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Myocardial Infarction Acute Coronary Syndrome Myocardial Infarction (MI) or Acute Coronary Syndrome (ACS) MI is a result of reduced blood flow through one of the coronary arteries. This causes myocardial ischemia, injury, and necrosis. Acute Coronary Syndrome This term covers a range of thrombotic coronary artery diseases, including unstable angina, ST elevation myocardial infarction (STEMI or Q wave MI), and non ST elevation myocardial infarction (NSTEMI or non-Q wave MI). Patients with ACS have some degree of coronary artery occlusion. Acute Coronary Syndrome Diagnosis Includes a complete history, physical examination, electrocardiogram, and serial cardiac enzymes. Differentiating ACS from non-cardiac chest pain is the primary challenge. Symptoms SOB/Dyspnea Chest pain Nausea/vomiting Orthopnea Diaphoresis Palpitations Apprehension Fatigue Pain in jaw, neck, upper arm Diaphoresis Lightheadedness or dizziness Syncope Risk Factors High blood pressure Elevated serum triglyceride levels, low density lipoprotein, high cholesterol, and homocysteine levels and decreased serum high-density lipoprotein levels Cigarette smoking Lack of physical activity Obesity Type 2 Diabetes Older age >45 men, >55 women Family history of chest pain, heart disease, or CVA Stress Use of amphetamines or cocaine Excessive intake of saturated fats, carbohydrates, or salt Causes ACS may develop slowly over time by the building up of plaques in the coronary arteries. These plaques, are made of fatty deposits, causing the arteries to narrow and make it more difficult for blood to flow through them. This buildup of plaque is known as atherosclerosis. Eventually, this buildup means that your heart can’t pump enough oxygen-rich blood to the rest of your body, causing chest pain (angina) or a MI. Trigger Mechanism of Ischemia Passive collapse of a vessel near a stenotic region Spasm, related to sympathetic tone Plaque rupture produces an ulcerated area that attracts platelets Platelets attracted to plaque cause a production of a powerful vasoconstrictor (thromboxane A2) Protective mechanisms are prostacyclin and nitric oxide are made by the endothelium and are vasodilators and plaque inhibitors Vasospasm Occurrences -Occurs in large or small arteries -Usually occurs near an artery damaged by plaque Factors that precipitate vasospasm -Cold exposure -Anxiety, fear -Exercise, hyperventilation, cocaine abuse Factors that prevent vasospasm -nitroglycerin, calcium channel blockers -Endothelial factor Law of Supply and Demand If myocardial oxygen demand increases, so must oxygen supply To effectively increase oxygen supply, coronary perfusion must also increase Tissue hypoxia the most potent stimulus, causes coronary arteries to dilate and increases coronary blood flow Normal coronary vessels can dilate and increase blood flow five to six times above resting levels. However, stenotic,diseased vessels can’t dilate, so oxygen deficit may result Oxygen Balancing Act 4 major determinants of myocardial oxygen demand -heart rate -contractile force -muscle mass -ventricular wall tension Cardiac workload and oxygen demand increase if the heart rate speeds up or if the force of contractions becomes stronger. This can occur in HTN, ventricular dilation, or heart muscle hypertrophy. Oxygen Balancing Act When the myocardial cell is lacking in oxygen, the cells begin to suffer injury Normal circulation and oxygenation need to be restored Remember ischemia and injury ARE reversible. Infarct or cell death is NOT!! Tests and Diagnostics Electrocardiogram: Ischemia, Injury, Infarction BMP, CBC, Cardiac Biomarkers Echocardiogram CXR Nuclear myoview CT angiogram Coronary artery calcium scoring Coronary angiogram (cardiac Catheterization) Acute Myocardial Infarction