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INTRODUCTION
Coronary Artery Disease leading cause of morbidity & mortality in industrialised nations. Although decrease in cardiovascular mortality still major cause of morbidity & burden of disease. South African perspective of cardiovascular disease: A World in One Country - Yusuf et al Epidemiological transitions of cardiovascular disease.
HIGH RISK POPULATION FOR CAD/ACS: INDIAN/WHITE/COLOURED INCREASING rate in Black population lifestyle/socioeconomic changes, urbanisation GF Jooste stats: 23.8% of admissions to resus. unit for chest pain/acs related (stats 1Jan 2009 28 Feb 2009) 150/628 entries. In US 2004 1.56 million admissions for ACS 669 000 for unstable angina, 896 000 for MI Higher prevelance for NSTEMI.
DEFINITIONS
CAD is a continuum of disease. Angina -> unstable angina -> AMI -> sudden cardiac death Acute coronary syndrome encompasses unstable angina, NSTEMI, STEMI Stable angina transient episodic chest pain d/t myocardial ischaemia, reproducible, frequency constant over time.usually relieved with rest/NTG. Classification of angina Canadian Cardiovascular Society classification.
CLASS 2
SLIGHT LIMITATION OF PHYSICAL ACTIVITY PAIN OCCURS WITH WALKING, CLIMBING STAIRS,STRESS SEVERE LIMITATION OF DAILY ACTIVITY PAIN OCCURS ON MINIMAL EXERTION
CLASS 3
CLASS 4
UNSTABLE ANGINA Pain occurring at rest duration > 20min, within one week of first visit New onset angina ~ Class 2 severity, onset with last 2 months Worsening of chest pain increase by at least 1 class, increases in frequency, duration Angina becoming resistance to drugs that previously gave good control. NB! ECG normal, ST depression(>0.5mm), T wave changes
ACUTE MYOCARDIAL INFARCTION ECC/ACC DEFN rise and fall in cardiac enzymes with one or more of the following: Ischaemic type chest pain/symptoms ECG changes ST changes, pathological Q waves Coronary artery intervention data Pathological findings of an acute MI NSTEMI = UNSTABLE ANGINA SYMPTOMS/FINDINGS + POSITIVE CARDIAC ENZYMES STEMI = ST ELEVATION ON ECG + SYMPTOMS
WHY IS IT IMPORTANT TO RECOGNISE PATIENTS WITH UNSTABLE ANGINA?? 5 -17% suffer an MI within a week after admission. 3 -15% die within a year.
ACS PATHOPHYSIOLOGY
Distruption of coronary artery plaque -> platelet activation/aggregation /activation of coagulation cascade -> endothelial vasoconstriction ->intraluminal thrombus/embolisation -> obstruction -> ACS
APPROACH
Identifying those with chest pain suggestive of IHD/ACS. Thorough history required: Character of pain Onset and duration Location and radiation Aggravating and relieving factors Autonomic symptoms
TYPICAL VS ATYPICAL HISTORY Failure to recognise symptoms other than chest pain -> approx 2 hr delay in seeking medical attention
CHARACTERISTICS OF TYPICAL ANGINAL CHEST PAIN (ADAPTED FROM ROSENS, EMERGENCY MEDICINE)
CHARACTERISTIC TYPE OF PAIN SUGGESTIVE OF ANGINA DULL PRESSURE/CRUSHING PAIN 2-5 MIN, <20 MIN GRADUAL SUBSTERNAL, NOT TENDER TO PALP. WITH EXERTION/ACTIVITY LESS SUGGESTIVE OF ANGINA SHARP/STABBING
AUTONOMIC SYMPTOMS
PRESENT USUALLY
ABSENT
ATYPICAL PAIN
RISK FACTORS FOR DEVELOPING ATYPICAL PAIN: Diabetes, females, non white patients, elderly, dementia, no prior history of MI ATYPICAL SYMPTOMS: GIT symptoms Syncope SOB Pleuritic/positional pain Chest wall tenderness No chest pain/symptoms NRMI 2 STUDY MI without chest pain -> increased risk of death (23% vs 9%) More complications hypotension,heart failure, stroke Delayed ED presentation, delayed intervention
Reasons : Provides prognostic information Determines treatment and level of intervention -> low risk patients early discharge, high risk -> admission to high care
Helps decongest the ED and make available medical resources to more needy patients
Risk stratification should be ongoing at admission, 6-8 hrs, 24hrs, discharge
ECG
First point of entry into ACS algorithm Abnormal or normal Neither 100% sensitive or 100% specific for AMI Single ECG for AMI sensitivity of 60%, specificity 90% Represents single point in time needs to be read in context
Normal ECG does not exclude ACS 1-6% proven to have AMI, 4% unstable angina
GUIDELINES: Initial 12 lead ECG goal door to ECG time 10min, read by experienced doctor (Class 1 B) If ECG not diagnostic/high suspicion of ACS serial ECGs initially 15 -30 min intervals (Class 1 B) ECG adjuncts leads V7 V9, RV 4 (Class 2a B) Continuous 12 lead ECG monitoring reasonable alternative to serial ECGs (Class 2a B)
BIOCHEMICAL MARKERS
IDEAL MARKER: High concentration in myocardium Myocardium specific Released early in injury Proportionate to injury Non expensive testing Troponins CKMB Myoglobin Other markers
TROPONINS T/I
Troponin T vs I both equivalent in diagnostic and prognostic abilities ( except in renal failure Trop T less sensitive) Elevation ~ 2hrs to 12hrs ~30 40% of ACS patients without ST elevation had normal CKMB but elevated troponins on presentation Meta-analysis (Heindereich et al) odds of death increased 3 to 8 fold with positive troponin
MYOGLOBIN
Rapid release within 2 hours Not cardiac specific Rule out for NSTEMI rather than rule in.
