eISSN: 1896-9151
ISSN: 1734-1922
Archives of Medical Science
Current issue Archive Manuscripts accepted About the journal Special issues Editorial board Abstracting and indexing Subscription Contact Instructions for authors Ethical standards and procedures
SCImago Journal & Country Rank
1/2005
vol. 1
 
Share:
Share:
more
 
 

REVIEW PAPER
Defects of coagulation and antiphospholipid antibodies in patients up to 40 years old with acute coronary syndrome

Agnieszka Dębska

Arch Med Sci 2005; 1, 1: 34-36
Online publish date: 2005/05/06
Article file
- Defects.pdf  [0.05 MB]
Get citation
ENW
EndNote
BIB
JabRef, Mendeley
RIS
Papers, Reference Manager, RefWorks, Zotero
AMA
APA
Chicago
Harvard
MLA
Vancouver
 
 
Submitted: 3 February 2005
Accepted: 5 April 2005



Corresponding author:
Małgorzata Lelonek, MD PhD
Department of Cardiology
1st Chair of Cardiology
and Cardiac Surgery
Medical University of Lodz
Sterlinga 1/3
91-425 Lodz, Poland
Phone: +48 42 633 96 30
Phone/fax: + 48 42 636 44 71
E-mail: mlelonek@poczta.fm
agndebska@wp.pl



Introduction
An analysis of acute coronary syndromes’ (ACS) prevalence focuses attention on an important and interesting clinical problem, which refers to increasing frequency of ischemic incidents in young patients. The literature shows comparisons of risk factors, symptomatology, clinical courses, therapeutic management and prognosis in relation to older patients.

Israeli scientists have analyzed a clinical course of ischemic episodes in fifteen young patients (mean age – 28 years), hospitalized in the cardiologic department in years 1993-2000. In 7 of these patients atheromatous changes in coronary arteries and also a special role of classical risk factors for coronary disease have been documented [1]. The remaining patients had normal coronary arteries and a complete diagnosis has confirmed a significance of trombophilia, arterial spasm caused by abuse of alcohol, withdrawal and hormonal disorders (hyperthyroidism). All the patients have presented a typical chest pain. A better prognosis has referred to patients without coronary arteries’ lesion. It has been connected with: a good left ventricular ejection fraction (LVEF) evaluated on follow-up echocardiography, an absence of hemodynamic complications and a lack of recurrent ACS in about four years. Four out of seven patients have shown incidents of ACS [1].
Very often clinicians find it difficult to arrive at the diagnosis of ACS in young patients, so a necessity for finding different than classical cardiac risk factors has occurred. On the basis of biochemical investigations performed among 127 males hospitalized with a first MI, Japanese scientists have formed a conclusion. It relates to the importance of hyperhomocysteinemia in the pathogenesis of early ACS [2]. They have also shown evidence of the essential role of tissue factor, tissue plasminogen activator (t-Pa) – their concentration has a positive correlation with hyperhomocysteinemia and influences coagulation cascade [2].
Other disorders of coagulation activation can be also considered in the case of MI. Increased levels of thrombin-antithrombin complexes, a lower concentration of factor VIIa and elevated tissue factor pathway inhibitor antigen can be responsible for ACS [3].
In 99 male patients with MI a connection between Bc1I polymorphism in the fibrinogen beta – chain gene (Bc1I bFb), plasma fibrinogen concentration and the number of abnormal coronary arteries has been determined in a comparison of healthy volunteers [4]. In patients with MI the prevalence of Bc1I bFb polymorphism was significantly higher than in the control group and has correlated with the increased level of plasma fibrinogen. Investigations have not confirmed a relationship between number of atheromatous coronary arteries and Bc1I bFb polymorphism [4].
Other polymorphisms have been also documented as a non-classical cardiac risk factors in young sick persons. In clinical investigations the role of following polymorphisms was observed: in the prothrombin gene – G20210A, in the thrombopoetin gene, in the Apo B (connexion with an increased level of LDL-ch), in the Apo E, in the CD 14 gene (C-260T) and in the E Selectin gene [5].
Articles on the role of antiphospholipid syndrome in the pathogenesis of ACS more often occur in the literature. Its clinical manifestation is caused by the presence of antiphospholipid antibodies (APA) and is characterized by: arterial embolism, recurrent venous thromboses and premature births or miscarriages [6]. APA can activate various cells: thrombocytes, monocytes and endothelial cells. This syndrome was diagnosed in 21-year-old female, who had experienced a TIA (transient ischemic attack) and half a year later – an ACS with thrombocytopenia [6]. So, there is a necessity of paying attention to APA as a risk factor of ACS, especially in young patients with thromboembolic incidents in anamnesis. In these clinical situations APA are determined in 10 – 20 % of cases [6]. Also, the role of APA has been detected in an ischemic stroke’s occurrence without identifiable risk factors for atherosclerosis [7].
An increased concentration of Lp (a), i.e. lipoprotein (a) can also be an important predictor of ACS [8]. This is strongly stressed in young patients after MI. In this group a high level of Lp (a) is a hereditary susceptibility, which has been confirmed by investigations made among their first – degree relatives. There is also a correlation between a higher level of Lp (a) and elevated interleukin-6 (IL-6) concentration in MI. An abnormal IL-6 often coexists with abdominal obesity and increased concentration of fibrinogen, which has been documented in the group of young women at mean age 40 [9].
An investigation of a coexistence of prothrombotic coagulation defects and the most common cardiac risk factor – smoking – has proved that in this situation the risk of MI increases 12 – fold in young women in comparison with a control, healthy group. Also, smoking women with the presence of factor V Leiden have a two times higher possibility of ACS’ occurrence [10].
A syndrome of protein C deficiency can play an important role in the pathogenesis of ACS, even in very young sick persons. Literature reports a special case of a 19-year-old man, who was diagnosed as anterior wall MI. Angiographically there was a total occlusion of LAD (left anterior descending coronary artery). Not for the first time an abnormal concentration of protein C has been presented as a cause of ACS in young age [11].
It is important to pay attention to the use of anabolic steroids as a predictor of ACS in the group of young patients. Steroids can cause a state of hipercoagulation and lipid disorders [12]. A case of a 27-year-old man with a dramatic course of MI caused by LAD occlusion has been described. He had been using anabolic steroids regularly for 10 years. Despite treatment by PTCA and intra-aortic balloon support in this case a serious myocardial lesion has developed [12].