Artery Specific Symptomology Left Main Coronary Artery Extensive anterior wall infarct EKG Location - V1-V6 Complications Sudden cardiac death Dysrhythmias Ventricular rupture/aneurysm Ventricular septal defect Congestive heart failure Cardiogenic shock Artery Specific Symtomology Left Anterior Descending (LAD) Artery Septal/Anterior wall infarct (or combination of both) EKG Location – V1, V2 (septal); V3, V4 (anterior) Complications Dysrhythmias Ventricular aneurysm Congestive heart failure Cardiogenic shock Left Anterior Descending Artery (LAD) LAD Supplies -Anterolateral myocardium -Apex -Interventricular septum -Typically supplies 45-55% of LV -RBB -Anterior fascicle of the LBB Artery Specific Symptomology Right Coronary Artery (RCA) -Inferior/Posterior wall infarct (or both) -RV -ECG locationII,III,aVF RCA Complications Dysrhythmias Papillary muscle rupture with mitral regurgitation CHF Right ventricular failure Right Coronary Artery RCA Supplies -RA and RV -Inferior and posterior walls of the LV -SA node in 55% of people -AV node in 90% of people -Posterior fascicle of the LBB Artery Specific Symptomology Left Circumflex Artery Lateral wall infarct EKG Location– High: I, aVL; Low: V5, V6 Complications Dysrhythmias Congestive heart failure Circumflex Artery Supplies -Lateral wall of LV -Inferior and posterior wall of LV (10% of population) -Septal perforator of LBB -SA (45% of population) -AV node (10% of population) STEMI (ST Elevation MI) Occurs with myocardial injury Occurs when tissue is damaged, before it becomes necrotic and has no electrical activity Defined as elevation in two or more leads Elevation is at least 1 mm per lead Q Waves and MI Small Q waves (septal depol) are usual in leads I, aVL, V5, and V6 (the lateral leads) Q criteria for MI -duration >/= 0.04 sec or -amplitude >/= ¼ of the R wave in the same lead Present when damage involves the entire thickness of the myocardial wall NSTEMI (Non ST Elevation MI) Smaller area of damaged heart muscle from sub-total occlusion of coronary artery No ST elevations on the 12 lead ecg Mechanisms of ST Depression K+ is lost from the ischemic tissue Positive ion loss produces a current vector toward the endocardium, opposite of the mean QRS vector This appears as ST depression on the ecg Complications of an MI Dysrhythmias Ventricular or atrial rupture/aneurysm Ventricular septal defect Congestive heart failure/pulmonary edema Cardiogenic shock Sudden cardiac death Pericarditis Mural thrombi causing cerebral or pulmonary emboli Papillary muscle rupture with acute mitral regurgitation Psychological problems Electrical Conduction System ST Segment Changes Primary ST Segment Depression Ischemic Heart Disease 12 Lead ECG’s Rate Rhythm Intervals Axis Hypertrophy Ischemia/Infarct ECG Changes In ACS Ischemia: T wave abnormality, flat or down-sloping T wave Injury: ST segment elevation Infarction: Q wave Normal 12 Lead ECG I aVR V1 V4 II aVL V2 V5 III aVF V3 V6 Main Arteries and Areas They Perfuse Inferior……………………………………RCA, LCx Inferior RV……………………………..Proximal RCA Inferoposterior……………………….RCA, LCx Isolated RV…………………………….LCx Isolated Posterior………………….RCA, LCx Anterior………………………………….LAD Anteroseptal…………………………..LAD Anteroseptal-lateral……………….Proximal LAD Anterolateral, inferolateral, or posterolateral…………………………LCx Indicative and Reciprocal Leads Area of Infarct Indicative leads Reciprocal leads Inferior II, III, aVF I, aVL Septal V1, V2 II, III, aVF Anterior V3, V4 II, III, aVF Lateral I, aVL, V5, V6 II, III, aVF Posterior V7, V8, V9 V1, V2 Lead Summary I Lateral aVR Circumflex Artery V1 Septal V4 Anterior LAD, RCA, Posterior, LM LAD, LM II Inferior aVL Lateral V2 Septal V5 Lateral RCA Circumflex LAD, LM Circumflex, LM III Inferior aVF inferior V3 Anterior V6 Lateral RCA RCA LAD, LM Circumflex, LM Normal Sinus