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ACUTE CORONARY SYNDROME BY: TIKAL KANSARA BARODA MEDICAL COLLEGE (BMC)
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Non-ST segment elevation myocardial infarction (NSTEMI)
ST segment elevation myocardial infarction (STEMI)ACUTECORONARY SYNDROME
ANATOMY OF CORONARY CIRCULATION
MYOCARDIAL INFARCTION
TREND OF DISEASE PROGRESSION
PATHOPHYSIOLOGY
http://upload.wikimedia.org/wikipedia/commons/thumb/f/f1/Atherosclerosis,_aorta,_gross_pathology_PHIL_846_lores.jpg/230px-Atherosclerosis,_aorta,_gross_pathology_PHIL_846_lores.jpg http://1.bp.blogspot.com/_TZRga5MgAqc/SlH2zWwQpnI/AAAAAAAAAMs/zOCV4MdVpZc/s400/atherosclerosis-1.jpg
http://www.nature.com/nature/journal/v420/n6917/images/nature01323-f1.2.jpg
http://www.live-in-green.com/features/images/diet_soda/atherosclerosis_development_process.jpg
RISKFACTORS
Intense exertion Physical Psycological Pneumonia Chlamydophiliapneumoniae CAUSES
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It occurs at rest (or with minimal exertion), usually lasting > 10 mins,
It is severe and of new onset,
It occurs in a cresendo pattern (i.e., distinctly more severe, prolonged, or frequent than previously)UNSTABLE ANGINA
UA occurs due to reduction in oxygen supply and/or by an increase in myocardial oxygen demand superimposed on an atherosclerotic coronary plaque, with varying degrees of obstruction. Plaque rupture or erosion with superimposed non occlusive thrombus (MC) Dynamic spasm Progressive mechanical obstruction Decreased supply v/s increased demand PATHOPHYSIOLOGY
http://drsvenkatesan.wordpress.com/2008/09/10/why-thrombolysis-is-contraindicated-in-unstable-angina/
A syndrome of ischemic pain that occurs at rest but not usually with exertion and is associated with transient ST-segment elevation. Due to focal spasm of an epicardial coronary artery, leading to severe myocardial ischemia. Focal spasm can be due to vasoconstrictor mitogens, leukotrienes, or serotonin. Associations – migraine, Raynauld’s Phenomenon, or aspirin-induced asthma. PRINZMETAL’SVARIANT ANGINA
UA + Raised cardiac markers NSTEMI
A 2007 consensus document classifies myocardial infarction into five main types: Type 1 – Spontaneous myocardial infarction related to ischemia due to a primary coronary event such as plaque erosion and/or rupture, fissuring, or dissection Type 2 – Myocardial infarction secondary to ischaemia due to either increased oxygen demand or decreased supply, e.g. coronary artery spasm, coronary embolism, anemia, arrhythmias, hypertension, or hypotension Type 3 – Sudden unexpected cardiac death, including cardiac arrest, often with symptoms suggestive of myocardial ischaemia, accompanied by presumably new ST elevation, or new LBBB, or evidence of fresh thrombus in a coronary artery by angiography and/or at autopsy, but death occurring before blood samples could be obtained, or at a time before the appearance of cardiac biomarkers in the blood Type 4 – Associated with coronary angioplasty or stents:  Type 4a – Myocardial infarction associated with PCI Type 4b – Myocardial infarction associated with stent thrombosis as documented by angiography or at autopsy Type 5 – Myocardial infarction associated with CABG
Chest pain Dyspnoea Epigastric discomfort Diaphoresis Pale cool skin Sinus tachycardia 3rd &/or 4th heart sound Basilar rales Occasionally, hypotension. CLINICAL FEATURES
Chest Pain
Electrocardiogram Cardiac biomarkers Cardiac imaging Nonspecific indices of tissue necrosis & inflammation DIAGNOSIS
UNSTABLE ANGINA ST- segment depression Transient ST-segment elevation T-wave inversion For patients presenting with clinical features of UA, the presence of new ST-segment deviation, even of 0.05 mV is important predictor of adverse outcome. ELECTROCARDIOGRAM
http://t2.gstatic.com/images?q=tbn:ANd9GcSZHFhpkVykyCcvRgdWTRm_5Z1DO6s95JfuivLOiRWojbnK2S_A
