Inferior Wall Myocardial Infarction

Dr.K.Prashanthi

Sir William Osler said, “Variability is the law of life, and as no two faces are the same, so no two bodies are alike, and no two individuals react alike and behave alike under the abnormal conditions which we know as disease

INTRODUCTION DEFINITION EPIDEMIOLOGY ETIOLOGY CLINICAL FEATURES DIAGNOSIS TREATMENT COMPLICATIONS CONCLUSION TAKE HOME MESSAGE

THE PIONEERS

EINTHOVEN

HAROLD ENSIGN BENNET PARDEE

PAUL DUDLEY WHITE

2D ECHO

PERCUTANEOUS TRANSLUMINAL ANGIOPLASTY

CHARLES THEODORE DOTTER

Balloon angioplasty

DR.ANDREAS GRUENTZIG

EXTERNAL DEFIBRILLATOR

DR.BERNARD LOWN

THE LIFE SAVING DRUGS

STREPTOKINASE

The saviour – ATROPINE

Coronary circulation

DEFINITION Criteria for Acute ,Evolving ,Recent MI : Either of the following criteria satisifies the diagnosis: 1.Typical rise and /or fall of biochemical markers

of myocardial necrosis with atleast one of the following :

A.Ischemic symptoms B.Development of the pathological q waves in the ECG. C.Ecg changes indicative of ischemia.(ST segment elev ation or depression). D.Imaging evidence of new loss of viable myocardium or new RWMA. 2.Pathological findings of an acute myocardial

infarction.

EPIDEMIOLOGY

Myocardial infarction is a common presentation of Ischemic heart disease.

Worldwide more than 3 million people have STEMIs and 4 million have NSTEMIs a year.

Coronary heart disease is responsible for 1 in 5 deaths in the United States.

EPIDEMIOLOGY-India In India, cardiovascular disease (CVD) is the leading

cause of death. 32% of all deaths in 2007 . Relatively new epidemic in India. Mortality estimates due to CVD vary widely by state,

ranging from 10% in Meghalaya to 49% in Punjab (percentage of all deaths). Punjab (49%), Goa (42%),

Tamil Nadu (36%) and Andhra Pradesh (31%) have the highest CVD related mortality estimates.

State-wise differences are correlated with prevalence of specific dietary risk factors in the states.

Moderate physical exercise is associated with reduced incidence of CVD in India (those who exercise have less than half the risk of those who don't).

EPIDEMIOLOGY Usually anterior wall MI is more than other segment MI because of

conjunction of HTN and diabetes along with the presence of hypercholeosterolemias in C.A.D -----Br heart journal 2000..ncbi.nch.gov/pmc

RVMI is present in one third of patients with IWMI ,but clinically significant in less than 50 % of the one third…. CMDT 2009.

AV block is more common than infranodal block and occurs in approximately 20% of IWMI. (infranodal – AWMI) ……… CMDT 2009 .

Sinus bradycardia is more common in IWMI (tahcycardia in AWMI) Posterior wall MI is assosciated with 5% of IWMI or lateral MI but

rarely occurs alone.

ETIOLOGY Atherosclerosis. 90% of MIs result from an acute

thrombus that obstructs an atherosclerotic coronary artery. Plaque rupture and erosion - the major triggers for coronary thrombosis.

CAD without atherosclerosis Secondary to vasculitis Ventricular hypertrophy Coronary artery emboli Congenital coronary anomalies Coronary trauma Primary coronary vasospasm (variant angina) Drug use (eg, cocaine, amphetamines, ephedrine) Arteritis Heavy exertion, fever, or hyperthyroidism Hypoxemia of severe anemia Aortic dissection with retrograde involvement of the

coronary arteries Infected cardiac valve through a patent foramen

ovale (PFO) Significant GI bleed CO Poisoning

Clinical features Prodromal symptoms: Fatigue, Chest discomfort, Malaise in the days preceding the event; May occur suddenly without warning

Nausea and/or abdominal pain often are present in infarcts involving the inferior or posterior wall.

CLINICAL FEATURES Symptoms: Chest pain > 30 min.

Character of the pain –retrosternal,constrciting,crushing,compressing sensation of heavy weight.

