1. SGD 1: AMI CL, 55y/o M, CEO, severe substernal chest heaviness

2. SALIENT FEATURES 55 y/o M, CEO severe substernal chest heaviness accompanied by nausea and vomiting History of having episodes of mild substernal chest tightness for the last 5 yrs a known hypertensive for 6 yrs (Usual BP: 130/80, Highest BP: 170/100) Irregular intake of Nifedipine 30mg

3. SALIENT FEATURES 40 pack years of cigarette smoking heavy alcohol beverage drinker Family History (+ ) premature CAD sister, 38 and brother, 45 (+ ) HTN father (+ ) DM mother

4. SALIENT FEATURES Soft S1 murmur on PE Laboratory tests 12 lead ECG: NSR, ST segment elevation I, aVL, V1-V6; ST segment depression II, III, aVF Troponin I – 1.5ng/mL CPK-MB – 256u/L CXR: cardiomegaly

5. SALIENT FEATURES Cont’d Echo –Doppler: Eccentric LVH w/ segmental wall motion abnormality Ejection fraction at 48% Doppler evidence off impaired LV relaxation Dilated LA Dilated Aortic Root Aortic Sclerosis

6. Diagnosis Ischemic Cardiac Disease with an Eccentric Left Ventricular Hypertrophy with segmental wall motion abnormality, a Dilated Left Atrium and Aortic Root, and Aortic Sclerosis with evident ST Elevation Myocardial Infarction (STEMI) and Normal Sinus Rhythm, of Class IV-D Functional Disability

7. 2. Differentiate between ATHEROGENESIS and ATHEROTHROMBOSIS

8. Atherogenesis The process of forming atheromas, plaques in the inner lining (the intima) of arteries. It involves elements of inflammation, a process that provides a unifying theme in the pathogenesis of atherosclerosis

9. Atherogenesis

10. Atherothrombosis Characterized by an unpredictable, sudden disruption (rupture or erosion/fissure) of an atherosclerotic plaque, which leads to platelet activation and thrombus formation. It is the underlying condition that results in events leading to myocardial infarction, ischemic stroke, and vascular death.

11. Atherothrombosis

12. What are the risk factors for CAD?

13. RISK FACTORS OF CAD Family history of premature CAD Sex (Male) Increasing age (>35 years old) Hyperlipidemia Hypertension Stress Diabetes mellitus Obesity Lack of regular exercise High - fat diet Cigarette smoking Too much alcohol

14. What risk factors are present in this patient?

15. RISK FACTORS PRESENT IN THE PATIENT (+) Family history of premature CAD (sister at age 38 and brother at age 45) Sex (Male) Age (55 years old) Known hypertensive for 6 years – Highest BP = 170/100 mmHg – Irregular intake of Nifedipine 30 mg Forty (40) pack years of cigarette smoking Stress – Occupation: CEO – Had an argument during regular board meeting Heavy alcoholic beverage drinker

16. 4. What are the WHO criteria for acute myocardial infarction? Are they present in this patient?

17. WHO CRITERIA FOR AMI (1979): 1. Clinical history of ischemic type of chest pain lasting for more than 20 minutes. A patient is diagnosed with myocardial infarction if two (probable) or three (definite) of the following criteria are satisfied:

18. WHO CRITERIA FOR AMI (1979): 2. Changes in serial ECG tracings. A patient is diagnosed with myocardial infarction if two (probable) or three (definite) of the following criteria are satisfied:

19. WHO CRITERIA FOR AMI (1979): 3. Rise and fall of serum cardiac biomarkers such as creatinine kinase- MB fraction and troponin. A patient is diagnosed with myocardial infarction if two (probable) or three (definite) of the following criteria are satisfied:

20. REDEFINED WHO CRITERIA FOR AMI (2000): Cardiac troponin rise accompanied by either:  Typical symptoms  Pathological Q waves  ST elevation or depression  Coronary intervention The WHO criteria were refined in 2000 to give more prominence to cardiac biomarkers.

21. IN THE PATIENT: Severe substernal heaviness (experienced about 1 hour) ST segment elevation I, aVL, V1-V6 Troponin I: 1.5ng/mL (NV: 0 – 0.4 ng/mL) CPK-MB: 256 u/L (NV: <1 u/L) ST segment depression II, III and aVF Clinical history of ischemic type chest pain lasting > 20 mins Changes in serial ECG tracings Rise and fall of cardiac biomarkers Cardiac troponin rise accompanied by ST depression CRITERIA:

22. 5.What are the clinical features(Sx and PE) of AMI? Are they present in this patient?

