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Войти в исследования Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology · 2026
LDL-cholesterol reduction is not associated with deterioration of cellular integrity after myocardial infarction - a longitudinal analysis.
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Jarosz Izabela, Mazur Michal, Popiolek-Kalisz Joanna
Аннотация
BACKGROUND: Intensive low-density lipoprotein cholesterol (LDL-C) lowering is a cornerstone of secondary prevention after myocardial infarction, but theoretical concerns persist regarding potential adverse effects of very low LDL-C on cellular membrane integrity. Phase angle at 50 kHz (PhA50), derived from bioelectrical impedance analysis (BIA), is a non-invasive marker reflecting cell membrane bioelectrical properties. This study assessed whether LDL-C reduction after myocardial infarction is associated with deterioration in PhA50.
METHODS: This longitudinal analysis included 45 patients undergoing outpatient cardiac rehabilitation after myocardial infarction. Lipid profile, body mass index (BMI), and PhA50 were assessed at rehabilitation entry and completion. Within-person changes were analyzed using paired tests. Associations between LDL-C reduction and change in PhA50 were examined using correlation and linear regression models adjusted for age, sex, BMI change, follow-up time, and baseline PhA50.
RESULTS: Median assessment interval was 55 [37-91] days. LDL-C decreased significantly from 131.42±36.32 mg/dL to 51.90±22.40 mg/dL (p < 0.001), corresponding to an approximate 60.5% reduction at the group level. PhA50 remained stable over follow-up (5.57 [5.08, 6.05] vs. 5.55 [5.12, 6.07] degrees; p = 0.332). LDL-C reduction was not correlated with change in PhA50 (R=-0.004; p = 0.981) and was not associated with ΔPhA50 in regression analyses. Age emerged as an independent inverse predictor of ΔPhA50 (p = 0.02).
CONCLUSIONS: Substantial LDL-C reduction after myocardial infarction was not associated with deterioration in BIA-derived PhA50, providing physiological reassurance regarding cellular integrity during intensive lipid lowering.
METHODS: This longitudinal analysis included 45 patients undergoing outpatient cardiac rehabilitation after myocardial infarction. Lipid profile, body mass index (BMI), and PhA50 were assessed at rehabilitation entry and completion. Within-person changes were analyzed using paired tests. Associations between LDL-C reduction and change in PhA50 were examined using correlation and linear regression models adjusted for age, sex, BMI change, follow-up time, and baseline PhA50.
RESULTS: Median assessment interval was 55 [37-91] days. LDL-C decreased significantly from 131.42±36.32 mg/dL to 51.90±22.40 mg/dL (p < 0.001), corresponding to an approximate 60.5% reduction at the group level. PhA50 remained stable over follow-up (5.57 [5.08, 6.05] vs. 5.55 [5.12, 6.07] degrees; p = 0.332). LDL-C reduction was not correlated with change in PhA50 (R=-0.004; p = 0.981) and was not associated with ΔPhA50 in regression analyses. Age emerged as an independent inverse predictor of ΔPhA50 (p = 0.02).
CONCLUSIONS: Substantial LDL-C reduction after myocardial infarction was not associated with deterioration in BIA-derived PhA50, providing physiological reassurance regarding cellular integrity during intensive lipid lowering.