Chapter 21 Marini Acute Coronary Syndromes

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CHAPTER 21 • Acute Coronary Syndromes

but can present on its own as a true posterior infarction. This may occur with either left cir- cumflex or distal RCA occlusion. 4. RV Infarcts: In about 30% of inferior wall infarctions, RV infarcts manifest on ECG as ST depressions in V 1 and V 2 and ≥ 1 mm ST ele- vations in right-sided chest leads, particularly V 3 R and V 4 R. Pure RV infarcts resulting from occlusion of RV marginal branch vessels may sometimes mimic an anterior MI by causing ST elevations in leads V 1 and V 2 . 5. New LBBB: New LBBB is typically seen with large MIs and carries an in-hospital mortality rate of 20% to 25%. There is a substantial ben- efit from reperfusion therapy (21% reduction in mortality at 7 weeks, which translates into 49 lives saved per 1,000 patients treated). How- ever, an MI may be missed in a significant num- ber of individuals with new complete LBBB, and therefore, they are less likely to get reper- fusion therapies than STEMI patients. Criteria for diagnosis of MI in the presence of LBBB are based on ST segment concordance or discord- ance: (1) greater than or equal to 1 mm con- cordant elevation, (2) greater than or equal to 5 mm discordant elevation, and (3) greater than 1 mm ST segment depressions in leads V 1 to V 3 . Presence of one or more of these criteria makes a diagnosis of AMI more likely with LBBB. 6. Normal ECG: ECG may be normal in high lateral wall infarctions, as this area may be elec- trocardiographically “silent.” Cardiac Enzymes Creatine Kinase Although now of secondary prominence to tropo- nins, traditional creatine kinase measurements con- tinue to be diagnostically helpful. Total CK and MB fractions begin to rise by 4 to 8 hours of onset of an MI, reach a peak by 18 to 24 hours, and return back to baseline by 48 to 72 hours. CK peaks earlier in non–Q wave infarctions and in patients who have received thrombolytic therapy to abort an acute infarction. The rapid washout of CK associated with thrombolysis may produce peak enzyme levels as early as 30 minutes after reperfusion. Peak CK activity correlates with the extent of muscle loss. Levels are checked every 8 hours, and three negative CK–MB levels help rule out an AMI. CK– MB levels greater than 3% of total CK levels are used to make a diagnosis of an AMI. The sensitivity

and specificity of CK–MB in the diagnosis of an AMI are lower than that of troponin. Thus, one may have a small infarct with normal CK–MB but slightly elevated troponins. Total CK may be mildly elevated by trivial skeletal muscle injury (e.g., severe exercise or intramuscular injection). Even though CK–MB is relatively specific for cardiac muscle, it may be released during massive skeletal or smooth muscle damage (e.g., rhabdomyolysis, polymyositis, small bowel surgery). Cardiac Troponins There are two types of cardiac troponin assays avail- able (T and I). Both are cardiac-specific regulatory proteins; troponin-I is in more widespread use. Highly sensitive and specific in making a diagnosis of AMI, their levels elevate within 6 to 8 hours of onset of an AMI, peak by 3 to 5 days, and gener- ally last for 7 to 12 days. Renal insufficiency slows their clearance. Thus, they aid in making a diagnosis of a remote MI. They are also helpful in making a diagnosis of an MI in certain situations like rhabdo- myolysis, polymyositis, and renal failure where the CK–MB levels may be elevated. Although sensitive, the serum aspartate amino- transferase is not sufficiently specific for diagnosis. Similarly, total lactic dehydrogenase (LDH) rises in most cases of MI but has a low specificity. Levels of the LDH-2 isoenzyme normally exceed those of the LDH-1 isoenzyme. Reversal of the ratio suggests MI. LDH begins to rise 12 to 24 hours after coro- nary occlusion, peaking at 2 to 4 days and resolving in 7 to 10 days. Because LDH rises later than cre- atine phosphokinase (CPK), it may be used to diag- nose infarction in patients presenting more than 24 hours after onset of symptoms. Accumulating expe- rience with troponin-I suggests it to be a sensitive and specific serum marker of myocardial damage. Echocardiography Although echocardiography cannot be considered a definitive test for ischemia, it is a helpful adjunc- tive technique. Echocardiography offers informa- tion that can help make a diagnosis of ischemia or infarction. A focal wall motion abnormality seen on the echocardiogram in the proper clinical setting can help make the diagnosis of acute ischemia or infarction, especially when the ECG is not help- ful. Echocardiography can also help in providing an explanation for hypotension or congestive symptoms in patients with an AMI (e.g., LV or RV dysfunction,