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{{Infobox_Disease |
__NOTOC__
  Name          = Myocardial infarction|
{{ST elevation myocardial infarction}}
  Image          = |
{{CMG}}; {{AE}} {{CZ}}
  Caption        = |
  DiseasesDB    = 8664 |
  ICD10          = {{ICD10|I|21||i|20}}-{{ICD10|I|22||i|20}} |
  ICD9          = {{ICD9|410}} |
  ICDO          = |
  OMIM          = |
  MedlinePlus    = 000195 |
  eMedicineSubj  = med |
  eMedicineTopic = 1567 |
  eMedicine_mult = {{eMedicine2|emerg|327}} {{eMedicine2|ped|2520}} |
  MeshID        = |
}}


'''For patient information click [[Heart attack (patient information)|here]]'''
==Overview==
 
In these chapters on ST elevation, the word risk factors refers to those epidemiologic and genetic variables that expose someone to a higher risk of developing atherosclerotic plaque.  The word triggers refer to those factors in the patients immediate history or environment that may have lead to rupture of the atherosclerotic plaque.
{{SI}}
{{WikiDoc Cardiology Network Infobox}}
{{CMG}}
 
'''Associate Editors-In-Chief:''' {{CZ}}
 
{{EH}}
 
==Risk factors vs Triggers of ST elevation MI==
 
In these chapters on ST elevation, the word ''risk factors'' refers to those epidemiologic and genetic variables that expose someone to a higher risk of developing atherosclerotic plaque.  The word ''Triggers'' refer to those factors in the patients immediate history or environment that may have lead to rupture of the atherosclerotic plaque.  Several [[ST elevation myocardial infarction triggers|triggers]] have been associated with an increased risk of developing ST elevation myocardial infarction (STEMI). These triggers include physical exertion, psychological stress, sexual activity, diurnal (daily) variations in cortisol and platelet aggregation and circannual (yearly) variations in lipids and infectious etiologies, exposure to pollution and or particulate matter, cocaine and ingestion of a recent fatty meal.


==Nomenclature==
Muller et al have developed the following nomenclature to categorize and analyze data pertaining to triggers of MI <ref name="pmid8113568">{{cite journal |author=Muller JE, Abela GS, Nesto RW, Tofler GH |title=Triggers, acute risk factors and vulnerable plaques: the lexicon of a new frontier |journal=J. Am. Coll. Cardiol. |volume=23 |issue=3 |pages=809–13 |year=1994 |month=March |pmid=8113568 |doi= |url=}}</ref>:
Muller et al have developed the following nomenclature to categorize and analyze data pertaining to triggers of MI <ref name="pmid8113568">{{cite journal |author=Muller JE, Abela GS, Nesto RW, Tofler GH |title=Triggers, acute risk factors and vulnerable plaques: the lexicon of a new frontier |journal=J. Am. Coll. Cardiol. |volume=23 |issue=3 |pages=809–13 |year=1994 |month=March |pmid=8113568 |doi= |url=}}</ref>:


:(1) '''Trigger:''' An activity that produces short-term physiological changes that may lead directly to onset of acute CVD.
:(1) Trigger: An activity that produces short-term physiological changes that may lead directly to onset of acute CVD.


:(2) '''Acute risk factor:''' A short-term physiological change, such as a surge in arterial pressure or heart rate, an increase in coagulability, or vasoconstriction, that follows a trigger and may result in disease onset.
:(2) Acute risk factor: A short-term physiological change, such as a surge in arterial pressure or heart rate, an increase in coagulability, or vasoconstriction, that follows a trigger and may result in disease onset.


:(3) '''Hazard period:''' The time interval after trigger initiation associated with an increased risk of disease onset because of the trigger. The onset and offset times of the hazard period, which could also be designated a “vulnerable period,” may be sharply defined, as in heavy exertion, or less well defined, as with respiratory infection. The duration of the hazard period may also vary, eg from < 1 hour during heavy physical exertion to weeks or months with bereavement.
:(3) Hazard period: The time interval after trigger initiation associated with an increased risk of disease onset because of the trigger. The onset and offset times of the hazard period, which could also be designated a “vulnerable period,” may be sharply defined, as in heavy exertion, or less well defined, as with respiratory infection. The duration of the hazard period may also vary, eg from < 1 hour during heavy physical exertion to weeks or months with bereavement.


:(4) '''Triggered acute risk prevention (TARP):''' Cardiovascular risk reduction that focuses on the short-term increase in risk associated with a trigger.
:(4) Triggered acute risk prevention (TARP): Cardiovascular risk reduction that focuses on the short-term increase in risk associated with a trigger.


