Diagnosis and Management of Acute Coronary Sndrome.pptx

PowerPoint presentation on presentations, diagnosis, and management of acute coronary syndromes

1. ACUTE CORONARY SYNDROME DR YUSUF ABAYOMI, MBBS DR EMEKEKWUE CHIMDALU, MD

2. 1 INTRO 2 EPI 3 PATHO 4 PREVENTION TABLE OF CONTENT What is Ischemic heart disease? What is acute coronary syndromes What is the disease burden? What is atherosclerosis? Causes of acute coronary syndrome How can acute coronary syndromes be prevented?

3. 8 PROGNOSIS 5 TYPES 6 Tests 7 TREATMENT AND COMPLICATIONS TABLE OF CONTENT Different types of ACS and how they present. Laboratory and imaging investigations Current mainstay of treatment? Sequalae of acute coronary syndromes What are the potential outcomes of patients who suffer ACS

4. INTRODUCTION Ischemic heart disease (IHD) is a condition that occurs when there is inadequate supply of blood and oxygen to a portion of the myocardium to meet it’s demands. Ischemic heart disease could be due to problems in the coronary arteries (termed coronary artery disease) or secondary to other problems such which do not directly affect coronary arteries (termed non-coronary IHD) Coronary artery disease is divided into stable angina and acute coronary syndrome

5. INTRODUCTION Acute coronary syndrome represent a group of conditions that occur due to the sudden onset of cardiac tissue ischemia secondary to impaired blood flow When this impairment in blood flow leads to death of cardiac myocytes, it is termed myocardial infarction.

6. INTRODUCTION

7. EPIDERMIOLOGY Ischemic heart disease and acute coronary syndrome cause more deaths and disability and incur greater economic costs than any other illness in the developed world . Globally, 197.2 million people live with ischemic heart disease. In the USA, about 20 million people have ischemic heart disease with 3-4% sustaining myocardial infarction.

8. EPIDERMIOLOGY It is the single largest cause of death in the UK being responsible for 1 in 5 male deaths and 1 in 10 female deaths (approximately 80,000 deaths) annually. In Nigeria, the incidence of ACS was 59.1 people per 100 000 hospitalized adults per year according to a 2021 study.   in-hospital mortality was 8.1%. Mortality rates at 30 days, 3 months, 6 months, and 1 year were 8.7%, 9.9%, 10.9%, and 13.3%, respectively This increase in Nigeria and other developing nations can be attributed to urbanization and incorporation of western diet and lifestyle.

9. EPIDERMIOLOGY Sudden cardiac death is a prominent feature of ischemic heart disease with every 1 in 6 coronary attacks presenting with death as the first, last and only symptom. Despite these statistics, it is worth noting that the epidemiologic data shows a decline in the rates of death due to ischemic heart disease. This can be attributed to earlier treatment and prevention by risk factor modification.

10. PATHOPHYSIOLOGY Central to understanding myocardial ischemia is the concept of myocardial supply and demand. Myocardial demand refers to the amount of work being carried out by the cardiac muscles at any point in time. Myocardial supply refers to the amount of oxygen and blood required by the cardiac muscles to sustain a particular amount of work being carried out by the myocytes.

11. PATHOPHSIOLOGY

12. PATHOPHYSIOLOGY

13. PATHOPHYSIOLOGY The normal coronary circulation is dominated and controlled by the heart’s requirement for oxygen. This need is met by the ability of the coronary vascular bed to vary it’s resistance (and therefore it’s blood flow) considerably. This allows the myocardium to extract a high and relatively fixed percentage of oxygen.

14. PATHOPHYSIOLOGY: ATHEROSCLEROSIS The most common cause of myocardial ischemia is atherosclerotic disease of an epicardial coronary artery (or arteries) sufficient enough to limit myocardial blood flow. This leads to inadequate perfusion of the myocardium supplied by the coronary artery.

