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CARDIOVASCULAR PATHOLOGY 2 - Coggle Diagram
CARDIOVASCULAR PATHOLOGY 2
ISCHEMIC CARDIOPATHY
insufficient oxygenated blood supply with respect to the functional demand
supply may decrease because of atherosclerosis of coronary arteries
hypertension can lead to atherosclerosis and hypertrophy
demand may increase because of myocardial hypertrophy
risk factors
modifiable
hyperlipidemia
hypertension
smoke
diabetes mellitus
diet
poor exercise
oral contraceptives
non-modifiable
age
sex
familiarity
mainly related to
CAD
impairment of blood flow through the coronary arteries
anomalous origin of coronary artery:
normally, coronary arteries originate from the sinuses of the aorta
they may originat from a single sinus, thus reducing the normal blood flow
coronary emboli:
mural left heart thrombosis
defect of the endocardial epithelial cells, leading to a sticky endocardium on which clots are created
vegetations due to endocarditis
common on the mitral valve
heart tumor
myocardial myxoma
coronary dissection:
it starts with a subadventitial hematoma, which might break, causing dissection
associated with Marfan syndrome and pregnancy
in the case of the coronary arteries the dissection is located in the subadventitial area, while in aortic dissection the blood flows along the wall between the internal 2/3 and the external 1/3 of the tunica media of the aorta (intramural)
unexpected death
during pregnancy, it may be due to hormonal changes, hemodynamic stress, changes in the autoimmune status
eosinophils and basophils inflammation reactive to internal hematoma
in survivors, hematoma organizes and shrinks
coronary arteritis:
middle-size vasculitis
polyarteritis nodosa: rare in the heart, more common in skin and kidneys
Kawasaki disease: more frequent
heart congenital anomalies
coronary atherosclerosis:
the most frequent cause of angina, AMI, chronic ischemic heart disease and sudden cardiac death
transient vasospasm (Prinzmetal angina):
acute reduction in blood perfusion to the myocardium
triggered by increased sympathetic stimulation of the coronaries, which can be worsened by mental stress and intranasal cocaine usage
microvessel disease
clinical syndrome of angina in the absence of obstruction of the coronary artery
functional impairment of pressure and flow in the very small myocardial vessels
there is no communication between large coronary arteries in the normal heart, but there are many anastomoses of the very small vessels
collateral circulation that may delay the appearance of ischemic heart symptoms
sometimes also association with
structural myocardial changes, e.g. LV hypertrophy
transplanted heart (--> cardiac allograft vasculopathy)
F>M (in particular, in post-menopausal periods)
ISCHEMIC CARDIOMYOPATHY
anatomo-clinical syndrome characterized by an imbalance between oxygenated blood supply and the need for oxygenation, usually due to decreased blood flow
entities
ANGINA PECTORIS
a pain that appears when there is an imbalance between oxygenated blood supply and functional demand
types
stable angina
pain appears under physical exertion
caused by stable atherosclerotic plaques
these plaques are encapsulated with a fibrous cap
reduction from 70%-75% of the coronary lumen
simple with lipid core and fibrous cap; calcifications
site
usually in the first 3-4 cm from the origin of the coronary
widespread in diabetic patients
unstable angina
momentary episodes of myocardial ischemia at rest
pain and ECG changes (ST depression)
possible elevation of serum troponin levels
rupture of the fibrous cap
lesion made of platelets and formation of mural thrombus, emboli or complete occlusion
necrotic microfoci
ACUTE MYOCARDIAL INFARCTION
death of myocardial tissue due to anatomical or functional occlusion of the lumen
classification
type I (spontaneous)
90%
acute coronary artery athero-thrombosis caused by atherosclerosis of the artery with a deposit of thrombus on it, occluding the lumen
type II
(secondary to ischemic imbalance)
imbalance between myocardial oxygen supply and/or demand
there may also be atherosclerosis, but with incomplete obstruction of the lumen
possible etiology
vasospasm
hypertrophy
(increased O2 demand)
type III
MI resulting in death when biomarker values are unavailable
type IVa
MI related to PCI
type IVb
MI related to stent thrombosis
type V
MI related to CABg
types
transmural AMI
the most frequent type
damage starts from endocardium to the epicardium, resulting in the entire wall thickness
subendocardial circumferential
damage located at the ventricles' lumen,
affecting endothelium and adjacent muscle tissue
complication: thrombus formation on the lumen, eventually resulting in emboli
causes
generalized hypoperfusion: it happens in conditions like hemodynamic shock and increase in metabolic demand
early reperfusion: can limit transmural infarction and cause subendocardial infarction
subpericardial MI
rare
seen in patients who died after resuscitation or in patients with septic shock ischemia
occlusion of smaller vessels by thromboembolism originating from coronary thrombi
atrial infarction
rare
combined with ventricular infarction
more common in the right atrium
complications: mural thrombosis and atrial rupture due to thin wall thickness, eventually resulting in cardiac tamponade
focal ischemic necrosis
generally due to increased catecholamine tone (due to pheochromocytoma or cocaine effect)
phases
metabolic phase: no alterations are seen, the tissue is metabolic --> high tissue lactate concentration can slow the rate of glycolysis and anaerobic ATP production, decrease IC pH and Ca2+ overload
functional phase: transient increase in IC Ca2+, leading to morphological alterations of myocytes --> myocytes hypertrophy, increase in contractile mass
reversible morphology: alterations are visible -->
swollen mitochondria: Ca2+ handling between sarcoplasmic reticulum and myofilament is distupted and Ca2+ is diverted to the mitochondria, causing swelling
necrosis: morphological alterations are no longer reversible vecause of necrosis
autopsy results
in the first 2 hours: no evidence unless evaluation is performed with electron microscopy (swelling of the sarcoplasm)
between 2 and 4 hours: signs can be recognized by using nitro blue tetrazolium chloride (it changes the colour of the healthy myocardium by redox reaction to blue; the affected area remains pale)
from the 4th hour: alterations in myocardial fibers in the form of "microfiber waviness"; loss of cross striations; C4D and C9 antibodies immunostaining acquires a brown colour
between 4 and 12 hours: macroscopic change in myocardial colour, areas of hemorrhage and of paleness; microscopic coagulative necrosis, eosinophilia, neutrophilic infiltrate
beween 12 and 24 hours: neutrophilic infiltrate, enzymes release, purulent necrosis development; later, macrophages arrive to clean the debris
after 20 days: scar tissue (connective dense scarring after >40 days)
reperfusion
spontaneous or induced
in the window of reversible damage (minutes) a recovery can be achieved, with stunned fibers still present
after 20 minutes: inneversible necrosis, but the damage can be stopped when there is only subenfdocardial damage, not transmural
complications
in the first hours (<2h)
arrhythmia, supraventricular tachycardia, ventricular fibrillation
not correlated with infarction extension
pump failure, cardiogenic shock, pulmonary edema, extended MI, death
correlated with infarction extension
1 week
wall break following colliquative necrosis
external: blood leaks in the pericardium, leading to cardiac tamponade
internal: breakage of the interventricular septum
incomplete: hematoma in the wall
papillary muscles involvement, leading to valvular insufficiency
wall aneurysm
when a large non-elastic scar is formed, tending to dilate over time due to the pressure
pericarditis
early
(first 4 days)
fibrinous pericarditis limited to the pericardium of the ischemic area
late
(Dressler type)
autoimmune pericarditis, with autoAbs reactive to necrosis
papillary muscle dysfunction
diffuse myocardial sclerosis
multiple small scars caused by a diffuse multifocal infarction
CHRONIC ISCHEMIC HEART DISEASE
causes
same as acute MI
pathogenesis
stable plaque, which reduces the coronary lumen and leads to focal necrosis
because of the presence of sclerosis, this area of the heart is tough
SUDDEN CARDIAC DEATH
natural, unexpected, fatal event occurring within one hour from symptoms onset in a healthy subject or in a subject with a mild disease
complication of IHD or a consequence of undiagnosed diseases
specific guidelines must be used to define the cause of the sudden death
Association for European CV Pathology