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NNEEDS MAJOR CONDENSING/SORTING OUT ESP NEAR THE END Add NICE GUIDELINES AT THE END ACUTE CORONARY SYNDROMES (ACS): -

CVD is the main cause of death in England and wales. Includes CHD, stroke and peripheral artery disease. CHD – most commonly caused by atherosclerosis which occurs when cholesterol deposits accumulate to form a plaque leading to a cascade of inflammatory processes

CVD risk factors: - Type 1 and 2 diabetes – complications are all CVD – HA & stroke are increased, blindness, peripheral neuropathy – micro and macrovascular complications. Or impaired glucose regulation - Ethnicity – ancestry from India, Pakistan, Bangladesh, Sri Lanka – may have same diet, age, level of exercise, smoking status as white caucasian, yet incidence of CVD would still be dramatically different. South Asians have incidence of CVD 30-40% higher- even considering dietary differences. - Increasing age, male gender (seems to be changing as more women in the workplace – maybe exposed to the same risk factors) - Lifetime smoking habit – including shisha, chewing tobacco – single biggest risk factor for CVD - High ratio of total cholesterol: HDL cholesterol – particularly LDL cholesterol, high systolic BP - Overweight/obesity – see NICE guidance on black/Asian patients – particularly central obesity - Sedentary lifestyle (inactive) – research behind taking 10,000 steps daily - Alcohol abuse – particularly binge drinking - Socioeconomic deprivation – deprived backgrounds, linked with dietary factors for example - Familial hypercholesterolaemia, familial mixed dyslipidemia, or other inherited dyslipidemias - Family history of premature CVD – parents who had a stroke/HA before age 55 - High triglycerides - Renal function - Left ventricular hypertrophy ACS: - Unstable angina - Non-ST elevation MI - ST elevation MI Diet high in sat fats over a number of years Spectrum of acute coronary cause excess fat to be deposited within coronary syndromes according to artery walls (supply the heart muscle with O2). ECG and biochemical The deposited fat will eventually rupture into the markers of myocardial lumen (before was on the wall of the inside of necrosis (troponin T, the coronary artery)– a sign of damage, platelets troponin I, and creatine will stick to where that fat has burst out – causes kinase MB), in patients presenting with acute a partial blockage – less blood flow therefore, cardiac chest pain. less oxygen to heart – symptoms of angina. Eventually, damage occurring significantly causing further problems/complete blockage. Partial – NSTEMI – typical symptoms of a HA – abnormal ECG, rise in troponin enzyme (incr when heart damage). Full blockage – typical symptoms, raised troponin, but ECG will show elevated ST if that blockage is left, can cause whole section of heart to die off- if that’s significant enough, can kill people.

Unstable angina and NSTEMI: these two can happen together - Symptoms are as a result of sudden plaque rupture leading to prolonged angina at rest/new onset severe angina. - Unstable angina pts have no evidence of myocardial necrosis - NSTEMI – some myocardial necrosis will be evident Diagnosis of ACS: (some pt get many symptoms at all) - Dependant on triad of clinical presentation don’t; ECG changes and biochemical cardiac markers (troponin) - Typical symptoms and history – severe chest pain > 20 mins, can radiate to left arm/jaw/neck, dyspnoea, fatigue - Resting 12 lead ECG (repeat every 15 mins whilst patient in pain). - Biochemical markers e.g. troponin I or T (released by myocardium as a sign of damage) – no such thing as normal/upper limit level - reference range varies depending on specificity of the test is & efficiency of equipment used in the hospital lab. ACS is defined as finding at least one troponin level above the 99th centile of troponin levels found in a normal population - cannot be taken in isolation, must be placed in context of clinical presentation and dynamic changes in troponin levels. For high sensitivity troponin tests, sample taken on admission then again at 3hrs after admission. If 3hr level is 20% above baseline, heart muscle damage is confirmed - FBC; serum electrolytes; blood glucose; lipid profile.