15. PATHOPHYSIOLOGY: ATHEROSCLEROSIS Atherosclerosis begins early in life with deposits of lipids in the vessel wall which tends to occur at sites of arterial shear stress such as bifurcations. It is also associated with abnormalities of endothelial function at that site. Plaques that are vulnerable to rupture are characterized by a lipid rich core, thin fibro-cellular cap, speckled calcification and inflammatory cells which release enzymes that degrade matrix proteins

16. RISK FACTORS FOR ATHEROSCLEROSIS NON-MODIFIABLE MODIFIABLE AGE (MOST IMPORTANT INDEPENDENT RISK FACTOR) SMOKING (MOST IMPORTANT MODIFIABLE RISK FACTOR) GENDER (PREMENOPAUSAL WOMEN HAVE LOWEST RISK) HYPERTENSION (ANTIHYPERTENSIVES REDUCE CVD MORTALITY, STROKE AND HEART FAILURE) FAMILY HISTORY AND GENETICS HYPERCHOLESTEROLEMIA RACE ( BLACK RACE AT INCREASED RISK) DIABETES MELLITUS HEMOSTATIC FACTORS (E.G ANTIPHOSPHOLIPID SYNDROME) PHYSICAL INACTIVITY OBESITY ALCOHOL INTAKE AND DIET

17. PATHOPHYSIOLOGY: ATHEROSCLEROSIS By reducing the lumen of the coronary arteries, atherosclerosis limits the appropriate increase in perfusion when the demand for more coronary blood flow occurs. The location of the obstruction determines the severity of the ischemia and clinical manifestations. More proximal arterial lesions usually lead to more ischemia and more severe disease than more more distal obstructions.

18. PATHOPHYSIOLOGY: ATHEROSCLEROSIS Progressive worsening of a stenosis in a proximal epicardial artery causes more distal vessels to vasodilate and reduce their resistance. When the distal vessels are maximally dilated, blood flow becomes dependent on the pressure in the coronary artery distal to the obstruction. In these circumstances, ischemia manifesting clinically as ST segment deviation can be precipitated by increases in myocardial oxygen demand caused by physical activity, emotional stress and/or tachycardia leading to poor myocardial contraction and relaxation and transient ventricular failure

19. RUPTURED ATHEROSCLEROTIC PLAQUE

20. PATHOPHYSIOLOGY:OTHER CAUSES OF MYOCARDIAL ISCHEMIA DECREASED OXYGEN SUPPLY INCREASED MYOCARDIAL DEMAND ANEMIA THYROTOXICOSIS CARBOXYHEMOGLOBINEMIA MYOCARDIAL HYPERTROPHY DUE TO AORTIC STENOSIS AND HYPERTENSION HYPOTENSION VASOSPASMS

21. PREVENTION Primary prevention aims to introduce lifestyle changes or therapeutic intervention to prevent ACS and other atherosclerotic diseases in the whole population of healthy individuals. Theses interventions include: Dietary and lifestyle changes Smoking: some countries have laws that prevent smoking in certain areas and this has been associated with decreased CVD risk Exercise: brisk walking, cycling, swimming for 20 minutes 2 to 3 times a week.

22. PREVENTION Secondary prevention involves instigating measures in individuals who have already had an event with the aim of reducing subsequent events. These include measures similar to those used in primary prevention as well as the use of medications to reduce the risk of subsequent events.

23. TYPES: STABLE ANGINA PECTORIS Occurs due to transient myocardial ischemia History Typically men > 50yrs or women > 60yrs complaining of chest discomfort Heaviness, pressure, squeezing, choking Rarely described as frank pain Clenched fist on sternum to localize pain (Levine sign) Lasts about 2 to 5 minutes, can radiate to either arm or shoulder, neck, jaw, teeth, epigastrium Mostly occurs during periods of exertion and relieved by rest and nitroglycerin

24. TYPES: STABLE ANGINA PECTORIS Some patients may report that discomfort occurs at a certain level of activity e.g. after climbing 2 flights of stairs Women, the elderly and diabetic patients may have atypical symptoms like dyspnea, nausea, fatigue, fearfulness.

25. TYPES: STABLE ANGINA PECTORIS Physical exam Usually unremarkable May have signs of atherosclerosis such as carotid bruits and diminished lower extremity pulses Signs of dyslipidemia such as xanthelasma and xanthomas Fundoscopy may reveal signs of hypertension such as increased light reflex and arteriovenous nicking Aortic stenosis causes a typical ejection murmur and should be excluded as it can also cause chest pain or discomfort in the absence of coronary arterosclerosis 3 rd and 4 th heart sounds may be heard due to transient left ventricular failure.

