REVUE MEDICALE

CLINICAL FEATURES —

 

 

History — Elements of the history that are critically important include characteristics of the discomfort, associated symptoms, precipitating factors, and information about social and family history.

Typical qualities of anginal pain — Clinicians should attempt to elicit information about the following characteristics of the discomfort:

●Quality − Angina is usually characterized more as a discomfort rather than pain. Terms frequently used by patients include squeezing, tightness, pressure, constriction, strangling, burning, heart burn, fullness in the chest, band-like sensation, knot in the center of the chest, lump in throat, ache, heavy weight on chest (elephant sitting on chest), like a bra too tight, and toothache (when there is radiation to the lower jaw) [17]. In some cases, the patient cannot qualify the nature of the discomfort, but places his or her fist in the center of the chest, known as the "Levine sign.”

It is generally not described as sharp, dull-aching, knife-like, stabbing, or pins and needles-like. In a report of patients presenting to the emergency department, "sharp" or "stabbing" pain was a low risk description, particularly when the pain was pleuritic or positional, was fully reproducible by palpation, and the patient had no history of angina or myocardial infarction [18]. No patient who presented with these findings had a cardiac etiology for the pain.

 

The following additional characteristics are typically seen:

•Angina is typically gradual in onset and offset, with the intensity of the discomfort increasing and decreasing over several minutes. In contrast, noncardiac pain is often of greatest intensity at its onset and often has an abrupt onset and offset.

 

•Since angina is a referred discomfort, patients tend to have the same quality of chest discomfort with recurrent ischemic episodes [13]. Generally, it is felt in the same location. The discomfort is generally the same prior to or with a myocardial infarction and is the same quality as prior to revascularization by either surgery (although the location may be different due to disruption of neural innervation of the heart) or percutaneous coronary intervention.

 

•Angina is a constant discomfort that does not change with respiration or position. It is also not provoked or worsened with palpation of the chest wall.

 

●Location and radiation − As noted above, angina is a referred pain due to involvement of a neural reflex pathway via the thoracic and cervical nerves. As a result, it is not felt in a specific spot, but is usually a diffuse discomfort that may be difficult to localize.

 

The patient often indicates the entire chest when asked where the discomfort is felt. Pain that localizes to one small area of the chest is more likely of chest wall or pleural origin rather than visceral.

Angina is referred to the corresponding dermatomes (C7-T4) that supply afferent nerves to the same segments of the spinal cord as the heart. Thus, angina often radiates to other parts of the body, including the upper abdomen (epigastric), shoulders, arms (upper and forearm), wrist, fingers, neck and throat, lower jaw and teeth (but not upper jaw), and rarely to the back (specifically the interscapular region) [19,20]. Radiation to both arms is a stronger predictor of acute myocardial infarction. The location and radiation of angina is usually the same each time. Occasionally, the location and radiation, but not quality, may be different after bypass surgery due to the disruption of the neural innervation of the heart.

Isolated back pain is unusual in patients with angina. However, it may be seen with an aortic dissection that also involves the coronary arteries. (See "Clinical manifestations and diagnosis of aortic dissection".)

●Provoking factors − Angina is often elicited by activities and situations that increase myocardial oxygen demand, including physical activity, cold, emotional stress, sexual intercourse, meals, or lying down (which results in an increase in venous return and increase in wall stress) [21-23]. Patients should be questioned about the use of cocaine or other recreational drugs, as they may trigger myocardial ischemia. (See "Evaluation and management of the cardiovascular complications of cocaine abuse", section on 'Myocardial ischemia'.)

 

Postprandial pain is generally considered to be gastrointestinal in origin. However, it may also be anginal, especially in patients with severe ischemia (eg, left main or three vessel coronary disease) [15].

●Timing − Angina occurs more commonly in the morning due to a diurnal increase in sympathetic tone. Enhanced sympathetic activity raises heart rate, blood pressure, vessel tone and resistance (resulting in a reduced vessel diameter that causes any fixed lesion to be more occlusive), and platelet aggregability (resulting in the release of vasoactive substances, such as serotonin and thromboxane A2) [8,9].

 

●Duration and relief − Classic angina is often relieved with termination of the provoking factor. Angina generally lasts for two to five minutes. It is not a fleeting discomfort, which lasts only for a few seconds or less than a minute, and it generally does not last for 20 to 30 minutes, unless the patient is experiencing an acute coronary syndrome, especially myocardial infarction.

 

Factors that reduce oxygen demand or increase oxygen supply will result in relief of angina. These include cessation of activity or termination of the provoking factor, use of nitroglycerin (which is a venodilator, reducing venous return, and a coronary artery vasodilator that increases coronary blood flow), and sitting up (which reduces venous return and preload).

Relief of chest discomfort with nitroglycerin is not specific for angina, since a similar response may be seen with esophageal spasm or other gastrointestinal problems as nitroglycerin also relaxes smooth muscle. In a review of 459 patients presenting to an emergency department with chest pain, the percentage of patients with relief of chest discomfort with nitroglycerin was similar among those with and without active coronary disease (35 versus 41 percent) [24].

