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Myocardial Infarction: Dept. of Pharmacology, GMC Amritsar 1

This document discusses the treatment of myocardial infarction (MI). It describes how MIs are classified based on ECG and troponin measurements. It outlines the initial treatment for MI, including morphine, aspirin, oxygen, and goals of relieving pain and decreasing mortality. It then discusses the subsequent management of proven MIs, focusing on treating complications and preventing future MIs. It provides details on thrombolytic therapy for treating MIs, describing various thrombolytic drugs, how they work, and their administration. It notes potential adverse effects of thrombolytic therapy and contraindications. The role of beta blockers, antiplatelet agents, and glycoprotein IIb/IIIa antagonists in treating MIs is also summarized

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70 views11 pages

Myocardial Infarction: Dept. of Pharmacology, GMC Amritsar 1

This document discusses the treatment of myocardial infarction (MI). It describes how MIs are classified based on ECG and troponin measurements. It outlines the initial treatment for MI, including morphine, aspirin, oxygen, and goals of relieving pain and decreasing mortality. It then discusses the subsequent management of proven MIs, focusing on treating complications and preventing future MIs. It provides details on thrombolytic therapy for treating MIs, describing various thrombolytic drugs, how they work, and their administration. It notes potential adverse effects of thrombolytic therapy and contraindications. The role of beta blockers, antiplatelet agents, and glycoprotein IIb/IIIa antagonists in treating MIs is also summarized

Uploaded by

Robert Katusabe
Copyright
© Attribution Non-Commercial (BY-NC)
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as PDF, TXT or read online on Scribd
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Myocardial Infarction

Dept. of Pharmacology, GMC Amritsar

The acute coronary syndromes (ACS) are classified on the basis of the ECG and Plasma troponin measurements into: 1. Pts. with ST elevation myocardial infarction (STEMI). 2. Non- ST elevation myocardial infarction (nonSTEMI) and positive troponin test. 3. Unstable angina by ECG & ve troponin test.

Dept. of Pharmacology, GMC Amritsar

Initial treatment before a definite diagnosis of AMI


Morphine or Diamorphine 2.5 5 mg i.v. Aspirin 150-300 mg orally. 60% oxygen. Immediate objective: Relief of pain Treatment to decrease mortality.
Dept. of Pharmacology, GMC Amritsar 3

Subsequent management of proven MI


Treatment of complications
1. Arrhythmias 2. Heart failure 3. Thromboemboli

Secondary prevention of future MI.

Dept. of Pharmacology, GMC Amritsar

Diagnosed STEMI
Institute myocardial reperfusion as early as possible by thrombolysis. Shift the patient to coronary care unit for thrombolysis. Non-STEMI patients may benefit those with LBBB. Only slight benefit to patients with Unstable Angina and pts. without ECG changes or with ST depression.
Dept. of Pharmacology, GMC Amritsar 5

Drugs That Produce Fibrinolysis


Fibrin - selective: Alteplase (rt-PA) Relteplase Recombinant prourokinase Non-fibrin selective: Streptokinase Anisteplase (APSAC, Anisoylated plasminogen streptokinase activator complex) Urokinase
Dept. of Pharmacology, GMC Amritsar 6

Drugs That Promote Fibrinolysis


Thrombolytics
Streptokinase Urokinase Anisteplase

Plasminogen in Blood Plasminogen binds to fibrin


Plasminogen formed On fibrin which it destroys

Bound to fibrin
Alteplase Prourokinase

Fibrin degradation Products GMC Dept. of Pharmacology, (FDP)


Amritsar

Thrombolytic Therapy
First infarct patient: Inj. Streptokinase 15,00,000 units i.v. infusion over 1 hr. For subsequent infarcts: Recombinant tissue plasminogen activator (rtPA or Alteplase) Alteplase and Stk. bind Plasminogen & convert it to Plasmin, which lyses Fibrin. Alteplase has much higher affinity for plasminogen bound to fibrin than in circulation.
Dept. of Pharmacology, GMC Amritsar 8

Streptokinase
47,000 dalton protein produced by haemolytic streptococci. Forms a stable non-covalent 1:1 complex with plasminogen. Converts plasminogen to plasmin. Loading dose 250,000 U; 2.5 mg i.v. to overcome plasma antibodies resulting from prior streptococcal infections. t1/2 40-80 min.
Dept. of Pharmacology, GMC Amritsar 9

Recombinant Tissue Plasminogen Activator (rt-PA or Alteplase)


