293. ischemic heart disease
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AcuteNon-ST Elevation Acute Coronary Syndrom- NSTE ACS
Unstable AnginaNon-ST elevation MI
ST Elevation Myocardial Infarct STMI
Stable AnginaClass1Class2Class3Class 4
Chronic
DefinitionsAcute coronary syndrome is defined as myocardial ischemia due to myocardial infarction (NSTEMI or STEMI) or unstable anginaUnstable angina is defined as angina at rest, new onset exertional angina (<2 months), recent acceleration of angina (<2 months), or post revascularization angina
CAUSES ACS
Thrombus formationDownstream embolizationDynamic Obstruction (Spasm –f.e. Prinzmetal ‘s Variant AnginaInvreased oxygen demand
DiagnosisDx of acute coronary syndrome is based on history, physical exam, ECG, cardiac enzymesPatients can then be divided into several groups
Non-cardiac chest pain (i.e., Gastrointestinal, musculoskeletal, pulmonary embolus) Stable angina Unstable angina Myocardial infarction (STEMI or NSTEMI) Other cardiac causes of chest pain (i.e., aortic dissection, pericarditis)
Diagnosis
Severe chest discomfortOccurs at restLasting >10 minRecent onset (up to 2 weeks)Crescendo pattern
Pathophysiology of ACSPlaque rupture and subsequent formation of thrombus – this can be either occlusive or non-occlusive (STEMI, NSTEMI, USA)Vasospasm such as that seen in Prinzmetal’s angina, cocaine use (STEMI, NSTEMI, USA)Progression of obstructive coronary atherosclerotic disease (USA)In-stent thrombosis (early post PCI)In-stent restenosis (late post PCIPoor surgical technique (post CABG)
Pathophysiology of ACS
Acute coronary syndromes can also be due to secondary causes
ThyrotoxicosisAnemiaTachycardiaHypotensionHypoxemiaAterial inflammation (infection, arteritis)
Date of download: 9/30/2015
From: Diagnosis of Stable Ischemic Heart Disease: Summary of a Clinical Practice Guideline From the American College of Physicians/American College of Cardiology Foundation/American Heart Association/American Association for Thoracic Surgery/Preventive Cardiovascular Nurses Association/Society of Thoracic SurgeonsAnn Intern Med. 2012;157(10):729-734. doi:10.7326/0003-4819-157-10-201211200-00010
Clinical Classification of Chest Pain
Table Title:
Copyright © American College of Physicians. All rights reserved.
Pre-test ProbabilityIn the absence of abnormal findings on physical exam, ECG, or enzymes, the pre-test probability of acute coronary syndrome must be determined by the clinician A good history is crucial (is the chest pain typical or atypical; what are the associated symptoms) Determination of risk factors is also crucial (male, age >55, smoking, DM, HTN, FamHx, hyperlipidemia, known CAD)
Treatment of ACS; Aspirin
Aspirin is an antiplatelet agent that initiates the irreversible inhibition of cyclooxygenase, thereby preventing platelet production of thromboxane A2 and decreasing platelet aggregationAdministration of ASA in ACS reduces cardiac endpoints
ACC/AHA Guidelines for Aspirin Therapy
Aspirin should be given in a dose of 75-325 mg/day to all patients with ACS unless there is a contraindication (in which case, clopidogrel should be given)
Treatment of ACS; Clopidogrel
Clopidogrel is a potent antiplatelet agentIt should be administered to all patients who cannot take ASAThe CURE trial suggests a benefit to adding Clopidogrel to ASA/Heparin in patients going for PCIGive 300 mg loading dose followed by 75 mg/day
AHA/ACC Guidelines for ClopidogrelClopidogrel should be administered to patients who cannot take ASA because of hypersensitivity or gastrointestinal intoleranceIn hospitalized patients in whom an early, noninterventional approach is planned, clopidogrel should be added to ASA as soon as possible on admission and administered for at least 1 month and up to 9 months. Do not use clopidogrel if there is any possibility patient may be candidate for CABG
