Impact of Lipoprotein(a) as a Residual Risk Factor in Long-Term Cardiovascular Outcomes in Patients With Acute Coronary Syndrome Treated With Statins

Takahashi, Daigo; Wada, Hideki; Ogita, Manabu; Yamaguchi, Kentaro; Nishio, Ryota; Takeuchi, Mitsuhiro; Shitara, Jun; Tsuboi, Shuta; Dohi, Tomotaka; Suwa, Satoru; Miyauchi, Katsumi; Daida, Hiroyuki; Minamino, Tohru

doi:10.1016/j.amjcard.2021.12.014

Cited by 12 publications

(9 citation statements)

References 24 publications

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“…Lp(a) accelerates the progression of low-attenuation coronary plaques (necrotic cores) [25]. As for patients with established cardiovascular disease, especially in young individuals, higher levels of Lp(a) are associated with an increased risk of MACE such as CAD death, myocardial infarction, and urgent revascularization [26][27][28].…”

Section: Discussionmentioning

confidence: 99%

Effect of an increase in Lp(a) following statin therapy on cardiovascular prognosis in secondary prevention population of coronary artery disease

Zhu

Fang

Gao

et al. 2022

BMC Cardiovasc Disord

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Background Lipoprotein (a) [Lp(a)] is an independent risk factor for coronary artery disease (CAD). Recent studies have indicated that statins tend to increase Lp(a) levels by 10–20%. However, the association of statin-mediated increases in Lp(a) levels with CAD has not been determined. Methods This study included 488 patients with acute coronary syndrome (ACS) who underwent percutaneous coronary intervention (PCI). Lp(a) levels were measured at baseline and 1 month after statin therapy. The study endpoints were major adverse cardiovascular events (MACE). Hazard ratios for the MACE were adjusted for potential confounder using Cox regression. Results After statin therapy, the mean level of Lp(a) increased by 19.3% from baseline. Lp(a) levels increased in 307 patients (62.9%) with a median elevation of 4.1 mg/dL. Patients with an increase in Lp(a) were at higher risk for MACE than those without an increase in Lp(a) (p = 0.044). Subgroup analyses revealed that a mild-to-moderate increase in Lp(a) was not associated with MACE, whereas there was a strong correlation between the highest quartile increase in Lp(a) (≥ 10.1 mg/dL) and MACE (HR = 2.29, 95%CI = 1.36–3.84, p = 0.002). This correlation was independent of baseline Lp(a) levels but not independent of on-statin Lp(a) levels. Conclusions Severe increases in Lp(a) following statin therapy raise the risk of MACE, but a mild-to-moderate increase in Lp(a) may not affect the cardiovascular prognosis of CAD patients. Even if the baseline Lp(a) levels are low, it is necessary to continue testing for Lp(a) concentration at least once after statin.

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Section: Discussionmentioning

confidence: 99%

Effect of an increase in Lp(a) following statin therapy on cardiovascular prognosis in secondary prevention population of coronary artery disease

Zhu

Fang

Gao

et al. 2022

BMC Cardiovasc Disord

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“…In contrast, a Chinese cohort study involving 1,008 patients with AMI aged ≥ 80 years between 2012 and 2018 found that baseline Lp(a) concentration was independently associated with the increased risk of cardiac death at 3 years. 15 Most recently, Takahashi et al 16 analyzed 1,131 Japanese patients with ACS between 2008 and 2017 and found that high Lp(a) levels are independently associated with increased incidence rates of major adverse cardiovascular events at a median follow-up of 2.2 years. However, they did not consider several hemodynamic parameters including systolic blood pressure, Killip classification on presentation, and left ventricular ejection fraction in the multivariable adjustments.…”

Section: Discussionmentioning

confidence: 99%

“… 11 12 However, the results of recent studies on the predictive value of baseline Lp(a) levels after index ACS events are conflicting. 13 14 15 16 Furthermore, the associated risk between high Lp(a) levels and acute myocardial infarction (AMI) reportedly varies markedly between ethnic groups. 17 Although LDL cholesterol has been proven to be a major causal factor for the development of atherosclerotic cardiovascular disease, the prognostic value of baseline LDL cholesterol after atherosclerotic cardiovascular events is different from what is expected: low baseline LDL cholesterol is associated with worse clinical outcomes.…”

