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Diagnosis?

• A 45 year old male, smoker presented with


chest pain lasting> 30 min and has a BP of
60/30. ECG shows widespread ST segment
depression. Echo shows an EF of 20%.
• What should be the treatment?
• PCI
Acute coronary syndromes
• Spectrum of clinical conditions ranging
from unstable angina to non-ST segment
elevation MI (ST segment elevation
generally absent), and ST segment elevation
infarction (persistent ST segment elevation)
and sudden cardiac death
Acute coronary syndromes
• Acute myocardial ischaemic states
• Chest pain is due to insufficient blood
supply to the heart muscle that results from
coronary artery disease
• A major cause of emergency medical care
and hospitalisation in the country
Unstable angina
• A clinical syndrome between stable angina and
acute MI
• Three main presentations
• Angina at rest—Also prolonged, usually > 20
minutes
• Angina of new onset—At least CCS class III in
severity
• Angina increasing—Previously diagnosed
angina that has become more frequent, longer in
duration, or lower in threshold (change in severity
by 1 class to at least CCS class III)
Unstable Angina/MI
• In the absence of specific ECG changes,
such as the development of new Q waves,
only serial measurements of serum levels of
cardiac enzymes, usually CPK and its MB
isoenzyme, can differentiate unstable angina
from myocardial infarction
Pathophysiology
• Initiation of the Cascade of Plaque
Fissure and Rupture
• Acute Thrombosis and Platelet
Aggregation
• Coronary Vasospasm
• Erosion of Coronary Plaque without
Rupture
Disruption of an atheromatous plaque

• Clinical spectrum in patients with ischemic chest


pain at rest ranges from unstable angina, due to the
partial occlusion of a coronary vessel, to acute
myocardial infarction, due to complete occlusion
• A coronary atherosclerotic plaque ruptures and a
mural or occlusive thrombus forms, interrupting
the perfusion of myocardial tissue
Spectrum of acute coronary syndromes according to electrocardiographic and
biochemical markers of myocardial necrosis (troponin T, troponin I, and creatine
kinase MB), in patients presenting with acute cardiac chest pain
Pathogenesis
• Fissuring or rupture of these plaques leads
to the local generation of thrombin and
deposition of fibrin