Treatment of ACS; NitratesNitroglycerin is considered a cornerstone of anti-anginal therapy, despite little objective evidence for its benefitBenefit is thought to occur via reduction in myocardial O2 demand secondary to venodilation induced reduction in preload as well as coronary vasodilation and afterload reductionTitrate to relief of chest pain; chest pain = death of myocardial cellsNo documented mortality benefit
Treatment of ACS; Beta Blockers
Beta Blockers reduce myocardial oxygen demand by reducing heart rate, contractility, and ventricular wall tensionAdministration of beta blockers in ACS reduces cardiac endpoints
AHA/ACC Guidelines for Beta Blocker Therapy
Intravenous beta blockers should be used initially in all patients (without contraindication) followed by oral beta blockers with the goal being decrease in heart rate to 60 beats per minuteA combination of beta blockers and nitrates can be viewed as first line therapy in all patients with ACS
Treatment of ACS; Heparin
Heparin (unfractionated heparin or UFH) has traditionally been the mainstay of therapy in acute coronary syndromes as its efficacy has been documented in several large, randomized trials
Treatment of ACS; LMWH
More recent studies indicate that low molecular weight heparin is also effective in the reduction of end points such as myocardial infarction or deathSome studies report that LMWH, when used in combination with ASA, may be superior to continuous infusion of Heparin
ACC/AHA Guidelines for Heparin Therapy
All patients with acute coronary syndromes should be treated with a combination of ASA (325 mg/day) and heparin (bolus followed by continuous infusion with goal of PTT 1-2.5X control) or ASA and low molecular weight heparin unless one of the drugs is contraindicated
Treatment of ACS; ACE-I
The best documented mechanism by which these agents act is to reduce ventricular remodeling over days to weeks after myocardial damage. However, there is data that a mortality benefit exists when these agents are used early in the course of ACSAdministration of ACE-I in ACS reduces cardiac endpoints
AHA/ACC Guidelines for ACE-I Therapy
ACE-I should be administered to all patients in the first 24 hours of ACS provided hypotension and other clear cut contraindications are absent
Treatment of ACS; Statins
Statins may be of benefit in ACSPossible mechanisms include plaque stabilization, reversal of endothelial dysfunction, decreased thrombogenicity, and reduction of inflammation
TIMI Risk Score
Age >65 yrsDaily ASA Therapy (>7 days prior to event)Symptoms of Unstable AnginaDocumented CAD (stenosis > 50%)3 or more traditional cardiac risk factorsElevated cardiac enzymesECG changes
TIMI Risk Score
Score of 3 or less = low riskScore of 4-5 = intermediate risk (use IIBIIIA)Score of 6-7 = high risk (use IIBIIIA)
Treatment of ACS; Emergent Revascularization
In the setting of STEMI primary PCI is associated with better outcomes than thrombolysisEmergent PCI is also indicated in the setting of a new LBBB
PCI Trials
PAMI (PTCA vs. thrombolysis)Netherlands Trials (PTCA vs. thrombolysis)GUSTO IIB (PTCA vs. thrombolysis)DANAMI-2 (stenting vs. thrombolysis)STAT (stenting vs. thrombolysis)
AHA/ACC Guidelines for Primary PCIPrimary PCI is indicated as an alternative to thrombolysis when the following criteria are met:
STEMI or new LBBBCan undergo PCI within 12 hours of the onset of symptomsThe MD doing the intervention does more than 75 PCI’s/yrThe procedure is done in a center that does more than 200 PCI’s/yr and has surgical backup
Conclusions; Approach to Chest Discomfort
Good History and Physical (note time and duration of symptoms)Careful evaluation of ECG (compare to previous when possible)Check Cardiac EnzymesMonitor on TelemetryOxygen
Conclusions; Treatment of NSTEMI/USA
ASANTG (consider MSO4 if pain not relieved)Beta BlockerHeparin/LMWHACE-I+/- Statin+/- Clopidogrel (don’t give if CABG is a possibility)+/- IIBIIIA inhibitors (based on TIMI risk score)
Conclusions; Treatment of STEMI ASANTG (consider MSO4 if pain not relieved)Beta BlockerHeparin/LMWHACE-I+/-Clopidogrel (based on possibility of CABG)IIBIIIA +/- StatinActivate the Cath Lab!!!
