Coronay Artery Disease

Dr. Bibek Poudel

Department of Medicine
City Medical College Hospital
 Coronary Artery Disease(CAD) is the commonest cause of angina and acute
coronary syndrome(ACS).
 It is one of the leading cause of death in the world.
 In vast majority of the patient, it is caused by Atherosclerosis but rarely it can
occur due to aortitis, vasculitis and autoimmune connective tissue diseases.
 ATHEROSCLEROSIS

 Atherosclerosis is a progressive infllammatory disorder of the arterial wall that is characterised by focal lipid-rich deposits
of atheroma that remain clinically silent until they become large enough to impair tissue perfusion, or until ulceration and
disruption of the lesion occurs resulting in thrombotic occlusion or diistal embolisation of the vessel.
 Pathophysiology: The development of atherosclerosis follows endothelial dysfunction, with increased permeability and
accumulation of oxidized lipoproteins, which are taken up by macrophages at focal sites within the endothelium to produce
lipid-laden foam cells. Release of cytokines, such as platelet-derived growth factor and transforming growth factor beta
(TGF-β), by monocytes, macrophages or the damaged endothelium promotes further accumulation of macrophages, as well
as smooth muscle cell migration and proliferation. The proliferation of smooth muscle with the formation of a layer of cells
covering the extracellular lipid separates it from the adaptive smooth muscle thickening in the endothelium. Collagen is
produced i n larger and larger quantities by the smooth muscle and the whole sequence of events cumulates as an ‘advanced
or raised fibrolipid plaque’. The ‘advanced plaque’ may grow slowly and encroach on the lumen, or become unstable,
undergo thrombosis and produce an obstruction (‘complicated plaque’).
ANGINA PECTORIS

 Angina pectoris is a symptom complex characterized by transient myocardial

ischaemia, which occurs whenever there is imbalance between myocardial
oxygen supply and demand.

 Two types: Stable Angina and Unstable Angina

STABLE ANGINA
 STABLE ANGINA

• Characterized by: central chest pain, discomfort or breathlessness

that is precipitated by – physical exertion, cold exposure, heavy
meals, intense emotion and relieved by rest. The pain is
tightening, squeezing or choking in nature and usually lasts for 2-
5 minutes.

• When the patient is asked to localize the sensation, he or she

typically places a hand over the sternum, sometimes with a
clenched fist, to indicate a squeezing, central, substernal
discomfort (Levine’s sign).

• Look for signs of anaemia and thyrotoxicosis as they may

precipitate angina
Investigations

1. ECG/EKG: A 12-lead ECG recorded at rest may be normal in patients with typical angina pectoris. Therefore an
exercise ECG is commonly performed. The ischemic ST-segment response generally is defined as flat or downsloping
depression of the ST segment >0.1 mV below baseline.
2. If diagnosis is unclear, CT coronary Angiography is the imaging investigation of first choice.
3. Stress Echocardiography
4. Myocardial perfusion scanning: A perfusion defect present during stress but not at rest provides evidence of reversible
myocardial ischaemia), whereas a persistent perfusion defect seen during both phases of the study is usually indicative
of previous MI.
5. Other baseline investigations for assessing risk factors: CBC,CRP, RBS, Urine R/E, Fasting lipid profile, Chest X-ray.
Management

 General Measures: a) Reassurance and explaination.

b) Complete cessation of smoking.
c) Identification and treatment of aggravading factors like anemia.
 Management of Dyslipidemia: All patients should be prescribed a statin, even if the serum cholesterol
concentration is normal.
 Antiplatelet drugs: Aspirin 75mg or Clopidogrel 75mg once daily should be prescribed.
Acute Coronary Syndrome(ACS)

 ACS encompasses both unstable angina and MI.

