Myocardial Infarction • What is Myocardial Infarction? Myocardial Infarction is a result of critical imbalance between coronary blood supply and myocardial demand (myocytes die due to myocardial ischemia ) .
BHF Heart Statistics Incidence of myocardial infarction, by sex and age, England 2010
MI pathophysiology : • Rupture or erosion of coronary artery plaque can produce prolong occlusion that leads to myocardial necrosis within 15 – 30 min
Continuous ischemia produce extend infraction zone to subendocardial myocardium which leads to ( Trans mural Q wave MI ) • Early reperfusion may salvage region of myocardium and reduce future mortality and morbidity .
Risk factor for death in 30 days : • 50 % of MI pt dead within 1-month . • 50 % dead in first 2 hrs • With pre-thrombolytic therapy the 50 % reduced to 20 % . • But with modern therapy it dropped to 6-7 % .
HTN DM • HTN is risk factor for MI, stroke and heart failure • Treatmentof HTN to optimal levels reduces the risk • DM is considered an IHD equivalent • Even when glucose level are under control • Almost 75% of DM die of some form of cardiovascular disease
Elevated cholesterol levels • LDLcholesterol is the most important • Low HDLcholesterol • Hypertriglyceridemia • Increased total to HDL cholesterol ratio
Tobacco • Cigarette or pipes smoking • Also passive smoking • A smoker’s risk of heart attack is more than twice that of a nonsmoker • The risk in who quit smoking ( two years ) was reduced
Obesity • Increased body fat especially in waist area is a risk for IHD • Excess weight increase the for DM type 2, raises blood pressure and increase blood cholesterol and triglyceride levels and it lowers HDL cholesterol • Studies have shown that loss of 10 to 20Ib can significantly reduce the risk
Exercise • Sedentary lifestyle is a risk for IHD • Exercise has a protective effect • It can help by control DM, obesity, lower blood pressure and increase HDL cholesterol
Major uncontrollable • Age • 4/5 who die of IHD are age 65 or older • Sex • Man more than women • Heredity • Family history
Symptoms : • The most common presenting symptom of MI is chest pain, which is often described as severe retrosternal chest pain of a crushing or squeezing nature. • Other clues to the differential diagnosis of chest pain are that the pain may radiate to the arms (commonly the left arm), shoulders, neck and/or jaw. • Similar to angina in location and radiation but it occurs at rest or with less activity and lasts > 30 minutes .
Associated symptoms : • Nausea and vomiting are also common and may be caused by severe pain, vagal stimulation or a decreased cardiac output. • Sever weakness, Dizziness, and palpitation. • There is profuse sweating which may drench the bed clothes .
Signs : • Pallor • Sweating • Tachycardia • Raised JVP • 3rd heart sound • Hypotension • Oliguria • Fever due to tissue damage .
INVESTIGATIONS Elecrtocardiography: The ECG is the main diagnostic test in acute MI
ST segment elevation – this is due to full-thickness myocardial injury greater than 1 mm in two or more consecutive leads. Reciprocal ST segment depression may be present at the same time and represents the mirror image of the ST elevation as seen from the opposite side of the heart. • Over 24 h the ST elevation resolves and the T waves begin to invert. • Q waves develop within 24–72 h of MI.
ECG changes in non-ST-elevation myocardial infarction • These are variable and the absence of Q waves does not necessarily indicate that full-thickness infarction has not occurred. The conventional view used to be that this represented subendocardial damage only. • The ECG changes tend to be in the form of persistent T wave inversion accompanied by an increase in cardiac enzymes.
Cardiac Enzymes • Troponin T and troponin I • Troponin T and troponin I are proteins that form part of the myocardial cell structure. Release of these proteins into the bloodstream indicates that there has been myocardial cell damage. The levels rise within 2–4 h of the onset of MI and remain elevated for up to 14 days. • However, the test is so sensitive that it may be positive in a variety of pathological (i.e. PE, pericarditis, tachyarrhythmias, sepsis) and non-pathological situations (i.e. after running a marathon). Renal failure reduces the excretion of troponin and will raise plasma levels, however a raised troponin in patients with end-stage renal failure is still an indicator of coronary risk and should not be ignored
Creatinekinase • The MB isoenzyme of creatinekinase (CK) increases and falls within 72 h. The source of CK-MB isoenzyme is cardiac muscle, whereas CK-MM is found in skeletal muscle and CK-BB is in brain and kidney. . The CK-MB isoenzymedoes not begin to increase until at least 4 h after infarction and is, therefore, no longer used to make the initial diagnosis in most cases.
