This patient is suspected to have angina pectoris. Would you like to ask her a few questions and perform

a relevant examination, to confirm these suspicions'?



· 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



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


· Previous myocardial infarction (see pp 45-52).


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).


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


· 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


· 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.


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.


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: