Acute Myocardial Infarction

(AMI)

Yang HaiBo MD
Department of cardiology,
1st affiliated hospital of ZZU
 Incidence & mortality
Incidence 0.2 ～ 0.6‰.yr
Mortality 30 (Pre-CCU)
15 （ CCU ）
12 （ βblocker ）
8 （ thrombolysis ）
80% （ cardiogenic shock ）
U.S.A 2.25 million
Risk factors

Hyperlipemia

Obesity

Hypertension

Smoking etc
Basic Mechanism
Pathophysiology of ST -Elevation
ST-Elevation
Myocardial Infarction
Generally caused by a Results from stabilization of a
completely occlusive platelet aggregate at site of
thrombus in a coronary artery plaque rupture by fibrin mesh

platelet
RBC
fibrin mesh
GP IIb-IIIa
 Thrombus propagation.

A, Left anterior descending coronary artery cut open longitudinally, showing a dark
(red) stagnation thrombosis propagating upstream from the initiating
rupture/platelet-rich thrombus at the arrow.
B, The right coronary artery cut open longitudinally, showing a huge stagnation
thrombosis propagating downstream from the initiating rupture/platelet-rich
thrombus at the arrow.
 ROSS PATHOLOGICAL CHANGES

• On gross inspection, AMI may be divided into tw

o major types:
(1) transmural infarcts, in which myocardial necr
osis involves the full thickness (or nearly full thic
kness) of the ventricular wall, and (2) subendoca
rdial (nontransmural) infarcts, in which the necro
sis involves the subendocardium, the intramural
myocardium, or both without extending all the w
ay through the ventricular wall to the epicardium
 Symptom

Presymptoms
• Initial onset angina
• Accelerated angina
• Nausea 、 Vomit 、 Bradycardi
a
• Heart failure 、 Arrhythmia
•
 Symptom
• Acute chest pain
〉 30min
dull or sharp burning pain
chest distress
• GI symptom nausea, vomit
• Slight fever
• Arrhythmia
• Hypotension ,Shock ,Heart Failure
 Sign

• S1 decreased ， S4
• Pericardial friction rub
• Systolic murmur
• Arrhythmia
ECG evolution
 localization
• Anterior Septal infarction:V1,V2
• Anterior infarction: V3,V4
• Anterolateral infarction: V3-V6,avl,I
• Inferior infarction：II,III,AVF
• Extensive anterior infarction: I, avl
V1-V6
• Posterior infarction ： V7-V9 ,
reciprocal change in leads V1,V2
Enzyme changes
 Enzyme changes
Time to
Time to Time to
return to
Initial peak
normal
elevation elevation
range
cTnI 3~12 24h 5~10d
cTnT 3~12 12h~2d 3~14d
CK <6h 24h 3~4d
CK-MB 4~6h 16~24h 3~4d
AST 6~12h 24~48h 3~6d
LDH 8~10h 2~3d 1~2w
• The classic World Health Organization
(WHO) criteria for the diagnosis of AMI
require that at least two of the following
three elements be present: (1) a history of
ischemic-type chest discomfort, (2)
evolutionary changes on serially obtained
ECG tracings, and (3) a rise and fall in
serum cardiac markers.
 Complication
• Dysfunction or rupture of papill
ary muscle
• Rupture of the heart
• Embolism
• Ventricular aneurysm
• Postinfarction syndrome
Emergency therapy

Thrombolysis
Aspirin
Nitrate
β- blocker
 Thrombolytic therepy
Urokinase (UK)——1.0 ～ 1.5 million unit （ 30min ）

Streptokinase (SK)—— 1.5 million unit （ 60min ）

Recombinant tissue plasminogen activator (rt-PA)

——100mg (90min)
Indication for thrombolysis
• Chest pain >30 min ， can’t relieve
by nitroglycerin
• Elevated ST >0.2mv
• Duration < 12h
• Duration >12h ， serious chest pa
in , elevated ST
• Age < 65yr ～ 70yr
 Contraindication
• Recent surgery or hemorrhage
• History of cerebrovascular accident
• Hemorrhage disease
• SBP>180mmHg
• Shock , refractory to medicine
 Evaluation of reperfusion
• Indirect index
chest pain relieved in 2h
ST segment declined in 2h >50%
the peak of enzyme advanced:
（ CK-MB 〈 14h ）
arrhythmia of reperfusion （ PVB,VT)
• Direct index
coronary atery angiography
Coronary artery angiography
Intervention therapy
 Intervention therapy

After therapy Before therapy

Flow chart showing postulated sequence of events from an unstable atherosclerotic plaque
to death. The original paradigm emphasizing early reperfusion is shown at the left; the
expanded paradigm illustrating the benefits of late reperfusion is shown at the right.
 CABG
(Coronary artery bypass graft)

Bypass

Bypass

Bypass
 Right ventricular infarction

• Posterior & inferior MI

• Right sided Heart failure
• Cardiac output (CO) decreased
• ECG: V3R ～ V5R ST elevation>1mm

• Treatment :Volume expansion

A, The impact of medical therapy for AMI on short-term mortality. In the pre-CCU era AMI
short-term mortality (30-day) was estimated to be 30 percent. Implementation of the CCU
concept with defibrillation, sophisticated hemodynamic monitoring, and beta blockade red
uced this to 15 percent. A further mortality reduction was ushered in by the reperfusion er
a; combinations of thrombolysis, primary percutaneous transluminal coronary angioplasty
, and aspirin are now employed. B, Cumulative incidence of CHD death as function of tim
e period of initial Q-wave MI.