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Etapele de evolutie ale ATS

Placa rupta
Cea mai frecventa patogenie a placii aterosclerotice rupte este inflamatia cauzata de -stimuli noninfectiosi(lipide oxidate) -stimuli infectiosi ce determina expansiunea placii si destabilizarea ei Macrofagele si limfocitele T se activeaza (cele de la nivelul placii) si creste expresia unor enzime cum ar fi metaloproteinazelor ce determina ruptura placii .

Ischemie acuta coronariana


Durere coronariana sau echivalente Supradenivelare ST , subdenivelare ST, inversiune unde T Plus sau minus enzime

Frecventa accidentului coronarian


Studiul MONICA sponsorizat de OMS - 7 milioane de oameni intre 35-64 ani ; inceput in 21 tari din 1980 - frecventa mare a ACS in Anglia SUA Finlanda Australia Polonia -frecventa mai mica in China Franta Spania Elvetia unele zone din Italia

Accidentul coronarian acut


Angina pectorala instabila = risc mare in lipsa tratamentului de infarct Infarctul NSTEMI

Infarctul STEMI

Definitia anginei instabile


Angina instabila = tablou clinic de durere coronariana fara modificare enzimatica la doua determinari de troponina si/sau CKMB in primele 6 ore

Angina pectorala instabila


Angor de novo Angina agravata Angina de repaus Angor precoce post infarct Angor la pacientul cu by-pass

Cauzele acidentului coronarian


1. Trombus sau tromboembolism la nivelul placii rupte sau erodate

2. Embolism din placa erodata (fara tromb)


3.Obstructie dinamica 4. Obstructie mecanica aterosclerotica progresiva 5.Inflamatia atrerei coronare 6.Disectie a arterei coronare(la femei in peripartum) 7. Angina secundara( de obicei la cei cu stenoze aterosclerotice usoare) cresterea necesarului de O2 la
- febrili , hipertiroidieni - hipotensiune - anemie , hipoxie

Patogenia anginei instabile


Discrepanta dintre oferta(glucoza acizi grasi liberi O2) si cerere =1/3 din angine Ruptura placii Tromboza Vasoconstrictie Recurenta tranzitorie a vasoconstrictiei

Cerere crescuta datorita cresterii muncii miocardului(frecventa cardiaca inmultit cu tensiunea sistolica) sau cresterea stresului pe perete este responsabila de aproape toate anginele stabile dar si probabil de 1/3 din anginele instabile Acumularea celulelor spumoase este caracteristica placii . LDL oxidat din celulele spumoase este citotoxic procuagulant si chemotactic. O data cu cresterea placii producerea proteazelor de catre macrofage ca si producerea de elastaza de catre neutrofile determina subtierea capsulei fibrimusculare care acopera inima lipidica Creserea instabilitatii placii alaturi de trauma peretelui prin flux determina fisurarea placii si ruptura in special la jonctiunea placii cu peretele normal Fisura nu determina tablou clinic dar ruptura da Plachetele adera si se agregheaza la zona de continuitate creiata si elibereaza tromboxan si adenozina si substante care determina vasoconstrictie si producere de trombina .Trombina determina continuarea activarii trombocitelor

Simptomele clinice ale ACS


Tipice -durere cu caracterele durerii coronariene dar mai lunga Atipice Indigestie greturi sau varsaturi asociate unui disconfort toracic Durere epigastrica cu modificare ecg Dispnee persistenta Slabiciune astenie modificarea constientei la un batrin sau la un diabetic eventual dispnee asociata Greturi si varsaturi asociate dispneei sau

Consideratii speciale
Femeile au mai frecvent durere atipica Diabeticii au simptome atipice datorita disfunctiei tesutului autonom Batrinii au simptome atipice cum ar fi slabiciune generalizata , accident vascular cerebral , sincopa modificarea constientei.

Diagnostic
Clinic ECG subdenivelare ST -tranzitorie = angor -stabila = suspect NSTEMI Enzime de citoliza miocardica -absente = angor -prezente =NSTEMI

Differential Diagnosis of Prolonged Chest Pain


AMI Aortic dissection Pericarditis Atypical angina pain associate with hypertrophic cardiomyopathy Esophageal, other upper gastrointestinal, or biliary tract disease Pulmonary disease
pneumothorax embolus with or without infarction pleurisy: infectious, malignant, or immune disease-related

Hyperventilation syndrome Chest wall


skeletal neuropathic

Psychogenic

Investigatiile obligatorii in API


serial cardiac markers

hemogloblin,
serum chemistry lipid panel within 24 hours of presentation

Brain natriuretic peptide (BNP) independent predictor of short-

and long-term mortality and risk of CHF in patients presenting with unstable angina. Elevated BNP levels have also been linked to more significant coronary artery lesions in patients with unstable angina, including greater LAD involvement
Elevated serum CRP levels on admission indicate worse short- and long-term mortality in patients with unstable angina. Patients with elevated CRP levels at time of discharge are at greater risk for recurrent MI.

