Angina IHD ACS STEMI NSTEMI UA PCI Thrombolysis CABG

2. Content
 Introduction
 Initial management
 How to diagnosis
 Other Managements
 Complications
 Summary

3. IschemicHeart
Disease
STABLE
ANGINA
AcuteCoronary
Syndrome
STEMI
NSTEMI
Unstable
Angina

4. Angina
Origin
The term derives from the Latin angere ("to
strangle") and pectus ("chest"), and can therefore
be translated as "a strangling feeling in the chest".

6. Risk factors for CAD
A- Non modifiable risk factors:
1. Age: more than 45 in male; more 55 in female.
2. Male gender.
3. Family history.
B- Modifiable factors for CAD:
1. Hyperlipidemia: is a major risk factor for atherosclerosis,
2. Hypertension: roughly half of hypertensive patients will die of IHD or congestive heart failure.
3. Diabetes Mellitus: 2 folds increase in CAD.
4. Smoking: most powerful preventable risk factor, 3 folds increase in CAD.
5. Obesity: BMI more than 30 .
6. Decreased Physical activity

7. Precipitating factors:
 Anemia
 Fever
 Thyrotoxicosis.
 LV hypertrophy
 Tachycardia.

9. Initial management of ACS
 All patients with suspected ACS should have continuous ECG
monitoring and access to a defibrillator.
 Rapid examination to exclude hypotension, note the presence of
murmurs, and identify and treat acute pulmonary edema.
 Secure IV access.
 12 Lead ECG should be obtained and reported within 10 minutes of
presentation.
 Give the following:
• Oxygen (initially only 28% if history of COPD)
• Morphine 2.5–10 mg IV prn for pain relief + metoclopramide 10 mg IV
• Aspirin 300 mg po + Ticagrelor 180 mg
• Nitroglycerin, unless hypotensive
• B-blocker: eg metoprolol 50mg/12h
• Heparin IV
• Atorvastatin 80 mg qd

10. Cont…
 Take blood for the following:
• CBC/chemistries Supplement K+ to keep it at 4–5 mmol/L
• RBS acutely post-MI, even in nondiabetics, it will be high,
reflecting a stress-catecholamine response.
• Biochemical markers of cardiac injury (S.troponin).
• Lipid profile Total cholesterol <150, LDL <100, HDL >50,
triglycerides <200.
 Send for CXR to assess cardiac size and pulmonary edema and to
exclude mediastinal enlargement.

11. Conditions mimicking pain in ACS
• Pericarditis
• Dissecting aortic aneurysm
• Pulmonary embolism
• Esophageal reflux, spasm, or rupture
• Biliary tract disease
• Perforated peptic ulcer
• Pancreatitis

12. STEMI diagnosis
It is based on a combination of:
1. History.
2. ECG.
3. Biochemical markers of cardiac injury.

13. Presentation of STEMI
 Chest pain is usually similar in nature to angina, but of greater in
severity and longer duration (>30 min) and is not relieved by
sublingual (SL) nitroglycerin.
Associated features are nausea and vomiting, sweating,
breathlessness, and extreme distress.
 The pain may be atypical (e.g., epigastric) or radiate to the back.
 Diabetics and elderly or hypertensive patients may suffer painless
(“silent” infarcts) and/or atypical infarction. Presenting features
include:
• Breathlessness from acute pulmonary edema.
• Syncope or coma from arrhythmias.
• Acute confusional states (mania/psychosis).
• Diabetic hyperglycemic crises.
• Hypotension or cardiogenic shock.
• Central nervous system (CNS) manifestations resembling stroke
secondary tosudden reduction in cardiac output.
• Peripheral embolization.

14. ECG changes
• ST-segment elevation occurs within minutes and may last for up to 2 weeks.
ST elevation of >2 mm in 2 chest leads and >1 mm in 2 limb leads. Persisting
ST elevation after 1 month suggests formation of LV aneurysm.
• Non-diagnostic changes, but ones that may be ischemic, include new LBBB
or RBBB, tachyarrhythmias, transient tall-peaked T waves or T-wave
inversion, axis shift (extreme left or right), or AV block.
• Pathological Q waves should be 25% of the R wave, 0.04 s in duration, with
negative T waves.
• ST-segment depression in a second territory (in patients with ST-segment
elevation) is secondary to ischemia in a territory other than the area of
infarction (often indicative of multivessel disease) or reciprocal electrical
phenomena.
• PR-segment elevation/depression abnormal atrial rhythms such as atrial
fibrillation (AF) or flutter, wandering atrial pacemaker, and AV nodal rhythm.
• T-wave inversion generally persists after the ST elevation has resolved.

