Cardiovascular Pathology and Exercise (SPE3ESP) PDF

latrobe.edu.au SPE3ESP Cardiovascular pathology and exercise La Trobe University CRICOS Provider Code Number 00115M 1...

latrobe.edu.au SPE3ESP Cardiovascular pathology and exercise La Trobe University CRICOS Provider Code Number 00115M 1 latrobe.edu.au Lecture outcomes By the end of this lecture, you should be able to:  Discuss the stages of atherogenesis in relation to cardiovascular function and disease  Describe key features of common cardiovascular pathologies  Interpret global and national prevalence of cardiovascular disease and related mortality  Explain the modifiable and non-modifiable cardiovascular disease risk factors  Analyse the mechanisms of aerobic and resistance exercise related to cardiovascular function, structure, disease and outcomes  Understand the indications, assessment and exercise prescription for cardiac rehabilitation  Explain the relationship between exercise and blood pressure  Justify the rationale for exercise prescription and referral for hypertension 2  latrobe.edu.au Cardiovascular disease La Trobe University CRICOS Provider Code Number 00115M 3 latrobe.edu.au Coronary (ischaemic) heart disease (CHD/IHD) Cerebrovascular Cardiomyopathy disease Cardiovascular disease Cardiovascular  Cardiovascular disease (CVD) is an umbrella term for Congenital disease Hypertension the group of disorders of the heart and blood vessels heart disease (CVD)  Leading cause of morbidity and mortality worldwide  World Health Organisation Global Action Plan is Peripheral focused on 4 main health-related behaviours: Rheumatic vascular heart disease disease Tobacco use, physical activity, diet and alcohol (PAD) Heart failure 4  latrobe.edu.au Global prevalence  Estimated 422 million cases worldwide  Highest prevalence observed in low and middle income countries (LMIC) 5 latrobe.edu.au Global mortality  Accounts for ~1/3 all deaths globally (70-80% LMIC)  40-80% decline in mortality in high income countries – From 2015 data, trends have plateaued 6  Prevalence (CVD type) Ischemic heart disease (IHD):  High prevalence, increases with age  Leading cause of all health loss globally Peripheral artery disease (PAD):  Largest proportion of CVD cases  Lowest burden Roth et al., 2017 7 latrobe.edu.au Mortality (CVD type) IHD:  Leading cause of death in the world  Death rate ↑ from 40 years Stroke:  Highest prevalence and mortality rate in Oceania Roth et al., 2017 8  latrobe.edu.au In Australia… 1n 2017-18… ~5.6% (1.2 million) Australian adults report 1 or more conditions related to heart or vascular disease  Prevalence of CVD is higher among: – Men (6.5%, compared to women 4.8%) – Increased age (26% of people ≥75 years have CVD) – Socioeconomically disadvantaged – Indigenous Australians 9 latrobe.edu.au CVD mortality rates In Australia:  1.4 x higher for males, compared to females  1.7 x higher among Indigenous Australians, compared with non-Indigenous Australians  ↑ with age  ↑ with remoteness and socioeconomic disadvantage  CVD deaths by type: – 42% ischaemic heart disease – 20% stroke 10  latrobe.edu.au Burden of disease In Australia:  IHD = leading cause of burden in adults  Total burden has decreased over time  In 2015–16, ~9% of total expenditure in the Australian health system was attributed to CVD (~$10.4 billion) 11 latrobe.edu.au Pathophysiology: Atherosclerosis  An artery is made up of 3 layers: – Intima: closest to the lumen, comprised of endothelium – Media: middle layer, consists of smooth muscle cells – Adventitia: vessel wall layer, made up of connective tissue, nerves. Atherosclerosis: a disease of the arteries characterised by the deposition of plaque on the inner walls  Plaque: fatty deposits, compromised of cholesterol, fatty substances, cellular waste products, calcium and fibrin (clotting material). 12  latrobe.edu.au Endothelial dysfunction Endothelium maintains vascular tone and permeability through vasodilation.  Releases nitric oxide (NO) = major vasodilating substance.  Laminar shear stress ↑ production of NO Endothelial dysfunction is characterised by ↓ vasodilation and ↑ inflammation.  