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Unstable angina pectoris

Definition

Angina pectoris is a term that refers to myocardial ischemia (lack of oxygenated blood to heart muscle) that results in a classic picture with central chest tightness or heaviness brought on by exertion and relieved by rest.

Unstable angina refers to any of the following:

1. Angina of recent onset
2. Angina increasing in severity or frequency or duration.
3. Angina at rest or minimal exertion.

Other types of angina:

• Stable angina
• Prinzmetal's angina (rare)
• Decubitus angina (precipitated by lying flat)

Epidemiology and statistics

• Prevalance of Angina: 6.4 million Americans (National Health and Nutrition Examination Survey III, 1988-94)

• Prevalance Rate: approx 1 in 42 or 2.35% or 6.4 million people in USA

• 1 million hospitalized patients each year carry a primary diagnosis of unstable angina.

• Mean age - 62 years

• Percentage of patients older than 65 years - 44%

• The overall incidence of death as a result of Ischemic heart disease is 0.5 in 1000.

• The incidence of death in the early weeks following hospitalization is approximately 4%, and the incidence of MI is approximately 10%.

Causes

• Usually atheroma

• Anemia

• Thyrotoxicosis

• Arteritis

• Hypertrophic obstructive cardiomyopathy

Risk Factors

Certain risk factors increase the incidence of this disease and its complications.

1. Age: the incidence increases with age, the incidence being 1.5 in 1000 at the age of 50. The mean age is 62 years old with 40% of patients over the age of 65.
2. Gender: Males are more prone than females (especially premenopausal women). Males are 5 times more prone to develop the disease at the age of 50.
3. Serum cholesterol: A ratio of LDL to HDL of greater than 4:1 increases the risk dramatically. Conversely, a higher HDL level seems to offer protection. Serum cholesterol levels should be kept below 200mg/dL.
4. Smoking: increases the incidence by 60%.
5. Hypertension: whether systolic or diastolic tends to increase the risk.
6. Diabetes mellitus: is known to increase the incidence of IHD both in males and females.
7. Family history: a familial predisposition is known to exist and is in part due to inheritance of the above risk factors.
8. Oral contraceptives is associated with an increased incidence of myocardial infarction.
9. Gout, Type A personality, premature arcus corneae, obesity, hypertriglyceridemia and diagonal ear lobe crease have all been reported to increase the risk of developing ischemic heart disease.

Clinical suspicion

• Patients presenting with typical symptoms (central chest  tightness or heaviness which is brought on by exertion and relieved by rest. It may radiate to the arms, the neck, jaw or teeth.) + risk factors are confirmed 90% of the time to be angina.

• Patients with non typical symptoms + no risk factors are confirmed <25% to be angina.

• Associated symptoms include dyspnea, nausea, sweatiness, faintness.

Diagnosis

• ECG shows down-slope of the ST segment during an attack or stress test.
• The principle problem is to differentiate between those with unstable angina and those with non-Q wave myocardial infarction. This is established by finding elevated enzymes in cases of myocardial infarction.

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Treatment

1. Keep in mind the risk of myocardial infarction with unstable angina (10-20% in untreated patients and 5-7% if treated).
2. Hospitalization, rest, correct precipitating and risk factors (e.g. lipid lowering therapy “lowers the mortality”).
3. Treatment of ischemia:
   IV nitroglycerin is preferred due to easy establishment of drug levels. Start at 10 ug/mint & increase by 5ug/mint to a level that abolishes chest pain but does not compromise the circulation. After 24hrs asymptomatic patients should be switched to long acting nitrate preparation. Sublingual nitroglycerin can be given in symptomatic patients up to every 1/2 hour. For prophylaxis of asymptomatic patients switch to isosorbide mononitrate. Always leave a nitrate free period of 8 hours to avoid tolerance.
   Beta blockers (atenolol 50-100mg/day) are given because this combination reduces the risk of MI.
   2^nd line Ca++ channel blocker (diltiazem 90mg/day or amlodipine 5mg/day) is given if there is a contraindication to the use of beta blockers and is given only to relieve ischemic symptoms as this drug does not reduce the incidence of MI.

4. Inhibition of thrombosis: heparin and aspirin reduce risk of MI and subsequent death. Combination is better than single drug alone. Heparin is given a bolus of 80 units/kg followed by 18units/kg/hr infusion. A heparin ampoule is 5000 U and the antidote is protamine sulfate 50mg over 10 mints IV. APTT is monitored q6hrs until a therapeutic level of 1.5-2 X the control level. Heparin is usually given for 48hrs or until angiography is performed. An alternative is low molecular weight heparin SC 1mg/kg SC without monitoring APTT.
   Aspirin is given 160-325mg qd reduces mortality by 34%. Ticlopidine in patients who are unable to take this.
   GP IIb/IIIa can be given starting 4 days before PTCA and continuing for 12 hours after (abciximab).
   The above 3 elements (triple antithrombotic therapy) provide the most effective therapy in preventing infarction.

5. Symptomatic: morphine reserved for pain that is refractory to medical treatment (it also has a mild VD effect).
6. Special situations:
   Thrombolytic agents are used only in patients with persistant ST segment elevation or new LBBB. It increases the risk of MI.
   Intra-aortic balloon counterpulsation only used to stabilize patients indicated for PTCA or CABG.

Subsequent treatment

1. Approximately 80% will respond to aggressive medical treatment.
2. Those who are asymptomatic after 48hrs of drug therapy should be stratified by stress testing (details). Those with markedly positive stress tests should be referred to the angiography department.

Patients with refractory ischemia, or elevation of baseline enzymes have an increased risk of cardiac death and should be referred for coronary angiography and possible revascularization.

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