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  1. Stable and acute Ischemic Heart Disease Gobezie T §CHD §1
  2. Introduction  Coronary heart disease (CHD) is the most common type of heart disease and cause of heart attacks.  also known as atherosclerotic heart disease,  coronary artery disease (CAD), or  ischemic heart disease (IHD)  Coronary artery disease is the narrowing or blockage of the coronary arteries,  usually caused by atherosclerosis. 2
  3. ETIOLOGY Angina pectoris.  Coronary atherosclerosis.  Coronary artery spasm.  Coronary artery embolism or thrombosis.  This can cause chest pain called angina. 3
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  6. PATHOPHYSIOLOGY….(2)  Progressive decrease in vessel radius associated with  coronary atherosclerosis impairs coronary blood flow and causes angina pectoris  when myocardial oxygen demand ↑s, as with exertion.  Angina pectoris may occur because of  abrupt reduction in blood flow due to • coronary thrombosis (unstable angina) or localized vasospasm (variant or Prinzmetal angina) • without increased oxygen demand. 6
  7. Risk factors Non-modifiable risk factors (those that cannot be changed) include:  Male gender.  Advanced age.  Family history of heart disease 7
  8. Risk factors… Modifiable risk factors (you can treat or control) include:  Cigarette smoking and exposure to tobacco smoke  High blood cholesterol and high triglycerides  HTN (130/80 mm/Hg or higher)  Uncontrolled diabetes  Physical inactivity  Being overweight (BMI 25-29 or being obese (BMI >30 kg/m2)  Uncontrolled stress or anger  Diet high in saturated fat and cholesterol 8
  9. Classification  IHD  Stable angina  Acute coronary syndrome • Unstable angina • non ST elevation MI • ST elevation MI 9
  10. Grading of Angina Pectoris by the Canadian Cardiovascular Society Classification System Class Description of Stage Class I Ordinary physical activity does not cause angina, such as walking, climbing stairs. Angina occurs with strenuous, rapid, or prolonged exertion at work or recreation. Class II Slight limitation or ordinary activity. Angina occurs on walking or climbing stairs rapidly, walking uphill, walking or stair climbing after meals, or in cold, or in wind, or under emotional stress, or only during the few hours after wakening. Walking more than 2 blocks on the level and climbing more than 1 flight of ordinary stairs at a normal pace and in normal condition. Class III Marked limitations of ordinary physical activity. Angina occurs on walking 1 to 2 blocks on the level and climbing 1 flight of stairs in normal conditions and at a normal pace. Class IV Inability to carry on any physical activity without discomfort— anginal symptoms may be present at rest. 10
  11. Clinical Presentation  Symptoms  sensation of pressure/burning over or near sternum; often but not always radiating • left jaw, shoulder, arm  chest tightness, shortness of breath  visceral pain: lasts 0.5 to 30 min  precipitating factors: exercise, cold environment, walking after a meal, emotional upset, fright, anger, coitus  relief with rest, nitroglycerin 11  Signs  abnormal precordial systolic bulge  abnormal heart sounds  Typically no abnormal laboratory tests  Likely to have abnormal tests for IHD risk factors  History of chest pain
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  13. Desired Outcomes Alleviate acute symptoms of myocardial ischemia  Reduce the number of ischemic episodes as well as  increasing the amount of exertion or exercise a patient can accomplish before inducing an ischemic episode.  Slow the progression of atherosclerosis and  preventing complications of such as MI, HF, stroke, & death. Avoid or minimize adverse treatment effects. 13
  14. General Treatment  Identification & treatment of aggravating conditions  Anemia  Thyrotoxicosis  Aortic valve diseases  Obesity  Prevention & control of HTN, dyslipidemia, and DM.  Avoidance of drugs that may be detrimental. 14
  15. Treatment General Approach to Treatment The primary strategies for preventing ACS and death are to:  Modify cardiovascular risk factors;  Slow the progression of coronary atherosclerosis; and  Stabilize existing atherosclerotic plaques.  Non-pharmacologic therapy 15
  16. Non-pharmacologic therapy  Surgical revascularization plays an important role in the treatment of SIHD.  The most common revascularization procedures are coronary artery bypass grafting (CABG) surgery or percutaneous coronary intervention (PCI) with or without stent placement 16
