Medical Management of MYOCARDIAL INFARCTION

Supervisor: BRIG Khuram Shahzad

Prepared By:

• Kasim Yar Hiraj
• Muhammad Faizan Absar
• Muhammad Saad Shahid
• Muhammad Sarmad Iqbal
• Muhammad Tauseef
• Muhammad Shaheer Mannan
• Mustafa Sajjad Cheema
• Muhammad Usman Gondal

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HISTORY

Biodata:

• Name: XYZ
• Age: 30
• Gender: Male
• Marital Status: Married
• Occupation: NCB
• Residence: Saddar, Lahore
• Date of Presentation: 29-12-2019
• Mode of Presentation: Emergency

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Presenting Complaint:

• Pain in Chest for last 6 hours

History of presenting complaint

Pain

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• Sudden in onset
• Crushing sensation of pain
• Central Chest
• Continuous
• Severe
• Radiating to the left arm
• Associated with vomiting, shortness of breath and sweating
• No aggravating or relieving factors
• Not associated with fever, nausea
• Not associated with tachycardia or dyspnea.�

Review of Systems:�

• CVS: Shortness of breath and chest pain present; no palpitation or swelling
• CNS: No headache, weakness, numbness, fits, visual changes or blackout
• GIT: No nausea, vomiting, abdominal pain, heartburn, dysphagia, diarrhea, constipation, jaundice, loss of appetite, weight gain/loss.
• Genitourinary: No flank pain or urinary complains.
• Respiratory: no cough or wheeze.

Past Medical and Surgical History:�

• No History of Cardiovascular Diseases.
• He is a known Diabetic for 5 years.
• Takes Oral Hypoglycemic: Metformin.
• History of Surgery post-Bilateral Renal Calculi in 2012.

Personal History:�

• No History of Smoking.
• No History of Substance Abuse.
• No History of Drug Allergy.
• Belongs to Lower Middle Class.
• Lives in Government House.
• Has access to Filtered Water.

Family History:�

• No Family History of Cardiovascular Diseases.
• Father died in Childhood due to Fever.
• Mother died due to Breast Cancer.
• 1 Sister died due to Breast Cancer.
• All other Siblings were normal without Genetically or Medical Defects.

EXAMINATION

General Physical Examination

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Our patient is a young man of average build, lying uncomfortably in bed, visibly distressed and anxious; well oriented in time place and person.

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General Physical Examination�

Vitals:

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• Blood pressure – 120/77 mmHg
• Heart rate – 72 beats/min
• Respiratory rate – 20 breaths/min
• Temperature – 93 Farenheit
• Oxygen saturation – 98%

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continued…

• Oral hygiene was satisfactory
• No central or peripheral cyanosis
• No jaundice
• No palpable lymph nodes
• No clubbing, koilonychia or leukonychia
• No palpable Osler’s, Heberden’s and Bouchard’s nodes
• No pedal or sacral edema

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Findings were not remarkable

SYSTEMIC EXAMINATION-CVS

• Inspection-
• No chest deformity
• No scars
• No visible pulsations
• Palpation
• JVP was not raised
• Apex beat was heard in the 4^th intercostal space, 1cm lateral of midline
• Parasternal heave was absent

Systemic examination - CVS

• Auscultation
• S1 and S2 heart sounds.
• No added sounds or murmur
• No thrill
• No pericardial rub

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SYSTEMIC REVIEW�

Findings were unremarkable

• GIT: No nausea, vomiting, abdominal pain, heartburn, dysphagia, diarrhea, constipation, jaundice, loss of appetite, weight gain/loss
• Genitourinary: No flank pain or urinary complains
• CNS: No headache, weakness, numbness, fits, visual changes, blackout
• CVS: Shortness of breath and chest pain. No palpitation or edema
• Respiratory: No cough or wheeze.

Differential Diagnosis

• Acute Myocardial infarction
• Acute Pericarditis
• Pneumothorax
• peptic ulcer
• Herpes zoster

Provisional Diagnosis

Acute myocardial infarction

Investigations

• Blood sample taken and sent to lab
• ECG was performed immediately

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ECG

ECG FINDINGS

• St segment elevation in Inferior leads II, III, aVF

Laboratory Investigations

Complete Blood Count

Cardiac Markers

Renal Profile

Liver Profile, Serum

Lipid Profile

Diabetic Profile

Echo

Echocardiography Report

Observation and comments

• Left ventricle ejection fraction = 50 %
• LV: Mild Inferior Wall hypokinesia
• Fair LV systolic function
• MV: Leaflets are thin with normal mobility and coaptation
• AV: 3 thin cusps with normal excursion and coaptation
• TV: Structurally normal
• PV: structurally normal
• IAS: Intact
• IVS: Intact

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Continued….