C-reactive protein (CRP)


Imaging Studies:
Perform chest radiography to evaluate patients for signs of
CHF and for other causes of chest symptoms such as pneumothorax, pulmonary infection or masses, pulmonary hypertension, and mediastinal widening. If available on a prompt basis, echocardiography can provide a quick evaluation of left ventricular function for prognosis (worse when LVEF is <40%) or for diagnosis, such as when new segmental wall motion abnormality is detected (eg, in postinfarction or postrevascularization chest pain in which baseline left ventricular function is known).
Important causes of chest pain, such as aortic stenosis and HOCM, can be readily detected by echocardiography. Transesophageal echocardiography, CT angiography (CTA), or magnetic resonance angiography (MRA) is invaluable when aortic dissection is being ruled out.

MRI has emerging applications for identifying ischemia (space-time maps


of impaired blood arrival), infarction (wall thinning, scar, delayed enhancement), and wall motion abnormalities that may be coupled with coronary artery assessment with MRA in the future.

Scintigrafia
Triaj in urgenta - Valoare negativa a eco - Slaba probabilitate eco Extinderea IM Elemente de prognostic(riscul post infarct)

Angina pectorala instabila


Trat. 1. Invaziv 2. conservator Antiplachetar top:bivalirudina , fondaparina(pt cei cu risc de hemoragie fara trat invaziv) , enoxaparina

Metode de apreciere a riscului de moarte sau infarct in angina instabila Calcul scor TIMI Calcul scor GRACE Alte elemente

Scorul de risc TIMI (moarte , infarct in urmatoarele 14 zile) un punct pentru fiecare 1) virsta>65 ani 2) peste 3 factori de risc 3) stenoza coronariana >50% cunoscuta 4) modificare a ST 5) angina severa >2 epis. dureroase /24h 6) folosirea aspirinei ultimile 7 zile 7) crestere enzimatica

Scorul TIMI
Cei cu scor 3-7 au risc mare si vor fi tratati cu inhibitori de glicoproteina IIIb si vor fi coronarografiati

Probabilitatea de a fi ACS
Mare (85-99%) apreciata pe prezenta urmatoarelor elemente Istorie de infarct in antecedente sau de MS resuscitata sau de angina pectorala Durere anginoasa clara la barbat de 60 ani sau femeie de 70 ani Modificari hemodinamice tranzitorii sau modificari tranzitorii ale ECG Durere cu supradenivelare ST tranzitorie ST-supradenivelat sau subdenivelat mai mult de 1mm Unde T negative , simetrice in derivatii multiple precordiale

Probabilitate de ACS
Mica (1-14%) absenta probabilitatii mari sau medii plus
Durere toracica nespecifica Un factor de risc altul decit diabetul Unde T inversate dar mai putin de 1mm in derivatii cu unde R dominante ECG normal

Probabilitate de ACS
Intermediar (15-84%) include urmatoarele
Angina clara la barbati sub 60 ani sau femei sub 70 ani Angina probabila la barbati de 60 ani sau femei de 70 ani angina Durere toracica nespecifica la un diabetic Durere toracica nespecifica in prezenta a 2-3 factori de risc dar nu diabet Boli vasculare extracardiace ST depression 0.05 to 1 mm Inversiune unde T cel putin 1mm in derivatii cu unde R dominante

Alti factori indicatori de risc de moarte


o Subdenivelare peste 1mm

Troponina pozitiva NSTEMI


o Durere refractara la medicatie Semne de IC o Depistare disfunctiei de VS o Instabilitate hemodinamica o Angina recurenta in ciuda tratamentului intensiv o Insuficienta mitrala noua sau TPV recurenta

Tratamentul medicamentos
Aspirina plus sau minus Clopidogrel Betablocante Heparina Statine Nitrati Blocante de calciu Inhibitori de glicoproteina IIa/IIIb Inhibitori enzima de conversie