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  18. Drug therapy  Treatment Improve mortality in patients with SIHD by providing guideline-directed medical therapy (GDMT).  Anti-platelet agents  ACE inhibitors/ARBs  Statins  B-blockers  Calcium channel blockers  Nitrates 18
  19. Antiplatelet Agents  platelets adhere to the site of atherosclerotic plaque rupture activated, Aggregated stimulate thrombus formation and ACS. o Guideline recommendations:  Aspirin 75–162 mg daily for all pnts, continued indefinitely in the absence of contraindications, particularly in patients with a Hx of MI.  Clopidogrel is a reasonable when aspirin is contraindicated.  Tt with aspirin (75–162 mg/d) and clopidogrel 75 mg/d might be reasonable in certain high-risk patients with SIHD. 19
  20. ACE Inhibitors  ACEIs have demonstrated the ability to:  stabilize coronary plaque,  provide restoration or improvement in endothelial function,  inhibition of vascular smooth muscle cell growth,  ↓ed macrophage migration, and  possibly possess some antioxidant activities. 20
  21. Risk factor modification. Lipid management: Statins  Guidelines recommend  All patients with known atherosclerotic CVD, such as SIHD, should receive high-intensity statin therapy. High-intensity statin options: • Atorvastatin 40 or 80 mg (preferred dose) daily. • Rosuvastatin 20 (preferred dose) or 40 mg daily.  Patients over the age of 75 years, or those who cannot tolerate high-intensity statin, should receive moderate- intensity statin. • Moderate-intensity statin options: • Atorvastatin 10–20 mg, Rosuvastatin 5–10 mg. • Simvastatin 20–40 mg, Pravastatin 40 mg, Lovastatin 40 mg. 21
  22. Risk factor modification….  Blood pressure management.  Drug selection in SIHD includes agents typically used to treat other aspects of the disease. • βBs, ACEIs & CCBs can be added if additional therapy needed. • Thiazide diuretics could also be an option.  Smoking cessation.  Nicotine replacement therapy.  Sustained release bupropion. 22
  23. Treatment for Symptom relief.  βBs: Effective in reducing both symptomatic and silent episodes of myocardial ischemia.  CCBs: Effective at reducing angina episodes, Reduction in MVO2  Can be used safely in many patients with CIs to βB therapy.  Short-acting nitrates: First-line for acute attacks. NG SL 2–5 min prior to activities prevent predicted attacks.  Long-acting nitrates: Use is limited to tolerance.  Ranolazine.  Option for patients who cannot tolerate any of the traditional agents due to hemodynamic or other adverse effects. 23
  24. Short-acting nitrates. Nitroglycerin to Relieve Acute Symptoms  Short-acting nitrates are first-line treatment to terminate acute episodes of angina.  All patients with a history of angina should have sublingual nitroglycerin tablets or spray to relieve acute ischemic symptoms. Nitrates  primarily cause venodilation reductions in preload  decrease in ventricular volume and wall tension  reduction in myocardial oxygen demand.  At higher doses, nitrates may also cause arterial dilation & 24
  25. Long-Acting Nitrates (LANs)  Isosorbide dinitrate, in a sublingual form, has a longer half- life with anti-anginal effects lasting up to 2 hours.  for patients with more frequent attacks, LANs is recommended.  The major limitation of nitrate therapy is the development of tolerance with continuous use.  Provide nitrate-free interval of 10–14 hrs per day or longer to maintain efficacy. 25
  26. Beta-Blockers  Stimulation of the β1-and β2- receptors in heart ↑ HR and cardiac contractility.  βBs ↓ myocardial oxygen demand by Antagonizing β1-and β2- Stimulation Lowering BP and ventricular wall tension.  βBs may ↑ ventricular wall tension.  However, the net effect of β-blockade is usually a reduction in myocardial oxygen demand  βBs with intrinsic sympathomimetic activity produce lesser reductions in myocardial oxygen demand and should be avoided in patients with IHD.  Other βBs appear equally effective at controlling symptoms of 26
  27. Calcium Channel Blockers  Inhibition of calcium entry into the vascular smooth muscle cells leads to systemic vasodilation and reductions in afterload.  Inhibition of calcium entry into the cardiac cells leads to reductions in cardiac contractility. Reduction in wall tension Reduction in myocardial oxygen demand  Nondihydropyridine CCBs further ↓ myocardial oxygen demand.  Due to their negative chronotropic effects, verapamil & diltiazem are generally more effective anti-anginal agents than dihydropyridine CCBs. 27
