Proprotein convertase subtilisin-kexin type 9 (PCSK9) inhibitors are a novel group of hypolipidemic drugs that are recommended particularly for high-risk hypercholesterolemia patients, including those with primary hypercholesterolemia (PH), where lifelong exposure to high low-density lipoprotein (LDL) cholesterol levels results in an elevated risk of atherosclerosis at an early age. The onset and progression of atherosclerosis is significantly influenced by activated platelets. Oxidized LDL influences platelet activation by interacting with their surface receptors and remodeling the composition of their cell membrane. This results in platelet aggregation, endothelial cell activation, promotion of inflammation and oxidative stress, and acceleration of lipid accumulation in atherosclerotic plaques. PCSK9 inhibitors reduce platelet activation by both significantly lowering LDL levels and reducing the LDL receptor-mediated activation of platelets by PCSK9. They also work synergistically with other hypolipidemic and antithrombotic drugs, including statins, ezetimibe, acetylsalicylic acid, clopidogrel, and ticagrelor, which enhances their antiplatelet and LDL-lowering effects. In this review, we summarize the currently available evidence on platelet hyperreactivity in PH, the effects of PCSK9 inhibitors on platelets, and their synergism with other drugs used in PH therapy.

The application of unattended blood pressure measurement (uAOBPM) for resting heart rate (RHR) assessment is unknown. To assess the agreement between RHR measured during uAOBPM and other methods, the authors conducted a comparability study with office blood pressure measurement (OBPM), ambulatory blood pressure monitoring (ABPM), and electrocardiogram (ECG) in a group of 110 participants referred for ABPM. RHR measured with uAOBPM (70.8 ± 12.5 bpm) was significantly lower than OBPM (72.8 ± 12.6 bpm) but higher than measured by 24 h ABPM (67.5 ± 10.2 bpm). There was no significant difference was found between RHR measured by uAOBPM and daytime ABPM (70.3 ± 11.2 bpm) or ECG (69.1 ± 11.6 bpm). Using Bland‐Altman statistics, the authors discovered a small difference in agreement between RHR measured by uAOBPM and daytime ABPM (bias: 0.4 with 95% confidence interval: ‐0.8 to 1.6 bpm), with a poorer agreement with OBPM (bias ‐2 with 95% confidence interval: ‐2.8 to ‐1.3 bpm) and ECG (bias 1.6 with 95% confidence interval: 0.5 to 2.7 bpm). The authors found significant agreement between uAOBPM and ECG in identifying subjects with RHR > 80 bpm OBPM, with Cohen's kappa coefficients of 0.783 and 0.671, respectively. Their findings indicate that RHR measured with uAOBPM remains in acceptable agreement with OBPM, ABPM, and ECG, the best agreement obtained with RHR from daytime ABPM.