CAD Investigation, Management and

Complications
Stable Angina

Investigation of Stable Angina Blood works

Details
Blood work CBC, RFT, FBS, HbA1c, Lipid profile, troponin if unstable
12 Lead ECG Exclude ACS
Pathological Q wave, left ventricular hypertrophy, BBB
Echocardiography Regional wall motion abnormalities, left ventricular ejection fraction,
diastolic function, alternative causes of chest pain.
Ambulatory ECG Paroxysmal arrhythmia
CXR Heart failure, pulmonary disease
CTCA CT calcium score 0: Unlikely angina, except in young might be soft plaque
CT calcium score 1- 400: CT coronary angiogram
CT calcium score > 400: Invasive coronary angiogram or functional imaging

Management of Stable Angina

Ticagrelor is the only antiplatelet that is given twice a day
 Acute Coronary Syndrome (ACS)

▪ Stable angina happens due to atherosclerosis.

▪ Unstable angina happens due to rupture plaque.
▪ STEMI: due to endocardial infarction
▪ NSTEMI: due to subendocardial infarction
ECG in STEMI
12-lead Precordial lead placement
▪ V1: 4th ICS, RIGHT margin of the sternum
▪ V2: 4th ICS along the LEFT margin of the sternum
▪ V4: 5th ICS, mid-clavicular line
▪ V3: midway between V2 and V4
▪ V5: 5th ICS, anterior axillary line (same level as V4)
▪ V6: 5th ICS, mid-axillary line (same level as V4)

ECG evolution during a STEMI

1. T wave is the first to change and last to normalize:

▪ 1st – “T” goes up (hyperacute tall T waves)
▪ then – “T” goes down (T wave inversion)
▪ lastly – “T” comes to place (T wave normalizes)

2. ST elevation:
▪ Appears after T wave goes up.
▪ Normalizes before T wave normalizes.

3. Q wave:
▪ Appears after ST elevation.
▪ Never returns to normal (persists) – also seen in old MI.
Localization of STEMI in ECG:
▪ Just remember that all the precordial leads are left-sided and hence, to detect the right
sided infarction, we need to place the leads on right side of chest.
As the precordial leads are placed sequentially to left, assign 2 precordial leads to each going
from medial to lateral:
A. V1 and V2: Septum
B. V3 and V4: Anterior part of left ventricle
C. V5 and V6: Lateral part of left ventricle
For limb leads: If you need a mnemonic for this:
A. aVF (‘F‘ stands for floor i.e. inferior part of left ventricle)
B. aVL (‘L‘ stands for lateral i.e. lateral part of left ventricle)

Reciprocal changes in STEMI: PAILS mnemonic

▪ Posterior ST Elevation – Anterior ST depression
▪ Anterior ST Elevation – Inferior ST depression
▪ Inferior ST Elevation – Lateral ST depression
▪ Lateral ST Elevation – Septal ST depression
▪ Septal ST Elevation – Posterior ST depression
▪ In Right sided infarction, you see reciprocal changes in V1-V4

ECGs

PVCs

▪ Anterolateral MI

Anterolateral MI
Inferior MI- in inferior MI always rule out RV infarction, Posterior MI and heart block

In patients with inferior STEMI, right ventricular infarction is suggested by:

▪ ST elevation in V1
▪ ST elevation in V1 and ST depression in V2 (highly specific for RV infarction)
▪ Isoelectric ST segment in V1 with marked ST depression in V2
▪ ST elevation in III > II
Diagnosis is confirmed by the presence of ST elevation in the right-sided leads (V3R-
V6R)
ST elevation in V4R has a sensitivity of 88%, specificity of 78% and diagnostic accuracy of
83% in the diagnosis of RV MI