  28. Calcium Channel Blockers  CCBs are recommended as initial treatment in IHD when βBs are contraindicated or not tolerated.  In addition, CCBs may be used in combination with βBs when initial treatment is unsuccessful. A long-acting dihydropyridine CCB is preferred. Amlodipine and felodipine possess less negative inotropic effects and appear to be safe in left ventricular systolic dysfunction.  Finally, there is some evidence that short acting CCBs (particularly short acting nifedipine & nicardipine) may ↑ risk of CV events. 28
  29. Treatment: Special Considerations  Variable threshold angina and Prinzmetal’s angina.  Nitrates & CCBs are effective agents for reducing vasospasm.  Most patients respond well to SL NTG for acute attacks. Nifedipine, verapamil, & diltiazem are all equally effective as single agents for initial management of coronary vasospasm. Dose titration is important to maximize the 29
  30. Acute Coronary Syndromes 30
  31. Acute coronary syndromes  Unstable angina (UA)  Myocardial infarction (MI): Non-ST-Segment Elevation MI (NSTEMI & UA), ST-Segment Elevation MI (STEMI)  The cause of an acute coronary syndrome is  the rupture of an atherosclerotic plaque with subsequent platelet adherence, activation, and aggregation, and the activation of the clotting cascade. • Ultimately, a clot forms composed of fibrin and platelets. 31
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  34.  Unstable angina  Angina with at least one of the three features • It occurs at rest, lasts >10 min • Severe & of new onset, with in the past 4-6 wks.  NSTEMI  UA + elevated cardiac biomarkers  STEMI: NSTEMI + ST elevaiton 30 day mortality rate is 30 %, ½ of it occurs before the patient reaches the hospital 34
  35. Risk Stratification 35  TIMI Risk Score for NSTE-ACS  Risk of death, MI, or urgent need for revascularization as follows: (One point for each of seven)  Age >65 years  >3 CHD risk factors: (smoking, hypercholesterolemia, HTN, DM, Fx of premature CHD death/events)  Known CAD (50% or greater stenosis of at least one major coronary artery on coronary angiogram)  Aspirin use within the past 7 days  Two or more episodes of chest discomfort within past 24 hours  ST-segment depression 0.5 mm or greater  Positive biochemical marker for infarction  TIMI Risk Score (5-7 points= High, 3-4 =Medium, 0-2= Low-
  36. Acute Coronary Syndromes: Treatment DESIRED OUTCOMES The short-term goals of Rx for ACS patient are as follows:  Early restoration of blood flow to the infarct-related artery to prevent infarct expansion (in case of MI) or prevent complete occlusion and MI (in unstable angina)  Prevention of death and other complications  Prevention of coronary artery reocclusion  Relief of ischemic chest discomfort  resolution of ST-segment and T-wave changes on the ECG. Long-term desired outcomes are  control of CV risk factors, 36
  37. General approach….  STEMI, • immediate primary PCI with balloon angioplasty or stent placement is reperfusion treatment of choice when patient presents within 12 hours of symptom onset.  NSTE ACS at low risk:  Obtain serial biochemical markers.  High-risk NSTE ACS:  early coronary angiography (within 24 hours) & revascularization if significant stenosis is found. 37
  38. Early Pharmacotherapy for STE ACS  In Emergency department (ED):  Morphine PRN  Oxygen (if SO2<90)  sublingual ± IV NTG  DAT: (ASA+P2Y12Is)  Anticoagulant (UFH or enoxaparin/fondaparinux/ bivalirudin)  β-blocker (in ED, within first 24 h)  Fibrinolysis 38
  39. Tt Algorism for STE MI 39
  40. Fibrinolytic Therapy Administer within 30 min of arrival of STE ACS patients if  Presenting to hospital within 12 hours of onset of chest discomfort  and have at least 1 mm of STE . Also consider in STE ACS patients  presenting within 12–24 hours of onset of chest discomfort  and have persistent symptoms of ischemia  and at least 1 mm of STE in two or more contiguous leads. 40
  41. Thrombolytics Drug Fibrin Specificity Dose Streptokinase (SK) (Streptase) + 1.5 MU in 50 mls NS/D5W IV over 60 mins Tissue plasminogen activator (tPA) (Alteplase) +++ IV Bolus: 15 mg, 0.75 mg/Kg over 30 mins (max: 50mg), 0.5mg/Kg over 1 hr (max 35mg) (max dose 100 mg) Reteplase (rPA) (Retevase) ++ 10 U IV push over 2 min, repeat after 30 min Tenecteplase (TNK) (TNKase) ++++ Single IV bolus given over 5 s based on weight < 60Kg: 30 mg IV Bolus 60-70Kg: 35 mg IV Bolus 71-80Kg: 40 mg IV Bolus 81-90Kg: 45mg IV Bolus > 91Kg: 50mg IV Bolus 41 alteplase, reteplase, & tenecteplase are acceptable as first-line agents.
