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Research team fall 2012 cardiovascular physiology
- 1. Introduction Heart and Stress Reactivity Hypothesis Key Studies
- 2. Introduction TODAY’S OUTLINE - Quiz - Reading ?’s Heart and Stress - Outline Stress and death, hypertension, inflammation Heart & Reactivity Hypothesis Stress Defined, mechanisms Key Studies Reactivity Monkeys, humans Hypothesis Take home message Heart disease, the leading cause of death in all Key Studies Western countries, is primarily the result of stress
- 3. Introduction Systems Organized By Stress Response - Quiz - Reading ?’s Central Nervous System - Outline Peripheral Nervous System Endocrine System Heart & (Autonomic, Somatic) Stress Cardiovascular System Digestive System Reactivity Lymphatic & Immune System Integumentary System Hypothesis Respiratory System Urinary System Musculoskeletal System Reproductive System Key Studies
- 4. Introduction STRESS AND DEATH 1900 2000 Heart & • Pneumonia & • Heart Disease Stress Influenza • Cancer - Stress & Death - Hypertension • Tuberculosis • Stroke - Inflammation • Gastroenteritis • Pulmonary Disease Reactivity • Heart Disease Hypothesis Infectious diseases Lifestyle and Stress Key Studies
- 5. Introduction Circulatory System Movement of blood to feed tissue and Heart & remove waste Stress • Closed system of arteries, veins, - Stress & Death capillaries (pressurized) - Hypertension • System moves through various - Inflammation organs for: oxygen, nutrition, Reactivity waste removal Hypothesis • How hormones get around The Heart • Pumps blood through the entire Key Studies system
- 6. Introduction Heart & Stress - Stress & Death - Hypertension - Inflammation Reactivity Hypothesis Key Studies
- 7. Introduction Tobacco Use (24%) Heart & Stress High Blood - Stress & Death Pressure (20%) Premature - Hypertension Stress Death - Inflammation Low Physical Reactivity Activity (10%) Hypothesis Obesity Key Studies (11%)
- 8. Introduction HYPERTENSION Heart & 115/75 and lower: Normotension Stress - Stress & Death 120/80 to 139/89: Pre-hypertension - Hypertension - Inflammation 140/90 and higher: Hypertension Reactivity Hypothesis Key Studies
- 9. Introduction HYPERTENSION Heart & Stress Blood Pressure Risk of Death from Heart Disease 120-129/80-84 101% more likely - Stress & Death - Hypertension 130-139/85-89 177% more likely - Inflammation 140-159/90-99 364% more likely >160/100 468% more likely Reactivity Hypothesis Key Studies
- 10. Introduction HYPERTENSION Heart & Stress - Stress & Death - Hypertension - Inflammation Reactivity Hypothesis Key Studies
- 11. Introduction HYPERTENSION Heart & Stress Of those with hypertension: - Stress & Death 50% take medications - Hypertension 33% of those taking medications have BP - Inflammation under control Reactivity Hypothesis Key Studies
- 12. Introduction HYPERTENSION Chronic stress leads to chronic elevations in blood pressure Heart & Stress - Stress & Death Chronic elevations in blood pressure lead to increased - Hypertension stress on blood vessels - Inflammation Blood vessels respond by increasing cell wall muscles Reactivity Hypothesis which decreases vessel diameter and makes vessel walls more rigid This vessel wall remodeling leads to permanent Key Studies hypertension
- 13. Introduction HYPERTENSION 90% of diagnosed cases of hypertension are Heart & ‘primary hypertension’ Stress Means that there is no physical disease - Stress & Death - Hypertension cause for the hypertension - Inflammation Reactivity 10% of diagnosed cases of hypertension are Hypothesis ‘secondary hypertension’ Secondary to a physical disease process such as kidney disease Key Studies
- 14. Introduction HYPERTENSION Heart & Stress - Stress & Death - Hypertension - Inflammation Reactivity Hypothesis Key Studies
- 15. Introduction INFLAMMATION Bifurcation Heart & Stress Hypertension contributes to cell wall damage - Stress & Death - Hypertension - Inflammation Inflammation response is body’s way to heal damage (cholesterol used in healing process) Reactivity Hypothesis CRP is a marker of inflammation CRP and cholesterol together best predict heart Key Studies disease
- 16. Introduction ISCHEMIA Cardiac ischemia: lack of oxygen to heart muscle Heart & Stress Results from blocked coronary vessels - Stress & Death - Hypertension - Inflammation Ambulatory studies: ischemia very common Reactivity Hypothesis Angina Key Studies
- 17. Introduction LEFT VENTRICULAR HYPERTROPHY Left ventricular hypertrophy is enlargement Heart & Stress (hypertrophy) of the muscle tissue that makes up the wall of your heart’s main pumping chamber (left - Stress & Death - Hypertension ventricle) - Inflammation Increased systemic pressure from constricted blood Reactivity Hypothesis vessels causes the heart to increase in muscle mass and decrease in flexibility (heart has to work harder to move blood because of increased pressure) Key Studies Left ventricle of heart has to move blood against higher pressure
- 18. Introduction LEFT VENTRICULAR HYPERTROPHY Heart & Stress - Stress & Death - Hypertension - Inflammation Reactivity Hypothesis Key Studies
- 19. Introduction SNS/PNS BALANCE Optimal health requires SNS and PNS to work Heart & Stress together in a balanced way - Stress & Death - Hypertension Chronic stress leads to increased SNS activation and - Inflammation decreased PNS activation Reactivity Hypothesis The role of the PNS in heart health is currently a hot topic (breathing techniques and meditation increase PNS function) Key Studies
- 20. Introduction REACTIVITY HYPOTHESIS Fight or Flight Psychological Stress Heart & Stress Reactivity Hypothesis - Defined - Mechanisms What happens during psychological stress – muscles do not need excess blood? Key Studies
- 21. Introduction REACTIVITY HYPOTHESIS Heart & Stress Reactivity Hypothesis - Defined - Mechanisms ? Key Studies
- 22. Introduction REACTIVITY HYPOTHESIS Larger, longer, and more frequent cardiovascular Heart & responses to stress will produce “wear-and- Stress tear” on the body leading to disease Reactivity Hypothesis - Defined - Mechanisms Key Studies
- 23. REACTIVITY HYPOTHESIS Introduction Cardiovascular Reactivity Heart & Stress Reactivity Hypothesis - Defined - Mechanisms Time of Stress Response Key Studies
- 24. REACTIVITY HYPOTHESIS Introduction Response Magnitude Heart & Larger responses hypothesized to produce Stress more damage Reactivity Hypothesis Response Duration - Defined Amount of time in a reactive state - Mechanisms 1. Stress Duration Key Studies 2. Recovery Duration
- 25. REACTIVITY HYPOTHESIS Introduction Shear Stress Heart & Rapid increase in velocity of blood flow at Stress bifurcations causes vascular injury and Reactivity plaque formation Hypothesis - Defined - Mechanisms Key Studies
- 26. REACTIVITY HYPOTHESIS Introduction An example of wear-and-tear Heart & Stress Reactivity Hypothesis • Injury to the • Inflammation • Fibrous cap - Defined arterial wall and immune forms over - Mechanisms lining response to more severe injury injuries that rupture into the • Swelling begins Key Studies lumen. to occlude the lumen.