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Management of NSTEMI: Treatment aims for acute management: provision of supportive care, pain relief during acute attack, prevention of further cardiac events Treatment: (Most of these pts won’t have PCI - may have a stent if in hosp and ECG isn’t looking great – blockage checked out to see if its more than a partial blockage). Paramedics do this to keep the patient alive. Infusions are started when they reach hospital) Oxygenation if hypoxia, pulmonary oedema, or continuing myocardial ischaemia = check oxygen sat is > 94%, if not then oxygen via nasal cannula 2-4L/min and titrate to 94-98%. Coronary vasodilation (pain relief)– GTN 2-10mg IV (maintain systolic BP >90mmHg) or sublingual 300mcg to- 1mg *Paramedic can give GTN spray to get fast absorption into the systemic circulation – relieve some pressure in heart – nitrates are venous dilators, will dilate blood vessels leading to the heart – reduces pressure and it reduces preload to the heart (less strain)* Analgesia – diamorphine 2mg-5mg slow IV injection/morphine 2.5mg-5mg IV bolus Antiplatelet therapy – aspirin 300mg stat & clopidogrel 300mg stat (given within 24 hours) Continue clopidogrel for at least 1 month and up to 12 months (platelets less sticky) Fondaparinux 2.5mg once daily SC injection – max 8 days (sooner if discharged) – It is an anticoagulant and given to enhance antiplatelet effect Given to pts without a high bleeding risk unless angiography is planned within 24hrs of admission. Stop if patient troponin negative. Beta Blockers IV metoprolol 5mg for ongoing chest pain, hypertension, tachycardia then oral treatment (reduction of myocardial energy consumption) Antiemetic - IV metoclopramide (cyclizine oral/IM if no heart failure, do not give IV). (diamorphine can cause nausea) Metoclopramide is preferred choice. Ondansetron is linked with arrhythmias, QT prolongation so less used Continue electrocardiogram (ECG) monitoring for arrhythmias – look out for cardiac arrest Assess risk of future adverse cardiovascular events using an established risk scoring system that predicts 6-month mortality (for example, Global Registry of Acute Cardiac Events [GRACE]). If risk score is >1.5% offer clopidogrel 300mg stat then

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75mg od for 12 months. Consider IV eptifibatide or tirofiban as part of the early management for ptswho have an intermediate or higher risk of adverse cardiovascular events (predicted 6 month mortality above 3.0%) and who are scheduled to undergo angiography within 96 hours of hospital admission. Management of STEMI: STEMI can be defined as the presentation of ischaemic symptoms in the presence of ST-segment elevation, with a rise of biomarkers of myocardial necrosis and progress to Qwave MI. Immediately assess eligibility for coronary perfusion therapy (mechanical PCI/pharmacological reperfusion) - offer coronary angiography (procedure using contrast dye, usually containing iodine, and x-ray pictures to detect blockages in the coronary arteries) with follow on PCI as the preferred reperfusion for pts with acute STEMI if: Presentation is within 12hrs of symptom onset and primary PCI can be delivered within 120 mins of the time when fibrinolysis could have been given. In patients who cannot be offered PCI within 120mins of diagnosis/blockage cannot be cleared with PCI/pt refused surgery for stent/unsure if NSTEMI/STEMI, a thrombolytic drug should be administered along with either unfractionated heparin (for maximum 2 days), a low molecular weight heparin (e.g. enoxaparin, dalteparin), or fondaparinux. Thrombolytics: tenecteplase/streptokinase/alteplase Indication for tenecteplase: For patient with persistent STEMI or LBBB (Left bundle branch block) within 12 hours on onset of symptoms - 30mg-50mg given over 10 seconds as IV bolus and initiated within 6hrs of symptom onset ST elevation should resolve within 30-60 mins following thrombolysis with resolution of symptoms. Risk of haemorrhagic stroke with thrombolysis is 0.5%-1% - high risk, hence why not used as much. Other reasons: patient had recent surgery, ulcer, so it can be contraindicated. Therefore, thrombolytics is risky, hence why PCI is preferred. Whole point is to increase blood flow to heart and save as much of the heart. Absolute contraindications: haemorrhagic stroke/stroke of unknown origin at any time ischaemic stroke in previous 6 months central nervous system (CNS) trauma or neoplasms recent major trauma/surgery/head injury (within preceding 3 weeks) gastrointestinal (GI) bleeding within the last month known bleeding disorder, aortic dissection, non-compressible punctures (e.g. liver biopsy, lumbar puncture [LP]) Relative contraindications: transient ischaemic attack (TIA) in preceding 6 months oral anticoagulant therapy pregnancy or within 1-week post-partum refractory hypertension (systolic blood pressure [BP] 180mmHg and/or diastolic BP 110mmHg)