  42. Aspirin Early aspirin administration to all patients without contraindications within the first 24 hours of hospital admission In patients undergoing PCI, aspirin prevents acute thrombotic occlusion during the procedure. In patients experiencing ACS, an initial dose ≥160 mg nonenteric aspirin is necessary to achieve rapid platelet inhibition.  This first dose can be chewed in order to achieve high blood concentrations and rapid platelet inhibition. 42
  43. Thienopyridines.  Should be used as soon as possible concomitantly with aspirin to prevent subacute stent thrombosis and longer term CV events.  Recommended duration is 12 months following PCI for STEMI receiving a bare metal stent or drug-eluting stent.  Clopidogrel 43
  44. Glycoprotein (GP) IIb/IIIa receptor inhibitors.  Do not give GPIs to STEMI patients who will not undergo PCI.  If UFH is selected for primary PCI in STEMI, add GPIs  to UFH (in addition to a thienopyridine and aspirin)  to reduce likelihood of reinfarction for patients not given fibrinolytics.  Abciximab 0.25 mg/kg IV bolus given 10–60 min before start of PCI, followed by 0.125 mcg/kg/min (maximum 10 mcg/min) for 12 hours.  Eptifibatide 180 mcg/kg IV bolus, repeated in 10 min, followed by infusion of 2 mcg/kg/min for 18–24 hours after PCI.  Tirofiban 25 mcg/kg IV bolus, followed by an infusion of 44
  45. Anticoagulants  Patients undergoing primary PCI  UFH or bivalirudin is preferred;  In fibrinolysis,  UFH, enoxaparin, or fondaparinux may be administered. 45
  46. Anticoagulants….UFH dosing  UFH dose for primary PCI:  50–70 units/kg IV bolus if GPI is planned and 70– 100 units/kg IV bolus if no GPI is planned;  give supplemental IV bolus doses to maintain the target activated clotting time (ACT).  UFH dose for STEMI with fibrinolytics:  60 units/kg IV bolus (max 4000 units), followed by continuous infusion of 12 units/kg/h (max. 1000 units/h).  Adjust to maintain target aPTT 1.5–2 times control (50–70 s). 46
  47. Dosing…for others  Enoxaparin dose for STEMI:  1 mg/kg SC Q 12–24 hours depending on renal function.  For STEMI patients receiving fibrinolytics, enoxaparin 30 mg IV bolus is followed immediately by 1 mg/kg SC Q12h if < 75 years (0.75 mg/kg SC Q12h if ≥75 years).  Bivalirudin dose for PCI in STEMI:  0.75 mg/kg IV bolus then 1.75 mg/kg/h continuous infusion.  Discontinue at end of PCI or continue at 0.25 mg/kg/h if prolonged anticoagulation is necessary.  Fondaparinux dose for STEMI:  2.5 mg IV bolus, followed by 2.5 mg SC daily starting on hospital day 2. 47
  48. Nitrates  One SL NTG tablet (0.4 mg) should be administered every 5 minutes for up to three doses to relieve myocardial ischemia.  ACEIs or βBs, should not be withheld for nitrates use because the mortality benefit of nitrates is unproven.  IV NTG initiated in all ACS with persistent ischemia, HF, or uncontrolled high BP in the absence of CIs.  IV NTG continued for approximately 24 h after ischemia relieved  The most significant adverse effects of nitrates are  tachycardia, flushing, headache, and hypotension.  Nitrate CI with oral PDE-5 inhibitors, such as sildenafil 48
  49. β-Blockers  A βB should be administered early in the care of patients with STE ACS and continued indefinitely.  Early administration of a βB within the first 24 hours of hospitalization in patients lacking a contraindication is a quality care indicator. 49
  50. BB…  Target resting HR is 50–60 beats/min; initial IV therapy may be omitted, if appropriate.  Metoprolol 5 mg by slow (over 1–2 min) IV bolus, repeated Q 5 min for a total initial dose of 15 mg; follow in 1–2 hours by 25–50 mg orally every 6 hours.  Propranolol 0.5–1 mg slow IV push, followed in 1–2 hours by 40–80 mg PO every 6–8 hours.  Atenolol 5 mg IV dose, followed 5 min later by a second 5 mg IV dose, then 50–100 mg PO daily beginning 1–2 h after the IV dose.  For at least 3 years for normal EF, indefinitely if 50