- 27. REACTIVITY HYPOTHESIS Introduction Amount of Cardiovascular Reactivity: Heart & Frequency of stressors Stress Reactivity to stressors Reactivity Hypothesis Recovery from stressors - Defined - Mechanisms Key Studies
- 28. DISCUSS WITH NEIGHBOR Introduction How does cardiovascular reactivity affect physical health? Heart & Stress Reactivity Hypothesis - Defined - Mechanisms Key Studies
- 29. Cynomolgus Monkeys Introduction Develop atherosclerosis Heart & Highly social Stress Display complex patterns of social interaction reminiscent of humans Reactivity Hypothesis Form social status hierarchies composed of Key Studies dominants and subordinates - Monkeys - Humans Use aggression to establish/ maintain order
- 30. Video clip Introduction Macaque plaque Heart & Stress Reactivity Hypothesis Key Studies - Monkeys - Humans
- 31. Introduction Bowman Gray Model Bowman Gray Medical School First experimental investigations of stress, Heart & CVR, and disease Stress Paradigm 1 Reactivity Atherogenic diet Hypothesis Housed in small groups (4-5) Key Studies Randomly assigned to - Monkeys conditions - Humans
- 32. Introduction Bowman Gray Model Stable environment Same members live together for Heart & study duration Stress Single establishment episode Low Stress Reactivity Hypothesis Unstable environment Members transferred monthly Key Studies Need to re-establish hierarchy - Monkeys - Humans High stress
- 33. Introduction Bowman Gray Model Study 1 Do animals in the high stress condition develop Heart & more disease than animals in the low stress Stress condition? Results Reactivity Animals in the unstable condition had more Hypothesis disease at study end than those in the stable condition Key Studies - Monkeys - Humans
- 34. Introduction Bowman Gray Model Study 2 Do the previous results depend on a high-fat Heart & diet? Stress 4 conditions Regular diet/ stable grouping Reactivity Hypothesis Regular diet/ unstable grouping High-fat diet/ stable grouping Key Studies High-fat diet/ unstable grouping - Monkeys - Humans
- 35. Introduction Bowman Gray Model Study 2 Do the previous results depend on a high-fat diet? Heart & Results Stress Monkeys on the high-fat diet developed more disease than those on low-fat diet Reactivity Hypothesis Monkeys in the unstable condition developed more disease than monkeys in the stable condition Key Studies Monkeys in the high-fat / unstable condition - Monkeys developed the most disease - Humans
- 36. Introduction Bowman Gray Model Study 3 Does the SNS mediate the CVR-disease relationship? Heart & Procedure Stress Half were given an SNS blocker (beta-blocker) All monkeys were then treated as previously Reactivity Hypothesis Key Studies - Monkeys - Humans
- 37. Introduction Bowman Gray Model Study 3 Does the SNS mediate the CVR-disease relationship? Heart & Results Stress Animals given SNS-blocker: Displayed less CVR to threat Reactivity Hypothesis Developed less disease than those not on drug Key Studies Displayed less aggression than those not on drug - Monkeys - Humans
- 38. Reactivity Hypothesis Introduction Does stress lead to the development of disease? Yes, animals in the high stress condition developed more disease than low stress condition Heart & Stress Do the previous results depend on a high-fat diet? No, animals in high stress condition developed more Reactivity disease regardless of disease [however, high-fat diet Hypothesis increased disease risk] Key Studies Does higher CVR predict more disease? - Monkeys Yes, animals responding more strongly to threat - Humans developed more disease
- 39. Reactivity Hypothesis Introduction Does stress lead to the development of disease in humans? Yes, reactivity/recovery to lab stressors predicts Heart & Stress future hypertension Does the SNS mediate the CVR-disease relationship in humans? Reactivity Hypothesis Yes, increased SNS activity drives relationship Key Studies Does higher CVR predict more disease in humans? - Monkeys Yes - Humans
- 40. FOR NEXT TIME Introduction Next research team meeting we will look at cardiovascular assessment Heart and Stress For Next Time Read: Cardiovascular Psychophysiology Reactivity Hypothesis (Berntson, et al., 2007) Physiological Measures (Diamond) Key Studies