Aspirina
Doza de atac 160-325 mg Doza ulterioara 150 mg/zi Reduce infarctul (tromboza ulterioara) si moartea cardiaca cu 40-50% la 30 zile Efect in 30 min
Contraindicatie la intoleranta sau suspiciune de singerare sau
sindrom hemoragipar cunoscut Cit timp? indefinit

Clopidogrel 75x4 in prima zi apoi 75mg

Tratamentul cu Plavix
Clopidogrel
intoleranta la aspirina combinat cu aspirina pare ca are efect mai bun (studiul CURE) in primele 24 ore in ceea ce priveste toate evenimentele cv la pacientii supusi tratamentului invaziv (studiul PCI CURE and CREDO) Doza 300 mg la internare si ulterior 75 mg/zi (o tableta)

Tratament cu betablocante
Administrat iv o fiola de 5mg Metoprolol repetat la 5 min pina la 15 mg Continuat 100-200 mg pos

Tratament cu betablocante
Beta-blocante
Several controlled trials have demonstrated the benefits of beta-blockers in the treatment of MI. Early use of IV beta-blockers (e.g., metoprolol) is preferred as it is associated with a lower rate of recurrent MI or death when compared to later therapy. After initial treatment, patient may be switched to oral regimen for chronic therapy.

Tratamentul cu antagonisti de glicoproteina


1. Pacientii supusi tratamentului invaziv abciximab eptifibatide tirofiban, (reduc 30-day mortality and infarction) of approximately 30-50%. 2. Pacientii cu risc mare care sunt tratati medical din diverse motive 5-7%,reducere evenimente cv

Tratamentul cu nitrati
Nitrates
IV nitrate agents may be used in the treatment of ischemic chest pain, symptoms of heart failure, or hypertension but are not associated with appreciable long-term clinical benefit. These agents are contraindicated for those with right ventricular infarction, hypertrophic cardiomyopathy, and severe aortic stenosis.

HMG coenzyme A reductase inhibitors3-hydroxy-3-

Tratamentul cu statine

methylglutaryl coenzyme A (HMG-CoA reductase),

Multiple large, randomized, secondary prevention trials including the Heart Protection Study have demonstrated significant mortality benefit from statin therapy. Recent results from the MIRACL and Pravastatin or Atorvastatin Evaluation and Infection Therapy (PROVE-IT) TIMI trials suggest that early initiation of antilipidemic agents (statins) in patients with ACS can decrease adverse events within a relatively short term. The PROVE IT-TIMI 22 trial demonstrated a benefit from statin therapy even in ACS patients presenting with relatively low serum LDL-C levels (LDL-C<100 mg/dL suggesting that the target LDL-C level should be less than 80 mg/dL in these patients. Statin therapy should be initiated before hospital discharge and clinical benefit may be gained by starting within 24-96 hours of admission.

Agregarea si adeziunea trombocitelor se realizeaza prin interventia factorului von Willebrant si a unui receptor membranar de tip glicoproteina = IIa/IIIb Substantele care inhiba acest receptor abciximab eptifibatid tirofiban

Tratament alternativ la heparina


Direct thrombin inhibitors
Direct thrombin inhibitors, such as hirudin, lepirudin, or bivalrudin, are potential alternatives to heparin. These agents are much more costly than conventional anticoagulation agents and are associated with higher rates of bleeding. Direct thrombin inhibitors should not be routinely used in the treatment of unstable angina but may be of clinical benefit in special circumstances (eg, heparininduced thrombocytopenia).

An early invasive strategy in patients with unstable angina/nonST-segment elevation MI and any of the following high-risk indicators. (level of evidence: A
Recurrent angina/ischemia at rest or with low- level activities despite intensive anti-ischemic therapy Elevated TnT or TnI New or presumably new ST-segment depression Recurrent angina/ischemia with CHF symptoms, an S3 gallop, pulmonary edema, worsening rales, or new or worsening MI High-risk findings on noninvasive stress testing Depressed LV systolic function (eg, EF < 0.40 on noninvasive study) Hemodynamic instability Sustained ventricular tachycardia PCI within 6 months Previous CABG

Tratament invaziv
Pacientii cu risc moderat sau mare de evenimente cardiovasculare fac coronarografie in urmatoarele 48 ore (The TACTICS/TIMI-18 trial showed that this early invasive strategy reduced 30-day rates of death, MI, or rehospitalization for unstable angina from 19.4% to 15.9%, or a relative risk reduction of 18%.