26. TYPES: NON ST-SEGMENT ELEVATED ACUTE CORONARY SYNDROMES One or more of the following three processes leads to coronary artery thrombosis Plaque fissure with inflammation Plaque fissure without inflammation Plaque erosion Leads to subendocardial ischemia or infarction. Two types differentiated by the presence or absence of elevated cardiac enzymes Unstable angina Non ST-segment elevated myocardial infarction

27. TYPES: NON ST-SEGMENT ELEVATED ACUTE CORONARY SYNDROMES History Chest discomfort which occurs at rest or with minimal exertion and usually lasts > 10 minutes Of relatively recent onset (< 2 weeks) More severe, prolonged or frequent than previous anginal episodes Anginal equivalents may occur in the elderly, women and diabetic patients

28. TYPES: NON ST-SEGMENT ELEVATED ACUTE CORONARY SYNDROMES Physical examination Large areas of ischemia or necrosis may lead to physical exam findings of diaphoresis, pale cool skin, sinus tachycardia, 3 rd and/or 4 th heart sounds, basilar crepitations or hypotension

29. TYPES: ST-SEGMENT ELEVATED MYOCARDIAL INFARCTION (STEMI) Occurs due to rupture or erosion of a vulnerable plaque leading to occlusion of the artery and myocardial necrosis in 15 – 30 minutes. Transmural ischemia History Severe chest pain or discomfort usually lasting for >20 minutes Does not respond to rest or sublingual glyceryl nitrate and usually requires opiate analgesia May radiate to the arms, elbows, shoulders, jaw Atypical symptoms may also be present, especially in elderly and diabetic patients

30. TYPES: ST-SEGMENT ELEVATED MYOCARDIAL INFARCTION (STEMI) Physical examination Pale, clammy, sweaty extremities Thready pulse Tachycardia hypotension

31. INVESTIGATIONS: ELECTROCARDIOGRAM An ECG in patients with chest pain should be performed within 10 minutes of first contact with the emergency medical team The initial ECG maybe normal or non-diagnostic in 1/3 of cases Hence, the ECG should be repeated every 15 minutes if initially normal and patient is still in pain

32. INVESTIGATIONS: ELECTROCARDIOGRAM

33. INVESTIGATIONS: ELECTROCARDIOGRAM LOCATION AFFECTED LEADS AFFECTED ARTERIES ANTERO-SEPTAL V1, V2, V3 LEFT ANTERIOR DESCENDING ARTERY ANTERO-LATERAL V4, V5, V6 LEFT ANTERIOR DESCENDING ARTERY LATERAL V5, V6, I, AVL LEFT CIRCUMFLEX ARTERY, LEFT ANTERIOR DESCENDING ARTERY INFERIOR II, III, AVF RIGHT CORONARY ARTERY, LEFT CIRCUMFLEX ARTERY POSTERIOR RECIPROCAL CHANGES ON V1 AND V2 RIGHT CORONARY ARTERY, LEFT CIRCUMFLEX ARTERY

34. INVESTIGATIONS: ELECTROCARDIOGRAM Stable angina, unstable angina, NSTEMI ST segment depression (>1mm for > 60 -80ms after the end of the QRS complex) T wave inversions tachycardia

35. INVESTIGATIONS: ELECTROCARDIOGRAM STEMI ST segment elevation (2mm or more above the isoelectric line) Left bundle branch block Should be repeated every 15 minutes if initially normal and patient still in pain Transient ST elevation can be seen with coronary vasospasms

36. INVESTIGATIONS: CARDIAC BIOMARKERS Cardiac troponins Cardiac troponins I, C, and T are proteins that form the microfilaments of cardiac myocytes and are important for cardiac contraction They get released into the bloodstream during periods of infarction There is no rise in unstable angina Levels of troponin T and I increase within 3 to 6 hrs of infarction, peak at 36hrs and remain elevated for 2 weeks If initially negative, repeat in 3hrs Also provides prognostic information as a higher levels carry higher mortality risk

