SIHD and angina : presentation and investigation Flashcards
Definition of angina?
“Angina”, more correctly (angina pectoris):
“ a discomfort in the chest and/or adjacent areas associated with myocardial ischaemia but without myocardial necrosis”
Pathophysiology of myocardial ischaemia and resultant anginal symptoms?
Mismatch between supply of O2 and metabolites to myocardium and the myocardial demand for them.
By far most commonly due to: a reduction in coronary artery blood flow to the myocardium, caused by:
Obstructive coronary atheroma (Very common)
Spasm of a portion of coronary artery (Uncommon)
Abnormal coronary flow (Uncommon).
What is supply demand mismatch due to?
by far most commonly due to reduction i n coronary artery blood flow to myocardium
uncommonly due to reduced oxygen transport
uncommonly due to pathologically increased myocardial oxygen demand
What is coronary atheroma? (most common cause)
When there is increased myocardial oxygen demand the increase of coronary blood flow is obstructed and this leads to myocardial ischaemia and then angina symptoms.
Myocardial oxygen demand increases in situations where HR and BP rise for example: exercise, anxiety/emotional stress and after a large meal.
How does stable angina present?
upper left side of chest
When do people experience symptoms?
blocking >70% lumen
How to diagnose stable angina?
Essential to establish the characteristics of patients pain to differentiate from other causes of chest pain:
Site of pain (watch for patient gestures): retrosternal
Character of pain: often tight band/pressure/heaviness.
Radiation sites: neck and/or into jaw, down arms.
Aggravating e.g. with exertion, emotional stress & relieving factors e.g. rapid improvement with GTN or physical rest.
What features make the diagnosis of angina less likely?
Sharp/‘stabbing’ pain; pleuritic or pericardial.
Associated with body movements or respiration.
Very localised; pinpoint site.
Superficial with/or without tenderness.
No pattern to pain, particularly if often occuring at rest.
Begins some time after exercise.
Lasting for hours.
What are the other diagnoses for chest pain?
Cardiovascular causes:
Aortic dissection (intra-scapular “tearing”), pericarditis.
Respiratory:
Pneumonia, pleurisy, peripheral pulmonary emboli (pleuritic)
Musculoskeletal:
Cervical disease, costochondritis, muscle spasm or strain
GI causes:
Gastro-oesphageal reflux, oesophageal spasm, peptic ulceration, biliary colic, cholecystitis, pancreatitis
What are the definitions of severity?
I Ordinary physical activity does not cause angina, symptoms only on significant exertion.
II Slight limitation of ordinary activity, symptoms on walking 2 blocks or > 1 flight of stairs.
III Marked limitation, symptoms on walking only 1-2 blocks or 1 flight of stairs.
IV Symptoms on any activity, getting washed/dressed causes symptoms.
Risk factors for coronary artery disease & ASCVD?
Non-modifiable
Age, gender, creed, family history & genetic factors.
Modifiable
Smoking
Lifestyle- exercise & diet
Diabetes mellitus (glycaemic control reduces CV risk)
Hypertension (BP control reduces CV risk)
Hyperlipidaemia (lowering reduces CV risk)
Examination of stable angina?
Tar stains on fingers.
Obesity (centripedal).
Xanthalasma and corneal arcus
(hypercholesterolaemia).- yellow deposits around eye
Hypertension.
Abdominal aortic aneurysm arterial bruits, absent or reduced peripheral pulses.
Diabetic retinopathy, hypertensive retinopathy on fundoscopy.
signs of exacerbating or associated conditions?
Pallor of anaemia
.
Tachycardia, tremor, hyper-reflexia of hyperthyroidism.
Ejection systolic murmur, plateau pulse of aortic stenosis
Pansystolic murmur of mitral regurgitation, and
Signs of heart failure such as basal crackles, elevated JVP, peripheral oedema.
Investigations for stable angina?
Electrocardiogram
normal in over 50% of cases.
may be evidence of prior myocardial infarction i.e. pathological Q-waves.
may be evidence of left ventricular hypertrophy i.e. high voltages, lateral ST-segment depression or “strain pattern”.
Bloods
Full blood count, lipid profile and fasting glucose; Electrolytes, liver & thyroid tests would be routine.
CXR
Often helps show other causes of chest pain and can help show pulmonary oedema.
Exercise tolerance test/ETT
Often can confirm diagnosis of angina.
