DR.N.H.

SARMA

ISCHEMIC HEART DISEASE

RIGHT
CORONARY LEFT
ARTERY CORONAR
Y ARTERY

LEFT
CIRCUMFLEX
ARTERY

LEFT
ANTERIOR
DESCENDING
BRANCH
(LAD)
ISCHEMIC HEART DISEASE COMPRISES :

 ANGINA PECTORIS
 ACUTE MYOCARDIAL INFARCTION(MI)
 CHRONIC MYOCARDIAL INFARCTION
 SUDDEN CARDIAC DEATH.

ACUTE CORONARY SYNDROME INCLUDES THE

LIFE THREATENING CONDITIONS
LIKE :
 UNSTABLE ANGINA
 ACUTE MYOCARDIAL INFARCTION(MI)
 SUDDEN CARDIAC DEATH(SCD).
 ACUTE MYOCARDIAL INFARCTION(MI) IS THE
MOST COMMON DANGEROUS EFFECT OF
ATHEROSCLEROTIC CORONARY ARTERIES.

 GOOD COLLATERAL CIRCULATION IN THE

CORONARIES USUALLY PREVENTS A SEVERE
EFFECT ON THE HEART
ACUTE MYOCARDIAL INFARCTION (MI)

 INCIDENCE: CORRELATES WITH PREVALENCE

OF ATHEROSCLEROSIS IN THAT POPULATION.

 AGE: USUALLY OLD AGE AROUND OR AFTER

45 YRS.BUT CAN OCCUR AT ANY AGE!!!!

 SEX: MORE COMMON IN MALES. DURING

REPRODUCTIVE YRS FEMALES ARE LESS
AFFECTED BUT AFTER MENOPAUSE (AFTER
60YRS AGE) FEMALES ARE EQUALLY
AFFECTED.
OPATHOGENESIS
 SEVERE ATHEROSCLEROSIS OF ONE OR MORE
BRANCHES OF CORONARY ARTERY IS SEEN IN
>90% OF CASES.

I.MYOCARDIAL ISCHEMIA CAN BE PRODUCED BY:

1. CORONARY BLOOD FLOW TO HEART DUE TO
ATHEROSCLEROSIS, OBSTRUCTION OR
COMPRESSION.
2. MYOCARDIAL DEMAND.
3. HYPERTROPHY OF THE HEART NEEDING MORE
BLOOD SUPPLY.
II.COMPLICATED ATHEROSCLEROTIC PLAQUE IN THE
CORONARY ARTERY. THE MAIN COMPLICATIONS ARE
- SUPERIMPOSED THROMBUS
- HEMORRHAGE INTO THE PLAQUE.
>90 % OF MI PATIENTS HAVE SUPERIMPOSED
THROMBUS
SO PTs ARE GIVEN FIBRINOLYTIC AGENTS
IMMEDIATELY AFTER MI IS DETECTED!!!!!

III. PLAQUE RUPTURE CAN ATTRACT PLATELETS AND

LEAD TO FORMATION OF THROMBUS OVER PLAQUE.
IV. NON ATHEROSCLEROTIC CAUSES WHICH CAN LEAD
TO MI ARE:
- CORONARY VASOSPASM, ARTERITIS, COMPRESSION
FROM OUTSIDE, EMBOLISM, THROMBUS FORMATION.

V. IN SUB ENDOCARDIAL INFARCTS MYOCARDIAL HYPO

PERFUSION IS THE CAUSE.USUALLY THERE IS NO
SUPERIMPOSED THROMBUS IN THESE CASES.
IN TRANSMURAL INFARCTS CORONARY
ATHEROSCLEROSIS WITH SUPERIMPOSED THROMBUS
IS ALWAYS PRESENT.
TYPES OF INFARCTS
1.ACCORDING TO THE ANATOMIC LOCATION:
-LEFT VENTRICLE, RIGHT VENTRICLE, ATRIAL.
- ANTERIOR, POSTERIOR,LATERAL ,SEPTAL AND
COMBINATION OF ANY OF THE ABOVE. MOST COMMON
LOCATION IS ANTERIO LATERAL PART OF THE LEFT
VENTRICLE

2. ACCORDING TO THE EXTENT OF THE INVOLVEMENT:

- TRANSMURAL
-SUBENDOCARDIAL

3. AGE OF THE INFARCT:

- RECENT
- OLD
MOST COMMON LOCATION OF THE INFARCT

MOST FREQUENTLY LOCATED IN THE LEFT VENTRICLE.

