Lipoprotein a is strongly associated with myocardial infraction
Answers
Answered by
1
Lipoprotein(a) [Lp(a)], a particle comprised of LDL and covalently bound apolipoprotein(a), [1] is considered a pro-atherogenic, pro-thrombotic risk factor for coronary heart disease (CHD) [2]. Mechanistically, it may be pro-atherogenic because excess Lp(a) preferentially binds proinflammatory oxidized phospholipids and is taken up into the sub-endothelial arterial space [3]. At the same time, it may be prothrombotic because apolipoprotein(a) is similar to plasminogen and may interfere with plasminogen’s antithrombotic function [2].
Clinically, both prospective and retrospective studies [2,4] as well as a large meta-analysis [5] have found overall positive associations of Lp(a) levels with CHD. However, many studies show significant heterogeneity in relationships to CHD and CHD risk equivalents, especially with respect to gender and race [6,7], with higher Lp(a) levels but lower Lp(a) related CHD risk in blacks [8,9].
Although Lp(a) is present in atherosclerotic plaque [10], it has variable relationships with measures of subclinical atherosclerosis. There have been conflicting data for coronary artery calcification (CAC) with both positive [11,12] and negative [13,14] findings. Furthermore, none of these studies had large numbers of type-2 diabetic individuals. It is known that Lp(a) function and atherogenicity may be modified by glycation in the milieu of overt diabetes [15]. We therefore investigated the relationship of Lp(a) with CAC, across race, gender and diabetes status using two large cross sectional studies of individuals without known CHD—one recruited on the basis of family history of CHD and the other on the basis of type-2-diabetes. We hypothesized that Lp(a) would have stronger association with CAC in diabetic individuals, and that this relationship would be modified in race and gender subgroups.
Clinically, both prospective and retrospective studies [2,4] as well as a large meta-analysis [5] have found overall positive associations of Lp(a) levels with CHD. However, many studies show significant heterogeneity in relationships to CHD and CHD risk equivalents, especially with respect to gender and race [6,7], with higher Lp(a) levels but lower Lp(a) related CHD risk in blacks [8,9].
Although Lp(a) is present in atherosclerotic plaque [10], it has variable relationships with measures of subclinical atherosclerosis. There have been conflicting data for coronary artery calcification (CAC) with both positive [11,12] and negative [13,14] findings. Furthermore, none of these studies had large numbers of type-2 diabetic individuals. It is known that Lp(a) function and atherogenicity may be modified by glycation in the milieu of overt diabetes [15]. We therefore investigated the relationship of Lp(a) with CAC, across race, gender and diabetes status using two large cross sectional studies of individuals without known CHD—one recruited on the basis of family history of CHD and the other on the basis of type-2-diabetes. We hypothesized that Lp(a) would have stronger association with CAC in diabetic individuals, and that this relationship would be modified in race and gender subgroups.
Answered by
2
Explanation:
Answer:
The myocardial infection ( MI) commonly known as heart attack, occurs when a portion of heart is deprived of oxygen due to blockage of a coronary artery.
Similar questions