Physiological conc. 5-10 ng/ml. Therapeutic infusion conc. 300-3000 ng/ml. Half life 5-10 min. Lysis thrombi during AMI. Accelerated regimen for coronary thrombolysis is 15 mg iv bolus followed by 0.75 mg/kg over 30 min. (Max 50 mg) & 0.5 mg/kg (upto 35 mg) over following Dept. of Pharmacology, GMC 10 hour. Amritsar

Thrombolytic Therapy
Timing of administration; Earlier the better Within Ist 3 hrs up to 12 hrs. Ant. MI pts. benefit most when treated within 4 hrs of onset. i.v. infusion over 1-3 hrs. Thrombolysis & Aspirin lowers the risk of stroke by limiting size of the infarct or by reducing thromboembolic episodes or by both.
Dept. of Pharmacology, GMC Amritsar 11

Recent studies suggest that: Angioplasty with / without stent placement is superior to thrombolytic therapy. Concurrent administration of Low-dose aspirin improves the efficacy of thrombolytic therapy of MI.

Dept. of Pharmacology, GMC Amritsar

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Thrombolytic Therapy
ADRs: Bleeding Nausea, Vomiting Multiple micro emboli Cardiac arrhythmias Allergy Streptokinase & Anisteplase are antigenic and anaphylactic reactions with rash, urticaria & hypotension. Avoid reuse b/n 5 days & 12 mths.
Dept. of Pharmacology, GMC Amritsar 13

Haemorrhagic diathesis Pregnancy Recent symptoms of peptic ulcer / GI bleeding. Recent stroke (Previous 3 mths) Recent surgery (Previous 10-14 days) Prolonged CPR (currently) Proliferative Diabetic retinopathy. Severe uncontrolled hypertension. Aortic dissection Acute pancreatitis. Pharmacology, GMC Dept. of
Amritsar

Contraindications to Thrombolysis

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Role of -Blockers
Reduce mortality due to prevention of cardiac rupture. Inj. Atenolol 50 mg i.v. Tab. Atenolol 50 mg orally daily. Usual CIs to -Blockers apply.

Dept. of Pharmacology, GMC Amritsar

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Role of antiplatelet agents


Glycoprotein IIb / IIIa receptor expression of cell surface. This expression is the final common pathway to platelet aggregation and thrombus formation. This receptor binds fibrinogen with high affinity. Specific monoclonal antibody Abciximab. Specific antagonists Eptifibatide. Tirofiban.
Dept. of Pharmacology, GMC Amritsar 16

Clopidogrel inhibits APD-dependent platelet aggregation. Clopidogrel more efficacious than Aspirin for prevention of ischaemic stroke or cardiovascular death in patients at high risk. Clopidogrel- Thienopyridine derivative.

Dept. of Pharmacology, GMC Amritsar

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Glycoprotein(GP) IIb / IIIa Antagonists


Abciximab is a human-murine chimeric monoclonal antibody Fab fragment that binds to GP IIb / IIIa complex with high affinity & slow dissociation rate. It produces immediate & profound antiplatelet activity that lasts for 12-36 hrs after termination of infusion. Inj. Abciximab 0.25 mg/kg i.v. bolus. Inj. Abciximab 0.125 g/kg/min infusion for 12hrs Dept. of Pharmacology, GMC 18
Amritsar

This reduces risk for death, MI or need for CABG surgery & maintains benefit upto 3yrs. Dose causes & maintains blockade of >80% receptors causing >80% reduction in aggregation. Combined with low dose of thrombolysis in AMI. Used as a single agent in stroke.
Dept. of Pharmacology, GMC Amritsar 19

Competitive inhibitors of GP IIb / IIIa


Epifibatide heptapeptide Tirofiban ] Non Lamifiban ] peptide
Lower affinity & Higher dissociation rates than Abciximab. Platelet aggregation returns to normal 30 min to 4 hrs after discontinuation. Effective in acute coronary syndromes.
Dept. of Pharmacology, GMC Amritsar 20

ADRs: 1) Haemorrhage Transfuse platelets after cessation of Abciximab necessary for life threatening or refractory bleeding. After transfusion, antibody redistributed to transfused platelets, reduce mean level of receptor blockade & improves platelet function. 2) Thrombocytopenia Occurs 1 hr to days after commencing treatment in 1% pts. o Platelet counts at 2-4 hrs. o Daily platelet count. o If severe, stop therapy. If necessary, transfuse platelets. Dept. of Pharmacology, GMC 21
Amritsar

Competitive inhibitors of GP IIb / IIIa

Thank You

Dept. of Pharmacology, GMC Amritsar

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