Background: Low admission low-density lipoprotein cholesterol (LDL-C) is paradoxically associated with worse outcomes after acute coronary syndrome, but this may reflect confounding rather than causation. We examined the paradox in statin-naïve patients. Methods: We studied 388 statin-naïve patients with a first ST-segment elevation myocardial infarction (STEMI) treated with primary percutaneous coronary intervention (PCI) and followed for up to five years. Admission LDL-C was analyzed continuously and as three categories (130 mg/dL), with all-cause mortality assessed using Kaplan–Meier, Cox regression, restricted cubic splines, and landmark sensitivity analyses. Results: Crude mortality was highest in the lowest LDL-C group (20.0% vs. 8.3% vs. 10.7%; p = 0.014), and LDL-C < 100 mg/dL predicted higher mortality (hazard ratio 2.03, 95% CI 1.02–4.03). After adjustment, this remained non-significant across the parsimonious and fully adjusted models (adjusted HR 1.27–1.43, all 95% CIs including 1); older age, lower ejection fraction, and diabetes were independent predictors of death. The lowest stratum also had lower albumin and higher CONUT scores, consistent with a frailty phenotype. Conclusions: In statin-naïve STEMI patients undergoing primary PCI, the lipid paradox reflected age- and frailty-related confounding rather than protection; low admission LDL-C marks a higher-risk phenotype and should not discourage guideline-directed lipid-lowering therapy.

Background: Benidipine is a long-acting calcium channel blocker used for the treatment of hypertension and chronic coronary syndrome. Although it effectively lowers blood pressure (BP), the relationship between BP reduction and improvement in angina-related health status during benidipine therapy remains uncertain. This study evaluated changes in BP and patient-reported angina-related health status in a large real-world cohort. Methods: This prospective, multicenter, observational cohort study included 1659 patients with hypertension and/or chronic coronary syndrome who underwent baseline clinical assessment before initiation of benidipine therapy and were reassessed after 3 months. Changes in systolic and diastolic BP and Seattle Angina Questionnaire-7 (SAQ-7) scores were evaluated. Multivariable linear regression analyses were performed to identify predictors of BP reduction and symptomatic improvement. A propensity score-matched analysis according to coronary artery disease (CAD) status was conducted to further explore differences in treatment response. Results: The mean age was 62.2 ± 12.2 years, and 54.0% of participants were women. Systolic BP decreased by 13.8 mmHg and diastolic BP by 6.7 mmHg (both p < 0.001). Mean SAQ-7 score increased by 8.1 points (p < 0.001), exceeding the established threshold for clinically meaningful improvement. Baseline SAQ-7 score showed the strongest association with change in SAQ-7, whereas baseline systolic BP was the strongest predictor of BP reduction. The correlation between changes in systolic BP and SAQ-7 was weak (r = 0.058, p = 0.023). In the propensity score-matched cohort (n = 732), BP reduction was similar regardless of CAD status, whereas improvement in SAQ-7 was greater in patients without obstructive CAD. Conclusions: In this multicenter real-world cohort, benidipine therapy was associated with significant BP reduction and clinically meaningful improvement in angina-related health status over 3 months. Symptomatic improvement showed only a weak association with BP reduction. These findings should be interpreted within the limitations of an observational study and warrant confirmation in controlled comparative studies.