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
What pathological features may be seen with hypertension
Hyaline arteriosclerosis - Homogenous pink hyaline thickening of vessels
Narrowing of lumen
Hyperplasic arteriosclerosis - laminated thickening of the walls (looks like onion skin)
Necrotising arteriolitis - seen in malignant hypertension
Nephrosclerosis
List the main diagnostic cardiovascular interventions
Angiography
Electrophysiology studies
Measuring intravascular pressure and O2 saturations
Intravascular ultrasound or echocardiography
Cardiac biopsy
What are the common causes of cardiogenic shock
MI is most common
Heart failure
Medication side effect
Anything that prevents good blood flow - PE etc.
What is Dressler’s syndrome
A type of pericarditis caused by the body’s immune response to damage to the heart or pericardium
Occurs after an MI,
Describe 1st degree AV block
PR interval of longer than 0.2 seconds
Most commonly due to inferior infarction
It isn’t usually serious and the progression to full heart block or ventricular asystole is very rare
What are the complications of valve replacement
All those associated with catherisation or open surgery
Also infective endocarditis, systemic emboli and valve failure
How does hypertension kill
Via heart failure
MI - causes plaque rupture and clots vessel
Causes stroke due to atherosclerosis
Necrotic damage to vessels lead to clots/infarcts
Causes aortic dissection
What is an aneurysm
A localised or diffuse dilation of an artery with a diameter at least 50% greater than its normal size
All layers of vessel affected but develop after issues in the media
What are the clinical features of acute mitral regurgitation following MI
Pansystolic murmur
Evidence on echo
Describe the structure of the adventitia
Consists of loose connective tissue, collagenous and elastic fibres
Can contain nerve fibers (nervi nervorum)
What is valvuloplasty/ valve replacement/repair used for
Used in the treatment of almost all valve diseases
e.g. aortic and mitral regurgitation and stenosis
In hypertensive heart disease, as the heart cells hypertrophy you also get additional capillaries to supply them – true or false ?
False
The lack of new capillaries causes the additional ischemia
What are the risk factors for primary hypertension
Obesity Lack of physical activity Older age Stress and anxiety High salt diet Alcohol Smoking
What are the risk factors for AAA
Male sex
Smokers
Rarely occur in the under 50s
Atherosclerosis
Describe the structure of fatty streaks in vessels
Are mainly composed of lipid-filled foamy macrophages
There is a subendothelial accumulation of these foam cells in intima without necrotic core or fibrous cap
They begin as small flat yellow macules and then coalesce into elongated streaks
What are the risk factors for ventricular free wall rupture
> 70yrs
Female
No previous acute MI (no preconditioning)
Q waves
Hypertension during STEMI
Corticosteroid/NSAID use
Fibrinolytic therapy >14 hrs after STEMI onset
How can pain type/location indicate location of aortic dissection
Anterior chest pain – anterior arch or aortic root
Neck or jaw pain indicates that the aortic arch and great vessels are involved
Tearing”/”ripping” pain in intrascapular area – descending aorta
What are accelerated junctional rhythms
Arrhythmia where there is increased automaticity of the junctional tissue that leads to an increased heart rate of 70-130bpm
What are supraventricular tachyarrhythmias
Tachyarrhythmias that originate above the ventricles in the atria or AV node
Broad term
What are the clinical features of hypertension
Hypertension itself is a clinically silent disease
Only sign will be your raised BP when measured
Will eventually cause symptomatic disease like HF or MI
What are the clinical features of a ventricular septal rupture
Chest pain SOB Hypotension Biventricular failure - oedema Shock holosystolic murmur
How does polyarteritis nodosa present
Rapidly accelerating hypertension due to renal artery involvement
Abdo pain & bloody stools due to GI lesions
Peripheral neuritis
Diffuse myalgias.