CKMB
Used in conjunction with troponins Useful in diagnosing re-infarction
OTHER MARKERS
INDICATORS OF INFLAMMATION OR ACTIVATION OF COAGULATION CASCADE: Myeloperoxidase, soluble CD40 ligand, IL6, hsCRP, d dimer, prothrombin fragment 1 & 2 Elevated before onset of irreversible injury Lack specificity Complex lab assays
B type Natriuretic Peptide: released from heart muscle in response to increased ventricular wall stress. Studies BNP not a specific marker but a strong predictor of ACS especially in patients with chest pain, no ECG changes, non diagnostic troponins. Also positive in heart failure, PE, atrial arrythmias, renal failure Pregnancy Associated Plasma Protein A (PAPP-A): Released when plaque ruptures Predictor of ischaemia
HEART FATTY ACID BINDING PROTEIN (HF ABP) Identifies AMI <4hrs after onset Protein involved in myocardial lipid synthesis, but also expressed outside heart Therefore may be sensitive but not specific for injury Possible role in multi-marker strategy IMAGING MODALITIES Cardiac MRI Multidetector CT for coronary calcification Coronary CT angiography Undergoing clinical evaluation
2007 ACC/AHA guidelines: Cardiac biomarkers measured in all patients with suspicion of ACS (Class 1 B) Troponin preferred marker( Class 1 B) If troponin negative within 6 hours of onset, repeat 8-12hours later(Class 1 B) Remeasuring of positive biomarkers to determine infarct size/necrosis (Class 2a B) Patients presenting within 6 hours of symptom onset myoglobin in conjunction with troponin measured (Class 2b B) 2hr delta CKMB/Delta troponin considered in <6hr presentation (Class 2b B) BNP level for global risk assessment(Class 2b B) Class 3 AST/LDH/CK without CKMB
TIMI RISK SCORE increase in mortality with increasing score ~40% all cause mortality at 14 days for patients requiring urgent revascularisation
2007 ACS/AHA GUIDELINES: Risk stratification models useful in decision making with regard to treatment options ( Class 2a B) TIMI vs GRACE vs PURSUIT PURSUIT & GRACE risk scores allow better discrimination of in hospital and 1 year mortality in patients compared to TIMI. (Andrew et al, Risk scores for risk stratification in ACS ) Whats appropriate in our setting???
