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CORONARY ARTERY DISEASE/MI

CORONARY ARTERY DISEASE/MI. By Henri Godbold MD Med Peds Noon Conference 9/21/2006. ETIOLOGY. Manifestation of atheroma with preserved caliber of lumen Rupture of the plaque’s fibrous cap causing a thrombosis

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CORONARY ARTERY DISEASE/MI

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  1. CORONARYARTERYDISEASE/MI By Henri Godbold MD Med Peds Noon Conference 9/21/2006

  2. ETIOLOGY • Manifestation of atheroma with preserved caliber of lumen • Rupture of the plaque’s fibrous cap causing a thrombosis • The clot overwhelms the endogenous fibrinolytic mechanism may propagate and lead to occlusion

  3. CLINICALMANEFESTATIONS • Transient ischemic cardiac events if prolonged can lead to necrosis and scarring with or without MI • Patients can present with cardiomegaly and heart failure secondary to ischemia of damage left ventricle

  4. ANGINA • Chest pain caused by mismatch of myocardial O2 supply & demand • Classified as: • Stable (usually from concentric plaque) • Usually 2º atherosclerotic obstruction • Unstable (usually from an ulcerated, ruptured plaque)-nidus for platelet aggregation • New onset or increased frequency • Only about 20% of pts. with ischemic ST changes have classic angina

  5. ANGINA TREATMENT • Modify risk factors & correct aggravating factors (anemia, HTN, drug abuse, non-compliance) • Emphasize meds. known to prolong survival post-MI • ASA also should be standard therapy • CCRB and nitrates may be useful for symptoms • Careful with combining meds. with similar effects (ie. Beta blockers, and verapamil)

  6. Nausea and vomiting Edema Orthropnea Paroxysmal nocturnal dyspnea Positional pain ASSOCIATEDSYMPTOMS • Dyspnea • Diaphoresis • Dizziness • Syncope • Palpations • Deep breathing pain

  7. Absolute FH smoking DM HTN Hyperlipidemia (LDL> 130, HDL<35) AGE (men>45,Female>55) Relative Obesity sedentary life stress postmenopausal state CARDIACRISKFACTORS OTHER • Hx CVA and PVD disease

  8. ROLEOFINFLAMATIONASARISKFACTOR • Vascular injury • Lipid peroxidation: along with the effects of HTN, DM, and smoking amplify the harmful effects of oxidized LDL cholesterol • Chronic inflammation promoting athersclerotic plaque which rupture and thrombose in vessels

  9. CIRCULATING MEDIATOR Inflammatory process: • Acutephasereactants • Cell adhesion molecules • Inflammatory Markers- • C-reactive protein (CRP) • IL-6 • serum amylase A • TNF alpha • selectins • macrophage inhibitor cytokines 1 • CD40 ligands

  10. Characteristic of CRP • High sensitivity • Assay well standardized • Widely available • Strong predictor of future myocardial infarctions and stroke • High plasma concentration are associated with a 1.5-to-7 fold increase in the relative risk of symptomatic atherosclerosis

  11. Role of homocysteine in risk stratification • Statistically significant but modest increase in risk of CAD events • Folic acid can reduce serum elevation • Neither prospective or randomized trails show reduction in elevation reduces CHD risk • Routine measurement are not warranted

  12. MANAGEMENT APPROACH • Goals are reduce coronary morbidity and mortality via: • Primary prevention: reducing risk of first event • Secondary prevention: reducing risk of event in person with established disease

  13. Correct reversible risk factors: smoking, hypertension, uncontrolled DM, obesity, stress, life style modification • Risk Stratification (Table 27.4)

  14. CAD Risk Association with Lipoprotein Cholesterol Abnormalities

  15. DIAGNOSIS • First step: estimate pretest probability base on know CV risk factor(age, gender) and symptoms) Is as follows: • Low(<10%): - Asymtomatic men and women of all ages - Women younger than 50 yrs or order with typical angina

  16. Intermediate (10%-90%): • Men of all ages with atypical angina • Women 50yrs or older with atypical angina • Women 30-59yrs with typical angina • High (>90%): • Men 40yrs or older with typical angina • Women 60yrs or older with typical angina

  17. TESTING MODALITIES Cardiac Stress Testing: • Preferred approach to assessing CAD in patients with suspected or known disease • Goal to induce myocardial ischemia by increasing myocardial oxygen demand • Indicated for the diagnosis of myocardial ischemia • Indicated for ECG abnormalities WPW, >1mm resting ST depression, LBBB • After cardiac catherization to identify if ischemia is present in the distribution of the coronary lesion identified

