INTRODUCTION

Myocardial infarction (MI)

refers to the process by which
areas of myocardial cells in the
heart are permanently destroyed.

It occurs when myocardial

tissues are abruptly and
severely deprived of oxygen.
DEFINITION
Myocardial infarction is a
diseased condition which is
caused by reduced blood flow
in a coronary artery due to
atherosclerosis and occlusion
of an artery by an embolus or
thrombus.
LOCATION / TYPES OF MYPCARDIAL INFARCTION
 Obstruction of the left anterior descending artery (LAD)
results in anterior or septal wall MI.
Contd…..
 Obstruction of the circumflex artery results in posterior
wall MI or lateral wall MI.
 Obstruction of the right coronary artery results in inferior
wall MI.
ETIOLOGY
 ETIOLOGY

NON-MODIFIABLE MODIFIABLE
RISK RISK
FACTORS FACTORS
NON-MODIFIABLE RISK
FACTORS
AGE: More than 40 years.

FAMILY HISTORY:
Myocardial infarction can
be inherited from parents
to children.

GENDER: Myocardial
infarction is 3 times more in
men than women.
MODIFIABLE RISK FACTORS
PATHOPHYSIOLOGY
 Causative factor: Obesity ,DM,SMOKING ,HT etc..

Atherosclerosis of coronary artery

Narrowing of lumen

ed heart insufficient blood flow to myocardium

Contractility ed O2 demand of myocardial cells

Inadequate creates an O2 deficit

Blood supply
myocardial cell death inflammation
Oliguria
CK-MB & Troponine released Fever
 Anaerobic glycolysis

Accumulation of lactic acid

Irritation of myocardial nerve fibers

Transmission of pain to myocardium

Chest pain & radiation towards shoulder & arm

Stimulation of vomiting SNS Stimulation
center
increased
Nausea & Vomiting catecholamine

Diaphoresis Increased
(perfuse sweating) Heart Rate

Cold & Clammy skin

“Cold Sweat”
 PAIN
Characteristics: Severe, immobilizing
chest pain.
Usually described as heaviness, pressure,
tightness, burning.
Location: Substernal, Retrosternal or
Epigestric.
Radiation: It may radiate to neck, jaw,
arm or back.
Duration: Lasts for 20 minutes or more.
 NAUSEA & VOMITING

Stimulation of vomiting center by severe pain causes

nausea & vomiting.

FEVER
100.4 to 102.2°F
It is due to inflammatory process caused by
Myocardial cell death.
SYMPATHETIC NERVOUS SYSTEM
STIMULATION

Increased catecholamine releases.

Diaphoresis (perfuse sweating).

Cold & clammy skin (“cold sweat”).

CARDIOVASCULAR MANIFESTATIONS
Hypotension

Decrease cardiac output

Shock

Urine output (Oliguria): <30ml/day.

Dyspnoea
DIAGNOSTIC TESTS
CONTD…..
 Electrocardiogram-
ECG provides information that
assists in diagnosing acute MI.
 The classic ECG changes are-
 T wave inversion
 ST segment elevation
 Abnormal Q wave
 ANGIOGRAPHY

To detect percentage of blockage & type of MI.

CHEST X-RAY
To detect cardiomegaly.
Positron emission tomography- (PET scan)
It is used to evaluate cardiac metabolism & to assess
tissue perfusion.
DRUG THERAPY IN MYOCARDIAL INFRACTION
Pharmacological therapy in MI has following
objectives.
1.To reduce pain, anxiety and apprehension .
2.Oxygenation .
3.Maintenance of blood volume, tissue perfusion, and
microcirculation .
4.correction of acidosis.
5.Prevention and treatment of arrhythmias.
6.To manage cardiac output .
7. Prevention of thrombus extension, embolism, venous
thrombosis
8.Thrombolysis and reperfusion.
9.Prevention of remodeling and subsequent CHF
10.Prevention of future attacks