  51. Calcium Channel Blockers  Administration of CCBs in the setting of STE ACS is reserved for patients who have contraindications to βBs and is given for relief of ischemic symptoms.  In patients prescribed CCBs for treatment of hypertension who are not receiving βBs and who do not have a contraindication to βBs, the CCB should be discontinued and a βB initiated.  Nifedipine should be avoided because it has demonstrated reflex sympathetic activation, tachycardia, and worsened myocardial ischemia. 51
  52. Early pharmacotherapy for NSTE- ACS  Generally similar to that of STEMI  all patients with NSTE-ACS should be tted in the ED with  Morphine PRN in refractory patients  IN Oxygen (if O2 saturation <90)  sublingual ± IV NTG (IV in selected patients )  DAT (Aspirin with P2y12 inhibitors)  Anticoagulant (UFH or enoxaparin/fondaparinux/bivalirudin)  PO β-blocker (in ED, within first 24 h) (IV in selected pnts)  High-risk patients should proceed to early angiography and may receive a GPI (optional with either UFH or enoxaparin but should be avoided with bivalirudin). 52
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  54. Fibrinolytic Therapy  is not indicated in any patient with NSTE-ACS  because increased mortality has been reported with fibrinolytics compared with controls in clinical trials in (patients with normal or ST-segment depression ECGs).3 54
  55. Aspirin  Reduces the risk of death or developing MI by about 50% (compared with no antiplatelet therapy) in patients with NSTE-ACS.  Therefore, aspirin remains the cornerstone of early treatment for all patients with ACS.  Dosing of aspirin for NSTE-ACS is the same as that for STEMI. 55
  56. Anticoagulants  UFH 60 units/kg IV bolus (max. 4000 units), followed by a continuous IV infusion of 12 units/kg/h (max. 1000 units/h); titrate to maintain aPTT between 1.5 and 2 times control.  Duration: continued for  up to at least 48 hours for UFH,  until the patient is discharged from the hospital (or 8 days, whichever is shorter) for either enoxaparin or fondaparinux, or  until the end of PCI or angiography procedure (or up to 72 hours following PCI for bivalirudin). 56
  57. Nitrates  Similar indication and dose recommendation to STE ACS  BBs  Recommendations are similar to STE ACS  Calcium Channel Blockers  Should not be administered to most patients.  Agent selection and indication for NSTE-ACS is identical to STEMI 57
  58. SECONDARY PREVENTION FOLLOWING MI  The long-term goals following MI are as follow: 1. Control modifiable CHD risk factors 2. Prevent development of systolic heart failure 3. Prevent recurrent MI and stroke 4. Prevent death, including sudden cardiac death 58
  59. Late hospital care/secondary prevention agents for both types of MI 59 All patients (ABAS) 1. Antiplatelet (ASA indefinitely +P2Y12 inhibitors ≥ 12 months) 2. BBs (within 24 hours of ED visit) indefinitely if no CI 3. ACEIs/ARBs 4. Statins (high-intensity) 5. NTG PRN On selected pnts 1. Aldosterone antagonists 2. Clopidogrel 3. warfarin
  60. Anticoagulants  Warfarin should be considered in selected patients following an ACS,  patients with an LV thrombus,  patients demonstrating extensive ventricular wall- motion abnormalities on cardiac echocardiogram, and  patients with a history of thromboembolic disease or chronic atrial fibrillation. 60
  61. EVALUATION OF THERAPEUTIC OUTCOMES Monitoring parameters for efficacy of therapy include:  relief of ischemic discomfort;  return of ECG changes to baseline; and  absence or resolution of heart failure signs. 61

Notes de l'éditeur

  1. CONDITION/DISORDER SYNONYMS Angina pectoris. Coronary artery disease. DEFINITION Lack of oxygen and decreased or no blood flow to myocardium resulting from coronary artery narrowing or obstruction.