Inferior MI and posterior MI

Leads V7-9 are placed on the posterior chest wall in

the following positions:
▪ V7 – Left posterior axillary line, in the same horizontal
plane as V6.
▪ V8 – Tip of the left scapula, in the same horizontal plane
as V6.
▪ V9 – Left paraspinal region, in the same horizontal plane
as V6.
Posterior MI
Clinical Significance of Posterior MI
▪ Posterior infarction accompanies 15-20% of STEMIs, usually occurring in the
context of an inferior or lateral infarction.
▪ Isolated posterior MI is less common (3-11% of infarcts).
▪ Posterior extension of an inferior or lateral infarct implies a much larger
area of myocardial damage, with an increased risk of left ventricular
dysfunction and death.
▪ Isolated posterior infarction is an indication for emergent coronary
reperfusion. However, the lack of obvious ST elevation in this condition
means that the diagnosis is often missed.
How to spot posterior infarction
▪ As the posterior myocardium is not directly visualised by the standard 12-
lead ECG, reciprocal changes of STEMI are sought in the anteroseptal leads
V1-3.
Posterior MI is suggested by the following changes in V1-3:
▪ Horizontal ST depression
▪ Tall, broad R waves (>30ms)
▪ Upright T waves
▪ Dominant R wave (R/S ratio > 1) in V2
In patients presenting with ischaemic symptoms, horizontal ST depression in
the anteroseptal leads (V1-3) should raise the suspicion of posterior MI
The anteroseptal leads are directed from the anterior precordium towards the internal surface
of the posterior myocardium. Because posterior electrical activity is recorded from the anterior
side of the heart, the typical injury pattern of ST elevation and Q waves becomes inverted:
▪ ST elevation becomes ST depression
▪ Q waves become R waves
▪ Terminal T-wave inversion becomes an upright T wave.
ECG changes in NSTEMI
▪ ST depression in 70-80%
▪ T wave inversion in 10-20%
▪ Combined ST depression and T wave inversion
▪ Normal ECG

Cardiac Enzymes

Management of ACS
Percutaneous Coronary Intervention
▪ PCI is the process of dilating a coronary artery stenosis by introducing an inflatable
balloon and metallic stent into the arterial circulation via the femoral, radial or brachial
artery.
▪ Complications of PCI include bleeding, haematoma, dissection and pseudoaneurysm
from the arterial puncture site, although use of the radial artery reduces these risks and
is the standard technique.
▪ Serious complications include acute myocardial infarction (2%), stroke (0.4%) and death
(1%).

Fibrinolysis
▪ Fibrinolytic agents enhance the breakdown of occlusive thromboses by the activation of
plasminogen to form plasmin.
▪ Fibrinolysis is still used if PCI is unavailable.
▪ Prompt reperfusion therapy (door to needle time < 30 minutes) will reduce the death
rate following MI.
▪ For patients who fail to reperfuse by 60–90 minutes, as demonstrated by 50% resolution
of the ST-segment elevation, re-thrombolysis or referral for rescue coronary angioplasty
is recommended.

Fibrinolysis
▪ Fibrinolytic agents enhance the breakdown of occlusive thromboses by the activation of
plasminogen to form plasmin.
▪ Fibrinolysis is still used if PCI is unavailable.
▪ Prompt reperfusion therapy (door to needle time < 30 minutes) will reduce the death
rate following MI.
▪ For patients who fail to reperfuse by 60–90 minutes, as demonstrated by 50% resolution
of the ST-segment elevation, re-thrombolysis or referral for rescue coronary angioplasty
is recommended.
Coronary Artery Bypass Grafting
▪ With CABG, autologous veins or arteries are anastomosed to the ascending aorta and
to the native coronary arteries distal to the area of stenosis.

The other medications in treatment of ACS:

▪ Beta blocker
▪ ACEI/ARBs
▪ Statin
▪ As a general rule all ACS patient should be loaded with DAPT (Dual antiplatelet
therapy), so given a high dose of aspirin and another anti-platelet at the time of
presentation and then regular doses thereafter.

Complications of Myocardial Infarction

Heart Failure
▪ Cardiac failure post STEMI is a poor prognostic feature that necessitates medical and
invasive therapy to reduce the death rate.
▪ The Killip classification is used to assess patients with heart failure post-MI:
▪ Killip I – no crackles and no third heart sound
▪ Killip II – crackles in < 50% of the lung fields or a third heart sound
▪ Killip III – crackles in > 50% of the lung fields
▪ Killip IV – cardiogenic shock.
Myocardial rupture and aneurysmal dilatation
▪ Rupture of the free wall of the left ventricle is usually an early, catastrophic and fatal
event.
▪ The patient will have a haemodynamic collapse, then an electromechanical cardiac arrest.
▪ A sub-acute rupture may allow for pericardiocentesis followed by surgical repair of the
rupture.
▪ Aneurysmal dilatation of the infarcted myocardium is a late complication that may
require surgical repair.

Ventricular septal defect

▪ A ventricular septal defect (VSD) may occur in 1–2.0% of patients with STEMI, and may
be associated with delayed or failed fibrinolysis.
▪ However, mortality is very high and there is a 12-month inoperative mortality of 92%.
▪ An intra-aortic balloon pump (IABP) and coronary angiography may allow patient
optimization prior to surgery.