“punched out” ulceration if cutaneous involvement
Which patients are most vulnerable to infectious vasculitis
Immunocompromised patients
How may an ascending aortic aneurysm affect surrounding structures
May compress/erode into sternum & ribs causing pain + fistula
Can compress SVC or airway
Rupture into pericardium causing tamponade
Dissect into aortic valve (aortic insufficiency)
Dissect into coronaries - MI
Describe the epidemiology of MI
Over 9 million deaths worldwide attributed to IHD
Prevalence declining in high-income countries, but increasing in low- and middle-income countries
Define atherogenesis
The process of forming plaques in the intima layer of arteries
Define arteriosclerosis
A generic term used for hardening of arteries and arterioles
What increases your risk of complications from PCI
Older age
CKD
Having heart failure at the time of procedure
Extensive heart disease and/or multiple blocked arteries
Describe the epidemiology of aortic dissection
Approx. 4,000 people/year affected in UK
More common in black ethnic groups vs. white; lowest incidence in Asian population.
More common in M vs. F
Peak age range is 50-65 (unless Marfan’s as thats 30-40)
What causes eosinophilic granulomatous and polyangiitis (EGPA)
Likely a consequence of overreaction to normal allergic stimuli
MPO-ANCAs present in few cases
Describe microinfarcts
Multiple small areas of necrosis within the myocardium
Caused by occlusion of intramural vasculature sparing the major coronary arteries e.g. vasospasm, vasculitis, cocaine
What are the modifiable risk factors for plaque formation
Hyperlipidemia (hypercholesterolemia) Hypertension Smoking Diabetes Inflammation
What causes hypertensive heart disease
Hypertension
Develop left ventricular hypertrophy as a result of increased pressure load
How may an aortic arch aneurysm affect surrounding structures
May compress brachiocephalic vein or airway
May stretch left recurrent laryngeal causing hoarseness
Risk of cerebral ischaemia
What are the most common causes of left sided heart failure
IHD
Hypertension
Aortic and mitral valvular diseases
Primary myocardial diseases
Do fatty streaks impact blood flow
No
The lesions are not raised so don’t impact flow
What is cardiogenic shock
When your heart cannot pump enough blood and oxygen to the vital organs
Medical emergency
What are the histological features of atheromatous plaques
Fibrous cap
Beneath and to the side of fibrous cap is a more cellular area containing macrophages, T lymphocytes and SMCs
Central necrotic core containing abundant lipids, debris from dead cells, foam cells, fibrin, thrombus, other plasma proteins
On the periphery you will have neovascularization
What are the risk factors for MI
Modifiable: HTN, hypercholesterolemia, obesity, smoking, diabetes
Non-modifiable: Age, FHx, PMHx of IHD, male sex (at younger ages)
IHD is the leading cause of mortality and morbidity worldwide - true or false
True
How can an MI cause pericarditis
The pericardial tissue above the infarcted myocardium becomes inflamed
Occurs 24-96 hours post MI
What are the main subtypes of small vessel vasculitis
ANCA associated - GPA, EGPA, MPA
Immune complex mediated - SLE vasculitis, IgA mediated (e.g. HSP), cryoglobulin vasculitis, Goodpasture’s disease
List the main complications of an ICD or pacemaker
Venous thrombosis Malignant arrhythmia Skin infection Pericarditis Pneumothorax
What is the Crawford classification
Way of classifying descending thoracic (thoracoabdominal) aneurysms
Type I – from left subclavian artery to abdominal aorta (above renal arteries)
Type II – from left subclavian artery to aortic bifurcation
Type III – from mid-distal descending thoracic aorta to the aortic bifurcation
Type IV – upper abdominal aorta and all or none of the infrarenal.
What are the 4 main outcomes of hypertensive heart disease
Die of something unrelated
Die IHD – i.e. MI
Die from renal damage or stroke
Progress to cardiac failure
What is the mortality rate of AAA
> 50% don’t survive a rupture
Very quickly fatal if they rupture
Describe how congenital heart defects can be repaired
In general all require surgical intervention to either reroute blood flow or close pathways that should not be there.
