pathology cvs ischemic heart disease. title : done by
TRANSCRIPT
YSTEMICISTS
Pathology CVS
Title : Ischemic heart disease.
Done by: Farah Al-Fraihat .
A man may die, nations may rise and fall ..But an idea lives on
Ischemic heart disease
IHD is synonymous with coronary artery disease (CAD) ,
obstructive atherosclerotic more than 90% of cases due to
: , other vascular disease
- Increased demand (e.g., with increased heart rate or
hypertension)
- Diminished blood volume (e.g., with hypotension or shock)
- Diminished oxygenation (e.g., due to pneumonia or CHF)
- Diminished oxygen-carrying capacity (e.g., due to anemia
or carbon monoxide poisoning).
Clinically :
Ischemia induces pain but is insufficient to cause myocyte death .
Angina pectoris
Ischemia sufficient to cause cardiomyocyte death .
Acute MI
Progressive cardiac decompensation after acute MI , or secondary to accumulated small ischemic insults , precipitates mechanical pump failure .
Chronic IHD with CHF
Lethal arrhythmia , After MI Sudden cardiac death Catastrophic manifestations of unstable angina , acute MI and SCD .
Acute coronary syndrome
Pathogenesis : Inadequate coronary perfusion relative to
myocardial demand.
- If obstruction occludes more than 70% of a lumen: stable
angina.
- If occludes 90% or more of vascular lumen: unstable
angina.
- Slow rate atherosclerosis, over years : collateral perfusion
can subsequently protect against MI even if the vessel
eventually becomes completely occluded.
- Acute coronary blockage: no time for collateral flow to
develop and infarction results
* Angina Pectoris*
Intermittent chest pain , Ischemia-induced release of
adenosine, bradykinin, and other molecules that stimulate
the autonomic afferents.
IMPORTANTTYPES :
Episodic chest pain associated : Typical or Stable angina) 1
with particular levels of exertion , Crushing or squeezing
substernal sensation, that can radiate down the left arm or
to the left jaw (referred pain), Pain relieved by rest
(reducing demand) or by drugs such as nitroglycerin
(vasodilator) .
Unstable angina ( crescendo ) 2
Increasingly : angina )
frequent pain, precipitated by
progressively less exertion or even occurring at rest ,
Associated with plaque disruption and superimposed
thrombosis, and/or vasospasm .
Caused by , Occurs at rest: Prinzmetal or variant angina) 3
coronary artery spasm , Completely normal vessel can be
affected , Responds to vasodilators such as nitroglycerin and
calcium channel blockers.
* Myocardial infarction (MI )*
Heart attack , necrosis of heart muscle due to ischemia , any
age ( rises with increasing age and with increasing
atherosclerotic risk factors ) , Vast majority of MIs are
caused by acute coronary artery thrombosis , Preexisting
atherosclerotic plaque serves as the nidus for thrombus
generation , 10% of MIs : occurs in the absence of occlusive
atherosclerosis, Embolization from mural thrombi .
Myocardial response to Ischemia :
Within seconds of vascular obstruction : aerobic glycolysis
ceases --> Drop in ATP --> accumulation of lactic acid in
cardiac myocytes .
Within a minute of onset ischemia : RAPID loss of
contractility .
within few minutes : myofibrillar relaxation , glyogen
depletion , cell swelling .
all of above are reversible .
Severe ischemia lasting 20-40 minutes ( irreversible damage
and coagulative necrosis .
If myocardial blood flow is restored before irreversible
injury occurs, cell viability can be preserved , This is the
rationale for early diagnosis and prompt intervention by
thrombolysis or angioplasty to salvage myocardium .
Irreversible : occur in the
subendocardial zone ( last area
to receive blood delivered by the
epicardial vessels , Exposed to
relatively high intramural
pressures, which act to impede
the inflow of blood.
With more prolonged ischemia, a
wave front of cell death moves,
with the infarct usually achieving
its full extent within 3 to 6 hours.
Patterns :
The location, size, and morphologic features of an acute MI
depend:
- The size and distribution of the involved vessel
- The rate of development and the duration of the occlusion
- Metabolic demands of the myocardium
- Extent of collateral supply .
Involve the full Transmural infarctions :. 1
thickness of the ventricle , ST segment
elevations on ECG .
: limited to the Subendocardial infarctions . 2
inner third of myocardium , NON- ST elevation
infarcts .
Vessels involved in MI :
- 40% to 50% of all MI: proximal left anterior descending
(LAD) artery occlusion
Infarction of the anterior wall of the LV, the anterior two
thirds of the ventricular septum, and most of the heart apex
- 30% to 40%: Proximal right coronary artery (RCA)
Affects much of the RV
- 15% to 20% : proximal left circumflex (LCX) artery
Infarction of the lateral LV
Morphology : ( Depend on age of the injury )
Grossly : Infarcts more than 3 hours old can be visualized by
, a triphenyltetrazolium chlorideexposing myocardium to
substrate for lactate dehydrogenase , this enzyme is
depleted in the area of ischemic necrosis and the infracted
area is unstained ( pale ) .