Mitral regurgitation
▪ Severe mitral regurgitation can occur early in the course of STEMI.
▪ Three mechanisms may be responsible for the mitral regurgitation, and a TOE may be
necessary to confirm the aetiology:
▪ Severe left ventricular dysfunction and dilatation, causing annular dilatation of the valve
and subsequent regurgitation
▪ Myocardial infarction of the inferior wall, producing dysfunction of the papillary muscle
that may respond to coronary intervention
▪ Myocardial infarction of the papillary muscles, producing sudden severe pulmonary
oedema and cardiogenic shock (IABP, coronary angiography and early surgery may
improve patient survival).

Cardiac arrhythmias
▪ Ventricular tachycardia and ventricular fibrillation are common in STEMI, particularly
with reperfusion. Cardiac arrest requires defibrillation.
▪ Atrial fibrillation occurs frequently, and treatment with beta-blockers and digoxin may
be required. Cardioversion is possible but relapse is common.
▪ Bradyarrhythmias can be treated initially with i.v. atropine 0.5 mg. Temporary
transcutaneous or transvenous pacemaker insertion may be necessary in patients with
symptomatic heart block.

Conduction disturbances
▪ These are common following MI.
▪ AV block may occur during acute MI, especially of the inferior wall (the right coronary
artery usually supplies the sinoatrial and atrioventricular nodes).
▪ Heart block, when associated with haemodynamic compromise, may need treatment
with atropine or a temporary pacemaker.
▪ Such blocks may last for only a few minutes, but frequently continue for several days.
▪ Permanent pacing may need to be considered if heart block persists for over 2 weeks.
 Post-MI pericarditis and Dressler syndrome
▪ This occurs in about 20% of patients in the first few days following MI.
▪ It is more common with anterior MI and STEMI with high serum cardiac enzymes, but its
incidence is reduced to 5–6% with thrombolysis.
▪ Pericarditis may also be present later on in the recovery phase after infarction.
▪ It is usually a feature of Dressler syndrome, an autoimmune response to cardiac damage
occurring 2–10 weeks' post infarct.
▪ Autoimmune reaction to myocardial damage is the main aetiology, and antimyocardial
antibodies can often be found.
▪ Recurrences are common.

Post-ACS lifestyle modification

▪ After recovery from an ACS, patients should be encouraged to participate in a cardiac
rehabilitation programme that provides education and information appropriate to their
requirements. An exercise programme forms part of the rehabilitation.
▪ Dietary recommendations include calorie control of obesity, increased fruit and
vegetables, reduced trans and saturated fats, and reduced salt intake in patients with
hypertension.
▪ Alcohol consumption should be maintained within safe limits (≤ 21 units/week for men
or ≤ 14 units for women) and avoid binge drinking.
▪ Patients should be physically active (30 min of moderate aerobic exercise 5 times per
week).
▪ Patients should stop smoking (nicotine patches and buprenorphine are safe).
▪ A healthy weight BMI < 25 kg/m2 should be maintained.
▪ Blood pressure and diabetes control.
▪ Pharmacotherapy for CAD
Theopoetic goal Drug class Example agent Specific Indication
Antiplatelet Aspirin: 75–162 mg PO once daily Recommended for all
agents Clopidogrel: in patients with contraindications patients with CAD
to aspirin→ 75 mg PO once daily
Dual antiplatelet therapy with aspirin and
Secondary clopidogrel may be used in certain
prevention circumstances.
ACEIs or Preferred: ACE inhibitors, e.g., lisinopril (2.5– Indicated in patients with
ARBs 10 mg PO once daily), ramipril concomitant:
Alternative: ARBs, e.g., losartan (25–100 mg Hypertension
PO once daily), valsartan (20–160 mg PO Diabetes mellitus
twice daily) LVEF ≤ 40%
Chronic kidney disease
Secondary Beta Carvedilol (6.25–25 mg PO every 12 hour) Consider for all patients
prevention and Blocker Metoprolol (usual dosage 50–100 mg PO with stable angina.
antianginal every 12 hours)
treatment Bisoprolol (usual dosage 2.5–10 mg PO once
daily)
Antianginal Nitrates Short-acting nitrate: nitroglycerin sublingual Short-acting nitrates:
treatment tablets→ 0.3–0.6 mg sublingual at first sign of Can prevent exertional
angina; may repeat every 5 minutes for up to angina
15 minutes Suitable for relief of
Long-acting nitrates: acute angina
Isosorbide dinitrate→ 5–40 mg PO 2–3 times Long-acting nitrates:
daily adjunctive or alternative
Isosorbide mononitrate→ 30–60 mg PO once long-term treatment to
daily beta blockers in patients
with stable angina.