Cardiorespiratory
Coronary artery disease
Coronary artery disease (CAD) remains a major cause of morbidity and mortality in developed countries.
One million people in the USA sustain myocardial infarction yearly. A major increase in incidence is occurring in developing countries.
Death rate has declined in developed countries by 30% in last 10yr.
50% of deaths with acute myocardial infarction occur within 1h attributable to ventricular fibrillation.
Clinical presentation of coronary heart disease
Stable angina pectoris: predictable onset of anginal symptoms on exercise or stress following imbalance of increased myocardial demand over supply.
Unstable angina and non-ST elevation myocardial infarction (non-STEMI): new onset, changing pattern or episodes of angina at rest. May be associated with release of cardiac enzymes. Troponin T and I used to make diagnosis or to exclude myocardial damage.
STEMI: presentation with rest pain, typical serial electrocardiogram (ECG) changes and enzyme release. Complicated by arrhythmias, associated with myocardial damage and left ventricle (LV) dysfunction or failure.
Sudden death associated with acute infarction or as an arrhythmic event.
Cardiac failure secondary to recurrent infarction or ischaemic cardiomyopathy.
Pathophysiology
Development of atheromatous plaques
Long pre-clinical phase of development with rapid change at time of plaque rupture.
Principally affect the proximal portions of coronary arteries, therefore, large muscle beds influenced by stenosis or occlusion.
Human coronary arteries are end arteries with little collateral development unless stimulated by reversible myocardial ischaemia or previous occlusion and infarction.
Distribution of arterial narrowing’s confers prognosis. Increasing mortality through single, double, and triple vessel or left main disease.
Plaque dynamics
Thrombogenic lipid rich core covered with fibrous cap of smooth muscle and inflammatory cells.
Inflammation may occur stimulated by oxidized lipid accumulation in the intima. CRP is an inflammatory marker. If elevated confers increased risk of further events.
Macrophages and T-lymphocytes are present in fatty streaks and mature plaques, cytokines, and growth factors are secreted.
Adhesion molecules interact with inflammatory cells.
Plaque rupture leads to platelet deposition and thrombus formation which may precipitate total obstruction and infarction.
Unstable plaques may be angiographically insignificant but can rapidly progress in significance.
Plaques may stabilize after rupture.
CAD is episodic in clinical presentation.
Aetiology
Atheroma associated with risk factors; subject to primary and secondary prevention.
Class 1 interventions
Hypertension.
Hypercholesterolaemia.
Cigarette smoking.
Cardiac protection with aspirin, beta-blockers, and angiotensin converting enzyme (ACE) inhibitors.
Class 2 interventions
Diabetes.
HDL and triglycerides.
Physical inactivity.
Obesity.
Moderate alcohol consumption.
Class 3 interventions
Diet.
Psychosocial factors.
Investigations
History of cardiac pain
Resting ECG.
Exercise stress testing for exercise capacity and evidence of myocardial ischaemia (ST depression).
Increasing use of functional imaging testing with pharmacological challenge.
Radionuclide scanning for distribution of perfusion defects and assessment of LV function.
Echocardiography for assessment of LV function. Stress echo techniques may be applied.
Multislice CT coronary angiography used as baseline noninvasive examination for anatomy.
Coronary arteriography to determine anatomical distribution of obstructive lesions and for coronary interventions.
Treatment of coronary heart disease
Pharmacological agents
Nitrates: act as venous dilators, reduce preload and systolic wall stress, used sublingually, orally, or by parenteral route in unstable patients. Tolerance may occur.
Beta blockers: act on cardiac beta receptors, reduce HR, contractility, systolic wall stress, and BP at rest and on exercise. Used to alter supply-demand ratio in stable angina, and after myocardial infarction as secondary prevention for anti-arrhythmic action. Consider other agents to reduce heart rate.
Calcium channel blockers: vasodilating action on coronary and peripheral arteries. Main therapy for increased vasoactivity such as Prinzmetal angina.
Nicorandil: potassium channel blocker, vasodilating action, but no tolerance. Action may be related to preconditioning.
Anti-platelet therapies: given as long-term therapy, (aspirin) as adjunct to coronary artery intervention acutely (abciximab) or as continuing treatment (clopidigrel, tigagretor).