===Traditional risk factors for atherosclerosis===
==Risk Factors==
===Traditional Risk Factors for Atherosclerosis<ref name="pmid11368702">{{cite journal |author= |title=Executive Summary of The Third Report of The National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, And Treatment of High Blood Cholesterol In Adults (Adult Treatment Panel III) |journal=JAMA |volume=285 |issue=19 |pages=2486–97|year=2001 |month=May |pmid=11368702 |doi= |url=http://jama.ama-assn.org/cgi/pmidlookup?view=long&pmid=11368702}}</ref>===
Risk factors for [[atherosclerosis]] are generally risk factors for myocardial infarction:
Risk factors for [[atherosclerosis]] are generally risk factors for myocardial infarction:
*Advancing age
*Advancing age
Line 50: Line 29:
*Elevated [[homocysteine]]
*Elevated [[homocysteine]]


 
===Genetic Disorders===
===Genetic disorders===
*Mendelian inherited conditions
*Mendelian inherited conditions
:[[Familial mixed hyperlipidaemia]]
:[[Familial mixed hyperlipidaemia]]
Line 61: Line 39:
:[[Sitosterolemia]]
:[[Sitosterolemia]]


====Family history and heart disease====
====Family History and Heart Disease====
According to present trends in the United States, half of healthy  40-year-old  males and 1 in 3 healthy 40-year-old women will develop coronary artery disease (CAD) in the future.<ref>{{cite journal |author=Rosamond W, Flegal K,  Friday G |title=Heart disease and stroke statistics--2007 update: a  report from the American Heart Association Statistics Committee and  Stroke Statistics Subcommittee |journal=Circulation |volume=115 |issue=5  |pages=e69–171 |year=2007 |month=February |pmid=17194875  |doi=10.1161/CIRCULATIONAHA.106.179918 |url=http://circ.ahajournals.org/cgi/content/full/115/5/e69/TBL3179728}}</ref> This chance  is greater when a family history of heart disease is involved.  
According to present trends in the United States, ''half'' of healthy  40-year-old  males and 1 in 3 healthy 40-year-old women will develop [[coronary artery disease]] (CAD) in the future.<ref>{{cite journal |author=Rosamond W, Flegal K,  Friday G |title=Heart disease and stroke statistics--2007 update: a  report from the American Heart Association Statistics Committee and  Stroke Statistics Subcommittee |journal=Circulation |volume=115 |issue=5  |pages=e69–171 |year=2007 |month=February |pmid=17194875  |doi=10.1161/CIRCULATIONAHA.106.179918 |url=http://circ.ahajournals.org/cgi/content/full/115/5/e69/TBL3179728}}</ref> This chance  is greater when a [[family history]] of [[heart disease]] is involved.  
 
Studies  have reported that the risk of CAD increases two- to sevenfold when  there is a genetic link. <ref>{{cite journal |author=Khaw KT, Barrett-Connor E |title=Family  history of heart attack: a modifiable risk factor? |journal=Circulation  |volume=74  |issue=2  |pages=239–44  |year=1986  |month=August  |pmid=3731415  |doi=  |url=}}</ref>  The studies by Nora and Nora (1978a) evaluated a large number of  patients with congenital heart disease. Results show that about 8% of  the defects were primarily genetics-related, 2% were environmental  (caused by drugs, viruses, maternal nutrition, maternal metabolism, or  fetal  hemodynamics) and 90% were multifactorial (due to a combination of  environmental and genetic factors). The study also noted that there is a  two- to threefold increase in the recurrence risk for congenital heart  disease when two of the family members are affected. This is  particularly the case when the parent is severely affected or when the  affected members are child and parent. Second cousins have a 1 in 23  chance of sharing a particular gene and third cousins have a 1 in 128  likelihood. <ref>http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=cm&part=A540#A556</ref>
 
===Endocrine conditions===
 
[[Diabetes]] mellitus type 2
[[Primary hyperparathyroidism]]


===Rheumatologic and Autoimmune conditions===
Studies have reported that the risk of [[CAD]] increases ''two- to sevenfold'' when there is a genetic link. <ref>{{cite journal |author=Khaw KT, Barrett-Connor E |title=Family  history of heart attack: a modifiable risk factor? |journal=Circulation  |volume=74  |issue=2  |pages=239–44  |year=1986  |month=August  |pmid=3731415  |doi=  |url=}}</ref>  The studies by Nora and Nora (1978a) evaluated a large number of  patients with [[congenital heart disease]].<ref>http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=cm&part=A540#A556</ref> Results show that about '''8%''' of the defects were primarily genetics-related, 2% were environmental (caused by drugs, viruses, maternal nutrition, maternal metabolism, or fetal [[hemodynamics]]) and '''90%''' were multifactorial (due to a combination of environmental and genetic factors). The study also noted that there is a ''two- to threefold increase'' in the recurrence risk for [[congenital heart disease]] when two of the family members are affected. This is particularly the case when the parent is severely affected or when the affected members are child and parent. The risk for a [[myocardial infarction]] is ''two to three times greater'' in a first-degree relative than in a person with no [[family history]] of [[heart disease]]. This fact speaks in particular to the early presentation of [[CAD]] in patients with no other risk factors. Second cousins have a ''1 in 23'' chance of sharing a particular [[gene]] and third cousins have a ''1 in 128'' likelihood.