17. Biochemical markers of
cardiac injury
1. CK (creatine kinase) (22 to 198 U/L)
• Levels twice the upper limit of normal are considered abnormal.
• Serum levels rise within 4–8 hours post-STEMI and fall to normal within
3–4 days.
• False-positive rates of ~15% occur in patients with alcohol intoxication,
muscle disease or trauma, vigorous exercise, convulsions, IM injections,
hypothyroidism, pulmonary embolism (PE), and thoracic outlet syndrome.
2. Cardiac troponins (TnT, TnI) (<0.4 ng/mL)
• Highly sensitive and specific.
• Serum levels start to rise by 3 hours post-MI and elevation may persist up
to 7–14 days. This is advantageous for diagnosis of late MI.
• Troponins can also be elevated in nonischemic myocyte damage, such as
myocarditis, cardiomyopathy, and pericarditis.

18. STEMI: reperfusion by
primary PCI
Primary PCI criteria:
1. Presented before 120 min of onset.
2. A primary PCI program is available.
3. Can undergo catheterization without delay.
Indication for primary PCI
1. All patients with chest pain and ST-segment elevation or new LBBB
2. Patients in whom thrombolysis is contraindicated.
 Primary PCI compared to thrombolysis is:
• More cost-effective in the long term.
• Significant savings from fewer days (72 hours if no complications) in the
hospital.
• Less need for readmission.
• Less heart failure.

19. Cont…
Complications
1. Bleeding from arterial puncture site.
2. Stroke.
3. Recurrent infarction.
4. Need for emergency coronary artery bypass grafting
(CABG).
5. Death is (~1%).
Peri-primary PCI low-molecular-weight (LMW) or unfractionated
(UF) heparin, antiplatelet agents (e.g., gpIIb/IIIa inhibitors)
should be given.
Rescue PCI
Should be reserved for patients who remain symptomatic
post-thrombolysis (failure to reperfuse) or develop
cardiogenic shock.

21. STEMI: reperfusion therapy
(thrombolysis)
 Reperfusion occurs in 50%–70% of patients who receive thrombolysis
within 4 hours of onset of pain.
 Indications for thrombolysis
1. Patients with chest pain <12 hours and ST-segment elevation or new
LBBB.
2. Didn’t meet criteria of primary PCI.
Absolute contraindications to thrombolysis
• Active internal bleeding
• Suspected aortic dissection
• Recent head trauma and/or intracranial neoplasm
• Previous hemorrhagic stroke at any time
• Previous ischemic stroke within the past 1 year
• Previous allergic reaction to fibrinolytic agents
• Trauma and/or surgery within past 2 weeks at risk of bleeding

22. Cont…
Complications of thrombolysis
1. Bleeding is seen in up to 10% of patients. (Recombinant tissue-
type plasminogen activator (rtPA)).
2. Intracranial hemorrhage is seen in ~0.3% of patients treated with
SK and in ~0.6% with rtPA.
3. Hypotension during the infusion is common with SK.
4. Allergic reactions are common with SK and include a low-grade
fever, rash, nausea, headaches, flushing, and, rarely (0.1%),
anaphylaxis.
5. Reperfusion arrhythmias (most commonly a short, self-limiting
run of idioventricular rhythm) may occur.
6. Systemic embolization may occur from lysis of thrombus within
the left atrium, LV, or aortic aneurysm.

23. Other managements
 Control of cardiac pain
1. Oxygen should be administered at 2–5 L/min for at least 2–3 hours.
Hypoxemia is frequently seen (70%) In patients with refractory
pulmonary edema, endotracheal intubation may be necessary. Beware
of CO2 retention in patients with COPD.
2. Morphine 2.5–10 mg IV may be repeated after 5 min, unless there is
evidence of emerging toxicity (hypotension, respiratory depression).
(reversal with naloxone 400 µg to 2 mg IV).
Nausea and vomiting should be treated with metoclopramide (10 mg IV).
3. Nitrates (sublingual or IV) (50 mg in 50 mL normal saline at 1–10
mL/hr) titrated to pain and keeping SBP >100 mmHg.
Common side effects are headache and hypotension.
 Correction of electrolytes
Both low potassium and low magnesium may be arrhythmogenic and
must be supplemented.

24. Cont…
 B-Blocker (23% mortality decrease)
All patients should have early B-blockade.
Use a short-acting agent IV initially metoprolol 5 mg If hemodynamic
stability continues 15–30 minutes after the last IV dose, start
metoprolol 50 mg po bid. Continue for 1 year.
Absolute contraindications: heart rate (HR) <50, systolic blood
pressure (SBP) <90 mmHg, moderate to severe heart failure, AV
conduction defect, severe airways disease.
 Calcium antagonists (Amlodipine)
These are best avoided, especially in the presence of LV
impairment.
Used if B blockers are contraindicated.

