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Jan16
ACUTE CORONARY SYNDROME
ACUTE CORONARY SYNDROME
Dr.S.ABBAS ALI
MD, DFM, DNB, MNAMS
FCGP, MCCP (Cardiology)
PGDHSc(Ultrasonography)
PGDHSc(Echocardiogram)
DEFINITION
ACS includes Unstable angina and evolving MI which share a common underlying pathology – plague rupture, thrombosis and inflammation. It results from reduction of flow through the affected epicardidal coronary artery. The flow reduction may be caused by completely occlusive thrombus or sub totally occlusive thrombus. A totally occlusive thrombus results in STEMI and a sub totally occlusive thrombus results in NSTEMI. Management of ACS is beyond the limit of Family physician and during evolution history and all risk factors should noted and diagnosed confidently and then refer to tertiary health care.
RISK FACTORS
NON MODIFIABLE MODIFIABLE Controversial risk factors
Age
Gender
Family history of IHD or premature death or MI in first degree relative Smoking
Hypertension
Diabetes
Hyperlipidemia
Obesity
Sedentary life styles
Poor oral hygiene
Cocaine use
Stress
Type A personality Raised Apolipoprotein
Raised homocysteine
Raised fibrinogen
Hyperinsulinemia
ACE genotype
TYPES
• STEMI (ST segment elevation MI)- results from totally occlusive thrombus of epicardial coronary artery.
• NSTEMI (non ST segment elevation MI) – results from subtotal occlusion of epicardial coronary artery.
ST SEGEMENT ELEVATION MYOCARDIAL INFARCTION
PATHOPHYSIOLOGY
1. There is total occlusion of the epicardial coronary
artery
2. The thrombus is fibrin rich hence called red
thrombus. Fibrinolytics are drug of choice
3. there is macro-infarction and time bound necrosis
of myocardium
4. Early reperfusion is the key to treatment
CLINICAL FEATURES
• Sudden onset of chest pain – substernal may radiate, pain lost for 30 minutes and it is not relieved by rest or sublingual nitrates. There may be associated dyspnoea, sweating, weakness, vomiting along with clinical features of cardiac failure.
• ECG FEATURES: patients with STEMI present with ST segment elevation. Many may ultimately develop a Q wave on the ECG. Those who undergo a successful fibrinolysis or primary PCI may not develop a Q wave on the ECG. A new onset LBBB with classical chest pain is also considered STEMI Fibrinolysis or primary PCI is the treatment of choice.
TREATMENT – immediate in the first 30 minutes
• If the chest pain is typical ACS give 325 mg of aspirin (not enteric coated) to be chewed (if there is no aspirin allergy)
• Clopidogrel 300 mg stat
• Sub lingual nitrates if HR >50 and <100/minute ; SBP >90 or if there is no BP fall of > 30 from base line (b) no prior sildenefil intake for 24 hours or Tadalafit for 48 hours © No RV infarction
• Sedation IV morphine 5-10mg +metoclopramide 10mg iv (not IM because of risk of bleeding with thrombolysis)
• Arrange emergency ambulance
• Re-assurance
• O2 inhalation – in icu
• Firbrinolytics or primary PCI
NON ST SEGMENT ELEVATION MYOCARDIAL INFARCTION
PATHOPHYSIOLOGY
• It results from sub-total critical occlusion of the epicardial coronary artery
• The thrombus is platelet rich hence called white thrombus. Hence fibrinolytics are contraindicated. Anticoagulants (UFH/LMWH), antiplatelets and other cardiac medications are treatment of choice
• The distinction between USA/NSTEMI is made by the presence or absence of serum cardiac marker such as Treponin
• There is a micro-infarction, hence treponin is done.
• The myocardium is still viable with high possiblity of developing necrosis, if the occlusion becomes total
• The risk determines intervention
CLINICAL FEATURES:
• PAIN is similar to anginal pain but may be more severe usually lasting upto 20 minutes. Pain is present at rest, there may be decreasing tolerance for exertion,
• clinical signs may be unremarkable. If some patients with large area of myocardial ischaemia or a large NSTEMI the physical findings can include diaphoresis, pale cool skin, tachycardia, S3,S4 or murmur of papillary dysfunction, basal rales and some time hypotension resembling large STEMI
DIAGNOSIS
For diagnosis at least three of four diagnostic tool required for general physician.
• Clinical history
• ECG
• Cardiac biomarkers
• Stress testing or angiography (optional)
ECG: In UA, ST-segment depression, transient ST-segment elevation, and/or T-wave inversion occur in 30 to 50% of patients. These patients do not develop Q waves. Both are differentiated by presence of treponin in blood. If Treponin levels are high then it is called NSTEMI and If treponin levels were normal then it is called Unstable angina. In patients with the clinical features of UA, the presence of new ST-segment deviation, even of only 0.05 mV, is an important predictor of adverse outcome. T-wave changes are sensitive for ischemia but less specific, unless they are new, deep T-wave inversions ( 0.3 mV).
CARDIAC ENZYMES OR CARDIAC BIOMARKERS
• Treponin T and I: cardiac Treponin T and I are the most sensitive and specific markers of myocardial necrosis. Serum levels increase within 3-12 hours from the onset of chest pain. If normal after 6 hours and ECG normal the risk of missing MI is very tiny.
• CK-MB: the levels raise with in 3-12 hours.
• Myoglobin: the levels raise with 1-4 hours from the onset of chest pain. They highly sensitive but not specific.
OTHER INVESTIGATIONS REQUIRED
x-ray chest PAview
haemogram
lipid profiles
liver profiles
serum electrolytes
blood sugar fasting and pp
HBA1c
Serum calcium Serum uric acid
FT4 FT3 TSH
Blood urea@serum creatinine
Serum Vitamin D
Serum B12
Serum testosterone
Prothrombin time and APTT
TREATMENT – IMMEDIATE WITH IN 30 MINUTES
• If the chest pain is typical ACS give 325 mg of aspirin (not enteric coated) to be chewed (if there is no aspirin allergy)
• Clopidogrel 300 mg stat
• Sub lingual nitrates if HR >50 and <100/minute ; SBP >90 or if there is no BP fall of > 30 from base line (b) no prior sildenefil intake for 24 hours or Tadalafit for 48 hours © No RV infarction
• Sedation IV morphine
• Re-assurance
• Firbrinolytics should not be given. LMWH or UFH or Fondaprinax can be given
• Conservative or invasive tretment depends upon risk stratification (TIMI score)
TIMI SCORE: TIMI risk score is simple tool composed of 7 (1 point) risk indicators rated on presentation
• Age 65 years or above
• At least 3 risk factors of CAD
• Prior coronary stenosis of 50% or more
• ST Segment deviation on ECG presentation
• At least 2 anginal events in prior 24 hours
• Use of aspirin in prior 7 days
• Elevated serum cardiac biomarkers


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