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Biomedical subjects

R Darioli

Publications and source records attributed to R Darioli.

At least 19 recordsLinked to original sources
PubMed2006

[Evolution of cardiac risk factors management among patients aged 65 years and older with coronary artery disease].

The aim of this retrospective study was to compare the appropriateness of cardiac risk factors (CV-RF) management in a Swiss cardiac rehabilitation center. The comparison of the control of CV-RF among 342 patients with coronary artery disease (CHD) aged > or =65 years was improved. The CV-RF management has globally improved during the two periods of observation (1994-95 and 1999-2000). Nevertheless, according to the recommendations published between 1994 and 1999, an underuse of the cardioprotective agents was still observed. Using a standardized protocol for the management of CHD which allows the benchmarking among the network of cardiac rehabilitation centers network could increase the quality of care for such high risk patients.

Aged↗
PubMed2006

[Early detection of atherosclerosis].

According to the guidelines, the global assessment of cardiovascular risk is based on traditional risk factors. The emergence of new cardiovascular risk factors may be helpful. However, at every level of risk factor exposure, there is a substantial variation of atherosclerosis. Thus, subclinical disease measurements, representing the end result of risk exposure may be useful for improving cardiovascular risk prediction. In comparison to the ankle-brachial index, the high resolution B-mode ultrasound is a more promising tool to detect early atherosclerosis both on carotid and femoral arterial wall in asymptomatic patients. It appears as a new approach to predict the risk of cardiovascular disease and to monitor the cardiovascular therapy.

Atherosclerosis↗
PubMed2005

[Statins in older patients: limits to prescription?].

Cardio-vascular diseases are a major contributor to mortality, morbidity and functional decline in the elderly population. Hypercholesterolemia remains a major risk factor in older persons, but treatment decisions are difficult because of the paucity of data specific to this segment of the population. While evidence seems strong enough to support treating patients with cardio-vascular diseases (secondary prevention) up to their eighties, the question remains open whether to treat asymptomatic older patients (primary prevention) or those in their nineties.

Age Factors↗
PubMed2005

[Alcohol and risk of coronary heart disease].

More than 60 prospective cohort studies have shown a consistent association between regular and moderate alcohol consumption and decrease in risk of coronary heart disease, ischemic stroke and heart failure by 20 to 40% as compared to heavy alcohol intake or drinking no alcohol. Lower protective effects were found in young, in women and in men living outside the Mediterranean area. Moreover, some biological characteristics of alcohol, particularly red wine, could interfere with the athero-thrombotic process and contribute to increase the plausibility for the protective effects of alcohol on cardiovascular diseases. However, the results of meta-analyses also demonstrate harmful effects in relation with dose and pattern of alcohol consumption. In regard to the available scientific data, alcohol consumption cannot be include in the recommendations for the prevention of cardiovascular diseases. On the other hand alcohol should not be prohibited when consumption remains mild to moderate.

Alcohol Drinking↗
PubMed2004

[Homocystein and cardiovascular risk: is dosage useful?].

Hyperhomocysteinemia represents an independent risk factor for atherothrombotic disease. Physiopathological mechanisms of accelerated progression of atherosclerosis in presence of hyperhomocysteinemia are complex. Herein we report a clinical case which emphasis the importance of screening elevated homocystein in the absence of conventional risk factors in patients who suffer from premature atherosclerosis.

Adult↗
PubMed2001

Premature atherosclerosis in HIV-infected individuals--focus on protease inhibitor therapy.

OBJECTIVE: Lipid disorders associated with the use of protease inhibitors may contribute to the premature development of atherosclerosis. The purpose of the present study was to determine whether the administration of a protease inhibitor-containing regimen to middle-aged (30-50 years) HIV-infected individuals for 6 months or longer is associated with an increased prevalence of atherosclerosis. METHODS: High-resolution B-mode ultrasound imaging was used to visualize the femoral and carotid arteries of 68 HIV-negative and 168 HIV-infected individuals, including 136 patients who had received protease inhibitors for 26.8 +/- 8.9 months (mean +/- SD). Atherogenic plaques were defined as a thickening of the intima-media > or = 1200 mm. RESULTS: The proportion of participants with one or more plaques was higher in the HIV-infected group in comparison with the HIV-negative group (55 versus 38%; P = 0.02), and so was the prevalence of cigarette smoking (61 versus 46%; P = 0.03) and hyperlipidaemia (56 versus 24%; P < 0.001). The presence of plaque was independently associated with age, male gender, plasma low-density lipoprotein cholesterol levels and smoking. In univariate logistic regression analysis, an association was also found with HIV infection. Among HIV-infected subjects protease inhibitor therapy was not associated with the presence of plaque. CONCLUSIONS: A large proportion of the middle-aged HIV-infected individuals examined during this study had one or more atherosclerotic plaques within the femoral or carotid arteries. The presence of peripheral atherosclerosis within this population is not associated with the use of protease inhibitors, but rather with 'classic' cardiovascular risk factors such as smoking and hyperlipidaemia, which are amenable to interventions.

