Acute coronary syndrome

Acute coronary syndrome (unstable coronary artery disease) includes both unstable angina and non-Q-wave myocardial infarction.

Clinical features

• increased severity or frequency of the patient's pre-existing angina within the last month;

• rapidly worsening chronic stable angina (crescendo angina);

• new onset of angina pectoris;

• angina at rest;

• post-infarction angina (more than 24 hours after myocardial infarction);

• non-Q-wave myocardial infarction.

Objective examination. During attack of chest pain the patient's condition is grave, forced sitting position, the face is pale with acrocyanosis. The border of relative cardiac dullness displaced outside.

In auscultation both heart sounds are decreased, S³ or S⁴ gallop may be detected during an episode of pain. Mitral regurgitation murmur appears. Arrhythmia is often observed. Blood pressure tends to have less level, than in period free of pain. The signs of congestion failure present: enlarged liver, pedal edema.

Additional methods of examination

Clinical blood analysis is without change, seldom may be slight leukocytosis.

Biochemical blood analysis: commonly there are the signs of disorders of lipid profile: increased level total cholesterol, triglycerides, low density lipoprotein cholesterol.

Small rises in the serum levels of biochemical markers of cardiac injury (creatine kinase, creatine kinase MB), troponin-T or troponin-I reflect the development of small foci of myocardial necrosis, minor creatine kinase, creatine kinase MB, which are usually accompanied by elevated troponin-T levels, indicate an increased risk of future events, despite stabilization of their clinical condition. Cardiac troponin-I is not detectable in the absence of cardiac injury. Because of the lag period before a rise becomes detectable, at least two samples, taken at an interval of 12-24 hours, should always be tested.

Elevated fibrinogen levels at the time of admission are associated with an increased risk of death, myocardial infarction or spontaneous ischemia in patients with unstable angina.

The acute-phase proteins C-reactive protein is sensitive, but non-specific, markers of inflammation. There is much evidence to suggest a role for inflammation in the etiology of unstable angina and myocardial infarction and level of this protein have been observed to be elevated in some patients with acute coronary syndrome. C-reactive protein levels 3 mg/1, as detected by means of sensitive radioimmunoassay, indicate an increased risk of subsequent cardiac events m patients with acute coronary syndrome.

Instrumental examination. ECG monitoring is regarded as an essential part of routine management. All patients with suspected acute coronary syndrome should be admitted to the coronary unit for 12-24 hours of ECG monitoring (Holter monitoring). Admission ECG finding in acute coronary syndrome: ST-segment depression, ST-segment elevation (transient), T-wave inversion, normal ECG.

A normal ECG recorded when the patient is pain free not exclude the diagnosis of acute coronary syndrome, although a normal ECG recorded during an episode of pain makes the diagnosis unlikely, and is associated with an excellent prognosis. Following abnormalities of ECG support a diagnosis of acute coronary syndrome: ST-segment depression >0,5 mm, ST-segment elevation >1mm, T-wave inversion. Transient elevation of the ST-segment which settles, either spontaneously or in response to nitrate treatment, is fully consistent with the diagnosis acute coronary syndrome. Isolated T-wave inversion on the initial ECG is a relative by benign sign, and is associated with a low risk of future myocardial infarction or death. A total of more than 60 minutes of ischemia during Holter monitoring is associated with a poor prognosis. However, T-wave inversion and change of ST-segment must be considered in the context of the whole clinical picture taking into account the patient's age, presence of other risk factors, levels of biochemical markers of cardiac injury. Exercise testing undertaken either before or shortly after hospital discharge, is a minimum requirement for patients. Once the patient has been pain-free for 24-48 hours and the ECG stable the risks associated with performing an exercise test are very low. Severe ischemia and low exercise tolerance in a patient who has had either unstable angina or non-Q-wave myocardial infarction is associated with a poor short-term prognosis.

Echocardiography should be performed in all patients in order to evaluate the left ventricular function.

Stress echocardiography can be performed either during or immediately after dynamic exercise or under pharmacological stress administration of dipyridamole or dobutamine. Patients who are unable to perform an exercise test can be usefully assessed by pharmacological induced stress echocardiography.

Myocardial perfusion scintigraphy (tallium or technetium scan) may be particularly valuable in patients who are unable to exercise. Such techniques can outline perfusion defects.