37. INVESTIGATIONS: CARDIAC BIOMARKERS Creatinine kinase – myocardial band (CK-MB) An enzyme located in myocytes (skeletal and cardiac) that adds a phosphate group to creatinine Levels elevated in infarction Levels also elevated in conditions affecting skeletal muscles such as rhabdomyolysis, statin use, hypothyroidism etc. Not as specific and sensitive as cardiac troponins CK-MB levels start to climb at about 3 – 6hrs, peaking about 12 hours, and remains elevated for 1 to 2 days Not as good as troponin at detecting initial infarction but better for detecting re-infarction

38. INVESTIGATIONS Chest radiograph May demonstrate pulmonary edema if infarction has lead to pulmonary congestion Heart size is usually normal but there might be cardiomegaly due to pre-existing myocardial damage

39. INVESTIGATIONS Echocardiography Not routinely done for the diagnosis of MI but can be used when other diagnostic tests are inconclusive Detects ventricular wall motion abnormalities Also used to evaluate complications of MI such as mural thrombus, septal rupture, pericardial effusion e.t.c

40. INVESTIGATIONS Coronary angiogram Should be considered with a view of revascularization in the moderate to high risk patient including those who have failed medical treatment Used to visualize coronary arteries and identify points of obstruction Shows disease that may be amenable to percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG)

41. TREATMENT All patients with suspected acute coronary syndrome should be admitted urgently to the hospital due to the risk of death and recurrent infarction during the early unsteady phases. Adequate medical therapy can reduce the incidence of these complications by at least 60%. Patients should ideally be managed in a dedicated cardiac unit where necessary expertise, monitoring, and resuscitation facilities are available.

42. TREATMENT: ACUTE MANAGEMENT Analgesia Relieves stress and lowers adrenergic drive, thereby reducing vascular resistance, blood pressure and infarct size Intravenous morphine 5 – 10mg or intravenous diamorphine 2.5 – 5mg Should be given with an antiemetic (initially iv metoclopramide 10mg) Analgesia should be administered and titrated until the patient is comfortable

43. TREATMENT: ACUTE MANAGEMENT 2. Reperfusion Therapy: PCI is indicated for new bundle branch block or ST elevation in 2 contiguous leads of 1mm or more in limb leads or 2mm or more in the chest leads It is the treatment of choice in patients who present within the first 12hrs Should be considered within the first 24hrs even if the patient has re-perfused spontaneously or with thrombolytic therapy Improves mortality in STEMI patients with more than 95% 1 year survival rates in clinical trials Preserves LV function, reduces progression to heart failure and recurrent MI No immediate mortality benefit and hence not used in NSTEMI and unstable angina

44. TREATMENT: ACUTE MANAGEMENT 3. Thrombolysis Used if PCI cannot be done in a timely manner Although the survival advantage is not as good as primary PCI, mortality is reduced and maintained for at least 10 years Benefit greatest in the first 12hrs, especially first 2hrs Human tissue plasminogen activator analogues: Tenecteplase, Alteplase Major hazard in bleeding (4 extra cerebral hemorrhages per 1000 patients treated, 0.5 – 1% incidence of other major bleeds) Emergency PCI can be used if thrombolysis fails or is contraindicated

45. TREATMENT: ACUTE MANAGEMENT 4. Antiplatelets Oral aspirin 75 – 325mg daily has a 25% relative risk reduction in mortality First tablet (300mg) should be given within first 12 hours and then continued indefinitely P2y12 antagonists should be used with aspirin for up to 12 months Ticagrelor 180mg, followed by 90mg twice daily Prasugrel 60mg, followed by 10mg dly Clopidogrel 300mg, followed by 75mg dly

46. TREATMENT: ACUTE MANAGEMENT 5. Anticoagulants Anticoagulants reduce the risk of thromboembolic complications and prevent re-infarction Low molecular weight heparin (enoxaparin 1mg/kg twice daily) Unfractionated heparin, fondaparinux Continue for 8 days OR until discharge OR until coronary revascularization has been completed Oral anticoagulants can be considered in patients with persistent atrial fibrillation or extensive anterior wall infarction with mural thrombus GP IIb/IIIa receptor antagonists (abciximab, tirofiban) are reserved for those with heavy thrombus burden on angiography and for complications of PCI (e.g. distal embolization)

