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BY:TIKAL KANSARA
BARODA MEDICAL COLLEGE (BMC)
Unstable AnginaNon-ST segment elevation myocardial
infarction (NSTEMI)ST segment elevation myocardial
infarction (STEMI)
ACUTE CORONARY SYNDROME
ANATOMIC REGION OF HEART
CORONARY ARTERY (MOST LIKELY ASSOCIATED)
Inferior Right coronary
Anteroseptal Left anterior descending
Anteroapical Left anterior descending (distal)
Anterolateral Circumflex
Posterior Right coronary artery
Ischemic Discomfort
Acute Coronary Syndrome
No ST elevation
Unstable Angina NQMI
ST elevation
QwMI
MYOCARDIAL INFARCTION
Stable Angina
Unstable Angina
NSTEMI
STEMI
TREND OF DISEASE PROGRESSION
ETIOPATHOGENESIS OF ISCHEMIC HEART DISEASE
Coronary Atherosclerosis
Superadded changes in coronary atherosclerosis• Acute Changes• Plaque haemorrhage• Fissuring• Ulcerations• Coronary artery thrombusNon-atherosclerotic changes• Vasospasm • Stenosis of ostia• Arteritis• Embolism• Aneurysm.• Compression
INITIAL LESIONS• Macrophages• Foam cells
FATTY STREAKS • Multiple layers of foam cells
INTERMEDIATE LESIONS• Lipid-laden cells • Extracellular lipid droplets
ATHEROMATOUS LESION
• Intra & extra cellular lipid pool
FIBROFATTY LESIONS• Fibrous cap • Lipid core
Complicated lesions
• Ulceration• Harmorrhage• Hematoma• Thrombosis
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
NON-MODIFIABLE MODIFIABLE
AgeSexFamily HistoryGenetic FactorsPersonality (?)
Cigarette smokingHigh blood pressureHigh LDL cholesterolObesityDiabetes Sedentary HabitsStress High Alcohol Intake
RISK FACTORS
Intense exertionPhysicalPsycological
PneumoniaChlamydophilia pneumoniae
CAUSES
Unstable Angina is defined as angina pectoris or equivalent ischemic discomfort with at least one of the three features: 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 spasmProgressive mechanical obstructionDecreased 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’S VARIANT 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 PCIType 4b – Myocardial infarction associated with stent thrombosis as documented by angiography or at autopsy
Type 5 – Myocardial infarction associated with CABG
Chest painDyspnoeaEpigastric discomfortDiaphoresisPale cool skinSinus tachycardia3rd &/or 4th heart soundBasilar ralesOccasionally, hypotension.
CLINICAL FEATURES
Condition Duration Quality Location Associated Features
Stable Angina
2 – 10 mins Pressure, tightness, heaviness, squeezing, burning
Retrosternal – radiation to left arm, also from chin to umbilicus
Exertion, cold, stressS4 gallop, MR during pain
Unstable Angina
10 – 20 mins
Similar but of more intensity
Similar to angina
Similar to angina, but occurs at lower levels of exertion or even at rest
Myocardial Infarction
Variable; often more than 30 mins
Similar but of more intensity
Similar to angina
Unrelieved by nitroglycerinEvidence of heart failure or arrhythmias
Chest Pain
ElectrocardiogramCardiac biomarkersCardiac imagingNonspecific indices of tissue necrosis &
inflammation
DIAGNOSIS
UNSTABLE ANGINA
ST- segment depressionTransient ST-segment elevationT-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 INFARCTIONST-segment elevation, in patients with total
occlusionThen, presence of Q-wavesIn partial occlusion, Q-waves may not be
present.If no ST-segment elevation, but cardiac
markers raised, then, diagnosis of NSTEMI is made.
ELECTROCARDIOGRAM
Location of infarctionLeads showing primary changesTypical changes
Anterior infarctionAntero-septal V1, V2, V3
AnteriorSome of V1-V3 plus some of V4-V6
Anterior extensive V1, V2, V3, V4, V5, V6,I, aVLAntero-lateral V4, V5, V6, I, aVL, possibly IIHigh lateral aVL and/or IInferior infarctionInferior II, III, aVF
Infero-lateral (= apical)II, III, aVF, V5, V6 & sometimes also I, aVL
Infero-septal II, III, aVF, V1, V2, V3Other changes
Posterior infarctionV1, V2 (inverse of usual changes elsewhere)
Subendocardial infarctionAny lead (usually multiple leads)
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
http://www.learntheheart.com/AnteriorSTEMI.jpg
ANTERIOR WALL MI
http://www.learntheheart.com/Case1.html
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)
Differentiates between UA & NSTEMIRaised in state of infarction, not in angina.Markers commonly used are:
CK-MBTroponin
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
TEST SENSITIVITY AND SPECIFICITY
APPROXIMATE PEAK
Troponin test The most sensitive and specific test for myocardial damage. 12 hours
Creatine Kinase (CK-MB) test
It is relatively specific when skeletal muscle damage is not present.
