BY:TIKAL KANSARA

BARODA MEDICAL COLLEGE (BMC)

Unstable AnginaNon-ST segment elevation myocardial

infarction (NSTEMI)ST segment elevation myocardial

infarction (STEMI)

ACUTE CORONARY SYNDROME

ANATOMY OF CORONARY CIRCULATION

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

http://www.texasheartinstitute.org/HIC/Anatomy/coroanat.cfm

http://www.le.ac.uk/pa/teach/va/anatomy/case1/frmst1.html

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