Predilection for left side. Radiates to the ulnar aspect of the left arm Tingling sensation of the wrist and fingers. In some patients, the symptom is epigastric, with a feeling of indigestion or of

fullness and gas. Nausea,Vomitings Profound weakness Dizziness Palpitations, Cold perspiration Sense of impending doom.

occurs most often in the early morning hours, -- increase in catecholamine-induced platelet aggregation and ↑ serum concentrations of plasminogen activator inhibitor-1 (PAI-1) that occur after awakening.

In general, the onset is not directly associated with severe exertion. Instead, it is concomitant with exertion.

The immediate risk of myocardial infarction increases 6-fold on average post MI,CAD and by as much as 30-fold in sedentary people. ncbi.nbl.com

Anginal equivalent --abdominal pain,jaw pain,sharp pain in women,elderly.

High index of suspicion women, diabetics, older patients, dementia, history of heart failure, cocaine users, hypercholesterolemia, positive family history for early coronary disease ---- any first-degree

Male aged≤ 45 years, female relative aged ≤ 55 years who MI

Silent MI Half of myocardial infarctions are clinically silent in that they do not

cause the classic symptoms described above and consequently go unrecognized by the patient.

In as many as 25% of elderly patients, a population in whom 50% of myocardial infarctions occur; in such patients, the diagnosis is often established only retrospectively, by applying electrocardiographic criteria or by scanning the patients using 2-dimensional (2D) echocardiography or magnetic resonance imaging (MRI).

On clinical evaluation, ventricular aneurysms may be recognized late, with symptoms and signs of heart failure, recurrent ventricular arrhythmia, or recurrent embolization.

Physical examination

Physical examination findings can vary; comfortable in bed, with normal examination results, may be in severe pain, with significant respiratory distress and a need for ventilatory support.

Ongoing pain --- pale and diaphoretic. Hypotension may indicate ventricular dysfunction due to ischemia. Hypotension in the setting of myocardial infarction usually

indicates a large infarct secondary to either decreased global cardiac contractility or a right ventricular infarct.

Signs Bradycardia Hypotension----due to parasympathetic

hyperactivity. Increased respiration – cheynes stokes –anxiety

and pain. Raised JVP.--- RVMI.—kussmaul’s sign Clear lung fields. On cardiac auscultation--S4 is almost universally

present in patients in SR with STEMI.but non specific.

S3 ,S4 heard along the left sternal border and increases on inspiration.—RVMI –RVF

IWMI with RVMI

The evidence of right ventricular ischemia should be sought in all patients with acute inferior MI at the time of admission. RT precordial leads, in particular lead V4R must be recorded in all patients with inferior MI. –ACC guidelines

1-mm ST segment elevation in the right precordial lead V4R is the single most predictive ECG finding in patients with right ventricular ischemia This finding, however, may be transient; half of the patients show resolution of ST elevation within 10 hours of the onset of symptoms .

IWMI with RVMI Distention of neck veins is commonly described as a sign of failure of

the RV. Impaired right ventricular diastolic function also leads to systemic

venous hypotension, edema, and hepatomegaly with abdominojugular reflux, which may result in saline-response underfilling of the LV and a concomitant reduction in cardiac output.

Peripheral cyanosis, edema, pallor, diminished pulse volume, delayed rise, and delayed capillary refill may indicate vasoconstriction, diminished cardiac output, and right ventricular dysfunction or failure.

Diagnosis ECG Cardiac imaging Cardiac biomarkers

Troponin T levels CKMB,CK Myoglobin levels

CBP ESR LDH Lipid profile CRP MRI ,technetium 99m pyrophosphate scintigraphy Scintigraphy with thallium 201 Hemodynamic assessement with PA catheter---cardiogenic

shock

ECG Most important tool in the initial evaluation Triage of patients in whom an ACS is suspected. Confirmatory of the diagnosis - 80% of cases. In Inferior myocardial infarction, record a right-sided ECG to rule out

right ventricular infarct. Daily serial ECGs for the first 2-3 days and additionally as needed.

High probability of myocardial infarction is indicated either by ST-segment elevation greater than 1 mm in 2 anatomically contiguous leads ,2mm in chest leads or by the presence of new Q waves.

intermediate probability of myocardial infarction are ST-segment depression, T-wave inversion, and other nonspecific ST-T wave abnormalities.

low probability of myocardial infarction are normal findings on ECGs however, normal or nonspecific findings on ECGs do not exclude the

possibility of myocardial infarction.

Inferior wall MI –ST segment elevation of > 1mm in inferior leads with reciprocal ST segement depression in anterior leads.

