Myocardial infarction: Difference between revisions
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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".<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. | |||
{{seealso|Acute coronary syndrome}} | {{seealso|Acute coronary syndrome}} | ||
The prevalence and severity of myocardial infarctions have decreased over the decades.<ref name="pmid20142444">{{cite journal| author=Roger VL, Weston SA, Gerber Y, Killian JM, Dunlay SM, Jaffe AS et al.| title=Trends in incidence, severity, and outcome of hospitalized myocardial infarction. | journal=Circulation | year= 2010 | volume= 121 | issue= 7 | pages= 863-9 | pmid=20142444 | The prevalence and severity of myocardial infarctions have decreased over the decades.<ref name="pmid20142444">{{cite journal| author=Roger VL, Weston SA, Gerber Y, Killian JM, Dunlay SM, Jaffe AS et al.| title=Trends in incidence, severity, and outcome of hospitalized myocardial infarction. | journal=Circulation | year= 2010 | volume= 121 | issue= 7 | pages= 863-9 | pmid=20142444 | ||
| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&email=badgett@uthscdsa.edu&retmode=ref&cmd=prlinks&id=20142444 | doi=10.1161/CIRCULATIONAHA.109.897249 | pmc=PMC2827641 }} <!--Formatted by http://sumsearch.uthscsa.edu/cite/--></ref> | | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&email=badgett@uthscdsa.edu&retmode=ref&cmd=prlinks&id=20142444 | doi=10.1161/CIRCULATIONAHA.109.897249 | pmc=PMC2827641 }} <!--Formatted by http://sumsearch.uthscsa.edu/cite/--></ref> | ||
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===Laboratory tests=== | ===Laboratory tests=== | ||
{{main|Troponin}} | {{main|Troponin}} | ||
[[Clinical practice guideline]]s 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.<ref name="pmid17692738" | [[Clinical practice guideline]]s 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.<ref name="pmid17692738" /> | ||
Still accepted, although less sensitive and specific than troponins, is the MB isoenzyme of [[creatine kinase]]. Urine [[myoglobin]] is a supplementary, sensitive, but not specific test. | Still accepted, although less sensitive and specific than troponins, is the MB isoenzyme of [[creatine kinase]]. Urine [[myoglobin]] is a supplementary, sensitive, but not specific test. | ||
| Line 79: | Line 79: | ||
==Treatment== | ==Treatment== | ||
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. | 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. | ||
Cell therapy: | |||
* Bone marrow cell (BMC), delivered | |||
** Intracoronary administration | |||
** Endomyocardial injection | |||
** Transendocardial injection | |||
* Skeletal myoblast | |||
===NSTEMI=== | ===NSTEMI=== | ||
[[Clinical practice guideline]]s by the [[American Heart Association]] address the treatment of NSTEMI.<ref>{{Cite journal | [[Clinical practice guideline]]s by the [[American Heart Association]] address the treatment of NSTEMI.<ref>{{Cite journal | ||
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|pmid=19923169 | |pmid=19923169 | ||
| url = http://circ.ahajournals.org/cgi/content/abstract/CIRCULATIONAHA.109.192663v1 | | url = http://circ.ahajournals.org/cgi/content/abstract/CIRCULATIONAHA.109.192663v1 | ||
}}</ref><ref name="pmid17692738" | }}</ref><ref name="pmid17692738" /> | ||
====Medications==== | ====Medications==== | ||
=====Adrenergic beta-antagonists===== | =====Adrenergic beta-antagonists===== | ||
According to the [[clinical practice guideline]]s of the American College of Cardiology/American Heart Association, [[adrenergic beta-antagonist]]s (beta-blockers, "should begin within a few days of the event, if not initiated acutely, and should be continued indefinitely."<ref name="pmid17692738" | According to the [[clinical practice guideline]]s of the American College of Cardiology/American Heart Association, [[adrenergic beta-antagonist]]s (beta-blockers, "should begin within a few days of the event, if not initiated acutely, and should be continued indefinitely."<ref name="pmid17692738" /> | ||
=====Platelet ADP receptor blockers===== | =====Platelet ADP receptor blockers===== | ||
| Line 149: | Line 157: | ||
==References== | ==References== | ||
{{reflist|2}} | {{reflist|2}}[[Category:Suggestion Bot Tag]] | ||
Latest revision as of 12:00, 22 September 2024
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".[1] The coronary arteries are the blood vessels that supply the heart muscle.
- See also: Acute coronary syndrome
The prevalence and severity of myocardial infarctions have decreased over the decades.[2]
Pathophysiology
Most myocardial infarctions are due to atherosclerosis. However, usually infarction occur where stenoses are less than 70%.[3]
Stunned myocardium
The area of damage in the heart that results from decreased blood supply is usually larger than the infarct.[4] 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[6] | |
|---|---|---|---|
| Non-ST segment elevation myocardial infarction (NSTEMI) |
"ST-segment depression or prominent T-wave inversion"[5] | 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.[5] NSTEMI is usually caused by a grayish-white thrombus that is platelet-rich.[6]
- Secondary
Secondary NSTEMI may be due to:[5]
- "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.[6] Most of these patients progress to a Q-wave myocardial infarction.[5]
Q-wave myocardial infarction
A q-wave infarction is a transmural infarction and is usually caused by occlusion of an epicardial coronary artery.[7]
Diagnosis
There is no single test that will confirm or rule out MI. Multiple tests, but above all, clinical judgment, are necessary.
History
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.
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.[8]
Reduction on pain on administration of nitroglycerin is strongly suggestive of coronary disease, although relief is more striking with angina pectoris than with an MI.
Electrocardiography
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.