Conclusions
Consecutive clinical studies prove that in the group of young patients up to 40 years old ACS is observed mainly in men, accompanied by ST segment elevation. The common anatomical localization is an anterior wall of heart muscle. In coronary angiography atheromatous changes are rarely revealed or there is a single vessel disease. It is connected with a decreased necessity of revascularization, also made by surgical procedures. It results in a smaller frequency of reoclusion, rare complications after an ischemic episode and a better prognosis. In connexion with a variety of cardiac risk factors investigated in young patients, there is a need of a detailed diagnosis and suitable treatment in comparison with older than 40 years old patients.
References
1. Gotsman I, Lotan C, Mosseri M. Clinical manifestations and outcome of myocardial infarction in very young patients. Isr Med Assoc J 2003; 5: 633-6.
2. Ogawa M, Abe S, Saigo M, Biro S, Toda H, Matsuoka T et al. Homocysteine and hemostatic disorder as a risk factor for myocardial infarction at a young age. Thromb Res 2003; 109: 253-8.
3. Brodin E, Borvik T, Sandset PM, Bonaa KH, Nordoy A, Hansen JB. Coagulation activation in young survivors of myocardial infarction (MI) – a population-based case-control study. Thromb Haemost 2004; 92: 178-84.
4. Lewandowski K, Kwasnikowski P, Elikowski W, Zawilska K. Myocardial infarction in patients aged lees than 40 years. Frequency of Bc1I polymorphism in the fibrinogen beta-chain gene and plasma fibrinogen. Kardiol Pol 2003; 59: 205-12.
5. Incalcaterra E, Hoffman E, Averna MR, Caimi G. Genetic risk factors in myocardial infarction at young age. Minerva Cardioangiol 2004; 52: 287-312.
6. Rank A, Lindner L, Hiller E. 21-year-old patient with myocardial infarct, transient cerebral ischemia and thrombocytopenia. Internist (Berl) 2003; 44: 349-53.
7. Singh K, Gaiha M, Shome DK, Gupta VK, Anuradha S. The association of antiphospholipid antibodies with ischemic stroke and myocardial infarction in young and their correlation: a preliminary study. J Assoc Physicians India 2001; 49: 527-9.
8. Isser HS, Puri VK, Narain VS, Saran RK, Dwivedi SK, Singh S. Lipoprotein (a) and lipid levels in young patients with myocardial infarction and their first-degree relatives. Indian Heart J 2001; 53: 463-6.
9. Salobir B, Sabovic M. Possible vascular-bed-specific role of interleukin-6 in young women with history of myocardial infarction, lacunar cerebral infarction and deep vein thrombosis. Cytokine 2004; 25: 265-72.
10. Tanis BC, Bloemenkamp DG, van den Bosch MA, Kemmeren JM, Algra A, van de Graaf Y et al. Prothrombotic coagulation defects and cardiovascular risk factors in young women with acute myocardial infarction. Br J Haematol 2003; 122: 471-8.
11. Peterman MA, Roberts WC. Syndrome of protein C deficiency and anterior wall acute myocardial infarction at a young age from a single coronary occlusion with otherwise normal coronary arteries. Am J Cardiol 2003; 92: 768-70.
12. Halvorsen S, Thorsby PM, Haug E. Acute myocardial infarction in a young man who had been using androgenic anabolic steroids. Tidsskr Nor Laegeforen 2004; 22: 170-2.





Copyright: © 2005 Termedia & Banach. This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) License (http://creativecommons.org/licenses/by-nc-sa/4.0/), allowing third parties to copy and redistribute the material in any medium or format and to remix, transform, and build upon the material, provided the original work is properly cited and states its license.
Quick links
© 2020 Termedia Sp. z o.o. All rights reserved.
Developed by Bentus.
PayU - płatności internetowe