• advanced liver disease, infective endocarditis (IE), active peptic ulcer, refractory resuscitation *most effective in clearing blockage – PCI/angioplasty. Thin tube is threaded into the femeral artery, up to the heart into coronary arteries to see where the blockage is. If there is a blockage, a balloon angioplasty is where the fat is squeezed, and blockage is cleared – a spring is placed where the blockage has now been cleared to prevent it from collapsing (damaged blood vessels normally collapse in on themselves so have to keep it open) – this is a stent (for life)– keeps it open and blood

flowing. This is more effective than thrombolysis – bleeding risk. Act quickly – longer wait = more damage. Acute manage of STEMI: • Immediate acute management: aim to provide supportive care, pain relief, promote reperfusion and reduce mortality • General oxygenation – Check oxygen saturation is between >94%. If not then oxygen via nasal cannula 2-4L/min and titrate to 94-98%. • Coronary vasodilation (pain relief)– GTN 2-10mg IV (maintain systolic BP >90mmHg) or sublingual 300mcg to- 1mg • Analgesia – diamorphine 2-5mg slow IV injection or morphine 2.5mg-5mg IV bolus. • Antiplatelet therapy- Aspirin 300mg stat + Clopidogrel 300mg stat (given within 24 hours). Continue clopidogrel for at least 1 month and up to 12 months. – to prevent blockage from increasing • Myocardial energy consumption – beta blockers IV metoprolol 5mg for ongoing chest pain, hypertension and tachycardia then oral treatment. – reduce angina pain, vasodilatory effect • Antiemetic – IV metoclopramide (cyclizine oral/im if no heart failure, do not give IV). – feeling sick because of the morphine • Continue electrocardiogram (ECG) monitoring for arrhythmias Secondary prevention of ACS: this is after a cardiac event, every pt will be at least on all these drugs unless there is a contraindiciation - Lifestyle advice and cardiac rehab – LT things Cardioprotective diet: Total fat ≤30% and saturated fats ≤7% of total energy intake: reduce their saturated fat intake, increase their mono-unsaturated fat intake with olive oil, rapeseed oil or spreads based on these oils and to use them in food preparation, choose wholegrain varieties of starchy food, 5 portions fruit and vegetables per day, 2 portions of fish per week (at least 1 of oily fish), 4-5 portions of unsalted nuts, seed and legumes per week, reduce sugar intake and intake of food products containing refined sugars including fructose. Alcohol: limit to 3-4 units/day max for men, women: 2-3 units/day. Avoid binge drinking. Later guidance has changed this to max 14 units/week in all groups Exercise: Advise people at high risk of or with CVD to do the following every week: At least 150 mins moderate intensity aerobic activity or 75 mins of vigorous intensity aerobic activity (or a mix of the above). Muscle strengthening exercises 2 days or more a week Encourage people who are unable to perform moderate-intensity physical activity because of comorbidity, medical conditions or personal circumstances to exercise at their maximum safe capacity. Weight management: advice to maintain healthy weight. => signpost patients to NHS choices for CVD diet and advice is there. Give patients resources, can refer on to other resources like weight management, smoking cessation (offer support and referral or pharmacotherapy), alcohol consumption. Can target these patients for MURs - Antiplatelet therapy (ongoing) NSTEMI: aspirin 75mg daily & clopidogrel 75mg daily (continued for upto 12 months) STEMI: aspirin 75mg daily orally + clopidogrel 75mg daily orally (clopidogrel as a treatment option for at least 1 month and for up to 12 months). Continue clopidogrel for up to 12 months in people who have had a STEMI and medical management with or without reperfusion treatment with a fibrinolytic agent Offers clopidogrel as a treatment option for up to 12 months in people who have had a STEMI and received a bare-metal or drug-eluting stent (in addition to aspirin) - Drug eluting stent: drugs are embedded into it. Stents are associated with being pro-thrombotic so in the first couple of months,

antiplatelets are attracted – possible blockage – hence why 2 anti-platelets are offered *Two antiplatelets are used to try and maintain platelets from not sticking – prevents blockages reforming – clopidogrel is only continued for up to 12 months as some people have a high bleed risk, GI ulcers - Aspirin is lifelong. Other antiplatelets can be given instead of clopidogrel e.g. ticagrelor, prasugrel. As clopidogrel is a pro-drug - must be converted to its active form – lack of enzymes in some pts = inefficient conversion = not full antiplatelet effect. Ticagrelor - already in its active form = better response from some pts (its 2 nd line to clopidogrel as very expensive- same duration- up to 12 months). Cardiologist- if someone has a secondary cardiac event and they have been on clopidogrel, they can switch to ticagrelor Tirofiban: Gp IIb/IIIa inhibitors act by inhibiting the final common pathway of platelet aggregation and play an important role in the management of acute coronary syndromes* SLIDE 20 - Cholesterol lowering drugs: Use on non-HDL rather than LDL. Non-HDL cholesterol = total cholesterol - HDL cholesterol. * Total cholesterol = LDL (bad which causes blockages) + HDL (good which we want more of) + triglycerides (also want less of)* LDL cholesterol is not directly measured - calculated using a fasting sample and requires triglyceride levels to be Measure total cholesterol, HDL cholesterol and non-HDL cholesterol at 3 months of treatment and aim for >40% reduction in non-HDL cholesterol- if not achieved, discuss adherence and timing of dose, optimise adherence to diet and lifestyle measures, consider increasing dose if on < 80 mg and if at higher risk due to comorbidities (risk score or using clinical judgement). Annual medication reviews - discuss medicines adherence and lifestyle modification and address CVD risk factors - annual non-fasting blood test for non-HDL cholesterol to discuss during review If stable on a low/ middle-intensity statin - discuss benefits and risks of changing to high-intensity statin (when they have a medication review) => drugs which lower cholesterol prevent blockages – SLIDE 29 Advice and monitoring: - Well tolerated - worried about s/e on muscle and liver abnormalities - baseline ALT/AST taken before treatment. Liver transaminase is measured within 3 months of starting treatment, at 12 months, but not again unless clinically indicated. Only exclude from therapy if liver transaminase levels are raised >3 x upper limit of normal (ULN). - Do not stop statins because of an increase in BG/HbA1c. - Contraindicated in pregnancy- teratogenic, do not restart until breastfeeding is finished.