Thrombolytic therapy: administered to patients with ST elevation myocardial infarction presenting early in absence of facilities for primary reperfusion therapy with angioplasty.
Interventions
Coronary interventions may be applied to each of the clinical presentations. Choice of intervention is determined by coronary artery anatomy on angiography.
Coronary artery bypass surgery generally applied to patients with left main or triple vessel involvement.
Increasing application of percutaneous coronary intervention (PCI) with balloon angioplasty and stenting in patients with stable angina with severe symptoms, unstable presentations, or in ST elevation myocardial infarction (primary angioplasty).
Primary angioplasty is treatment of choice if possible within 90min of attendance at a PCI equipped centre or within 120min of first presentation. Intervention associated with better short- and long-term outcomes with this system.
Exercise and coronary artery disease
Potential benefits of exercise
Reduced body weight and component of fat.
Increased exercise capacity and endurance Increased VO2 max by 10-15%.
Increased A-VO2 diff at maximal exercise.
Reduced total cholesterol and low density lipoprotein (LDL).
Reduction in triglycerides.
Enhanced fibrinolysis.
Improved endothelial dysfunction, decreased systemic inflammation.
Exercise prescription
Used as major component of rehabilitation following acute myocardial infarction.
May be applied to subjects with stable angina. Should have pre participation exercise test.
Non-pharmacological management of angina leads to increased functional capacity and angina threshold.
Potential adverse effects
Enhanced catecholamine release, increased HR contractility, and systolic wall tension; main determinants of myocardial oxygen consumption.
Potassium release may predispose to arrhythmias.
Rise in free fatty acids.
Enhanced platelet activation during exercise.
May induce onset of angina, myocardial infarction, or sudden death.
Physical inactivity, exercise, and coronary artery disease
Epidemiological observations
Occupational physical activity protective. IHD less in bus conductors than drivers, but drivers obese, raised cholesterol, and BP.
Sedentary workers who participate in vigorous exercise have 50% fewer coronary heart disease (CHD) events than inactive colleagues.
Indirect relationship of level of exercise and CHD; 3 times mortality in light workers compared to heavy workers. Shows dose-response for positive effects of exercise.
Lifelong exercise protective, late exercisers assume low risk.
Leisure time vigorous exercise protective.
General increased level of cardiovascular fitness protective against coronary events.
Cardiac rehabilitation
Definition
A long-term process by which patients with cardiac disease are encouraged and supported by multidisciplinary professionals to achieve optimal physical and psychosocial health. Used as vehicle for paint specific secondary prevention.
Evidence of benefit
In patients with myocardial infarction. Individual studies of exercise-based or comprehensive cardiac rehabilitation programmes are equivocal, but meta-analyses confirm 20-25% reduction in mortality and 28% reduction in fatal re-infarction at 2-3yr. No effects on non-fatal re-infarction or revascularization.
30-50% increase in exercise capacity and peak oxygen uptake of 10-20%. May not be sustained in long term.
Improved sub-maximal exercise capacity, reduced rate of perceived exertion, and delayed onset of lactate threshold.
Delayed onset of angina by reduced rate pressure product.
Improved psychological well-being and quality of life.
Improved physical activity but long term effects determined by compliance.
Programme of exercise and information sessions that help patient to get back to everyday life as quickly as possible.
It aims to help by understanding the problem, aiding recovery from a heart attack or surgery, make changes to lifestyle to improve heart health and reduce the risk of further clinical events.
Phases of rehabilitation
Phase 1: in-patient
Key elements are evaluation, reassurance, education, risk factor assessment, mobilization, and discharge planning. Applied after myocardial infarction, unstable angina, cardiac surgery, or angioplasty, or cardiac failure. To engage the patient and partner and identify particular problems prior to hospital discharge, and tailor the rehabilitation programme according to individual needs. Can be used after a step change in clinical condition. Encourage a positive attitude and introduce educational material.
Exercise prescription
Engage in self-care activities, general range of motion exercise, and walk short distances.
Phase 2: early outpatient recovery after discharge
Programme commencing 2-4 weeks after discharge lasting 4-12 weeks. Support from hospital or community-based health professionals through home visits or telephone contact. Education for risk factor modification and behavioural change. Medical evaluation for future management.
Exercise prescription
Undertake daily living activities and gradually increase the duration, frequency, and intensity of walking to increase functional and endurance activity.
