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level: ANGINA & MI

Questions and Answers List

level questions: ANGINA & MI

QuestionAnswer
Atherosclerosis: Unmodifiable Risk Factorsfamily predisposition (premature atherosclerosis eg MI<55yrs) age : >40yrs M >50yrs F male gender genetic abnormalities
Atherosclerosis: Modifiable Risk Factors -1st lineDyslipidemia Hyperfibrinogenemia Cigarette/ cigar smoking Arterial Hypertension Diabetes Mellitus (NB: MI risk ↑es 4x, if >3 ↑es 10x )
Atherosclerosis: Modifiable Risk Factors - 2nd lineObesity (BMI >30% above normal) Physical inactivity Mental stress + Type A personality Hyperuricemia - strengthen the impact of 1st line factors
Atherosclerosis: Pathogenesis1- Endothelial injury due to risk factors or trauma 2- LDLs accumulate & aggregate, entering tunica intima 3- Macrophages oxidise LDLs via free radicals 4- Oxidised LDLs stimulate further leukocyte recruitment via chemoattractants releases by endothelial & SM cells 5- Monocytes engulf LDLs; accumulation of lipids and fatty streak development; cause cytotoxic damage to endothelial cells and cause dysfunction 6-Intimal smooth muscle proliferation &↑leukocyte recruitment result in atherosclerotic plaque formation 7- If plaque reaches coronary arteries, it can keep growing and cause stenosis OR rupture off; thrombosis/ embolism OR cause aneurysm by wall damage 8- ↓ O2 supply to myocardium, cellular acidosis and lactate release; in time it can cause ischemia and is called IHD
Stable Angina Pectoris : definitionPain >1month, not progressing & no exact time of disease beginning
Stable Angina Pectoris : PAIN symptomsPAIN 1) type: pressure/heaviness/squeezing/tightness/burning/numbness 2) when: physical or emotional exertion/cold/rich meals/tobacco/anger 3) where: sub/parasternal; mostly left or both sides/ levine's sign (between epigastrium and neck) 4) radiation: inner arm to forearm/wrist/left shoulder/epigastrium, sometimes neck/mandible/upper back 5) duration: 0.5-5 mins but sometimes 10-15 mins 6) relief: rest/sublingual nitroglycerine (1-3mins), elimination of factor
Stable Angina Pectoris : other symptoms & signsOther symptoms (Dyspnea, nausea, anxiety, cold sweats, general weakness, tremor, clouding of consciousness) Signs (pallor, ↑ HR/BP, diffuse apex beat, gallop rhythm, paradoxical S2 due to prolonged LV ejection & mid-late systolic apical murmur due to ischemia of papillary muscles) on palpation: ectopic systolic bulging / paradoxic movement
Stable Angina Pectoris : ClassificationClass I (only rapid/strenuous/ prolonged exertion); Rare Class II (high but usual everyday physical load ); More frequent w/ nervous tension Class III (low/moderate physical load); sometimes 1st hours of awakening Class IV (slight tension, even at rest)
Stable Angina Pectoris: Diagnostic Criteria1- Typical anginal pain 2- Ischemia on ECG at rest or exertion 3- Significant CA stenosis >75%
Stable Angina Pectoris: Diagnosis- Clinical signs - Blood test (for risk factors/causes & DDx): CBC, lipids, electrolytes, Thyroid, Troponin, CRP, sugar, liver enzymes, Creatinine kinase & uric acid - ECG (rest+24 hr - ST changes, T inversion,↓R, arrhythmia, BBB) - Exercise Stress test: pathological if ST changes >1mm + anginal pain - Xray (heart): degree of myocardial hypertrophy, the signs of left ventricular failure - Echo (regional wall abnormality) - SPECT w/Thallium, PET, multi-slice CT - Angiography (MRI or Invasive)
Stable Angina Pectoris: Treatment objectives- To alleviate /prevent angina attack & improve QoL - To perform timely diagnosis of acute MI - To prevent sudden ischemic death
Stable Angina Pectoris : Treatment - lifestyle changesChange lifestyle to improve prognosis: - quit smoking - nutrition: reduce fat/salt/alcohol intake & more fruit/veg, - if obese: reduce calories + exercise - if HTN: reduce salt/alcohol - exercise Modify RFS: ( Lipid management: diet & anti-lipid drugs, BP: antihypertensives, DM, Weight, thromboses: reduce fats/smoking/aspirin)
