Lesson topic №24. ОКС (Acute Coronary Syndrome )

Laboratory Studies

Electrocardiography

Recording an ECG during an episode of the presenting symptoms is valuable.

Transient ST-segment changes (>0.05 mV) that develop during a symptomatic period

and that resolve when the symptoms do is strongly predictive of underlying coronary

artery disease and has prognostic value. Comparison with previous ECGs is often helpful.

Alternative causes of ST-segment and T-wave changes are left ventricular aneurysm,

pericarditis, Prinzmetal angina, early repolarization, Wolff-Parkinson-White syndrome,

drug therapy (eg, with tricyclic antidepressants, phenothiazines).

Measurement of cardiac enzyme levels

Measure cardiac enzyme levels at regular intervals, starting on admission and

continuing until the peak is reached or until 3 sets of results are negative. Biochemical

biomarkers are useful for both diagnosis and prognostication (see Media file 1).

This plot shows changes in cardiac markers over time after the onset of symptoms.

Peak A is the early release of myoglobin or creatine kinase isoenzyme MB (CK-MB) after acute myocardial infarction (AMI).

Peak B is the cardiac troponin level after infarction.

Peak C is the CK-MB level after infarction.

Peak D is the cardiac troponin level after unstable angina.

Data are plotted on a relative scale, where 1.0 is set at the myocardial-infarction cutoff concentration.

Courtesy of Wu et al (1999). ROC = receiver operating characteristic.

Measurement of CK-MB levels

oCK-MB, the isoenzyme specific to the heart muscle, was the principal biomarker of cardiac injury until troponin supplemented it.

o

oIn the setting of myocardial infarction, plasma CK-MB concentrations typically rise about 4-6 hours after the onset of chest pain. They peak within 12-24 hours and return to baseline levels within 2448 hours.

oSerial measurements obtained every 6-8 hours (at least 3 times) are warranted until peak values are determined.

oClinical settings other than acute coronary syndrome, such as trauma, heavy exertion, and skeletal muscle disease (eg, rhabdomyolysis) may elevate CK-MB values.

o

oThe area under the concentration-time curve for CK-MB created with serial measurements of blood enzyme levels provides a reliable estimate of the size of the infarct.

oDetermination of subforms of CK-MB (CK-MB2 that is more specific to heart muscle) may improve the sensitivity of this test.

Measurement of troponin levels

o Troponin is part of the contractile apparatus of the myocyte associated with tropomyosin and actin and myosin

filaments. Troponin has 3 subunits: TnT, TnI, and TnC. TnI and TnT are normally not detectable in the blood.

o Measurement of troponin level has both diagnostic and prognostic value.

o Positive troponin levels are virtually diagnostic of myocardial infarction in the most recent revisions of the ACC/AHA guidelines, as they are without equal in terms of combined specificity and sensitivity in diagnosing

myocardial infarction.

oElevated troponin levels might help in identifying patients who might greatly benefit from aggressive antiplatelet and other adjunctive therapy.5

oTroponin levels are typically measured serially along with CK values.

Measurement of myoglobin levels

oMyoglobin is not cardiac specific, but it may be detected as early as 2 hours after myocardial necrosis starts.

oMyoglobin results should be supplemented with other more specific cardiac biomarkers, such as CK-MB or troponin.

oMyoglobin values have a high negative predictive value when blood is sampled in the first 4-8 hours after onset.

CBC determination

The CBC helps in ruling out anemia as a secondary cause of acute coronary syndrome. Leukocytosis has prognostic value in the setting of acute myocardial infarction.

Basic metabolic panel

Close monitoring of potassium and magnesium levels is important in patients with acute coronary syndrome because low levels

may predispose them to ventricular arrhythmias. Routine measurement of serum potassium levels and prompt correction are

recommended.

A creatinine level is also needed, particularly if cardiac catheterization is considered. Use of N -acetylcysteine and adequate

hydration can help prevent contrast material–induced nephropathy.

New biomarkers

Levels of brain natriuretic peptide (BNP) and N-terminal pro-BNP (NT-pro-BNP) are elevated in acute MI and provide predictive information for risk stratification across the spectrum of acute coronary syndrome.7,8

In the future, a combination of levels of troponin (a biomarker of myocardial necrosis), NT-pro-BNP (an indicator of elevated left ventricular end-diastolic pressure and wall stress), and C-reactive protein (CRP, an estimate of extent of systemic inflammation)

may prove useful for predicting the outcome of patients with acute coronary syndrome.

Routine measurement of BNP and CRP levels in patients with acute coronary syndrome is not warranted at this time.

Imaging Studies

Chest radiography

Chest radiography helps in assessing cardiomegaly and pulmonary edema. A chest radiograph may also assist in diagnosing concomitant disease (eg, pneumonia in an elderly patient) as a precipitating cause of acute

coronary syndrome.

Echocardiography

An echocardiogram may play an important role in the setting of acute coronary syndrome. Regional wall-motion abnormalities can be identified. Echocardiograms are especially helpful if the diagnosis is questionable.

An echocardiogram can also help in defining the extent of the infarction and assess overall function of the left

and right ventricles. In addition, an echocardiogram can help identify complications such as acute mitral

regurgitation, left ventricular rupture, and pericardial effusion.

Absence of segmental wall-motion abnormality on echocardiography during active chest discomfort is a highly

reliable indicator of a nonischemic origin of symptoms.

Myocardial perfusion imaging

Myocardial perfusion is a valuable method for triaging patients with chest pain in the emergency department.

Myocardial perfusion imaging at rest is highly sensitive for detecting acute myocardial infarction, and it can be

supplemented with provocative testing after infarction is excluded.

Results of clinical trials can be applied only in centers with proven reliability and experience.

The sensitivity of single photon emission computed tomography (SPECT) is sufficient to detect infarcts of at least

10 g, but MRI with gadolinium enhancement may depict infarcts as small as 1–5 g.

Cardiac angiography

Cardiac catheterization helps in defining the patient's coronary anatomy and the extent of the disease.

Patients with cardiogenic shock, intractable angina despite medication, severe pulmonary congestion, or right ventricular infarction should immediately undergo cardiac catheterization.

For high-risk patients with acute coronary syndrome without persistent ST elevation, angiography with

glycoprotein IIb/IIIa inhibition has been recommended.

Most patients benefit from angiography when they have a TIMI risk score of less than 3 points (see Table).

After the diagnosis of acute coronary syndrome is established, risk stratification based on

TIMI risk scores and the GRACE risk of death can be useful in making clinical decisions

regarding the need for an invasive approach.

Patients are at higher risk if the following findings are present:

Clinical instability

Accelerating chest pain in the 48 hours before presentation

Prolonged ischemic chest pain

Clinical evidence of heart failure

Hypotension

Ventricular tachycardia

ECG changes of ischemia

Positive cardiac biomarkers

TIMI risk score of more than 3 points (see the Table above) or a GRACE risk of death more than 4%.