10–24 hours
Lactate dehydrogenase (LDH)
LH is not as specific as troponin. 72 hoursAspartate transaminase (AST)
Myoglobin (Mb) low specificity for myocardial infarction 2 hours
Ischemia-modified albumin (IMA)
low specificity
Pro-brain natriuretic peptideGlycogen phosphorylase isoenzyme BB
high sensitivity and specificity early after chest pain 7 hours
2D-EchocardiographyEasySafeQuickCannot differentiate between old myocardial
scar & acute severe ischemia.Other uses:
Ventricular aneurysmPericardial effusionLV 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 ECHOCARDIOGRAPHYTo detect serious complications of STEMI:
Ventricular septal defectMitral regurgitation
PERFUSION IMAGING99mTc-sestamibi or 201Tl reveals a defect
“cold spot” in 1st few hours after the transmural infarct.
Radionucleotide ventriculography, 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 THERAPY
Nitrates
B-blockers
Calcium channel blockers
Morphine sulfate
ANTI-THROMBOTIC THERAPY
Oral antiplatelet therapy
Aspirin
Clopidogrel
Intravenous antiplatelet therapy
Abciximab
Eptifibatide
Tirofiban
Heparins
Heparin
Enoxaparin
Fondaparinux
Bivalirudin
MEDICAL MANAGEMENT
DRUG CATEGORY
CLINICAL CONDITION
WHEN TO AVOID
DOSAGE
NITRATES Primary treatment protocol
•Hypotension•Patients receiving sildenafil or PDE-5 inhibitor.
5-10 ug/min IV continuous infusionTitrate to 75-100 ug/min
BETA BLOCKERS
Unstable Angina
•PR interval >0.24 sec•2nd or 3rd heart block•HR < 60/min•BP < 90 mmHg•LVF with CCF•Airway disease
METOPROLOL5 mg increments, repeat every 5 mins for a max of 15 mgOral 25-50 mg after 1-2 hrs, every 6 hrsESMOLOLInitial 0.1 mg/kg/min IVS;lowly increase by 0.05 mg/kg/min
ANTI-ISCHEMIC TREATMENT
DRUG CATEGORY
CLINICAL CONDITION
WHEN TO AVOID
DOSAGE
CALCIUM CHANNEL BLOCKERS
Not relieved or unable to tolerate nitrates & B-blockers or in whom they are contraindicated
Pulmonary OedemaLVF (for diltiazem & Verapamil)
Varies with the agent used
MORPHINE SULPHATE
Not releived by 3 sublingual nitrates or whose symotoms recur after anti-ischemic therapy
•Hypotension•Respiratory depression•Confusion•Obtundation
2-5 mg IV Repeated every 5-30 mins
ORAL ANTIPLATELET THERAPY
ASPIRIN Initial 162-325 mg followed by 75-162 mg
CLOPIDOGREL Loading dose – 300 mgMaintenance dose – 75 mg/day
ANTI-THROMBOTIC THERAPY
INTRAVENOUS ANTIPLATELET THERAPY
ABCIXIMAB 0.25 mg/kg bolus then 0.125 ug/kg/min for 12-24 hrs
EPTIFIBATIDE 180 Ug/kg bolus then infusion 2.0 ug/kg/min for 72-96 hrs
TIROFIBAN 0.4 ug/kg/min for 30 mins then infusion 0.1 ug/kg/min for 48-96 hrs.
HEPARINS
HEPARIN Bolus 60-70 U/kg IV then 12-15 U/kg/hr titrated for aPTT 50-70 sec
ENOXAPARIN 1 mg/kg SC every 12 hrs.
FONDAPARINUX 2.5 mg SC qd
BIVALIRUDIN Initial bolus 0.1 mg/kg/hr then infusion 0.25 mg/kg/hr.
INITIAL MANAGEMENT•Pre-hospital care•Emergency department•Control of symptoms
HOSPITAL PHASE MANAGEMENT
•Limitation of infarct size•Activity, diet, bowel & sedation
PHARMACOTHERAPT•Anti-thrombotics•B-Blockers•ACE-I•IV nitroglycerin
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 therapyNitroglycerin SLMorphineIV B-Blockers
INITIAL MANAGEMENT
Further line of management depends on selection of either reperfusion therapy by fibrinolysis or primary PCI.
Fibrinolysis includes :
HOSPITAL CARE
DRUG DOSAGE
tPA 15 mg – bolus50 mg over 30 mins35 mg over 60 mins
Streptokinase 1.5 MU IV over 60 mins
rPA 10 MU – bolus over 2-3 mins10 MU – bolus 30 mins later
Percutaneous coronary interventionAngioplastyStenting
PRIMARY PCI : without prior fibrinolysisSECONDARY PCI : prior fibrinolysis
http://www.umm.edu/graphics/images/en/19006.jpg
CORONARY ARTERY BYPASS GRAFT (CABG)
http://www.daviddarling.info/images/coronary_artery_bypass.jpg
THANK YOU
TIKAL KANSARAINTERN
CIVIL HOSPITALAHMEDABAD