Rhythm Primary ST Segment Depression Ischemic Heart Disease Inferior Wall MI Anterioseptal Wall MI Transmural Acute Anterior MI Acute Anterior Wall Infarction Old Inferior Wall Infarction Acute Inferior Wall Infarction Old Inferior Wall Infarction + Afib + PVC’s Pharmacological Management MONA Morphine is used for pain relief Oxygen may reduce ischemic injury Nitrates are used to vasodilate coronary arteries Aspirin dissolves fibrin in the clot and prevents platelet aggregation Morphine Usually given 2-4mg IV for continued angina after use of nitrates Causes venodilation, decreases HR, BP, workload of your heart, which decreases the amount of oxygen that your heart needs Decreases anxiety-Antiolytic CAUTION use of other analgesics such as NSAIDS…can increase mortality, HF, reinfarction Oxygen Indications -Respiratory distress -Keep oxygen saturations >90% -Prevent hypoxemia Nitroglycerine Used for treating chest pain and angina temporarily widening narrowed blood vessels by vasodilating the arteries. This improves blood flow to and from your heart. NTG is most valuable in increasing oxygen supply if good collateral circulation exists. It also increases venous and arterial dilation. Nitroglycerine (NTG) Indications -Relief ongoing ischemic discomfort -Control of Hypertension -Management of pulmonary congestion Avoid if: -BP <90mmHg -Recent use of phosphodiestrase inhibitors within 24-48 hours (ex. Viagra, Cialis, Levitra) -Suspect RV infarction Aspirin Decreases platelet aggregation, helping to keep blood flowing through narrowed coronary arteries. One of the first medications given in the setting of suspected ACS. It should be chewed so it is absorbed in the blood stream more quickly. Beta Blockers Beta Blockers -Relax your heart muscle - Slow your heart rate and decrease your blood pressure -Increase the blood flow through your heart, decreasing chest pain and the potential for damage to your heart during a heart attack. -Decrease myocardial workload & myocardial oxygen demand by decreasing HR and contractility. Beta Blockers Oral BB therapy within first 24 hrs unless contraindicated -No signs of heart failure or low output state -No increased risk of cardiogenic shock Beta Blockers Carvedilol (Coreg) non selective, + alpha blocking Labetalol non selective, + alpha blocking Nadolol (Corgard) non selective Pindolol (Visken) non selective Propanolol (Inderal LA) non selective Sotalol (Betapace) non selective Atenolol (Tenormin) B1 selective Metoprolol (Lopressor, Toprol XL) B1 selective Nebivolol (Bystolic) B1 selective Acebutolol (Sectral) B1 selective Angiotensin-converting enzyme (ACE) inhibitors and Angiotensin Receptor Blockers (ARBs) Indications for ACE/ARB - allow blood to flow from your heart more easily - Low Ejection Fraction - Lower blood pressure and may prevent a second heart attack - Reduce mortality by about 20% when used on a long-term basis in high risk post infarct patients - Early initiation in key in the potential benefit of early ventricular remodeling. ACE/ARB’s Give within the first 24 hours -Anterior infarction -Pulmonary congestion or ejection fraction </= 40% -Can cause hyperkalemia, renal insufficiency, cough or angioedema ACE/ARB’s Benazepril (Lotensin) Captopril (Capoten) Enalapril (Vasotec) Fosinopril (Monopril) Lisinopril (Prinivil,zestril) Moexipril (Univasc) Perindopril (Aceon) Quinapril (Accupril) Ramipril (Altace) Tradolapril (Mavik) Candesartan (Atacand) Irbesartan (Avapro) Telminsartan (Micardis) Valsartan (Diovan) Losartan (Cozaar) Olmesartan (Benicar) Calcium Channel Blockers Contraindicated in STEMI, low EF: Negative inotrope which decreases contractility Used for persistent symptoms of USA and NSTEMI when Beta Blockers are contraindicated Coronary vasodilator, smooth muscle relaxant, negative inotrope, negative