Atypical features — Specific chest pain characteristics can be used to help differentiate cardiac from noncardiac causes (table 2A-B). (See "Diagnostic approach to chest pain in adults".)

In two systematic reviews, the following characteristics were found to be more typical of nonischemic chest discomfort [25,26]:

●Pleuritic pain, sharp or knife-like pain related to respiratory movements or cough.

●Primary or sole location in the mid or lower abdominal region.

●Any discomfort localized with one finger.

●Any discomfort reproduced by movement or palpation.

●Constant pain lasting for days.

●Fleeting pains lasting for a few seconds or less.

●Pain radiating into the lower extremities or above the mandible.

 

However, some patients with an acute coronary syndrome present with atypical types of chest pain. In one study, acute ischemia was diagnosed in 22 percent of patients who presented with sharp or stabbing pain and 13 percent who presented with pleuritic-type pain [18].

In addition, some patients who appear to have a noncardiac cause of chest pain have other serious conditions including acute aortic dissection, pulmonary embolism, tension pneumothorax, myocarditis, perforating peptic ulcer, and esophageal rupture (table 2A-B) [27]. It is essential to consider these alternate diagnoses to avoid potentially dangerous errors in management, such as the administration of thrombolytic therapy to a patient with an aortic dissection. (See "Differential diagnosis of chest pain in adults".)

Associated symptoms — Angina is often associated with other symptoms. The most common is shortness of breath or wheezing, which may reflect mild pulmonary congestion [20,28]. Pulmonary congestion is due to an elevation in left ventricular end diastolic pressure related to failure of the myocardium to relax normally in diastole (as relaxation or lusitropy is energy dependent). The resulting diastolic “stiffness” or diastolic dysfunction results in an increase in left ventricular end diastolic pressure, left atrial pressure, and pulmonary venous pressure, which is transmitted to the pulmonary vessels. (See "Clinical manifestations and diagnosis of heart failure with preserved ejection fraction".)

Other symptoms may include belching, nausea, indigestion, diaphoresis, dizziness, lightheadedness, clamminess, and fatigue. However, these symptoms may be seen with other etiologies for chest pain, especially gastrointestinal causes. (See "Differential diagnosis of chest pain in adults".)

It is common for patients with diabetes mellitus, who often have autonomic (sympathetic) dysfunction, to experience "silent ischemia" or best termed “discomfortless ischemia.” In this situation, they may experience the above symptoms associated with ischemia in the absence of the chest discomfort due to failure of transmission of neural impulses from the heart to the spinal cord. (See "Silent myocardial ischemia: Epidemiology and pathogenesis".)

Social and family history — Many patients who are ultimately diagnosed with myocardial ischemia have key pieces of information in the social and family histories. For example, risk factors for coronary artery disease are often present in individuals with angina due to coronary artery disease. (See "Overview of the risk equivalents and established risk factors for cardiovascular disease", section on 'Established risk factors for atherosclerotic CVD'.)

The family history may reveal members with premature cardiovascular disease or hypertrophic cardiomyopathy. (See "Genetics of hypertrophic cardiomyopathy".)

Physical examination — Ischemia can produce impairment in myocardial function, which may result in the following findings on physical examination. All disappear with resolution of the ischemia. Some patients have none of these features.

Increase in heart rate — Ischemia can raise the heart rate even if the patient is receiving a beta blocker or calcium channel blocker. The increase in heart rate is induced by reflex sympathetic nervous system activation as a response to ischemia.

Elevation in blood pressure — Ischemia often causes a hypertensive blood pressure response. The elevation in blood pressure is induced by both sympathetic activation in response to ischemia and stimulation of the left anterior descending coronary artery chemoreceptor. This chemoreceptor is stimulated by serotonin secreted as a result of platelet aggregation, which often occurs in association with angina.

New heart sounds — Ischemia-induced myocardial dysfunction can lead to changes in the normal heart sounds. The second heart sound may become paradoxically split due to delayed relaxation of the left ventricular myocardium and delayed closure of the aortic valve. There may also be a third or fourth heart sound. (See "Auscultation of heart sounds".)

New/changed murmurs — Impaired myocardial function may result in a new mitral regurgitation murmur, which appears to be due to papillary muscle dysfunction causing apical tethering or tenting of the leaflets, or changes in the intensity or timing of pre-existing murmurs. (See "Ischemic mitral regurgitation" and "Auscultation of cardiac murmurs".)

Precordial pulsation — Palpation of the chest wall may reveal abnormal pulsations that correlate with transient left ventricular dysfunction. An area of dyskinesis may develop, especially at the apex of the left ventricle or at the anterior axillary line (location of the left ventricular wall), reflecting disease of the left anterior descending coronary artery. (See "Examination of the precordial pulsation".)

