[Lifestyle intervention for the prevention of cardiovascular disease].
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Cardiovascular Diseases↗
Biomedical subjects
J J van Doormaal
Publications and source records attributed to J J van Doormaal.
[Lifestyle intervention for the prevention of cardiovascular disease].
The high cardiovascular disease prevalence in western countries is largely attributable to the contemporary lifestyle. Interventions in the area of nutrition and physical activity have been shown to be effective in the prevention of cardiovascular disease. Successful implementation of lifestyle intervention programmes may be just as effective as drug treatment. In combination with drug treatment, intervention in the area of nutrition and physical activity is the recommended treatment for patients at a high risk of cardiovascular disease. Addition of new drugs to those presently available is associated with low absolute risk reductions and high costs, particularly in the presence of successful lifestyle interventions.
Cardiovascular Diseases↗
[Clinical reasoning and decision-making in practice. A 31-year-old woman with transient monocular blindness and polycythaemia].
A 31-year-old woman presented with recurrent transient monocular blindness. As transient ischaemic attacks were suspected further investigations were targeted at evaluation of premature atherosclerotic lesions in the internal carotid artery. Initially laboratory tests were not performed. After referral to a cardiovascular-disease prevention outpatient clinic, laboratory evaluation disclosed a marked isolated polycythaemia that turned out to be secondary to right-left shunting through multiple pulmonary arteriovenous malformations. The ultimate diagnosis was hereditary haemorrhagic telangiectasia. Later on, physical signs such as telangiectasia and central cyanosis were noticed. In the clinical decision-making process, laboratory tests associated with causes of transient monocular visual loss were not carried out and therefore clues important for the ultimate diagnosis were not obtained. In only a minority of young patients with transient monocular visual loss can this be ascribed to premature atherosclerosis. For these reasons, a proper physical examination and laboratory tests directed towards other causes must be part of the initial diagnostic work-up in young patients with visual disturbances and suspected transient ischaemic attacks.
Adult↗
Low diagnostic value of fasting and post-methionine load homocysteine tests. A study in Dutch subjects with homocysteine test indications.
BACKGROUND: Homocysteine is a cardiovascular disease risk factor. We investigated, both in subjects with past plasma total homocysteine (tHcy) test indications and healthy adults, the diagnostic value of a fasting (tHcy) (f-tHcy) and the added value of a post-methionine-load tHcy (postload-tHcy). METHODS: Plasma homocysteine cut-off values were retrospectively used for hyperhomocysteinemia assessment in 3477 subjects with past tHcy test indications and 177 apparently healthy subjects. Cut-off values were based on reference limits (f-tHcy < or = 15.0; postload-tHcy < or = 50.0 micro mol/l), relative risk (f-tHcy < or = 12.0, postload-tHcy < or = 38.0; or f-tHcy < or = 10.0 micro mol/l) and vitamin-optimized reference limits (f-tHcy < or = 9.3; postload-tHcy < or = 35.1 micro mol/l). RESULTS: Use of the American Heart Association 10 micro mol/l f-tHcy cut-off value gave hyperhomocysteinemia prevalences of 65% in subjects with past tHcy test indications and 50% in healthy subjects. The combination of the vitamin-optimized reference limits for f-tHcy and postload-tHcy gave a hyperhomocysteinemia prevalence of 79% in subjects with tHcy test indications, of which only 5% was on account of increased postload-tHcy. Corresponding values for healthy subjects were 68% and 3%, respectively. CONCLUSIONS: Employment of a 10 micro mol/l (American Heart Association) or 9.3 micro mol/l (vitamin-optimized reference) cut-off value leaves no indications for tHcy testing from an evidence-based point-of-view.
Adult↗
Antineutrophil cytoplasmatic antibodies in patients with premature atherosclerosis: prevalence and association with risk factors.