chronotrope, negative dromotrope Used for chronic recurrent symptoms of angina, treatment of HTN and arrhythmias Different Classes of Calcium Channel Blockers Dihydropyridine CCB’s used to reduce SVR and arterial pressure, but not used to treat angina Amlodipine (Norvasc) Felodipine (Plendil) Nicardipine (Cardene, Madipine) Nisoldipine (Sular) Nifedipine (Procardia, Adalat) Non-Dihydropyridine are relatively selective for myocardium, reducing myocardial oxygen demand & reverse coronary vasospasm & are often used to treat angina Verapamil (Calan) Benzothiazepine CCB selective for vascular calcium channels, reduce arterial pressure Diltazem (Cardizem) Antiplatelet Therapy Platelet Aggregation Inhibitors ASA Plavix (clopidogrel)Now generic Effient (prasugrel) Brilinta (ticagrelor) Ticlid (ticlopidine) -Used to prevent platelet aggregation. Heparin gtt may be prescribed to prevent clotting or extension of clot. Brilinta (Ticagrelor)/Antiplatelet MOA: Reduces platelet activation and aggregation Proven superior to clopidogrel across a broad range of ACS patients at reducing thrombotic CV events, including CV death Discontinue at least 5 days prior to any surgery Anticoagulants Unfractionated Heparin (UFH) Enoxaparin (Lovenox) Fondaparinux Glycoprotein IIb/IIIa inhibitors Unfractionated Heparin (UFH) Acute treatment of thromboembolic disorders Administered intravenously Monitored by PTT Short biologic half life of approximately 1 hour Enoxaparin (Lovenox) MOA: binds to antithrombin III, inhibits thrombin and Factor Xa (low molecular weight heparin) Indications for USA, NSTEMI, STEMI 1mg/kg SC Q12 hours Half-life 4.5-7 hours No monitoring Fondaparinux (Arixtra) Similar to enoxaparin in reducing ischemic events Substantially reduces major bleeding Can be used as treatment against HIT Given subcutaneously Long half life 17-21 hours No monitoring Glycoprotein IIb/IIIa Inhibitors Inhibits platelet aggregation Helps prevent occlusion of the coronary arteries, reducing the incidence of ischemic events Used in treating patients with USA Usually administered in combination with angioplasty with or without PCI Given in combination with heparin or ASA to prevent clotting before and during invasive heart procedures Examples -Abciximab (ReoPro) -Eptifibatide (Integrilin) -Tirofiban (Aggrastat) Fibrinolytics Drug that works to break up clots, “clot buster” Best outcome if administered within 12 hours or less after the onset of the symptoms Examples -Streptokinase (not used much anymore) -Tissue plaminogen activator (tPA, Alteplase -Urokinase -Retaplase -Tenecteplase Hospital Care Anti-Thrombotic Therapy Immediate ASA Clopidogrel, if ASA contraindicated ASA + clopidogrel for up to 1 month, if medical therapy or PCI planned Heparin (IV unfractionated, LMW) with antiplatelet agents above Enoxaparin preferred over UFH unless CABG is planned within 24 hours or with renal insufficiency Stress Testing Types of Stress Tests -Exercise -Vasodilators: Dypyridamole, Lexiscan, Adenosine, Dobutamine -Dobutamine or exercise Stress Echocardiogram Measure of Induced Ishemia -ECG changes with exercise or vasodilator -Perfusion defects with radionuclide myocardial perfusion imaging -Wall motion abnormalities with echocardiography Resting and Stress Myocardial Perfusion Imaging Reperfusion Pharmacologic Fibrinolysis Percutaneous coronary intervention Possible surgical measures Cardiac Catheterization Laboratory • In the cath lab the patient undergoes angioplasty ▫ Balloon-tipped catheter threaded through the femoral artery ▫ Threaded to the site of the blockage and inflated to remove the clot restoring normal blood flow ▫ Metal stents are often placed to keep the arteries open ▫ IABPs, Impella ventricular assist devices and temporary pacemakers are also placed if necessary Treatment of AMI in the Cardiac