SALIENT
FEATURES
History
· Have you ever had any
pain or discomfort in the chest'?
· How would you describe
the chest discomfort (heavy, burning, tightness, stabbing, pressure)'?
· Do you get this on
walking at ordinary pace on the level or does it come on when you walk uphill
or
hurry'?
· When you get the
pain/discomfort, do you stop, slow down or continue at the same pace?
· Does the pain/discomfort
go away when you stand still'? (It is typically relieved by rest or
nitroglycerine
within 10 minutes.)
· Where do you get this
pain? (Angina is a visceral sensation and is poorly localized, therefore
patients
rarely point to the
location of their discomfort with one finger.)
· Does it radiate
elsewhere (e.g. arms, jaw, epigastrium)?
· Does food or cold
weather bring on the pain'?
· Ask about risk factors
such as smoking, diabetes, hypertension, family history of ischaemic heart
disease.
Examination
Typically no signs are
manifest, but patients should be examined for evidence of the following:
· Hypertension (see pp
27-30).
· Hyperlipidaemia (see pp
440-1).
· Diabetes (see pp
518-23).
· Left ventricular outflow
obstruction (aortic stenosis, hypertrophic
cardiomyopathy).
· Previous myocardial
infarction
DIAGNOSIS
This patient has angina
pectoris (lesion) which is due to atherosclerotic coronary artery disease
(aetiology). She is in
Canadian Cardiovascular Society functional class II (functional status).
QUESTIONS
How is
angina graded by the Canadian Cardiovascular Society?
There are four functional
classes:
· Class I: Angina
occurs only with strenuous or rapid or prolonged exertion.
· Class II: There
is slight limitation of ordinary activity (e.g. climbing more than one flight
of ordinary
stairs at a normal pace
and in normal conditions).
· Class III: There
is marked limitation of ordinary activity (e.g. climbing more than one flight
in normal
conditions).
· Class IV:
Inability to carry out any physical activity without discomfort - anginal
syndrome may be
present at rest.
What is the
mechanism of angina pectoris?
It commonly results from
increased myocardial oxygen demand triggered by physical activity, but it can
also be caused by
transient decreases in oxygen delivery due to coronary vasospasm. Unstable
angina is
caused by non-occlusive
intra-coronary thrombi.
How would
you investigate a patient with angina pectoris?
· Haemoglobin: anaemia
aggravates angina.
· Rest ECG: to detect left
ventricular hypertrophy, prior Q-wave MI or ST-T changes.
· Rest echocardiogram:
done only when there is clinical suspicion of aortic stenosis or hypertrophic
cardiomyopathy.
· Exercise ECG: to
precipitate symptoms, to document workload at onset and to record any
associated ECG abnormality
(?> I mm of horizontal or downsloping ST-segment depression or
elevation for ?> 60 to
80 ms after the end of the QRS complex) or arrhythmia.
· Exercise myocardial
perfusion imaging or exercise echocardiography in patients who have one of
the following baseline ECG
abnormalities: (a) LBBB, (b) more than 1 mm of rest ST depression, (c)
electronically paced
ventricular rhythm, and in patients with prior revascularization (PTCA or CABG)
or in whom consider-ations
of functional significance of lesions or myocardial viability are important.
· Coronary angiography:
provides detailed anatomical in/ormation about site and severity of luminal
narrowing due to coronary
atherosclerosis and less common non-atherosclerotic causes such as
coronary artery spasm,
coronary anomaly, primary coronary artery dissection and radiation-induced
coronary vasculopathy.
How would
you treat a patient with chronic stable angina pectoris?
Mnemonic ABCDE
(Circulation 1999; 99: 2829-48):
· Aspirin, Anti-anginal
therapy and ACE-inhibitor therapy. Aspirin has been shown to reduce the
incidence of non-fatal
myocardial infarction and the overall incidence of cardiac events, although
overall death rate and the
incidence of fatal myocardial infarction were similar to those obtained with
placebo in the Swedish
Angina Pectoris Aspirin Trial (SAPAT) study. Ramipril up to 10 mg once a day
should be offered to all
patients in view of the new HOPE trial.
· Beta-blocker and Blood
pressure.
· Cigarette smoking and
Cholesterol.
· Diet and Diabetes.
· Education and Exercise.
Percutaneous transluminal
coronary angioplasty (with or without coronary stent)
· Complementary to drug
treatment and surgery: no improvement in survival.
· Best results are
achieved in discrete single-vessel coronary artery disease.
· The restenosis rate is
-30% at 6 months; for balloon angioplasty with stenting. restenosis is lower, -20%.
· The ACME (Angioplasty
Compared to Medicine) study showed that PTCA can offer better symptomatic
relief than medical
therapy in patients with single-vessel coronary artery disease, but is a much
more
expensive procedure and is
associated with complications (including emergency and elective coronary
by-pass and second PTCA).
· The RITA (Randomized
Intervention Treatment of Angina) study compared PTCA with coronary artery
bypass graft (CABG) and
found that both procedures have similar prognostic implications with risk of
death or myocardial
infarction similar in the two groups, but more patients in the PTCA group
required a
second revascularization
procedure and more antianginal therapy.
Coronary artery bypass
grafting
· This has prognostic
value in patients with left main-stem coronary stenosis or three-vessel
coronary
artery disease and
impaired left ventricular function.