OBJECTIVES: Autoimmunity is suggested to play a role in premature atherosclerosis. Antineutrophil cytoplasmatic antibodies (ANCA) are a group of autoantibodies found in several inflammatory disorders in which they supposedly amplify the inflammatory process. In this study the hypothesis is tested that ANCA play a role in premature atherosclerosis. DESIGN: Cross-sectional study followed by nested case-control study. In a total of 286 consecutive patients with premature atherosclerosis (age < 55 years) ANCA were tested. Within the same cohort, a nested case-control study in 16 ANCA-positive patients and 32 ANCA-negative controls matched for sex, and site of atherosclerosis, was executed. SETTING: University hospital outpatient clinic for lipids and premature atherosclerosis. SUBJECTS: A total of 286 consecutive patients with premature atherosclerosis (age < 55 years). RESULTS: Prevalence of ANCA was 5.6% (16 of 286). All cases had perinuclear ANCA (pANCA); no cytoplasmatic ANCA was found. Mean age was 42 +/- 7 in the ANCA-positive vs. 42 +/- 9 years in the ANCA-negative group (P=ns). More female parents were ANCA-positive (8M/8F vs. 200M/70F, P=0.03). Patients with ANCA had more often peripheral vascular disease (37.5 vs. 15.2%, P=0.03). In the case-control study levels of Lp(a) were higher (43.8 vs. 15.6% >300 mg x L(-1), P=0.05), whereas levels of HDL-c were lower in ANCA-positive patients (0.84 +/- 0.26 vs. 1.06 +/- 0.27 mmol x L(-1), P=0.01). Markers of inflammation, C-reactive protein (CRP) and serum amyloid A (SAA), did not differ, nor did antibodies against oxidized-LDL and malondialdehyde (MDA)-LDL, markers for the extent of atherosclerosis. CONCLUSIONS: Our results suggest that ANCA do not appear to play a major role in premature atherosclerosis as there was no increased prevalence of the autoantibody. Moreover, no differences in the incidence of classical cardiovascular risk factors nor in serum levels of markers of inflammation were found between the ANCA-positive group as compared with the ANCA-negative group.
Adult↗
Effects of initial and long-term lipid-lowering therapy on vascular wall characteristics.
Several studies have demonstrated the beneficial effects of 3 hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors on vascular properties, but little is known about treatment intensification. We compared patients in whom statins were started (INITIAL, n=30) for hypercholesterolaemia (>6.5 mmol l(-1)) with a matched patient group of long-time statin users, with similar baseline characteristics for lipids, intima-media thickness (IMT), and pulse wave velocity, in whom treatment with statins was intensified (LONG-TERM, n=54). At baseline and after 1 year, lipid profile, IMT of the carotid and femoral arteries, aortic distensibility using pulse-wave velocity and various properties of the peripheral vascular bed using a recently developed bio-impedance method were measured. After 1 year the relative changes in lipid profile were significantly better in the INITIAL compared with the LONG-TERM-group. The relative changes in IMT of the mean internal carotid and common femoral arteries significantly differed between the INITIAL and LONG-TERM-group (-8 and +11%, -11 and +22%, respectively). After 1 year, in both groups, most other vascular wall characteristics were unaltered compared with baseline. In conclusion, the beneficial structural alterations of the vascular wall were greater after starting than after intensifying already existing lipid-lowering treatment. This suggests that other effects of HMG-CoA reductase inhibitors than lipid-lowering alone must be involved in vascular changes.
Adult↗
No long-lasting or intermittent mast cell activation in acute coronary syndromes.