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.[5]
Still accepted, although less sensitive and specific than troponins, is the MB isoenzyme of creatine kinase. Urine myoglobin is a supplementary, sensitive, but not specific test.
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.
Treatment
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.
Cell therapy:
- Bone marrow cell (BMC), delivered
- Intracoronary administration
- Endomyocardial injection
- Transendocardial injection
- Skeletal myoblast
NSTEMI
Clinical practice guidelines by the American Heart Association address the treatment of NSTEMI.[9][10][5]
Medications
Adrenergic beta-antagonists
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."[5]
Platelet ADP receptor blockers
Thienopyridine ADP blockers such as clopidogrel, ticlopidine, and the prodrug prasugrel may help especially for patients undergoing percutaneous coronary intervention (PCI).
Glycoprotein IIb/IIIa inhibitors
Glycoprotein IIb/IIIa inhibitors (GPIs) may be helpful.
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."[5] 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.[11][12] 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.[13]
STEMI
Clinical practice guidelines by the American College of Chest Physicians address management of STEMI.[14]
Medications
Platelet ADP receptor blockers
Thienopyridine ADP blockers such as clopidogrel, ticlopidine, and the prodrug prasugrel may help especially for patients undergoing percutaneous coronary intervention (PCI).
Platelet glycoprotein IIb/IIIa inhibitors
Glycoprotein IIb/IIIa inhibitors (GPIs) may be helpful.
Invasive treatment
Percutaneous transluminal coronary angioplasty with stenting has less restenosis than angioplasty alone according to the CADILLAC randomized controlled trial.[15]
Primary angioplasty is better than thrombolysis if the angioplasty can be performed with less than a 90 minute delay.[16]
Non-beneficial treatments
Glucose-insulin-potassium
Glucose-insulin-potassium (GIK) infusion does not benefit patients according to a randomized controlled trial.[17] However, there are concerns about the design of the trial.[18]
Historical treatments
Prior to the availability of percutaneous transluminal coronary angioplasty, treatment at home had similar efficacy to hospitalization.[19]
Complications
Dysrhythmia
Pump Failure
References
- ↑ National Library of Medicine. Myocardial infarction. Retrieved on 2007-10-28.
- ↑ Roger VL, Weston SA, Gerber Y, Killian JM, Dunlay SM, Jaffe AS et al. (2010). "Trends in incidence, severity, and outcome of hospitalized myocardial infarction.". Circulation 121 (7): 863-9. DOI:10.1161/CIRCULATIONAHA.109.897249. PMID 20142444. PMC PMC2827641. Research Blogging.
- ↑ Little WC, Constantinescu M, Applegate RJ, Kutcher MA, Burrows MT, Kahl FR et al. (1988). "Can coronary angiography predict the site of a subsequent myocardial infarction in patients with mild-to-moderate coronary artery disease?". Circulation 78 (5 Pt 1): 1157-66. PMID 3180375. [e]
- ↑ 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]
- ↑ 5.0 5.1 5.2 5.3 5.4 5.5 5.6 5.7 5.8 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
- ↑ 6.0 6.1 6.2 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.
- ↑ Kushner, Frederick G.; Mary Hand, Sidney C. Smith, Spencer B. King, Jeffrey L. Anderson, Elliott M. Antman, Steven R. Bailey, Eric R. Bates, James C. Blankenship, Donald E. Casey, Lee A. Green, Judith S. Hochman, Alice K. Jacobs, Harlan M. Krumholz, Douglass A. Morrison, Joseph P. Ornato, David L. Pearle, Eric D. Peterson, Michael A. Sloan, Patrick L. Whitlow, David O. Williams (2009-11-18). "2009 Focused Updates: ACC/AHA Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction (Updating the 2004 Guideline and 2007 Focused Update) and ACC/AHA/SCAI Guidelines on Percutaneous Coronary Intervention (Updating the 2005 Guideline and 2007 Focused Update): A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines". J Am Coll Cardiol: j.jacc.2009.10.015. DOI:10.1016/j.jacc.2009.10.015. Retrieved on 2009-11-19. Research Blogging.
- ↑ Kushner, Frederick G.; Mary Hand, Sidney C. Smith, Spencer B. King, Jeffrey L. Anderson, Elliott M. Antman, Steven R. Bailey, Eric R. Bates, James C. Blankenship, Donald E. Casey, Lee A. Green, Judith S. Hochman, Alice K. Jacobs, Harlan M. Krumholz, Douglass A. Morrison, Joseph P. Ornato, David L. Pearle, Eric D. Peterson, Michael A. Sloan, Patrick L. Whitlow, David O. Williams (2009-11-18). "2009 Focused Updates: ACC/AHA Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction (Updating the 2004 Guideline and 2007 Focused Update) and ACC/AHA/SCAI Guidelines on Percutaneous Coronary Intervention (Updating the 2005 Guideline and 2007 Focused Update). A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines". Circulation: CIRCULATIONAHA.109.192663. DOI:10.1161/CIRCULATIONAHA.109.192663. PMID 19923169. Retrieved on 2009-11-19. Research Blogging.
- ↑ 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]
- ↑ Montalescot G, Cayla G, Collet JP, Elhadad S, Beygui F, Le Breton H et al. (2009). "Immediate vs delayed intervention for acute coronary syndromes: a randomized clinical trial.". JAMA 302 (9): 947-54. DOI:10.1001/jama.2009.1267. PMID 19724041. Research Blogging.
- ↑ 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.
- ↑ Mather HG, Morgan DC, Pearson NG, Read KL, Shaw DB, Steed GR et al. (1976). "Myocardial infarction: a comparison between home and hospital care for patients.". Br Med J 1 (6015): 925-9. PMID 1268490. PMC PMC1639298.