Background <p>Lipoprotein(a) [Lp(a)] is causally linked to cardiovascular disease, but its role in the progression of coronary artery disease (CAD) remains uncertain. We investigated the association of Lp(a) levels with both functional severity and progression of coronary atherosclerosis, as assessed by angiography-derived quantitative flow ratio (QFR).</p> Methods <p>We retrospectively enrolled 290 patients who underwent serial coronary angiography and had baseline Lp(a) measurement. The global QFR, representing the total physiological burden, was calculated as the sum of the QFR values in the 3 major coronary arteries. Functional atherosclerotic progression was defined as a decline in global QFR.</p> Results <p>At baseline, patients with elevated Lp(a) (≥ 30&#xa0;mg/dL) had a lower global QFR compared to those with Lp(a) &lt; 30&#xa0;mg/dL (2.46 [2.20, 2.64] vs. 2.61 [2.44, 2.73]; P &lt; 0.001). The prevalence of functional significant multivessel disease was also higher in the elevated Lp(a) group (31.4% vs. 12.3%, P &lt; 0.001). Over a median follow-up of 12&#xa0;months, the global QFR declined more rapidly in the high Lp(a) group compared to the low Lp(a) group (−0.03 [−0.08, 0] vs. −0.01 [−0.05, 0.02], P = 0.027). Multivariable logistic regression confirmed that elevated Lp(a) is independently associated with functional disease progression (adjusted odds ratio 2.06, 95% confidence interval 1.13–3.73; P = 0.018).</p> Conclusions <p>Among patients with established CAD, Lp(a) is associated with high physiological atherosclerotic burden and accelerated progression of coronary physiology. These findings provide a pathophysiological insight into the link between Lp(a) and the residual cardiovascular risk, underscoring its potential as a therapeutic target.</p>

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Association of lipoprotein(a) with severity and progression of coronary artery disease: a serial QFR study

  • Wen Ye,
  • Jiapeng Chu,
  • Deqiang Yuan,
  • Yian Yao,
  • Xuebo Liu,
  • Wenwen Yan

摘要

Background

Lipoprotein(a) [Lp(a)] is causally linked to cardiovascular disease, but its role in the progression of coronary artery disease (CAD) remains uncertain. We investigated the association of Lp(a) levels with both functional severity and progression of coronary atherosclerosis, as assessed by angiography-derived quantitative flow ratio (QFR).

Methods

We retrospectively enrolled 290 patients who underwent serial coronary angiography and had baseline Lp(a) measurement. The global QFR, representing the total physiological burden, was calculated as the sum of the QFR values in the 3 major coronary arteries. Functional atherosclerotic progression was defined as a decline in global QFR.

Results

At baseline, patients with elevated Lp(a) (≥ 30 mg/dL) had a lower global QFR compared to those with Lp(a) < 30 mg/dL (2.46 [2.20, 2.64] vs. 2.61 [2.44, 2.73]; P < 0.001). The prevalence of functional significant multivessel disease was also higher in the elevated Lp(a) group (31.4% vs. 12.3%, P < 0.001). Over a median follow-up of 12 months, the global QFR declined more rapidly in the high Lp(a) group compared to the low Lp(a) group (−0.03 [−0.08, 0] vs. −0.01 [−0.05, 0.02], P = 0.027). Multivariable logistic regression confirmed that elevated Lp(a) is independently associated with functional disease progression (adjusted odds ratio 2.06, 95% confidence interval 1.13–3.73; P = 0.018).

Conclusions

Among patients with established CAD, Lp(a) is associated with high physiological atherosclerotic burden and accelerated progression of coronary physiology. These findings provide a pathophysiological insight into the link between Lp(a) and the residual cardiovascular risk, underscoring its potential as a therapeutic target.