[[Systemic lupus erythematosus]]
Genetic [[hypertension]] and [[hyperlipidemia]] are strong predictors of familial [[heart disease]].<ref>http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=cm&part=A540#A556</ref> Hypertensive people are ''twice as likely'' to have a [[family history]] of the condition than are normotensives. Genetic [[hypertension]] is an example of a polygenic mode of inheritance that reflects cellular sodium transport defects and an abnormal response to psychogenic stress. There is indication that [[Pheochromocytoma]], a rare cause of [[hypertension]], may be familial as well.


==Risk factor modification==
====Endocrine Conditions====
While family history, along with age and sex, is uncontrollable<ref name="Framingham1998"/>,
* [[Diabetes]] mellitus type 2 ([[NIDDM]])
many of the risk factors for heart disease can be eliminated by maintaining a healthy lifestyle. These modifiable
* [[Primary hyperparathyroidism]]
risk factors include: obesity, blood pressure, cigarette smoking and plasma cholesterol.<ref>{{cite  journal |author=Khaw KT, Barrett-Connor E |title=Family  history of heart attack: a modifiable risk factor? |journal=Circulation  |volume=74  |issue=2   |pages=239–44  |year=1986  |month=August  |pmid=3731415  |doi=  |url=}}</ref> 


A study published in Circulation shines some light on the  importance of eliminating these controllable risk factors in people with  a family history
====Rheumatologic and Autoimmune Conditions====
of heart disease. Data demonstrated that in men with a  genetic link to heart disease, an estimated 68% of the
* [[Systemic lupus erythematosus]] ([[SLE]])
excess deaths  were due to the addition of smoking, a modifiable risk factor;  concluding that the risk of heart
disease in men with a family  history of the condition is significantly related to the additional risk  factors he
accumulates.


==Socioeconomic factors==
===Socioeconomic Factors===
Socioeconomic factors such as a shorter education and lower income (particularly in women), and living with a partner may also contribute to the risk of MI.<ref name="Nyboe-1989">{{cite journal | author=Nyboe J, Jensen G, Appleyard M, Schnohr P. | title=Risk factors for acute myocardial infarction in Copenhagen. I: Hereditary, educational and socioeconomic factors. Copenhagen City Heart Study. | journal=Eur Heart J | year=1989 | volume=10 | issue=10 | pages=910-6 | id=PMID 2598948}}</ref>  To understand epidemiological study results, it's important to note that many factors associated with MI mediate their risk via other factors. For example, the effect of education is partially based on its effect on income and marital status.<ref name="Nyboe-1989"/>
Socioeconomic factors such as a shorter education and lower income (particularly in women), and living with a partner may also contribute to the risk of MI.<ref name="Nyboe-1989">{{cite journal | author=Nyboe J, Jensen G, Appleyard M, Schnohr P. | title=Risk factors for acute myocardial infarction in Copenhagen. I: Hereditary, educational and socioeconomic factors. Copenhagen City Heart Study. | journal=Eur Heart J | year=1989 | volume=10 | issue=10 | pages=910-6 | id=PMID 2598948}}</ref>  To understand epidemiological study results, it's important to note that many factors associated with MI mediate their risk via other factors. For example, the effect of education is partially based on its effect on income and marital status.<ref name="Nyboe-1989"/>