Phase 3: intermediate outpatient
Generally comprises an exercise training programme undertaken in hospital gym with self-monitoring. Can be accommodated in community or home-based setting. Generally up to 12 weeks.
Exercise prescription
20-30min of low to moderate intensity aerobic exercise, e.g. walking, cycling, circuit training on 3 days a week and moderate intense physical activity, e.g. walking, on days when not participating in formal exercise programme.
Phase 4: long-term maintenance
Continued education after exercise period. Long-term rehabilitation may involve self-help groups, exercise leaders, or buddy programme. Community-based programme out of the hospital setting with most care delivered in primary care. Patient’s clinical status, medication, and risk factor modification undertaken by GP or other health care professional.
Exercise prescription
A minimum of 20min of moderate intensity exercise on 3 days per week, and/or accumulate 30min or more of moderate intensity physical activity on at least 5 days a week. Use of local facilities.
Components at all phases
Education to improve adherence to preventive therapies.
Smoking cessation.
Counselling.
Exercise training.
Psychology.
Secondary prevention.
Secondary prevention
Rehabilitation now used as vehicle for delivery, and exercise is one component. Encourage life style changes including diet and smoking.
Target risk factors with pharmacological agents to treat:
Hypercholesterolaemia.
Hypertension.
Diabetes.
Use of anti-platelet compounds, beta-blockers, and ACE inhibitors.
The multidisciplinary team includes doctors, nursing staff, physiotherapists, dieticians, and exercise consultants. Co-ordinate the programme for the maximum benefit of the individual.
Adherence strategies
High level of dropouts (9-49% from short supervised programmes). Factors include social class, angina, reduced ejection fraction, inactive leisure habits, current smoking, transport problems, medical problems, work, or domestic commitments, lack of motivation, inconvenient timing of programmes, anxiety, and depression.
Factors to improve maintenance of exercise
Compliance improved by addressing travel problems.
Membership of cardiac support groups and buddy systems.
Community programmes.
Home based programmes using local facilities.
Use of electric or paper resources. Information from National Audit of Cardiac Rehabilitation.
Exercise referral
Exercise referral has now been widened to a larger group of subjects. With recognition that most individuals do not take adequate exercise, exercise prescription is now more widely applied.
Physical activity guidelines: exercise prescription for healthy adults
1990 American College of Sports Medicine (ACSM) exercise recommendation to improve and maintain cardio-respiratory fitness a minimum of 3 times 20 min of continuous moderate to vigorous intensity aerobic exercise per week. (60-90% of maximum HR or 50-85% of maximum aerobic capacity.)
1995 ACSM and Center for Disease Control (CDC) physical recommendation to promote health and prevent disease. Accumulate at least 30min of moderate intensity physical activity on five or more days per week. This activity would include alterations of daily routine of walking short distances or climbing stairs, and includes activities such as gardening, housework, or washing the car.
Physical Activity Guidelines for Americans 2008:
Children and adolescents (6-17 yrs) should do 1h or more of physical activity every day. Most activity should be moderate or vigorous intensity aerobic physical activity. Vigorous intensity and muscle strengthening and bone strengthening activity should occur on at least 3 days a week.
Adults (18-64 yrs) Should do 2h and 30min a week of moderate intensity or 1h and 15min a week of vigorous intensity aerobic physical activity in episodes of at least 10min. Additional health benefits may occur by doubling the duration of exercise activities. Muscle strengthening exercises should be performed on 2 or more days a week.
Benefits of exercise
Mechanism of increased exercise capacity
Peripheral effects of skeletal muscle and vascular adaptations; increase in a-vO2 diff, increased extraction, increased blood flow, and aerobic metabolism in skeletal muscle, increased fibre area, capillary density, and oxidative activity. Cardiac effects increased ejection fraction, cardiac output, stroke volume.
Clinical benefits
Lower risk of early death, heart disease, stroke, type 2 diabetes, high BP, adverse blood lipid profile, metabolic syndrome, colon, and breast cancers.
Prevention of weight gain, weight loss when combined with diet, improved cardiovascular and muscular fitness, prevention of falls/reduced depression and better cognitive function
New patient groups
Sedentary low risk groups have risk factors but no clinical symptoms nor overt disease. After screening for symptoms these patients are seen for exercise consultation.