Stable Angina Pectoris : Drug therapy & RevascularisationDrug therapy (nitrates + anti-ischemic improve quality of life, others for prognosis) 1- ↑O2 supply, = Nitrates (nitroglycerin, glycerol trinitrate, isosorbide mono/di nitrate), ACE inhibitors (captopril),Revascularization procedures (PCI, CABG) 2-↓ O2 demand = Nitrates, B-blockers (B1-metaprolol / B1&2-propanolol), Ca+ channel blockers (amlodapine), IF inhibitor (Ivabradine), Non-nitrate Anti-anginals (Ranolazine) 3- Myocyte metabolism adaptation= Anti-ischemic drugs (Trimetazidine, mildronate) 4- Prevention of adverse outcomes= Antiplatelet therapy to prevent TE (aspirin/clopidogril), Influenza vaccine, Statins (fluvastatin), RAAS blockade therapy 5- improve QoL + Prognosis( B-blockers, ACEI, Statins, Aspirin, CCBs)
Unstable Angina: Definitionmyocardial ischemia at rest or w/ minimal exertion in the absence of myocardial necrosis ECG: ST segment depression + inverted T wave (acute ischemia)
NSTEMI: Definitionmyocardial necrosis in clinical setting consistent with acute myocardial ischemia
Acute Coronary Syndromes : Types- Unstable Angina - Non-ST-Segment Elevation MI (NSTEMI) - ST-Segment Elevation (STEMI)
NSTE- ACS: Pathogenesis4 processes: 1- rupture of unstable atheromatous plaque 2- coronary arterial vasoconstriction 3- imbalance between the supply and demand of myocardium for oxygen 4- gradual intra-luminal narrowing of an epicardial coronary artery because of progressive atherosclerosis or post-stent restenosis can occur simultaneously in any combination
Unstable Angina: Clinical presentation-Prolonged (>20mins) anginal pain at rest: retrosternal sensation of pressure/ heaviness radiating to left arm, neck or jaw - sweating, pallor - nausea, abdominal pain, vomiting - dyspnea, syncope - Atypical symptoms: epigastric pain, indigestion - Physical exam: stable or in shock; excited/flashy/sweaty , BP↓ or↑, tachy/bradycardia auscultation : gallop rhythm,, systolic murmur, pericardial friction sound (if pericarditis)
MI: Clinical Presentation- Pressure/ tightness in chest with radiation. - shortness of breath - diaphoresis (ex. sweating due to sympathetic innervation) - nausea and vomiting (parasympathetic response) - anxiety
NSTE-ACS: Diagnostic Criteria1- Troponin elevation (not specific) 2- typical ischemic symptoms or ECG ischemic changes (ST depression of T wave inversion) 3- Imaging tests: echocardiography , coronary angiography
NSTE- ACS: Diagnosis1- Clinical signs 2- ECG: ST changes - >1mm height), T inversion (if LBBB, ECG not useful) for MI: pathological Q waves 3- Biomarkers - < x5 ↑ troponin = Unstable Angina > x5 ↑ troponin = NSTEMI 4- Chest Xray - acute left ventricular insufficiency (due to stasis or edema) & heart dilation 5- Transthoracic echo - check LV structure (volume, size) and function (segment contractility, diastolic dysfunction), MI complications (rupture, aneurysm, thrombus, heart valves, pericardial effusion)
NSTE-ACS: GRACE Risk Score (Mnemonic - CBCSTEAK)- Creatinine - Systolic BP - Cardiac arrest at admission - ST deviation - Troponin, (elevated cardiac biomarkers) - Elevated pulse rate - Age - Killip classification (I- no HF, II- rales/JVD, III- Pulmonary edema, IV- Cardiogenic shock/hypotension)
NSTE-ACS: TIMI Risk ScoreTIMI (each one is 1 point) - Mnemonic - AASSKPR Age ≥65, ≥3 CAD risk factors (hypertension, hypercholesterolemia, diabetes, current smoker,family history of CAD) Known CAD (stenosis >50%) Aspirin use in past 7 days Severe angina (>2 episodes in 24 hrs) ST changes ≥ 0.5 mm Positive cardiac marker
NSTE-ACS: High Risk Patients- Recurrent ischemia - Dynamic ST changes - Early post-infarction angina, - Elevated troponins - Hemodynamically unstable - Major ventricular arrhythmias - Diabetes, - GRACE score >140 (Death/MI 30d. 12-30%)
NSTE-ACS: Low Risk Patients- No recurrent ischemia - Isoelectric ST segment - Only negative T wave or normal ECG - Normal biomarker levels at baseline & after 6-12 hours - GRACE score <109 (Death/ MI 30d. <2%)
NSTE-ACS : Invasive strategy criteria- Immediate (<2hrs) for very high risk criteria - Early (<24hrs) for High risk criteria - Invasive (<72hrs) for intermediate risk criteria - Selective invasive for low risk criteria
