ACS

Date: 05/03/2014

Date: 05/03/2014
Cardiology
Cardiology
Medicine
Medicine
Pgs. Num: 8
Pgs. Num: 8
Lec: 2
Lec: 2
Dr. Muzahim
Dr. Muzahim

Acute coronary syndrome

Objectives
Definition
Pathophysiology
Clinical Features
Investigations
Management
Complications
Secondary prevention
Prognosis
Definition
Acute coronary syndrome is used to describe a spectrum of disease that encompasses unstable angina & myocardial infarction, ischaemia with no myocardial damage, ischaemia with minimal myocardial damage, partial thickness (non-ST elevation) myocardial infarction, and full thickness (ST elevation, Q wave) myocardial infarction
Pathophysiology
This may present as a new phenomenon or against a background of chronic stable angina. The lesion is usually a complex ulcerated or fissured atheromatous plaque with adherent platelet-rich thrombus and local coronary artery spasm
It is important to appreciate that this is a dynamic process whereby the degree of obstruction may either increase, leading to complete occlusion of the vessel, or regress due to the effects of platelet disaggregation and endogenous fibrinolysis.
In acute MI , thrombus is almost always present at the site of rupture or erosion of an atheromatous plaque .
The thrombus may undergo spontaneous lysis over the course of the next few days, although by this time irreversible myocardial damage has occurred.
The process of infarction progresses over several hours & most patients present when it is still possible to salvage myocardium & improve outcome.
UNSTABLE ANGINA
Unstable angina is a clinical syndrome that is characterized by new-onset or rapidly worsening angina (crescendo angina), angina on minimal exertion or angina at rest. The condition shares common pathophysiological mechanisms with acute myocardial infarction


Approximately 12% of patients with well-characterized unstable angina progress to acute infarction or death, and almost one-third will suffer a recurrence of severe ischaemic pain, within 6 months of the index event
Evolving transmural infarction is characterized by persistent ST elevation, new Q waves or new left bundle branch block.
In patients with unstable angina or partial thickness (non-Q wave or non-ST elevation) myocardial infarction, the ECG may show ST/T wave changes including ST depression, transient ST elevation and T-wave inversion; the T-wave changes are sometimes prolonged.
MYOCARDIAL INFARCTION (MI)
ANATOMY OF CORONARY ARTERIES

Clincal Features:

Symptoms
Prolonged cardiac pain Chest, throat, arms, epigastrium or back .
Anxiety and fear of impending death
Nausea and vomiting
Breathlessness
Collapse/syncope
Physical signs
Signs of sympathetic activation
Pallor, sweating, tachycardia
Signs of vagal activation
Vomiting, bradycardia
Signs of impaired myocardial function
Hypotension, oliguria, cold peripheries
Narrow pulse pressure
Raised jugular venous pressure
Third heart sound
Quiet first heart sound
Diffuse apical impulse
Lung crepitations
Signs of tissue damage
Fever
Signs of complications, e.g. mitral regurgitation, pericarditis.
Investigations:
Electrocardiography
The ECG is usually helpful in confirming the diagnosis. It may be difficult to interpret if there is
1. bundle branch block
2. evidence of previous MI.
Only rarely is the initial ECG entirely normal, but in up to one-third of cases the initial ECG changes may not be diagnostic.


Typical ECG changes in MI

T-inversion

The plasma biochemical markers
The biochemical markers that are most widely used in the detection of MI are:
1. Creatine kinase (CK) (CK-MB).
rise at 4-6 hours, and falls to normal within 48-72 hours.
2. Cardiospecific proteins, troponins T and I.
released within 4-6 hours and remain elevated for up to 2 weeks.