Line 95: Line 62:
Inflammation in [[Periodontium|periodontal]] disease may be linked coronary heart disease, and since [[periodontitis]] is very common, this could have great consequences for [[public health]].<ref name="Janket-2003">{{cite journal | author=Janket SJ, Baird AE, Chuang SK, Jones JA. | title=Meta-analysis of periodontal disease and risk of coronary heart disease and stroke. | journal=Oral Surg Oral Med Oral Pathol Oral Radiol Endod. | year=2003 | volume=95 | issue=5 | pages=559-69 | id=PMID 12738947}}</ref>  [[Serology|Serological]] studies measuring [[antibody]] levels against typical periodontitis-causing [[bacteria]] found that such antibodies were more present in subjects with coronary heart disease.<ref name="Pihlstrom-2005">{{cite journal | author=Pihlstrom BL, Michalowicz BS, Johnson NW. | title=Periodontal diseases. | journal=Lancet | year=2005 | volume=366 | issue=9499 | pages=1809-20 | id=PMID 16298220}}</ref>  Periodontitis tends to increase blood levels of CRP, [[fibrinogen]] and [[cytokines]];<ref name="Scannapieco-2003">{{cite journal | author=Scannapieco FA, Bush RB, Paju S. | title=Associations between periodontal disease and risk for atherosclerosis, cardiovascular disease, and stroke. A systematic review. | journal=Ann Periodontol | year=2003 | volume=8 | issue=1 | pages=38-53 | id=PMID 14971247}}</ref>  thus, periodontitis may mediate its effect on MI risk via other risk factors.<ref name="D'Aiuto-2006">{{cite journal | author=D'Aiuto F, Parkar M, Nibali L, Suvan J, Lessem J, Tonetti MS. | title=Periodontal infections cause changes in traditional and novel cardiovascular risk factors: results from a randomized controlled clinical trial. | journal=Am Heart J | year=2006 | volume=151 | issue=5 | pages=977-84 | id=PMID 16644317}}</ref>  [[Medical research|Preclinical research]] suggests that periodontal bacteria can promote aggregation of [[platelets]] and promote the formation of [[foam cell]]s.<ref name="Lourbakos-2001">{{cite journal | author=Lourbakos A, Yuan YP, Jenkins AL, Travis J, Andrade-Gordon P, Santulli R, Potempa J, Pike RN. | title=Activation of protease-activated receptors by gingipains from Porphyromonas gingivalis leads to platelet aggregation: a new trait in microbial pathogenicity. | journal=Blood | year=2001 | volume=97 | issue=12 | pages=3790-7 | format=PDF | url=http://bloodjournal.hematologylibrary.org/cgi/reprint/97/12/3790.pdf | id=PMID 11389018}}</ref><ref name="Qi-2003">{{cite journal | author=Qi M, Miyakawa H, Kuramitsu HK. | title=Porphyromonas gingivalis induces murine macrophage foam cell formation. | journal=Microb Pathog | year=2003 | volume=35 | issue=6 | pages=259-67 | id=PMID 14580389}}</ref>  A role for specific periodontal bacteria has been suggested but remains to be established.<ref name="Spahr-2006">{{cite journal | author=Spahr A, Klein E, Khuseyinova N, Boeckh C, Muche R, Kunze M, Rothenbacher D, Pezeshki G, Hoffmeister A, Koenig W. | title=Periodontal infections and coronary heart disease: role of periodontal bacteria and importance of total pathogen burden in the Coronary Event and Periodontal Disease (CORODONT) study. | journal=Arch Intern Med | year=2006 | volume=166 | issue=5 | pages=554-9 | id=PMID 16534043}}</ref>
Inflammation in [[Periodontium|periodontal]] disease may be linked coronary heart disease, and since [[periodontitis]] is very common, this could have great consequences for [[public health]].<ref name="Janket-2003">{{cite journal | author=Janket SJ, Baird AE, Chuang SK, Jones JA. | title=Meta-analysis of periodontal disease and risk of coronary heart disease and stroke. | journal=Oral Surg Oral Med Oral Pathol Oral Radiol Endod. | year=2003 | volume=95 | issue=5 | pages=559-69 | id=PMID 12738947}}</ref>  [[Serology|Serological]] studies measuring [[antibody]] levels against typical periodontitis-causing [[bacteria]] found that such antibodies were more present in subjects with coronary heart disease.<ref name="Pihlstrom-2005">{{cite journal | author=Pihlstrom BL, Michalowicz BS, Johnson NW. | title=Periodontal diseases. | journal=Lancet | year=2005 | volume=366 | issue=9499 | pages=1809-20 | id=PMID 16298220}}</ref>  Periodontitis tends to increase blood levels of CRP, [[fibrinogen]] and [[cytokines]];<ref name="Scannapieco-2003">{{cite journal | author=Scannapieco FA, Bush RB, Paju S. | title=Associations between periodontal disease and risk for atherosclerosis, cardiovascular disease, and stroke. A systematic review. | journal=Ann Periodontol | year=2003 | volume=8 | issue=1 | pages=38-53 | id=PMID 14971247}}</ref>  thus, periodontitis may mediate its effect on MI risk via other risk factors.<ref name="D'Aiuto-2006">{{cite journal | author=D'Aiuto F, Parkar M, Nibali L, Suvan J, Lessem J, Tonetti MS. | title=Periodontal infections cause changes in traditional and novel cardiovascular risk factors: results from a randomized controlled clinical trial. | journal=Am Heart J | year=2006 | volume=151 | issue=5 | pages=977-84 | id=PMID 16644317}}</ref>  [[Medical research|Preclinical research]] suggests that periodontal bacteria can promote aggregation of [[platelets]] and promote the formation of [[foam cell]]s.<ref name="Lourbakos-2001">{{cite journal | author=Lourbakos A, Yuan YP, Jenkins AL, Travis J, Andrade-Gordon P, Santulli R, Potempa J, Pike RN. | title=Activation of protease-activated receptors by gingipains from Porphyromonas gingivalis leads to platelet aggregation: a new trait in microbial pathogenicity. | journal=Blood | year=2001 | volume=97 | issue=12 | pages=3790-7 | format=PDF | url=http://bloodjournal.hematologylibrary.org/cgi/reprint/97/12/3790.pdf | id=PMID 11389018}}</ref><ref name="Qi-2003">{{cite journal | author=Qi M, Miyakawa H, Kuramitsu HK. | title=Porphyromonas gingivalis induces murine macrophage foam cell formation. | journal=Microb Pathog | year=2003 | volume=35 | issue=6 | pages=259-67 | id=PMID 14580389}}</ref>  A role for specific periodontal bacteria has been suggested but remains to be established.<ref name="Spahr-2006">{{cite journal | author=Spahr A, Klein E, Khuseyinova N, Boeckh C, Muche R, Kunze M, Rothenbacher D, Pezeshki G, Hoffmeister A, Koenig W. | title=Periodontal infections and coronary heart disease: role of periodontal bacteria and importance of total pathogen burden in the Coronary Event and Periodontal Disease (CORODONT) study. | journal=Arch Intern Med | year=2006 | volume=166 | issue=5 | pages=554-9 | id=PMID 16534043}}</ref>