23. Symptoms and PE of AMI Chest pain – described as a pressure sensation, fullness, or squeezing in the midportion of the thorax – may radiate to the arms, jaw or teeth, shoulder, and/or back Associated diaphoresis or sweating palpitations, weakness Substernal chest pain for >30 mins and diaphoresis strongly suggests STEMI Presence of a precipitating factor: – Vigorous physical activity – Emotional stress – Illness: medical or surgical

24. Symptoms and PE of AMI Associated with dyspnea or shortness of breath Associated epigastric discomfort with or without nausea and vomiting Syncope or near-syncope without other cause Impairment of cognitive function without other cause lightheadedness or loss of consciousness a look of anxiety, or a sense of impending doom or death It may occur at any time of the day, but most appear to be clustered around the early hours of the morning, are associated with demanding physical activity, or both

25. PE Signs of ventricular dysfunction: – (+) S3 and S4 – Decreased intensity of S1 – Paradoxical splitting of S2 Transient midsystolic or late systolic apical systolic murmur (mitral valve apparatus dysfunction) Anterior infraction (1/4 of pxs): sympathetic hyperactivity – Tachycardia, hypertension Posterior infarction (1/2 of pxs): parasympathetic hyperactivity – Bradycardia, hypotension Carotid pulse decreased in volume (reduced stroked volume) 1 st week after STEMI: temp. up to 38 ⁰C in transmural STEMI: (+) pericardial friction rub Symptoms and PE of AMI

26. Symptoms and PE seen in AMI wc is present in our patient (+) precipitating factor – Emotional stress: started after argument during board meeting (+) Chest pain (severe substernal chest heaviness) not relieved by rest (+) weakness, sweating ( due to sympathetic activity), nausea, vomiting anxiety Soft S1

27. What is the ECG pattern of STEMI and NSTEMI?

28. STEMI ECG FINDINGS ST-segment elevation of at least 1 mm in two or more limb leads

29. STEMI ECG FINDINGS At least 2 mm ST segment elevation in two or more precordial leads

30. Non-ST Elevation Myocardial Infarction Example of an acute coronary syndrome closely related to unstable angina Difference primarily in whether the ischemia is severe enough to cause sufficient myocardial damage to release detectable quantities of a marker of myocardial injury Diagnosis of NSTEMI is established if a patient with the clinical features of UA develops evidence of myocardial necrosis, as reflected in elevated cardiac biomarkers

31. Pathophysiology Most commonly caused by a reduction in oxygen supply and/or by an increase in myocardial oxygen demand superimposed on an atherosclerotic coronary plaque, with varying degrees of obstruction

32. History and Physical Exam Clinical Hallmark: chest pain – typically located in the substernal region or sometimes in the epigastrium, that radiates to the neck, left shoulder, and left arm Large area of myocardial ischemia or a large NSTEMI – Diaphoresis – pale cool skin – sinus tachycardia – a third and/or fourth heart sound – basilar rales – sometimes hypotension

33. ECG NSTEMI In UA, – ST-segment depression – transient ST-segment elevation – T-wave inversion

34. Non-ST Elevation Infarction ST depression & T-wave inversion The ECG changes seen with a non-ST elevation infarction are: Before injuryNormal ECG ST depression & T-wave inversion ST returns to baseline, but T-wave inversion persists IschemiaInfarction Fibrosis

35. Classify AMI as to location based on ECG.

36. ACUTE ANTERIOR MYOCARDIAL INFARCTION

37. ACUTE INFERIOR MYOCARDIAL INFARCTION

38. POSTEROLATERAL MYOCARDIAL INFARCTION

39. What is the location of the AMI in this patient based on his ECG?

40. Early Management of AMI Key points Recognition of symptoms by the patient and prompt seeking of medical attention Rapid deployment of emergency medical team capable of performing resuscitative measures Expeditious transport of patient to hospital Early treatment without more delay

41. Early Management of AMI Goals of Management Control of cardiac discomfort Rapid identification of patients in need of urgent reperfusion therapy

42. Early Management of AMI Treatment: 1. Aspirin- rapidly inhibits COX-1 in platelets and reduces thromboxane A2. - chewed 160- 325 mg tablet 2. Presence of hypoxemia- Oxygen supplementation (2-4 L/ min) 3. Nitroglycerin(sublingual) – 3 doses of 0.4 mg at 5 min intervals to relieve chest pain and decrease preload and dilate infarcted coronary or collateral vessels.