Catheterization Laboratory Angioplasty and stent implantation Mechanical thrombus extraction Blood thinners -ASA -Thienopyridines (clopidogrel) -GPIIb/IIIa inhibitors (abciximab) -Low molecular weight heparin Anatomy Cardiac Catheterization Left Coronary System Right Coronary System Cardiac Catheterization Acute Myocardial Infarction Thrombus in the Left Main Coronary Artery Plain old Balloon Angioplasty (POBA) 1977 POBA first trialed In the past, plain old ballon angioplasty or POBA, had the potential to cause elastic recoil effect Occurred in approximately 5-10% of patients within the first few hours or even minutes of surgery After the procedure the coronary artery experienced rebound and subsequent occlusion This often lead to complications including MI Balloon Angioplasty Angioplasty Causes Neointimal hyperplasia is the immune system’s reaction to the intrusion of angioplasty Damage incurred on the endothelial barrier at the site of balloon inflation, the extracellular matrix can become exposed Leads to hyperproliferation of smooth muscle cells A response prompted by growth factors and proteoglycans These cells move into the intima, where they cluster and form a lesion Angioplasty Continued The lesions become thickened and scarred The artery undergoes a subsequent remodeling of its structure End result is redevelopment of arterial blockage and obstructed flow, in other words restenosis Stents In 1994, J & J produced the PalmzSchatz Balloon expandable stent. The first approved by the FDA. In the past decade, over 25 companies have used various materials and designs in the construction of the bare metal stents (BMS). Over time, stents have achieved greater durability and flexibility PCI Procedural refinements: Stents Expandable metal mesh tubes that buttresses the dilated segment, limit restenosis. Drug eluting stents: further reduce cellular proliferation in response to the injury of dilatation Drug Eluding Stents Balloon Deployment of Stent Bare Metal Stents Tubular, lattent structure assembled by a range of metals. Should be spring like and flexible, conforming to the shape of the arterial wall Primary goal of the stent is to hold the inner wall in its newly compressed position, retaining the enlarged diameter Stent diameter range from 2mm-4mm, depending on the diameter of the vessel Bare Metal Stents Stents eliminated the concern for plain old balloon angioplasty’s elastic recoil effect Incidence of restenosis dropped to around 25% of patients, in-stent restenosis, or ISR within 3-6 months after surgery Again, this resulted from the body’s tendency toward neointimal hyperplasia Working with BMS’s, Interventional Cardiologists used various techniques to attempt to decrease the effects of restenosis by the use of brachytherapy, dose of radiation emitted from a catheter that inhibits cell division at the occluded site or anti-platelet drugs Bare Metal Stents and Restenosis Multiple strategies attempted to prevent restenosis (1990-1999): -thromboxane A2 receptor blockade -ACE inhibitors (Cilazapril) -Enoxaparin, low molecular weight heparin -Tirofiban -Abciximab Mostly Unsuccessful!! Bare Metal Stents and Restenosis Intra-Coronary Radiation(1999-2002) -Most useful for treatment of restenosis -Less useful in prevention Drug Eluting Stents (DES) First used in 2003 The interest in these anti-platelet drugs, coupled with the desire to eliminate ISR, inspired the development of DES’s This therapy involves coating the outside of a standard coronary stent with a thin polymer containing medication that can prevent scarring at the site of the intervention. Examples of Drug Eluting Stents Two FDA approved compounds: Paclitaxel anti-proliferative agent extracted from bark of Pacific Yew blocks cell mitosis Sirolimus immunosuppressive agent isolated from soil on Easter