BACKGROUND: Unstable coronary syndromes, such as acute myocardial infarction and unstable angina pectoris are mostly due to rupture of an atherosclerotic plaque. Recently mast cells were found to participate actively in the inflammatory process of atherosclerosis by excreting proteolytic and pro-inflammatory substances with the ability to cause plaque instability and rupture. Mast cell activity can be determined by measuring serum levels of tryptase, as has been demonstrated in patients with anaphylaxis and mastcytosis. HYPOTHESIS: Acute coronary events (acute myocardial infarction and unstable angina pectoris) are associated with increased mast cell activity, reflected by elevated serum tryptase levels. METHODS: Serum levels of tryptase were determined in the following three groups of patients: 13 patients with acute myocardial infarction, 10 patients with unstable angina pectoris, and 14 patients without ischaemic cardiovascular disease who were used as controls. Patients with known IgE mediated allergic diseases and/or anti-histaminical drugs were excluded. RESULTS: The groups were comparable for sex, blood pressure, smoking and cholesterol levels. The controls tended to be younger (P=0.05). Levels of tryptase did not differ between patients with acute myocardial infarction (7.9+/-4.6 microg/l), unstable angina pectoris (6.0+/-2.1 microg/l) or controls (6.9+/-4.1 microg/l), nor could a relation with levels of C-reactive protein be demonstrated. CONCLUSION: Serum levels of tryptase are not elevated in patients with acute coronary syndromes. This implies that increased mast cell activity, if any, in unstable coronary syndromes is not reflected systemically. Other, more specific methods will be needed to determine the activity of the mast cell in vivo.
Adult↗
Secondary prevention with fluvastatin decreases levels of adhesion molecules, neopterin and C-reactive protein.
BACKGROUND: Treatment of hypercholesterolaemia with HMG-CoA reductase inhibitors results in an earlier reduction of morbidity and mortality than expected from trials using conventional cholesterol-lowering therapies. Possible explanations for this effect include stimulation of angiogenesis, improvement of endothelial function, plaque stabilisation, inhibition of coagulation and/or thrombocyte aggregation and inhibition of the inflammatory response associated with atherosclerosis. METHODS: We investigated whether statins exert their effects by inhibition of endothelial activation, inflammation and/or monocyte/macrophage activation by measuring plasma levels of soluble cell adhesion molecules, neopterin and C-reactive protein upon treatment with fluvastatin for a period of 12 months in patients with established atherosclerosis and hypercholesterolaemia. RESULTS: Blood samples were taken at baseline and at 3 and 12 months after starting treatment with fluvastatin 80 mg daily. Upon treatment, a reduction of s-ICAM-1 (956.3+/-123.6 vs. 745.4+/-127.4 vs. 674.9+/-70.8 ng/ml, P<0.05) and s-E-selectin (58.6+/-6.7 vs. 47.0+/-6.1 vs. 44.9+/-3.2 ng/ml, P<0.01) was observed. In addition, levels of neopterin decreased, albeit transiently (7.1+/-0.7 vs. 6.0+/-0.5 vs. 6.5+/-0.8 nmol/l, P=0.02), suggesting a reduction in monocyte/macrophage activity. Moreover, we found a decrease in levels of C-reactive protein during follow-up (5.21+/-2.0 vs. 3.18+/-0.7 vs. 1.95+/-0.3 mg/l, P<0.05), compatible with a reduction in inflammatory activity. CONCLUSION: We conclude that statins have a combined beneficial effect on monocyte/macrophage activity, endothelial function and systemic inflammatory activity.
Journal Article↗
Influence of vitamin-optimized plasma homocysteine cutoff values on the prevalence of hyperhomocysteinemia in healthy adults.
