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Coronary heart disease is a common and serious condition in patients aged over 80 years. The presenting clinical symptoms are all the more atypical and the prognosis poorer when it occurs in patients with multiple comorbid diseases. The presence of comorbidities dictates the need for a standardized geriatric assessment to screen for the existence of underlying frailty. The available scientific data were obtained during studies that included few subjects aged over 80 years. These recommendations are therefore mainly extrapolated from results obtained in younger populations. The pharmacological management and revascularization strategy for coronary heart disease in octogenarians is basically the same as in younger subjects. Epidemiological studies all concur that available therapies are underutilized despite the fact that this population has a high cardiovascular risk. Specific precautions for use must be respected because of the comorbidities and age-related changes in pharmacokinetics or pharmacodynamics. Generally, the therapeutic strategy in coronary heart disease is based not on the patient's real age, but rather on an individual analysis taking into account the severity of the coronary disease, comorbidities, the risk of drug misadventures, patient life expectancy and quality of life.

We evaluated the prevalence, risk factors and impact on all-cause mortality of the metabolic syndrome (MetS) and its components in a large French population. The study population consisted of subjects aged 40 years or more who volunteered for a free health check-up at the IPC Center (Investigations Préventives et Cliniques, Paris) between 1999 and 2002. There were 40 977 men (53.2 +/- 9.1 years) and 21 277 women (55.9 +/- 10.3 years). The cutoff date for mortality data was March 2004. The mean follow-up period was 3.57 +/- 1.12 years. During this period, 271 men and 87 women died. MetS was defined according to NCEP-ATP III criteria. Cox regression models were used to evaluate the risk of death [hazards ratio (95% CI)]. MetS was present at baseline in 11.8% of men and 7.6% of women. The prevalence of MetS increased from 9% in men aged 40 to 49 years to 12.5% in men aged 70 years. In women, the prevalence rose from 4.9% to 11.3%, respectively. From 1999 to 2002, the prevalence of MetS increased from 11.0% to 12.8% in men and from 7.2% to 8.8% in women. The following clinical and biological parameters were significantly associated with MetS in men and women, after adjustment for age: lower physical activity, lower vital capacity ratio, higher pulse pressure and heart rate, higher gamma-glutamyl transpeptidase, ASA and ALA transaminase and alkaline phosphatase levels, higher uricemia, leukocyte and globulin levels, dental and gingival inflammation, and higher stress and depression scores. After adjustment for age, the excess risk of all-cause mortality in subjects with MetS compared to subjects without MetS was 1.82 (1.35-2.43) in men and 1.80 (1.01-3.19) in women. After adjustment for age, gender, smoking, cholesterol, physical activity, socioeconomic status and prior cardiovascular disease, the risk of all-cause mortality was 1.69 (1.28-2.22) in the entire population. In order to evaluate the impact of each Mets component, and combinations of three MetS components, on all-cause mortality, a control group of subjects with no MetS components was used. After adjustment for age and gender, the risk of death associated with each MetS component was 2.36 (1.65-3.37) for high waist circumference, 2.08 (1.44-3.01) for elevated triglyceride levels, 1.71 (1.07-2.72) for low HDL-cholesterol levels, 1.75 (1.29-2.38) for elevated arterial pressure, and 2.93 (2.04-4.22) for elevated glucose levels. Waist circumference + elevated triglycerides + elevated glucose was the three-component combination with the strongest impact [HR = 4.95 (2.92-8.37)]. In this large French population, in which MetS was moderate, MetS was associated with other hemodynamic, hepatic, inflammatory and psychological risk factors, and with a 70% increase in all-cause mortality. The three-component combination most strongly associated with mortality was high waist circumference + elevated glucose + elevated triglycerides.

Background: The results of experimental studies have suggested that matrix metalloproteinases (MMPs) and their inhibitors, the tissue inhibitors of metalloproteinases (TIMPs), are involved in vascular remodeling. In a population-based study, we report the relationships of serum TIMP-1 with carotid intima-media thickness, carotid plaques and aortic arterial stiffness., Methods: Free health examinations were performed on 238 men free of coronary heart diseases (aged 56.5 +/- 10.4 years, 57.1% were hypertensive). Carotid-femoral pulse-wave velocity (PWV) was used to assess aortic stiffness. Carotid ultrasound examination included measurements (at sites free of plaques) of intima-media thickness (IMT) at the common carotid arteries (CCA) and assessment of atherosclerotic plaques in the extracranial carotid arteries., Results: The percentage of subjects with plaques was lower in subjects with low TIMP-1 values (P for trend = 0.0001). In multivariate analysis adjusted for age, body mass index, smoking habits, total cholesterol, triglycerides, C-reactive protein, heart rate, diabetes and systolic blood pressure, the odds ratio of carotid plaques in subjects with high values of TIMP-1 (tertile 3) compared to those with low values (tertile 1) was 2.89 (95% confidence interval 1.12-7.47, P < 0.01). TIMP-1 was positively associated with CCA-IMT and PWV in univariate analysis. However, the associations disappeared once age and systolic blood pressure were taken into account in the multivariate analysis., Conclusion: This study shows that there is a differential association of TIMP-1 with PWV, CCA-IMT and carotid plaques. Our results suggest that TIMP-1 might be involved in plaque formation.

Purpose: In rats, chronic aldosterone administration with high diet intake increases aortic stiffness independent of mechanical stress. In hypertensive humans, enhanced plasma aldosterone and arterial stiffness are positively associated. Whether the aldosterone synthase gene polymorphism (ASGP) CYP11B2 influences the age-related changes in blood pressure (BP) and arterial stiffness in hypertensive subjects has never been investigated., Methods: In 425 untreated hypertensive men and women, ASGP was evaluated together with aortic pulse wave velocity (PWV). In 191 of these subjects, cardiac haemodynamics were measured using echo-Doppler techniques., Results: In the overall population, independently of sex, the TC and CC genotypes of ASPG had significantly higher heart rate (HR) (P < 0.05) and lower stroke index (P < 0.01) than the TT genotype, but did not affect BP. In men, the adjusted slopes of the curves relating age to PWV and HR were significantly steeper (P = 0.04; P = 0.002) for the TC and CC than for the TT genotype. Such gene-related differences were not observed for the age-systolic BP relationship., Conclusion: In hypertensive subjects, the TC and CC genotypes of ASGP involve, by comparison with the TT genotype, significantly higher HR and reduced stroke index. In men with the C allele, the reduced stroke index (cardiac effect) compensates for the steep increase of PWV with age (arterial effect), thus modulating the cardiovascular phenotype and explaining the lack of increased incidence of systolic hypertension. The results are consistent with a local role of endogenous aldosterone on both heart and vessels.