Background and objectives: Nutritional disorders are common in patients with heart failure (HF) and are associated with reduced functional capacity and poor prognosis. In this study, we evaluated the prognostic, nutritional and functional impact of a structured nutritional intervention in patients with chronic HF at risk of malnutrition. Methods: This is a prespecified subanalysis of the randomized controlled trial Prognostic And Clinical iMpAct of a Nutritional intervention in patients with chronic HF (PACMAN-HF). Ambulatory patients with chronic HF at risk of malnutrition were identified using the Mini Nutritional Assessment (MNA) questionnaire and randomized to receive either an individualised nutritional intervention (intervention group) or standard care (control group). We evaluated the frequency of malnutrition risk and the impact of the intervention on clinical outcomes, defined as a composite of all-cause mortality or time to first HF hospitalisation, as well as nutritional status and functional capacity at 3- and 12-month follow-ups. Results: A total of 225 patients were screened. Of these, 72 (32%) were identified as being at risk of malnutrition and 64 (28.4%) met the inclusion criteria and were randomized (31 in the intervention group and 33 in the control group). There were no significant differences between the groups in terms of all-cause mortality or time to first HF hospitalisation (HR = 0.34 [0.11–1.09]; p = 0.072). At 12 months, the intervention group demonstrated a significant improvement in functional capacity, with an increase of 31.3 metres in the 6-minute walk test (6MWT) (p = 0.002), whereas no significant change was observed in the control group. Nutritional status improved significantly in the intervention group (MNA score +4.12, p < 0.001) and declined in the control group (−1.15, p = 0.029). At 12 months, body mass index, tricipital skinfold thickness, arm circumference, and serum albumin levels increased in the intervention group. Conclusions: A structured and individualised nutritional intervention significantly improved nutritional status and functional capacity over 12 months, although it did not impact major clinical outcomes.
Background/Objectives: Achieving guideline-recommended low-density lipoprotein cholesterol (LDL-C) targets in patients with chronic coronary syndrome (CCS) remains challenging despite intensive lipid-lowering therapy. Bempedoic acid (BA) offers an oral therapeutic option, although data on its clinical performance and patient-level determinants of response in real-world Spanish settings are limited. Methods: We conducted a prospective multicentre study across the four healthcare areas of Cáceres province, Spain, including consecutive CCS patients with LDL-C ≥ 55 mg/dL despite stable intensive lipid-lowering therapy. BA 180 mg/day was added to background treatment. Lipid parameters, metabolic profile, and safety outcomes were assessed after a median follow-up of 28 weeks (IQR 23–47). Multivariable analyses were performed to identify factors associated with of LDL-C reduction and target attainment. A total of 118 patients were analyzed for outcomes. Results: A total of 118 patients (mean age 62.4 ± 10.0 years; 79.2% male) were included. BA reduced LDL-C by 22.8% (−16.36 mg/dL; p < 0.001), enabling 48.3% of patients to achieve LDL-C < 55 mg/dL. Higher baseline LDL-C (β = −0.515; p = 0.001) and the presence of diabetes mellitus (B = 13.8 mg/dL; p = 0.024) were independently associated with greater LDL-C reduction. Notably, 56.3% of patients presented with elevated baseline lipoprotein(a) levels (>50 mg/dL), describing a high underlying burden of residual risk. BA was well tolerated, with a modest increase in uric acid levels but no gout events and a high treatment persistence rate (94.4%). Conclusions: In a real-world CCS population receiving intensive lipid-lowering therapy, BA provides clinically meaningful LDL-C reduction with a favorable safety profile in this multicentre cohort from Cáceres province. Patients with higher baseline LDL-C and diabetes derive greater benefit, supporting a more personalized approach to therapy. These findings reinforce the role of BA in Spanish patients as an intermediate step in lipid-lowering strategies before escalation to more costly therapies, addressing the scarcity of local real-world data.
Background: Hepatic cholesterol synthesis inhibition is a cornerstone of atherosclerotic cardiovascular disease (ASCVD) prevention. Despite intensive lipid-lowering therapy, many very-high-risk patients with chronic coronary syndrome (CCS) fail to achieve recommended LDL-C targets. Bempedoic acid (BA), a liver-activated ATP citrate lyase (ACLY) inhibitor, suppresses cholesterol biosynthesis upstream of HMG-CoA reductase and may have metabolic and renal effects. Methods: We conducted a prospective, single-centre, real-world study including consecutive CCS patients with LDL-C ≥55 mg/dL despite stable intensive lipid-lowering therapy (high-intensity statin plus ezetimibe or PCSK9 inhibitor plus ezetimibe in statin-intolerant patients). BA 180 mg/day was added to background therapy. Lipid parameters, uric acid, and renal function were assessed at baseline and ≥8 weeks. Multivariable regression analyses identified predictors of LDL-C reduction and target attainment. Results: Among 118 patients with complete follow-up (mean age 62.4 ± 10.0 years; 79.2% male), BA reduced LDL-C by 22.8% (−16.36 mg/dL; p < 0.001), enabling 48.3% to achieve LDL-C < 55 mg/dL. Total and non–HDL cholesterol decreased significantly, whereas triglycerides and fasting glucose remained unchanged. HDL-C showed a modest reduction. Uric acid increased by 0.96 mg/dL without gout events, and renal function changes were small and clinically non-relevant. Higher historical untreated LDL-C and diabetes mellitus independently predicted greater LDL-C reduction; higher historical LDL-C and baseline uric acid predicted LDL-C goal attainment. Conclusions: ACLY inhibition with BA provides clinically meaningful LDL-C reduction in intensively treated CCS patients, revealing a cardiometabolic phenotype with proportional lipid responsiveness and modest urate changes. BA represents an effective translational strategy linking hepatic cholesterol metabolism to clinical lipid optimization in very-high-risk patients.