Definition of MI - Acute Myocardial lnfarction
1. Evidence of myocardial necrosis: cardiac biomarker values (preferably cardiac troponin [cTn]) and with at least one of the following. Symptoms of ischemia. New or presumed new significant ST-T changes or new LBBB. Development of pathologic Q waves on ECG. Imaging evidence of new loss of viable myocardium or new regional wallmotion abnormality. Identification of an intracoronary thrombus by angiography or autopsy. Cardiac death with symptoms suggestive of myocardial ischemia andpresumed new ischemic ECG changes of new LBBB , but death occurredbefore cardiac biomarkers were obtained or before cardiac biomarkervalues would be increased. Percutaneous coronary intervention (PCI)-related MI is arbitrarily de 有ned by elevation of cTn val ues (>5 x 99th percentile U RL) in patients with normal 七 as 巳 line val ues ( 王 99th percentile URL) or a rise of cTn val ues >20% ifthe baseline val ues are elevated and a re s 旧 ble or 句 I ling. In addition , either(i) symptoms sugg 巳 stive of myoca rdial ischemia , or (ii) new ischemic ECGchanges , or (iii) angiographic 白 ndings consistent with a procedural complication , or (iv) imaging demonstration of new loss of viabl 巳 myocardium ornew regional wall motion a bnormality a re required. Stent thrombosis associated with MI when detected by coronary angiography or autopsy in the setting of myocardial ischemia and with a rise and/or fal l of cardiac biomarker val ues with at least one value abo 、 e the 99thpercentile URL. Coronary artery bypass grafting (CAßG)-r 巳 lated MI is a rbitrarily definedby elevation of cardiac biomarker values (> 1 0 x 99th percentile U RL) inpatients with normal baseline cTn values ( 呈 99th percentile U RL). In addition , either (i) new pathologic Q w 讥 es or new Lßßß , or (ii) angiog日 phicdocumented new graft or new native coronary artery Occlu5ion , or (iii)imaging evidence of n 巳 N 1055 of viable myocardium or new regional wallmotion abnorma
Criteria for Prior Myocardial l nfarctionAny one of the fol lowing criteria meets the diagnosis for prior MI. Pathologic Q waves with or without 5ym 仁 tom5 in the ab5 巳nce of nonischemlc caU5 巴 5. I maging evidence of a region of 1055 of viable myocardium that i5 thinnedand fails to contract , in the absence of a noni5chemic cause.. Pathologic 有 ndings of a prior M
CLASSIFICATION OF MYOCARDIAL INFARCTlON
Type 1: Sponta neous Myocardial lnfarctionType 2: Myocardial l nfarction Secondary to an Ischemic ImbalanceType 3: Myocardial l nfarction Resulting in Death When Biomarker Values Are UnavailableType 4a: Myocardia 川 nfarction Related to Percutaneous Coronary Intervention (PCI)Type 4b: Myocardial lnfarction Related to Stent ThrombosisType 5: Myocardial l nfarction Related to Coronary Artery Bypass Grafting (CABG)
Date of download: 9/30/2015
From: Diagnosis of Stable Ischemic Heart Disease: Summary of a Clinical Practice Guideline From the American College of Physicians/American College of Cardiology Foundation/American Heart Association/American Association for Thoracic Surgery/Preventive Cardiovascular Nurses Association/Society of Thoracic SurgeonsAnn Intern Med. 2012;157(10):729-734. doi:10.7326/0003-4819-157-10-201211200-00010
Pretest Likelihood of Coronary Artery Disease in Symptomatic Patients According to Age and Sex
Copyright © American College of Physicians. All rights reserved.
Complications
Ventricular DisfunctionHemodinamic AssessmentHypovolemiaCardiogenic shockArrhythmias, conduction disturbancesPericarditisAneurism
Complications MIComplication Type Manifestations
Ischemic Angina, reinfarction, infarct extensionMechanical Heart failure, cardiogenic shock, mitral
valve dysfunction, aneurysms, cardiac rupture
Arrhythmic Atrial or ventricular arrhythmias, sinus or atrioventricular node dysfunction
Embolic Central nervous system or peripheral embolization
Inflammatory Pericarditis
Date of download: 9/30/2015
From: Diagnosis of Stable Ischemic Heart Disease: Summary of a Clinical Practice Guideline From the American College of Physicians/American College of Cardiology Foundation/American Heart Association/American Association for Thoracic Surgery/Preventive Cardiovascular Nurses Association/Society of Thoracic SurgeonsAnn Intern Med. 2012;157(10):729-734. doi:10.7326/0003-4819-157-10-201211200-00010
Comparing Pretest Likelihoods of Coronary Artery Disease in Low-Risk Symptomatic Patients and High-Risk Symptomatic Patients
Table Title:
Copyright © American College of Physicians. All rights reserved.
