Two years after the publication of the 2013 guidelines for the management of arterial hypertension of the European Society of Hypertension (ESH) and the European Society of Cardiology (ESC),1 the ESH and the European Union Geriatric Medicine Society have created a common working group to examine the management of hypertensive subjects aged >80 years. The general term hypertension in the elderly is not sufficiently accurate because it mixes younger old patients (60–70 years) with the oldest old. Our group believes that the management of hypertension in individuals aged ≥80 years should be specifically addressed. Although arbitrary, this cutoff value identifies a population that is expanding faster than any other age group with a 50% increase of life expectancy during the past 50 years2,3; furthermore, the incidence and prevalence of comorbidities, frailty, and loss of autonomy greatly increases after the age of 80 years4; finally, although there is limited evidence on the management of hypertension in this age group, the latest clinical studies indicate that in these patients, treatment may not be the same as in patients in the lower age strata. The aim of this Working Group was to discuss more in-depth treatment aspects of hypertensive patients aged ≥80 years or older, with special focus on the difficulties and uncertainties posed by very old frail individuals. We focused, in particular, on the following points of the 2013 ESH/ESC guidelines: Benefits of treatment. Blood pressure (BP) thresholds and targets. The choice of treatment

There is an increasing proportion of the general population surviving to old age with significant chronic disease, multi-morbidity, and disability. The prevalence of pre-frail state and frailty syndrome increases exponentially with advancing age and is associated with greater morbidity, disability, hospitalization, institutionalization, mortality, and health care resource use. Frailty represents a global problem, making early identification, evaluation, and treatment to prevent the cascade of events leading from functional decline to disability and death, one of the challenges of geriatric and general medicine. Cardiac arrhythmias are common in advancing age, chronic illness, and frailty and include a broad spectrum of rhythm and conduction abnormalities. However, no systematic studies or recommendations on the management of arrhythmias are available specifically for the elderly and frail population, and the uptake of many effective antiarrhythmic therapies in these patients remains the slowest. This European Heart Rhythm Association (EHRA) consensus document focuses on the biology of frailty, common comorbidities, and methods of assessing frailty, in respect to a specific issue of arrhythmias and conduction disease, provide evidence base advice on the management of arrhythmias in patients with frailty syndrome, and identifies knowledge gaps and directions for future research.

OBJECTIVE—The aim was to evaluate the impact of specific component combinations of the metabolic syndrome on all-cause mortality risk in a large French cohort. RESEARCH DESIGN AND METHODS—The population was composed of 39,998 men (aged 52.6 ± 8.3 years) and 20,756 women (aged 54.7 ± 9.2 years) who were examined at the Investigations Préventives et Cliniques Center from 1999 to 2002. Mean follow-up was 3.57 ± 1.12 years. Metabolic syndrome was defined according to three definitions: the National Cholesterol Educational Program (NCEP 2001), the revised NCEP (NCEP-R; American Heart Association/National Heart, Lung, and Blood Institute 2005), and the International Diabetes Federation (IDF 2005). Subjects with metabolic syndrome were compared with subjects without metabolic syndrome and with subjects with no metabolic syndrome components using Cox regression models. RESULTS—The prevalence of metabolic syndrome increased from 10.3% (NCEP) to 17.7% (NCEP-R) and 23.4% (IDF). After adjustment for age, sex, classical risk factors, and socioprofessional categories, and compared with subjects without metabolic syndrome, the risk of all-cause mortality was 1.79 (95% CI 1.35–2.38), 1.46 (1.14–1.88), and 1.32 (1.04–1.67) with the NCEP, NCEP-R, and IDF definitions, respectively. Among the combinations significantly associated with all-cause mortality, the following three-component combinations and the four-component combination were more highly significant than other combinations (P < 0.05): elevated waist circumference plus elevated glucose, plus either elevated blood pressure or elevated triglycerides, and the combination of all four of these. CONCLUSIONS—In a large middle-aged French population, four specific components of metabolic syndrome are associated with a much higher mortality risk. These results may have a significant impact on detecting high-risk subjects suffering from metabolic disorders and underline the fact that metabolic syndrome is a nonhomogeneous syndrome.

Angiotensin-converting enzyme inhibitors improve arterial stiffness independently of blood pressure reduction. Since we have recently shown that in hypertensive individuals the A ¹¹⁶⁶ C polymorphism of the angiotensin II type 1 receptor (AT ₁ -R) is an independent determinant of aortic stiffness, we designed the present study to assess the influence of this polymorphism on the changes of aortic stiffness after chronic treatment with the angiotensin-converting enzyme inhibitor perindopril and the calcium channel blocker nitrendipine. Forty perindopril- and 42 nitrendipine-treated hypertensive individuals were studied. We evaluated aortic stiffness by measuring the carotid-femoral pulse wave velocity. Carriers of the AT ₁ -R C allele showed higher baseline values of pulse wave velocity than AA homozygotes ( P <.05). In the perindopril group, a threefold greater reduction in pulse wave velocity was observed in carriers of the C allele than in AA homozygotes (−2.85±0.62 versus −0.94±0.32 m/s, respectively; P <.001), whereas in the nitrendipine group, pulse wave velocity decreased only in AA homozygotes and not in AT ₁ -R C carriers (−1.38±0.35 versus +0.04±0.60 m/s, respectively; P <.01). These results indicate that according to the AT ₁ -R A ¹¹⁶⁶ C genotype, an angiotensin-converting enzyme inhibitor and a calcium channel blocker affect pulse wave velocity in opposite ways. Since some evidence shows that increased pulse wave velocity may enhance cardiovascular risk, it might be useful for physicians to consider the AT ₁ -R genotype when prescribing an angiotensin-converting enzyme inhibitor or calcium channel blocker to a hypertensive individual.