  2. Race. African Americans have more severe high BP than Caucasians and therefore have a higher risk of heart disease. Heart disease risk is also higher among Mexican Americans, American Indians, and some Asian Americans. This is partly due to higher rates of obesity and diabetes in these populations.
  3. Response to nitroglycerin or rest. Cardiac enzymes are normal in stable angina; troponin T or I, myoglobin, and creatinine kinase myocardial band (CK-MB) may be elevated in unstable angina
  4. Prevent acute coronary syndromes and death; Alleviate acute symptoms of myocardial ischemia Prevent recurrent symptoms of myocardial ischemia; and Avoid or minimize adverse treatment effects.
  5. Door-to-balloon time is a phrase that denotes the time between the arrival of a patient with STEMI in the emergency room until the time that a balloon is inflated in the occluded, culprit coronary artery.
  6. ACC/AHA for the use of antiplatelet agents in the management of SIHD include a Class I recommendation for the use of aspirin 75 to 162 mg daily. 1 Aspirin should be continued indefinitely in the absence of contraindications (LOE A). Clopidogrel is considered an appropriate alternative when aspirin is contraindicated (LOE B). The guidelines state that treatment with aspirin (75-162 mg daily) and clopidogrel 75 mg daily might be reasonable in certain high-risk patients with SIHD (Class IIb, LOE B recommendation).
  7. ecommendations from the ACC/AHA include a Class I recommendation to use ACE inhibitors in all patients with SIHD who also have HTN, DM, HFrEF, or chronic kidney disease, unless contraindicated (LOE A). 1 ARBs are recommended for the same patient populations if they are intolerant to ACE inhibitors (LOE A). It is a Class IIa recommendation to use ACE inhibitors in patients with both SIHD and other vascular diseases (LOE B), and ARBs in these patients if intolerant to ACE inhibitors (LOE B).
  8. regimens. 47 Current guidelines recommend that all patients with known ASCVD, such as SIHD, should receive high-intensity statin therapy to achieve a 50% or more reduction in LDL-C. 48 Patients over the age of 75 years, or those who cannot tolerate high-intensity statin therapy, should receive moderate-intensity statin therapy to achieve a 30% to 50% reduction in LDL-C. In patients with clinical ASCVD who do not achieve a 50% reduction in LDL-C or who have an LDL ≥100 mg/dL (2.59 mmol/L) on high-intensity statin therapy, the additional nonstatin therapies such as ezetimibe, bile-acid sequestrates, or PCSK9-inhibitors may be considered
  9. Drugs used to treat HTN in patients with SIHD commonly include agents that can be used to treat the symptoms of the disease. β-blockers are often used to control angina symptoms and they also lower BP. Patients may also be on ACE inhibitors to reduce CV risk. Like HTN, the glycemic target for patients with DM, including those with SIHD, is the subject of considerable debate. Studies have found that achieving an A1c of less than 7% (53 mmol/mol Hgb) reduces microvascular complications from DM such as retinopathy, nephropathy, and neuropathy. Metformin is the drug of first choice for the treatment of DM type 2, including patients with SIHD.
  10. . All patients with CAD should have access to SL NTG tablets or spray for the treatment of acute episodes of angina.