43. Early Management of AMI 4. Nitroglycerin (intravenous)- given when there is return of chest pain accompanied with ST- segment of T-wave shifts. 5. Beta-blockers- diminish myocardial O2 demand and ischemia, reduces the risk of ventricular fibrillation. 6. Reperfusion therapy- by fibrinolysis or primary Percutaneous Coronary Intervention. - done if ST- segment elevation is at least 2mm in 2 contiguous precordial leads and 1 mm in 2 adjacent limb leads present

44. 8. What are the possible complications of AMI?

45. Complications Ventricular remodeling left ventricle undergoes a series of changes in shape, size, and thickness in both the infarcted and noninfarcted segments Precedes clinically evident CHF in months to years after infarction Progressive dilation and its clinical consequences may be ameliorated by therapy with ACE inhibitors and other vasodilators (e.g., nitrates). Ventricular premature beats – Infrequent, sporadic ventricular premature depolarizations occur in almost all patients with STEMI and do not require therapy. – hypokalemia and hypomagnesemia are risk factors for ventricular fibrillation in patients with STEMI; the serum potassium concentration should be adjusted to approximately 4.5 mmol/L and magnesium to about 2.0 mmol/L.

46. Complications Ventricular tachycardia and fibrillations – Within the first 24 h of STEMI, ventricular tachycardia and fibrillation can occur without prior warning arrhythmias. – The occurrence of ventricular fibrillation can be reduced by prophylactic administration of intravenous lidocaine. – Ventricular arrhythmias, including the unusual form of ventricular tachycardia known as torsades des pointes, may occur in patients with STEMI as a consequence of other concurrent problems (such as hypoxia, hypokalemia, or other electrolyte disturbances) or of the toxic effects of an agent being administered to the patient (such as digoxin or quinidine)

47. Complications Accelerated idioventricular rhythm (AIVR, "slow ventricular tachycardia") – Ventricular rhythm with a rate of 60–100 bpm, occurs in 25% of patients with STEMI. – Often occurs transiently during fibrinolytic therapy at the time of reperfusion. – Benign and does not presage the development of classic ventricular tachycardia. – Most episodes do not require treatment if the patient is monitored carefully, as degeneration into a more serious arrhythmia is rare. Sinus bradycardia – Treatment of sinus bradycardia is indicated if hemodynamic compromise results from the slow heart rate. Atropine is the most useful drug for increasing heart rate and should be given intravenously in doses of 0.5 mg initially.

48. Complications Recurrent chest discomfort – Recurrent angina develops in ~25% of patients hospitalized for STEMI. – Higher in patients who undergo successful fibrinolysis. – Since recurrent or persistent ischemia often heralds extension of the original infarct or reinfarction in a new myocardial zone and is associated with a near tripling of mortality after STEMI, patients with these symptoms should be referred for prompt coronary arteriography and mechanical revascularization. – Repeat administration of a fibrinolytic agent is an alternative to early mechanical revascularization. Pericarditis – Pericardial friction rubs and/or pericardial pain are frequently encountered in patients with STEMI involving the epicardium. – It is important to diagnose the chest pain of pericarditis accurately, since failure to recognize it may lead to the erroneous diagnosis of recurrent ischemic pain and/or infarct extension, with resulting inappropriate use of anticoagulants, nitrates, beta blockers, or coronary arteriography. – Pain radiating to either trapezius muscle is helpful since such a pattern of discomfort is typical of pericarditis but rarely occurs with ischemic discomfort. – Managed with aspirin (650 mg four times daily). Anticoagulants should not be used since it can produce tamponade

49. Complications Thromboembolism – Clinically apparent thromboembolism complicates STEMI in ~10% – Embolic lesions are found in 20% of patients in necropsy series, suggesting that thromboembolism is often clinically silent. – Considered to be an important contributing cause of death in 25% of patients with STEMI who die after admission to the hospital. – Arterial emboli originate from LV mural thrombi, while most pulmonary emboli arise in the leg veins. – Occurs in association with large infarcts (especially anterior), CHF, and a LV thrombus detected by echocardiography. – Arterial embolism often presents as a major complication, such as hemiparesis when the cerebral circulation is involved or hypertension if the renal circulation is compromised. – Systemic anticoagulation for 3–6 months is probably prudent Left Ventricular Aneurysm – dyskinesis or local expansile paradoxical wall motion – Complications of LV aneurysm do not usually occur for weeks to months after STEMI they include CHF, arterial embolism, and ventricular arrhythmias. – Apical aneurysms are the most common and the most easily detected by clinical examination. – The physical finding of greatest value is a double, diffuse, or displaced apical impulse. Ventricular aneurysms are readily detected by two-dimensional echocardiography, which may also reveal a mural thrombus in an aneurysm. – readily detected by two-dimensional echocardiography