Seminar 2 - Heart Disease Flashcards
Describe a subendothelial infarct
Do not involve the full thickness of the myocardium
Regional – transient or partial occlusion of a coronary vessel
Seen in nSTEMIs
Can be circumferential if there is global hyperperfusion
What are the 3 types of ventricular free wall rupture
Type 1 – abrupt slit like tear that is full thickness and occurs in first 24hrs
Type 2 - erosion of myocardium at infarction site (occurs 1-3 days post-MI)
Type 3 – severely expanded rupture that occurs at border between infarct and normal (occurs late)
Describe the structure of the intima layer of blood vessels
It is the thinnest innermost layer
Consists of a single layer of endothelial cells attached to basement membrane
A thin layer of extracellular matrix
Describe the gross appearance of an aortic dissection
Entry ± exit tear creating true and false lumen (double-barrelled aorta).
True lumen lined by intima; false lined by/contained within media
How do you diagnose a ventricular free wall rupture
Echocardiography is gold standard
Should show a pericardial effusion with signs of an impending tamponade
What are the main inflammatory complications of MI
Pericarditis
Dressler’s syndrome
How can atherosclerosis lead to aortic aneurysm
It thickens the intima layer of aorta
This leads to ischaemia of inner media layer as further for O2 and nutrients to travel
This leads to loss of smooth muscle cells which weakens the vascular wall
What are the microscopic features of hypertensive heart disease
Myocyte transverse diameter increases
Interstitial fibrosis is present
What are the main ventricular arrhythmias that can be caused by an MI
Premature ventricular contractions - may be a warning of more serious one incoming Ventricular fibrillation - needs defib Accelerated idioventricular rhythm Nonsustained ventricular tachycardia Sustained ventricular tachycardia
Describe the aetiology of MI
Type 1 – An acute coronary artery event e.g. plaque rupture, dissection
Type 2 – Due to mismatch in the supply/demand for oxygen
Describe the epidemiology of heart failure
Estimated that as many as 920,000 people are living with heart failure in the UK
Aging population and people living longer with heart disease has caused increase in prevalence
Mortality is still high
How do you manage stable angina
Lifestyle modifications
Pharmacological – GTN, beta-blockers
CABG or PCI in patients with chronic, limiting systems
How can you manage hypertensive heart disease
Good BP control can decrease risk and cause regression
If it progresses to HF you manage as that
May require ICD or pacemaker in late stages of HF
What is vasculitis
Vessel wall inflammation with clinical manifestation from affected tissues
Usually also have signs of systemic inflammations such as fever, myalgia and malaise
What is the most serious complication of acute MI
Ventricular free wall rupture
Second most common cause of death - usually immediate
How can you treat an aortic aneurysm
EVAR or open repair
Better short-term survival from EVAR but the long-term rates of mortality are similar.
Higher rates of secondary intervention for EVAR.
Describe acute mitral regurgitation following MI
Mechanical complication occurring 7-10 days post MI
Caused by infero-posterior infarction causing rupture/necrosis of valve structures
Describe the structure of the media
Has smooth muscle cells and an external elastic membrane
Fenestrated lamellae of elastin and collagen interposed between SMCs
What are the non-modifiable risk factors for plaque formation
Genetic abnormalities,
Family history
Increasing age
Male gender (females fairly protected pre-menopause)
Describe the medium/muscular arteries
Have more SMCs and less elastin in media
Prominent internal and external elastic membrane
Includes the smaller branches of the aorta like the coronary arteries
Which drugs can lead to drug hypersensitivity vasculitis
Penicillin
Streptokinase
How do you manage hypertension
First line management is lifestyle changes
2nd line is to start stepwise drug management
What are the microscopic features of an MI
First 24hrs - Wavy fibres with loss of striations and nuclei
3-4 days - signs of inflammation such as neutrophils and exudate
7-10 - Presence of macrophages with areas of granulation tissue and hyperaemia
After 2 months you get fibrous scarring
Describe the pathogenesis of hypertensive heart disease
Hypertension is the main driving process
New sarcomeres are laid down which increases ventricular wall width
The O2 and nutrient supply of the heart increases due to hypertrophy but the capillaries don’t increase = ischemia
This leads to interstitial fibrosis which impedes diastole causing ischaemia and HF
What are the potential complications of cardiogenic shock
If not treated quickly, cardiogenic shock can lead to life-threatening organ failure or brain injury.