• This in turn promotes platelet adhesion and


aggregation, vasoconstriction, and the
formation of partially or totally occlusive
intracoronary thrombus
Pathophysiologic Events Culminating in the Clinical Syndrome of Unstable Angina
Diagram of an unstable plaque with superimposed luminal thrombus
Distal embolisation of a platelet-rich thrombus causing occlusion of intramyocardial
arteriole (arrow). Such an event may result in micro-infarction and elevation of
markers of myocardial
Diagnosis
• Unstable angina and non-ST segment
elevation MI are closely related conditions
• Clinical presentations may be
indistinguishable
• Distinction depends on whether the
ischaemia is severe enough to cause
myocardial damage and the release of
detectable quantities of markers of myocyte
necrosis
Diagnosis
• The initial diagnosis is made on the basis of
a patient's history, ECG and the presence of
elevated plasma concentrations of
biochemical markers
• An ECG may be normal or show minor
non-specific changes
• Transient ST-segment elevation of > 0.5
mm that resolves spontaneously or after
nitrate is given
Diagnosis
• Transient or persistent ST-segment
depression of > 0.5 mm
• Bundle branch block
• T-wave inversion of > 1 mm within 12
hours before or after chest pain, or
• Raised serum concentration of CK-MB
• Cardiac troponins are the preferred markers
• More specific and reliable than CK or
CKMB
Right coronary artery angiogram in patient with non-ST segment elevation myocardial
infarction (top left), showing hazy appearance of intraluminal thrombus overlying a severe
stenosis (arrow). Abciximab was given before direct stenting (top right), with good
angiographic outcome (bottom)
Diagnosis
• Physical examination may exclude
important differential diagnoses
• Pleuritis, pericarditis, or pneumothorax, as
well as revealing evidence of ventricular
failure and haemodynamic instability
• Look for risk factors
Management
• All patients suspected of having ACS
should be managed as medical emergencies
and monitored in the CCU and assessed by
a cardiologist on the day of presentation
• Baseline tests must include 12 lead ECG,
CXR, and haemoglobin and markers of
myocardial damage, preferably cardiac
troponin T or I
Medical treatment
• Medical treatment includes bed rest,
oxygen, opiate analgesics to relieve pain,
anti-ischaemic and anti-thrombotic drugs
• Should be started at once on admission and
continued in those with probable or
confirmed unstable angina or non-ST
segment elevation myocardial infarction
Management
• Medical Therapy
• Antiplatelet Therapy
• Aspirin
• Clopidogrel
• Ticlopidine
• Platelet Glycoprotein IIb/IIIa Receptor
Antagonists
Antithrombin Therapy
• Heparin- Unfractionated, Low-
Molecular-Weight Heparins
• Direct Thrombin inhibitors
• Conventional Antianginal Therapy
• Beta-Blockers
• Nitrates
• Calcium-Channel Blockers
• Coronary Revascularization
Revascularization/reperfusion
• Cardiogenic shock
• Overt heart failure/severe LV dysfunction
• Recurrent/persistent angina despite
intensive medical therapy
• Hemodynamic instability due to mechanical
complications (VSD,Acute MR)
• Unstable arrhythmias (AF, sustained V
arrhythmias)
Treatment for angina
• Aspirin 300 mg followed by a low
dose of 75-150 mg daily
• Clopidogrel 600 mg followed by 75
mg per day (aspirin intolerance)
• Anti-ischemic
• Intravenous nitroglycerin
• Beta Blockers should also be given
Treatment for angina

• Rate limiting calcium antagonists can be


used if beta blockers are contraindicated or
are already being used
• Antithrombotic drugs
• Aspirin, clopidogrel, I/V unfractionated
heparin or LMWH and glycoprotein IIb/IIIa
inhibitors
Antithrombotic treatment
• Ideally, patients should be given LMWH
(enoxaparin) according to their weight
• If LMWH is unavailable, unfractionated
heparin may be used
• Intravenous heparin is given as a bolus dose
of 5000 U, followed by an infusion at a rate
of 1250U per hour, with the APTT
maintained in the range of 50 to 70 seconds
Antithrombotic treatment
• LMWH should be given for at least two
days, and for up to eight days or longer in
cases of
• Recurrent ischaemia or
• Where myocardial revascularisation is
delayed or contraindicated
Anti platelet agents
• Ticlopidine and clopidogrel, are antiplatelet
agents that inhibit the platelet aggregation
induced by adenosine diphosphate, thereby
reducing ischemic events
• Aspirin blocks the thromboxane-mediated
pathway
Subsequent management
• Patients should be observed over the next
eight to 12 hours
• When patients have been free from
symptoms and ischaemic ECG changes for
>48 hours, and any intravenous treatments
and heparin have been stopped for >24
hours, risk assessment with stress testing
should be performed unless contraindicated
Subsequent management
• Long term treatment with aspirin,
clopidogrel (especially after stenting),Beta
blockers, ACE inhibitors
• Aggressive modification of risk factors
• Smoking should be strongly discouraged
 Statins should be used to lower blood lipid
levels
• Antihypertensive & antidiabetic drugs
Summary
• The diagnosis of unstable angina or non-ST
segment elevation myocardial infarction
demands urgent hospital admission and
coronary monitoring. A clinical history and
examination, 12 lead electrocardiography, and
measurement of troponin concentration are the
essential diagnostic tools. Bed rest, aspirin,
clopidogrel, heparin, antianginal drugs, and
opiate analgesics are the mainstay of initial
treatment.

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