BACKGROUND: Hyperhomocysteinemia is a cardiovascular disease (CVD) risk factor. We determined plasma homocysteine (Hcy) reference values at optimized vitamin status and investigated their influence on the prevalence of hyperhomocysteinemia in healthy adults. Results were compared with those obtained using European Concerted Action Project (ECAP) cutoff values. METHODS: Healthy adults (n = 101) received folic acid (5 mg/day) and vitamin B(12) (1 mg/day) for 2 weeks and the same dosages of folic acid and vitamin B(12) plus vitamin B(6) (1 mg. kg(-1). day(-1)) during the following 2 weeks. Hcy concentrations, both fasting and 6-h post-methionine load, were determined at baseline and after 4 weeks. RESULTS: Baseline (4 weeks) fasting and 6-h postload Hcy reference values were 4.7-14.6 (4.1-9.3) and 18.8-49.7 (12.9-35.1) micromol/L, respectively. Mean fasting and 6-h postload Hcy decreased after 4 weeks of vitamin supplementation by 3.5 micromol/L (33.5%) and 8.5 micromol/L (26.3%), respectively. The percentages of subjects exhibiting significant decreases in fasting Hcy following vitamin supplementation were 88% (all subjects), 92% (non-vitamin users), and 72% (vitamin users). The prevalences of hyperhomocysteinemia with use of ECAP cutoff values were 29% for all groups, 29% for men, 27% for premenopausal women, and 53% for postmenopausal women. With vitamin-optimized cutoff values, prevalences were 58%, 58%, 76%, and 89%, respectively. Use of vitamin-optimized cutoff values increased the diagnostic value of fasting Hcy and decreased that of a 6-h postload Hcy compared with use of ECAP cutoff values. CONCLUSIONS: Use of vitamin-optimized cutoff values gives rise to high hyperhomocysteinemia pretest probabilities in the general population and, therefore, precludes any meaningful role for Hcy testing. Future demonstration of a beneficial effect of decreasing Hcy on CVD risk would justify use of vitamin-optimized cutoff values for assessment of CVD risk.
Adolescent↗
[Pregnancy in women with diabetes mellitus type I: maternal and perinatal complications, in spite of good blood glucose control].
OBJECTIVE: To examine the maternal and neonatal outcome of pregnancies of women with type I diabetes mellitus. DESIGN: Retrospective. METHODS: The medical records of pregnancies (> or = 16 weeks) in women with type I diabetes mellitus between 1986/'97 were studied in University Medical Center Utrecht, Academic Hospital Groningen and Isala Clinics, location 'De Weezenlanden', Zwolle, the Netherlands. RESULTS: During the study period, 172 women had 220 pregnancies: 212 single and 8 twin pregnancies. The mean age was 29.1 years (SD: 4.1), the mean duration of standing of the diabetes was 12 years (range: 1-32) and the mean concentration of glycosylated haemoglobin (HbA1c) was 6.3% at 10 weeks of pregnancy. The incidence of children with congenital malformations was 4 times higher (n = 19; 9.0%) than that in the Dutch population (2%). Macrosomia occurred in 92 children (43.4%) and perinatal mortality in 7 (3.3%). Maternal hypertensive complications occurred in 39 single pregnancies (18.4%), which is 2-3 times more often than in the Dutch population. CONCLUSION: In type I diabetic women maternal complications, perinatal morbidity and mortality are increased, despite near optimal glycaemic control.
Adult↗
[Obstetric problems followed by stroke].
Obstetrical problems sometimes portend manifestations of atherosclerosis, as illustrated by two case reports. The first patient had the combination of hyperhomocysteinaemia due to chronic vitamin deficiencies in the diet, and smoking. The second was also a smoker and had a genetically determined mild hyperhomocysteinaemia, aggravated by chronic vitamin deficiencies resulting from poor dietary habits; she also had an increased folic acid requirement because of use of anti-epileptic drugs in combination with a familial predisposition for premature atherosclerotic manifestations. The first patient had four pregnancies, two of which ended in intrauterine foetal death due to placental infarction, and one in the birth of a dysmature boy. The second patient's four pregnancies ended twice in abortion and twice in the birth of a dysmature child; in one of the latter cases placental infarction was observed. Both women subsequently suffered cerebrovascular accidents while in addition, older cerebral infarctions were found to be present. Women with recurrent abortion, pre-eclampsia, placental infarction, placental detachment and foetal growth retardation should be examined, even if other risk factors are also present, for (mild) hyperhomocysteinaemia, and treated for it with vitamin suppletion (folic acid, vitamins B6 and B12), even although admittedly more research is necessary to make certain that such treatment has a preventive effect on the manifestations of this disorder.
Abortion, Habitual↗
A frequent mutation in the lipoprotein lipase gene (D9N) deteriorates the biochemical and clinical phenotype of familial hypercholesterolemia.
