Lipoprotein(a) Interactions With Low‐Density Lipoprotein Cholesterol and Other Cardiovascular Risk Factors in Premature Acute Coronary Syndrome (ACS)

Afshar, Mehdi; Pilote, Louise; Dufresne, Line; Engert, James C.; Thanassoulis, George

doi:10.1161/jaha.115.003012

Cited by 67 publications

(46 citation statements)

References 46 publications

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“…Clinical studies and meta‐analysis also suggest that it might be important to predict the risk of AAA, and the present study by Afshar et al10 further extends the current knowledge suggesting that high Lp(a) might be an important biomarker of premature ACS in young individuals (<55 years), especially with simultaneous high LDL‐C levels. Further studies are still required to enable an understanding of all of the aspects of Lp(a) (patho)physiology, its functions, predictive values in different conditions, the “gold standard” method for its measurement, and whether it is possible to reduce the cost of this method to enable its widespread use.…”

supporting

confidence: 83%

“…The interaction with high Lp(a) was stronger at increasing LDL‐C levels (LDL‐C >3.5, adjusted odds ratio 1.87; LDL‐C >4.5, adjusted odds ratio 2.72), and became attenuated at LDL‐C ≤3.5 mmol/L (OR 1.16; P =0.447). No other risk factors investigated, such as age, sex, smoking, hypertension, diabetes, familial hypercholesterolemia, and body mass index were associated with high Lp(a) 10. The authors confirmed that in relatively young ACS patients (<55 years), high Lp(a) was strongly associated with high LDL‐C levels, and Lp(a) confers greater risk for premature ACS when LDL‐C is elevated.…”

mentioning

confidence: 72%

“…Taking the abovementioned into account, the study by Afshar et al10 in this issue of the Journal of the American Heart Association ( JAHA ) is of special interest and importance. The authors verified the current recommendations for Lp(a) and suggested that treatment should focus on the control of other risk factors first, including lowering LDL‐C, and assumed that identifying interactions between Lp(a) and other risk factors could identify individuals at increased risk for Lp(a)‐mediated disease 10.…”

mentioning

confidence: 99%

“…The authors confirmed that in relatively young ACS patients (<55 years), high Lp(a) was strongly associated with high LDL‐C levels, and Lp(a) confers greater risk for premature ACS when LDL‐C is elevated. Therefore, especially in individuals with high Lp(a) (>50 mg/dL) and concomitant elevations in LDL‐C >3.5 mmol/L, intensive LDL‐C lowering may be warranted to reduce the risk of premature ACS 10. Obviously this study needs to be confirmed in larger well‐designed controlled trials; however, even based on these results, we can say that Lp(a) might be an important predictor of premature ACS in young patients with cardiovascular risk 10.…”

mentioning

confidence: 99%

“…Therefore, especially in individuals with high Lp(a) (>50 mg/dL) and concomitant elevations in LDL‐C >3.5 mmol/L, intensive LDL‐C lowering may be warranted to reduce the risk of premature ACS 10. Obviously this study needs to be confirmed in larger well‐designed controlled trials; however, even based on these results, we can say that Lp(a) might be an important predictor of premature ACS in young patients with cardiovascular risk 10. This study clearly confirms that elevated Lp(a) might often be present in relatively young individuals without any other important risk factors.…”

mentioning

confidence: 99%

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Lipoprotein (a)—We Know So Much Yet Still Have Much to Learn …

Banach

2016

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supporting

confidence: 83%

mentioning

confidence: 72%

mentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Lipoprotein (a)—We Know So Much Yet Still Have Much to Learn …

Banach

2016

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Effect of C-Reactive Protein on Lipoprotein(a)-Associated Cardiovascular Risk in Optimally Treated Patients With High-Risk Vascular Disease

