation of genetic linkage of the disease locus to the Harvey Ras-1 gene (HRAS 1) on chromosome 11p15.5. More recently loci on chromosomes 3, 4, and 7 have also been found to be linked to LQTS, thus demonstrating heterogeneity in the causes for this disease. The present study performed sequence analysis on the HRAS 1 gene in patients with congenital and acquired LQTS to determine the frequency of HRAS 1 mutations in patients with this disease. In neither group were no mutations identified in the coding regions or in the splice donor and acceptor sites. Alleles characterized by a T to C transition in exon 1 and an insertion/deletion polymorphism upstream of exon 1 showed no significant difference in their frequencies between LQTS patients and normal controls. No quantitative influence of the such characterized genotypes on the QT duration was observed. These results demonstrate that structural mutations in the HRAS 1 gene are not a frequent cause of LQTS. Also, since there was no association of different alleles at the HRAS 1 locus with changes in QT duration, it appears unlikely that this gene is a major contributor to this disease.

Alleles↗