==Controversial risk factors==
===Controversial Risk Factors===
[[Baldness]], [[Gray hair|hair greying]], a diagonal [[Earlobe|earlobe crease]]<ref name="Lichstein-1974">{{cite journal | author=Lichstein E, Chadda KD, Naik D, Gupta PK. | title=Diagonal ear-lobe crease: prevalence and implications as a coronary risk factor. | journal=N Engl J Med | year=1974 | volume=290 | issue=11 | pages=615-6 | id=PMID 4812503}}</ref> and possibly other [[skin]] features are independent risk factors for MI. Their role remains controversial; a common denominator of these signs and the risk of MI is supposed, possibly genetic.<ref name="Miric-1998">{{cite journal | author=Miric D, Fabijanic D, Giunio L, Eterovic D, Culic V, Bozic I, Hozo I. | title=Dermatological indicators of coronary risk: a case-control study. | journal=Int J Cardiol | year=1998 | volume=67 | issue=3 | pages=251-5 | id=PMID 9894707}}</ref>
[[Baldness]], [[Gray hair|hair greying]], a diagonal [[Earlobe|earlobe crease]]<ref name="Lichstein-1974">{{cite journal | author=Lichstein E, Chadda KD, Naik D, Gupta PK. | title=Diagonal ear-lobe crease: prevalence and implications as a coronary risk factor. | journal=N Engl J Med | year=1974 | volume=290 | issue=11 | pages=615-6 | id=PMID 4812503}}</ref> and possibly other [[skin]] features are independent risk factors for MI. Their role remains controversial; a common denominator of these signs and the risk of MI is supposed, possibly genetic.<ref name="Miric-1998">{{cite journal | author=Miric D, Fabijanic D, Giunio L, Eterovic D, Culic V, Bozic I, Hozo I. | title=Dermatological indicators of coronary risk: a case-control study. | journal=Int J Cardiol | year=1998 | volume=67 | issue=3 | pages=251-5 | id=PMID 9894707}}</ref>


==Sources==
==Risk Factor Modification==
*The 2004 ACC/AHA Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction <ref name="pmid15339869">{{cite journal |author=Antman EM, Anbe DT, Armstrong PW, Bates ER, Green LA, Hand M, Hochman JS, Krumholz HM, Kushner FG, Lamas GA, Mullany CJ, Ornato JP, Pearle DL, Sloan MA, Smith SC, Alpert JS, Anderson JL, Faxon DP, Fuster V, Gibbons RJ, Gregoratos G, Halperin JL, Hiratzka LF, Hunt SA, Jacobs AK |title=ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Revise the 1999 Guidelines for the Management of Patients with Acute Myocardial Infarction) |journal=Circulation |volume=110 |issue=9 |pages=e82–292 |year=2004 |month=August |pmid=15339869 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=15339869}}</ref>
While family history, along with age and sex, is uncontrollable<ref name="Framingham1998"/>, many of the  risk factors for heart disease can be eliminated by maintaining a  healthy lifestyle. In fact, a person's daily habits significantly affect  the risk of heart  disease due to genetic predisposition. Studies have shown that deaths  can be avoided by attending to the controllable risk factors. Such risk  factors include: obesity, blood pressure, cigarette smoking and plasma  cholesterol.<ref>{{cite   journal |author=Khaw KT, Barrett-Connor E |title=Family    history of heart attack: a modifiable risk factor?|journal=Circulation   |volume=74    |issue=2    |pages=239–44    |year=1986    |month=August   |pmid=3731415    |doi=   |url=}}</ref>  
 
A study published in Circulation shines some light on the  importance of eliminating these controllable risk factors in people  with  a family history of heart disease. Data demonstrated that in men  with a  genetic link to heart disease, an estimated 68% of the excess  deaths  were due to the addition of smoking, a modifiable risk factor;  concluding that the risk of heart disease in men with a family  history of the condition is significantly related to the additional  risk  factors he accumulates.