Renal function and electrolytes • These are important in all patients who have MI. Renal function may be deranged or may worsen due to poor renal perfusion in cardiogenic shock. Hypokalaemia may predispose to arrhythmias and must be corrected because acute MI is in itself a proarrhythmogenic condition.
Full blood count • Anaemia may precipitate an acute MI in a patient who has angina. There is often a leucocytosis after acute MI.
Serum cholesterol • This should be measured within 24 h of an MI; hypercholesterolaemia is a risk factor for MI and needs to be treated. Cholesterol level falls to an artificially low level 24 h after MI, so after this time a true reading can only be obtained 2 months after MI.
Chest radiography • This should be performed on all patients who have acute MI. Points to note are:• • Widening of the mediastinum – suggests a likelihood of aortic dissection, which is an absolute contraindication for thrombolysis. • • • Signs of pulmonary oedema – signify the need for antifailure therapy (intravenous diuretics, oxygen and possibly a nitrate infusion).
- Rapid history . - Intravenous access. Investigations : - blood ( cardiac markers , CBC , creatinine , electrolytes , glucose , lipids ) - ECG ( cardiac monitor and 12-lead, repeat after 15-30 min if not diagnostic and persistent chest pain).
Treatment : - Oxygen : nasal canula 2-4 L / min - Glyceryltrinitrate : 2-10 mg/h ( iv – buccal or sublingual ) ( maintain systolic BP above 90 mmHg ) - Aspirin : 300 mg , then 75-100 mg p.o. daily ( give PPI with dyspepsia history ) - Clopidogrel : 300 mg p.o. loading dose , then 75 mg p.o. daily.
- Diamorphine or morphine : 2.5 – 5 mg i.v , with metoclopramide 10 mg i.v. - reperfusion therapy for patients presenting within 12 hours of onset : * Primary angioplasty with GP 11b / 111a inhibitors e.g. abciximab , eptifibatide , tirofiban. *Or thrombolysis e.g. streptokinase : 1.5 million units in 100 ml 0.9% NaCl over 1 h by i.v infusion pump. ( others : alteplase , tenecteplase , reteplase )
- β blocker : atenolol 5 mg i.v. repeated after 15 min or metoprolol 5mg i.v. repeated after 15 min . ( avoid in hypotension , heart failure , asthma , bradycardia) . - Insulin infusion if blood glucose > 11 mmol/L , aim of 7-10 mmol/L . - Treat the complications.
Subsequent management of uncomplicated infarction : - Repeat ECG , cardiac markers and electrolytes at 24 and 48 hours after admission. - Initiate secondary prevention therapy : aspirin , clopidogrel , statin , metoprololand ACE inhibitors . - Transfer from CCU to medical ward after 48 hours. - Mobilize gradually and discharge from hospital after 5 days.
Discharge medication The patient should get mediations once he got discharged, In particularly after preparing for discharge. Those medications include : 1- Antiplatelet medication 2- Beta blocker 3- statins 4- ACE inhibitors and AR blockers
Risk factor modification 1- smoking cessation. Proved to reduce risk of subsequence M.I by 50% within one year. 2- Long term glycemic control Goal is to maintain HbA1c less than 7% 3- control hypertension. 4- exercise ( end point breathlessness- fatigue) 5- Stress management
IF patient free of complication discharge within 3-5 days and if not until become stable.
Instruction before discharge : Initially ambulation limited to home. No lifting of heavy weight . Control risk factor . Cardiac rehabilitation. Avoid effort for 6 to 8 weeks. Be on medication
How is High risk patient • Age > 70 . • Female . • Prior angina or previous MI. • History of DM,HTN and non-cardiac vascular disease . • On ECG: anterior MI , increase number of leads showing ST elevation. • Ejection fraction <40 %
Complication • Early Within 2-3 days • Later Within 3- 5 days • late Within weeks
Early complication • Cardiac arrhythmias • Cardiac failure • Pericarditis ( common with anterior MI)
Cardiac arrhythmias • Ventricular ectopics • Ventricular tachycardia • Ventricular fibrillation • Atrial fibrillation • Sinus bradcardia • Heart block
Later complication • Recurrent infraction. • Angina . • Thromboembolism . • Mitral valve regurgitation. (papillary muscle damage ) • VSD. (interventricular septum rupture )
Late complication • post- myocardial infarction syndrome. • Shoulder – hand syndrome . • Ventricular aneurysm. • Recurrent cardiac arrhythmias.
post- myocardial infarction syndrome.(Dressler’s syndrome) • About 5% • Auto-immune response to damaged cardiac tissue or pericardium • Fever, malaise, chest pain .arthralgias • Antimycardial antibody may found • Aspirin 600-900mg /4-6H