The D9N substitution is a common mutation in the lipoprotein lipase (LPL) gene. This mutation has been associated with reduced levels of HDL cholesterol and elevated triglycerides (TG) in a wide variety of patients. We investigated the influence of this D9N mutation on lipid and lipoprotein levels and risk for cardiovascular disease (CVD) in patients with familial hypercholesterolemia (FH). A total of 2091 FH heterozygotes, all of Dutch extraction, were screened for the D9N mutation using standard polymerase chain reaction techniques, followed by specific enzyme digestion. A total of 94 FH subjects carried the D9N mutation at a carrier frequency of 4.5%. Carriers of other common LPL mutations, such as the N291S and the S447X were excluded. Clinical data on 80 FH individuals carrying the D9N were available and were compared with a FH control group matched for age, sex, and body mass index (n=203). Analysis revealed significantly higher TG (P=0.01) and lower HDL-cholesterol levels (P=0.002). Dyslipidemia was more pronounced in D9N carriers with higher body mass index. Moreover, FH patients carrying this common LPL mutation were at higher risk for CVD, (odds ratio=2.8; 95% CI, 1.43 to 5.32; P=0.002). The common D9N LPL mutation leads to increased TG and decreased HDL plasma levels in patients with FH. These effects are most apparent in those FH heterozygotes with an increased body mass index. Furthermore, this mutation, present in 4.5% of Dutch FH heterozygotes, leads to increased risk for CVD.
Adolescent↗
[Recommended dietary allowance of folic acid is insufficient for optimal homocysteine levels].
OBJECTIVE: To determine the effect of short term supplementation of vitamin B6 (pyridoxine) followed by folic acid in apparently healthy volunteers on the fasting plasma homocysteine concentrations (hyperhomocysteinaemia is an independent risk factor for premature atherosclerosis). DESIGN: Prospective, descriptive. SETTING: Academic Hospital Groningen, the Netherlands. METHODS: Apparently healthy Dutch volunteers, aged 20-75 years, were supplemented with vitamin B6 1 mg/kg/day during 7 days followed by folic acid 5 mg/day during another 7 days. On days 0, 7 and 14 the fasting plasma homocysteine concentrations were measured. A change of an individual's plasma homocysteine level was considered statistically significant if the change in percentage exceeded 2.8 times the sum of the analytical and the intraindividual biological variation. RESULTS: There were 103 participants, 45 males and 58 females, with average ages of 43 and 44 years, respectively (on day 7, data were available on 101 participants). Baseline folic acid concentrations of all participants were above the lower limit of the reference range. Eight and two of them had vitamin B6 and vitamin B12 concentrations below the reference range, respectively. Plasma homocysteine was inversely related to plasma levels of folic acid and vitamin B12 at that moment. During vitamin B6 supplementation the mean plasma homocysteine level did not change; one participant exhibited a significant plasma homocysteine decrease. During folic acid supplementation the mean plasma homocysteine decreased from 11.7 mumol/l (SD: 5.6) to 9.1 (SD: 3.4); 40 participants (40%) exhibited significant plasma homocysteine decreases. At the end of the study plasma homocysteine was still related to plasma vitamin B12. CONCLUSION: The folic acid status of the participants at baseline was not associated with the lowest plasma homocysteine levels. Since atherosclerosis risk may increase continuously with increasing plasma homocysteine, it may be wise to keep plasma homocysteine levels as low as possible. To reach this goal, the recommended dietary allowance of folic acid may have to be increased.
Adult↗
Influence of fasting on circulating levels of alpha-tocopherol and beta-carotene. Effect of short-term supplementation.
We investigated the influence of fasting on the levels of alpha-tocopherol in plasma, erythrocytes and platelets, and on plasma beta-carotene. Six apparently healthy adults were subjected to 17-h feed-fasting experiments at various days before, during and after supplementation with alpha-tocopherol (455 mg/day, 41 days) and beta-carotene (25 mg/day, 24 days). Adipose tissue alpha-tocopherol and beta-carotene were measured at regular intervals. Supplementation increased alpha-tocopherol and beta-carotene in all compartments, except for beta-carotene in adipose tissue. Discontinuation caused a rapid return to baseline, except for adipose tissue alpha-tocopherol and plasma beta-carotene. Fasting caused linear increases of free fatty acids, consistent (but small) increases of plasma alpha-tocopherol and inconsistent increases of plasma beta-carotene. There were no fasting-related changes in other compartments. We conclude that fasting is unable to increase alpha-tocopherol and beta-carotene in circulating lipoproteins and cells to a considerable extent, both at baseline levels and after short-term supplementation. Maintenance of high levels may necessitate regular high oral intakes.
