A case of heterozygous familial hypercholesterolemia requiring strict low-density lipoprotein cholesterol management with proprotein convertase subtilisin/kexin 9 inhibitor after coronary artery bypass grafting.

Heterozygous familial hypercholesterolemia (HeFH) is a common, autosomal dominant, genetic disease that results in premature atherosclerotic cardiovascular disease secondary to high-level low-density lipoprotein cholesterol (LDL-C) exposure. We present a 68-year-old male patient with HeFH who was diagnosed with acute coronary syndrome at 9 months after coronary artery bypass grafting, although his LDL-C level was decreased to 77 mg/dL from 213 mg/dL. The emergency coronary angiography revealed that all bypass grafts were occluded, and the large atherosclerotic plaque burden was observed even in right internal thoracic artery (RITA) by intravascular ultrasound examination. Emergency percutaneous coronary intervention (PCI) was performed to his RITA bypass graft. After strict LDL-C management with proprotein convertase subtilisin/kexin 9 (PCSK-9) inhibitors, re-stenosis was not observed at the PCI site and the atherosclerotic plaque burden in his graft drastically disappeared. The high-risk HeFH patients, including those suffering from coronary bypass graft stenosis despite receiving medical therapy, might need stricter management of lipid profile with PCSK-9 inhibitors. .

Baseline low-density lipoprotein cholesterol predicts the benefit of adding ezetimibe on statin in statin-naïve acute coronary syndrome.

We aimed to evaluate the effect of baseline low-density lipoprotein cholesterol (LDL-C) on the outcomes of patients with the acute coronary syndrome (ACS) receiving pitavastatin monotherapy or the combination of pitavastatin + ezetimibe. In the HIJ-PROPER study, 1734 ACS patients with dyslipidemia were randomly assigned to receive pitavastatin or pitavastatin + ezetimibe therapy. Statin-naïve participants (n = 1429) were divided into two groups based on the median LDL-C level (131 mg/dL) at enrollment. The primary endpoint was a composite of all-cause death, non-fatal myocardial infarction, non-fatal stroke, unstable angina, and ischemia-driven coronary revascularization. The median follow-up was 3.2 years. In the < 131 mg/dL group (n = 686), LDL-C changes were - 34.0% and - 49.8% in the pitavastatin monotherapy and pitavastatin + ezetimibe-treated groups (P < 0.0001), respectively; in the ≥ 131 mg/dL group (n = 743), LDL-C changes were - 42.9% and - 56.4% (P < 0.0001, respectively. Kaplan-Meier analyses revealed that the primary endpoint was not significantly different between the treatment groups for the < 131 mg/dL group, however, it was significantly lower in patients treated with pitavastatin + ezetimibe in the ≥ 131 mg/dL group (Hazard ratio = 0.72, 95% confidence interval = 0.56-0.91, P = 0.007, P value for interaction = 0.012). Statin-naïve ACS patients with baseline LDL-C < 131 mg/dL did not clinically benefit from pitavastatin + ezetimibe, while patients with baseline LDL-C ≥ 131 mg/dL treated with pitavastatin + ezetimibe showed better clinical results than those treated with pitavastatin monotherapy.Clinical Trial Registration: Original HIJ PROPER study; URL: http://www.umin.ac.jp/ctr . Unique Identifier; UMIN000002742, registered as an International Standard Randomized Controlled Trial.

The Effective Use of Digoxin in a Patient with Metastatic Breast Cancer and Anthracycline-induced Cardiomyopathy.

Anthracyclines have cardiotoxic side effects. Cardioprotective drugs such as angiotensin-converting enzyme inhibitors and beta-blockers are therefore recommended for patients with anthracycline-induced cardiomyopathy. We herein present a 54-year-old woman with recurrent metastatic breast cancer who developed heart failure (HF) with a left ventricular ejection fraction (LVEF) of 22% after undergoing epirubicin chemotherapy. However, her HF symptoms and low LVEF persisted despite 5 months of cardioprotective therapy and additional oral pimobendan. Pimobendan was discontinued because of ventricular arrhythmia and hypotension. After the start of low-dose (0.125 mg daily) digoxin, her LVEF increased to 42%, and her HF symptoms improved with no adverse events.