Serum level of lipoprotein (a) is inversely associated with the development of coronary collateral circulation

Aras, Dursun; Geyık, Bilal; Topaloğlu, Serkan; Ergün, Kumral; Ayaz, Selime; Maden, Orhan; Yıldız, Ali; Balcı, Mustafa; Özeke, Özcan; Korkmaz, Şule

doi:10.1097/00019501-200603000-00010

Cited by 12 publications

(10 citation statements)

References 26 publications

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“…The contribution of Lp(a) to cardiovascular diseases differs among races [46], [47], but stratification was of minimal concern in the present study because all the subjects were Japanese.…”

Section: Discussionmentioning

confidence: 89%

Low Lipoprotein(a) Concentration Is Associated with Cancer and All-Cause Deaths: A Population-Based Cohort Study (The JMS Cohort Study)

et al. 2012

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Background Experimental studies support the anti-neoplastic effect of apo(a), but several clinical studies have reported contradictory results. The purpose of this study was to determine whether a low lipoprotein(a) [Lp(a)] concentration is related to mortality from major causes of death, especially cancer. Methods The subjects were 10,413 participants (4,005 men and 6,408 women) from a multi-center population-based cohort study in Japan (The Jichi Medical School cohort study). The average age at registration was 55.0 years, and the median observation period was 4,559 days. As the estimated hazard ratio was high for both the low and very high Lp(a) levels, we defined two Lp(a) groups: a low Lp(a) group [Lp(a)<80 mg/L] and an intermediate-to-high Lp(a) group [Lp(a)≥80]. Participants who died from malignant neoplasms (n = 316), cardiovascular disease (202), or other causes (312) during the observation period were examined. Results Cumulative incidence plots showed higher cumulative death rates for the low Lp(a) group than for the intermediate-to-high Lp(a) group for all-cause, cancer, and miscellaneous-cause deaths (p<0.001, p = 0.03, and p = 0.03, respectively). Cox proportional hazards analyses with the sex and age of the participants, body mass index, and smoking and drinking histories as covariates showed that a low Lp(a) level was a significant risk for all-cause, cancer, and miscellaneous-cause deaths (p<0.001, p = 0.003, and p = 0.01, respectively). The hazard ratio (95% CI) [1.48, 1.15–1.92] of a low Lp(a) level for cancer deaths was almost the same as that for a male sex (1.46, 1.00–2.13). Conclusions This is the first report to describe the association between a low Lp(a) level and all-cause or cancer death, supporting the anti-neoplastic effect of Lp(a). Further epidemiological studies are needed to confirm the present results.

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“…The contribution of Lp(a) to cardiovascular diseases differs among races [46], [47], but stratification was of minimal concern in the present study because all the subjects were Japanese.…”

Section: Discussionmentioning

confidence: 89%

Low Lipoprotein(a) Concentration Is Associated with Cancer and All-Cause Deaths: A Population-Based Cohort Study (The JMS Cohort Study)

et al. 2012

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“…In their study, in addition to the inhibition of activation of transforming growth factor (TGF-β), Lp(a) inhibited angiogenesis, as it stimulated the proliferation of vascular smooth muscle cells. Aras et al (19) established a strong negative correlation between Lp(a) and vascular endothelial cell growth factor (VEGF). High level of Lp(a) negatively affects the formation of coronary collateral vessels in humans by reducing the production or bioactivity of VEGF; however, this was found only in 60 patients.…”

Section: Discussionmentioning

confidence: 99%

“…However, the correlation between Lp(a) and collateral circulation is yet an enigma. Aras et al (19) observed a strong negative correlation between Lp(a) and vascular endothelial cell growth in only 60 CAD patients. Therefore, the current study was undertaken to assess whether the Lp(a) concentration was associated with the extent of angiographically visible coronary collateral vessels in patients with high-grade coronary artery stenosis or occlusion in a large Chinese cohort treated for the disease.…”

Section: Introductionmentioning

confidence: 99%

Lipoprotein(a) as a predictor of poor collateral circulation in patients with chronic stable coronary heart disease

