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

2. CL, 55y/o CEO, severe substernal chest heaviness
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. CL, 55y/o CEO, severe substernal chest heaviness
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. CL, 55y/o CEO, severe substernal chest heaviness
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. CL, 55y/o CEO, severe substernal chest heaviness
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. CL, 55y/o CEO, severe substernal chest heaviness
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. 3. What are the risk factors for CAD?

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

14. 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

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

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

17. WHO CRITERIA FOR AMI (1979):
A patient is diagnosed with myocardial infarction if two (probable) or three (definite) of the following criteria are satisfied:
2. Changes in serial ECG tracings.
The current guidelines for the ECG diagnosis of acute myocardial infarction require at least 1 mm (0.1 mV) of ST segment elevation in the limb leads, and at least 2 mm elevation in the precordial leads. These elevations must be present in anatomically contiguous leads.[59] (I, aVL, V5, V6 correspond to the lateral wall; V1-V4 correspond to the anterior wall; II, III, aVF correspond to the inferior wall.)

18. WHO CRITERIA FOR AMI (1979):
A patient is diagnosed with myocardial infarction if two (probable) or three (definite) of the following criteria are satisfied:
3. Rise and fall of serum cardiac biomarkers such as creatinine kinase-MB fraction and troponin.
The horizontal line depicts the upper reference limit for the cardiac biomarker in the lab. The URL is that value representing the 99th percentile of a reference control group without STEMI. The kinetics of release of CK-MB and cardiac troponin in patients who do not undergo reperfusion are shown in the solid green and red curves as multiples of the URL. Note that when px with STEMI undergo reperfusion, as depicted in the dashed green and red curves, the cardiac biomarkers are detected sooner, rise to a higher peak value, but decline more rapidly, resulting in a smaller area under the curve and limitation of infarct size.

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

20. IN THE PATIENT: CRITERIA:
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
The current guidelines for the ECG diagnosis of acute myocardial infarction require at least 1 mm (0.1 mV) of ST segment elevation in the limb leads, and at least 2 mm elevation in the precordial leads. These elevations must be present in anatomically contiguous leads.[59] (I, aVL, V5, V6 correspond to the lateral wall; V1-V4 correspond to the anterior wall; II, III, aVF correspond to the inferior wall.)

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

22. 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

23. 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

24. Symptoms and PE of AMI 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)
1st week after STEMI: temp. up to 38 ⁰C
in transmural STEMI: (+) pericardial friction rub

25. Symptoms and PE seen in AMI which 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

26. 6. What is the ECG pattern of STEMI and NSTEMI?

27. CL, 55y/o CEO, severe substernal chest heaviness
Normal ECG PAttern

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. CL, 55y/o CEO, severe substernal chest heaviness
STEMI
ST segment elevation
Q – wave inversion

31. 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

32. 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
Four pathophysiologic processes that may contribute to the development of UA/NSTEMI have been identified: (1) plaque rupture or erosion with superimposed nonocclusive thrombus, believed to be the most common cause—NSTEMI may occur with downstream embolization of platelet aggregates and/or atherosclerotic debris; (2) dynamic obstruction [e.g., coronary spasm, as in Prinzmetal's variant angina (p )]; (3) progressive mechanical obstruction [e.g., rapidly advancing coronary atherosclerosis or restenosis following percutaneous coronary intervention (PCI)]; and (4) secondary UA related to increased myocardial oxygen demand and/or decreased supply (e.g., tachycardia, anemia).

33. 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

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

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

36. Classify AMI as to location based on ECG.

37. CL, 55y/o CEO, severe substernal chest heaviness
Location
Leads
Vessel
Anterior
V3-V4
LCA
Septal
V1-V2
LAD
Inferior
II, III, AVF
RCA
Lateral
V5-V6
L circumflex
Posterior
II, III, AVF, rV4 or marked depression V1-V4

38. ACUTE ANTERIOR MYOCARDIAL INFARCTION

39. ACUTE INFERIOR MYOCARDIAL INFARCTION

40. POSTEROLATERAL MYOCARDIAL INFARCTION

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

42. CL, 55y/o CEO, severe substernal chest heaviness

43. Location of AMI based on ECG –ANTERIOR

44. CL, 55y/o CEO, severe substernal chest heaviness
ECG of the Patient
ST segment depression on II, III and aVF
Marked ST elevation on I, aVL, V1-V6

45. 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

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

47. Early Management of AMI
Treatment: 1. Aspirin- rapidly inhibits COX-1 in platelets and reduces thromboxane A2. - chewed 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.

48. 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

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

50. Complications Ventricular remodeling Ventricular premature beats
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.

51. 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)

52. 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.

53. 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.

54. CL, 55y/o CEO, severe substernal chest heaviness
Complications
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

55. 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

56. Complications 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