Describe the epidemiology of hypertension
More common in African American and afro Caribbean
Prevalence between men and women varies with age (younger men, older women)
More common in lower socioeconomic countries
26% of the worlds population has hypertension
When might an aortic dissection be painless
In those with neurologic complications from the dissection and in those with Marfan syndrome
How do blood vessels receive O2 and nutrients
Adequate diffusion of oxygen and nutrients from the lumen sustains thin-walled vessels and innermost smooth muscle cells
In larger and medium sized vessels the vasa vasorum pefrfuse the outer half to 2/3 of the media
Describe how PCI/ coronary angioplasty is carried out
A catheter is inserted into the femoral or radial artery and then passed up to the coronary arteries under x-ray guidance
A contrast dye (usually iodine based) is injected at the site to properly identify the blockage
To unblock the artery a balloon at the end of the catheter is inflated to widen it.
A small mesh stent can be deployed at this point to keep the artery open
What are the clinical features of heart failure
Shortnss of breath Orthopnoea Fatigue Reduced exercise tolerance Ankle/sacral oedema Elevated JVP Lung crackles Murmur
What are the 3 classic features of stable angina
Constricting/ crushing chest pain +/- radiation to L arm, jaw, neck Brought on by physical (or emotional) exertion
Resolved within minutes of rest or GTN
How does smoking increase your risk of atherosclerosis
Increases level of multiple inflammatory markers
Increases oxidative modification of LDL
How does ventricular free wall rupture cause death
Leads to cardiac tamponade
Death is usually sudden
How do you diagnose a ventricular septal rupture
Echocardiography with colour flow Doppler imaging + cardiac catheterisation
Very specific and sensitive
Describe the mechanisms of infection that can lead to infectious vasculitis
Direct invasion of infectious agents
Part of a localised infection, e.g. a bacterial pneumonia
Haematogenous spread of microorganisms during septicaemia or embolization from infective endocarditis
Describe the natural progression of an MI
Starts with ischaemia - thrombus blocks coronary artery
Within minutes you get hypoxic injury (reversible) due to loss of flow - leads to decrease systolic function
After around 20mins necrosis occurs - starts just below endocardium and extends superficially through the myocardium. Microvasculature is also damaged.
Without intervention infarction occurs (death of tissue) after 3-6 hours - can span the wall of the heart, leading to sustained dysfunction, scarring and cardiogenic shock, which can be fatal
What is cardiac output
Amount of blood pumped per ventricle per minute
Determined by SV x HR
How do you manage an aortic dissection
Surgical – area of aorta with intimal tear is resected and replaced with a Dacron graft
Used for type A dissections or complicated type B
Endovascular therapy is becoming the preferred treatment for descending aortic dissection
Medical management for descending aortic dissections - reduce BP and force of contraction using B-blockers
What are the functions of Anti-neutrophil cytoplasmic antibodies (ANCAs)
They can directly activate neutrophils
Stimulate the release of ROS and proteolytic enzymes
This causes destructive interactions between inflammatory cells and endothelial cells in the vessels
What are the complications of infectious vasculitis
Vascular infections weaken arterial walls
This can result in a mycotic aneurysm or induce thrombosis and subsequent infarction
What are the symptoms of cardiogenic shock
Hypotension HR slows Confusion Loss of consciousness Sweaty skin Rapid breathing
Describe the microscopic features of an aortic dissection
Cystic medial degeneration
Elastin fragmentation and areas without elastin that resemble cystic spaces (actually contain proteoglycans)
Characteristic absence of inflammation
List the main underlying mechanisms of non-infectious vasculitis
Immune complex deposition - seen in drug hypersensitivity vasculitis and vasculitis secondary to infection
Anti-neutrophil cytoplasmic antibodies (ANCAs) - PR3-ANCA and MPO-ANCA
Anti-endothelial cell antibodies - seen in Kawasaki disease
Which type of MI most commonly leads to accelerated junctional rhythms
Inferior MI
What are the clinical features of aortic dissection
Sudden onset severe chest pain (may get neck/jaw pain too)
Syncope & altered mental status
Hemianesthesia, hemiparesis or hemiplegia
Horner syndrome
SOB, haemoptysis & haemothorax - if pleural rupture or resp obstruction
Symptoms of CHF - SOB, orthopnoea, raised JVP etc.
Difference of BP >20mmHg between arms
Aortic regurgitation
How is valvuloplasty carried out
Replacement valve can be put in place via cardiac catherization and a balloon (e.g. TAVI) or is done as open surgery
Catheter based surgery is becoming increasingly popular, especially in
those considered too weak for open surgery
What is the internal elastic lamina
Boundary between intima and media
A lamella of fenestrated elastic material
What is a reperfusion injury
Occurs when blood supply is restored to ischaemic tissues
Can cause arrhythmia and local cell injury
Damage to microvasculature due to platelet activation
Release of toxic metabolites following periods of hypoxia can trigger apoptosis in nearby cells
Can lead to “stunned” myocardium – temporary loss of function following short-term ischaemia which resolves after several days
What are the macroscopic features of hypertensive heart disease
Grossly thickened left ventricle
In later stages it will dilate outwards
Describe the damage that essential hypertension can cause
Damages vessel walls leading to atheroma
Increases heart strain = LVH and heart failure
Causes arteriosclerosis and hyaline sclerosis of cerebral vessels which leads to clots, infarction and haemorrhage
Causes nephrosclerosis
Aortic dissection
What are the risk factors for acute mitral regurgitation following MI
Old age Female Large infarct Previous AMI Recurrent ischaemia CAD HF
List the main supraventricular tachyarrhythmias
Sinus Tachycardia - HR>100 with regular rhythm
Premature atrial contractions
Atrial flutter
Atrial fibrillation
Paroxysmal supraventricular tachycardia -intermittent episodes of abrupt onset and termination
What causes a sudden cardiac death
IHD is the leading cause
Congenital heart defects
Conduction defects
Hereditary conditions e.g. hypertrophic cardiomyopathy
Electrolyte disturbances e.g. hyperkalaemia
Recreational drug use
What are the complications of PCI
All of the general ones associated with catherisation
Can also lead to an MI or stroke (due to thrombus)
Kidney damage (via contrast reaction)
Stent thrombosis
Restenosis
What are the pathological features of eosinophilic granulomatous and polyangiitis (EGPA)
Associated with asthma and allergic rhinitis
Lung infiltrates
Peripheral eosinophilia
Extravascular necrotising granulomas
Eosinophilic infiltration of vessels and tissues.
Major one is that both granulomas and eosinophils present
What determines stroke volume
Na homeostasis and a and b adrenergic factors
What are the pathological features of polyarteritis nodosa
Segmental transmural necrotising inflammation
Aneurysms and/or thrombosis
Aneurysms can rupture or thrombose leading to ischaemia nd infarction
Presence of both early and late stage disease within the same or different vessels - suggests ongoing injury
Describe 2nd degree AV block
Intermittent blocks at the AV node
Characterised by narrow QRS
Two types:
1 = progressive lengthening of the PR until there is a dropped beat (more common)
=Associated with inferior infarction
2= some action potentials fail to get through the AV node
=associated with anterior infarction
What location is classically involved in Takayasu arteritis
The aortic arch
Affected in 50% of cases
How does AAA correspond to rupture risk
The larger the AAA the more likely it is to rupture
<4cm has no risk
Anything above this risk rises
What are the respiratory tract features of granulomatosis with polyangiitis (GPA)
Can get sinusitis with mucosal granulomas
Ulcerative lesions of the nose, palate, or pharynx
Accompanying vasculitis
Haemoptysis
Cavitating lesions on x-ray
Describe the aetiology of Kawasaki disease
A variety of infectious (mostly viral) agents trigger the disease in genetically susceptible individuals
It is a delayed type hypersensitivity response to vascular antigens
Cytokine production and polyclonal B-cell activation result in autoantibodies to ECs and SMCs that precipitate the vasculitis
What are the renal features of granulomatosis with polyangiitis (GPA)
Can have mild focal glomerular necrosis with isolated capillary thrombosis
Or can have more advanced lesions with diffuse necrosis and parietal cell proliferation resulting in crescent formation
What is cardiac catherterisation
Interventional procedure where a catheter is inserted into the coronary vessels via the femoral or radial artery.