This surgery can sometimes be performed via catheter (ASD and VSD) whilst others are more complex procedures that require open surgery
What are the clinical features of hypertensive heart disease
Mainly asymptomatic when compensated
Symptoms occur when progresses to heart failure
May have AF if atria dilated
What are some of the complication of surgical aortic dissection repair
Deep hypothermic arrest usually required for repair - risk of CNS complications if prolonged MI Respiratory and renal failure Stroke Paraplegia.
What are the 2 main bradyarrhythmia’s caused by MI
Sinus bradycardia - seen after inferior/posterior MI
Junctional bradycardia
Describe the structure of capillaries
Have an endothelial lining but no media
Variable numbers of pericytes (cells that resemble SMCs) lie deep to the endothelium
They have thin walls and slow flow (good for gas exchange)
What is the natural history of hypertension
Most will be asymptomatic for a large period of time
Progresses to cause IHD, PVD, cardiac failure etc
If untreated it can be fatal via MI, stroke etc
Describe coronary thrombectomy
A catheter-based operation where blood clots are removed from the coronary arteries
It is often performed before further procedures such as PCI/angioplasty to reduce risk of the clot being dislodged and blocking another area
What are the symptoms of Takayasu arteritis
Characteristically ocular disturbance and weakening of pulses in upper extremities.
Other symptoms reflect the location of narrowed vessels (e.g. renal arteries with systemic hypertension)
How does a ruptured AAA present
Abdominal or back pain with pulsatile abdominal mass
Transient hypotension - can lead to shock and loss of consciousness
What are the main subtypes of aneurysm
True aneurysm – all 3 layers of vessel intact and blood flow contained
False (pseudoaneurysm) – breach in vessel wall but surrounding structures / layers of wall keep it contained
Saccular – small sac forms off aortic wall, uncommon but high rupture risk
List the main therapeutic cardiovascular interventions
Radiofrequency ablation PCI/coronary angioplasty Valvuloplasty/valve replacement/repair Coronary thrombectomy Congenital heart defect repair
How does hypertension increase your risk of atherosclerosis
Increase arterial wall tension leads to a disturbed repair processes
What are the symptoms of MI
Ischaemic chest pain Dyspnoea Nausea Sweating Pallor light-headedness
Women more likely to present ‘silently’ with atypical symptoms
List the main physiological compensatory mechanisms of the heart in response to heart failure
Frank Starling mechanism - increased filling volume dilates the heart which enhances contractility and stroke volume.
Activation of neurohumoral systems - norepinephrine released which increases HR, strength of contractions and vascular resistance
- RAAS activated which promotes fluid retention, increasing circulatory volume and vascular tone
- ANP released to counteract RAAS
Myocardial adaptations - ventricular remodelling in response to the increased mechanical load
How does unstable angina present
sudden onset or deterioration of angina-like symptoms
Describe the structure of veins
When compared to arteries at the same branching level they have larger diameters, larger lumens and thinner and less well-organized walls
Reverse flow is prevented in the extremities by venous valves
What conditions come under ischaemic heart disease
Stable angina Unstable angina MI - STEMI and NSTEMI Chronic IHD - congestive heart disease Sudden cardiac death
What can cause an aortic dissection
Congenital problems - Marfan’s, Ehler’s Danlos, PCKD etc.
Can occur with increasing age - loss of elasticity
Hypertension, CAS or hypercholesterolemia
Pregnancy is a risk factor
Cocaine use
Deceleration injury - trauma
Syphilis
Iatrogenic - post cardiac surgery and fluoroquinolone antibiotics
What are the acute coronary syndromes
Unstable angina
MI - STEMI and NSTEMI
What are the ENT features of granulomatosis with polyangiitis (GPA)
Nose bleeds Deafness Recurrent sinusitis Nasal crusting Collapse of nose due to ischaemia called “saddle nose”
How do you treat a ventricular free wall rupture
Emergency surgical repair when haemodynamically stable
Pericardiocentesis for tamponade
What causes microscopic polyangiitis (MPA)
Associated with MPO-
ANCA
There is recruitment and activation of neutrophils within affected vascular beds which leads to vasculitis
Which vessles are typically affected in polyarteritis nodosa
Typically renal, cutaneous and visceral vessels but spares the pulmonary circulation.
