Pathology of Ischemic Heart Disease Flashcards
Cardiac Failure Definition
The clinicopathologic state where the heart is unable to pump blood at the rate required for normal function and metabolism
Cardiac failure may be acute or chronic and may affect one or both ventricles (i.e. called biventricular failure)
This entails increase in the ventricular wall
thickness as well as the mass of the heart
It is only when the hypertrophic ventricles no
longer can compensate for the increased
demand, that the ventricles dilate, i.e. failure
Categories of Cardiac Failure
- Low-output or high output failure
- Systolic or diastolic failure
- Right or left heart failure
Low-output, high-output, systolic and diastolic
failure are considered functional definitions
Low-Output Cardiac Failure:
The heart itself is incapable of pumping normally and this is seen in cases of abnormal myocardial function or valvular lesions
High-Output Cardiac Failure
The heart is pumping normally, but cannot meet the
excessive demand for blood by the body and this is encountered in cases of anaemia or hyperthyroidism
Systolic Failure:
The heart is unable to contract forcefully enough in order to pump blood into the systemic circulation
Diastolic Failure:
Although the systolic function is normal, the heart cannot relax adequately during diastole to fill with blood, and thus a smaller volume of blood is pumped
into the circulation during systole
Right Ventricular Failure:
Can be classifies as either Acute or Chronic
- Acute failure occurs after massive pulmonary
embolism, resulting in sudden death - Chronic failure may be secondary to mitral stenosis
or lung disease (cor pulmonale), resulting in neck
vein distention, liver congestion (so-called nutmeg
liver) and peripheral oedema
Important to note that the normal heart
muscle has a large functional reserve (600%),
allowing the ventricles to compensate for the
increased functional demands, i.e. ventricular
hypertrophy
Causes:
- LV hypertrophy: systemic hypertension, aortic stenosis and incompetence, mitral incompetence, coarctation of the aorta, severe anaemia, severe hyperthyroidism.
- RV hypertrophy: pulmonary hypertension (lung diseases, mitral stenosis, LV failure), pulmonary stenosis, VSD, ASD, PDA.
CARDIAC FAILURE
Left-Ventricular Failure:
Can be classified as either Acute and Chronic:
- Acute failure occurs after massive myocardial
infarction, resulting in severe dyspnoea, pulmonary
oedema and death - Chronic failure may be secondary to systemic
hypertension or chronic ischaemic heart disease
(IHD), which leads to chronic lung congestion (socalled ‘brown induration’ of the lungs) and with
time, right ventricular failure
The pathological causes of Heart Failure can broadly be categorised as:
Ischaemic heart disease (IHD)
Hypertensive heart disease
Valvular heart disease
Primary (non-ischaemic) myocardial disease
Congenital heart disease
Ischemic Heart Disease:
Definition
IHD encompasses the conditions that arise owing to an imbalance between the supply and demand of oxygen an nutrients to the heart muscle it is also termed coronary artery disease (CAD)
Ischemic Heart Disease:
Aetiology
Coronary artery atherosclerosis
Coronary vasospasm
Narrowing of the coronary ostia
Coronary artery vasculitis
AETIOLOGY OF IHD
• coronary vasospasm
▪ results in the temporary reduction of luminal
caliber
▪ may aggravate the local mechanical forces that
result in plaque fracture
AETIOLOGY OF IHD • narrowing of coronary ostia ▪ aortic atherosclerosis ▪ syphilitic mesaortitis (a form of tertiary syphilis) AETIOLOGY OF IHD • other rare causes include ▪ shock (diffuse subendocardial infarction) ▪ aortic stenosis ▪ embolism ▪ dissecting aneurysm ▪ congenital abnormalities of coronary arteries ▪ severe anaemia CLINICAL FEATURES OF IHD
Aetiology of IHD:
Coronary Artery Atherosclerosis
Coronary artery atherosclerosis:
- fixed coronary atherosclerosis
- progressive coronary atherosclerosis
acute disruption of the atherosclerotic plaque
causing partial or total occlusion of the coronary
artery lumen, i.e.:
❑rupture or ulceration of plaque with superimposed
thrombosis (‘crack’ or ‘facture’ theory) or
❑haemorrhage into a plaque
Aetiology of IHD:
Coronary Vasospasm
Results in the temporary reduction of luminal
caliber and may aggravate the local mechanical forces that result in plaque fracture
Aetiology of IHD:
Narrowing of Coronary Ostia
Aortic atherosclerosis
Syphilitic mesaortitis (a form of tertiary syphilis)
Aetiology of IHD:
Rare causes
Aortic stenosis
Embolism
Shock-Diffuse subendocardial infarction
Dissecting Aneurysm
Congenital abnormalities of coronary arteries
Severe anaemia
The clinical manifestations that an individual
develops is determined by:
Cause of the ischaemia
The degree of ischaemia
The collateral circulation
The mass of the ventricle
Clinical Features of IHD
The clinical manifestations of ischaemic heart
disease include the following
- Angina pectoris
- Acute myocardial infarction
- Chronic ischaemic heart disease
- Sudden cardiac death
Angina Pectoris
Defined as a sudden transient retrosternal
chest pain usually elicited by physical exertion
and relieved with rest
No myocardial pathology demonstrable
Acute Myocardial Infarction
Acute myocardial infarction can be defined as
a localized area of ischaemic necrosis in heart
muscle resulting from a sudden reduction in
coronary blood flow
The lay term is ‘heart attack
Acute Myocardial Infarction:
Incidence
Very common
Responsible for approximately 25% of deaths in Western countries
In South Africa, mainly White and Indian
population, and mostly males
Age incidence in males after 40 years, and females
after 55 years
Sometimes familial
Acute Myocardial Infarction:
Aetiology
Coronary atherosclerosis with acute disruption of
the atherosclerotic plaque, i.e. usually
superimposed thrombosis or sometimes
haemorrhage into plaque
The result is total occlusion of the vascular lumen
with interruption of blood flow to the cardiac
muscle, which undergoes ischaemic necrosis (i.e.
