22. It occurs in a cresendo pattern (i.e., distinctly more severe, prolonged, or frequent than previously)UNSTABLE ANGINA
23. 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
25. 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 â migraine, Raynauldâs Phenomenon, or aspirin-induced asthma. PRINZMETALâSVARIANT ANGINA
27. A 2007 consensus document classifies myocardial infarction into five main types: Type 1 â Spontaneous myocardial infarction related to ischemia due to a primary coronary event such as plaque erosion and/or rupture, fissuring, or dissection Type 2 â 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 â 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 â Associated with coronary angioplasty or stents: Type 4a â Myocardial infarction associated with PCI Type 4b â Myocardial infarction associated with stent thrombosis as documented by angiography or at autopsy Type 5 â Myocardial infarction associated with CABG
31. 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
36. 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
40. 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.
43. 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
44. 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
51. DOPPLER ECHOCARDIOGRAPHY To detect serious complications of STEMI: Ventricular septal defect Mitral regurgitation PERFUSION IMAGING 99mTc-sestamibi or 201Tl reveals a defect âcold spotâ in 1st few hours after the transmural infarct. Radionucleotideventriculography, with 99mTc-labeled RBCs, detects wall motion abnormalities & reduction in ventricular ejection fraction.
54. Coronary angiography showing lesions in the circumflex artery http://www.tkd.org.tr/TKD_DATA/dergi/images/2004-04-91s.gif
55. 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
62. 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
63. Further line of management depends on selection of either reperfusion therapy by fibrinolysis or primary PCI. Fibrinolysis includes : HOSPITAL CARE