Lesions occur at vessel bifurcations
Which arteries are most affected by giant cell arteritis
Arteries in the head - temporal, ophthalmic and vertebral
Aorta can also be affected
Temporal is easiest to biopsy
Describe the natural history of aortic dissection
Rupture of dissection
Then it bleeds into pericardial, pleural, or peritoneal cavities
If not treated it will cause death
List the Stanford classification for aortic dissection
Type A – ascending aorta involved.
(DeBakey I and II)
- usually need surgical management
Type B – descending aorta involved.
(DeBakey III)
-managed medically in most circumstances
What are the 2 main pathological mechanisms of vasculitis
Immune mediated
Infection-induced inflammation
Important to determine type so that it is treated correctly
How common are arrhythmias after MI
Almost all will get some type arrhythmias - usually in 1st 24hrs
Risk of serious one is greatest in first hour
Most others are benign
What are the major symptoms of eosinophilic granulomatous and polyangiitis (EGPA)
Associated with asthma and allergic rhinitis
Palpable purpura
GI bleeding
Renal disease (focal segmental glomerulosclerosis).
Cardiomyopathy - major cause of morbidity and death
Describe the small arteries and arterioles
Small arteries have 3-8 layers of smooth muscle cells
Arterioles have only 1 or 2 layer
Found within tissues or organs
How do you treat cardiogenic shock
Treatment aims to restore blood flow and protect organs from damage
What causes primary hypertension
Most cases are essential (no exact known cause)
Probably linked to genetic factors and environmental factors
Describe the aetiology of polyarteritis nodosa (PAN)
It is immune complex mediated
1/3rd of patients have chronic hepatitis B – HBsAg-HbsAb complexes in organs
Describe the large/elastic arteries
They are conducting arteries
Layers of elastin fibers and smooth muscle cells allow them to expand during systole & recoil during diastole
Includes the aorta and it’s major branches and the pulmonary arteries
Which vasculitis is MPO-ANCA associated with
Microscopic polyangiitis (MPA) and eosinophilic granulomatosis with polyangiitis (EGPA)
Used to be called p-anca
Describe the pathogenesis of the formation of atheromatous plaques
Endothelial injury/dysfunction causes increased permeability, leukocyte adhesion and thrombosis
Get accumulation of lipoproteins (mainly LDL) in vessel wall
Monocytes adhere to the endothelium and then migrate to intima and become macrophages and foam cells
Platelets adhere
Factor release from activated platelets, macrophages and vascular wall cells leads to SMC recruitment
SMC proliferate and covert fatty streak to plaque
Recruitment of T cells
Lipid accumulation both extracellularly and within cells
Calcification of the ECM and necrotic debris
Describe a transmural infarct
Infarct spans the full width of the myocardium
Occurs due to permanent/ sustained occlusion of major coronary vessel(s)
Commonly LAD, RCA or LCA
Seen in STEMIs
How do mechanical complications of MI arise
They develop due to a complete lack of perfusion leading to necrosis, wall thinning, increased wall stress and ventricular dilatation, and finally wall disruption and rupture.
Low incidence but often fatal
How does Dressler’s syndrome present
Usually 2-3 weeks post MI
Fever
Chest pain
Other pericarditis symptoms
What is a intraventricular block
Also called bundle branch blocks
Conduction from the bundle of His is blocked
Can occur in L or R bundle
Describe the mortality rates of thoracic aortic aneurysms
Ascending – lowest rate after repair.
Descending – medium risk after repair.