High-risk patient groups have evidence of previous disease with a previous history of angina, myocardial infarction, or revascularization, but no ongoing exercise programme. Appropriate programmes of exercise are prescribed after pre-participation health and symptom questionnaires and exercise testing.
Information regarding facilities and sources
Exercise networks and sites of delivery are collated and advertised in public places, primary care facilities, and websites to provide the widest possible public access.
Exercise and adult congenital heart disease
The live birth incidence of congenital heart disease is 7-8 cases/1000 and 96% survive into adult life. Survival patterns have changed and exercise plays a role in assessment. Common heart defects include atrial septal defect, ventricular septal defect, patent ductus arteriosis, coarctation of the aorta with or without additional disease, valvular aortic stenosis, pulmonary stenosis, Fallot’s tetralogy, and transposition of the great arteries. Many have interventions, but some complicated disease states have palliation and supportive therapy, including those with pulmonary hypertension including Eisenmenger circulation.
Areas for advice include employment, insurance, and driving. In particular we are concerned with advice re-exercise, activity level, sports participation, and the risk of sudden death.
Patient groups include:
No previous surgery, but may be needed in future, e.g. aortic stenosis.
Previous surgery with possible risk of arrhythmia, e.g. Fallot’s tetralogy.
Patients with palliation, further intervention required, e.g. Mustard procedure for transposition of great arteries (TGA).
Inoperable subjects, consideration of heart- or heart-lung transplant.
Uses of exercise testing
To evaluate symptoms and perception of functional capacity and decide if exercise prescription is indicated.
To identify underlying cardiac lesion severity. Abnormal ventilatory response to exercise relates to cyanosis and predicts survival. Low peak oxygen uptake predicts hospitalization or death over the following year.
To assess effectiveness of treatment or interventions.
To assess functional capacity prior to recreational or athletic activity.
Information available from exercise testing
Functional capacity including workload, oxygen consumption and anaerobic threshold.
Heart rhythm including atrial and ventricular arrhythmias induced by exercise or heart block.
BP response on exercise. (May induce fall in obstructive lesions or abnormal rise in patients with coarctation, with or without previous intervention.)
Induction of myocardial ischaemia in patients with valvular disease.
Causes of limitation of exercise capacity
Limitation of rise in cardiac output; Fontan repair, obstructive lesions of valves or ventricular outflow tract, or regurgitant lesions.
Associated with chronotropic incompetence, inadequate stroke volume, and ventricular filling.
Inadequate peripheral compensation and conditioning.
Associated pulmonary disease.
Psychological barriers of perceived limitations.
Exercise prescription
Individual programme for each patient.
Use of prescreening exercise test and use of target HR.
Advice regarding type and duration of exercise according to nature of structural lesion.
Education regarding symptoms and heart rhythm.
Maintenance of fluid balance and avoidance of hypotension.
Guidelines for exercise and sport in congenital heart disease
Advice should be in keeping with the nature of the exercise challenge, including whether the exercise is recreational or competitive, and also including the personality of the participant.
Factors will include type, intensity, and duration of training and competition related to individual sports.
Special consideration of the influence of bodily contact in subjects with valve replacements.
Special limitation in sports if risk of loss of consciousness.
Classification of sports is required in terms of isotonic and isometric components.
High risk
Compromised ventricular function.
Significant cardiomyopathy.
Critical obstructive lesions.
Severe regurgitant lesions.
Severe pulmonary hypertension.
Exercise induced ventricular arrhythmias.
Light exercise permitted
Moderate obstructive lesions.
Moderate regurgitant lesions.
Moderate pulmonary hypertension.
Systemic hypertension.
Uncorrected cyanotic heart disease.
Minimal restriction to exercise
Mild obstructive lesions.
Mild regurgitant lesions.
Shunts in the absence of pulmonary vascular disease.
Corrected cyanotic patients with minimal anatomical abnormality.
Factors in individual congenital conditions
Coarctation of the aorta
Pulmonary stenosis
Determine if mild, moderate, or severe. If major obstruction, gradient > 50mmHg then recommend mild intensity of exercise and short duration. May be unrestricted post operation.
