Myocardial infarction: Difference between revisions
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A '''myocardial infarction''', or "heart attack", is defined as "gross necrosis of the myocardium, as a result of interruption of the blood supply to the area".<ref>{{cite web |url=http://www.nlm.nih.gov/cgi/mesh/2007/MB_cgi?mode=&term=unstable+angina |title=Myocardial infarction|author=National Library of Medicine |accessdate=2007-10-28 |format= |work=}}</ref> The [[coronary artery|coronary arteries]] are the blood vessels that supply the heart muscle. | A '''myocardial infarction''', or "heart attack", is defined as "gross necrosis of the myocardium, as a result of interruption of the blood supply to the area".<ref>{{cite web |url=http://www.nlm.nih.gov/cgi/mesh/2007/MB_cgi?mode=&term=unstable+angina |title=Myocardial infarction|author=National Library of Medicine |accessdate=2007-10-28 |format= |work=}}</ref> The [[coronary artery|coronary arteries]] are the blood vessels that supply the heart muscle. | ||
Revision as of 07:52, 30 May 2009
A myocardial infarction, or "heart attack", is defined as "gross necrosis of the myocardium, as a result of interruption of the blood supply to the area".[1] The coronary arteries are the blood vessels that supply the heart muscle.
Pathophysiology
Most myocardial infarctions are due to atherosclerosis.
Stunned myocardium
The area of damage in the heart that results from decreased blood supply is usually larger than the infarct.[2] 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.
Classification
| Electrocardiogram | Serum biomarkers | Typical appearance of culprit vessel at angioscopy[4] | |
|---|---|---|---|
| Non-ST segment elevation myocardial infarction (NSTEMI) |
"ST-segment depression or prominent T-wave inversion"[3] | Elevated | Primary NSTEMI: Nonocclusive grayish-white thrombus (platelet-rich) Secondary NSTEMI: no thrombus |
| ST segment elevation myocardial infarction (STEMI) |
ST-segment elevation | Elevated | Occlusive reddish thrombus (fibrin-rich) |
| Q-wave myocardial infarction | Q-waves | Elevated | Occlusive reddish thrombus (fibrin-rich) |
Non-ST segment elevation myocardial infarction (NSTEMI)
- Primary
NSTEMI is usually due to coronary artery narrowing.[3] NSTEMI is usually caused by a grayish-white thrombus that is platelet-rich.[4]
- Secondary
Secondary NSTEMI may be due to:[3]
- "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)
STEMI is usually caused by a reddish thrombus that is fibrin-rich.[4] Most of these patients progress to a Q-wave myocardial infarction.[3]
Q-wave myocardial infarction
A q-wave infarction is a transmural infarction and is usually caused by occlusion of an epicardial coronary artery.[5]
Diagnosis
History and physical examination
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.[6]
Laboratory tests
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.[3][7]
Treatment
NSTEMI
Clinical practice guidelines address the treatment of NSTEMI.[3]
Medications
Invasive treatment
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."[3] 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.[8][9]
STEMI
Clinical practice guidelines by the American College of Chest Physicians address management.[10]
Medications
Invasive treatment
Stenting has less restenosis that angioplasty according to the CADILLAC randomized controlled trial.[11]
Primary angioplasty is better than thrombolysis if the angioplasty can be performed with less than a 90 minute delay.[12]
Non-beneficial treatments
Glucose-insulin-potassium
Glucose-insulin-potassium (GIK) infusion does not benefit patients according to a randomized controlled trial.[13] However, there are concerns about the design of the trial.[14]
Complications
Dysrhythmia
Pump Failure
References
- ↑ National Library of Medicine. Myocardial infarction. Retrieved on 2007-10-28.
- ↑ Solomon SD, Glynn RJ, Greaves S, et al (2001). "Recovery of ventricular function after myocardial infarction in the reperfusion era: the healing and early afterload reducing therapy study". Ann. Intern. Med. 134 (6): 451–8. PMID 11255520. [e]
- ↑ 3.0 3.1 3.2 3.3 3.4 3.5 3.6 3.7 Anderson JL, Adams CD, Antman EM, et al (2007). "ACC/AHA 2007 guidelines for the management of patients with unstable angina/non-ST-Elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines for the Management of Patients With Unstable Angina/Non-ST-Elevation Myocardial Infarction) developed in collaboration with the American College of Emergency Physicians, the Society for Cardiovascular Angiography and Interventions, and the Society of Thoracic Surgeons endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation and the Society for Academic Emergency Medicine". J. Am. Coll. Cardiol. 50 (7): e1–e157. DOI:10.1016/j.jacc.2007.02.013. PMID 17692738. Research Blogging.
