- Sudden injury to the myocardium resulting from decreased coronary perfusion
- Heaviness, pressure, squeezing, or tightness in the chest for > 30 min
- Discomfort radiates to arms, neck, or jaw
- Diaphoresis, nausea, emesis
- Dyspnea
- Dizziness
- Arrhythmia, cardiac arrest
- Almost always caused by thrombotic occlusion
- Most elderly patients present with shortness of breath, and many present with dizziness or symptoms of arrhythmia
- In one fourth of patients, symptoms are mild or absent
- Esophagitis
- Pulmonary embolism
- Aortic dissection
- Spontaneous pneumothorax
- Pericarditis
- Cholecystitis
Clinical Definition of MI (American College of Cardiology)
- Acute, evolving, or recent MI
- Biochemical markers of myocardial necrosis (i.e.,
typical rise and gradual fall of troponin or more rapid rise and fall of
creatine kinase–myocardial band [CK-MB]) with at least one of the
following:
- Ischemic symptoms
- Development of pathologic Q waves on the ECG
- ECG changes indicative of ischemia (i.e., ST segment elevation or depression)
- Coronary artery intervention (e.g., primary coronary angioplasty)
- Pathologic findings of an acute MI
- Biochemical markers of myocardial necrosis (i.e.,
typical rise and gradual fall of troponin or more rapid rise and fall of
creatine kinase–myocardial band [CK-MB]) with at least one of the
following:
- Established MI
- Development of new pathologic Q waves on serial ECGs; patient may or may not remember previous symptoms; biochemical markers of myocardial necrosis may have normalized, depending on the length of time that has passed since the infarct developed
- Pathologic findings of a healed or healing MI
- History and physical exam are useful for excluding other causes of chest pain rather than confirming MI
- Vital signs often normal, but sinus tachycardia may be present
- Patient may be anxious and distressed
- Hypertension or hypotension may be present
- Pulse may be rapid or slow
- Lung exam is typically normal
- Cardiac exam may reveal dyskinetic apical pulsation, third or fourth heart sound, murmur of ischemic mitral regurgitation, abnormal splitting of second heart sound
- Hypertension or hypotension may be present
ECG
- Elevated ST segment indicates > 90% likelihood of MI and high risk of mortality
- CK-MB assays: lack specificity, because CK and CK-MB levels require ≥ 3 hr of profound ischemia to rise
- Myoglobin level: rises more rapidly than CK but also lacks specificity
- Troponin level: cardiac-specific; elevated level predicts subsequent cardiac events
- Echocardiography: treatment should not be delayed for echocardiography when symptoms and ECG indicate acute MI; may be useful in patients with left bundle branch block or abnormal ECGs without ST segment elevation whose symptoms are atypical and in whom the diagnosis is uncertain
- Radionuclide imaging: sensitive and specific for MI
- Generally recommended before discharge from the hospital to assess functional capacity and ability to return to activities of daily living and work
- Contraindications: spontaneous postinfarction angina, congestive heart failure, hypotension, malignant ventricular arrhythmia; perform coronary angiography instead
- Patients who have received thrombolytic therapy: recommended only for those with hemodynamic instability or those with spontaneous or exercise-induced ischemia following uncomplicated MI
- Patients who have not received thrombolytic therapy: may be helpful for those with hemodynamic compromise, postinfarction chest pain, or possible multivessel disease or reduced ventricular function
Emergent Therapy
- Evaluate symptomatic patients < 10 min after arrival in ER
- Avoid delay in treatment
- Assess heart rate and BP
- Perform 12-lead ECG
- Administer oxygen for the first several hours after admission
- Administer analgesia immediately
- Administer aspirin as soon as MI is diagnosed, and continue indefinitely
- Administer sublingual nitroglycerin if BP > 90 mm Hg
- Admit to hospital with continuous ECG monitoring
- Admit high-risk patients to CCU
- Best therapy achieves coronary patency most rapidly, depending on the capabilities of the institution
- Should be administered < 60 min after presentation, < 30 min if possible
- Indications
- ST segment elevation in ≥ 2 leads and < 12 hr of chest pain
- Classic symptoms of infarction and a bundle branch block that precludes detection of ST segment elevation
- 6–12 hr of chest pain on presentation
- Contraindications
- Significant bleeding
- Risk of intracerebral bleeding (e.g., advanced age, low body weight, hypertension, warfarin use, previous stroke, GI bleeding, recent surgery)
- Thrombolytic agents
- Front-loaded, weight-adjusted t-PA and I.V. heparin: moderately superior to other thrombolytic regimens but much more expensive; associated with a greater frequency of intracerebral hemorrhage than streptokinase
- Streptokinase and I.V. heparin: contraindicated in patients who have recently received a dose of streptokinase
- Streptokinase and subcutaneous heparin
- Combination of I.V. t-PA and streptokinase given concurrently with I.V. heparin
- Reteplase (recombinant t-PA): given as two boluses, together with aspirin and I.V. heparin; as effective as t-PA
- Combination therapy: a thrombolytic agent plus a glycoprotein IIb/IIIa inhibitor; not currently indicated
- Preferred therapy for acute MI at institutions where it can be performed without delay; associated with lower morbidity and mortality than thrombolytic therapy alone
- Alternative treatment strategy for patients with ST segment elevation MI initially assessed at a hospital without on-site cardiac surgery facilities
- Combined use of stents and platelet glycoprotein inhibitors may normalize antegrade blood flow and reduce need for repeat procedures the following year
- Achieves reperfusion more slowly than thrombolytic therapy and primary coronary angioplasty
- Should be reserved for patients in whom primary coronary angioplasty is precluded or has failed and those with a ventricular septal defect, severe mitral regurgitation, or myocardial rupture
- I.V. heparin: recommended for patients with suspected MI who are not treated with thrombolytics; should be discontinued > 24 hr before discharge
- Low-molecular-weight heparin: may be as effective as unfractionated heparin; optimal dose is unknown; avoid in renal failure
- Direct thrombin inhibitors: bivalirudin may reduce incidence of reinfarction but has been associated with increased bleeding events
- Beta blockers: recommended for all patients with acute MI and without contraindications as early as possible, whether or not they receive reperfusion therapy; patients with the largest infarctions benefit the most; continue indefinitely in the absence of contraindications or side effects
- ACE inhibitors: use in all patients with significant ventricular dysfunction (i.e., ejection fraction < 40%) contraindications; begin within the first 48 hr of infarction and increase cautiously to avoid hypotension
- I.V. nitroglycerin: indicated in patients with persistent/recurrent chest pain after reperfusion therapy and those who do not receive reperfusion therapy
- Prophylactic antiarrhythmic therapy: not recommended for patients without malignant ventricular ectopy
- Calcium channel antagonists: indicated in patients with ischemia that persists despite use of aspirin, beta blockers, nitrate therapy, and I.V. heparin
- Magnesium: indicated in patients with MI who have torsade de pointes–type ventricular tachycardia and those with magnesium deficiency
- Measure cholesterol < 24 hr after presentation; prescribe HMG-CoA reductase inhibitors for those patients with LDL level ≥ 130 mg/dl
- Exercise
- Weight reduction in overweight patients
- Avoidance of dietary saturated fat and cholesterol
- Smoking cessation
- Dose: 81–162 mg
- When used before discharge, can help identify patients at increased risk for sudden cardiac death
- Routine antiarrhythmic therapy not recommended
- Treatment of hypertension and hypercholesterolemia
- Smoking cessation
- Cardiac rehabilitation
- Exercise program