Adult↗
PubMed2001

Plasma apolipoprotein(a) co-deposits with fibrin in inflammatory arthritic joints.

Extravascular coagulation and diminished fibrinolysis are processes that contribute to the pathology of both inflammatory arthritis and atherosclerosis. We hypothesized that, given its homology with plasminogen, apolipoprotein (apo) (a), the distinctive glycoprotein of the atherogenic lipoprotein (Lp) (a), may be equally implicated in inflammatory arthritis. We detected the presence of apo(a) as part of Lp(a) in human arthritic synovial fluid. The abundance of apo(a) in synovial fluid rose in proportion to plasma apo(a) levels and was higher in inflammatory arthritides than in osteoarthritis. In addition, apo(a) immunoreactive material, but not apo(a) transcripts, was detected in inflammatory arthritic synovial tissues. These data indicated that synovial fluid apo(a) originates from circulating Lp(a) and that diffusion of Lp(a) through synovial tissue is facilitated in inflammatory types of arthritis. In synovial tissues, apo(a) co-localized with fibrin. These observations could be reproduced in a model of antigen-induced arthritis, using transgenic mice expressing human Lp(a). Although in this mouse model the presence of apo(a) did not change the severity of arthritis, the co-localization of apo(a) with fibrin in synovial tissue suggests that, in humans, apo(a) may modulate locally the fibrinolytic activity and may thus contribute to the persistence of intra-articular fibrin in inflammatory arthritis.

Animals↗
PubMed2001

Epidemiology of cardiovascular risk factors among schoolchildren in Sousse, Tunisia.

BACKGROUND: In Tunisia, where the epidemiological transition phenomenon is well established, there are no data available at the population level on the cardiovascular disease (CVD) risk profile for children, although it is well known that risk factor development takes place in childhood. METHODS: We report an epidemiological survey based on a representative sample of 1569 urban schoolchildren of Sousse in Tunisia to assess the following CVD risk factors: hypertension, hypercholesterolaemia and other lipid disorders, obesity and tobacco consumption. RESULTS: The main results showed that girls had significantly higher levels of body mass index (BMI), diastolic blood pressure (DBP), total cholesterol, low-density lipoprotein (LDL) cholesterol and high-density lipoprotein (HDL) cholesterol than boys, who however had significantly higher levels of systolic blood pressure (SBP). Total cholesterol was significantly correlated to BMI and decreased with age. Obesity (BMI = 27) was found in 7.9% of the study population and was significantly higher for girls (9.7%) than for boys (6%): chi 2 = 9.02, DF = 2, P = 0.011. Overweight (BMI = 25) was also significantly higher for girls (16%) than for boys (11.1%): chi 2 = 8.21, DF = 1, P = 0.0041. Smoking habit concerned 7.6% of the study population; it was significantly higher for boys (14.7%) than for girls (1.1%): chi 2 = 103.4, DF = 1, P < 0.00001. CONCLUSION: This study showed to some extent that Tunisia's urban population of schoolchildren is exposed early to CVD risk factors and all should be done to avoid the worsening of this profile. These results will serve as a baseline for assessment of future trends in the risk factors studied.

Adolescent↗
PubMed2000

Inactivated hepatitis A vaccine booster given >/=24 months after the primary dose.

We investigated what happens with the immune response when people come back for their booster dose of inactivated hepatitis A vaccine later than the recommended time of 6-12 months after the primary dose. We recruited a group of 124 travellers who received either the primary doses of Havrix 720 (two doses) or of Havrix 1440 (one dose) >/=24 months before study entry. They received a booster dose of Havrix 1440 and blood was drawn 1 month later. As a control group, we recruited a group of 125 travellers who followed a recommended schedule with a primary dose at month 0 and a booster dose at months 6-12. For both study groups, the GMTs increased dramatically and similarly upon the booster immunisation. Although significantly more late travellers (32%) had lost detectable antibodies than controls (11%) before administration of the booster dose, all these subjects showed an anamnestic response to the booster dose. Delaying the booster dose up to 66 months after primary vaccination did not seem to influence the immunogenicity of the booster dose. However, the recommended 6-12-month interval remains if detectable antibody titers are to be warranted constantly.

Adult↗
PubMed2000

[Evaluating the efficacy and tolerance of atorvastatin in hyperlipidemia in general practice (SWITCH Study)].

