Expansions of cytotoxic CD4+CD28− T-cells drive excess cardiovascular mortality in rheumatoid arthritis and other chronic inflammatory conditions and are triggered by CMV infection

A large proportion of cardiovascular pathology results from immune-mediated damage, including systemic inflammation and cellular proliferation, which cause a narrowing of the blood vessels. Expansions of cytotoxic CD4+ T-cells characterized by loss of CD28 (‘CD4+CD28− T-cells’ or ‘CD4+CD28null cells’) are closely associated with cardiovascular disease (CVD), in particular coronary artery damage. Direct involvement of these cells in damaging the vasculature has been demonstrated repeatedly. Moreover, CD4+CD28− T-cells are significantly increased in rheumatoid arthritis (RA) and other autoimmune conditions. It is striking that expansions of this subset beyond 1-2% occur exclusively in CMV-infected people. CMV infection itself is known to increase the severity of autoimmune diseases, in particular RA and has also been linked to increased vascular pathology. A review of the recent literature on immunological changes in cardiovascular disease, RA, and CMV infection provides strong evidence that expansions of cytotoxic CD4+CD28− T-cells in RA and other chronic inflammatory conditions are limited to CMV-infected patients and driven by CMV-infection. They are likely to be responsible for the excess cardiovascular mortality observed in these situations. The CD4+CD28− phenotype convincingly links CMV infection to cardiovascular mortality based on a direct cellular-pathological mechanism rather than epidemiological association

Effects of chronic congestive heart failure on 24-hour blood pressure and heart rate patterns: a hemodynamic approach.

For 29 patients with congestive heart failure (CHF), 24-hour noninvasive ambulatory blood pressure (ABP) and heart rate (HR) measurement profiles were described, using the periodogram method, and were compared with the same findings in 22 matched controls. Right-sided heart catheterization was performed in all patients. The mean cardiac index was 2.2 L/min/m2 (range 1.3 to 2.9 L/min/m2). More severe CHF, as assessed by cardiac index, pulmonary artery wedge pressure, and right atrial pressure, correlated significantly with a reduction in the amplitude of the circadian ABP and HR rhythms (0.38 less than r less than 0.63; p less than 0.05). Moreover, a reduced increase in cardiac index during cycloergometric exercise in 11 CHF patients correlated with a blunting of the circadian systolic ABP and HR profiles (0.57 less than r less than 0.90; p less than 0.05). Our results indicate that there is a reduction in the amplitude of the circadian BP and HR rhythms related to the severity of CHF.Comparative StudyJournal Articleinfo:eu-repo/semantics/publishe

Analysis of climate change, high-flows and low-flows scenarios on the Meuse basin: WP1 report - Action 3

AMICE: Adaptation of the Meuse to the Impact of Climate Evolutio