Right ventricular - RV4, RV5 Posterior wall - R/S ratio greater than 1 in V1 and V2; T-wave

changes (ie, upright) in V1,ST segment elevation in V8, and V9 Right ventricular myocardial infarction commonly is manifested by

ST-segment elevation or Q waves detectable in right-sided precordial leads.

2D ECHO RWMA RV dysfunction. Assess the LV function secondary to RVMI --- in case of refractory to

IV Fluids --- to rule out cardiogenic shock. MRI with gadolinium contrast enhacement –most sensitive –2 gm of

MI can be detected. Techntium scan – hot spot with calcium – insensitive to small

infarctions. Thallium scan –cold spots in regions of diminished perfusion –does

not differentiate old from new.

Cardiac markers Troponin T and troponin I Highly specific monoclonal antibodies - not normally detectable in the

blood of the healthy individuals but may increase after STEMI to levels greater than 20 times.

Normal troponin T 0-0.1 µg/l,I --- 0 – 0.08 µg/l Cut off for MI t>0.1µg/l, I . 0.4 µg/l CK, CK MB --- CK rises within 4-8 hrs and returns to normal by 48-

72 hrs. A ratio (relative index) CKMB mass :CK actvity > 2.5 suggests but

not diagnostic of acute MI rather than the skeletal source of CKMB elevation.

Treatment golden period is 1 hr ….Door to needle time -30 min,door to balloon time is <90 min < 6 hrs PCI = thrombolysis <6 hrs with hypotension,cardiogenic shock PCI < 6 hrs with hypotension ,no PCI center Give IV fluids -- Then thrombolysis with cardiac monitoring. In presenceof bradycardia Give atropine In presence of CHB Temporary pacemaker

Management

1.Aspirin Block the formation of thromboxane A2 in the platelets by COX inhibition. Dose is 160-325 mg. 2.Clopidogrel Thienopyridine class antiplatelet agent Inhibits P2Y12 subtype of ADP receptor 300 mg CLARITY trial –loading dose of 300 mg,75 mg /day therafter along with

thormbolysis---coronary patency –no increase in bleed. COMMIT/CCS2 trial in china Clopidogrel to be added to apsirin to all patients with STEMI

regardless of whether or not perfusion is given and continued for atleast 14 days,and generally for 1 year.

Reperfusion therapy Limitation of the infarct size PCI -- Fibrinolysis Option depends upon the duration and the availability of the PCI

nearby. < 6 hrs ---PCI – fibrinolysis >6 hrs --- PCI > fibrinolysis The patient at discharge should be sent for angiography in case of

absence of PCI not done < 6 hrs….but thrombolysis given, for the evaluation of the vessel blockage …and extent of vessel disease,.

Thrombolysis/fibrinolysis To maintain the patency of the coronary artery. Fibrinolytics agents used : Tissue plasminogen activator Tenectplase Reteplase Alteplase ---GUSTO trial tpA---- 15 mg bolus followed by 50 mg intravenously IV over the first

30 min followed by 30 mg over the next 60 min. Tenectplase – IV bolus of 0.53 mg/kg over 10 sec Reteplase – 10 MU bolus given over 2 -3 min followed by 2nd 10 MU

units 30 min later. Streptokinase--- 15 MU given over 1 hr –hypotension.

Contraindications and complications

Absolute – cerebrovascular hemorrhage ,ischemia,marked hypertensionSBP > 180mm Hg,DBP > 110 mmHg,aortic dissection,active internal bleeding.

Relative --- pregnancy,hemorrhagic diabetic retinopathy,active peptic ulcer disease,severe HTN ,allergic reactions .<5 days- 2yrs.,trauma within 2-4 weeks,major surgery within 3 weeks,traumatic CPR ,current use of anticoagulants INR >2-3.

Antithrombotic agents Goal is to maintain the patency of the infarct related artery in

conjunction with reperfusion related strategies. UFH --- 60 U/kg followed by infusion of 12 U/kg/hr The APTT should be 1.5 – 2 times the control value. LMWH – enoxaparin 30 mg IV bolus –1mg/kg every 12 hrs---

ASSENT 3 trial. Decreased the death at day 30 compared to UFH –EXTRACT trial OASIS 6 trial – fondaparinux given at dose of 2.5 mg /day reduced

death and reinfarction .no benefit in patients udergoing PCI –catheter thrombosis..