Other blood tests

Leucocytosis is usual, reaching a peak on the first day.
Erythrocyte sedimentation rate (ESR) becomes raised and may remain so for several days.
C-reactive protein (CRP) is also elevated in acute MI.
Chest X-ray
This may demonstrate pulmonary oedema that is not evident on clinical examination The heart size is often normal but there may be cardiomegaly due to pre-existing myocardial damage.
Echocardiography
EARLY MANEGMENT OF ACS
Provide facilities for defibrillation
Immediate measures
High-flow oxygen
I.v. access
ECG monitoring
12-lead ECG
I.v. analgesia (opiates) and antiemetic
Aspirin 300 mg
Reperfusion
Primary PCI or thrombolysis
Detect and manage acute complications
Arrhythmias
Ischaemia
Heart failure
Thrombolytic Treatment in Acute Myocardial Infarction
Prompt thrombolytic treatment (within 12 hours, and particularly within 6 hours, of the onset of symptoms) reduces mortality in patients with acute myocardial infarction and ECG changes of ST elevation or new bundle branch block . Intracranial haemorrhage is more common in people given thrombolysis with one additional stroke for every 250 people treated.
Relative Contraindication to Thrombolytic Therapy (Potential Candidates For Primary Angioplasty)
Active internal bleeding
Previous subarachnoid or intracerebral haemorrhage
Uncontrolled hypertension
Recent surgery (within 1 month)
Recent trauma (including traumatic resuscitation)
High probability of active peptic ulcer
Pregnancy
N.B: Primary PCI is more effective than thrombolysis for the treatment of acute myocardial infarction
N.B: Death, non-fatal re-infarction and stroke are reduced from 14% with thrombolytic therapy to 8% with primary PCI.
Maintaining vessel patency
1.Antiplatelet therapy
Aspirin 75-300 mg daily Orally improves survival (30% reduction in mortality) on its own. The first tablet (300 mg) should be given orally within the first 12 hours and the therapy should be continued indefinitely if there are no unwanted effects.
Clopidogrel the early use (within 12 hours) of 600 mg,150 mg daily for 1 week & 75 mg daily confers a further reduction in mortality with no evidence of increased adverse bleeding events.
Ticagrelor ( 180 mg followed by 90 mg 12-hourly), is more effective than Clopidogrel in reducing vascular death.
2. Anticoagulant (Heparin)
Subcutaneous heparin (12 500U twice daily), given in addition to oral aspirin, may prevent reinfarction after successful thrombolysis and reduce the risk of thromboembolic complications.
Fractioned LMWH or a pentasaccharide(subcutaneous fondaparinux 2.5 mg daily) have the best safety & efficacy profile, with LMWH (S.C Enoxaparin 1 mg/kg 12-hr) being a reasonable alternative given for 8 days or until discharge from hospital.
A period of treatment with warfarin should be considered if there are :
A. Persistent atrial fibrillation
B. Evidence of extensive anterior infarction,
C. or if echocardiography shows mobile mural thrombus.
because these patients are at increased risk of systemic thromboembolism
Adjunctive therapy
Beta-blockers
Intravenous β-blockers (e.g. atenolol 5-10 mg or metoprolol 5-15 mg given over 5 minutes) relieve pain, reduce arrhythmias and improve short-term mortality in patients who present within 12 hours of the onset of symptoms, but should be avoided if there is heart failure, atrioventricular block or severe bradycardia. Chronic oral β-blocker therapy improves long-term survival and should be given to all patients who can tolerate it.
Nitrates and other agents
Sublingual glyceryl trinitrate (300-500 μg) is a valuable first-aid measure in threatened infarction,
Intravenous nitrates (nitroglycerin 0.6-1.2 mg/hour or isosorbide dinitrate 1-2 mg/hour) are useful for the treatment of left ventricular failure and the relief of recurrent or persistent ischaemic pain.
No evidence of a survival advantage from the routine use of oral nitrate therapy, oral calcium antagonists or intravenous magnesium in patients with acute MI.


Complications of Infarction
1. Arrhythmias
Common Arrhythmias in MI:
Ventricular fibrillation
Ventricular tachycardia
Accelerated idioventricular rhythm
Ventricular ectopics
Atrial fibrillation
Atrial tachycardia
Sinus bradycardia (particularly after inferior MI)
Heart block
2. Other complications
Mechanical (Papillary muscle dysfunction, rupture of inter-ventricular septum and rupture of the ventricle and cardiac temponade).
Acute circulatory failure.
Thromboembolic phenomenon (like stroke and ischaemic leg).
Ischaemia (post infarct angina).
Pericarditis.
Impaireds ventricular function, remodelling and ventricular aneurysm.

LATE MANAGEMENT OF MYOCARDIAL INFARCTION

Risk stratification and further investigation
1. Lifestyle modification
Stop smoking
Regular exercise
Diet (weight control, lipid-lowering)
2. Secondary prevention drug therapy
Antiplatelet therapy (aspirin and/or clopidogrel)
β-blocker
ACE inhibitor
Statin
Additional therapy for control of diabetes and hypertension
Rehabilitation