Elevated levels of serum lipids and lipoproteins are known to play a major role in the development of atherosclerosis and subsequent coronary heart disease (CHD). In controlled clinical studies, atorvastatin (Sortis), a new 3-hydroxy-3-methyl-glutaryl-coenzyme-A (HMG-CoA)-reductase inhibitor, proved to be a very effective and safe lipid-lowering agent. The aim of this open-label, multicentre study (without a control group) was to confirm the efficacy and safety of atorvastatin in a private practice group, including 181 Swiss cardiologists, internists, and general practitioners. A total of 877 hyperlipidaemic patients requiring treatment participated in this study. To evaluate the effectiveness of the treatment with atorvastatin over a period of 12 weeks, total plasma cholesterol (TC), HDL cholesterol, LDL cholesterol and triglycerides (TG) were determined every 4 weeks. The initial atorvastatin dose was 10 mg in 78% of patients and 20 mg in 22%. The dose was doubled every 4 weeks until the target values of TC < or = 5.2 mmol/l and TC/HDL < or = 5 were reached. After 12 weeks of treatment with atorvastatin the mean reduction in TC, TC/HDL, LDL and TG compared to baseline levels was 33, 37, 42, and 25% respectively. At the same time the HDL concentration was increased by 9%. These results were evidenced in patients with existing coronary heart disease, in high risk patients without manifest coronary heart disease and in patients with significantly elevated lipid levels (TC > 7.8 mmol/l, TC/HDL > 6.5). After treatment with atorvastatin for 12 weeks, 59% of patients had reached the therapeutic target of TC < or = 5.2 mmol/l. The target of TC/HDL < or = 5 was reached by 79%. Atorvastatin was almost without exception well tolerated, the most frequently reported side effects being nausea, myalgia, and headache. In this open-label multicentre study atorvastatin was found to be effective and well tolerated. The observed reduction in the lipid and lipoprotein concentration is in accordance with the results of published controlled studies. The lipid and lipoprotein concentrations were decreased significantly in patients with slight to moderate elevation of lipid levels as well as in those with significantly raised values.

Adult↗
PubMed2000

[Pharmacoeconomic evaluation of pravastatin in coronary secondary prevention in patients with myocardial infarct or unstable angina pectoris. An analysis based on the LIPID Study].

BACKGROUND: Secondary coronary prevention with lipid lowering drugs have become a major issue in health policy formulation due to the large upfront investment in drug therapy. The recently completed LIPID trial with pravastatin in secondary prevention immediately raise the question whether pravastatin might be cost-effective in Switzerland. METHODS: We conducted a cost-effectiveness analysis from the perspective of third party payers. The following costs were included in the analysis: daily treatment costs of pravastatin, non fatal myocardial infarction, coronary bypass operations and stroke. Life years gained was obtained by applying the declining exponential approximation of life expectancy. All calculations were standardized to 1000 treated patients. RESULTS: The net costs of treating 1000 patients (i.e. drug costs minus the costs of sequelae and interventions) are Fr. 3.6 Mio. In addition, a total of 430 life-years may be saved through treatment. The corresponding cost-effectiveness of pravastatin treatment is Fr. 8341 (nominal) Fr. 6985 (discounted). CONCLUSIONS: The results suggest that the cost-effectiveness of pravastatin in secondary prevention lie well within the threshold of other commonly accepted medical interventions and may be considered an economically viable approach for secondary coronary prevention.

Angina, Unstable↗
PubMed2000

Major reduction in plasma Lp(a) levels during sepsis and burns.

Plasma levels of lipoprotein(a) [Lp(a)], an atherogenic particle, vary widely between individuals and are highly genetically determined. Whether Lp(a) is a positive acute-phase reactant is debated. The present study was designed to evaluate the impact of major inflammatory responses on plasma Lp(a) levels. Plasma levels of C-reactive protein (CRP), low density lipoprotein cholesterol, Lp(a), and apolipoprotein(a) [apo(a)] fragments, as well as urinary apo(a), were measured serially in 9 patients admitted to the intensive care unit for sepsis and 4 patients with extensive burns. Sepsis and burns elicited a major increase in plasma CRP levels. In both conditions, plasma concentrations of Lp(a) declined abruptly and transiently in parallel with plasma low density lipoprotein cholesterol levels and closely mirrored plasma CRP levels. In 5 survivors, the nadir of plasma Lp(a) levels was 5- to 15-fold lower than levels 16 to 18 months after the study period. No change in plasma levels of apo(a) fragments or urinary apo(a) was noticed during the study period. Turnover studies in mice indicated that clearance of Lp(a) was retarded in lipopolysaccharide-treated animals. Taken together, these data demonstrate that Lp(a) behaves as a negative acute-phase reactant during major inflammatory response. Nongenetic factors have a major, acute, and unexpected impact on Lp(a) metabolism in burns and sepsis. Identification of these factors may provide new tools to lower elevated plasma Lp(a) levels.