Yang

Guo

et al. 2017

Braz J Med Biol Res

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As a mechanism compensating for obstructive coronary artery disease, coronary collateral circulation (CCC) has attracted cardiologists for a long time to explore its potential impact. In the present study, Chinese patients suffering from ≥95% coronary stenosis, as diagnosed by angiography, have been investigated for the correlation between CCC and lipoprotein(a) [Lp(a)] levels. A cohort of 654 patients was divided into four categories according to Rentrop grades 0, 1, 2, and 3. Lp(a) levels were divided into model 1, discretized with critical values of 33 and 66%, and model 2, discretized with a cutoff value of 30.0 mg/dL. Furthermore, we evaluated the correlation between CCC and serum Lp(a) levels. The four groups had significantly different Lp(a) levels (25.80±24.72, 18.99±17.83, 15.39±15.80, and 8.40±7.75 mg/dL; P<0.001). In model 1, concerning R0, the risk in the third Lp (a) tertile (OR=3.34, 95%CI=2.32-4.83) was greater than that in the first tertile. In model 2, concerning R0, the risk in Lp(a) >30.0 group (OR=6.77, 95%CI=4.44-10.4) was greater than that of Lp(a) <30.0 mg/dL. The worst condition of CCC can be predicted independently by Lp(a) levels. In addition to clinical usage, Lp(a) levels can also be utilized as biological markers.

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“…Although the distribution of serum Lp(a) levels is very skewed, elevated circulating Lp(a) has emerged as an independent and causal cardiovascular risk factor and an important predictor of adverse outcomes for both general and higher risk populations [12], especially when low-density lipoprotein cholesterol (LDL-C) levels are elevated [13]. Previous studies with a small sample size have suggested an inverse relation between serum levels of Lp(a) and development of coronary collateral circulation [14, 15], with high levels of Lp(a) associated with reduced production and bioactivity of vascular endothelial growth factor [14, 16]. Hypercholesterolemia particularly with high levels of LDL-C and/or low levels of high-density lipoprotein cholesterol (HDL-C) is an established coronary risk factor that induces endothelial cell dysfunction and impairs collateral vessel growth [17].…”

Section: Introductionmentioning

confidence: 99%

Lipoprotein (a) interactions with cholesterol-containing lipids on angiographic coronary collateralization in type 2 diabetic patients with chronic total occlusion

Shen

Chen

Dai

et al. 2019

Cardiovasc Diabetol

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Background We investigated whether or to what extent the interaction of lipoprotein (a) [Lp(a)] with cholesterol-containing lipids was associated with angiographic coronary collateralization in type 2 diabetic patients with chronic total occlusion. Methods Serum levels of Lp(a), total cholesterol, low-density lipoprotein–cholesterol (LDL-C), high-density lipoprotein–cholesterol (HDL-C), and triglyceride were determined and non-HDL-C was calculated in 706 type 2 diabetic and 578 non-diabetic patients with stable coronary artery disease and angiographic total occlusion of at least one major coronary artery. The degree of collaterals supplying the distal aspect of a total occlusion from the contra-lateral vessel was graded as poor (Rentrop score of 0 or 1) or good coronary collateralization (Rentrop score of 2 or 3). Results For diabetic and non-diabetic patients, Lp(a), total cholesterol, LDL-C, and non-HDL-C levels were higher in patients with poor coronary collateralization than in those with good collateralization, whereas HDL-C and triglyceride levels were similar. After adjustment for potential confounding factors, tertiles of Lp(a), total cholesterol, LDL-C and non-HDL-C remained independent determinants for poor collateralization. A significant interaction between Lp(a) and total cholesterol, LDL-C or non-HDL-C was observed in diabetic patients (all P interaction < 0.001) but not in non-diabetics. At high tertile of total cholesterol (≥ 5.35 mmol/L), LDL-C (≥ 3.36 mmol/L) and non-HDL-C (≥ 4.38 mmol/L), diabetic patients with high tertile of Lp(a) (≥ 30.23 mg/dL) had an increased risk of poor collateralization compared with those with low tertile of Lp(a) (< 12.66 mg/dL) (adjusted OR = 4.300, 3.970 and 4.386, respectively, all P < 0.001). Conclusions Increased Lp(a) confers greater risk for poor coronary collateralization when total cholesterol, LDL-C or non-HDL-C are elevated especially for patients with type 2 diabetes. Electronic supplementary material The online version of this article (10.1186/s12933-019-0888-z) contains supplementary material, which is available to authorized users.

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Serum level of lipoprotein (a) is inversely associated with the development of coronary collateral circulation

Cited by 12 publications

References 26 publications

Low Lipoprotein(a) Concentration Is Associated with Cancer and All-Cause Deaths: A Population-Based Cohort Study (The JMS Cohort Study)

Low Lipoprotein(a) Concentration Is Associated with Cancer and All-Cause Deaths: A Population-Based Cohort Study (The JMS Cohort Study)

Lipoprotein(a) as a predictor of poor collateral circulation in patients with chronic stable coronary heart disease

Lipoprotein (a) interactions with cholesterol-containing lipids on angiographic coronary collateralization in type 2 diabetic patients with chronic total occlusion

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