  18. Exercise Stress Test • Preferred to pharmacologic stress • Provides data on exercise capacity and hemodynamic response to exercise • Patients with normal baseline ECG, ischemia can be detected using ECG monitoring • Patient with abnormal baseline ECG, who undergo pharmacologic or exercise stress testing, either echocardiographic or radionuclide imaging is needed to detect ischemia

  19. Stress Echo • Detects provoked regional ventricular wall motion abnormality • Uses myocardial perfusion imaging: • Sestambi(Cardiolite) radionuclide tracer, decrease uptake represent the area of ischemia measure by scintigraphy • Vasodilator agents: Adenosine, Persantine and dobutamine

  20. Postitron Emission Tomography(PET) • More specific and sensitive than conventional nuclear imaging • Can combine high resolution CT imaging of anatomy and function for noninvasive assessment of coronary disease

  21. Coronary Angiography • Invasive • Pretest probability of disease is high • Stress test is positive • Symptomatic presentation despite a negative stress test • Diagnosis and therapy can be preformed simultaneosly (i.e. percutaneous revascularization)

  22. Indication Revascularization in Patient with Chronic Stable Angina CABG is recommended for • Left main coronary artery stenosis • 3-vessel CAD(greatest survival benefit with EF <50%) • 2-vessel CAD and proximal LAD stenosis with LV EF <50% or ischemia on noninvasive testing • 1-2 vessel CAD w/o prox LAD stenosis who survived sudden cardiac death or sustain VT

  23. Percutaneous Coronary Intervention (PCI) is recommended for • Nondiabetics w/ 2-vessel CAD • Proximal LAD stenosis • Normal LV function w/ anatomy amenable to PCI

  24. Either CABG or PCI recommended • 1 or 2 vessel CAD w/o prox LAD stenosis and high risk criteria on noninvasive testing • Prior CABG or PCI w/ recurrent stenosis and a large area of ischemia or high risk criteria on noninvasive testing • Symptoms refractory to medical therapy with an acceptable risk of revascularization

  25. TREATMENT • Vigorouslifestylemodification- low fat and cholesterol diet; regular exercise; and smoking cessation • Aspirin- antiplatelet • Statin- lipid-lowering • Betablocker and CCB- reducing myocardial oxygen consumption • ACE inhibitor-especially patients w/ DM and /or left ventricle systolic dysfunction

  26. Nitrates: reduce angina by peripheral venodilation and coronary artery dilation • To avoid tolerance need atleast 8hrs daily free period • Do not use in patients receiving phosphodiesterase type 5 inhibitors( sildenafil, vardenafil, tadalafil) lead to life threatening hypotension

  27. HyperlipidemiaDrugs HMG-CoAreductaseinhibitor (Statins) • First line • Inhibits intracellular cholesterol and increaseclearenceLDL • Starting dose 10-20mg/d w/ max dose 80mg/d • Adverse effects hepatocellular dysfunction and myositis • Monitor transaminases intially then f/u measurements 6 month and 1 year

  28. Bile Acid Sequestrants • Interrupt enterohepatic circulation in the gut • Highly effective used in combination in those high risk patients • Side effects constipation, bloating, heartburn and nausea

  29. Ezetimibe • Block absorption from the gut • Inhibits cholesterol transport by interfering with specific transporters proteins and dose not interfering w/ other drugs and fat-soluble vitamins • Lowers LDL by 15 to 20%; If use with statin, provides additional 15% reduction

  30. Niacin( B-complex vitamin) • Inhibits mobilization of free FA from fat cells to the liver • Raises HDL 15% to 35% • Lowers triglycerides 20% to 50% and LDLs 5% to 25% • Side affects flushing, pruritis, PUD, hyperglycemia, rashes

  31. Fibrates(Gemfibrozil and Fenofibrate) • Not first-line • Decreases VLDL synthesis enhancing clearance • Raises HDL cholesterol • Well tolerated except in combo w/ statins possible rhabdomyolysis

  32. Nonprescriptions dietary Supplements Omega-3 Fish Oils • Decreases VLDL, and platelet inhibition Antioxidant vitamins • Capable of increasing LDL resistance to oxidative changes and reduce the risk of arterial wall injury Garlic, Fiber, and Red yeast extract

  33. TreatmentThresholds Recommendation of NCEP Panel • High risk or CAD plus multiple risk factor • LDL cholesterol threshold 100mg/dl, treatment goal <70mg/d • Moderately high risk(no CAD, multiple risk factor and 10 yr CAD risk 10%-20%) • LDL cholesterol threshold 130mg/dl, treatment goal <100mg/dl