  11. Provide some ↑ in supply by inducing coronary vasodilation & preventing vasospasm.
  12. ACS is classified according to electrocardiogram (ECG) changes into STEMI or NSTE-ACS (NSTEMI and UA) (Fig. 17-1).3 A STEMI occurs when symptoms of myocardial ischemia occur in conjunction with new STE with subsequent release of biomarkers of myocardial necrosis, mainly troponins T or I.2 Image not available. A STEMI typically results in an injury that transects the thickness of the myocardial wall. Following a STEMI, pathologic Q waves are frequently seen on the ECG, indicating transmural MI, whereas such an ECG manifestation is seen less commonly in patients with NSTEMI.3 NSTEMI is limited to the subendocardial myocardium and is not as extensive as STEMI. NSTEMI differs from UA in that ischemia is severe enough to produce myocardial necrosis resulting in the release of a detectable amount of troponins T or I, from the necrotic myocytes in the bloodstream.
  13. NSTEMI differs from UA in that ischemia is severe enough to produce myocardial necrosis resulting in the release of a detectable amount of troponins T or I, from the necrotic myocytes in the bloodstream.
  14. Patients with STEMI are of the highest priority and should be emergently referred to the cardiac catheterization lab for primary PCI Patients with NSTE-ACS will undergo additional risk stratification to determine the best approach, which is usually an early invasive approach (eg, PCI) for intermediate- and high-risk patients or a more conservative, ischemia-guided management plan without planned PCI for those with either the lowest risk for coronary event or contraindications to the invasive procedure itself Regardless of treatment strategy planned (early invasive approach or ischemia-guided approach), general treatment measures for intermediate- and high-risk patients include admission to the hospital, oxygen administration, antithrombotic t/t initiated
  15. Short-term desired outcomes in a patient with ACS are: (a) early restoration of blood flow to the infarct-related artery to prevent infarct expansion (in the case of MI) or prevent complete occlusion and MI (in UA); (b) prevention of death and other MI complications; (c) prevention of coronary artery reocclusion; and as evidence of restoration of coronary artery blood flow; (d) relief of ischemic chest discomfort; and (e) resolution of ST-segment and T-wave changes on the ECG. Long-term desired outcomes are control of CV risk factors, prevention of additional CV events, including reinfarction, stroke, and HF, and improvement in quality of life.
  16. Selecting evidence-based therapies for patients without contraindications results in lower mortality.17,18 General treatment measures for all STEMI and high- and intermediate-risk NSTE-ACS patients include admission to hospital, oxygen administration (if oxygen saturation is low, less than 90%), continuous multi-lead ST-segment monitoring for arrhythmias and ischemia, frequent measurement of vital signs, bed rest for 12 hours in hemodynamically stable patients, avoidance of the Valsalva maneuver (prescribe stool softeners routinely), and pain relief
  17. THROMBINS2 (Thienopyridine, Heparin, Reninangiotensin-aldosterone system, Oxygen, Morphine, β-blocker, Intervention [eg, PCI], Nitroglycerin, Statin/Salicylate [eg, aspirin])
  18. aOptions after coronary angiography also include medical management alone or CABG surgery. bClopidogrel preferred P2Y12 inhibitor when fibrinolytic therapy is utilized in DAT. No loading dose recommended if age older than 75 years. cGiven for up to 48 hours or until revascularization-SC UFH. dSC enoxaparin/fondaparinux: Given for the duration of hospitalization, up to 8 days or until revascularization. eIf pretreated with UFH, stop UFH infusion for 30 min prior to administration of bivalirudin (bolus plus infusion). fIn patients with STEMI receiving a fibrinolytic or who do not receive reperfusion therapy, administer clopidogrel for at least 14 days and ideally up to 1 year. (CI, contraindication; FMC, first medical contact; GPI, glycoprotein IIb/IIIa inhibitor)
  19. The mortality benefit of fibrinolysis is highest with early administration and diminishes after 12 hours.2 The use of fibrinolytics between 12 and 24 hours after symptom onset should be limited to patients with ongoing ischemia. Given within 30 min of arrival for patients presenting within 12 hours of onset of chest discomfort to a hospital not capable of primary PCI and cannot be transferred and undergo PCI within 120 min of medical contact. Also consider for patients with persistent ischemic symptoms who present within 12 to 24 hours of symptom onset. Consult product information for list of absolute and relative contraindications.