Section: Introductionmentioning

confidence: 99%

Baseline Lipoprotein(a) Levels and Long-Term Cardiovascular Outcomes After Acute Myocardial Infarction

et al. 2023

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Background Lipoprotein(a) is a known independent risk factor for atherosclerotic cardiovascular disease. However, the prognostic impact of the baseline lipoprotein(a) levels on long-term clinical outcomes among patients with acute myocardial infarction remain unclear. Methods We analyzed 1,908 patients with acute myocardial infarction from November 2011 to October 2015 from a single center in Korea. They were divided into 3 groups according to their baseline lipoprotein(a) levels: groups I (< 30 mg/dL, n = 1,388), II (30–49 mg/dL, n = 263), and III (≥50 mg/dL, n = 257). Three-point major adverse cardiovascular events (a composite of nonfatal myocardial infarction, nonfatal stroke, and cardiac death) at 3 years were compared among the 3 groups. Results The patients were followed for 1094.0 (interquartile range, 1,033.8–1,095.0) days, during which a total of 326 (17.1%) three-point major adverse cardiovascular events occurred. Group III had higher rates of three-point major adverse cardiovascular events compared with Group I (23.0% vs. 15.7%; log-rank P = 0.009). In the subgroup analysis, group III had higher rates of three-point major adverse cardiovascular events compared with group I in patients with non-ST-segment elevation myocardial infarction (27.0% vs. 17.1%; log-rank P = 0.006), but not in patients with ST-segment elevation myocardial infarction (14.4% vs. 13.3%; log-rank P = 0.597). However, in multivariable Cox time-to-event models, baseline lipoprotein(a) levels were not associated with an increased incidence of three-point major adverse cardiovascular events, regardless of the type of acute myocardial infarction. Sensitivity analyses in diverse subgroups showed similar findings to those of the main analysis. Conclusion Baseline lipoprotein(a) levels in Korean patients with acute myocardial infarction were not independently associated with increased major adverse cardiovascular events at 3 years.

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“…Lp(a) accelerates the progression of low-attenuation coronary plaques (necrotic cores) [25]. As for patients with established cardiovascular disease, higher levels of Lp(a) are associated with an increased risk of MACE such as CAD death, myocardial infarction, and urgent revascularization [26,27].…”

Section: Effect Of Statins On Lp(a) Levelsmentioning

confidence: 99%

Effect of an increase in Lp(a) following statin therapy on cardiovascular prognosis in secondary prevention population of coronary artery disease

Zhu

Fang

Gao

et al. 2022

Preprint

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Background It is frequently observed in clinical trials that statins lead to an increase in Lp(a), and recent studies have indicated that statins tend to increase Lp(a) levels by 10–20%. Lp(a) is an independent risk factor for coronary artery disease (CAD). However, the association of statin-mediated increases in Lp(a) levels with CAD has not been determined. Methods This study included 488 patients with acute coronary syndrome (ACS) who underwent percutaneous coronary intervention (PCI). Lp(a) levels were measured at baseline and 1 month after statin therapy. The study endpoints were major adverse cardiovascular events (MACE). Hazard ratios for the MACE were adjusted for potential confounder using Cox regression. Results After statin therapy, the mean level of Lp(a) increased by 19.3% from baseline. Lp(a) levels increased in 307 patients (62.9%) with a median elevation of 4.1 mg/dL. Individuals with an increase in Lp(a) were at higher risk for MACE than those without an increase in Lp(a) (p = 0.044). Subgroup analyses revealed that a mild-to-moderate increase in Lp(a) was not associated with MACE, whereas there was a strong correlation between the highest quartile increase in Lp(a) (≥ 10.1mg/dL) and MACE (HR = 2.29, 95%CI = 1.36–3.84, p = 0.002). This correlation was independent of baseline Lp(a) levels but not independent of on-statin Lp(a) levels. Conclusions Substantial increases in Lp(a) following statin therapy raise the risk of MACE, but a mild-to-moderate increase in Lp(a) hardly affects the cardiovascular prognosis of CAD patients. Even if the baseline Lp(a) levels are low, it is necessary to continue testing for Lp(a) concentration at least once after statin.

show abstract

Impact of Lipoprotein(a) as a Residual Risk Factor in Long-Term Cardiovascular Outcomes in Patients With Acute Coronary Syndrome Treated With Statins

Cited by 12 publications

References 24 publications

Effect of an increase in Lp(a) following statin therapy on cardiovascular prognosis in secondary prevention population of coronary artery disease

Effect of an increase in Lp(a) following statin therapy on cardiovascular prognosis in secondary prevention population of coronary artery disease

Baseline Lipoprotein(a) Levels and Long-Term Cardiovascular Outcomes After Acute Myocardial Infarction

Effect of an increase in Lp(a) following statin therapy on cardiovascular prognosis in secondary prevention population of coronary artery disease

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