Arch – highest risk (25%) and complicated to operate on
What are the triad of features of granulomatosis with polyangiitis (GPA)
Acute necrotising granulomas of the URT, the LRT or both;
Necrotising granulomatous vasculitis, most prominent in the lungs and upper airways;
Focal necrotising, often crescentic, glomerulonephritis
How does Kawasaki disease present
Conjunctival & oral erythema Blistering oedema of the hands and feet Desquamative rash Cervical lymphadenopathy May have an MI if coronary arteritis causes aneurysms that rupture or thrombose
Give 2 examples of medium vessel vasculitis
Polyarteritis nodosa (PAN) Kawasaki disease
What is malignant hypertension
Systolic >200, Diastolic > 120
Causes death in 1-2 years
Can arise from essential hypertension
Define atherosclerosis
A disease of arteries which leads to the formation of lipid-laden lesions called atherosclerotic or atheromatous plaques in the vessel wall
How can aortic dissection cause death
Hypotension, shock, eventual death from exsanguination.
Hemi pericardium & tamponade
Occlusion of coronary ostia leads to MI
Or severe aortic insufficiency - disrupts the valve
Involvement of spinal arteries causes transverse myelitis
How do you treat a ventricular septal rupture
Get the patient haemodynamically stable - vasodilator, diuretics etc
Then surgical repair
What are the 3 main layers found in arteries and veins
Intima
Media
Adventitia
More distinct in the arteries
What are the clinical features of a ventricular free wall rupture
Acute: severe chest pain, haemodynamic collapse,
Subacute: syncope, hypotension, shock, arrhythmia, chest pain
Define sudden cardiac death
Unexpected death from cardiac causes without prior symptoms or within an hour of symptoms presenting
What is the aim of PCI/coronary angioplasty
Aims to increase blood flow to the heart itself by opening the coronary vessels
What are the histological features of Takayasu arteritis
Histologically indistinguishable from GCA
Get intimal thickening and lumen narrowing
As disease progresses, collagenous scarring plus chronic inflammatory infiltrates occur in all 3 layers of vessel wall.
What are the main complications of hypertension treatment
Only really due to drug reactions
Diuretics = hypokaleamia and arrhythmia
Ace inhibitor = angioneurotic oedema
ARB = renal dysfunction
List the main diagnostic cardiovascular tests
ECG - assesses electrical signals
Echo - US scan of heart
Chest X-ray - Little detail but shows gross features
CT - more detail on structure and function
CT angiography - contrast-enhanced imaging of the coronary arteries
MRI
What is total peripheral resistance
Resistance of all the vasculature in the systemic circulation
Controlled mainly by neuronal and hormonal control of arterioles (vasoconstriction vs dilation)
What are the most common causes of right sided heart failure
Left sided heart failure
Lung disorders resulting in pulmonary hypertension
What are the complications of congenital heart defect repair surgery
Can lead to arrhythmia as cardiac surgery can cause scarring in or around the heart
These areas of fibrosis prevent the electrical signals from passing through the myocytes properly
What causes an AV block
Occur when the electrical conduction is delayed at the AV node or doesn’t pass through the AV node at all
Can occur post-MI
How can hypertension lead to aortic aneurysm
significantly narrows arterioles of the vasa vasorum which causes ischaemia of the media
This leads to loss of smooth muscle cells which weakens the vascular wall
What causes angina pectoris
90% of cases due to atherosclerosis
Other causes include vasospasm, spontaneous thrombosis/ embolism, coronary artery dissection, microvascular dysfunction
How may an aortic arch aneurysm affect surrounding structures
Trachea, bronchus, oesophagus, vertebral body, spinal column can be compressed/eroded into
How does hypertensive heart disease cause death
Mainly through cardiac failure and sudden cardiac death
Becomes ischemic due to tissue hypertrophy
Can’t dilate as well due to fibrosis so can’t fill properly = more ischaemia and SV/CO
How do you treat AV blocks
1st degree - no treatment unless associated with sinus bradycardia and hypotension. In this case atropine can be given.