  20. although the risk of major bleeding, particularly gastrointestinal bleeding, appears to be reduced by using lower doses of aspirin, low-dose aspirin, taken chronically, is not free of adverse effects. Patients should be counseled on the potential risk of bleeding. Aspirin therapy should be continued indefinitely
  21. Clopidogrel. For patients with aspirin allergy, use 300–600 mg loading on day 1, followed by 75 mg/day, continued indefinitely. For patients treated with fibrinolytics and in those receiving no revascularization, use 75 mg or 300 mg on day 1 followed by 75 mg/day for up to 1 year plus aspirin 75–325 mg once daily. For patients undergoing primary PCI, Use 300–600 mg loading followed by 75 mg/day plus aspirin 81 mg once daily.
  22. UFH, administered as an IV bolus followed by a continuous infusion, is a first-line anticoagulant for treatment of patients with STE ACS, both for medical therapy and for patients undergoing PCI. Anticoagulant therapy should be initiated in the emergency department and continued for at least 48 hours in selected patients who will be bridged over to receive chronic warfarin anticoagulation following acute MI If a patient undergoes PCI, UFH is discontinued immediately after the procedure.
  23. UFH, administered as an IV bolus followed by a continuous infusion, is a first-line anticoagulant for treatment of patients with STE ACS, both for medical therapy and for patients undergoing PCI. Anticoagulant therapy should be initiated in the emergency department and continued for at least 48 hours in selected patients who will be bridged over to receive chronic warfarin anticoagulation following acute MI If a patient undergoes PCI, UFH is discontinued immediately after the procedure.
  24. Nitrates promote the release of nitric oxide from the endothelium, which results in venous and arterial vasodilation at higher doses. Venodilation lowers preload and myocardial oxygen demand. Arterial vasodilation relieves coronary artery vasospasm, dilating coronary arteries to improve myocardial blood flow and oxygenation.
  25. non-DHP CCBs (eg, diltiazem, verapamil) to treat angina symptoms in patients with ACS who have a contraindication, have intolerance, or are refractory to β-blockers in the absence of left ventricular dysfunction, risk factors for cardiogenic shock, and atrioventricular conduction defects
  26. Similar to STE ACS treatment with a few exceptions fibrinolytic therapy contraindicated GP IIb/IIIa receptor blockers (abciximab, eptifibatide) administered to high-risk patients undergoing invasive method, like coronary angiography Morphine is administered to patients with refractory angina as an analgesic and a venodilator that lowers preload. These agents should be administered early, while the patient is still in the emergency department.
  27. Analgesia and anti-emetics The pain of myocardial infarction is usually severe and requires potent opiate analgesia. Intravenous diamorphine 2.5–5 mg (repeated as necessary) is the drug of choice and is not only a powerful analgesic but also has a useful anxiolytic effect. The use of opiates may be associated with nausea and vomiting which can be prevented with anti-emetic drugs such as cyclizine 50 mg or metoclopramide 10 mg given intravenously. Opiate analgesia may also be associated with arterial hypoxaemia (see above). For some patients the psychological stress of a coronary event and the environment of a coronary care unit can provoke severe anxiety; the use of diazepam 2–5 mg orally as an anxiolytic and hypnotic may be useful.
  28. SL NTG followed by IV NTG for patients with persistent ischemia, HF symptoms, or uncontrolled HTN; continue IV NTG for about 24 hours after ischemia relief. Dose similar to STE ACS BBs Recommendations are similar to STE ACS In absence of CIs, initiate oral βBs within 24 hours of admission to all patients and continue indefinitely. Consider IV βBs for hemodynamically stable patients who present with persistent ischemia, HTN, or tachycardia. βBs are continued indefinitely in patients with LVEF < 40% (0.40) & for at least 3 years in normal LV function. Calcium Channel Blockers Should not be administered to most patients. Second-line tt for CIs to βBs and those with continued ischemia despite βB and nitrate therapy. Agent selection for NSTE-ACS is identical to STEMI either diltiazem or verapamil preferred unless LV systolic dysfunction, bradycardia, or heart block, and then either amlodipine or felodipine is preferred. Immediate-release nifedipine is contraindicated, especially in the absence of a βB.
  29. All patients at discharge: ASA/clopidogrel β-blocker Statins /high intensity/ ACE inhibitor or ARB NTG