Heart - Pathology
Syndrome StenosesPlaque
Disruption Plaque-Associated ThrombusStable angina >75% No NoUnstable angina Variable Frequent Non-occlusiveTransmural MI Variable Frequent Occlusive
Subendocardial MI
Variable Variable Widely variable
Sudden death severe Frequent Often small
Heart - PathologyIschemic Heart Disease
Angina PectorisChest discomfort = prolonged, recurrent, different qualitiesCause = transient myocardial ischemia( seconds to minutes)Patterns
Stable = 75% vessel block, transient ( <15 minutes), aggravated by exertion, relived by rest & Nitroglycerin (VD)Prinzmetal = coronary spasm, episodic, Typical EKG change – ST elevation, Relived by VD but not restUnstable = 90% vessel block or Acute plaque change ( superimposed thrombus), prolonged ( >15 min.), not relived by rest, VD, Pre-infarction Angina
MI - Types
TransmuralFull thickness
Superimposed thrombus in atherosclerosis
Focal damage
Sub-endocardialInner 1/3 to half of ventricular wallDecreased circulating blood volume( shock, Hypotension, Lysed thrombus)Circumferential
Heart - PathologyIschemic Heart Disease
MI= Also called Heart attackIncidence = disease of old
elderly (45% in 65 yrs. old) young ( 10% in 40yrs. Old),
Sex = Male > FemaleEthnic = same in African & AmericanRisk factors
Major modifiable- DM, HTN, Smoking, HypercholesterolemiaHRT for Postmenopausal females – will not protect the heart
Heart - PathologyIschemic Heart Disease
MIPathogenesis
Coronary vessel occlusionAtherosclerosis with thrombus = MC cause ( 90% cases)Others = vasospasm (10%)
Most important mechanism = dynamic changes in the plaque (rather than plaque size), Plaque disruption PLTS aggregation thrombus and VC (happens in minutes)Irreversible changes = after 30 minutes of ischemia
ATP < 10% of normalMechanism of cell death = necrosis ( Coagulative)
Heart - PathologyIschemic Heart Disease
MI -Morphologylight microscopy
First 12 hrs. after MI – no changeUp to 3 days = Coagulative necrosis, neutrophils1-2 weeks = Granulation tissue≥ 3 weeks = fine scar≥ 2 months = dense scar
EM – membrane disruption and Mitochondrial densitiesSpecial stain = TTC ( Triphenyl Tetrazolium chloride),
Detects and stains Mahogany brown with Lactate dehydrogenaseUnstained area = infarctionMahogany brown = viableWhite, glistening= scar
Most common and nonspecific change in ischemia = sub-endocardial myocyte vacuolization
MI- Microscopic features
One-day-old infarct
coagulative necrosis
wavy fibers
Up to 3 days duration
Neutrophilic infiltrate
1 -2 weeks
Granulation tissueScar
>3 weeks
Heart - PathologyIschemic Heart Disease
MI –ReperfusionMechanisms
Intrinsic Extrinsic =
Thrombolytic drugs = < 1hr. After onset of MIPTCA/CABG = > 1hr. After onset of MI
Target = clot lysis and restoration of blood flowPost- reperfusion changes =
Contraction bands = hyper contracting myocytes, Stunned myocardium = transient, protective dysfunctionReperfusion damage = mostly apoptosis by free radicals ( unlike MI)
Heart - PathologyIschemic Heart Disease
MI = ClinicalSilent MI = DM, Elderly, Cardiac transplantation recipients,Typical features = Rapid, weak pulse and sweating profusely (diaphoretic), Dyspnea, chest painLab=
Diagnostic Best markers = Troponins ( T & I), both sensitive and cardio – specificNext best – CK-MB
PredictiveCRP- >3mg/l – highest risk
Heart - PathologyIschemic Heart Disease
MI –ComplicationsIn 75% of Patients with MIPoor prognosis in = elderly, females, DM, old case of MI, Anterior wall infarct – worst, posterior –worse, Inferior wall – best
1. Arrhythmia = Ventr. Fibrillation – MC arrhythmia lead to sudden death in MI patients, before they reach hospital2. pump failure – LVF, cariogenic shock, if >LV wall infarcts, lead to death ( 70% of hospitalized MI patients)3.Ventricular rupture = Free or lateral LV wall – MC site, later cause false aneurysm, 4.True aneurysm = rupture is very rare5.Pericarditis = Dressler’s syndrome ( Late MI complication)6.Recurrence