MANAGEMENT ALGORITHM
MANAGEMENT UPDATE
2007ACS/AHA GUIDELINES: Rapid catergorisation of patient (Class 1 C) Possible ACS, non diagnostic ECG/biomarkers observed in facility with cardiac monitoring (Class 1 C) Alternative to in patient treatment: for those with 12hr ECG/markers negative stress ECG in 72hrs (Class 1 C) Giving precautionary treatment for those for OPD stress (Class 1 B)
INITIAL INVASIVE VS INITIAL CONSERVATIVE STRATEGY CLASS 1 RECOMMENDATIONS: Early invasive strategy for refractory angina, hemodynamic instability (LOE B) Early invasive strategy for stabilised patients with elevated risk for clinical events. High risk factors include:
Recurrent angina, ischaemia at rest or minimal activity Elevated troponins New ST depression Signs of heart failure/worsening mitral regurg. Ventricular tachycardia Prior CABG PCI in last 6 months High TIMI/GRACE scores LVEF < 40%
CLASS 2b May opt for initial conservative strategy in stabilised high risk patients dependent on patient/physician preference (LOE B) CLASS 3 Invasive strategy -not recommended in patients with multiple co morbidities, low risk patients, patients not consenting.(LOE C)
CLASS 2a In patients managed conservatively who develop recurrent ischaemia on clopidogrel/ASA/Anticoagulant can add glycoprotein inhibitor. (LOE C) Invasive strategy can use clopidogrel + glycoprotein inhibitors(LOE C) CLASS 2b In patients managed conservatively can add glycoprotein inhibitor therapy, in addition to aspirin & anticoagulant (LOE B)
For initial conservative strategy: Aspirin + Clopidogrel + anticoagulant administered for 1 month(LOE A), continued ideally up to 1 year(LOE B) If initial conservative strategy selected but patient has recurrent ischaemic symptoms/heart failure/arrythmias diagnostic angiography recommended. Clopidogrel or Glycoprotein 2b/3a inhibitors should be added before angiography.
ANTICOAGULANT THERAPY
CLASS 1 Anticoagulant therapy should be added as soon as possible For patients undergoing angiography/PCI enoxaparin/UFH (LOE A) of Bivalirudin/ fondaparinux (LOE B) For conservative strategy: enaxaparin, UFH (LOE A), fondaparinux For patients with increased risk of bleeding with conservative strategy fondaparinux
CLASS 2a Enoxaparin /fondaparinux vs UFH Enoxaparin/fondaparinux preferred except in those undergoing CABG within 24hrs (LOE B)
ADDITIONAL MANAGEMENT
STRESS TEST should be performed for those managed conservatively. If stress test positive/ high risk needs diagnostic angiography(Class 1 LOE A) If classed as low risk need to continue aspirin indefinitely ( LOE A) Clopidogrel for at least 1 month(LOE A), ideally up to 1 year(LOE B)
STEMI
PHARMACOLOGICAL UPDATE: ANALGESIA changes from 2004 guidelines MORPHINE: still remains Class 1 C for STEMI, titrated doses
NSAIDS/COX 2 INHIBITORS: those on it should have it discontinued ( increased risk of mortality, re infarction, heart failure, myocardial rupture) Class 1 C
NSAIDS should not be administered in hospital for MI (Class 3)
BETA BLOCKERS Modified recommendation Oral Beta Blockers should be initiated in first24rs, if no contraindications (heart failure, risk of cardiogenic shock) Class 1 B Patients with early contraindications -> re- evaluated later for possible use Role of IV B blockers used in hypertensive patients with STEMI Class 2a B Class 3 LOE A IV B blockers should not be administrated to patients with heart failure, risk of cardiogenic shock
No major changes to reperfusion strategies. Emphasis on decreasing ischaemic time. Increase use of prehospital 12 lead ECG emphasised. In PCI capable hospital door to PCI time 90 min (Class 1 A) In non PCI capable hospital door to needle time 30 min or timeous transfer to PCI capable hospital. (Class 1 B)
REPERFUSION STRATEGY
FIBRINOLYTICS