• Ra: Normal Sized
• RV: Normal sized with good global systolic function
• LA: Normal Sized
• IVC: >50% inspiratory collapse
• No Clot seen
• No pericardial effusion see
• No coarctation of aorta/PDA
• NO diastolic dysfunction dysfunction

Definitive Diagnosis

Acute Inferior Wall ST elevated Myocardial Infarction

Management

Emergency management

• Tablet Aspirin 300 mg chewed
• Tablet Clopidogrel 75 mg x 8 PO
• Tablet Nitroglycerin sublingual
• Infusion Heparin

Intervention

Percutaneous coronary intervention (PCI)

• Also known as Coronary angioplasty
• A percutaneous technique for treating myocardial infarction
• Coronary catheterization is used to visualize blood vessels on x-ray imaging
• Angioplasty is performed using a balloon catheter which is introduced into the obstructed artery to relieve narrowing.

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Primary PCI is the urgent use of PCI in people with acute myocardial infarction (heart attack) especially where there is evidence of heart damage on ECG (ST elevation)

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Femoral�-Shock�-Negative Allen’s test

Left Radial�-Older )>65 y�-Female�-Shorter stature�-Lower BMI�-Previous CABG

Arterial Access for Primary PCI

Right Radial�(default)

Procedure:

• PCI was done through RCA
• GIUDING JR 4/6 F
• WIRE SION
• BALOON 2/12
• STENT 3/26 DEPLOYED AT 14
• TIMI # 3

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Normal Left coronary system

Normal Left coronary system

Total Occlusion of RCA

GIUDE wire in RCA

Stent placement in RCA

Final Result:�blood flow resumed

Post-treatment condition of patient

• Result of PCI:
• Excellent result with no residual stenosis
• Patient was shifted to CCU – 1
• Infused with tirofoban for 24 hours
• GPIIb/IIIa Inhibitor

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Patient’s condition at the time of discharge

• Patient was clinically stable
• Asymptomatic
• General condition was good
• Patient had no respiratory distress

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Drugs prescribed at the time of Discharge

• Tab Aspirin CV 100mg 1+0+0
• Tab Clopidogrel 75mg 1+0+0
• Tab Bisoprolol 5mg 1+0+0
• Tab Perindopril 4mg 0+0+1
• Tab Atorvastatin 40mg 0+0+1
• Tab Pantoprazole 40mg 1+0+0
• Tab Sitaglumet 50/500 1+0+1

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Follow-Up Instructions

• Patient advised to:
• Continue aspirin lifelong
• Clopidogrel for 1 year
• Follow up in cardiac clinic after 2 weeks
• Resume normal activities and desk job
• Avoid strenuous activity which might cause breathlessness and exertion

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Case Discussion�

Pathophysiology �

What is Myocardial Infarction?

Myocardial Infarction is defined by the demonstration of myocardial cell necrosis due to significant and sustained ischemia.

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Detection of a rise and/or fall of cardiac biomarker values (preferably cardiac troponin) with at least one value above the 99^th centile upper reference limit, with at least one of the following:

1. Symptoms of ischemia

2. New significant ST segment-T wave changes

3. Development of pathological Q waves in the ECG

4. Imaging evidence of new loss of viable myocardium

5. Identification of an intracoronary thrombus

Criteria for diagnosis of MI

Pathogenisis

A brief review of the cardiac blood supply

Left Circumflex Artery�-Left atrium and ventricle

Right Coronary Artery

-Right atrium �-Right ventricle

Right Marginal Artery�-Right ventricle �-Apex

Left Anterior Descending Artery�-Right ventricle �-Left ventricle �-Interventricular septum

Left Marginal Artery �-Left ventricle

TRANSMURAL INFARCTS

SUBENDOCARDIAL INFARCTS

Types of infarcts

• According to anatomic region of the heart involved:
• Anterior
• Posterior
• Lateral
• Septal
• Circumferential
• Combinations: Anterolateral, posterolateral, anteroseptal

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Progression of myocardial necrosis after coronary artery occlusion

Biochemical changes in acute MI

Ischemic myocardium�Anaerobic glycolysis�Increased accumulation of lactate�Decrease in pH�Lysosomal enzymes activated�Disintegration of myocardial proteins�Cell death and necrosis�

Clinical manifestations�(chest pain)

Release of intracellular contents into blood �(Biochemical markers)

ECG changes

• ST elevation
• Q and T wave �changes

• Pain
• Severe, crushing, substernal
• May radiate to neck, jaw, epigastrium, left arm
• May last several minutes to hours
• Not relieved by nitroglycerin or rest
• Pulse may be rapid or weak
• Breathlessness
• Low grade fever
• Narrow pulse pressure
• Raised JVP
• Hypotension

Clinical Features of Myocardial Infarction

Sympathetic activation:

• Pallor
• Sweating
• Tachycardia

Clinical Features of MI contd.