25. Cont…
 ACE inhibitors (Captopril)
• All patients with STEMI/LBBB infarction should receive an ACE
inhibitor within the first 24 hours of presentation.
 Statins (HMG-CoA reductase inhibitors)
High-dose statins (e.g., atorvastatin 80 mg qd) have been shown to
reduce mortality and recurrent MI in the acute setting. Continue
for life.
 Anticoagulation
 LMWH
LMWH can be used at a prophylactic dose to prevent thromboembolic
events. (e.g., enoxaparin 30 mg IV bolus, then 1 mg/kg SC q12h).
• Anticoagulation should be continued for 8 days or until hospital
discharge.

26. Cont…
 Antithrombotic therapy (antiplatelets)
1. Aspirin (25% reduction in mortality)
(irreversible inhibition of cyclooxygenase enzyme)
(300 mg initially, then 75 mg daily) continued indefinitely (unless there
are contraindications.
2. Thienopyidines (ADP receptor blocker)
Clopidogrel In combination with aspirin (dual therapy), (600 mg, then
150 mg daily for a week, then 75 mg daily)
Ticagrelor (180 mg, then 90 mg twice daily) is more effective.
Continued for at least 1 month and ideally for 12 months (if there was
intervention).
3. Glycoprotein (gp) IIb/IIIa inhibitors (e.g. abciximab)
These are recommended routinely in the context of STEMI patients
treated with primary PCI and high risk NSTEMI.

27. Surgery for acute STEMI
CABG in the context of an acute STEMI is of value in the following situations:
1. High-risk coronary anatomy (Triple vessel disease) on catheterization (left
main stenosis, left anterior descending [LAD] ).
2. Complicated STEMI (acute mitral regurgitation, or ventricular rupture)

28. NSTEMI/UA: diagnosis
It is based on a combination of:
1. History.
2. ECG.
3. Biochemical markers of cardiac injury.

29. Presentation of
NSTEMI/Unstable angina
 New-onset angina (in a patient without prior
angina)
 Rest angina (angina when patient is at rest; may
occur in a patient with prior stable, exertional
angina)
 Increasing angina (crescent) (in a patient with
previously diagnosed angina for whom angina has
become more frequent or longer in duration or
requires a lower threshold to elicit)

30. Cont…
 Serial ECGs
1. ST-segment depression of >0.05 mV is highly specific of
myocardial ischemia (unless isolated in V1–V3, suggesting a
posterior STEMI).
2. T-wave inversion is sensitive but nonspecific for acute
ischemia unless very deep (>0.3 mV).
3. Rarely, Q waves
 Serial biochemical markers of cardiac injury
• These are used to differentiate between NSTEMI and UA.
• We recommend levels at 0, 6, and 12 hours after the last
episode of pain.
• A positive biochemical marker is diagnostic of NSTEMI. If
serial markers over a 24-hour period from the last episode of
chest pain remain negative, UA is diagnosed.

31. Management notes
 ACE inhibitors
Unlike patients with STEMI, no significant prognostic benefits,
 Thrombolysis
There is no evidence to benefit in patients with NSTEMI.

33. Discharge and secondary
prevention

34. Complications of MI
1. Arrhythmia:
 Transient supraventricular arrhythmia occur in 1/3 of patients.
 Unstable VT should be treated urgently with DC shock.
2. Bradyarrhythmia:
 Sinus bradycardia:
 1st degree & mobitz type 1:usually with INF.MI.
 Mobitz type II & complete heart block:
- Usually with anterior MI, carry bad prognosis & need
pacemaker.

35. Cont…
3. Right ventricular infarction:
• As hypotension , raised JVP, clear lungs.
• ECG: inferior MI+ ST elevation in V4.
• Treatment: IV fluid(NS), Inotropic agents, Usually improve with
time.
4. Papillary muscle rupture & VSD:
Usually present as cardiogenic shock. Need surgical
treatment.
5. Free wall rupture:
6. Cardiac aneurysm:
7. Pericarditis: Central chest pain, relieved by sitting forwards.
ECG: saddle-shaped ST elevation.
Treatment: NSAIDS. Echo to check for effusion

39. References
1. Oxford American Handbook of Cardiology
2. OXFORD HANDBOOK OF CLINICAL MEDICINE NINTH EDITION
3. Davidsons Principles and Practice of Medicine 22ed
4. Davidson’s Essentials of Medicine 2nd Edition
5. Medscape
6. Netter's Essential Physiology - 2nd Edition