*The 2007 Focused Update of the ACC/AHA 2004 Guidelines for the Management of Patients with ST-Elevation Myocardial Infarction <ref name="pmid18071078">{{cite journal |author=Antman EM, Hand M, Armstrong PW, ''et al'' |title=2007 Focused Update of the ACC/AHA 2004 Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines: developed in collaboration With the Canadian Cardiovascular Society endorsed by the American Academy of Family Physicians: 2007 Writing Group to Review New Evidence and Update the ACC/AHA 2004 Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction, Writing on Behalf of the 2004 Writing Committee |journal=Circulation |volume=117 |issue=2 |pages=296–329 |year=2008 |month=January |pmid=18071078 |doi=10.1161/CIRCULATIONAHA.107.188209 |url=}}</ref>
==References==
==References==
{{reflist|2}}
{{reflist|2}}
==External links==
* [http://hp2010.nhlbihin.net/atpiii/calculator.asp?usertype=pub Risk Assessment Tool for Estimating Your 10-year Risk of Having a Heart Attack] - based on information of the [[Framingham Heart Study]], from the United States [[National Heart, Lung and Blood Institute]]
* [http://www.nlm.nih.gov/medlineplus/heartattack.html Heart Attack] - overview of resources from [[MedlinePlus]].
* [http://ww2.heartandstroke.ca/Page.asp?PageID=1975&ArticleID=5288 Heart Attack Warning Signals] from the Heart and Stroke Foundation of Canada
* [http://www.regionalpci-stemi.org/index.html Regional PCI for STEMI Resource Center] - Evidence based online resource center for the development of regional PCI networks for acute STEMI
* [http://www.stemisystems.org/ STEMI Systems] - Articles, profiles, and reviews of the latest publications involved in STEMI care. Quarterly newsletter.
* [http://d2b.acc.org/ American College of Cardiology (ACC) Door to Balloon (D2B) Initiative.]
*[http://www.americanheart.org/heartattack American Heart Association's Heart Attack web site] - Information and resources for preventing, recognizing and treating heart attack.
{{STEMI}}


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Latest revision as of 00:17, 30 July 2020

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2]

Overview

In these chapters on ST elevation, the word risk factors refers to those epidemiologic and genetic variables that expose someone to a higher risk of developing atherosclerotic plaque. The word triggers refer to those factors in the patients immediate history or environment that may have lead to rupture of the atherosclerotic plaque.

Nomenclature

Muller et al have developed the following nomenclature to categorize and analyze data pertaining to triggers of MI [1]:

(1) Trigger: An activity that produces short-term physiological changes that may lead directly to onset of acute CVD.
(2) Acute risk factor: A short-term physiological change, such as a surge in arterial pressure or heart rate, an increase in coagulability, or vasoconstriction, that follows a trigger and may result in disease onset.
(3) Hazard period: The time interval after trigger initiation associated with an increased risk of disease onset because of the trigger. The onset and offset times of the hazard period, which could also be designated a “vulnerable period,” may be sharply defined, as in heavy exertion, or less well defined, as with respiratory infection. The duration of the hazard period may also vary, eg from < 1 hour during heavy physical exertion to weeks or months with bereavement.
(4) Triggered acute risk prevention (TARP): Cardiovascular risk reduction that focuses on the short-term increase in risk associated with a trigger.

Risk Factors

Traditional Risk Factors for Atherosclerosis[2]

Risk factors for atherosclerosis are generally risk factors for myocardial infarction:

Genetic Disorders

  • Mendelian inherited conditions
Familial mixed hyperlipidaemia
LDL receptor deficiency
  • Autosomal dominant conditions
Pseudoxanthoma elasticum dominant type 1
  • Autosomal recessive conditions
Cystathionine beta-synthase deficiency
Sitosterolemia

Family History and Heart Disease

According to present trends in the United States, half of healthy 40-year-old males and 1 in 3 healthy 40-year-old women will develop coronary artery disease (CAD) in the future.[5] This chance is greater when a family history of heart disease is involved.

Studies have reported that the risk of CAD increases two- to sevenfold when there is a genetic link. [6] The studies by Nora and Nora (1978a) evaluated a large number of patients with congenital heart disease.[7] Results show that about 8% of the defects were primarily genetics-related, 2% were environmental (caused by drugs, viruses, maternal nutrition, maternal metabolism, or fetal hemodynamics) and 90% were multifactorial (due to a combination of environmental and genetic factors). The study also noted that there is a two- to threefold increase in the recurrence risk for congenital heart disease when two of the family members are affected. This is particularly the case when the parent is severely affected or when the affected members are child and parent. The risk for a myocardial infarction is two to three times greater in a first-degree relative than in a person with no family history of heart disease. This fact speaks in particular to the early presentation of CAD in patients with no other risk factors. Second cousins have a 1 in 23 chance of sharing a particular gene and third cousins have a 1 in 128 likelihood.