When NO production is impaired, this can result in – Vasoconstriction (e.g. hypertension) – Inflammation  Changes in endothelial function occur prior to the development of atherosclerotic plaques 13 latrobe.edu.au Vascular modifications Stage Characteristics 1. Plaque formation Endothelial dysfunction Fatty streak formation Foam cell formation 2. Plaque progression Fibrous cap atheroma 3. Plaque disruption Rupture, leading to clinical complication Atherosclerotic plaques may be:  Stable: remain static, grow slowly  Unstable: vulnerable to spontaneous rupture 14  latrobe.edu.au Mechanisms of plaque rupture  Plaque rupture occurs where the fibrous cap is thinnest  Rupture of may occur spontaneously, or be triggered by an increase in emotional or physical stress – High blood pressure – ↑ heart rate (a) normal artery (b) partially blocked artery (c) significantly blocked artery 15 latrobe.edu.au Ischaemic heart disease  IHD = coronary artery/coronary heart disease  Ischaemia: inadequate circulation to an area due to occlusion of the blood vessels There are 2 forms of IHD:  Angina: temporary chest pain or a sensation of pressure that occurs during ischaemia – Angina pectoris (stable): Chest pain/discomfort provoked by similar amounts of activity or stress – Unstable angina: Changing pattern of symptoms  Myocardial infarction (MI): myocardial cell death due to prolonged ischaemia 16  latrobe.edu.au Stroke Stroke: brain tissue damage/death due to loss of blood supply (cerebral infarction)  Ischaemic stroke (~80%) – Blockage of artery to the brain  Haemorrhagic stroke (~20%) – Rupture of blood vessel in or around the brain. 17 Peripheral artery disease (PAD)  Abnormal narrowing of arteries other than those that supply the heart/brain  Claudication: reproducible discomfort/fatigue in the muscles that occurs with exertion and is relieved within 10 minutes of rest  Severity based on presence of signs and symptoms Stage Symptoms 1 Asymptomatic 2 Intermittent claudication (2a) Distance to pain onset > 200m (2b) Distance to pain onset < 200m 3 Pain at rest 4 Gangrene, necrosis, tissue loss 18  latrobe.edu.au Risk factors Non-modifiable Modifiable Age Metabolic Sex Behavioural Family history Environmental Ethnicity Psychosocial and socioeconomic Strength Over 70% of CVD worldwide is caused by modifiable risk factors 19 latrobe.edu.au Modifiable risk factors Metabolic Metabolic: Blood pressure, diabetes, non-HDL cholesterol, abdominal obesity Behavioural: Smoking, physical activity, diet, alcohol use Strength: Grip strength Behavioural Strength Environmental: Air pollution Psychosocial and socioeconomic: Mental ill health, education, access to health Psychosocial Environmental and care socioeconomic 20  latrobe.edu.au Blood pressure and blood lipids Blood pressure (BP)  Hypertension: ≥140/90 mmHg  24% of men and 21% of women worldwide  Strongest association with CVD  BP reduction reduces CVD risk in those with established hypertension Cholesterol  Non-high-density lipoprotein (HDL) cholesterol = Total cholesterol – HDL cholesterol  High non-HDL cholesterol associated with ↑ CVD events  Reducing low-density lipoprotein (LDL) ↓ risk of CVD 21 latrobe.edu.au Obesity/abdominal obesity  BMI 25 is a risk factor for CVD  Can be heterogeneity in the CVD risk profile in overweight individuals (location of adiposity matters!)  Accumulation of visceral fat associated with ↑ cardiometabolic risk – Indicated by waist-to-hip ratio and/or waist circumference  BMI and waist-hip ratio are highest in high income countries 22  Smoking, alcohol use Smoking  Tobacco use is strongly associated with CVD  30% of CVD mortality is attributable to smoking  No safe lower limit Joseph et al., 2017. Alcohol  Heavy alcohol intake is associated with CVD  ↓ in alcohol intake associated with ↓ in CVD risk  Beverage choice and drinking patterns Klatsky, 2015. 23 Diet Food sources  ↓ CVD risk – ↑ fruit and vegetable consumption – Fish consumption  ↑ CVD risk – Industrially produced trans fat – Refined CHO – Processed meats – Sugar-sweetened beverages associated with weight gain, obesity Dietary patterns  Adherence to Mediterranean diet ↓ CVD risk  Higher proinflammatory diet associated with ↑ CVD risk Li, J et al, 2020. 24  latrobe.edu.au Physical in/activity  Cardiovascular health is independently associated with physical in/activity  One third of adults are physically inactive  Estimated ~6% of IHD cases caused by physical inactivity.  In 2008, premature mortality as a result of physical inactivity accounted for over 5.3 million global deaths  Sedentary behaviour? 