Atrial septal defect
In those without surgery—a small shunt in absence of pulmonary hypertension, no limitation. If pulmonary hypertension, then low intensity. In those following surgery, if pulmonary vascular resistance remains low, then no restriction. If post-operative pulmonary pressure is elevated then restrict. Atrial arrhythmias may occur on exercise.
Ventricular septal defect
Advice depends on the size of defect and pulmonary vascular resistance. Post-operative advice depends on pulmonary artery pressure, exclusion of ventricular arrhythmias on exercise, and 24h monitoring.
Patients with associated pulmonary vascular disease
If severe, low level exercise may lead to marked dyspnoea. Exercise may increase the left to right shunt. Local tissue acidosis occurs. Exercise induced syncope may occur.
Tetralogy of Fallot
If uncorrected, advice depends on exercise capacity associated with the degree of obstruction to the right ventricular outflow tract and increase in right to left shunt. Particular risks may occur with isometric exercise.
After repair, exercise influenced if residual shunt, induced pulmonary regurgitation following outflow tract repair, stenosis of pulmonary artery at site of previous Blalock shunt, or induction of arrhythmias which may occur in any patient with previous ventriculotomy.
Transposition of great arteries (Mustard repair)
Venous pathway obstruction may reduce exercise capacity. Baffle leaks may induce desaturation on early phase of exercise.
Depression of systemic right ventricle limits increase in cardiac output.
Sinus node dysfunction. Atrial and ventricular tachyarrhthmias or abnormal atrioventricular (AV) conduction may occur. General guideline of no more than mild to moderate isotonic exercise.
Fontan circulation
Circulation devoid of a functional sub-pulmonary ventricle. Function depends on nature of sub-aortic ventricle, which may be morphological left or right. Exercise performance reduced with lowered aerobic capacity, HR reduction, and post-operative hypoxaemia. Exercise capacity may be improved by total caval pulmonary connection.
Marfan syndrome
Mutations in a single gene affects components of the extracellular matrix, leading to a disorder of the connective tissue.
Autosomal dominant disease of connective tissue with variable expressibility. Frequency 1 in 20,000; 25% represent new mutations.
Mutation on chromosome 15 in fibrillin-1 gene (FBN-1) affecting the extracellular matrix glycoprotein present in the aorta, suspensory ligament of the lens, and connective tissue of tendons and ligaments.
Molecular analysis of complement deoxynbp nucleic acid and deoxynbo nucleic acid on fibrillin 1 gene from skin fibroblasts culture shows reduced, absent, or structurally abnormal fibrillin and excessive transforming growth factor beta TGF-β.
Challenges
Diagnosis made on clinical grounds with abnormalities in two systems.
Genetic counselling, particular problems with pregnancy.
Life style advice, body habitus may allow sports participation, e.g. basketball or volleyball.
Cardiovascular surveillance aimed predominantly at aortic size and mitral valve.
Diagnosis
Skeletal system
Major criteria
Pectus carinatum, pectus excavatum requiring surgery.
Reduced upper to lower segment ratio or arm span to height ratio > 1.05.
Wrist and thumb signs.
Scoliosis of > 20° or spondylolisthesis.
Reduced extension at the elbows (<170°).
Pes planus.
Protrusion acetabulae (on X-ray).
Minor criteria
Pectus excavatum of moderate severity.
Joint hypermobility.
High-arched palate with crowding of teeth.
Typical facial appearance.
Ocular system
Major criteria
Ectopia lentis.
Minor criteria
Flat cornea (keratometry).
Increased axial length of globe (ultrasound).
Decreased miosis.
Family/genetic history
Major criteria
Having a parent, child or sibling who meets the diagnostic criteria independently.
Known mutation in fibrillin 1 gene.
Haplotype of FBN-1 is inherited and known to be associated with unequivocal Marfan syndrome in the family.
Cardiovascular system
Major criteria
Dilatation of ascending aorta including sinuses of Valsalva.
Dissection of ascending aorta.
Minor criteria
Mitral valve prolapse.
Unexplained dilatation of main pulmonary artery <40yr.
Calcification of mitral valve annulus <40yr.
Dilatation or dissection of descending thoracic or abdominal aorta <50yr.
Pulmonary system
Minor criteria
Spontaneous pneumothorax.
Apical blebs (chest X-ray).
Skin and integument
Minor criteria
Unexplained stretch marks.
Recurrent or incisional herniae.