Genetic hypertension and hyperlipidemia are strong predictors of familial heart disease.[8] Hypertensive people are twice as likely to have a family history of the condition than are normotensives. Genetic hypertension is an example of a polygenic mode of inheritance that reflects cellular sodium transport defects and an abnormal response to psychogenic stress. There is indication that Pheochromocytoma, a rare cause of hypertension, may be familial as well.

Endocrine Conditions

Rheumatologic and Autoimmune Conditions

Socioeconomic Factors

Socioeconomic factors such as a shorter education and lower income (particularly in women), and living with a partner may also contribute to the risk of MI.[9] To understand epidemiological study results, it's important to note that many factors associated with MI mediate their risk via other factors. For example, the effect of education is partially based on its effect on income and marital status.[9]

Women who use combined oral contraceptive pills have a modestly increased risk of myocardial infarction, especially in the presence of other risk factors, such as smoking.[10]

Inflammation is known to be an important step in the process of atherosclerotic plaque formation.[11] C-reactive protein (CRP) is a sensitive but non-specific marker for inflammation. Elevated CRP blood levels, especially measured with high sensitivity assays, can predict the risk of MI, as well as stroke and development of diabetes.[11] Moreover, some drugs for MI might also reduce CRP levels.[11] The use of high sensitivity CRP assays as a means of screening the general population is advised against, but it may be used optionally at the physician's discretion, in patients who already present with other risk factors or known coronary artery disease.[12] Whether CRP plays a direct role in atherosclerosis remains uncertain.[11]

Inflammation in periodontal disease may be linked coronary heart disease, and since periodontitis is very common, this could have great consequences for public health.[13] Serological studies measuring antibody levels against typical periodontitis-causing bacteria found that such antibodies were more present in subjects with coronary heart disease.[14] Periodontitis tends to increase blood levels of CRP, fibrinogen and cytokines;[15] thus, periodontitis may mediate its effect on MI risk via other risk factors.[16] Preclinical research suggests that periodontal bacteria can promote aggregation of platelets and promote the formation of foam cells.[17][18] A role for specific periodontal bacteria has been suggested but remains to be established.[19]

Controversial Risk Factors

Baldness, hair greying, a diagonal earlobe crease[20] and possibly other skin features are independent risk factors for MI. Their role remains controversial; a common denominator of these signs and the risk of MI is supposed, possibly genetic.[21]

Risk Factor Modification

While family history, along with age and sex, is uncontrollable[3], many of the risk factors for heart disease can be eliminated by maintaining a healthy lifestyle. In fact, a person's daily habits significantly affect the risk of heart disease due to genetic predisposition. Studies have shown that deaths can be avoided by attending to the controllable risk factors. Such risk factors include: obesity, blood pressure, cigarette smoking and plasma cholesterol.[22]

A study published in Circulation shines some light on the importance of eliminating these controllable risk factors in people with a family history of heart disease. Data demonstrated that in men with a genetic link to heart disease, an estimated 68% of the excess deaths were due to the addition of smoking, a modifiable risk factor; concluding that the risk of heart disease in men with a family history of the condition is significantly related to the additional risk factors he accumulates.

