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MIOCARDIAL INFARCTION

 

Myocardial infarction (MI) is the rapid development of myocardial necrosis caused by a critical imbalance between oxygen supply and demand of the myocardium. This usually results from plaque rupture with thrombus formation in a coronary vessel, resulting in an acute reduction of blood supply to a portion of the myocardium.

Although the clinical presentation of a patient is a key component in the overall evaluation of the patient with MI, many events are either "silent" or are clinically unrecognized, evidencing that patients and physicians often do not recognize symptoms of a MI. The appearance of cardiac markers in the circulation generally indicates myocardial necrosis and is a useful adjunct to diagnosis.

Cardiac markers help to categorize MI, which is considered part of a spectrum referred to as acute coronary syndrome that includes ST-elevation MI (STEMI), non–ST-elevation MI (NSTEMI), and unstable angina. This categorization is valuable because patients with ischemic discomfort may or may not have ST-segment elevations on their electrocardiogram. Those without ST elevations may ultimately be diagnosed with NSTEMI or with unstable angina based on the presence or absence of cardiac enzymes. Additionally, therapeutic decisions, such as administering an intravenous thrombolytic or performing percutaneous coronary intervention (PCI), are often made based on this categorization.

Pathophysiology

The most common cause of MI is narrowing of the epicardial blood vessels due to atheromatous plaques. Plaque rupture with subsequent exposure of the basement membrane results in platelet aggregation, thrombus formation, fibrin accumulation, hemorrhage into the plaque, and varying degrees of vasospasm. This can result in partial or complete occlusion of the vessel and subsequent myocardial ischemia. Total occlusion of the vessel for more than 4-6 hours results in irreversible myocardial necrosis, but reperfusion within this period can salvage the myocardium and reduce morbidity and mortality.

Nonatherosclerotic causes of MI include coronary vasospasm as seen in variant (Prinzmetal) angina and in patients using cocaine and amphetamines; coronary emboli from sources such as an infected heart valve; occlusion of the coronaries due to vasculitis; or other causes leading to mismatch of oxygen supply and demand, such as acute anemia from GI bleeding. MI induced by chest trauma has also been reported, usually following severe chest trauma such as motor vehicle accidents and sports injuries.

Lab Studies

  • Troponin is the preferred biomarker for diagnosis.

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    • Troponins have the greatest sensitivity and specificity in detecting MI. The test result is both diagnostic as well as prognostic of outcome.
    • Troponin is a contractile protein that normally is not found in serum. It is released only when myocardial necrosis occurs.
    • For early detection of myocardial necrosis, sensitivity of this laboratory test is superior to that of the creatine kinase-MB (CK-MB). Troponin I is detectable in serum 3-6 hours after an AMI and its level remains elevated for 14 days.
    • Troponin is also the optimum biomarker for the evaluation of patients with MI who have coexistent skeletal muscle injury.
  • Creatine kinase–MB level

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    • CK-MB levels begin to rise within 4 hours after injury, peak at 18-24 hours, and subside over 3-4 days. A level within the reference range does not exclude myocardial necrosis.
    • Occasionally, very small infarcts can be missed by CK-MB; therefore, a troponin level should be measured for patients suspected of having had MI who have negative serial CK-MBs.
  • Myoglobin levels

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    • Myoglobin, a low-molecular-weight heme protein found in cardiac and skeletal muscle, is released more rapidly from infarcted myocardium than troponin and CK-MB and may be detected as early as 2 hours after MI. Myoglobin levels rise early in the course of MI.
    • The marker has high sensitivity but poor specificity. When performed in conjunction with other studies, it may be useful for the early detection of MI.
  • Complete blood count

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    • CBC is indicated if anemia is suspected as a precipitant. Transfusion with packed red blood cells may be indicated.
    • Leukocytosis may be observed within several hours after an AMI. It peaks in 2-4 days and returns to levels within the reference range within 1 week.
  • Chemistry profile

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    • Potassium and magnesium levels should be monitored and corrected.
    • Creatinine levels must be considered before using an angiotensin-converting enzyme (ACE) inhibitor.
  • C-reactive protein (CRP) is a marker of acute inflammation. Patients without biochemical evidence of myocardial necrosis but with elevated CRP level are at increased risk of a subsequent ischemic event.
  • Erythrocyte sedimentation rate (ESR) rises above reference range values within 3 days and may remain elevated for weeks.
  • Serum lactate dehydrogenase (LDH) level rises above the reference range within 24 hours of MI, reaches a peak within 3-6 days, and returns to the baseline within 8-12 days.