· The risk of surgery is
related to the degree of impairment of left ventricular function.
Neurostimulation
This is useful in refractory
cases and involves the use of percutaneous electric nerve stimulation (TENS)
or spinal cord stimulation
(SCS).
Transmyocardial
revascularization
A laser is used to drill
tiny holes into the heart, providing symptomatic relief h-om refractory angina,
but
does not improve
cardiovascular function or reduce adverse ischaemic events.
ADVANCED-LEVEL
QUESTIONS
What is the
prognosis of patients with angina?
· Fourteen per cent of
patients with newly diagnosed angina pectoris progress to unstable angina,
myocardial infarction, or
death within I year.
· Mortality at coronary
artery bypass grafting with normal ventricular function is 1 %.
What is the
significance and the mechanism of postprandial angina?
The presence of
postprandial angina indicates severe coronary artery disease; one mechanism is
'intramyocardial steal'
with blood being distributed from the stenotic territories to the normal
territories
(Circulation 1998; 97:
1144-9). It results from the carbohydrate content of the meal (Am J
Cardio/ 1997;
79: 1397-1400) and can be
ameliorated by prior treatment with octreotide (Circulation 1996; 94:
1-730),
which prevents
postprandial vasodilatation of the superior mesenteric artery.
How would
you follow a patient with stable angina in your clinic?
· Patients with
successfully treated chronic stable angina pectoris should have a follow-up
evaluation every
4-12 months. During the
first year of therapy evalu-ations every 4-6 months are recommended. After the
first year of therapy,
annual evaluations are recommended provided the patient is stable and reliable
enough to call or make an
appointment when anginal symptoms become worse or other symptoms occur.
Patients who are
co-managed by their general practitioner and cardiologist may alternate these
visits
(Circulation 1999; 99:
282948).
· The ACC/AHA 'five
questions' that must be answered regularly during the follow-up of the patient
who is receiving treatment
for chronic stable angina (Circulation 1999; 99: 282948):
1. Has the patient
decreased the level of physical activity since the last visit?
2. Have the patient's
anginal symptoms increased in frequency and become more severe since the last
visit'? If the symptoms
have worsened or the patient has decreased physical activity to avoid
precipitating angina, then
he or she should be evaluated and treated according to either the unstable
angina or chronic stable
angina guidelines, as appropriate.
3. How well is the patient
tolerating therapy'?
4. How successful has the
patient been in reducing modifiable risk factors and improving knowledge
about ischaemic heart
disease'?
5. Has the patient
developed any new comorbid illnesses or has the severity or treatment of known
comorbid illnesses
worsened the patient's angina'?
What do you
understand by the term unstable angina?
This includes patients
with more severe or frequent angina superimposed on chronic stable angina,
angina at rest or minimal
exertion, or angina of new onset (within I month) which is brought about by
minimal exertion.
It is a potentially
dangerous condition and patients should be admitted to a coronary care unit and
begun on antianginal
therapy including beta-blockers, aspirin and intravenous nitrates. Intravenous
heparin should be started
in patients with rest angina of 48 hours duration and in those with chest pain
and ischaemic ECG changes
on admission. Most patients stabilize with this treatment, although some
may require intra-aortic
balloon counterpulsation before cardiac catheterization. A monoclonal antibody
7E3 against platelet
glycoprotein llb/IIIa, which prevents platelet adhesion and degranulation, is
undergoing evaluation in
the treatment of unstable angina.
What is
Prinzmetal's angina?
It is angina occurring at
rest, unpredictably, and associated with transient ST seg-ment elevation on the
ECG. Coronary vasospasm is
the cause, often in the presence of atherosclerosis.
How is
exercise testing useful in determining the prognosis of chest pain ?
A study at Duke University
used exercise testing to determine high- and Iow-risk subsets in patients with
chest pain suggestive of
ischaemic heart disease:
· Low-risk subset:
subjects who could complete 9 minutes of exercise using the Bruce protocol
without
evidence of ischaemic ST
segment changes and achieve a maximal sinus heart rate in excess of 160
beats per minute. These
were found to have a l-year survival rate of 99% and a 4-year survival rate of
93%. This .means that
cardgac ,.:atheterixation and CABG ,:an be deferre,J.
· High-risk subset: those
who were forced to stop exercising in stages I or Il (under 6 minutes);
survival rate was 85% at I
year and 63% at 4 years.
What do you
understand by the term 'syndrome X'?
· Syndrome X, or
microvascular angina, is the presence of classic angina and ST depression on
exercise stress testing
and a normal coronary angiogram in the absence of any other demonstrable
cardiac abnormalities.
· Reaven's syndrome or
'endocrine' syndrome X is the association of insulin resistance, hypertension,
and increased very low
density lipoprotein (VLDL) and decreased high density lipoprotein (HDL)
cholesterol concentrations
in the plasma.
Coronary artery bypass
grafting wasintroduced by R.G. Favalaro in 1969 while he was at the Cleveland
Clinic, USA (J Thorac
Cardiovasc Surg 1969; 58: 178-85).
Balloon angioplasty was
introduced by Arthur Gruntzig, a Swiss cardiologist, in 1977 (Lancet 1978; i:
263).