http://t0.gstatic.com/images?q=tbn:ANd9GcRfQ9vhakX9DUOOMFZ00KjaDgJfQIxB0kD8yBBr03hPn1N0mtnCIQ http://t1.gstatic.com/images?q=tbn:ANd9GcTpKHVspKnAzenrh8e3stJG5juj2g8nK3C8RZFD9dp_JYm6Auxe
http://www.cathlabtoday.com/wp-content/plugins/rss-poster/cache/9380f_0314-ECG-small-2.jpg
http://drsvenkatesan.files.wordpress.com/2008/09/ua.png?w=500&h=122
MYOCARDIAL INFARCTION ST-segment elevation, in patients with total occlusion Then, presence of Q-waves In partial occlusion, Q-waves may not be present. If no ST-segment elevation, but cardiac markers raised, then, diagnosis of NSTEMI is made. ELECTROCARDIOGRAM
http://www.google.co.in/imgres?imgurl=http://www.trialimagestore.com/imagesDW3/mi_article_ekgs/inf_mi_2_JPEG.jpg&imgrefurl=http://www.trialimagestore.com/article_myocardial_infarction_heart_attack.html&usg=__guojgJu9pYR2ImqurueusU1DsD8=&h=371&w=668&sz=77&hl=en&start=8&zoom=1&tbnid=lfmFcyE-pQuVvM:&tbnh=77&tbnw=138&ei=-_UJToOUGNDKrAem1YyvDw&prev=/search%3Fq%3Dst%2Belevation%2Bmi%26hl%3Den%26gbv%3D2%26biw%3D1366%26bih%3D661%26tbm%3Disch&itbs=1&biw=1366&bih=661
http://www.frca.co.uk/images_main/resources/ECG/ECGresource44.jpg
The EKG shows ST elevation in leads II, III, and aVF suggesting inferior wall myocardial infarction. Reciprocal changes (ST segment depression) may be seen in leads V1 and V2 in inferior wall myocardial infarction as in this patient. In addition there is ST elevation in lead V6 suggesting lateral wall involvement. Lateral infarction produces changes in leads I, avL and V5/6.
ANTERIOR WALL MI
ANTERIOR WALL MI http://www.learntheheart.com/AnteriorSTEMI.jpg
1) Sinus rhythm with 2nd degree type I AV block (Wenkebach)2) Inferior ST segment elevation MI (leads II, III, and aVF) with reciprocal ST depression (leads I and aVL) http://www.learntheheart.com/Case1.html
Differentiates between UA & NSTEMI Raised in state of infarction, not in angina. Markers commonly used are: CK-MB Troponin Troponin more specific and sensitive marker of myocardial necrosis. CARDIAC BIOMARKERS
http://upload.wikimedia.org/wikipedia/commons/thumb/8/80/AMI_bloodtests_engl.png/400px-AMI_bloodtests_engl.png
2D-Echocardiography Easy Safe Quick Cannot differentiate between old myocardial scar & acute severe ischemia. Other uses: Ventricular aneurysm Pericardial effusion LV thrombus CARDIAC IMAGING
http://www.users.interport.net/w/s/wsc1/www.westsubcardiology.com/pages/noninvasive/echo/echo1.jpg MITRAL REGURGITATION
IMAGE 1 OF 2…
IMAGE 2 OF 2…
DOPPLER ECHOCARDIOGRAPHY To detect serious complications of STEMI: Ventricular septal defect Mitral regurgitation PERFUSION IMAGING 99mTc-sestamibi or 201Tl reveals a defect “cold spot” in 1st few hours after the transmural infarct. Radionucleotideventriculography, with 99mTc-labeled RBCs, detects wall motion abnormalities & reduction in ventricular ejection fraction.
CORONARY ANGIOGRAPHY http://98.131.235.9/images/Normal-coronary-Angiogram.jpg
http://98.131.235.9/images/Diseased-left-coronary-Artery.jpg
Coronary angiography showing lesions in the circumflex artery http://www.tkd.org.tr/TKD_DATA/dergi/images/2004-04-91s.gif
Initial management aims at complete bed-rest with continuous ECG monitoring for ST-segment deviation & cardiac rhythm. Ambulation permitted onlyh if patients shows no recurrence of ischemia (discomfort or ECG changes) and does not develop biomarkers of necrosis for 12-24 hours. TREATMENT OF UA/NSTEMI
MEDICAL MANAGEMENT
ANTI-ISCHEMIC TREATMENT
ANTI-THROMBOTIC THERAPY
TREATMENT OF STEMI
Largely based on prevention of complications: Electrical complications (arrhythmias) Mechanical complications (pump failure) Identification of patients who needs quick reperfusion therapy Symptomatic relief: Aspirin  O2 therapy Nitroglycerin SL Morphine IV B-Blockers INITIAL MANAGEMENT
Further line of management depends on selection of either reperfusion therapy by fibrinolysis or primary PCI. Fibrinolysis includes : HOSPITAL CARE

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Acute coronary syndrome