a. platelet inhibitors.
b. beta blockers
c. control of hyperlipidemia .
1.To reduce pain anxiety and apprehension
1. After pain is not relieved by 3 doses of GTN given 5
min. apart , an opioid analgesic [morphine
/pethidine] or diazepam is administered parentally.
2.Prevention and treatment of arrhythmias.
Prophylactic i.v. infusion of beta blockers as soon as the
MI patient is seen ,reduces the incidence of arrhythmia
and mortality .
Beta blockers used early in evolving MI can reduce the
infract size and complications.
Tachyarrhythmias may be treated with i.v lidocaine,
procainamide, or amiodarone.
3. To manage cardiac output-
The objective is to increase c.o. and to decrease filling
pressure without increasing cardiac work or lowering
BP-
A. Furosemide- indicated if pulmonary wedge pressure
is > 20 mm Hg. It decreases cardiac preload.
B. Vasodilators – GTN or nitoprusside have been manily
used.
C. Inotropic agents- dopamin or dobutamine to
augment pumping action of heart.
4.Prevention of thrombus extension, embolism,
venous thrombosis-
1. Aspirin [162- 325 mg] as soon as MI is suspected. This is
continued at 80- 160 mg / day.
2. Anticoagulants [heparin followed by oral
anticoagulants ]are used to prevent deep vein thrombosis
and pulmonary or arterial embolism.
5.Thrombolysis and reperfusion
1. Fbrinolytic agents i.e. streptokinase /urokinase/
alteplase are used to achieve reperfusion of infracted
area
2.Thrombolysis should be started within 1- 2 hours of
MI symtom onset.
3. Primary percutaneous coronary intervention with
stenting is preferred revascularization procedure.
6.Prevention of remodeling and subsequent
CHF
1.ACE inhibitors/ARBs are of proven efficacy and
afford long- term survival benefit.
7.Prevention of future attacks-
Platelet inhibitors- asprine or clopidogrel.
Beta blockers- reduce risk of re infaraction, CHF, and
mortality.
Control of hyperlipidemia.
 SURGICAL MANAGEMENT

PTCA (Percutaneous
Transluminal Coronary
Angioplasty)
STENT PLACEMENT
 ATHERECTOMY

With Atherectomy the plaque is shaved off using a

type of rotational blade.
 CORONARY
ARTERY
BYPASS GRAFT
(CABG)
A portion of saphenous
vein from leg is
removed & is
anastmosed proximally
to the ascending aorta
& distally to coronary
artery.
Recent Advances in the Management of Acute
Myocardial Infarction
1. Optimsing the Outcomes Of PPCI

Thrombus aspiration during PPCI

Rheolytic thrombectomy (RT) before direct infarct artery stenting as compared
to direct stenting (DS) alone to improve the results of myocardial reperfusion
and clinical outcome in patients with acute myocardial infarction.
Intracoronary Gp IIb/IIIa inhibitors
Intracoronary administration of drugs increases local drug concentration
several fold. The increased concentration of Gp IIb/IIIa inhibitors like
Abciximab, Eptifibatide, Tirofiban are shown to improve the outcomes of
PCI safely and efficaciously in terms of reduction in infarct size,
peri-procedural MI .
Adenosine
Intracoronary administration of vasodilators such as adenosine during
and after PPCI has been shown to improve flow in the infarct-related
coronary artery and myocardial perfusion and reduces infarct size.
New oral anti-platelet drugs for AMI

Ticagrelor, unlike the thienopyridines Clopidogrel and Prasugrel, is not a pro-

drug and therefore has a faster onset of action with less variability than the
thienopyridines. It causes stronger platelet inhibition, particularly in the early
phase, and it is reversible, which maybe an advantage in reducing bleeding.
The ticagrelor group suffered fewer cardiovascular events, with the primary
end point of MI, stroke, or vascular death being significantly reduced without
any increase in major bleeding complications.
Cardioprotection Against Myocardial
Reperfusion Injury

The restoration of blood flow to ischemic myocardium sometimes leads

to myocardial injury termed as reperfusion injury which can be more
detrimental than ischemia itself and paradoxically reduce the advantage
of early restoration of blood flow. This type of injury is called as
Ischemic –Reperfusion injury.
a. The drugs which target these pathways are
cyclosporine, erythropoietin, glucagon-like peptide 1
and atrial nitriuretic peptides. The new strategies for protection
against reperfusion injury are Ischemic conditioning, targeting
the RISK [reperfusion injury salvage kinase]pathway, targeting
mitochondrial[phosphotyrosyl phosphatase activator] PTPa
b. The ischemic conditioning can be defined as preconditioning
when performed before reperfusion and post-conditioning . In clinical
practice the remote ischemic preconditioning is carried out with brief
occlusion of blood flow to either upper or lower limb by periodically inflating
and releasing the blood pressure cuff. The remote ischemic
preconditioning is believed to activate changes in intracellular
kinase and mitochondria that are cardio-protective..

c. The ischemic post-conditioning is carried out by transient

balloon occlusion of the infarct related artery. The remote
ischemic post-conditioning is carried out by transient occlusion
of other than the infarct related coronary artery.
Cardiac Repair and Regeneration

The Transplantation of Progenitor Cells And Regeneration Enhancement

in Acute Myocardial Infarction investigated both safety, feasibility, and
potential effects on parameters of myocardial function of intracoronary
infusion of either circulating progenitor cells (CPC) or bone
marrow-derived progenitor cells (BMC) in patients with acute myocardial
infarction (AMI).
Sono - thrombolysis

The use of Ultrasonic waves along with the fibrinolytic agent is

described as Sono-thrombolysis.

ST-segment resolution was better in patients who received

tenecteplase and sono-thrombolysis compared with those
who received tenecteplase alone.The exact mechanism of
benefit of sono-thrombolysis is not known, however the nitric
oxide release by vibrating endothelial cells and opening of
collateral channels have been contemplated
THANKS
THANKS