Selectively inhibits adenosine diphosphate (ADP) binding to platelet receptor and subsequent ADP-mediated activation of glycoprotein llb/llla complex, thereby inhibiting platelet aggregation

Transiently impaired contractile function of muscle that persists after the relief from ischemia is called stun, and long-term dysfunction of viable muscle is called hibernation
If a region is thin and akinetic (no motion), it is more likely to scar (dead myocardium) that if it is not. However, when in doubt, viability tests are appropriate

Infarct miocardic STEMI

Mortalitatea in AMI 9,5% Prevalenta in AMI 1,9 - 5,2% A scazut procentul STEMI dar a crescut procentul NSTEMI de la 45% la 65%(cauza, sensibilitatea troponinei)

Spontaneous coronary artery dissection remains an unusual cause of acute coronary syndrome. It should be included in the differential diagnosis of acute myocardial infarction, especially when it affects young, healthy females

Clasificarea infarctului de miocard


Tip 1=Im spontan declansat de eveniment coronarian primar(placa rupta) pe coronara sau pe stent Tip 2=Im declansat de ischemie secundara imbalantei dintre cerere si oferta (spasm, anemie, hipotensiune) Tip 3=moarte subita cu simptome de ischemie insotite de supradenivelare ST sau BRS nou , sau verificare coronarografica sau necroptica a unui tromb dar cu moarte inainte de verificare clinica Tip 4= a. asociat PTC b.asociat trombozei stentului Tip 5=Im asociat by-pas

Diagnosis of Acute MI
evaluation of cardiac enzymes - troponina Creatinine phosphokinase (CK) CK-MB elevated in first lactate dehydrogenase 24

Symptoms
ECG

Enzymatic Criteria for Diagnosis of Myocardial Infarction


Serial increase, then decrease of plasma CK-MB, with a change > 25% between any two values CK-MB > 10-13 U/L or > 5% total CK activity increasing MB-CK activity > 50% between any two samples, separated by at least 4 hrs if only a single sample available, CK-MB elevation > twofold beyond 72 hrs, an elevation of troponin T or I or LDH-1 > LDH-2

Manifestarea clinica
Depinde de marimea necrozei daca zona necrotica este mare sunt prezente semne de IVS sau si hipotensiune Depinde de starea irigarii muschiului in zone nonnecrotice - diabet Starea de stimulare a SNV - simpaticotonie : tahicardie , hipertensiune , transpiratii , agitatie - vagotonie : bradicardie , hipotensiune Virsta boli asociate

Manifestare clinica
Tipica=durere coronariana dar prelungita Atipica = dispnee 50% transpiratii 25% greturi si varsaturi 25% presincopa si sincopa 19% Manifestare atipica au diabeticii , batrinii,cei cu IC anterioara, negrii ,femeile

Retrospective study of confirmed MIs: 47% did not present with chest pain, Women and older patients more likely to present without chest pain. (Ann Emerg Med 40(2):180, 2002)

ECG in perspectiva trat trombolitic


1.Supradenivelare ST in doua derivatii alaturate 2mm in punctul J V1-V3(exista si alte cauze:repolarizarea pr4ecoce , pericardita ,BRS , HVS) - 1mm in alte derivatii 2. BRS nou criterii Sgarbossa=supradenivelare >1mm in derivatii cu R dominant ,>5mm in derivatii cu S dominant , subdenivelare >1mm V1-V3 3.Subdenivelarea ST in V1-V3 poate reprezenta AMI posterior

o This allows detection of the highest-risk chest pain syndrome in patients who may in fact be in the midst of acute MI and thereby allows immediate triage to revascularization therapy. This is manifested by an ST elevation, new left bundle-branch block (LBBB), or peaked T wave (early)type MI on ECG.

Other MI Locations
First, take a look again at this picture of the heart.

Lateral portion of the heart

Anterior portion of the heart

Inferior portion of the heart

Anterior MI
Remember the anterior portion of the heart is best viewed using leads V1- V4.
Limb Leads Augmented Leads Precordial Leads

Lateral MI
So what leads do you think the lateral portion of the heart is best viewed? Limb Leads Leads I, aVL, and V5- V6 Precordial Leads

Augmented Leads

Inferior MI
Now how about the inferior portion of the heart? Limb Leads Leads II, III and aVF Precordial Leads

Augmented Leads

Inferior Wall MI
This is an inferior MI. Note the ST elevation in leads II, III and aVF.

ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction.

Interpretation
Yes, this person is having an acute anterior wall myocardial infarction.

Anterolateral MI
This persons MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6, I, and aVL)!

Tratamentul trombolitic
Indicat la toti pacientii cu durere coronariana sau disconfort asociat cu supradenivelare ST in primele 12 ore de la debutul durerii

ContraindicatIons and Cautions for Fibrinolytic Used in Myocardial Infarction


Cautions / Relative Contraindications
Severe uncontrolled HTN on presentation (BP >180/110 mmHg) History of prior CVA or known intra-cerebral pathology not covered in contraindications Current use of anticoagulants in therapeutic doses (INR 23); no bleeding diathesis Recent trauma (within 2-4 weeks) including head trauma Noncompressible vascular punctures Recent (within 2-4 weeks) internal bleeding For streptokinase/anistreplase: prior exposure (especially within 5d-2 yrs) or prior allergic reaction Pregnancy Active peptic ulcer History of chronic hypertension

Angioplastia primara
Studiile PRAGUE 1 si 2 si DANAMI au demonstrat beneficiu la toti pacientii cu conditia incadrarii in intervalul de 90 min de la diagnostic Indicatie majora la cei cu soc cardiogen La cei cu contraindicatie de fibrinolitic

Fibrinolitice
Streptokinaza Alteplaza = Actilyse Reteplaza = Rapilysin 2 doze a 10 unitati la 30 min Tenecteplaza = Metalyse un singur bolus raportat la Kg

Nu se administreaza peste 75 ani Daca pacientul s-a prezentat la peste 4 ore de la debut folosesc ultimile doua Pot readministra fibrinoliticul daca nu am obtinut reperfuzie cu streptokinaza

Angioplastia facilitata
PTC post fibrinoliza la pacientii cu infarct mare

Evolutia IMA

Complicatiile STEMI
faza precoce aritmii ventriculare insuficienta ventriculara stinga insuficienta cardiaca soc cardiogen faza intermediara complicatii mecanice pericardita embolii faza tardiva anevrism insuf cardiaca

Initial Management in ED
Aspirin165-325 mg (chew and swallow) Sublingual NTG unless SBP <90 or HR <50 or >100: test for prinzmetals angina, reversible spasm, antiischemic, antihypertensive effects O2 by nasal prolongs, first 2-3 h in all; continue if PaO2 <90% Analgesia: small doses of morphine (2-4 mg) as needed Fibrinolysis or PCI if ST elevation > 1mV or LBBB (Goal: door-needle < 30 min or door-dilatation < 60-90 min)

Myocardial Infarction
Characteristics

associated with higher risk of reinfarction and death x EF<40% x ischemia during low intensity exercise x poor exercise capacity (<4 METS) x complex ventricular arrhythmias

Tratamentul complicatiior

Suspected pericarditis - ASA 650 mg q 4-6 hrs CHF - ACE inhibitor and diuretic as needed Shock - consider intra-aortic balloon pump + cath with PCI or CABG RV MI - fluids (NS) + inotropics if hypotensive

MI Management in 1st 24 Hours Limited activity for 12 hours, monitor 24 hours No prophylactic antiarrhythmics IV heparin if: a) large anterior MI; b) PTCA; c) LV thrombus; d) alteplase/reteplase use (for ~48 hours) SQ heparin for all other MI (7,500 u b.I.d.) Aspirin indefinitely IV NTG for 24-48 hrs if no / HR or BP IV beta-blocker if no contraindications ACE inhibitor in all MI if no hypotension

Infarctul de VD
- Il suspectez in infarctul inferior - Tablou clinic de insuficienta cardiaca dr jugulare turgescente hepatomegalie meteorism abdominal hipotensiune , soc semnul Kussmaul - ecg IMA in D2 D3 aVF plus ST supradenivelat V3r , V4r

Treatment Strategy for Right Ventricular Ischemia/Infarction


Maintain right ventricular preload
Volume loading (IV normal saline) Avoid use of nitrates and diuretics Maintain AV synchrony (AV sequential pacing for symptomatic high-degree heart block unresponsive to atropine) Prompt cardioversion for hemodynamically significant SVT

Inotropic support
Dobutamine (if cardiac output fails to increase after volume loading)

Exercise and Atherosclerosis


Independently reduces risk of CAD Slows rate of progression by acting on other risk factors Increases fibrinolytic activity May stimulate the formation of collateral vessels when one or more obstructive lesions are present