Used for diagnostic tests or therapeutic procedures.
What is the most common site of aortic dissection
Within first few cm of ascending aorta
Which population is most affected by Kawasaki disease
Infants and young children
80% of patients <4years
What equation is used to calculate BP
BP = CO x TPR
Anything that effects either aspect of the equation will effect BP
What are the subtypes of thoracic aortic aneurysms
Ascending aorta aneurysms - between aortic annulus and brachiocephalic artery
Aortic arch aneurysms
Descending thoracic aorta aneurysms
- Originates beyond the left subclavian artery, may extend into abdomen
If it extends into abdo it is called a thoracoabdominal aortic aneurysm
What are the main complications of cardiac catherisation
Haemorrhage at insertion site Contrast reaction Arrhythmias Pericardial effusion or tamponade Can develop angina, arterial dissection or thrombosis
How do you manage an MI
PCI, fibrinolysis, nitrates, dual antiplatelet therapy
Goal is to reperfuse damaged tissues to save injured myocardium
List the DeBakey anatomic classification for aortic dissection
Type I – intimal tear in ascending aorta, descending aorta is also involved.
Type II – only ascending aorta is involved.
Type III – only descending aorta involved.
IIIA – originates distal to left subclavian artery, extending as far as diaphragm.
IIIB – involves descending aorta below the diaphragm.
What can cause heart failure
Coronary Heart Disease (CHD) Hypertension Cardiomyopathy Valve dysfunction Cardiac arrhythmias Pericardial disease Infection
Other minor causes: anaemia, alcoholism, overactive thyroid, pulmonary hypertension
What are the risk factors for a ventricular septal rupture
>65yrs Female Single vessel disease Extensive MI Poor septal collateral circulation
How does MI lead to sinus tachycardia
The heart needs to compensate for an acute decrease in stroke volume caused by MI so it beats faster
How do you treat Dressler’s syndrome
Observe the patient for any signs of cardiac tamponade (can occur due to inflammatory fluids)
Rest
NSAIDs/steroids
What are the macroscopic features of an MI
No gross findings until at least 24hrs
Infarcted area will have a yellow-tan center (necrosis) with a hyperaemic border (seen day 3-10)
Older MI will have collagenous white scarring (after 2 months)
Hard to accurately age as changes over wide period
Describe the pathological features of giant cell arteritis
Focal destruction and fragmentation of elastic lamina (black line on slide)
Thickening of the intima
Lumen occlusion
Giant cells may be seen on biopsy
How do you treat acute mitral regurgitation following MI
Vasodilator therapy
Surgery
Where do most aneurysms occur
Abdominal aorta - AAA
Can affect SMA, IMA or renal artery due to direct extension or by occluding vessel ostia
What causes granulomatosis with polyangiitis (GPA)
T cell-mediated hypersensitivity response to normal microorganisms/debris.
PR3-ANCAs present in 95% of cases
Describe a ventricular septal rupture
Tear in the ventricular septum
Mechanical complication of MI
Infrequent but life threatening
Occur most commonly in the first 24 hours and then 3-5 days after
Which vasculitis is PR3-ANCA associated with
Granulomatosis with polyangiitis (GPA).
Used to be called c-ANCA
Describe the pathogenesis of aortic dissection
Reduced elasticity & distention of aorta (common in elderly)
Wall tension increased - can be due to increased diameter in aneurysm or hypertension
As tension increases the aorta dilates further
In most cases, the final trigger for the intimal tear is unknown
An exit tear creates a true and a false lumen (double-barrelled aorta).
What are the 2 subtypes of large vessel vasculitis
Giant cell arteritis
Takayasu arteritis
