(Angina of Effort, Heberden’s Angina)
ANGINA PECTORIS…..The word ‘angina’ means I cry.’ Angina pectoris is used to denote cardiac pain of short duration due to inadequate blood supply to the cardiac musculature. As a result of this, pain producing factors (some metabolites) accumulate and stimulate the nerve endings resulting in pain.
The most important symptom of Angina Pectoris is pain. This has got the following characteristics:
- Location: It is located commonly in the mid or upper sternal region in 80%-90% of cases. It may be felt over the left side of the chest. Left inframammary pain is, however, never due to Angina pectoris. It may uncommonly be felt on the right of the sternum or even in the epigastric region.
- Character: It is classically constricting, squeezing, pressingor crushing in character, and patients may describe thatthe chest is crushed in a vice. In the neck it is frequently described as choking in character. In the jaw it is described like toothache. The feeling in the arms is one of tingling in type. Sometimes it is described as gas or indigestion, tight, heavy or gripping in nature. When it is very severe a sense of impending death develops.
- Radiation: The pain of Angina pectoris is radiated along both the shoulders and upper arms between C8 to t4 dermatome more commonly on the left side. The pain may radiate up to elbow, wrist or even up to fourth and fifth fingers (not to the thumb usually as it is supplied by c5 and Cc). Sometimes it may radiate to the neck and upper jaw and throat and back interscapular region rarely abdomen. Occasionally pain may be felt in these radiation sites though central chest pain is absent. Again central chest pain may be present without any radiation.
- Provoking factors: It usually starts after exercise, e.g. walking uphill, walking against the wind, or walking upstairs. It may also be seen after heavy meals, exposure to cold weather, emotional upsets or even during sexual intercourse.
- Relieving factors: It usually disappear after taking rest or after taking nitroglycerin.
- Duration of pain is not more than 15 minutes usually, but its tempo is reached within 2-3 minutes. When attacks occur after a heavy meal or after emotional excitement the duration of Angina may be 15 to 20 minutes.
If the pain lasts for more than 30 minutes it may indicate unstable angina, myocardial infarction or other alternate possibility.
ON EXAMINATION (at the time of attack)
Patient may look pale and anxious. He is motionless and still, with a tightly closed fist kept over the precordium. Pulse rate may be increased and systolic and diastolic blood pressures may be little elevated. At the site of pain in the arms a few tender spots may be present.
Cardiac finding is usually nil except tachycardia; sometimes there may be evidence of cardiac enlargement or aortic second sound (A2) may be accentuated. Atrial sound (S,) may be palpable and audible, this may give rise to a gallop rhythm. Apical systolic murmur due to papillary muscle dysfunction, paradoxical splitting of the second heart sound, even precordial bulge may be present. Evidences of diabetes, xanthomatosis xanthelasma, Tendinous xanthoma, hypertension, thyrotoxicosis, myxoedema, orthostatic hypotension, aortic stenosis, aortic regurgitation, mitral stenosis, occlusive peripheral arteries, hypertrophic cardiomyopathy, mitral valve prolapse, peripheral arterial disease, etc. may be present. Supraventricular or ventricular arrhythmia may be present as a cause or effect relationship. Angina pectoris may be of different types.
This is classical angina pectoris which is prOvoked by effort or exercise, relieved by rest or by taking nitroglycerin, is short lasting and often recurrent. ECG shows ST segment depression.
It is of recent onset (less than 3 months), clinical picture is more severe but not so characteristic, pain may occur at rest at night, more frequent, usually 3 episodes per day and very often leads to myocardial infarction. It is of longer duration (15 minutes or more) and may not improve with nitrates. Patients with accelerated stable angina, i.e. when induced with minimal provocation, lasts longer, occurring at rest is also included under unstable angina. ECG shows transient ST and T changes simulating sub-endocardial injury pattern but serum enzymes remain at normal level. Coronary angiography shows significant obstruction (>80%) in one or more larger coronary arteries. There is controversy regarding the relative merits of medical and surgical treatment.
Variant Angina Pectoris (Prinzmetal’s angina)
It is more common in women under 50. The pain is typical but may occur at rest without any provocating factor. It characteristically occurs in the early morning often awakening the patient from sleep. No history of previous myocardial infarction is usually seen. It often recurs in cyclic fashion with waxing and waning and sometimes may have a fixed time each day. The ECG shows ST elevation as is seen in acute myocardial infarction transiently. Focal coronary spasm of proximal epicardial coronary arteries is the usual factor associated with various types of arrhythmias and conduction defects. Both surgical and medical treatment are advocated. Rapid relief of pain is observed with sublingual nitrates and nifedepine. B-blocker may increase coronary vasospasm though they are used in the management where spasm is associated with fixed stenosis.
This type of angina occurs when patient lies down. This is usually seen in presence of heart failure. In recumbent position the central blood volume is increased and myocardial tension is also increased. In such patients severe coronary artery disease is usually present.
This type of angina occurs at night awakening the patient from sleep as with variant angina. It is usually precipitated by vivid dreams. Severe coronary artery disease is usually associated with this condition.
Here pain of angina pectoris is same as in chronic stable angina but with normal coronary arteriogram. After exercise ECG shows ST segment depression. Possibly these patients have an abnormal coronary vascular reserve. In response to vasoconstrictive influences there may be an abnormal increase In coronary vascular reserve. In response to vasodilatation for increased myocardial oxygen demand. Probably some local factors which autoregulate coronary vascular resistance such as endothelium derived relaxing factor (EDRD), paracrine hormones and endothelin are responsible. Abnormalities in the release of these hormones or their effect on the smooth muscles is responsible for precipitating a clinical atack Long term prognosis is better in comparison to usual angina pectoris.