Adult↗
PubMed2000

[Reference values of intima-medial thickness of carotid and femoral arteries in subjects aged 20 to 60 years and without cardiovascular risk factors].

Many studies have shown a close correlation between intima-medial thickness of the carotid artery measured by high resolution ultrasonography and the presence of coronary artery disease or atherogenic risk factors. However, reference values for the value of intima-medial thickness (IMT) in healthy subjects have not yet been established. The aim of this study was, therefore, to determine the reference values of carotid (C-IMT) and femoral intima-medial thickness (F-IMT) with respect to age and gender in healthy subjects (53 women and 45 men) aged 20 to 60, with no family or personal history of cardiovascular disease or atherogenic risk factors, underwent high resolution colour echo-Doppler examination. The mean C-IMT was 556 +/- 57 microns in women and 573 +/- 70 microns in men (NS), and the femoral equivalent was 543 +/- 63 microns in women and 562 +/- 74 microns in men (NS). Between the ages of 20 and 60, the C-IMT increased by 1.8 microns per year (p < 0.03) in women and 3.4 microns (p < 0.001) in men, the variations being respectively 1.2 microns (NS) and 3.1 microns (p < 0.002) in the femoral artery. Multiple regression analysis including gender and individual values of age, body mass index and lipid profile confirmed that only age was significantly correlated to the increase in thickness. The authors conclude that the reference values of IMT do not differ with gender or site of analysis, but there is a slight influence with respect to age.

Adult↗
PubMed1999

Atherogenic dyslipidemia in HIV-infected individuals treated with protease inhibitors. The Swiss HIV Cohort Study.

BACKGROUND: Administration of protease inhibitors (PIs) to HIV-infected individuals has been associated with hyperlipidemia. In this study, we characterized the lipoprotein profile in subjects receiving ritonavir, indinavir, or nelfinavir, alone or in combination with saquinavir. METHODS AND RESULTS: Plasma lipoprotein levels were quantified in 93 HIV-infected adults receiving PIs. Comparison was done with pretreatment values and with 28 nonPI-treated HIV-infected subjects. An elevation in plasma cholesterol levels was observed in all PI-treated groups but was more pronounced for ritonavir (2.0+/-0.3 mmol/L [mean+/-SEM], n=46, versus 0.1+/-0.2 mmol/L in nonPI treated group, P<0.001) than for indinavir (0.8+/-0.2 mmol/L, n=26, P=0.03) or nelfinavir (1.2+/-0.2 mmol/L, n=21, P=0.01). Administration of ritonavir, but not indinavir or nelfinavir, was associated with a marked elevation in plasma triglyceride levels (1.83+/-0.46 mmol/L, P=0.002). Plasma HDL-cholesterol levels remained unchanged. Combination of ritonavir or nelfinavir with saquinavir did not further elevate plasma lipid levels. A 48% increase in plasma levels of lipoprotein(a) was detected in PI-treated subjects with pretreatment Lp(a) values >20 mg/dL. Similar changes in plasma lipid levels were observed in 6 children receiving ritonavir. CONCLUSIONS: Administration of PIs to HIV-infected individuals is associated with a marked, compound-specific dyslipidemia. The risk of pancreatitis and premature atherosclerosis due to PI-associated dyslipidemia remains to be established.

Adult↗
PubMed1999

Effect of cardiopulmonary bypass and heparin on plasma levels of Lp(a) and Apo(a) fragments.

Fragments of apolipoprotein(a) [apo(a)], the distinctive glycoprotein of lipoprotein(a) [Lp(a)], are present in human plasma and urine and have been implicated in the development of atherosclerosis. The mechanism responsible for the generation of apo(a) fragments in vivo is poorly understood. In this study, we examined the plasma levels of Lp(a) and apo(a) fragments [or free apo(a)] and urinary apo(a) in 15 subjects who underwent cardiac surgery necessitating cardiopulmonary bypass. We also measured the plasma concentration and activity of polymorphonuclear elastase, an Lp(a)-cleaving enzyme in vitro, and plasma levels of C-reactive protein. Despite a marked activation of polymorphonuclear cells and a pronounced inflammatory response, as documented by an 8-fold and a 35-fold increase in plasma levels of polymorphonuclear elastase and C-reactive protein, respectively, the proportion of plasma free apo(a) to Lp(a) and urinary excretion of apo(a) remained unchanged over a 7-day period after surgery, and polymorphonuclear elastase activity remained undetectable in plasma. No fragmentation of apo(a) was observed ex vivo in plasma samples collected before and after surgery. These data indicate that in this model, apo(a) is not fragmented in plasma and are consistent with the hypothesis that apo(a) fragments result from a constitutively active tissue mechanism that is not modified by cardiac surgery with cardiopulmonary bypass.

Aged↗