Puri

Nissen

Arsenault³

et al. 2020

JAMA Cardiol

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IMPORTANCE Although lipoprotein(a) (Lp[a]) is a causal genetic risk factor for atherosclerotic cardiovascular disease, it remains unclear which patients with established atherosclerotic cardiovascular disease stand to benefit the most from Lp(a) lowering. Whether inflammation can modulate Lp(a)-associated cardiovascular (CV) risk during secondary prevention is unknown.OBJECTIVE To examine whether Lp(a)-associated CV risk is modulated by systemic inflammation in optimally treated patients at high risk of CV disease. DESIGN, SETTING, AND PARTICIPANTS A prespecified secondary post hoc analysis of the double-blind, multicenter randomized clinical Assessment of Clinical Effects of Cholesteryl Ester Transfer Protein Inhibition With Evacetrapib in Patients at a High Risk for Vascular Outcomes (ACCELERATE) trial was conducted between October 1, 2012, and December 31, 2013; the study was terminated October 12, 2015. The study was conducted at 543 academic and community hospitals in 36 countries among 12 092 patients at high risk of CV disease (acute coronary syndrome, stroke, peripheral arterial disease, or type 2 diabetes with coronary artery disease) with measurable Lp(a) and high-sensitivity C-reactive protein (hsCRP) levels during treatment. Statistical analysis for this post hoc analysis was performed from September 26, 2018, to March 28, 2020. INTERVENTIONS Participants received evacetrapib, 130 mg/d, or matching placebo. MAIN OUTCOMES AND MEASURESThe ACCELERATE trial found no significant benefit or harm of evacetrapib on 30-month major adverse cardiovascular events (CV death, myocardial infarction [MI], stroke, coronary revascularization, or hospitalization for unstable angina). This secondary analysis evaluated rates of CV death, MI, and stroke across levels of Lp(a).RESULTS High-sensitivity C-reactive protein and Lp(a) levels were measured in 10 503 patients (8135 men; 8561 white; 10 134 received concurrent statins; mean [SD] age, 64.6 [9.4] years). In fully adjusted analyses, in patients with hsCRP of 2 mg/L or more but not less than 2 mg/L, increasing quintiles of Lp(a) were significantly associated with greater rates of death, MI, and stroke (P = .006 for interaction). Each unit increase in log Lp(a) levels was associated with a 13% increased risk of CV death, nonfatal MI, or stroke only in those with hsCRP levels of 2 mg/L or more (P = .008 for interaction). There was also a significant stepwise relationship between increasing Lp(a) quintiles and time to first CV death, MI, or stroke (log-rank P < .001) when hsCRP levels were 2 mg/L or more but not less than 2 mg/L. Sensitivity analyses in the ACCELERATE placebo-treated group yielded similar significant associations exclusively in the group with hsCRP of 2 mg/L or more.CONCLUSIONS AND RELEVANCE Elevated Lp(a) levels during treatment are related to CV death, MI, and stroke when hsCRP levels are 2 mg/L or more but not less than 2mg/L. This finding suggests a potential benefit of lowering Lp(a) in patients with residual systemic inflammation despite receipt of o...

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Risk factor profile and outcomes of premature acute coronary syndrome after percutaneous coronary intervention: A 1‐year prospective design

Fallahzadeh,

Mehraban,

Mahmoodi

et al. 2023

Clinical Cardiology

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BackgroundThe prevalence of acute coronary syndrome (ACS) among young adults (premature ACS) has dramatically increased in recent years, especially in developing countries. Yet, the data on these patients' attributed risk factors and outcomes are inconsistent. In this study, we aimed to investigate these data in a cohort of premature ACS cases who underwent percutaneous coronary intervention (PCI) compared to older patients.HypothesisWe hypothesize that premature ACS patients undergoing PCI will exhibit different risk factor profiles and outcomes compared to non‐premature patients. specifically, we anticipate that premature patients do not necessarily have better outcomes than non‐premature.MethodsOverall, 3142 and 10 399 patients were included in premature and non‐premature groups, respectively. Patients' pre‐operative, post‐operative, and follow‐up data were retrieved retrospectively from the Tehran Heart Center PCI databank.ResultsThe mean age of premature and non‐premature cohorts was 48.39 and 67 years, respectively. Patients were predominantly male in both groups. Family history of coronary artery disease (CAD), dyslipidemia, smoking, and opium addiction were more prevalent among the younger cohort. After adjustment, in‐hospital mortality in younger patients was considerably higher, with all‐cause mortality and major cardiovascular and cerebrovascular events (MACCE) exhibiting no noticeable difference among the two groups.ConclusionsRisk factor profile is different in young patients, and traditional cardiovascular risk factors, such as hypertension and diabetes mellitus, are more prevalent among older adults. Younger age is not equivalent to a better prognosis; hence, similar or even more caution should be taken into consideration regarding secondary prevention for these patients.

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Lipoprotein(a) Interactions With Low‐Density Lipoprotein Cholesterol and Other Cardiovascular Risk Factors in Premature Acute Coronary Syndrome (ACS)

Cited by 67 publications

References 46 publications

Lipoprotein (a)—We Know So Much Yet Still Have Much to Learn …

Lipoprotein (a)—We Know So Much Yet Still Have Much to Learn …

Effect of C-Reactive Protein on Lipoprotein(a)-Associated Cardiovascular Risk in Optimally Treated Patients With High-Risk Vascular Disease

Risk factor profile and outcomes of premature acute coronary syndrome after percutaneous coronary intervention: A 1‐year prospective design

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