ROLE OF INFLAMMATION IN HYPERTENSION. Dr Barasa FA Physician Cardiologist Eldoret
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1 ROLE OF INFLAMMATION IN HYPERTENSION Dr Barasa FA Physician Cardiologist Eldoret
2 Outline Inflammation in CVDs the evidence Basic Science in Cardiovascular inflammation: The Main players Inflammation as a driver of HTN Novel concepts and clinical applications of anti inflammatory drugs in HTN
3 NONE DISCLOSURES
4
5 Inflammation and CVD the evidence
6 JUPITER: Conclusions Primary Endpoint Among apparently healthy men and women with elevated hscrp but low LDL C, rosuvastatin reduced major cardiovascular events by 44%: Primary points myocardial infarction, stroke, arterial revascularization, hospitalization for unstable angina, or death from cardiovascular causes Benefits of rosuvastatin were consistent regardless of age, sex, region or ethnicity. Rates of hospitalization and revascularization were reduced by 47 percent within a two year period suggesting that the screening and treatment strategy tested in JUPITER is likely to be cost effective, benefiting both patients and payers.
7 Inflammation and CVD the evidence
8 HOPE 3 Strategy Hypothesis: Statins beneficial in intermediate risk individuals without CVD (elevated waist to hip ratio, history of a low level of HDL, current or recent tobacco use, dysglycemia, family history of premature CAD, mild renal dysfunction). Primary outcomes: composite of death from cardiovascular causes, nonfatal MI or nonfatal stroke. Pragmatic strategy: No Lipid or BP entry criteria or targets No Dose titration Infrequent safety monitoring Interventions: Fixed dose combination of Candesartan 16 mg + HCTZ 12.5 mg/day or Placebo; Rosuvastatin 10mg or placebo. 37
9 Hope3: Findings and Implications BP reduced 6.0/3.0 mmhg, but did not reduce significantly CV events 25% RRR in primary endpoints from statin use Consistent benefits regardless of: LDL C SBP Risk profile CRP Ethnicity Strategy used in HOPE 3 is simple, safe and effective and widely applicable 19
10 C reactive protein concentration and risk of cardiovascular events : 2010 Direct comparison of hscrp, systolic blood pressure, total cholesterol, and non HDLC Risk Ratio (95%CI) hscrp Systolic BP Total cholesterol Non HDLC 1.37 ( ) 1.35 ( ) 1.16 ( ) 1.28 ( ) Risk Ratio (95%CI) per 1 SD higher usual values Adjusted for age, gender, smoking, diabetes, BMI, BP, triglycerides, alcohol, lipid levels, and hscrp Emerging Risk Factor Collaborators, Lancet Jan 2010
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12 Cardiovascular inflammation: The basics Inflammation canopy has the leukocytes, the cytokines, chemokines, granulocytes and a quasiimmune cell type, the platelets. Role of platelet (beyond thrombosis) in regulating immune mechanisms is always underrated. Inflammation is a key component in the development of both atherosclerotic and non atherosclerotic CVDs. In atherosclerotic CVD, plaque stability is only a function of these players.
13 Causes of Inflammation: Initial Triggers?cigarette smoking,?processed food stuffs (junk)?inflammatory diseases eg RA, SLE, COPD.?Alcohol abuse?depression?type II Diabetes
14
15 Major players Angiotensin II : responsible for triggering vascular inflammation by inducing oxidative stress. Resulting in up regulation of pro inflammatory transcription factors such as NF κb (nuclear factor κb). These, in turn, regulate the generation of inflammatory mediators (adhesion molecule :VCAM 1 and ICAM 1 and cytokine expression in several cell types that lead to endothelial dysfunction and vascular injury. Ang II also stimulates the production of PAI 1 (plasminogen activator inhibitor 1) which contributes to the prothrombotic state as well as to atherosclerotic plaque rupture.
16 Cytokines Implicated in Hypertension Tumor necrosis factor Interleukin 17 Interferon Interleukin 6 Tissue growth factor Interleukin 10
17
18 C reactive protein: marker (or mediator?) of inflammation in hypertension In atherosclerotic plaques, appears to be involved in foam cell formation, promotes monocyte chemotaxis facilitation of LDL uptake by macrophages In endothelial cells, CRP facilitates the release of PAI 1 and ET 1, leading to increased the expression of cell adhesion molecules reduced NO bioavailability. In VSMCs, CRP induces the expression of AT1 receptors and AT1 receptor mediated ROS formation, which reduce NO bioavailability
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20 The Role of activated Platelet Major adhesion molecules expressed by platelets and play crucial role: P selectin: A membrane glycoprotein required for the adhesion of platelets to endothelium. Integrins ( αvβ3, α2β1, α5β1, αiibβ3 or GPIIb/IIIa. GPIIb/IIIa )Transmembrane receptors, important for cell to cell and cell to extracellular matrix [ECM] interactions. Chemokine receptors: CCR1, CCR3, CCR4, CXCR2, CXCR4, CXCR6 and CXCR7). These are G protein linked receptors that induce signal transduction by interacting with several cytokines and chemokines Intracellular Adhesion molecule 2 (ICAM2 or CD102): MIF (macrophage migration inhibitory factors): involved in monocyte recruitment and arrest.
21 Anti Inflammatory Drugs and Hypertension Not Routinely used: marginal Bp reduction coupled with significant systemic immunosuppresion. Mycophenolate mofetil (Blocks T/B cell proliferation beneficial in patients with Psoriasis/ RA. Tacrolimus (calcineurium inhibitor ) Vaccines (CYT006 Ang GB) targetting Ang II STATINS Low dose ASA
22 Conclusion Inflammation is emerging as both a cause and an effect of hypertension. Angiotensin II induced oxidative stress, endothelial dysfunction and Platelets are the key players associated with inflammation in hypertension. Statins are potent Anti inflammatory drugs that have shown significant CVD benefits beyond lipid lowering.
23 A cardiothoracic Surgeon s perspective Dr Dwight Lundell Popular Quote from his books I have peered inside thousands upon thousands of arteries. A diseased artery looks as if someone took a stiff brush and scrubbed repeatedly against its wall. Several times a day, every day, the foods we eat create small injuries compounding into more injuries, causing the body to respond continuously and appropriately with inflammation
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