Relies on ability to walk for long enough to produced sufficient CV stress.
Typical symptoms and ST-segment depression for positive test.
-ve ETT doesn’t exclude significant
coronary atheroma but if negative at high workload overall prognosis is good
Myocardial perfusion imaging
Superior to ETT in detection of CAD, localisation of ischaemia and assessing size of area affected.
Expensive, involves radioactivity; depending on availability used where ETT not possible/equivocal.
Either exercise or pharmacological stress: adenosine, dipyridamole or dobutamine
Computed tomography (CT) coronary angiography
When to refer people for invasive angiography?
Early or strongly positive ETT (suggests multi-vessel ds).
Angina refractory to medical therapy.
Diagnosis not clear after non-invasive tests.
Young cardiac patients due to work/life effects.
Occupation or lifestyle with risk e.g. drivers etc.
What is Cardiac catheterisation/coronary angiography?
Almost always done under local anaesthetic
Arterial cannula inserted into femoral or radial artery.
Coronary catheters passed to aortic root and introduced into the ostium of coronary arteries.
Radio-opaque contrast injected down coronary arteries and visualised on X-ray.
Treatment strategies of stable angina?
General measures.
Address ASCVD risk factors: BP, DM, Cholesterol, Lifestyle: physical activity & smoking.
Medical treatment.
Drugs to reduce disease progression & symptoms
Revascularisation (if symptoms not controlled).
Percutaneous coronary intervention (PCI) & coronary artery bypass grafting (CABG)
Medical treatment for influencing disease progression?
Statins: consider if total cholesterol >3.5 mmol/l.
Reduce LDL-cholesterol deposition in atheroma and also stabilise atheroma reducing plaque rupture and ACS.
ACE inhibitors: if increased CV risk and atheroma
Stabilise endothelium and also reduce plaque rupture.
Aspirin; 75mg or Clopidogrel if intolerant of aspirin.
May not directly affect plaque but does protect endothelium and reduces of platelet activation/aggregation.
Medical treatment for relief of symptoms?
ß-blockers; achieve resting hr <60 bpm.
Reduced myocardial work and have anti-arrhythmic effects
Ca2+ channel blockers; achieve resting hr <60 bpm.
Central acting eg diltiazem/verapamil if ß-blockers C-I.
Ik channel blockers; achieve resting hr <60 bpm.
Ivabridine is a newer medication which reduces sinus node rate
Medical treatment for relief of symptoms?
Ca2+ channel blockers; produce vasodilatation
Peripherally acting dihydropyridines e.g. amlodipine, felodipine.
Nitrates; produce vasodilatation
Used as short or prolonged acting tablets, patches or as rapidly acting sublingual GTN spray for immediate use.
K+ channel blockers; nicorandil
Nitrate molecule and K+ channel helpful in ‘pre-conditioning’.
Describe Percutaneous coronary intervention (PCI)
?
Percutaneous transluminal coronary angioplasty (PTCA) and stenting (now in ~95% procedures).
Similar beginnings to coronary angiography but cross stenotic lesion with guidewire and squash atheromatous plaque into the arterial walls with balloon and stent.
If stent used aspirin and clopidogrel taken together whilst endothelium covers the stent struts and it is no longer seen as a foreign body with associated risk of thrombosis
Is PCI effective?
PCI effective for symptoms, but
No evidence it improves prognosis in stable disease.
Small risk of procedural complication: death=0.1%, MI=0.2%, emergency CABG=0.05%
Risk of restenosis: varying from 10-15% with bare metal stents and <10% with drug eluting stents.
Also still need to continue disease modifying medication.
Describe CABG?
Coronary artery bypass surgery (CABG)
In diffuse multi-vessel CABG often best option for stable angina
‘Up front’ risks are significantly > PCI
death=1.3%, Q-wave MI=3.9%; these increase in presence of co-morbidity
But good lasting benefit- 80% symptom free 5 years later.
CABG may confer prognostic benefit in certain subgroups:
who derives prognostic benefit from CABG?
> 70% stenosis of left main stem artery
significant proximal three-vessel coronary artery disease
two vessel coronary artery disease that includes significant stenosis of proximal left anterior descending coronary artery and who have ejection fraction < 50%.
Patients must continue disease modifying medication and predictable deterioration in vein grafts after 10 years.
