'Lp(a)' Joins Other Serum Cholesterol Lipoproteins as Risk Determinant

Merz, Beverly

doi:10.1001/jama.1989.03420140013002

Cited by 7 publications

(5 citation statements)

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“…An atheromatous plaque could develop and fibrinolysis could be inhibited by competi tive inhibition of plasminogen. Together with other pos sible mechanisms [13], this hypothesis not only explains the apparent atherogenicity of Lp(a), but it also provides a long-sought link between thrombus and atheroma [ 8,12].…”

Section: Introductionmentioning

confidence: 92%

“…Currently Lp(a) levels are considered to be genetically determined, at least to a very large extent [7,8,[14][15][16]]. …”

Section: -----------------mentioning

confidence: 99%

“…In the last decade, lipoprotein(a) [Lp(a)] has emerged as another independent lipid risk determinant for both cor onary heart disease and peripheral artery disease [4][5][6][7][8]. It has been claimed that Lp(a) is as good a predictor of the severity of coronary disease in men as low-density lipoprotein and high-density lipoprotein [8].…”

Section: Introductionmentioning

confidence: 99%

“…Its lipid composition is very similar to that of low-density lipo protein, but it contains an additional apolipoprotein(a) linked to apolipoprotein B by a disulfide bridge [7,9], Sequencing of apolipoprotein(a) has revealed a striking homology to plasminogen [10,11], but apolipoprotein(a) has no proteolytic activity [7,8]. It has been hypothe sized that, like plasminogen, apolipoprotein(a) is at tracted by fibrin in a vessel wall injury, thereby fixing Lp(a) to the clot [8,12]. An atheromatous plaque could develop and fibrinolysis could be inhibited by competi tive inhibition of plasminogen.…”

Section: Introductionmentioning

confidence: 99%

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Lp(a) Lipoprotein in Patients with Acute Stroke

Asplund¹,

Olsson²,

Viitanen³

et al. 1991

Cerebrovasc Dis

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Serum lipoprotein(a) [Lp(a)] was determined in 205 patients (71 ± 10 years; mean age ± SD) with acute stroke and in 204 nonhospitalized referent subjects in the 60- to 80-year age range. Lp(a) levels were significantly higher in the stroke patients (median 87 vs. 63 mg/l; p = 0.002). Within the group of stroke patients, Lp(a) levels were similar among men and women, correlated modestly with age (r = 0.15; p = 0.04) and increased only marginally through the first days after stroke. Patients with concomitant ischemic heart disease tended to have higher Lp(a) than those without coronary disease (median 103 vs. 71 mg/l; p = 0.07). Hypertensive patients had higher levels than normotensives (97 vs. 73 mg/l; p = 0.02) and this relation between hypertension and Lp(a) was particularly strong among patients below 65 years of age (p = 0.01). Median Lp(a) level was 75 mg/l in patients not on beta blocker treatment, 103 mg/l in patients on selective beta blockers and 150 mg/l in those on nonselective beta blockers. In a multiple regression model, the use of beta blockers was a predictor of high Lp(a) levels (p = 0.03) that was independent of other clinical variables.

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Section: Introductionmentioning

confidence: 92%

“…Currently Lp(a) levels are considered to be genetically determined, at least to a very large extent [7,8,[14][15][16]]. …”

Section: -----------------mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Lp(a) Lipoprotein in Patients with Acute Stroke

Asplund¹,

Olsson²,

Viitanen³

et al. 1991

Cerebrovasc Dis

View full text Add to dashboard Cite

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“…It has been later found that apolipoprotein A (apoA) was linked to apoB100 of LDL by disulfide linkages (4). The apoA structural gene is located on chromosome 6 with the gene for plasminogen, indicating that both might have arisen from a common ancestral gene (5,6).…”

Section: Introductionmentioning

confidence: 99%

Lipoprotein (a), Lipid Profile and Mean Platelet Volume in Hypothyroid Patients in Sana'a, Yemen: A Case-Control Study

2016

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Objectives: This study aimed to measure lipoprotein (a) [Lp(a)], lipid profile and mean platelet volume (MPV) in hypothyroid patients compared to healthy controls.Methods: An unmatched case-control study was conducted involving 100 subjects (50 overt hypothyroidism patients and 50 healthy controls admitted to the University of Science and Technology Hospital, Al-Thawra Hospital and Al-Jomhori Hospital-Sana'a, Yemen during the period from May 2013 to March 2014. Data were collected by in-person interview using a structured questionnaire followed by weight and height measurements. Fresh blood samples were collected and analyzed using electrochemiluminescent, spectrophotometric and immunoturbidimetric methods for estimating Lp(a), lipid profile and MPV parameters. Results:Hypothyroid patients had a significantly higher concentration of Lp(a) compared to the control. Total cholesterol (TC), triglycerides and low-density lipoprotein-cholesterol (LDL-C) levels were also significantly higher in hypothyroid patients. Serum level of free triiodothyronine (FT3) was negatively correlated with Lp(a), p=0.007; p=0.012; p=0.013, respectively). However, serum thyroid-stimulating hormone was positively correlated with Lp(a), p=0.015; r=0.299, p=0.035; r=0.405, p=0.004, respectively) among hypothyroid patients. MPV levels, on the other hand, showed a strong positive correlation with (r=0.611, p=0.001). Conclusions:These findings indicate that overt hypothyroidism patients tend to have increased Lp(a) and atherogenic lipids that may contribute to increasing risk of atherosclerosis. However, hypothyroid patients showed no significant difference compared to the controls regarding the MPV

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