Clinical & Pathological Aspects of Cardiovascular Disease

• What is hypertension?

  Persistently raised blood pressure >140/90 mm Hg

  
  

  90% of time: no cause is found- primary hypertension

  10% of time: cause found- secondary hypertension
• What could be possible causes of secondary hypertension?

  Renal disease

  Pregnancy

  Drugs e.g corticosteroids

  Endocrine disease

  Coarctation of aorta
• How do you diagnose hypertension?

  Measurements of BP on at least 3 occasions over 3 month period & patients often require a 24 hr monitor
• How do you treat primary & secondary hypertension?

  Secondary:

  Treat cause if possible

  
  

  Primary:

  General advice (weight loss, reduce alcohol, exercise more etc.)

  Medical treatment (ACE inhibitors, angiotensin II receptor blockers, beta blockers, Ca channel blockers, diuretics)
• What are potential complications of hypertension if left untreated?

  Heart failure

  Stroke- cerebrovascular accident (CVA)

  Coronary artery disease/MI

  Renal failure

  Peripheral vascular disease
• What is the dental relevance of hypertension?

  -Patient may be taking aspirin

  -post-operative bleeding is more likely

  -Minimise stress and pain to minimise further increase in BP which may lead to stroke or myocardial infarction

  
• What is the dental relevance of medications being taken for hypertension?

  ACE inhibitors:

  Loss of taste, angioedema (swelling of blood vessels), lichenoid reactions

  Beta blockers:

  Lichenoid reactions

  Ca channel blockers:

  Gingival overgrowth

  Diuretics:

  Xerostomia

  
• What is the 'good' and 'bad' cholesterol?

  Good: HDL (protective and stops oxidation of LDL)

  Bad: LDL (low in protein, high in fat)
• What is atherosclerosis and what happens?

  Widely prevalent disease affecting large elastic & muscular arteries

  
  

  Thickenings of the intima: composed of lipid derived from plasma and deposits of extra connective tissue

  
  

  May calcify over time

  
• Atherosclerosis

  condition in which fatty deposits called plaque build up on the inner walls of the arteries
• Where are the common sites for atheromas?

  Aorta

  Carotid

  Coronary arteries
• How does an atheroma form?

  1. LDL into intima layer

  2. Oxidised and sends chemotactic messages to monocytes

  3. Macrophages enter intima and ingest LDL By binding through scavenger receptors

  4.This signals the stimulation of smooth muscle cell migration and connective tissue synthesis

  5.Death of lipid containing macrophages which causes spillage of lipid and cholesterol into the plaque

  
• Describe the sequence in progression from atheroma to atherosclerosis.

  
• What is hyperlipidaemia?

  Too many lipids in the blood
• What is familial hypercholesterolaemia?

  Inherited disorder of high LDL that can't be removed from circulation because of a decreased level of receptors (cells which aid in elimination via liver) for LDL cholesterol

  
  

  Heterozygotes have 50% reduction in receptors: disease development in 40s

  Homozygotes: disease development in 20s
• What are some risk factors for atherosclerosis?

  Sex: primarily a disease of men and older women

  Cigarette smoking: endothelial cell damage

  Diabetes: increased incidence of hyperlipidaemia & microvascular damage
• What happens after you have a substantial atherosclerotic plaque?

  Could be regression: change in lifestyle, HDL increase, antioxidants

  
  

  If no regression then:

  Interference with blood flow to target organ (ischaemia/infarction)

  Thrombosis: could lead to total occlusion

  Embolisation
• What is ischaemia?

  Restriction in supply of blood to the tissues causing a shortage of oxygen & glucose necessary for cellular metabolism
• What is an infarction?

  Tissue death caused by a lack of oxygen due to obstruction in blood flow
• What are clinical symptoms of ischaemia & infarction?

  
• What are some factors that will affect the chances of you getting ischaemia or an infarction from a significant atherosclerotic plaque?

  Collateral blood supply to that organ

  Speed of arterial occlusion

  Metabolic needs of tissue

  Degree of arterial blocking
• What is ischaemic heart disease (IHD) & what is the aetiology?