  34. Moderate risk with 2 or more CAD risk Factors (10yr risk probability is <10%) • LDL cholesterol cut off 160mg/dl • Fewer than 2 CAD risk factors • LDL cholesterol >190mg/dl require drug rx • Optional rx for levels between 160-190mg/dl

  35. Isolated low HDL cholesterol • Treatment with statin seems to lower CAD morbidity • Even though the strong inverse relationship between HDL levels and CHD risk, there is no data showing that raising HDL alone significantly reduces CAD mortality

  36. Primary Prevention • NECP target LDL Cholesterol <130mg/dl, ATPIII optimal level <100mg/dl and target of less than 100mg/dl for person with moderate high CAD risk • Secondary Prevention • LDL cholesterol < 100mg/dl with an optimal goal of <70mg/dl for very high risk patients

  37. ACUTE MYOCARDIAL INFARCTION(AMI) Overview • 15% are asymptomatic • Women more likely to have silent infarcts • Differential diagnosis of prolonged chest pain: AMI, aortic dissection, pericarditis, esophageal problems, biliary tree, pneumothorax, pulmonary embolism, pleurisy, chest wall problems, and psychogenic

  38. Arrhythmias in the first 48 hrs are due to ischemia • MR due to papillary muscle dysfuntion is seen with inferior wall MIs • VSD is seen with anterior and inferior MIs • Inferior MIs are associated with more stable arrhythmias • Anterior MIs can result with poorer prognosis associated with Mobitz II and BBBs • Both anterior and inferior MIs can result in septal wall rupture

  39. Acute Coronary Syndrome (ACS) NSTEMI(non Q wave MI)/UA: episodic cessation of coronary blood flow or vasospasms(prinzmetal’s) or drug induce, like cocaine • NSTEMI: Detectable release of biological markers(Tnp I, T, MB isoenzymes) hours after the onset of ischemic chest pain • Unstable angina(UA): no detectable markers released

  40. STEMI(Q wave MI) • most often by occlusive thrombus • Rule out other life-threatening conditions (i.e. aortic dissection, PE, tension pneumothorax, esophageal rupture, perforated ulcer) • Risk stratification-TIMI risk score • ID higher risk patients for adverse event particularly with anterior wall MIs • Cardiac marker helpful but do not delay implementation of reperfusion therapy, if not contraindicated

  41. TIMI RISK SCORE PATIENTS WITH DIAGNOSIS STEMI • PrognosticvariablesPoints Age >75 yrs 3 Age 65-75yrs 2 DM, HTN, or angina 1 • PE SBP <100mm Hg 3 HR > 100/min 2 Killip class II-IV 2 wt < 67kg (150 lb) 1

  42. PrognosticVariablesPoints Presentation Ant. ST elevation or LBBB 1 Time to reperfusion > 4 hrs 1 Risk score = total points (0-14) correlates 30-day mortality rate (%) with 0 risk=0.8%, 5 risk=12%, and >8 risk=36%

  43. Myocardial Infarction

  44. ST elevation: Q-wave(transmural infarct) or Non Q wave subendocardial infarct)MI • Not frequently seen • Earlist changes is hyperacute or peaked T waves • ST segment elevation in leads corresponding to involved region of myocardial damage • Initially J point elevation and concave ST segments

  45. Over time ST segments becomes convex or roundedupwards • ST segment indistinguishable from T waves • QRS-T complex resemble a monophasic action potential • Initial Q waves develop several hrs to days and the loss of R wave amplitude

  46. Abnormal Q wave criteria: • Q waves in leads V1 to V3 or a Q wave greater than or equal 30 msec in leads I, II, aVL, aVF, or V4 to V6 • Must be present in two contiguous leads and a depth greater than or equal 1mm • Overtime Ist 2 wks or several hrs after the event R wave amplitude is markly reduced • Q waves deepen

  47. Overtime, several hrs or weeks after the event • R wave amplitude is markedly reduced • Q-wave deepens • T waves become inverted

  48. Management of UA and NSTEMI

  49. STEMI/New LBBB **PCI within 12 hrs. of CP Onset and within 90 Minutes of arrival to ED

  50. STEMI/New LBBB • Consider emergent reperfusion (fibrinolytics or PCI) in ALL pts. that present with STEMI or new LBBB within 12 hrs. of onset of symptoms and who are < age 75 • Fibrinolytics • LBBB benefits most anterior>inferior (amt. of myocardium saved) • NSTEMI (not much myocardium lost), the risks of fibrinolytics outweighs the benefits • So, ONLY give fibrinolytics to STEMI or NEW LBBB or RBBB • Actually shown to increase mortality in NSTEMI

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