2nd degree type 1 - atropine if poor perfusion
2nd degree type 2 -Requires immediate treatment with atropine or a pacemaker
What is cardiac angiography
Injection of radiopaque dye into the arteries to assess the blood flow and structure of the heart
Used in diagnosis of coronary artery disease (if patient has symptoms or is high risk)
What are the major complications of microscopic polyangiitis (MPA)
Necrotising glomerulonephritis
Peripheral neuropathy (e.g. mononeuritis multiplex)
Pulmonary capillaritis.
What are the features of microscopic polyangiitis (MPA)
Segmental necrosis of the small vessel media
Spares medium and large vessels
No granulomatous inflammation.
All lesions tend to be of the same age in any given patient, suggesting a single episode of antibody or immune complex deposition
Similar features to GPA minus the granulomas
How does hyperlipidemia increase your risk of atherosclerosis
Modified LDL causes injury to endothelium and underlining smooth muscle
Oxidized LDL induces the expression of adhesion molecules and pro-inflammatory cytokines
How do you treat heart failure
Lifestyle changes - healthy diet, exercise, stop smoking Medication - wide range Pacemaker Surgery - bypass Treatment is required for life
What is PCI/coronary angioplasty used for
To treat symptoms of coronary heart disease or reduce tissue damage during or after a MI
Treatment of choice for a STEMI if it can be provided quickly (within 12 hours of symptoms or if it can be given within 120 mins of fibrinolysis)
How does an AAA present
Usually asymptomatic until they expand/rupture
Back, flank, abdominal or groin pain.
Local compression symptoms can be early satiety, nausea, vomiting, urinary symptoms, or venous thrombosis from venous compression
Embolic phenomena affecting the toes - blue toes
What causes an aneurysm
Defects in the synthesis & breakdown of connective tissues within a vessel wall
Insufficient connective tissue in vascular wall - Ehlers Danlos
Abnormal signaling of transforming growth factor-b - Marfan’s, Loeys-Dietz syndrome
Proteolytic degradation of aortic wall connective tissue - can be due to macrophages and cytokines
Loss of smooth muscle cells and increase in ECM (non-elastic) weakens vessel wall – atherosclerosis, hypertension, tertiary syphilis
Describe 3rd degree AV block
AKA complete heart block
No action potentials from the SA node get through the AV node
Can occur due to anterior or inferior infarctions
Define ischaemic heart disease
The term covers conditions caused by insufficient perfusion of
the myocardium, most commonly due to narrowing or occlusion
of the coronary arteries
Describe the macroscopic appearance of atheromatous plaques
Yellow-tan plaques
They are raised above the surrounding vessel wall - lumen is moderately compromised
Vary in size but can coalesce to form larger masses
How can you diagnose giant cell arteritis
MR angiography - thickened vessel walls and stenosis
PE CT - increased metabolic activity in large vessels
Temporal artery biopsy - may see giant cells
Claudicant symptoms in upper and lower limbs
How do you diagnose heart failure
Echo - most effective
Physicals exam - leg swelling, irregular heart, raised JVP etc.
Define heart failure
The condition in which the heart can no longer pump blood to adequately meet the metabolic needs of the peripheral tissues
Which other conditions can be caused by essential hypertension
IHD MI PVD Heart Failure Multi infarct dementia Renal disease - parenchymal ischemia and renal failure Aortic dissection
Describe the aetiology of giant cell arteritis
T-cell mediated response to an unidentified vessel wall antigen
Dendritic cells in the vessel wall activate CD4+ T cells
These recruit macrophages to the vessel wall
Proinflammatory cytokines (esp. TNF) and anti-EC antibodies are also released and contribute to thickening of intima and vessel lumen occlusion
This leads to granulomatous inflammation
What is the definition of hypertension
Blood pressure greater than 140/90 mm/Hg
