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ISCHAEMIC HEART DISEASE Acute Coronary Syndromes. JD Marx Department of Cardiology University of the Free State. Acute Coronary Syndromes. PATHOPHYSIOLOGY Intermittent, partial or total occlusion of coronary artery responsible for acute myocardial ischaemia Several factors play a role .
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ISCHAEMIC HEART DISEASEAcute Coronary Syndromes JD Marx Department of Cardiology University of the Free State
Acute Coronary Syndromes PATHOPHYSIOLOGY • Intermittent, partial or total occlusion of coronary artery responsible for acute myocardial ischaemia • Several factors play a role
Acute Coronary Syndromes PATHOPHYSIOLOGY Thrombosis Unstable angina MI Ischemic stroke/TIA Critical leg ischemia Intermittent claudication CV death ACS Atherosclerosis Stable angina intermittent claudication MI=myocardial infarction ACS=acute coronary syndromes TIA=transient ischemic attack CV=cardiovascular
Acute Coronary Syndromes • 1. Atherosclerotic Lesions in ACS • Vulnerable plaque present in most patients • Culprit lesions most often a low grade lesion
Acute Coronary Syndromes Multiple UnstableLesions
Acute Coronary Syndromes • 2. Inflammation in ACS 43% 29% 29% 25% RECURRENT UAP 6% 7% T LYMPHOCYTES
Acute Coronary Syndromes • 3. Thrombus in ACS • Thrombosis on ulcerated or ruptured plaque plays pivotal role • Platelet Thrombus • Fibrin Thrombus
Platelet Adhesion Tissue factor, vWF COLLAGEN I GP lb- IX GP Ia - IIa GP IIb - IIIa Plaque rupture, endothelial damage, fibrous cap erosion
Platelet Activation and Aggregation Platelet Thrombin PAR-1 Platelet Fibrinogen PAR-4 P2Y1 GP IIIa ADP GP IIb P2Y12 ThromboxaneA2 GP IIb TXA2-R GP IIIa Epinephrine Serotonin 5HT2A Anionic phospholipid surfaces GP VI Collagen GP Ia
Platelet Aggregation Hemisphere-shaped platelet Rolling ball-shaped platelet Spreading platelet Flowing disc-shaped platelet FIRM, BUT REVERSIBLE ADHESION IRREVERSIBLE ADHESION Scanning electron micrograph of discoid, dormant platelets Activated, aggregating platelets illustrating fibrin strands
Microembolization in Unstable Angina Courtesy of C. Michael Gibson, MS, MD, Director TIMI Data Coordinating Center, Brigham & Women’s Hospital, Associate Chief of Cardiology, Interventional Cardiologist, Beth Israel Deaconess Medical Center, Harvard Medical School.
Acute Coronary Syndromes • 3. Thrombus in ACS • Thrombosis on ulcerated or ruptured plaque plays pivotal role • Platelet Thrombus • Fibrin Thrombus
Acute Coronary Syndromes • 4. Coronary Artery Spasm in ACS Can play an important etiological role
Acute Coronary Syndromes PATIENT WITH MYOCARDIUM AT RISK CLINICAL PRESENTATION • Unstable Angina Pectoris • Angina of recent onset ( 1 month ) • Angina at rest • Worsening angina • Early post infarction angina • Non ST-segment elevation myocardial infarction • Cardiac enzymes elevated e.g. troponins,CK, MB-CK • ST-segment elevation myocardial infarction • Normal progression to Q-wave infarction
Acute Coronary Syndromes Unstable Angina Pectoris & Non ST-segment elevation infarction TREATMENT • Medical Stabilization • General • Hospitalization • Monitor as appropriate • Pain relief • Sedation as necessary Identify and treat precipitating factors e.g. anaemia, tachiarrhythmias
Acute Coronary Syndromes TREATMENT • Drugs • Antithrombotic • Antiplatelet e.g.. Aspirin • Anticoagulant e.g.. Heparin • Antianginal • Nitrates • β-Blockers • Calcium Antagonists • Disease Modifying Drug • Statins • ACE Inhibitors
Acute Coronary Syndromes TREATMENT • Coronary Angiography Evaluate coronary anatomy • Depending on clinical and anatomic findings an appropriate long term treatment is determined.
Acute Coronary Syndromes LONG TERM TREATMENT • Medical therapy • Coronary angioplasty • Coronary artery Bypass Graft surgery
Diffuse Disease MAHOMED
Right Coronary Artery Before PTCA After PTCA
Stenting LAD BEFORE STENT LAD AFTER STENT