Vagal activation:

• Vomiting
• Bradycardia

Complications: Immediate (hours)

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Arrhythmias

• Ventricular Fibrillation
• Atrial Fibrillation
• Atrioventricular Block
• Ventricular Tachycardia

Complications: Immediate

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Acute Heart Failure

Complications: Early (days)

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Recurrent Angina

Complications: Early

• Papillary Muscle Rupture
• Ventricular Septum Rupture
• Ventricular Rupture

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Complications: Late (weeks)

• Pericarditis
• Dressler’s Syndrome (characterized by persistent fever, pericarditis and pleurisy)
• Embolism
• Ventricular Remodeling
• Ventricular Aneurysm

Investigations in a case of Myocardial Infarction��

Classic Triad of Myocardial Infarction

Diagnosis

12- Lead ECG

ST-Elevation MI (STEMI)

Deep Q wave is an indicator of myocardial tissue death and will remain on the ECG.� A "pathological" Q wave is not "time-specific". It may be there from a previous heart attack and therefore is not part of the criteria for evaluating an Acute Myocardial Infarction.

STEMI vs. NSTEMI

Cardiac Biomarkers

Myocardial necrosis causes sarcolemmal disruption�

Release of intracellular macromolecules�

• Can be measured by serial blood testing
• Pattern and level of rise correlates with timing and size of MI
• Cardiac biomarkers assessed: Troponins and CK-MB

Laboratory Markers

Raised Troponin T and I

Increase within 3-6 hours

Peak at 36 hours

Remain elevated for 2 weeks

Other Lab Investigations

1. Presence of Leukocytosis on CBC.
2. Raised Erythrocyte sedimentation rate (ESR) and C-reactive proteins (CRP).
3. Lipids should be measured within 24 hours of presentation because there is often a transient fall in cholesterol for the 3 months following infarction

Imaging: Chest X-Ray

A chest X- ray may demonstrate:

• Pulmonary edema
• Cardiomegaly in the case of pre-existing myocardial damage

Imaging: Echocardiograph

• It is done to assess ventricular function
• It plays a crucial role in detecting important complications such as:
• Mural thrombus
• Cardiac rupture
• Mitral regurgitation
• Pericardial effusion

Imaging: Coronary Angiography

• Done to assess the coronary arteries.�
• Once the diagnosis for STEMI is established primary percutaneous intervention (PCI) can be performed in the same procedure

Management�

Acute MI is a medical emergency, needs to be treated promptly

MANAGEMENT

IMMEDIATE

UNRESOLVED

CASES

DRUGS

REPERFUSION PCI

SURGERY

Immediate: Non specific

• Maintain IV line
• Analgesia: IV Opiates (Morphine sulphate)
• Antiplatelet therapy:
• Aspirin 75 -325mg - within first 30 mins of pain
• Clopidogrel-600mg stat

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Contd.

• Antithrombotic therapy:
• HEPARIN 70-100 U/kg body weight or
• S/C ENOXAPARIN until revascularization

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• Vasodilators: S/L Glyceryl Trinitrate 300-500 micrograms

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Immediate: Specific

Patients with STEMI who present within 12 hours of onset of symptoms should be offered reperfusion therapy

REPERFUSION

THROMBOLYTIC THERAPY:

STREPTOKINASE

PERCUTANEOUS CORONARY INTERVENTION (PCI)

1. PCI/Angioplasty

• First treatment of choice
• Balloon angioplasty with or without stenting.
• Can establish revascularization in occluded vessel
• Non surgical technique

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2. Fibrinolytic Therapy(t-PA)

• 2^nd treatment modality, when PCI unavailable
• For lysis of clot- establish reperfusion
• Not used in NSTEMI, only STEMI
• Useful only if given within first 12 hours of onset of symptoms
• Provided – no contraindication to this therapy

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STREPTOKINASE/ALTEPLASE � (IV over 60-90 minutes)

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Contraindication of t-PA

• Haemorrhagic stroke anytime in life
• Ischemic stroke within last 3 months
• Active bleed
• Aortic dissection
• Recent spinal/cranial surgery
• Cerebrovascular tumours

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Late Therapy: Surgery

Coronary Artery Bypass Grafting

(CABG)

Indications:

• Graft taken from either leg vein or internal mammary artery
• Blocked vessel is identified
• Graft placed in between aorta and distal part of blocked vessel
• Blood flow established through this alternate route

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• Left main stem disease
• Triple vessel coronary artery disease.��

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CABG: Method

Late Management

• Lifestyle modifications
• Weight management
• Regular exercise
• Diet changes
• Cessation of smoking

Contd.

• Secondary prevention drug therapy
• Antiplatelet drugs (aspirin/clopidogrel)
• Beta blockers
• ACE inhibitors
• Statin drugs
• Mineralocorticoid receptor antagonist
• Additional therapy for control of DM and HTN�
• Devices to prevent sudden death
• Implantable cardiac defibrillator

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Thank You�Any Questions?