Executive summary Summary at National Guidelines Clearinghouse Cite error: Invalid
<ref>tag; name "pmid17692738" defined multiple times with different content Cite error: Invalid<ref>tag; name "pmid17692738" defined multiple times with different content - ↑ 4.0 4.1 4.2 Mizuno K, Satomura K, Miyamoto A, et al (January 1992). "Angioscopic evaluation of coronary-artery thrombi in acute coronary syndromes". N. Engl. J. Med. 326 (5): 287–91. PMID 1728732. [e]
- ↑ DeWood MA, Spores J, Notske R, et al (October 1980). "Prevalence of total coronary occlusion during the early hours of transmural myocardial infarction". N. Engl. J. Med. 303 (16): 897–902. PMID 7412821. [e]
- ↑ Bruyninckx R, Aertgeerts B, Bruyninckx P, Buntinx F (February 2008). "Signs and symptoms in diagnosing acute myocardial infarction and acute coronary syndrome: a diagnostic meta-analysis". Br J Gen Pract 58 (547): 105–11. DOI:10.3399/bjgp08X277014. PMID 18307844. Research Blogging.
- ↑ Braunwald E, Antman EM, Beasley JW, et al (2002). "ACC/AHA 2002 guideline update for the management of patients with unstable angina and non-ST-segment elevation myocardial infarction--summary article: a report of the American College of Cardiology/American Heart Association task force on practice guidelines (Committee on the Management of Patients With Unstable Angina)". J. Am. Coll. Cardiol. 40 (7): 1366–74. PMID 12383588. [e]
- ↑ Cannon CP, Weintraub WS, Demopoulos LA, et al (2001). "Comparison of early invasive and conservative strategies in patients with unstable coronary syndromes treated with the glycoprotein IIb/IIIa inhibitor tirofiban". N. Engl. J. Med. 344 (25): 1879-87. PMID 11419424. [e]
- ↑ Bach RG, Cannon CP, Weintraub WS, et al (2004). "The effect of routine, early invasive management on outcome for elderly patients with non-ST-segment elevation acute coronary syndromes". Ann. Intern. Med. 141 (3): 186-95. PMID 15289215. [e]
- ↑ Goodman SG, Menon V, Cannon CP, Steg G, Ohman EM, Harrington RA (June 2008). "Acute ST-segment elevation myocardial infarction: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition)". Chest 133 (6 Suppl): 708S–775S. DOI:10.1378/chest.08-0665. PMID 18574277. Research Blogging.
- ↑ Stone GW, Grines CL, Cox DA, et al (2002). "Comparison of angioplasty with stenting, with or without abciximab, in acute myocardial infarction". N. Engl. J. Med. 346 (13): 957-66. DOI:10.1056/NEJMoa013404. PMID 11919304. Research Blogging.
- ↑ Asseburg C, Vergel YB, Palmer S, et al (2007). "Assessing the effectiveness of primary angioplasty compared with thrombolysis and its relationship to time delay: a Bayesian evidence synthesis". Heart 93 (10): 1244–50. DOI:10.1136/hrt.2006.093336. PMID 17277350. Research Blogging.
- ↑ Mehta SR, Yusuf S, Díaz R, et al (2005). "Effect of glucose-insulin-potassium infusion on mortality in patients with acute ST-segment elevation myocardial infarction: the CREATE-ECLA randomized controlled trial". JAMA 293 (4): 437–46. DOI:10.1001/jama.293.4.437. PMID 15671428. Research Blogging.
- ↑ Cobb LA, Killip T, Lambrew CT, et al (2005). "Glucose-insulin-potassium infusion and mortality in the CREATE-ECLA trial". JAMA 293 (21): 2597; author reply 2598. DOI:10.1001/jama.293.21.2597-a. PMID 15928278. Research Blogging.