Invasive assessment of coronary microvascular dysfunction and cardiovascular outcomes across the full spectrum of CHD: a meta-analysis.

INTRODUCTION AND OBJECTIVES: Coronary microvascular dysfunction (CMD) is highly prevalent and is recognized as an important clinical entity in patients with coronary heart disease (CHD). Nevertheless, the association of CMD with adverse cardiovascular events in the spectrum of CHD has not been systemically quantified. METHODS: We searched electronic databases for studies on patients with CHD in whom coronary microvascular function was measured invasively, and clinical events were recorded. The primary endpoint was major adverse cardiac events (MACE), and the secondary endpoint was all-cause death. Estimates of effect were calculated using a random-effects model from published risk ratios. RESULTS: We included 27 studies with 11 404 patients. Patients with CMD assessed by invasive methods had a higher risk of MACE (RR, 2.18; 95%CI, 1.80-2.64; P<.01) and all-cause death (RR, 1.88; 95%CI, 1.55-2.27; P<.01) than those without CMD. There was no significant difference in the impact of CMD on MACE (interaction P value=.95) among different invasive measurement modalities. The magnitude of risk of CMD assessed by invasive measurements for MACE was greater in acute coronary syndrome patients (RR, 2.84, 95%CI, 2.26-3.57; P<.01) than in chronic coronary syndrome patients (RR, 1.77, 95%CI, 1.44-2.18; P<.01) (interaction P value<.01). CONCLUSIONS: CMD based on invasive measurements was associated with a high incidence of MACE and all-cause death in patients with CHD. The magnitude of risk for cardiovascular events in CMD as assessed by invasive measurements was similar among different methods but varied among CHD populations.

The association of lipoprotein (a) with coronary artery calcification: A systematic review and meta-analysis.

BACKGROUND AND AIMS: Coronary artery calcification (CAC) is a crucial pathophysiological characteristic of atherosclerosis. The association between lipoprotein (a) [Lp(a)] and CAC is inconsistent. We aimed to assess the relationship between Lp(a) and CAC by exploring the association between elevated Lp(a) and CAC prevalence, the relationship between Lp(a) level and CAC prevalence, and the correlation between elevated Lp(a) and CAC progression. METHODS: We searched the PubMed, Web of Science, and EMBASE databases up to November 01, 2023. Studies exploring the association between serum Lp(a) and CAC (quantified using the Agatston score) were included. Association between Lp(a) level or elevated Lp(a) (higher than the cutoff values of 30 mg/dL, 50 mg/dL, or the highest quartile ranging from 33 to 38.64 mg/dL) and prevalence [CAC score >0 or >100, log (CAC score+1) >0] or progression (an increase in CAC score >0 or ≥100) of CAC were analysed. Odds ratios and 95% confidence intervals were calculated using a random-effects model. RESULTS: 40,073 individuals from 17 studies were included. Elevated Lp(a) was associated with a higher prevalence of CAC (OR, 1.31; 95% CI, 1.06 to 1.61; p = 0.01). As a continuous variable, Lp(a) level was positively correlated with the prevalence of CAC (OR, 1.05; 95% CI, 1.02 to 1.08; p = 0.003). Furthermore, elevated Lp(a) was associated with greater CAC progression (OR, 1.54; 95% CI, 1.23 to 1.92; p = 0.0002). CONCLUSIONS: This meta-analysis suggested that Lp(a) is associated with prevalence and progression of CAC. Further studies are required to explore whether Lp(a)-lowering therapy could prevent or inhibit CAC, ultimately reducing coronary artery disease risk.