47. TREATMENT: ACUTE MANAGEMENT 6. Antianginals Sublingual glyceryl trinitrate (300-500mcg) is available as a first aid measure Iv nitrates (glyceryl trinitrate 0.6 – 1.2mg/ hr or isosorbide dinitrate 1 – 2mg/ hr ) are useful for the relief of recurrent or persistent ischemic pain IV beta-blockers (atenolol 5 – 10mg or metoprolol 5 – 15mg given over 5 minutes) relieves pain, reduces arrythmias and improves short term mortality in patients who present within 12hrs of symptom onset Beta-blockers should be avoided if there is heart failure, hypotension (SBP < 105mmhg), bradycardia (HR < 65b/m) or asthma

48. TREATMENT: ACUTE MANAGEMENT 6. Antianginals Calcium channel blockers (verapamil, diltiazem) can be used where beta-blockers are contraindicated

49. TREATMENT: LONG TERM MANAGEMENT RAAS Blockade Long term treatment with ACE inhibitors or ARBs counteract ventricular remodeling , improves survival, reduces MI, and avoids re-hospitalization. Caution in patients with hypovolemia or hypotension as these may be exacerbated by RAAS blockade Mineralocorticoids Antithrombotics Lipid lowering drugs Smoking cessation, dietary modification, exercise Rehabilitation Implantable defibrillators

50. TREATMENT: LONG TERM MANAGEMENT 7. Coronary artery bypass surgery This is a surgical procedure that aims to bypass narrowing's in heart arteries by using arteries or veins harvested from other parts of the body, thus restoring adequate blood supply to the previously ischemic heart. Usually reserved for complications of MI such as septal perforation or mitral regurgitation Operative mortality highest in the first two 72 hours

51. COMPLICATION MANIFESTATION TIMELINE Arrhythmic Heart blocks, atrial and ventricular arrythmias 1 to 3 days Ischemic Reinfarction, peri-infarct ischemia, infarct extension Most common in the initial few days Mechanical Mitral valve and chordae rupture/tear, ventricular septal defect (VSD), ventricular free wall rupture, tamponade, aneurysm Usually first week to first month Inflammatory Pericarditis, post-myocardial infarction (MI) Dressler syndrome First week to months (Dressler syndrome typically manifests days to weeks later) Systemic Cardiogenic shock, heart failure, embolic cerebrovascular accident, MI, and systemic and lower extremity embolism Within 24 hours.

52. PROGNOSIS The prognosis of patients is Who survive an ACS is related to the extent of residual myocardial ischemia, the degree of myocardial damage the presence of ventricular arrhythmias. In almost one-quarter of all cases of MI, death occurs within a few minutes without medical care. Half the deaths occur within 24 hours of the onset of symptoms and about 40% of all affected patients die within the first month. The prognosis of those who survive to reach hospital is much better, with a 28-day survival of more than 85%.

53. PROGNOSIS Patients with unstable angina have a mortality of approximately half that of patients with MI. Early death is usually due to an arrhythmia and is independent of the extent of MI. L ate outcomes are determined by the extent of myocardial damage, and unfavorable features include poor left ventricular function, AV block and persistent ventricular arrhythmias. The prognosis is worse for anterior than for inferior infarcts. Bundle branch block and high cardiac marker concentrations both indicate extensive myocardial damage. Old age, depression and social isolation are also associated with a higher mortality. Of those who survive an acute attack, more than 80% live for a further year, about 75% for 5 years, 50% for 10 years and 25% for 20 years

54. REFERENCES https://www.uptodate.com/contents/role-of-echocardiography-in-acute-myocardial-infarction https://pubmed.ncbi.nlm.nih.gov/34935419/ davidsons-principles-and-practice-of-medicine-2022-pdf-ghy-dr-notes.pdf dokumen.pub_kumar-amp-clarks-clinical-medicine-10th-edition-9780702078705.pdf harrison’s-principles-of-internal-medicine-21st-edition.pdf