Imaging Studies

  • Chest radiography

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    • Chest radiography may provide clues to an alternative or complicating diagnosis (eg, aortic dissection, pneumothorax). Other imaging studies such as a contrast chest CT scan or transesophageal echocardiography should be used to differentiate MI from aortic dissection in patients in whom the diagnosis is in doubt. Stanford type A aortic dissections may dissect in a retrograde fashion causing coronary blockage and dissection, which may result in MI. In one study, 8% of patients with Stanford type A dissections had ST elevation on ECG.
    • Chest radiography also reveals complications of MI such as pulmonary edema secondary to heart failure.
  • Echocardiography

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    • Use 2-dimensional and M-mode echocardiography when evaluating wall motion abnormalities and overall ventricular function.
    • Echocardiography can identify complications of MI (eg, valvular insufficiency, ventricular dysfunction, pericardial effusion).
  • Technetium-99m sestamibi scan

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    • Technetium-99m is a radioisotope that is taken up by the myocardium in proportion to the blood flow and is only minimally redistributed after initial uptake. This allows for time delay between injection of the isotope and imaging.
    • It has potential use in identifying infarct in patients with atypical presentations or in patients with ECGs that are not interpretable.
    • Normal scan findings are associated with an extremely low risk of subsequent cardiac events.
  • Thallium scanning: Thallium accumulates in the viable myocardium.
  • Perfusion imaging has been used in risk stratification after MI and for measurement of infarct size to evaluate reperfusion therapies. Novel "hot spot" imaging radiopharmaceuticals that visualize infarction or ischemia are currently undergoing evaluation and hold promise for the future. (See Myocardial Ischemia - Nuclear Medicine and Risk Stratification.)
  • Recent advances include dual-source 64-slice CT scanning that can do a full scan in 10 seconds and produce high-resolution images that allow fine details of the patient's coronary arteries to be seen. This technology allows for noninvasive and early diagnosis of coronary artery disease and thus earlier treatment before the coronary arteries become more or completely occluded. It allows direct visualization of not only the lumen of the coronary arteries but also plaque within the artery. Dual-source 64-slice CT scanning is being used with intravenous contrast to determine if a stent or graft is open or closed.
  • MRI can identify wall thinning, scar, delayed enhancement (infarction), and wall motion abnormalities (ischemia). Currently, this is not a primary diagnostic modality for MI, but coronary artery assessment may be enhanced by magnetic resonance angiography (MRA) in the future.

Other Tests

  • Electrocardiography

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    • An ECG should be obtained as soon as possible after presentation to the ED.
    • Approximately one half of patients have diagnostic changes on their initial ECG.
    • Because the symptoms of AMI can be subtle or protean, an ECG should be performed on any patient who is older than 45 years and is experiencing any form of thoracoabdominal discomfort, including new epigastric pain or nausea.
    • In younger patients, an ECG should be considered when suggestive symptoms are present or in patients with risk factors for early coronary artery disease. Younger patients are disproportionately represented in missed cases. An ECG is a rapid, low-risk, relatively low-cost measure.
    • Results that indicate high probability of MI are ST-segment elevation greater than 1 mm in 2 anatomically contiguous leads or the presence of new Q waves.
    • Results that indicate intermediate probability of MI are ST-segment depression, T-wave inversion, and other nonspecific ST-T wave abnormalities.
    • Results that indicate low probability of MI are normal findings on ECG; however, normal or nonspecific findings on ECG do not exclude the possibility of MI.
    • Localization of MI based on distribution of ECG abnormalities is as follows:
      • Inferior wall - II, III, aVF
      • Lateral wall - I, aVL, V4 through V6
      • Anteroseptal - V1 through V3
      • Anterolateral - V1 through V6
      • Right ventricular - RV4, RV5
      • Posterior wall - R/S ratio >1 in V1 and V2; T-wave changes (ie, upright) in V1, V8, and V9

Procedures

  • Percutaneous coronary interventions (PCIs) are a group of catheter-based technologies used to establish coronary reperfusion. Angiography provides essential knowledge of the extent of coronary disease and is performed prior to PCI. PCI may then be performed as a primary intervention or as an intervention after thrombolysis failure. Evidence suggests that primary PCI is more effective than thrombolysis and should be performed for confirmed STEMI, new or presumably new left bundle-branch block (LBBB), severe congestive heart failure, or pulmonary edema if it can be performed within 12 hours of symptom onset. Door-to-balloon time should be 90 minutes or less.
    • Percutaneous transluminal coronary angioplasty (PTCA) (balloon angioplasty) is the primary therapeutic modality used at centers where it can provide reperfusion as quickly as fibrinolytic therapy. In other centers, it is used selectively for patients failing to respond to thrombolytics.
    • PCI has fewer bleeding complications and recurrent ischemia when compared with thrombolysis. PCI restores coronary artery patency in more than 90% of patients.
    • A drawback of PCI is the need for 24-hour availability of an angioplasty suite with the required staff and the availability of backup cardiothoracic capabilities. Primary PCI for STEMI should be performed at hospitals with readily available cardiothoracic surgery. Readily available may be defined as the ability to transport patients quickly to a hospital with cardiothoracic capabilities.
  • Coronary artery bypass graft may be indicated based on angiographic findings.
  • Morbidity and mortality from MI are significantly reduced if patients and bystanders recognize symptoms early, activate the EMS system, and thereby shorten the time to definitive treatment. Trained prehospital personnel can provide life-saving interventions if the patient develops cardiac arrest. The key to improved survival is the availability of early defibrillation. Approximately 1 in every 300 patients with chest pain transported to the ED by private vehicle goes into cardiac arrest en route. Several studies have confirmed that patients with STEMI usually do not call 911; in one study, only 23% of patients with a confirmed coronary event used EMS.

Date: 2015-01-12; view: 1169


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