- 1 Pathophysiology
- 2 Classification
- 3 Diagnosis
- 4 Treatment
- 4.1 NSTEMI
- 4.2 STEMI
- 5 Complications
- 6 References
- See also: Acute coronary syndrome
A myocardial infarction, or "heart attack", is one type of acute coronary syndrome and is defined as "gross necrosis of the myocardium, as a result of interruption of the blood supply to the area". The coronary arteries are the blood vessels that supply the heart muscle.
The prevalence and severity of myocardial infarctions have decreased over the decades.
The area of damage in the heart that results from decreased blood supply is usually larger than the infarct. In other words, when the blood supply becomes inadequate (Ischemia) and the hard-working cardiac muscle cells are deprived of oxygen and nutrients, at least some of the affected muscle cells may be impaired by this loss rather than killed. By definition, if an infarct has occurred, at least some of these muscle cell have died- but many others may have become swollen or injured and yet, with restoration of the blood supply, are able to eventually recover.
|Electrocardiogram||Serum biomarkers||Typical appearance of culprit vessel at angioscopy|
| Non-ST segment elevation myocardial infarction
|"ST-segment depression or prominent T-wave inversion"||Elevated|| Primary NSTEMI: Nonocclusive grayish-white thrombus|
Secondary NSTEMI: no thrombus
| ST segment elevation myocardial infarction
|ST-segment elevation||Elevated|| Occlusive reddish thrombus |
|Q-wave myocardial infarction||Q-waves||Elevated|| Occlusive reddish thrombus |
Non-ST segment elevation myocardial infarction (NSTEMI)
Secondary NSTEMI may be due to:
- "increase myocardial oxygen requirements, such as fever, tachycardia, or thyrotoxicosis"
- "reduce coronary blood flow, such as hypotension"
- "reduce myocardial oxygen delivery, such as anemia or hypoxemia"
ST segment elevation myocardial infarction (STEMI)
Q-wave myocardial infarction
There is no single test that will confirm or rule out MI. Multiple tests, but above all, clinical judgment, are necessary.
Patients describe a wide range of symptoms, and the nature of onset. While the classic presentation includes a crushing substernal pain, pain radiating down the left arm, sweating, and anxiety, other patients could present with a sensation of pressure in the back. Many patients perceive the initial discomfort as gastrointestinal.
Recreational use of cocaine can trigger MIs even in the absence of atherosclerosis.
A helpful finding is reproduction of chest pain upon palpating the chest. In a patient whose other findings also suggest a non-cardiac course of their chest pain, this finding can help rule out coronary disease.
While the most emphatic confirmation of MI is ST segment elevation with the presence of Q waves, any ST abnormality including depression needs further evaluation. The basic QRS complex may, however, be normal in the early phases or throughout the episode.
Other electrocardiographic changes, such as runs of premature ventricular contractions in the presence of chest pain, are nonspecific, but certainly strong indicators of a need for further studies, such as troponins.
Clinical practice guidelines jointly written by multiple expert groups anchor the diagnosis on troponin blood assays obtained within 6 hours and again within 8-12 hours of a patient arriving for medical care.
In the past, elevations both in lactic dehydrogenase (LDH) and aspartate transaminase (ALT) (previously called [serum] oxalacetic transaminase] (SGOT) were the primary surrogates for destruction of the myocardium, but they are far less specific than the above methods. A refinement was separating the isoenzymes of LDH and testing for those most associated with myocardium.
Nitroglycerin, morphine and oxygen should be administered early in the workup, when there is even a strong suggestion of MI or angina. Unless there are strong contraindications such as allergy or hemorrhage, the patient should chew a 325-mg aspirin tablet.
- Bone marrow cell (BMC), delivered
- Intracoronary administration
- Endomyocardial injection
- Transendocardial injection
- Skeletal myoblast
According to the clinical practice guidelines of the American College of Cardiology/American Heart Association, adrenergic beta-antagonists (beta-blockers, "should begin within a few days of the event, if not initiated acutely, and should be continued indefinitely."
Platelet ADP receptor blockers
Glycoprotein IIb/IIIa inhibitors
Glycoprotein IIb/IIIa inhibitors (GPIs) may be helpful.
According to clinical practice guidelines, percutaneous transluminal coronary angioplasty (PTCA) is "indicated for patients with UA/NSTEMI who have no serious comorbidity and who have coronary lesions amenable to PCI and any of the high-risk features." High-risk features is later defined at "refractory angina or hemodynamic or electrical instability" or "elevated risk for clinical events" (high Thrombolysis in Myocardial Infarction (TIMI) risk score).
Among patients with unstable angina or NSTEMI, patients with ST-segment changes (e.g. depression or a transient elevation), a Thrombolysis in Myocardial Infarction (TIMI) risk score of 3 or more, elevated myocardial enzymes, and elderly patients may be most likely to benefit from invasive management (PTCA) according to the TACTICS randomized controlled trial. In patients without ST-segment elevation on the electrocardiogram, urgent angioplasty may occur anytime within the first 24 hours according to a randomized controlled trial.
Platelet ADP receptor blockers
Platelet glycoprotein IIb/IIIa inhibitors
Glycoprotein IIb/IIIa inhibitors (GPIs) may be helpful.
Primary angioplasty is better than thrombolysis if the angioplasty can be performed with less than a 90 minute delay.
- National Library of Medicine. Myocardial infarction. Retrieved on 2007-10-28.
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