Diagnostic criteria for Marfan syndrome
Negative family/genetic history
Major criteria in at least two different organ systems and involvement of a third system, or known genetic mutations plus one major criterion and involvement of a second organ system.
Positive family/genetic history
One major criterion in an organ system and involvement of a second organ system.
Cardiac problems
Early mortality in 4th and 5th decades.
Children are more affected by mitral valve disease.
Aortic problems progressively more likely in adolescents and older.
Mitral complications more common in females than males.
Higher risk of deterioration (25%) in this group of mitral valve prolapse than in normal population.
Mitral valve disease
Mitral annulus dilatation stretching, may occasionally rupture chordae. 10% have associated calcification. Repair of the valve is often successful.
Factors influencing the results of surgery: Valve cusp extremely redundant, marked chordal damage, degree of calcification. There is an increased risk of dehiscence of prosthetic valve if replacement required.
Aortic root involvement
May be dilated at birth, rate of progression variable. Prediction of dissection is difficult. Screening with trans-thoracic echo sufficient if dilatation limited to proximal ascending aorta. Usual rate of change is slow. If dilatation of descending aorta, trans-oesophageal echo and serial MRI required. Aortic valve regurgitation usually accompanies dilatation of 50mm. Consideration of surgical intervention if aorta 45mm
Positive family history may influence the decision
Treatment
Beta-blockers should be introduced as early as possible at the highest tolerated dose. Possible benefit of angiotensin 11 receptor blockers to reduce TGF-β.
Valve surgery
Approach to repair dilated aortic root, and preserve the aortic valve to avoid risks of endocarditis and anticoagulation.
Aortic root replacement
Elective root repair low operative mortality. Emergency results much poorer.
Aortic dissection
Most arise above the coronary ostium (type A Stanford). Some may extend the entire length (type 1 deBakey scheme). 10% distal to left subclavian (type B or 111). Rarely may be limited to abdominal aorta.
Pregnancy
High risk of affected child.
Dilatation of aortic root with aortic regurgitation and cardiac failure.
Heightened risk of dissection. In third trimester, at parturition, and first month post-delivery.
Risk highest if previous dilatation or dissection.
Risk much less if aorta <40mm.
Preconception counselling
If dilated or previous dissection consider termination.
Avoid physical activity.
Beta-blockade.
If problems elective section.
Indications for monitoring
Aortic root size must be monitored by echocardiography or MRI if echo window inadequate.
If aortic root diameter is 4cm then investigations should be undertaken 3-monthly and if diameter is 4.5cm then prophylactic surgery will be considered.
If aortic root is normal and no family history of sudden death then dynamic exercise may be undertaken in low and moderate static/low dynamic competitive sports, but isometric exercise should be avoided.
Hypertension and exercise
Prevalence
Diagnosis
To establish level of BP, 3 readings should be taken in a relaxed environment over 3 months. If borderline, 24h ambulatory monitoring should be performed or home BP recordings performed using automatic recorders by patients on 4 week days on four occasions These values correlate better with target organ damage.
Transient or persistent increases in BP may occur associated with stress, but have normal values at other times (e.g. white coat hypertension). This may occur in some 20% of subjects and is not related to cardiovascular events.
There is considerable variability over 24h with a normal nocturnal dip. Loss of dip associated with more serious target organ effects.
Exercise-induced hypertension may occur. Systolic BP rise > 60mmHg after 5min, > 70mmHg after 10min, or diastolic rise > 10mmHg at any time is associated with the development of hypertension and an increased risk of cardiovascular events.
Aetiology
Primary, essential, or idiopathic (90-95%).
Secondary, associated with (a) renal disease (b) endocrine abnormalities, including Cushing’s syndrome.
Coarctation of the aorta.
Pregnancy.
Natural history of hypertension and prognosis
Established increase in diastolic BP (5-10mmHg) associated with a 34-56% increase in cerebrovascular accidents and a 21-37% increase in CAD.
Absolute risk small 3.5% over 8yrs.
Symptoms and signs
Uncomplicated high BP asymptomatic.
End organ complications include left ventricular hypertrophy, abnormalities in renal function and hypertensive retinopathy.
Decision on treatment is based on the overall cardiovascular risk including total cholesterol, low HDL, cigarette smoking, glucose intolerance and left ventricular hypertrophy (LVH).Related posts:
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