Heart - PathologyIschemic Heart Disease
Sudden cardiac death = unexpected death in one hour due to cardiac causes with or without clinical symptomsCause – Atherosclerosis ( 90%), others (10%)
Romano- Ward syndrome – Long Q-T syndrome ( K+, Na+ channel defects)
Mechanism- Most likely due to arrhythmias ( VF)Patients – young athletes, with Pul. HTN, IHDMorphology
Prominent finding – increased heart massVacuolations in Sub – endocardial myocardium
Heart - Pathology
Ischemic Heart DiseaseChronic IHD = also called ischemic cardiomyopathyPatients = post heart transplant receipts, previous MI or CABG ptsCause =compromised ventricular functionMorphology =vacuoles, Myocyte HypertrophyDiagnosis= by exclusion
Date of download: 9/30/2015
From: Diagnosis of Stable Ischemic Heart Disease: Summary of a Clinical Practice Guideline From the American College of Physicians/American College of Cardiology Foundation/American Heart Association/American Association for Thoracic Surgery/Preventive Cardiovascular Nurses Association/Society of Thoracic SurgeonsAnn Intern Med. 2012;157(10):729-734. doi:10.7326/0003-4819-157-10-201211200-00010
Alternative Diagnoses to Angina for Patients With Chest Pain
Table Title:
Copyright © American College of Physicians. All rights reserved.
Date of download: 12/10/2015 Copyright © The American College of Cardiology. All rights reserved.
From: 2014 AHA/ACC Guideline for the Management of Patients With Non–ST-Elevation Acute Coronary Syndromes: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines
J Am Coll Cardiol. 2014;64(24):e139-e228. doi:10.1016/j.jacc.2014.09.017
Date of download: 12/10/2015 Copyright © The American College of Cardiology. All rights reserved.
From: 2014 AHA/ACC Guideline for the Management of Patients With Non–ST-Elevation Acute Coronary Syndromes: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines
J Am Coll Cardiol. 2014;64(24):e139-e228. doi:10.1016/j.jacc.2014.09.017
Global Registry of Acute Coronary Events Risk Calculator for In-Hospital Mortality for Acute Coronary Syndrome
Date of download: 12/10/2015 Copyright © The American College of Cardiology. All rights reserved.
From: 2014 AHA/ACC Guideline for the Management of Patients With Non–ST-Elevation Acute Coronary Syndromes: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines
J Am Coll Cardiol. 2014;64(24):e139-e228. doi:10.1016/j.jacc.2014.09.017
Algorithm for Management of Patients With Definite or Likely NSTE-ACS**See corresponding full-sentence recommendations and their explanatory footnotes.†In patients who have been treated with fondaparinux (as upfront therapy) who are undergoing PCI, an additional anticoagulant with anti-IIa activity should be administered at the time of PCI because of the risk of catheter thrombosis.ASA indicates aspirin; CABG, coronary artery bypass graft; cath, catheter; COR, Class of Recommendation; DAPT, dual antiplatelet therapy; GPI, glycoprotein IIb/IIIa inhibitor; LOE, Level of Evidence; NSTE-ACS, non–ST-elevation acute coronary syndrome; PCI, percutaneous coronary intervention; pts, patients; and UFH, unfractionated heparin.
Figure Legend:
Date of download: 12/10/2015 Copyright © The American College of Cardiology. All rights reserved.
From: 2014 AHA/ACC Guideline for the Management of Patients With Non–ST-Elevation Acute Coronary Syndromes: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines
J Am Coll Cardiol. 2014;64(24):e139-e228. doi:10.1016/j.jacc.2014.09.017
Stepped-Care Approach to Pharmacological Therapy for Musculoskeletal Symptoms in Patients With Known Cardiovascular Disease or Risk Factors for Ischemic Heart DiseaseASA indicates aspirin; COX-2, cyclooxygenase-2; GI, gastrointestinal; NSAIDs, nonsteroidal anti-inflammatory drugs; and PPI, proton-pump inhibitor.
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