ST elevation myocardial infarction risk factors: Difference between revisions
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==Risk factors vs Triggers of ST elevation MI== | ==Risk factors vs Triggers of ST elevation MI== | ||
Several | In these chapters, risk factors refer to those epidemiologic and genetic variables that expose someone to a higher risk of developing atherosclerosis. Triggers refer to those factors in the patients immediate history that may have lead to plaque rupture. | ||
Several 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 | |||
Muller et al have developed the following nomenclature to categorize and analyze data pertaining to triggers of MI [1]: | Muller et al have developed the following nomenclature to categorize and analyze data pertaining to triggers of MI [1]: | ||
Revision as of 16:27, 6 February 2009
| Myocardial infarction | |
| ICD-10 | I21-I22 |
|---|---|
| ICD-9 | 410 |
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Risk factors vs Triggers of ST elevation MI
In these chapters, risk factors refer to those epidemiologic and genetic variables that expose someone to a higher risk of developing atherosclerosis. Triggers refer to those factors in the patients immediate history that may have lead to plaque rupture. Several 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
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.
Traditional risk factors for atherosclerosis
Risk factors for atherosclerosis are generally risk factors for myocardial infarction:
- Advancing age
- Male gender[1]
- Cigarette smoking
- Hypercholesterolemia (more accurately hyperlipoproteinemia, especially high low density lipoprotein and low high density lipoprotein)
- Diabetes (with or without insulin resistance)
- High blood pressure
- Obesity[2] (defined by a body mass index of more than 30 kg/m², or alternatively by waist circumference or waist-hip ratio).
- Elevated homocysteine
Genetic disorders
- Mendelian inherited conditions
- Autosomal dominant conditions
- Pseudoxanthoma elasticum dominant type 1
- Autosomal recessive conditions
Cystathionine beta-synthase deficiency Sitosterolemia
Endocrine conditions
Diabetes mellitus type 2 Hyperparathyroidism, primary
Cardiac and vascular conditions
Atherosclerosis
Rheumatologic and Autoimmune conditions
Systemic lupus erythematosus
Risk factor modification
Many of these risk factors are modifiable, so many heart attacks can be prevented by maintaining a healthier lifestyle. Physical activity, for example, is associated with a lower risk profile.[3] Non-modifiable risk factors include age, sex, and family history of an early heart attack (before the age of 60), which is thought of as reflecting a genetic predisposition.[1]
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.[4] 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.[4]
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.[5]
Inflammation is known to be an important step in the process of atherosclerotic plaque formation.[6] 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.[6] Moreover, some drugs for MI might also reduce CRP levels.[6] 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.[7] Whether CRP plays a direct role in atherosclerosis remains uncertain.[6]
Inflammation in periodontal disease may be linked coronary heart disease, and since periodontitis is very common, this could have great consequences for public health.[8] Serological studies measuring antibody levels against typical periodontitis-causing bacteria found that such antibodies were more present in subjects with coronary heart disease.[9] Periodontitis tends to increase blood levels of CRP, fibrinogen and cytokines;[10] thus, periodontitis may mediate its effect on MI risk via other risk factors.[11] Preclinical research suggests that periodontal bacteria can promote aggregation of platelets and promote the formation of foam cells.[12][13] A role for specific periodontal bacteria has been suggested but remains to be established.[14]
Controversial risk factors
Baldness, hair greying, a diagonal earlobe crease[15] 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.[16]
See also
References
- ↑ 1.0 1.1 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.
- ↑ 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.
- ↑ Jensen G, Nyboe J, Appleyard M, Schnohr P. (1991). "Risk factors for acute myocardial infarction in Copenhagen, II: Smoking, alcohol intake, physical activity, obesity, oral contraception, diabetes, lipids, and blood pressure". Eur Heart J. 12 (3): 298–308. PMID 2040311.
- ↑ 4.0 4.1 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.
- ↑ 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.
- ↑ 6.0 6.1 6.2 6.3 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.
- ↑ 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.
- ↑ 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.
- ↑ Pihlstrom BL, Michalowicz BS, Johnson NW. (2005). "Periodontal diseases". Lancet. 366 (9499): 1809–20. PMID 16298220.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ Qi M, Miyakawa H, Kuramitsu HK. (2003). "Porphyromonas gingivalis induces murine macrophage foam cell formation". Microb Pathog. 35 (6): 259–67. PMID 14580389.
- ↑ 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.
- ↑ 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.
- ↑ 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.
External links
- 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
- Heart Attack - overview of resources from MedlinePlus.
- Heart Attack Warning Signals from the Heart and Stroke Foundation of Canada
- Regional PCI for STEMI Resource Center - Evidence based online resource center for the development of regional PCI networks for acute STEMI
- STEMI Systems - Articles, profiles, and reviews of the latest publications involved in STEMI care. Quarterly newsletter.
- American College of Cardiology (ACC) Door to Balloon (D2B) Initiative.
- American Heart Association's Heart Attack web site - Information and resources for preventing, recognizing and treating heart attack.