3 MOST COMMON AREAS OF MI ARE:

1.40-50% INVOLVE ANTERIOR PART OF LEFT VENTRICLE

APEX AND ANTERIOR 2/3rds OF INTERVENTRICULAR
SEPTUM.ANTERIOR DESCENDING BRANCH OF THE LEFT
CORONARY ARTERY IS AFFECTED IN THESE CASES.

2. 30-40% INVOLVE POSTERIOR PART OF LEFT VENTRICLE AND

POSTERIOR 1/3rds OF INTERVENTRICULAR SEPTUM.THERE IS STENOSIS
OF THE RIGHT CORONARY ARTERY.

3.15-20% INVOLVE LATERAL WALL OF LEFT VENTRICLE.THERE IS

STENOSIS OF LEFT CIRCUMFLEX CORONARY ARTERY.
GROSS & MICROSCOPIC FEATURES

 EARLY INFARCTS CAN BE DETECTED ON

GROSS EXAMINATION BY TTC TEST.
- IN THIS TEST ‘TRIPHENYL TETRAZOLIUM
CHLORIDE’ IS POURED ON THE HEART.THE
NORMAL AREA SHOWS PURPLE COLOR
BECAUSE OF THE PRESENCE OF
DEHYDROGENASES IN THE CELLS. WHERE
AS THE INFARCTED AREA REMAINS PALE OR
NO COLOR IS SEEN AS THE
DEHYDROGENASES FROM THE CELLS HAVE
COME OUT INTO THE BLOOD.
MORPHOLOGICAL CHANGES IN MYOCARDIAL INFARCTION
I.REVERSIBLE INJURY

TIME GROSS LIGHT MICRO EM

FEATURES
0-1/2 HR NONE NONE GLYCOGEN
LOSS AND
MITOCHONDRIAL
SWELLING
SARCOLEMMAL
DISRUPTION
CHROMATIN
CLUMPING
EFFLUX OF K+
AND INFLUX OF
Na+
MORPHOLOGY OF MYOCARDIAL INFARCTION
II.IRREVERSIBLE INJURY

TIME GROSS LIGHT MICRO EM

0-6 HRS NO CHANGES TTC NO CHANGES. MITOCHONDRIAL
TEST IS NEGATIVE STRETCHING & AMORPHOUS
WAVY FIBRES MAY DENSITIES
BE SEEN
6-12HRS DARK MOTTLING BEGINNING OF ---
COAGULATIVE
NECROSIS ,OEDE
MA AND
NEUTROPHIL
INFILTRATION
12-24 HRS DARK MOTTLING PROGRESSIVE ------
NECROSIS,
NEUTROPHILS
48-72 HRS MOTTLING WITH NECROSIS,LOSS -----
YELLOW TAN OF NUCLEI &
INFARCT CENTRE STRIATIONS,
NEUTROPHILS +++
MORPHOLOGY OF MYOCARDIAL INFARCTION
II.IRREVERSIBLE INJURY
TIME GROSS LIGHT MICRO EM
3-7 DAYS HYPEREMIC DISINTEGRATION OF ----
BORDER ,CENTRAL DEAD MYOFIBRES,DEAD
YELLOW AREA, NEUTROPHILS,PHAGOC
SOFT YTOSIS OF DEAD TISSUE
BY MACROPHAGES

7-10 DAYS BRIGHT YELLOW PHAGOCYTOSIS OF -----

TAN,SOFT AND DEAD CELLS. EARLY
RED-PURPLE GRANULATION TISSUE
PERIPHERY AT MARGINS

10-14 DAYS RED-GREY WELL ESTABLISHED ------

DEPRESSED GRANULATION TISSSUE
INFARCT BORDERS AND COLLAGEN
DEPOSITION

14-60 DAYS GREY WHITE SCAR COLLAGEN AND LOSS -----

OF CELLS

> 2 MONTHS COMPLETE SCAR COLLAGENISED TISSUE

POSTERIOLATERAL LEFT VENTRICULAR
PROMINENT CONTRACTION BANDS(EARLIEST MICROSCOPIC CHANGE)
MYOCARDIAL INFARCTION –EARLY CHANGES
MYOCARDIAL INFARCTION--EARLY CHANGES
2 WEEK OLD MYOCARDIAL INFARCTION
COLLAGEN REPLACEMENT OF INFARCTED AREA
SCAR TISSUE IN SUBENDOCARDIAL INFARCTION
INFARCTED AREA REPLACED BY SCAR TISSUE
CLINICAL DIAGNOSIS OF MYOCARDIAL INFARCTION

DIAGNOSIS OF MYOCARDIAL INFARCTION

IS BASED ON:
1. CLINICAL FEATURES

2. LABORATORY INVESTIGATIONS LIKE

- ECG
- SERUM ENZYME ASSESSMENT
CLINICAL FEATURES

 THE TYPICAL PRESENTATION OF MI IS: PATIENT

COMPLAINS OF SUDDEN LEFT SIDED CHEST PAIN
RADIATING TO THE LEFT SHOULDER AND ARM.