Use antacids and an H2 blocker as prophylactically

Asessment of reperfusion Early cessation of pain The resolution of the ST segment elevation at 90 min. 50% resolution of ST elevation can occur even without reperfusion –

still a strong predictor of better outcome. Reinfarction – recurrence of pain and ST segment elevation –angio

and PCI.

General measures Activity : Bed rest for the first 12 hrs. Diet : Clear liquids for the first 12 hrs . Fibre but low in sodium diet Bowels: Stool softeners are recommended Sedation: Lorazepam ,oxazepam,diazepam

3.Analgesics – morphine Very effective analgesic for pain assosciated STEMI Reduces sympathetically mediated arteriolar and venous constriction Reduces arterial pressure and cardiac output. Dose – 2- 8 mg repeated in 5-15 min. Hypotension and bradycardia – atropine 0.6mg 4.b blockers: If HR > 60 /min,BP > 100 mm Hg SBP Metoprolol 5 mg every 2-5 min ,3 doses. 5.nitrates: Should not be given in inferior wall MI –causes hypotension and bradycardia. If waxing and waning of pain ,systole > 100 mm Hg --- IV NTG. 5µg --- 200

µg /min

6.oxygen: By face mask/nasal prongs 2-4 lit /min 7.ACEI /ARBs: The benefits in EF < 40% ,presence of left heart

failure . SAVE ,AIRE,SMILE ,TRACE,GISI –III,ISIS 4 ---short

and long term benefits CURE trial clopidogrel 75 mg/day to be given

along with aspirin for 1 year in MI patients.

At discharge Aspirin Clopdiogrel H2 blockers ACEI /ARBS Stress testing –see for ST segment depression during submximal

exercise –positive send him for angiography---revascualrization.

TIMI grading Thrombolysis in myocardial infarction Grade 0 –complete occlusion of the infarct

related artery. Grade 1 – some penetration of the contrast

material beyond the point of obstruction,but without the perfusion of the distal coronary bed.

Grade 2 – perfusion of the entire infarct vessel into the distal bed but with flow that is delayed compared with that of the normal artery.

Grade 3 – full perfusion of the infarct vessel with normal flow.

GRACE score

Global Registry of Acute Coronary Events (GRACE) Hospital Discharge Risk Score Accurately Predicts Long-Term Mortality Post Acute Coronary Syndrome

Complications Post infarction ischemia RVMI VPCs AF AFL AIVR Sinus bradycardia Pericarditis Septum rupture Cardiogenic shock

Arryhthmias

Autonomic nervous system imbalance. Electrolyte disturbances Ischemia Slowed conduction in zones of ischemic

myocardium 1. Sinus bradycardia—50% CASES 2.PVCs 3.VT 4.VF 5.AIVR 6.AF AFL

Pericarditis Pericardial friction RUB and pericardial pain are frequently

encountered in patients with MI. Pain radiating to either trapezius muscle is typical. Rub -heard within 24 hrs or as late as 2 weeks…most commonly on

second or third day. Audible along the left sternal border or at the point of maximal

impulse. Anticoagulants should be stopped.

Lets have a look at the ECGs

Acute Inferior wall MI

Acute Inferolateral MI

Acute InferoPosterior Myocardial Infarction

RIGHT SIDED LEADS

Acute Inferior MI with RVMI

Acute Inferolateral MI with 2:1 AVblock

Acute inferior wall MI and complete AV block

Take home message Inferior wall MI presents with nausea and abdominal pain also. Inferior wall in 30-50% cases is assosciated with RV MI. Take right sided V4R in all the patients with IWMI. Presence of RVMI increases the mortality of the patients. IV fluids and inotropes,pacing play a equally contributing role in the

management of patients on presentation. Recurrence of IWMI at the same site is more than in the anterior

wall MI. Triad of raised JVP ,hypotension and clear lungs think of RVMI. PWMI in case of R wave in V1 with upright T wave and R/S ratio >1

V1 and V2..take leads V7-9.

References Braunwald – 7 th edition An Introduction to electrocardiography ---Schamroth ,7 th ed Marriott’s practical electrocardiography –Galen Basic and bedside electrocardiography –Romulo.F.Baltazar CMDT 2009 HARRISON’S 17 th ed http://www.ncbi.nlm.nih.gov/pmc/articles www.ecglibrary.com www.netterimages.com www.medscape.com www.americanjournalofcaridology.com

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