A_10%20_CVD%20part%201 - Cardiovascular Disease(CVD Outline...

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Unformatted text preview: Cardiovascular Disease (CVD) Outline 550 Epidemiology & Significance Deaths in Thousands 500 450 Hyperlipidemia/Atherosclerosis Hyperlipidemia/Atherosclerosis Other CVD issues Peripheral Artery Disease (PAD) Ischemic Heart Disease (IHD) ex. Myocardial Infarction Heart Failure (HF) ex. Congestive Heart Failure Coronary Artery Bypass Graft Pe r 1 00 ,0 0 0 P o pulation CVD Risk Factors Hypertension 400 350 79 80 85 90 Years Males Females 95 00 06 200 150 101.5 130.0 100 57.0 50 0 Coronary Heart Disease 41.1 41.1 39.0 22.9 31.6 Stroke Lung Cancer Breast Cancer White Females Black Females Metabolic Syndrome American Heart Association 2010 statistics AgeAge-adjusted death rates for CHD, stroke, lung and breast for white and black females (United States: 2006). Source: NCHS. CVD Risk Factors Age & Sex M 45 yr F 55 yr or premature menopause Family history of premature CHD Potentially Modifiable Factors Hypertension (>140/90 mm Hg) Hypertension (>140/90 mm Hg) Hyperlipidemia ( LDL cholesterol) Low HDL cholesterol (< 40mg/dl) (< Cigarette smoking Diabetes Life habit risk factors: overwt/obesity, inactivity, atherogenic diet Emerging risk factors: Lp(a), Hcys, CRP, IGT, TG LMCA – LEFT MAIN CORONARY ARTERY CIRC – CIRCUMFLEX CORONARY ARTERY LAD – LEFT ANTERIOR DESCENDING CORONARY ARTERY LMCA LAD CIRC 1 Table 13-6, p. 300 Hypertension, Obesity, and Inflammation: The Complex Designs of a Deadly Trio A. Rizvi, Metabolic Syndrome and Related Disorders 8:287-294, 2010 Hypertension Hypertension – Outline Hypertension Physiologic factors Medications Dietary management 2 Hypertension (HTN) Normal Blood Pressure: PrePre-Hypertension: 120/80 mm Hg 120-139 systolic / 80-89 diastolic mm Hg 12080- High Blood Pressure defined as: stage I Mild HTN arterial BP stage II Moderate stage III Severe 140 systolic/90 diastolic mm Hg 160/100 180/110 Untreated HTN is a risk factor for: Heart disease, Stroke, Renal disease Box 13-1, p. 289 Mean Arterial Blood Pressure • Cardiac Output – Heart rate & stroke volume – Sympathetic & Parasymp. Activity – Venous return – Blood Volume • Water & Na balance • Total Peripepheral Resistance – Arteriolar radius • Local metabolic control • Extrinsic vasoconstrictor control – Blood viscosity **Vasopressin, ReninAngiotensin, Aldosterone AntiAnti-Hypertensive Medications Table 13-1a, p. 291 3 Lifestyle Modifications Decrease weight if overweight Smoking cessation if smoker Limit alcohol Dec Decrease Sodium intake to 100 mmol/d ( 2.3 g/d Sodi intake to mmol/d g/d or or 6 g NaCl/d) Maintain adequate intake other minerals Potassium Calcium Magnesium 90-120 mmol/d 9020-30 mmol/d 2011.5-14.4 mmol/d 11.5(3.5-4.6 g/d) (3.5(0.8-1.2g/d) (0.8(0.28-0.35g/d) (0.28- Aerobic exercise Table 13-1b, p. 291 Table 13-4, p. 293 Table 13-2, p. 292 Dietary Approaches to Stop Hypertension Control American Diet Fruit/Vegetable Diet (37% total fat, 3.6 serv F/V, 2.5 serv meat, 0.4 serv dairy) (37% total fat, 8.5 serv F/V, 2.5 serv meat, 0.3 serv dairy, 0.6 serv nuts) 0.6 serv nuts) (27% total fat, 9.6 serv F/V, 1.6 serv meat, 2 serv low fat dairy, 0.7 serv nuts) DASH Diet DASH Diet Outcomes: Change in Blood Pressure: 5.5 mm HG systolic, 3.0 mm Hg diastolic on the Dash diet, intermediate results on F/V diet Box 13-4, p. 296 4 Dietary Approaches to Stop Hypertension Control American Diet DASH Diet (37% total fat, 3.6 serv F/V, 2.5 serv meat, 0.4 serv dairy) (27% total fat, 9.6 serv F/V, 1.6 serv meat, 2 serv low fat dairy, serv meat serv low fat dairy 0.7 serv nuts) DASH Sodium Diet Sodium Restricted Diets Typical levels of Na intake Ave. American intake No Added Salt MildMild-Moderate Restrict. Strict Severe 6-8 g/d 4g 2 -3 g 1g 0.5 g Three Na levels for each diet were compared: 3.3 g/d, 2.4 g/d, 1.5 g/d Outcomes: BP was seen with lower Na intake for both diets. BP effect was greater on DASH diet Biggest contributors: processed foods, snack items and table salt processed General recommendations: No salt at table, minimal salt in No cooking, avoid highly processed foods -- use more fresh foods & foods cooked at home from scratch, alternative seasonings (lemon, herbs, wine, KCl salt substitute if warranted) Pathogenesis of Atherothrombotic Disease Atherosclerosis & Hyperlipidemia Diabetes Risk Factors Hypertension Smoking Dyslipidemia Estrogen Withdrawal Homocysteine Atherosclerosis Physiological processes Oxidative Stress Endothelial Dysfunction [NO] Hyperlipidemia LDLLDL-Receptor Medications Dietary management Local mediators: Endothelin, AngII, TXA2, Superoxide anion, Catecholamines Smooth muscle cell proliferation Vasoconstriction t - PA PAI - 1 Platelet adhesion & aggregation Thrombosis Adhesion molecules Cytokines Growth factors Inflammation Vascular Lesion Progression Plaque Rupture Thrombosis and Vasospasm Coronary Events Figure 1. Initiation and progression of atherosclerotic lesions. LDL enters the subendothelial space and is oxidized. Oxidized LDL (OxLDL) promotes monocyte adhesion to injured or inflamed epithelium and migration into the artery wall, where monocytes differentiate into macrophages. OxLDL also binds to scavenger receptors (SRs) on macrophages. This binding triggers uptake of OxLDL, converting macrophages into lipid-laden foam cells. Subsequently, smooth muscle cells migrate into the subendothelial space, where they accumulate and produce extracellular matrix, two important components of more advanced atherosclerotic lesions. J Exptl Med 2006;203:813-816. 5 Advanced lesion 6 ...
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This note was uploaded on 11/21/2010 for the course NUT 116A 72876 taught by Professor Steinberg/stern during the Fall '10 term at UC Davis.

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