Palpation of the left anterior chest wall at the anterior axillary line may reveal an abnormal tapping in systole, which reflects the presence of an area of dyskinetic contraction or aneurysm. Transient right ventricular dysfunction may lead to a transient right ventricular heave or sternal pulsation.

Laboratory tests — For patients in whom the history and physical examination raise the possibility of myocardial ischemia as the cause of chest discomfort, an electrocardiogram should be obtained. An electrocardiogram obtained when the chest discomfort is present will often show J point and ST segment depression, which indicates subendocardial ischemia. When the patient is asymptomatic, the electrocardiogram may be entirely normal. (See "Electrocardiogram in the diagnosis of myocardial ischemia and infarction", section on 'Unexpected absence of diagnostic findings'.)

A chest radiograph is often ordered but is not likely to confirm or refute the diagnosis of myocardial ischemia. Generally, the radiography is performed to screen for other causes of chest pain (eg, enlarged aorta, broken rib). (See "Diagnostic approach to chest pain in adults", section on 'Other studies'.)

Cardiac biomarkers (eg, troponin) are often obtained in patients with angina. However, they are unlikely to be elevated in patients with intermittent and relatively brief angina episodes. They may be useful when the anginal episode is more prolonged. (See "Troponins as biomarkers of cardiac injury", section on 'Ischemia and troponin elevation'.)

DIAGNOSIS — The diagnosis of myocardial ischemia can often be made with a high likelihood based on the history, physical examination, and electrocardiogram. Such patients have classic angina (see 'Clinical Features' above), either a normal physical examination or features consistent with myocardial ischemia (see 'Physical examination' above), and an electrocardiogram that is normal in the absence of ongoing ischemia.

For example, in the patient with classic angina and multiple risk factors for coronary artery disease, the diagnosis is highly likely. Indeed, a history consistent with classical angina has a 93 percent predictive accuracy for the diagnosis of ischemia that is most often the result of coronary artery disease.

For some patients, additional testing is necessary to secure the diagnosis with certainty. Testing, particularly stress testing, is of value when the history is not completely consistent with angina or in a high-risk patient with symptoms that are atypical for ischemia.

We perform some type of stress testing in most patients for the purpose of prognosis. (See "Exercise ECG testing to determine prognosis of coronary heart disease".)

The choice of initial stress test, such as with exercise electrocardiogram (ECG), exercise with imaging, or pharmacologic stress testing with imaging, may be influenced the patient's resting ECG, physical ability to perform exercise, local expertise, and available technologies.

An electrocardiogram

to perform coronary angiography

 

 

ANTIANGINAL THERAPY — 

Beta blockers —first line therapy by reducing both heart rate and contractility

Atenolol (sectral) 100mg 0.5-2tab/day

Metoprolol (Lopressor, Seloken) 200mg 1/day

 

Calcium channel blockers — used in combination with beta blockers or as a substitute for a beta blocker when beta blockers are contraindicated or cause side effects.

Long-acting diltiazem  (Monotildiem 120mg od or verapamil (Isoptine 120mg tds)

or a second generation dihydropyridine (amlodipine  5mg od or felodipine) are preferred.

 

aspirine 75-325mg/d

 

Although a third class of antianginal drug can be added in patients who have limiting angina on two agents, many physicians would consider coronary angiography in such patients and revascularization if indicated.

 

Nitrates — first-line therapy for the treatment of acute anginal symptoms. for the prophylaxis of anginal episodes.

 

RNew therapy: Ranolazine (Ranexa))— 500 mg twice daily. For patients who remain symptomatic, 1000 mg twice daily may be used.

In patients with a history of chronic stable angina, including those who are stable after an acute coronary syndrome, ranolazine is effective at reducing anginal symptoms and improving exercise capacity, when added to standard antianginal therapy. It may also be an effective anti-arrhythmic agent, although that aspect of its activity needs more extensive clinical testing.

Ranolazine can be combined with beta blockers for relief of symptoms if initial monotherapy with beta blockers is unsuccessful.

As an initial test in patients who have survived sudden cardiac arrest or potentially life-threatening ventricular arrhythmia or in those who develop symptoms and signs of heart failure.

 

●When a patient’s clinical characteristics and the results of noninvasive testing indicate a high likelihood of severe ischemic heart disease.

 

We also agree with the following weaker recommendations for coronary angiography in patients with SIHD and:

●Depressed left ventricular systolic function (ejection fraction <50 percent) and moderate risk criteria on noninvasive testing with demonstrable ischemia.

 

●Inconclusive prognostic information after noninvasive testing or in patients for whom noninvasive testing is contraindicated or inadequate.

 

●An unsatisfactory quality of life due to angina, a left ventricular ejection fraction >50 percent, and intermediate risk criteria on noninvasive testing.

 

PREVENTATIVE THERAPIES —

Antiplatelet therapy — aspirin from 75 to 325 mg daily

Risk factor reduction —

Role of exercise — 

Influenza vaccine —