Island blocks cell progression by inhibiting DNA synthesis Current Drug Eluting Stents Cypher- Sirolimus(2003) Taxus- Paclitaxel(2004) Endeavor –Zotarilimus(2008) Xience V /Promus – Everolimus(2008) Drug Eluting Stents Future Use More complex coronary disease traditionally correlated with higher restenosis rates Lower restenosis rates with DES may improve outcome in more difficult patient groups Complex multivessel coronary disease Left main disease Disease in small vessels Long areas of stenosis Extreme vein-graft disease Coronary disease in diabetics Chronic total occlusions Vascular disease outside the heart ABSORB TRIAL Conventional stents are permanent ABSORB BVS is unique It gradually disappears over time Your artery does not need a permanent stent to remain open With ABSORB, your artery becomes free to move over time and meet the needs of your heart Processes needed to heal the plaque Resolution of inflammation Thrombus reorganisation Smooth muscle cell proliferation Re-endothelialisation Smooth muscle cell matrix synthesis Return of vasomotor regulation Drug eluting stents can inhibit all these processes + Foreign body reaction due to polymers giant cell inflammation Endothelialization BMS take about 30 days to reendothelialize DES can take up to one year or more to reendothelialize DES has a polymer coating and a drug, either sirolimus or paclitaxel, mixed into the polymer. This drug is delivered to the area of the opened artery over a period of a year or more An antiplatelet agent, Plavix or Effient, will be needed to decrease the tendency of their blood platelets to clot Cost of Dual Antiplatelet Therapy after DES $800- Bare metal stents $2400- Drug eluting stents + cost of dual antiplatelet therapy+ risk of bleeding Impella Ventricular Assist Device Bridges to aid in perfusion until a surgical procedure can be performed Assist device for either cardiogenic shock or porphylaxis http://www.abiomed.com/products/impella.cfm Impella Ventricular Assist Device • Provides up to 2.5 liters per minute ventricular unloading • Placed percutaneously via femoral artery • Threaded to and placed across aortic valve • Small catheter-mounted “impeller” motor blows blood across valve and into aorta •Effectively increases cardiac output and end organ perfusion • Decreases workload of the heart Impella Ventricular Assist Device Intra Aortic Balloon Pump “Counterpulsation Therapy” • 30-40cc balloon inserted to below aortic arch ▫ Rhythmic inflation/deflation in time with cardiac cycle ▫ Inflation during cardiac diastole – pushes blood back to aortic root to fill aortic arteries ▫ Deflation during cardiac systole – creates vacuum effect, helping to pull blood from the ventricle, decreasing cardiac workload and O2 consumption • Intra Aortic Balloon Pump Coronary Artery Bypass Grafting Failed PCI Persistent or recurrent ischemia not a candidate for PCI or fibrinolytic therapy or significant area myocardium at risk Cardiogenic shock within 36 hours of STEMI Severe multivessel or Left main disease Life-threatening ventricular arrhythmias in presence of >/= 50% left main and or tripple vessel disease Coronary Artery Bypass Grafting CABG 1967: Kolessov: LIMA LAD on a beating heart Favaloro: SVG on still heart Procedural refinements: arterial rather than vein grafts avoid the cardiopulmonary bypass machine smaller thoracotomy incision rather than sternotomy Discharge/Post Discharge Medications ASA if not contraindicated Clopidogrel, when ASA contraindicated ASA + Clopidogrel for up to 1 year Beta Blocker if not contraindicated Lipid Agents + diet, if LDL >130mg ACE inhibitor: CHF, EF <40%, DM, or HTN Nitrates Ranexa (Ranolazine) Indicated for chronic angina MOA: Unknown, reduces sodium induced calcium overload in myocytes Dosing 500mg-1000mg BID; max 2000mg/day QUESTIONS!!