MI: Definitionevidence of myocardial injury (elevated cTn values) w/ necrosis in a clinical setting consistent with myocardial ischemia
MI: CriteriacTn >99th percentile & at least one of the following: - symptoms of ischemia - ECG changes indicative of ischemia: sig ST/T changes or LBBB - Pathological Q wave - Imaging: new loss of myocardium or new regional wall abnormality -angiography/ autopsy: intracoronary thrombus
MI: CLASSIFICATIONType I : SPONTANEOUS MI- ischemia due to primary coronary event eg plaque rupture/erosion/fissure, coronary dissection, distal platelet embolism Type II: ischemia due to ↑O2 demand eg HTN or ↓supply eg coronary artery spasm/embolism/arrhythmia/hypotension Type III: related to sudden unexpected cardiac death ( w/ symptoms of myocardial ischemia + new ECG changes: ischemia or LBBB) Type IVa: associated with PCI (w/ symptoms of MI+ cTn values >5x URL) Type IVb: associated with documented stent thrombosis Type V: associated with CABG (w/ symptoms of MI+ cTn >5x URL)
MI : etipathogenesis- disruption of atherosclerotic plaque - leads to activation of thrombogenesis pathways: thrombus forms from platelet aggregates, fibrins & RBCs - complete occlusion of epicardial vessel leads to large zone of ischemia - if ischemia prolongs -> necrosis -> MI
Other causes of elevated troponin: Cardiac disorders- Heart failure - Cardiomyopathy ( hypertrophic, viral ) - Hypertension - Myocarditis, pericarditis - Infiltrative disorders eg amyloidosis - Injury - Cancer
Other causes of elevated troponin: Systemic disorders- Pulmonary embolism - Rhabdomyolysis - Toxicity eg anthracycline - Trauma - Renal failure - Sepsis - Stroke - Subarachnoid haemorrhage
ACS w/ ST elevation: Treatment- Stabilse patient : MONA - if <120 mins: Primary PCI strategy + Re-perfusion - if >120 mins: Fibrinolytic therapy for re-perfusions ( bolus of fibrinolytic eg Tenecteplase, alteplase, reteplase, streptokinase ) then either Routine or Rescue PI & Re-perfusion - Long term : B-blockers/ ACEI (if patient w/ HF, LV dysfunction or DM) & Statins- should be continued indefinitely
Peri-procedural anti-thrombotic medication in PCI- Aspirin: LD 162-325 mg/day then 75-100mg/day - P2Y12 inhibitor- Clopidogrel: LD 300-600mg/day then 75mg/day for at least 12m - Anti-coagulants: LMWH 1mg/kg or Unfractionated heparin or Bivalrudin - Glycoprotein IIb/IIIa inhibitors for high risk patients (recurrent ischemia, dynamic ECG changes or hemodynamically unstable) eg Abciximab, Tirofiban, Eftifibatide for 6-24hrs
Fibrinolytic therapy : contraindications- Aortic dissection - Previous hemorrhagic stroke - Previous ischemic stroke w/in 1 yr - Active internal bleeding - Intracranial tumour - Pericarditis
Myocardial Revascularisationrestoration of blood supply to ischemic myocardium to limit ongoing damage, reduce ventricular irritability & improve long-term and short-term outcomes in ACS patients Modes: - Fibrinolytic therapy, - PCI w/ or w/out stent placement - CABG
Myocardial Revascularisation: Unstable Angina NSTEMI- immediate perfusion not urgent - Angiography w/in 24-48hrs of hospitalisation to identify coronary lesions requiring PCI or CABG - Non-interventional approach & trail of medical management if angiography shows ( small area of myocardium at risk, lesion morphology not amenable to PCI, CA stenosis <50% or significant left main disease in CABG candidates) or patients are at high risk of procedure- related morbidity and mortality - if persistent chest pain despite meds -> Immediate PCI or CABG
MI: Early complications (<48hrs)1) Arrhythmias: ventricular fibrillation/flutter, ventricular extrasystoles, atrial fibrillation/flutter/premature beats , AV block( if inferior infarct), bradyarrhythmias 2) LV insufficiency/ Cardiogenic shock (SBP <90mmHg) 3) RV insufficiency 4) Acute pulmonary edema
MI: Late complications (>48hrs)1) Cardiac aneurysm 2) Pericarditis 3) Remodelling (hypertrophy) 4) Rupture of the heart 5) Arrhythmias 6) Heart failure - Stroke (emboli from LV) - Venous thrombosis