References

  1. ↑ Muller JE, Abela GS, Nesto RW, Tofler GH (1994). "Triggers, acute risk factors and vulnerable plaques: the lexicon of a new frontier". J. Am. Coll. Cardiol. 23 (3): 809–13. PMID 8113568. Unknown parameter |month= ignored (help)
  2. ↑ "Executive Summary of The Third Report of The National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, And Treatment of High Blood Cholesterol In Adults (Adult Treatment Panel III)". JAMA. 285 (19): 2486–97. 2001. PMID 11368702. Unknown parameter |month= ignored (help)
  3. ↑ 3.0 3.1 Wilson PW, D'Agostino RB, Levy D, Belanger AM, Silbershatz H, Kannel WB. (1998). "Prediction of coronary heart disease using risk factor categories" (PDF). Circulation. 97 (18): 1837–47. PMID 9603539.
  4. ↑ Yusuf S, Hawken S, Ounpuu S, Bautista L, Franzosi MG, Commerford P, Lang CC, Rumboldt Z, Onen CL, Lisheng L, Tanomsup S, Wangai P Jr, Razak F, Sharma AM, Anand SS; INTERHEART Study Investigators. (2005). "Obesity and the risk of myocardial infarction in 27,000 participants from 52 countries: a case-control study". Lancet. 366 (9497): 1640–9. PMID 16271645.
  5. ↑ Rosamond W, Flegal K, Friday G (2007). "Heart disease and stroke statistics--2007 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee". Circulation. 115 (5): e69–171. doi:10.1161/CIRCULATIONAHA.106.179918. PMID 17194875. Unknown parameter |month= ignored (help)
  6. ↑ Khaw KT, Barrett-Connor E (1986). "Family history of heart attack: a modifiable risk factor?". Circulation. 74 (2): 239–44. PMID 3731415. Unknown parameter |month= ignored (help)
  7. ↑ http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=cm&part=A540#A556
  8. ↑ http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=cm&part=A540#A556
  9. ↑ 9.0 9.1 Nyboe J, Jensen G, Appleyard M, Schnohr P. (1989). "Risk factors for acute myocardial infarction in Copenhagen. I: Hereditary, educational and socioeconomic factors. Copenhagen City Heart Study". Eur Heart J. 10 (10): 910–6. PMID 2598948.
  10. ↑ Khader YS, Rice J, John L, Abueita O. (2003). "Oral contraceptives use and the risk of myocardial infarction: a meta-analysis". Contraception. 68 (1): 11–7. PMID 12878281.
  11. ↑ 11.0 11.1 11.2 11.3 Wilson AM, Ryan MC, Boyle AJ. (2006). "The novel role of C-reactive protein in cardiovascular disease: risk marker or pathogen". Int J Cardiol. 106 (3): 291–7. PMID 16337036.
  12. ↑ Pearson TA, Mensah GA, Alexander RW, Anderson JL, Cannon RO 3rd, Criqui M, Fadl YY, Fortmann SP, Hong Y, Myers GL, Rifai N, Smith SC Jr, Taubert K, Tracy RP, Vinicor F; Centers for Disease Control and Prevention; American Heart Association. (2003). "Markers of inflammation and cardiovascular disease: application to clinical and public health practice: A statement for healthcare professionals from the Centers for Disease Control and Prevention and the American Heart Association" (PDF). Circulation. 107 (3): 499–511. PMID 12551878.
  13. ↑ Janket SJ, Baird AE, Chuang SK, Jones JA. (2003). "Meta-analysis of periodontal disease and risk of coronary heart disease and stroke". Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 95 (5): 559–69. PMID 12738947.
  14. ↑ Pihlstrom BL, Michalowicz BS, Johnson NW. (2005). "Periodontal diseases". Lancet. 366 (9499): 1809–20. PMID 16298220.
  15. ↑ Scannapieco FA, Bush RB, Paju S. (2003). "Associations between periodontal disease and risk for atherosclerosis, cardiovascular disease, and stroke. A systematic review". Ann Periodontol. 8 (1): 38–53. PMID 14971247.
  16. ↑ D'Aiuto F, Parkar M, Nibali L, Suvan J, Lessem J, Tonetti MS. (2006). "Periodontal infections cause changes in traditional and novel cardiovascular risk factors: results from a randomized controlled clinical trial". Am Heart J. 151 (5): 977–84. PMID 16644317.
  17. ↑ Lourbakos A, Yuan YP, Jenkins AL, Travis J, Andrade-Gordon P, Santulli R, Potempa J, Pike RN. (2001). "Activation of protease-activated receptors by gingipains from Porphyromonas gingivalis leads to platelet aggregation: a new trait in microbial pathogenicity" (PDF). Blood. 97 (12): 3790–7. PMID 11389018.
  18. ↑ Qi M, Miyakawa H, Kuramitsu HK. (2003). "Porphyromonas gingivalis induces murine macrophage foam cell formation". Microb Pathog. 35 (6): 259–67. PMID 14580389.
  19. ↑ Spahr A, Klein E, Khuseyinova N, Boeckh C, Muche R, Kunze M, Rothenbacher D, Pezeshki G, Hoffmeister A, Koenig W. (2006). "Periodontal infections and coronary heart disease: role of periodontal bacteria and importance of total pathogen burden in the Coronary Event and Periodontal Disease (CORODONT) study". Arch Intern Med. 166 (5): 554–9. PMID 16534043.
  20. ↑ Lichstein E, Chadda KD, Naik D, Gupta PK. (1974). "Diagonal ear-lobe crease: prevalence and implications as a coronary risk factor". N Engl J Med. 290 (11): 615–6. PMID 4812503.
  21. ↑ Miric D, Fabijanic D, Giunio L, Eterovic D, Culic V, Bozic I, Hozo I. (1998). "Dermatological indicators of coronary risk: a case-control study". Int J Cardiol. 67 (3): 251–5. PMID 9894707.
  22. ↑ Khaw KT, Barrett-Connor E (1986). "Family history of heart attack: a modifiable risk factor?". Circulation. 74 (2): 239–44. PMID 3731415. Unknown parameter |month= ignored (help)


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