25 latrobe.edu.au Women 26  latrobe.edu.au Prevention Over 70% of CVD worldwide is caused by modifiable risk factors 27 latrobe.edu.au Exercise and Cardiovascular Disease La Trobe University CRICOS Provider Code Number 00115M 28  latrobe.edu.au Exercise, physical activity and CVD 29 latrobe.edu.au The London Transport Workers Study Morris et al. (1953): Drivers vs. conductors of London buses  Medical records of 31,000 men (aged 35-64 years)  ↑ mortality in drivers vs. conductors Postal workers  ↓ mortality in active postmen vs. less active post-staff vs. sedentary telephonists First observation that PA can protect against CVD 30  latrobe.edu.au The ‘Harvard Alumni’ Study Paffenbarger et al. (1978, 1986)  Longitudinal  ~21,000 male Harvard alumni aged 35-74 Key findings:  64% ↑ risk of MI in individuals with low PA  31% ↑ risk of death in sedentary individuals  Estimated added longevity based on PA 31 latrobe.edu.au Back to the future… Lear et al., 2017:  130 843 participants without pre-existing CVD from 17 countries  Low PA (750 minutes/wk) Very High (1250 mins/week) Physical activity associated with ↓ risk of mortality and incident CVD in all regions of the world. High PA associated with lowest risk, benefit plateaus at very high PA. 32  latrobe.edu.au Exercise is medicine… at any dose?  There is a dose-response relationship between (aerobic) physical activity and cardiovascular health  Curvilinear relationship, ‘more is better’  ‘Extreme Exercise Hypothesis’ – Some studies report ↑ risk of disease/mortality at the highest exercise volumes – Suggest a revision of the dose-response association – Currently limited evidence to support this 33 latrobe.edu.au Mechanisms: Aerobic Exercise  Modifies metabolic risk factors 34  latrobe.edu.au Mechanisms: Aerobic Exercise  Induces antiatherogenic adaptations in vascular function and structure 35 latrobe.edu.au Mechanisms: Resistance Exercise  Low muscle mass and strength is associated with CVD development and mortality, and CVD-related outcomes  Resistance training may prevent CVD through proposed mechanisms Fiuza-Luces et al., 2018. 36  Exercise prescription and delivery 37 latrobe.edu.au Cardiac rehabilitation  A coordinated, multifaceted intervention designed to reduce risk, foster healthy behaviours (and compliance) to reduce disability and promote an active lifestyle for individuals with CVD – Inpatient / phase I – Outpatient / phase II  Reduces rate of morbidity and mortality by stabilising, slowing, or reversing the progression of atherosclerotic process 38  latrobe.edu.au Indications Contraindications Stable post myocardial infarction Unstable angina Stable angina Uncontrolled hypertension (resting systolic blood Post cardiac surgery incl. transplant pressure >180 mm Hg and/or resting diastolic blood Stable heart failure pressure >110 mm Hg) Heart transplantation Orthostatic blood pressure drop of >20 mm Hg with Valvular heart disease/surgery symptoms Peripheral arterial disease Significant aortic stenosis At risk for coronary artery disease with diagnoses of Uncontrolled arrhythmias diabetes mellitus, dyslipidaemia, hypertension, Uncontrolled sinus tachycardia (>120 beats/min) obesity Uncompensated heart failure Other individuals who may benefit from structured Third-degree atrioventricular block without exercise and/or individual education based on pacemaker referral Active pericarditis or myocarditis Recent embolism (pulmonary or systemic) Acute thrombophlebitis Aortic dissection Acute systemic illness or fever Uncontrolled diabetes mellitus 39 latrobe.edu.au Assessment Subjective Objective Medical and surgical history Cardiovascular Ax e.g. 12-lead ECG CVD risk factors Clinical exercise testing Current medications Strength Psychosocial factors esp support system Resting/exercise HR Resting/exericse BP Body weight Symptoms at rest (e.g., dyspnea, dizziness) Symptoms/evidence of exercise intolerance 40  latrobe.edu.au Exercise Prescription (Ex Rx) Aerobic Resistance Frequency Minimum 3d/wk; preferably ≥5 d/wk 2-3 d/wk Intensity With an exercise test: 40%-80% of exercise 10-15 repetitions of each exercise without capacity using HRR/VO2peak significant fatigue; Without an exercise test: HRrest +20 to +30 RPE 11-13 or 40%-60% of 1-RM. bpm or an RPE of 12-16 (6-20 scale) Time 20-60 min 1-3 sets; 8-10 different exercises focused on major muscle groups. Type e.g. arm ergometer, upright and recumbent Select equipment that is safe and cycles, recumbent stepper, rower, elliptical, comfortable for the patient to use. stair climber, treadmill 41 latrobe.edu.au Hypertension  Independent risk factor for MI, stroke, heart Category Systolic BP Diastolic BP failure and premature death (mmHg) (mmHg) Optimal