infarction)
ACUTE MYOCARDIAL INFARCTION
• infarcts may be classified as
▪ diffuse subendocardial
❑as a complication of shock, i.e. hypoperfusion which
results in ischaemic necrosis of subendocardial region of
the heart (watershed area)
❑involves the entire subendocardial region
❑rare
ACUTE MYOCAR
Classification of Infarcts
Diffuse subendocardial
Regional
Diffuse Subendocardial
As a complication of shock, i.e. hypoperfusion which
results in ischaemic necrosis of subendocardial region ofthe heart (watershed area)
Involves the entire subendocardial region
Rare
Regional
Involves only a part of the ventricular wall
-May be either transmural, i.e. almost the entire
ventricular wall thickness or regional subendocardial
-Transmural infarction is most common
The position of the regional infarct is determined by the anatomical pattern of coronary blood supply and the position of the occlusion
Left anterior descending artery:
-approximately 50% of cases
-anterior and anterior part of the septum (anteroseptal
infarction)
Right coronary artery
- approximately 35% of cases
- posterior (inferior) and posterior part of the septum
Circumflex artery
- approximately 15% of cases
- lateral infarction
Macroscopic appearance of Myocardial Infarctions
For 24 hours after the occlusion the muscle looks normal. It then becomes pale and swollen and after 3 - 4 days is yellow with a hemorrhagic border.
In transmural infarcts: fibrinous pericardial exudate. After 5 days a mural thrombus may begin to form. After 10 days the infarct becomes pale and after 3 - 6 weeks becomes a hard, grey-white scar.
Microscopic appearance of Myocardial Infarctions
0 - 12 hours :Looks normal
12 - 24 hours :Fibres eosinophilic, striations lost, nuclear changes
1 - 4 days :Neutrophils
4 - 14 days :Macrophages and granulation tissue
14 days + : progressive fibrosis with scarring
Complications of Myocardial Infarctions
Can be classified as Early(within the first 10 days) and Late
Early complications of Myocardial Infarctions
- Arrhythmias, especially VF
- Cardiogenic shock, seen in cases of massive
infarction - Softening of the heart muscle (called myomalacia
cordis) maximal at day 5 with:
-Ventricular rupture resulting in haemopericardium and
cardiac tamponade
-Tearing of the posterior papillary muscle resulting in
acute mitral incompetence
-Rupture of the IV septum causing an acquired VSD
ventricular rupture
- Mural thrombosis (also seen at day 5) with
subsequent systemic embolism
5.DVT with pulmonary thromboembolism (decreased
cardiac output and patient bedridden)
Late complications of Myocardial Infarction
- Ventricular aneurysm resulting in heart failure,
mural thrombi and arrhythmias (remember scar
tissue stretches, cannot contract, and does not
rupture) - Chronic heart failure
- Dressler syndrome (possibly autoimmune-related)
and characterized by fever, pericarditis and
effusions
Complications of myocardial infarcts with the mechanism involved in each:
Sudden death = Ventricular fibrillation
Arrhythmias = Ventricular fibrillation
Persistent pain = Progressive myocardial necrosis
Angina = Ischaemia of non-infarcted
cardiac muscle
Cardiac failure =Ventricular dysfunction
following muscle necrosis / arrhythmias
Mitral incompetence =Papillary muscle dysfunction,
necrosis or rupture
Pericarditis = Transmural infarct with inflammation of pericardium
Cardiac rupture = Weakening of wall following muscle necrosis and acute inflammation
Mural thrombosis = Abnormal endotheleal surface
following infarction
Ventricular aneurysm = Stretching of newly formed
collagenous scar tissue
Dressler’s syndrome = Autoimmune
Pulmonary emboli = Deep venous thrombosis in lower
limbs
Prognosis of Myocardial Infarction
Mortality is approximately 20%
Prognosis depends on the following:
- Size of the infarct
- Position of the infarct (anterior most dangerous)
- Complications
- Availability of specialized medical assistance
Chronic Ischemic Heart Disease
This is characterized by chronic left ventricular failure
Causes are:
-Previous infarct(s) that impair the ability of the
heart to function adequately as a pump
-Progressive coronary atherosclerosis that results
in interstitial myocardial fibrosis (which also
impairs the heart function)
Sudden Cardiac Death
This is defined as the sudden unexpected
death of a previously healthy individual
Almost always the result of ventricular
fibrillation caused by the following:
-Coronary atherosclerosis with or without
thrombosis
Coronary vasospasm
- Aortic stenosis
- Cardiomyopathy or myocarditis
- Cocaine abuse
-SADS – Sudden Adult (arrhythmic) Death Syndrome:
biochemical abn in sodium or potassium channels –
channelopathies - heritable
