Acute Coronary Syndrome

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CAUSES:

It occurs due to the complete blockage of a segment of one of the coronary artery due to a thrombussuperimposed on atheromatous plaques. The sudden complete ischemia leads to necrosis ofmyocardium (HEART ATTACK) which can be salvaged by early treatment . Acute coronary syndromerepresents a shift from one category to another as new ST-elevation can develop after presentation and cardiac markers can become abnormal with recurrent ischaemic episodes such as:

• UNSTABLE ANGINA AND NSTEMI :

The atherosclerotic lesion in unstable angina have complex morphology like ulcerated or fissured atheromatous plaques withsuperimposed plaques. Episodes of myocardial infarction are due to abrupt reduction in coronary blood flow caused by thrombosis or spasm.

NON ST -ELEVATION MYOCARDIAL INFARCTION (NSTEMI)- means unstable angina with evidence ofmyocardial damage/necrosis as evidence raised by CPK-MB or cardiac troponins.

• ST- ELEVATION MYOCARDIAL INFARCTION (SEMI):

It occurs due to occlusion of a coronary artery due to thrombosis. The thrombus is formed at the site of rupture of an atheromatous plaque in a coronary artery.

SYMPTOMS:

• NSTEMI: NON ST-ELEVATION MYOCARDIAL INFARCTION includes:

• Patients with recent onset angina pectoris within 6 weeks that is troublesome and frequent
• Patients with angina of any duration but occurs at rest.
• Patients of chronic stable angina with a recent increase in intensity, frequency or duration of pain.
• Patients with angina pectoris developing or becoming worse within days or weeks aftermyocardial infarction.

RISK FACTORS:

• Old age
• Males
• Family history
• Smoking, alcohol
• Hypertension
• Mental stress, sedentary lifestyle
• Obesity
• Diabetes mellitus
• Protein S and C deficiency

• MYOCARDIAL INFARCTION SYMPTOMS:

• Prolonged and severe chest pain radiating to left arm,throat, epigastrium and back
• Anxiety, fear apprehension of impeding death
• Dyspnoea,nausea,vomiting, sweating
• Giddiness or syncope or collapse.
• Cold extremities, pallor.

• STEMI (ST-ELEVATION MYOCARDIAL INFARCTION) SYMPTOMS:

• Pain is similar to typical angina but more severe and prolonged that radiates to left arm, chinneck, throat,epigastrium, back.
• Tightness and heaviness in the chest
• Patient feels breathless.
• In some cases, syncope can even occur due to complications like arrhythmias, hypotension.
• Cardiac failure or pump failure develops in patients with extensive acute anterior infarction which is the leading cause of death within first few hours of infarction.

DIAGNOSIS:

• ELECTROCARDIOGRAPHY (ECG): Most sensitive and specific method to diagnose.

EVOLUTION ofECG:

• WITHIN MINUTES: acute ST segment elevation >2mm in more than 2 leads.
• WITHIN HOURS: progressive loss of R wave andappearance of Q wave. Resolution of ST segment elevation starts. Terminal T wave inversion starts.
• WITHIN A DAY: Deep Q and T wave inversion.
• WITHIN SEVERAL WEEKS AND MONTHS: Q wave tends to persist but T wave change
• becomes less marked.

• BLOOD TESTS: Leukocytes may be present on the first day and ESR may be raised.

• PLASMA ENZYMES: The enzymes most widely used are CK, AST and LDH for diagnostic andprognostic values:

• CK: It starts to rise at 4-6 hours after infarction reaches at peak at 12 hours and falls to normal within 48-72 hours. CK-MB is more specific but is expensive but is useful for diagnosis of an early infarction.

• CARDIAC TROPONINS (T AND I): They are not detected normally in the blood of healthy person gets elevated to >20 times in patients with ST elevation AMI (STEMI) within 24 hours and elevated for 7-10 days.

• AST: It starts to rise after 12 hours after infarction reaches its peak on 1st or 2nd day and returns on 3rd and 4th day.

• LDH: It starts to rise after 12 hours, reaches its peak after 2-3 days and elevated till a week.

• CHEST X-RAY: This may detect acute pulmonary oedema or congestion which may not bedetected. Otherwise, it is helpful to detect pericardial effusion, cardiomegaly,etc.in these patients.

• ELECTROCARDIOGRAPHY:

It is a valuable technique for assessing ventricular function and detecting complications such as ventricular septalis or chordae tendinae rupture producing acute mild regurgitation and pericardialeffusion.

• RADIONUCLIDE SCANNING:

Radionuclide blood pool scan is useful to assess ventricular function.Infarct avid scanning is possible because some isotopes., pyrophosphate are taken up byfreshly infarcted myocardium, hence, is useful in diagnosis of those patients who have non-specificECG.

TREATMENT AND MANAGEMENT:

• Management of uncomplicated myocardial infarction:

The principal objectives of management of acute myocardial infarction are:

• To prevent sudden death from arrhythmias.
• To minimise or limit the mass/area of infarcted tissue.
• To relieve pain and alleviate anxiety.
• To detect early complications and to treat them.