AVAILABLE FIBRINOLYTICS: STREPTOKINASE 1.5mu infusion over 30min (1hour ACLS) rtPA accelerated infusion over 1.5hrs - 15mg IV bolus, 0.75mg/kg over 30 min, 0.5mg/kg over 1hr ANISTREPLASE 30 U IV over 5 min TENECTEPLASE 30 TO 50 MG RETEPLASE 10 U IV bolus, ffd. 10U IV after 30 min WHICH FIBRINOLYTIC TO USE??? GISSI 2 trial tPA vs Streptokinase , no difference in mortality, marginally higher stroke rate with tPA (1.3% vs 1%) GUSTO 1 trial early vessel patency post infract assoc. with better survival. Accl. tPA/heparin cf comb. Streptokinase/tPA/heprain cf strep with IV vs S/C heparin Outcome better flow rates with accl. tPA -> lower mortality rates
ASSENT 2 TRIAL tenecteplase vs aTPA - tenecteplase was equally or minimally more effective, especially in those presenting > 4hrs after symptom onset. Fibrinolysis combined with glycoprotein 2b/3a inhibitors no overall advantage (ASSENT 3, GUSTO 5 trials)
RESCUE PCI: CLASS 1 LOE B angiography with +/- PCI in patients (<75 yrs)with cardiogenic shock, severe heart failure, ventricular dysrythmias Class 2a persistent ischaemic symptoms post fibrinolysis, haemodynamic instability, electrical instability (LOE C) New recommendation PCI for failed fibrinolytic therapy (less than 50% decrease in ST elevation in worst lead, 90min post fibrinolytic therapy, or large area of myocardium injured) LOE B Class 3 angiography performed if invasive strategy contraindicated, or patient refusal (LOE C)
ANTICOAGULANT ADJUNCTS
NEW RECOMMENDATIONS: CLASS 1 Patients undergoing fibrinolysis should be kept on anticoagulants for atleast 48 hrs and preferably the duration of hospital stay. LOE A Anti coagulants with proven efficacy: Unfractionated Heparin - keeping aPTT 1.5 2 sec above control (LOE C) Enoxaparin (Clexane) initial dosage of 30mg IV bolus ffd by 1mg/kg 12hrly, caution in renal impairment (LOE A) Fondaparinux 2.5mg IV, ffd by 2.5mg dly S/C maintenance for duration of hospitalisation (LOE B)
ANTICOAGULANTS
CLASS 2a recommendation to use anticoagulants in STEMI without reperfusion. UFH (LOE B) LMWH (LOE C) Fondaparinux (LOE B)
THIENOPYRIDINES
CLASS I CLOPIDOGREL now recommended in all STEMI patients in addition to aspirin, whether undergoing reperfusion or not. Dosage 75mg daily(LOE A) Duration -14 days (LOE B) CLASS 2 A In patients < 75yrs Clopidogrel 300mg loading dose recommended(LOE C) Long term maintenance therapy should be considered, 75mg dly for 1 year (LOE C)
SECONDARY PREVENTION
INCREASED FOCUS ON SECONDARY PREVENTION: SMOKING CESSATION DIET MODIFICATION/WT CONTROL BP CONTROL LIPID MANAGEMENT
EXERCISE
DIABETES MANAGEMENT
Despite good reperfusion strategies approx. 1/3 of patients worldwide miss out. Attributed to delayed presentation, atypical presentation, complicated disease presentation, older age SYMPTOMS OF INFARCT BUT NO ESTABILISHED ECG CHANGES - keep in mind aortic dissection, GIT disease, other chest pathology
CONCLUSION
With increase burden of CVD, and lack of health resources risk stratification becomes important. Emphasis should also be placed on primary &secondary prevention of ACS. Early intervention helps prevent complications, decreases morbidity & mortality The way forward fully equipped CHEST PAIN OBSERVATION UNIT
REFERENCES
EDITORS MARX ET AL, ROSENS EMERGENCY MEDICINE: CONCEPTS AND CLINICAL PRACTICE, 6TH EDITION PAUL PD ET AL, KEY ARTICLES IN MANAGEMENT OF ACS & PCI -2007 UPDATE, PHARMACOTHERAPY 2007:27(12), 1722 -1750 WHITE HD, DEFINING THE LIMITS OF ACS, CARDIOLOGY AT THE LIMITS IV, EDITORS: OPIE LH, YELLON DM YUSUF S, THE GLOBAL EPIDEMIC OF ATHEROSCLEROTIC CARDIOVASCULAR DISEASE, CARDIOLOGY AT THE LIMITS IV, EDITORS: OPIE LH, YELLON DM FOX KA, MANAGEMENT OF ACS: AN UPDATE, HEART.2004 JUNE, 90(6):698 -706 ANDERSON ET AL, ACC/AHA 2007 GUIDELINES FOR MXN OF U/A,NSTEMI EXECUTIVE SUMMARY DOWNLOADED content.onlinejacc.org SIX AJ ET AL, CHEST PAIN IN THE ER: VALUE OF THE HEART SCORE, NETH. HEART J. 2008 JUNE,16(6):191 -196
ANTMAN EM ET AL, 2007 FOCUSSED UPDATE OF ACC/AHA 2004 GUIDELINES FOR MAXN OF PATIENTS WITH STEMI, DOWNLOADED http://circ.ahajournals.org McCANN CJ ET AL, NOVEL BIOMARKERS IN EARLY DIAGNOSIS OF AMI COMPARED WITH CARDIAC TROPONIN T, EUROPEAN HEART JOURNAL 2008,29(23): 2843 -2850 KING III SB ET AL, 2007 FOCUSSED UPDATE OF ACC..FOR PCI, JOURNAL OF AMERICAN COLLEGE OF CARDIOLOGY, VOL 51, NO 2, 2008