Reconfiguring Cardiac Rehabilitation to Achieve Panvascular Prevention: New Care Models for a New World.

Atherosclerotic cardiovascular disease (ASCVD) and its associated economic burden are increasing globally. Although cardiac rehabilitation is a vital component of secondary prevention with proven benefits, it is underutilized due to numerous barriers, especially in resource-limited settings. New care models for delivery of comprehensive prevention programs such as community-based, home-based, and "hybrid" models implementing m-health, e-health, and telemedicine need to be adopted. Such new care models should be offered to all patients with established ASCVD (coronary, cerebral, and peripheral) and additionally to those at high risk of developing ASCVD with multiple risk factors for panvascular prevention.

Translating guidelines to practice: findings from a multidisciplinary preventive cardiology programme in the west of Ireland.

AIMS: The aim of this observational, descriptive study is to evaluate the impact of an intensive, evidence-based preventive cardiology programme on medical and lifestyle risk factors in patients at high risk of developing cardiovascular disease (CVD). METHODS: Increased CVD risk patients and their family members/partners were invited to attend a 16-week programme consisting of a professional multidisciplinary lifestyle intervention, with appropriate risk factor and therapeutic management in a community setting. Smoking, dietary habits, physical activity levels, waist circumference and body mass index, and medical risk factors were measured at initial assessment, at end of programme, and at 1-year follow up. RESULTS: Adherence to the programme was high, with 375 (87.2%) participants and 181 (84.6%) partners having completed the programme, with 1-year data being obtained from 235 (93.6%) patients and 107 (90.7%) partners. There were statistically significant improvements in both lifestyle (body mass index, waist circumference, physical activity, Mediterranean diet score, fish, fruit, and vegetable consumption, smoking cessation rates), psychosocial (anxiety and depression scales and quality of life indices), and medical risk factors (blood pressure, lipid and glycaemic targets) between baseline and end of programme, with these improvements being sustained at 1-year follow up. CONCLUSIONS: These findings demonstrate how a holistic model of CVD prevention can improve cardiovascular risk factors by achieving healthier lifestyles and optimal medical management.

Modification of the transcriptomic response to renal ischemia/reperfusion injury by lipoxin analog.

BACKGROUND: Lipoxins are lipoxygenase-derived eicosanoids with anti-inflammatory and proresolution bioactivities in vitro and in vivo. We have previously demonstrated that the stable synthetic LXA4 analog 15-epi-16-(FPhO)-LXA4-Me is renoprotective in murine renal ischemia/reperfusion injury, as gauged by lower serum creatinine, attenuated leukocyte infiltration, and reduced morphologic tubule injury. METHODS: We employed complementary oligonucleotide microarray and bioinformatic analyses to probe the transcriptomic events that underpin lipoxin renoprotection in this setting. RESULTS: Microarray-based analysis identified three broad categories of genes whose mRNA levels are altered in response to ischemia/reperfusion injury, including known genes previously implicated in the pathogenesis of ischemia/reperfusion injury [e.g., intercellular adhesion molecule-1 (ICAM-1), p21, KIM-1], known genes not previously associated with ischemia/reperfusion injury, and cDNAs representing yet uncharacterized genes. Characterization of expressed sequence tags (ESTs) displayed on microarrays represents a major challenge in studies of global gene expression. A bioinformatic annotation pipeline successfully annotated a large proportion of ESTs modulated during ischemia/reperfusion injury. The differential expression of a representative group of these ischemia/reperfusion injury-modulated genes was confirmed by real-time polymerase chain reaction. Prominent among the up-regulated genes were claudin-1, -3, and -7, and ADAM8. Interestingly, the former response was claudin-specific and was not observed with other claudins expressed by the kidney (e.g., claudin-8 and -6) or indeed with other components of the renal tight junctions (e.g., occludin and junctional adhesion molecule). Noteworthy among the down-regulated genes was a cluster of transport proteins (e.g., aquaporin-1) and the zinc metalloendopeptidase meprin-1 beta implicated in renal remodeling. CONCLUSION: Treatment with the lipoxin analog 15-epi-16-(FPhO)-LXA4-Me prior to injury modified the expression of many differentially expressed pathogenic mediators, including cytokines, growth factors, adhesion molecules, and proteases, suggesting a renoprotective action at the core of the pathophysiology of acute renal failure (ARF). Importantly, this lipoxin-modulated transcriptomic response included many genes expressed by renal parenchymal cells and was not merely a reflection of a reduced renal mRNA load resulting from attenuated leukocyte recruitment. The data presented herein suggest a framework for understanding drivers of kidney injury in ischemia/reperfusion and the molecular basis for renoprotection by lipoxins in this setting.