- before treatment is started, creatine kinase level is measured in pts who had persistent generalised unexplained muscle pain – whether or not associated with previous lipid-lowering therapy If levels are more than 5 x ULN, re-measure after 7 days If levels are still 5 x ULN, do not start statin treatment If levels are raised but less than 5 x ULN, start statin treatment at a lower dose => Advise on warning signs – muscle pain/tenderness/weakness where exercise is not the cause – liver enzymes are then checked, must be significantly low for the doctor to do something - if muscle pain or weakness is reported, explore other possible causes and raised creatine kinase if they have previously tolerated statin therapy for more than 3 months. Do not measure creatine kinase levels if asymptomatic. Myopathy occurs in several different forms and the specific definition varies across studies: - Rhabdomyolysis is the most severe manifestation of myopathy associated with statins. It is often defined as a creatine kinase concentration at least 40 x ULN or increased creatine kinase in association with renal failure – most severe Risk factors for rhabdomyolysis; increasing age, renal impairment, drug interactions. - Myositis (myopathy) is defined as muscle pain in association with a creatine kinase concentration >10 x ULN - Myalgia refers to muscle pain without an increase in creatine kinase – least severe Common atorvastatin side effects (may affect up to 1 in 10 people) include: inflammation of the nasal passages, pain in the throat, nose bleed; allergic reactions; increases in blood sugar levels (if diabetes continue careful monitoring of blood sugar levels), increase in blood creatine kinase; headache; nausea, constipation, wind, indigestion, diarrhoea; joint pain, muscle pain and back pain; blood test results that show your liver function can become abnormal Muscle-related problems are most reported side effect of statins – studies have shown its not that common – slide 38. No clinical difference found between statins and placebo in causing myalgia in people with CVD at up to 6 years. High quality evidence showed that medium-intensity statin is more clinically effective when compared to high-intensity statin in showing less myalgia at up to 5 years Over a median 5 years of follow-up in the Heart Protection Study (HPS), 33% of patients allocated to simvastatin and placebo reported muscle pains at some point during the study, and no difference was seen between the groups. Large clinical trials showed that statins are generally well tolerated by most people who take them..Some side effects only apparent when medicines are used in the community by many pts (because of the rarity of some side effects) for a long time (slow onset of some s/e) as high doses are used cf to clinical trials by pts who are not typically inc in clinical trials (multiple medical conditions, use other medicines, differences in genetic make-up/ lifestyle, younger/older than those included in trials (all these factors might affect the risk of side effects - Advise about interactions with food/supplements (e.g. grapefruit juice) – should always consult the PIL/ pharmacist/prescriber before starting other drugs/supplements. - Pt should restart the statin if stopped taking it due to drug interactions or to treat illnesses. Ezetimibe: monotherapy is an option for treating primary (heterozygous-familial or non-familial) hypercholesterolaemia in adults in whom initial statin therapy is contraindicated/cannot tolerate. Co-administered when: serum total or LDL cholesterol concentration is not appropriately controlled either after appropriate dose titration of initial statin therapy or because dose titration is limited by intolerance to the initial statin therapy and a change from initial statin therapy to an alternative statin is being considered Do not offer these for primary of secondary prevention: Anion exchange resin – cholestyramine, fibrate (this is do not routinely offer), nicotinic acid, omega 3 fatty acid compounds (2 oily fish a week is better) Do not offer coenzyme Q10 or vitamin D to increase adherence to statin treatment.

- RAAS drugs: ACEI – offer to people who present acutely with an MI as soon as they are haemodynamically stable – contin...