Adult↗
Gamma-linolenic acid does not augment long-chain polyunsaturated fatty acid omega-3 status.
Augmentation of long chain polyunsaturated omega3 fatty acid (LCPUFA omega3) status can be reached by consumption of fish oil or by improvement of the conversion of alpha-linolenic acid (ALA) to LCPUFA omega3. Since gamma-linolenic acid (GLA) might activate the rate-limiting delta-6 desaturation, we investigated whether GLA augments LCPUFA omega3 status. Eight adults received 1.4 g GLA for 4 weeks and subsequently 2.2 g ALA+1.4 g GLA daily during another 4 weeks. Another seven adults received a daily oral dose of 2.2 g ALA for 4 weeks, and subsequently 2.2 g ALA+1.4 g GLA during another 4 weeks. ALA, or ALA+GLA, did not significantly augment EPA and DHA contents. We conclude that the LCPUFA omega3 status can not be improved by supplementation of low dose GLA, neither by co-supplementation of ALA. Poor conversion of ALA to LCPUFA omega3 may be caused by preferential beta-oxidation of ALA, negative feedback of arachidonic acid from the omnivorous diet, or by the low dietary ALA/LA ratio.
Adult↗
Plasma folic acid cutoff value, derived from its relationship with homocyst(e)ine.
We established the cutoff value for plasma folic acid, using plasma homocyst(e)ine as the functional marker. To do this, we investigated the relationship of the plasma folic acid of 103 apparently healthy adults with their fasting plasma homocyst(e)ine and with their plasma homocyst(e)ine 6 h after oral methionine challenge (100 mg/kg). We also studied the relationship of their plasma folic acid with the decline of fasting plasma homocyst(e)ine after 7 days of folic acid supplementation (5 mg/day). The three approaches suggested a cutoff value of 10 nmol/L. The chances of individuals to significantly (P <0.05) lower their plasma homocyst(e)ine after folic acid supplementation proved significantly higher at plasma folic acid concentrations < or = 10 nmol/L, as compared with folic acid concentrations above this value (odds ratio, 5.02; 95% confidence interval, 1.87-13.73). We suggest adopting a 10 nmo/L plasma folic acid cutoff value on functional grounds.
Adult↗
Pravastatin in diabetes-associated hypercholesterolemia.
Patients with diabetes mellitus (DM), type 1 and type 2, have an increased risk of coronary heart disease as a result of accelerated atherosclerosis. Dyslipidemia, often found in these patients, plays an important role in this process. This study investigates the efficacy and safety of lipid-lowering therapy with pravastatin, a 3-HMG-Coenzym A reductase inhibitor in hypercholesterolemic type-1 and type-2 diabetic patients. Of 49 patients (22 type-1 DM and 27 type-2 DM), 24 patients were treated with pravastatin, 20 mg/day, and 25 patients with placebo. After 24 weeks, total cholesterol (TC) was decreased by 22.2%, low-density lipoprotein (LDL) cholesterol by 25.8% and triglycerides (TG) by 13.6%. Pravastatin treatment did not induce a significant change in high-density (HDL) cholesterol levels. No differences in effects of pravastatin treatment on serum lipids and lipoproteins were found with respect to the diabetes type. No serious side effects occurred and pravastatin treatment did not cause any deterioration in glycemia control. The data suggest that pravastatin is effective and safe in the treatment of dyslipidemia in both type-1 and type-2 diabetic patients.
Adult↗
Fatal anaphylaxis after a yellow jacket sting, despite venom immunotherapy, in two patients with mastocytosis.
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Adult↗