  Inadequate oxygen supply to meet the demands of the heart

  
  

  Aetiology: atheromatous plaque within coronary arteries causing constriction to blood flow
• What are the modifiable & unmodifiable risk factors for IHD?

  Unmodifiable: age, male gender, family history

  
  

  Modifiable: hyperlipidaemia, smoking, hypertension, diabetes, obesity, lack of exercise, high alcohol intake, stress, OCP
• What is angina pectoris?

  Reduced oxygen perfusion of the cardiac muscle resulting in strangling feeling in the chest, breathlessness, pain radiating to the jaw & left arm

  
  

  Pain resolves in minutes following rest & GTN
• What is the dental relevance of angina?

  The medications for it:

  Aspirin- bleeding tendency

  Beta blockers/calcium channel blockers- mucosal disease

  Nicorandil- oral ulceration
• What are the symptoms & signs of a MI?

  Symptoms:

  Central strangling pain lasting longer than 15 minutes

  Pain radiates to the neck, jaw & left arm

  Nausea, vomiting

  
  

  Signs:

  Grey tinge

  Sweating

  Tachycardia (fast heart rate)

  
• How do you manage a MI?

  Sit patient up

  Calm & relaxed approach

  Dial for ambulance/crash team

  Administer oxygen & GTN (repeat every 10 mins)

  Aspirin 300mg PO crushed or chewed

  Entonox if available

  Monitor pulse & oxygen saturation
• What is the dental relevance of a MI?

  
• What is the difference between clotting & thrombosis?

  Clotting :-essential and beneficial activation of clotting cascade when there has been tissue injury-refers to activation of protein cascade leading to formation of fibrin

  Thrombosis:-Involves activation of both platelets and clotting cascade.-Haemostasis occurring at wrong place and time

  
• What is Virchow's triad?

  Factors that promote thrombosis

  
  

  1. Changes in the surface of the vessel

  2. Changes in the blood flow - stasis

  3. Changes in the constituents of the blood - hypercoagulation
• How can the vessel surface be changed and how does this promote thrombosis?

  -Splitting/fraying/ loss of surface endothelial cell layer

  
  

  -exposure of sub-endothelial tissues lead to platelet activation (promoting thrombosis)

  
  

  -Atheromatous plaque

  
  

  Surface can also be changed by burning/freezing: "frostbite" causes trauma to endothelium

  
  

  Chemical injury - injectable materials

  
  

  Inflammation (vasculitis)
• How could the blood flow change?

  DVT- deep vein thrombosis

  
  

  Patients with congestive cardiac failure (venous stagnation)

  
  

  Post myocardial infarction

  
  

  Atrial fibrillation

  
  

  Heart valve disease
• Where are arterial & venous thromboses more likely to occur?

  Arterial thrombosis in places where there's more turbulent flow

  
  

  Venous thrombosis in places where there's more sluggish/slow flow
• Why might the blood constituency change?

  Hypercoaguable state: haemostatic equilibrium is tilted in the favour of thrombosis

  
• What factors might result in increased plasma fibrinogen & factor VIIc concentrations?

  Increasing age

  Obesity

  Oral contraceptives

  Menopause

  Diabetes

  Smoking
• What 3 possible things could happen to a thrombus?

  Lysis

  Organisation/recanalisation

  Embolisation
• What is embolisation of a thrombus?

  Thrombi detach & travel at high speed through the circulation until a vessel is reached whose lumen is smaller than the size of the thrombus.

  
  

  This causes ischaemia or infarction at that site
• How does a pulmonary embolism occur?

  Venous thrombi will travel through vessels of increasing size through the right side of the heart and then sit in the lungs (in a pulmonary vessel)
• What are the types of emboli?

  Thrombus (99%)

  Infective (vegetations of infective endocarditis)

  Gaseous

  Fat

  Foreign material
• What is heart failure?

  The inability of the heart to pump sufficient blood to meet the needs of the tissues for oxygen and nutrients