EARLY MEDICAL MANAGEMENT:

ACCIDENTAL AND EMERGENCY TREATMENT:

• Aspirin 150-300mg to be chewed.
• Sublingual GTN O.4 -1 mg
• Oxygen through nasal cannula.
• Record 12- lead ECG,
• Thrombolysis, if facility exists.
• V beta blockers like metoprolol 5mg every 2-5 mins for 3 doses for chest pain,
• Procure I.V line and take blood samples for glucose, lipids, and complete hemogram
• Pain may be relieved by by I.V morphine plus metoclopramide as an antiemetic.
• Immediately shift the patient to ICU after bed rest.

IN HOSPITAL TREATMENT:

• HOSPITALIZATION AND STRICT BED REST: Ingeneral, all the patients with suspected

myocardial infarction should be admitted directly in ICCU if facility exists., The treatment in ICCU provides necessary expertise, monitoring and resuscitation facilities.

• ANALGESIA: Intravenous morphine sulphate 10 mg and an antiemetic -cyclizing 50 mg orprochlorperazihe 12.5 mg) should be administered through the L.V. cannula, repeated frequentlydepending on the response till good analgesia is achieved and patient feelsbetter. Intramuscular injection should be avoided if patient is receiving an anticoagulant or arrhythmia may appearthrombolytic therapy.

• ANTI PLATELET DRUGS: Low dose aspirin (75-150 mg) andclopidogrel (300mg stat, then 75mg) and prosugrel orally daily improves survival. Studies have shown30%reduction in mortality infarction patients receiving combination therapy. It also enhances the effect of thrombolytictherapy.
• OXYGEN THERAPY: should be administered by a face mask or nasal prongs for a day ortwo after infarction.

• THROMBOLYSIS (MYOCARDIAL REVASCULARISATION): to restore the patency of coronaryartery and it reduces the hospital mortality by < 6 hours by streptokinase - 1.5 million units in 100ml of saline given as IV infusion over 1 hour.

• ALTEPLASE:

It is a potent fibrinolytic drug but is expensive. It also prevents thromboembolic complications. It isless antigenic and does not cause hypotension. The current tPA regimen given, over 90 minutes (bolusdose of 15mg) followed by 50 mg over 30 minutes and then 35 mg over next 60 minutes) is widely accepted. The other drugs include reteplase(PA)given in double dose regimen (10 million units over 2-3

minutes followed by another dose of 10 million units after 30 minutes) andtenectaplase (TNK)given as abolus dose of 40 mg and then 0.5 mg/kg over 10 seconds.

• ANGIOPLASTY AND STENTING:

• Immediate angioplasty of the infarct related artery is relatively safe and superior to thrombolysis. Now-a-days, it is done early called primary angioplasty in MI. It is reserved for those patients where hazards ofthrombolysis are high. It is combined with placement of stent to channelize the blood flow. Rescueangioplasty for patients with failed thrombolysis.

• ANTICOAGULANTS:

• Subcutaneous heparin -7,500 units twice a day for 7-10 days can b employed in patients who do not receivethrombolytictherapy. Patients who receive thrombolytic therapy should receive immediate fulldoses of heparin. - 10,000 bolus plus 1000 U hourly. Nowadays low molecular heparin(enoxaparin 30 mg I.V bolus and 1mg /kg every 12 hourly is safe with less chances of bleeding

• BETA -ADRENERGIC BLOCKERS:It includes atenolol (5 -10 mg over 5 mins) or metoprolol( 5-15 mg over 5 mins) relieves pain and reduce arrhythmia .

• ACE INHIBITORS: given in patients with large infarct when EF are low < 40% on the first daysuch as captopril,enalapril.

• NITRATES AND OTHER AGENTS: sublingual glyceryl trinitrite - 0.4 mg is taken outside thehospital. I.V. Nitriglycerine - 0.6mg-1.2mg /hr or isosorbide dinitrite 1-2 mg/hr for left ventricular failure and pain.

• CALCIUM CHANNEL BLOCKERS: they are second or third line treatment of hypertension with ischemia like verapamil and diltiazem.

• ALDOSTERONE ANTAGONISTS:like spironolactone have been shown to reduce the risks ofmortality and in patients with L.V dysfunction.

• SEDATIVES: Diazepam 5 mg 3 or 4 times a day is quite effective.

• DIET:during first 4-5 days, a low calorie diet divided into multiple frequent small meals withrestriction of salts and cholesterol and saturated fats is preferred.

• LIPID LOWERING AGENTS: Lipid profile should be done. If LDL level is high, a statin (atorvastatin) should be given to bring LDL < 70 mg %.

PREVENTION / FOLLOW UP AFTER SURGERY:

• After surgery, remain on bed first 1-2 days.
• Avoid excessive talking and discussion on any subject
• Avoid smoking alcohol.
• Don’t read any news items that can precipitate anxiety or emotions
• Avoid straining during defecation or urination.
• Move the feet and legs while lying on the bed.
• A proper low calorie diet is a must.

COMPLICATIONS:

• Sudden death
• Post myocardial angina
• Acute circulatory failure
• Pericarditis
• Mural thrombosis and embolism