 OTHER MANIFESTATIONS CAN BE LOW GRADE

FEVER,
INDIGESTION, SHOCK,OLIGURIA,SWEATING AND
BREATHLESSNESS.
ECG CHANGES

 ‘ST’ SEGMENT ELEVATION

 ‘T’ WAVE INVERSION
 APPEARANCE OF DEEP ‘Q’ WAVES

NOTE: THESE FINDINGS ARE IN A TYPICAL

ANTERIOR LEFT VENTRICULAR INFARCTION.

DEPENDING ON THE LOCATION THE ECG

CHANGES VARY
‘T’ WAVE INVERSION(ARROWS)
SERUM ENZYMES WHICH ACT AS MARKERS OF
MYOCARDIAL INFARCTION

 CK-MB (CK-MB 1 AND CK-MB 2)

 LDH (LDH 1 AND LDH 2)
 CARDIAC TROPONINS.(I AND T)
 MYOGLOBIN –IT IS NOT SPECIFIC

OUT OF ALL THESE CARDIAC TROPONINS ARE

MORE SPECIFIC AS THEY START APPEARING
IMMEDIATELY AFTER INFARCTION AND ARE
PRESENT IN THE SERUM FOR 10-14 DAYS.
COMPLICATIONS OF MYOCARDIAL INFARCTION

 80-90% OF MI CASES DEVELOP MAJOR COMPLICATIONS

AND IN THIS AROUND 25% ARE FATAL.
THE COMPLICATIONS SEEN IN MI ARE:
- CARDIAC ARRHYTHMIAS.
- RUPTURE OF LEFT VENTRICLE AT THE SITE OF INFARCT
- CARDIAC TAMPONADE.
-RUPTURE OF PAPILLARY MUSCLE OR CHORDAE TENDINAE.
-LEFT VENTRICULAR ANEURYSM
- MURAL THROMBOSIS AND EMBOLISM
- SHOCK
- PERICARDITIS
- CONGESTIVE HEART FAILURE
- POST MYOCARDIAL SYNDROME(DRESSLER’S SYNDROME)
ANGINA PECTORIS

 Angina pectoris is a symptom complex of IHD

characterized by paroxysmal and usually recurrent
attacks of substernal or precordial chest
discomfort (variously described as
constricting,squeezing, choking, or knifelike) caused
by transient (15 seconds to 15 minutes)
myocardial ischemia that falls short of inducing
the cellular necrosis that defines infarction.
PATTERNS OF ANGINA PECTORIS
3 PATTERNS ARE SEEN:

1. STABLE OR TYPICAL ANGINA

2. PRINZMETAL OR VARIANT ANGINA

3. UNSTABLE OR CRESCENDO ANGINA

STABLE ANGINA
 the most common form and called typical angina
pectoris, appears to be caused by the reduction of
coronary perfusion to a critical level by chronic
stenosing coronary atherosclerosis;
 this renders the heart vulnerable to further
ischemia whenever there is increased demand,
such as that produced by physical activity,
emotional excitement, or any other cause of
increased cardiac workload. Typical angina
pectoris is usually relieved by rest (thereby
decreasing demand) or nitroglycerin, a strong
vasodilator. .
PRINZMETAL ANGINA
 Prinzmetal variant angina is an uncommon pattern
of episodic angina that occurs at rest and is due to
coronary artery spasm. Usually there is an elevated
ST segment on the
electrocardiogram (ECG), indicative of transmural
ischemia. Although individuals with this form of
angina may well have significant coronary
atherosclerosis, the anginal attacks are
unrelated to physical activity, heart rate, or blood
pressure. Prinzmetal angina generally responds
promptly to vasodilators, such as nitroglycerin and
calcium channel blockers.
UNSTABLE OR CRESCENDO ANGINA
 Unstable or crescendo angina refers to a pattern
of pain often occurs at rest, and tends to be of
more prolonged duration.
 unstable angina is induced by disruption of an
atherosclerotic plaque with superimposed partial
(mural) thrombosis or vasospasm (or both).
 unstable angina is often referred to as
preinfarction angina.