 Unstable angina is characterized by new-onset or rapidly worsening angina
(crescendo angina), angina on minimal exertion or angina at rest in the absence of
myocardial injury.
 Myocardial infarction (MI) is distinguished from unstable angina by the
occurrence of myocardial necrosis and is diagnosed when myocardial injury
occurs in the presence of clinical evidence of acute myocardial ischaemia.
 Pain in MI

 Criteria of MI pain: sudden, severe,central or diffuse chest pain

lasting for more than 30 min which is tightening, squeezing or
choking in nature, radiate to neck, lower jaw, left shoulder, medial
aspect of left arm and forearm, aggravaded by exertion, emotion or
stress, not relieved by NSAID, GTN or taking rest, associated with
sweating, vomiting and fear of impending death.
 Pain may be absent if Diabetic neuropathy, autonomous neuropathy,
leprosy, age >80 years.
 Investigations

 Serial ECG: Initial ECG may be normal or non

diagnostic in one third of the cases. It may be difficult
to interpret if there is BBB or previous MI. The earliest
ECG change is usually ST-segment deviation.
 Serial Cardiac Biomarkers: Troponin-I is more specific than other markers.

Enzyme Initial rise Peak Back to Normal

Myoglobin 2 hrs 6-9 hrs 1 day

CK-MB 4-6 hrs 12 hrs 48-72 hrs

Troponin-I 4-6 hrs 72 hrs 2 weeks

 CXR- exclude severe pneumonia, tension pneumothorax.
Cardiomegaly may be found.
 Echocardiography.
 Coronary Angiography.
Criteria for diagnosis of MI

 The term acute myocardial infarction (MI) should be used when there is acute myocardial injury with
clinical evidence of acute myocardial ischaemia and with detection of a rise and/or fall of cardiac troponin
values with at least one value above the 99th centile upper reference limit and at least one of the following
a. Symptoms of myocardial ischaemia
b. New ischaemic ECG changes
c. Development of pathological Q waves
d. Imaging evidence of new loss of viable myocardium or new regional wall motion .
abnormality in a pattern consistent with an ischaemic aetiology
e. Identifiation of a coronary thrombus by angiography or autopsy
Management of Acute MI

 Immediate admission of the patient in CCU.

 Anti- thrombotic therapy: Tab. Aspirin 300mg + Clopidogrel 600mg
 Analgesia: IV Morphine plus injectable antiemetics
 Anti-anginal therapy: sublingual GTN or injectable nitrates
 Immediate reperfusion therapy with PCI is indicated when the ECG shows new
bundle branch block or characteristic ST-segment elevation in two contiguous
leads of 1 mm or more in the limb leads or 2 mm or more in the chest leads. This
is the treatment of choice for those presenting within 12 hours of symptom onset.
 Thrombolytic therapy: If primary PCI cannot be achieved in a timely manner in
ST-elevated MI patients, thrombolytic therapy should be administered. The
benefit of thrombolytic therapy is greatest in those patients who receive treatment
within the first 12 hours and especially the first 2 hours. Streptokinase or Altepase
is used.
 LMW Heparin such as subcutaneous Heparin(Enoxaparin) is used in non ST-
elevayed MI.
 Renin Angiotensin Blockers: Long-termtreatment with ACE inhibitors such as enalapril (10 mg twice daily)
or ramipril (2.5–5 mg twice daily) can counteract ventricular remodelling, prevent the onset of heart failure,
improve survival, reduce recurrent MI and avoid rehospitalisation.
 Lipid lowering agents such as Atorvastatin
 Managent of associated risk factors such as DM
 Coronary Artery Bypass Graft(CABG) if indicated.
Complications of MI

# Cardiac Arrythmias # Papillary muscle rupture

# Recurrent angina # Ventricular septal rupture
# Acute Heart failure # Ventricular rupture
# Pericarditis # Embolism
# Dressler syndrome # Ventricular remodelling
# Ventricular Aneurysm
Prognosis of MI

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%. Patients with unstable angina have a mortality of approximately half that of patients with MI. Early death
is usually due to an arrhythmia.

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.