12 - 24 hours after MI: red-blue discoloration caused by
stagnated, trapped blood , then infarcts become soft ,
yellow-tan areas .
10 - 14 days: infarcts are rimmed by hyperemic (highly
vascularized) granulation tissue.
Over the succeeding weeks: fibrous scar
Microscopic : - Coagulative necrosis : 4-12 hours of
infarction ( wavy fibers ) , - acute inflammation : 1-3 Days
after MI , - Macrophages : 4-7 Days after MI , - infracted
zone replaced by granulation tissue : 1-2 weeks after MI ,
- Scarring advanced by the end of sixth week , Once an MI
is completely healed, it is impossible to distinguish its age:
Whether present for 8 weeks or 10 years, fibrous scars look
the same.
Clinically : severe crushing substernal chest pain that can
radiate to the neck , jaw , epigastrium or left arm , typically
lasts several minutes to hours and not relieved by
nitroglycerin or rest .
( common in DM and elderly ) % of MIs15-silent infarcts : 10
The pulse generally is rapid and weak, and patients are
often diaphoretic (sweaty) and nauseous .
With massive MIs (involving more than 40% of the left
ventricle): cardiogenic shock develops.
Electrocardiographic abnormalities : Q waves, ST segment
changes, and T wave inversions , Arrhythmias .
: Complications
- hospital death of MI : 7%
- out of hospital mortality is worse : - A third of persons with
(STEMIs) will die, usually of an arrhythmia within an hour of
symptom onset, before they receive appropriate medical
attention .
1 ) Contractile dysfunction
2 ) Papillary muscle dysfunction
3 ) myocardial rupture :
- 1-5% of MIs
- Within 3- 7 days after infarction
- Left ventricular free wall rupture is most common
- Ventricular septal rupture creates a VSD with left-to-right
shunting
- Papillary muscle rupture leads to severe mitral
regurgitation .
4 ) Pericarditis : fibrinous or fibrinohemorrhagic ( Dressler
syndrome ) 2-3 days after MI .
5 ) Chamber dilation .
6 ) Mural thrombus .
7 ) Ventricular aneurysm .
8 ) Progressive late heart failure .
9 ) Arrhythmias : Heart block of variable degree (including
asystole) , Bradycardia , Supraventricular tachyarrhythmias ,
Ventricular premature contractions , Ventricular tachycardia
, Ventricular fibrillation .
(ischemic Chronic ischemic heart disease*
)*cardiomyopathy
Progressive heart failure secondary to ischemic
myocardial damage , history of previous MI .
appears when compensatory mechanisms (e.g.,
hypertrophy) of residual viable myocardium begin to fail.
left ventricular dilation and hypertrophy, often with
discrete areas of gray-white scarring from previous healed
infarcts.
* deathSudden cardiac *
Sudden death, typically due to sustained ventricular
arrhythmias in individuals who have underlying structural
heart disease which may or may not have been symptomatic
in the past.
Coronary artery disease is the leading cause of death,
responsible for 80% to 90% of cases
SCD often is the first manifestation of IHD.
The ultimate mechanism of SCD most often is a lethal
arrhythmia (e.g., asystole or ventricular fibrillation).
-Hereditary (channelo atherosclerotic causes of SCD :-Non
pathies) or acquired abnormalities of the cardiac conduction
system, Congenital coronary arterial abnormalities , Mitral
valve prolapse , Myocarditis or sarcoidosis , Dilated or
hypertrophic cardiomyopathy ,Pulmonary hypertension.
* Hypertensive heart disease*
Major cardiac complications of hypertension, result from
pressure overload .
Myocyte hypertrophy is an adaptive response, but there
are limits .
Persistent hypertension eventually can culminate in
dysfunction, cardiac dilation, CHF, and even sudden death.
Systemic hypertension: affects the left side of the heart .
((1) left ventricular hypertrophy in the absence of other
cardiovascular pathology (e.g., valvular stenosis)
(2) a history or pathologic evidence of hypertension .. )
morphology :
left ventricular hypertrophy .
- No ventricular dilation until very late in the process
- Heart weight can exceed 500 g (normal, 320 - 360 g)
- Left ventricular wall thickness can exceed 2.0 cm (normal,
1.2 - 1.4 cm).
Microscopically :
- Transverse diameter of myocytes is increased
- Prominent nuclear enlargement and hyperchromasia
- Intercellular fibrosis .
Clinically :
- Compensated hypertensive heart disease typically is
asymptomatic
- The disease can comes to attention with the onset of atrial
fibrillation and/or CHF .
Pulmonary hypertension : can cause right-sided
hypertensive changes called cor pulmonale.
- Right ventricular hypertrophy and dilation, frequently
accompanied by right heart failure
- Cause of chronic cor pulmonale:
1- Primary disorders of the lung parenchyma
2- Disorder of pulmonary vasculature
- Acute : pulmonary embolism
Morphology :
- Acute cor pulmonale:
Right ventricle usually shows only dilation
If an embolism causes sudden death, the heart may even be
of normal size.
- Chronic cor pulmonale:
Right ventricular hypertrophy
When ventricular failure develops, the right ventricle and
atrium are dilated
.. THE END