Objective: Lipoprotein (a) (Lp[a]), which is a highly heritable trait, is associated with coronary artery disease (CAD). However, the insight into whether the association between Lp(a) and CAD differs according to the family history of CAD remains unclear. Methods: We investigated clinical data of 4,512 participants who underwent serum Lp(a) level measurement at Kanazawa University Hospital between 2008 and 2016. The association between Lp(a) and CAD according to CAD family history was investigated through logistic regression analyses. Results: CAD family history and Lp(a) levels were significantly associated with CAD development (odds ratio [OR], 1.32; 95% confidence interval [CI], 1.12–1.52; p<0.001 and OR, 1.13; 95% CI, 1.03–1.23; p<0.001 per 10 mg/dL, respectively). In patients without CAD family history, those with Lp(a) levels ≥30 mg/dL had higher CAD risk than those with Lp(a) levels <30 mg/dL (reference) (OR, 1.33; 95% CI, 1.05–1.61; p<0.001). In patients with CAD family history, those who had Lp(a) levels <30 and ≥30 mg/dL were both highly at risk for CAD (OR, 1.24; 95% CI, 1.04–1.44; p<0.001 and OR, 1.68; 95% CI, 1.34–2.02; p<0.001, respectively). Adding CAD family history and Lp(a) information to other conventional risk factors enhanced CAD risk discrimination (C-statistics: 0.744 [0.704–0.784] to 0.768 [0.730–0.806], and 0.791 [0.751–0.831], respectively; p<0.05 for both). Conclusion Lp(a) level was associated with CAD development regardless of CAD family history status.

Objective: Lipoprotein (a) (Lp[a]), which is a highly heritable trait, is associated with coronary artery disease (CAD). However, the insight into whether the association between Lp(a) and CAD differs according to the family history of CAD remains unclear. Methods: We investigated clinical data of 4,512 participants who underwent serum Lp(a) level measurement at Kanazawa University Hospital between 2008 and 2016. The association between Lp(a) and CAD according to CAD family history was investigated through logistic regression analyses. Results: CAD family history and Lp(a) levels were significantly associated with CAD development (odds ratio [OR], 1.32; 95% confidence interval [CI], 1.12–1.52; p<0.001 and OR, 1.13; 95% CI, 1.03–1.23; p<0.001 per 10 mg/dL, respectively). In patients without CAD family history, those with Lp(a) levels ≥30 mg/dL had higher CAD risk than those with Lp(a) levels <30 mg/dL (reference) (OR, 1.33; 95% CI, 1.05–1.61; p<0.001). In patients with CAD family history, those who had Lp(a) levels <30 and ≥30 mg/dL were both highly at risk for CAD (OR, 1.24; 95% CI, 1.04–1.44; p<0.001 and OR, 1.68; 95% CI, 1.34–2.02; p<0.001, respectively). Adding CAD family history and Lp(a) information to other conventional risk factors enhanced CAD risk discrimination (C-statistics: 0.744 [0.704–0.784] to 0.768 [0.730–0.806], and 0.791 [0.751–0.831], respectively; p<0.05 for both). Conclusion Lp(a) level was associated with CAD development regardless of CAD family history status.

Objective: Lipoprotein (a) (Lp[a]), which is a highly heritable trait, is associated with coronary artery disease (CAD). However, the insight into whether the association between Lp(a) and CAD differs according to the family history of CAD remains unclear. Methods: We investigated clinical data of 4,512 participants who underwent serum Lp(a) level measurement at Kanazawa University Hospital between 2008 and 2016. The association between Lp(a) and CAD according to CAD family history was investigated through logistic regression analyses. Results: CAD family history and Lp(a) levels were significantly associated with CAD development (odds ratio [OR], 1.32; 95% confidence interval [CI], 1.12–1.52; p<0.001 and OR, 1.13; 95% CI, 1.03–1.23; p<0.001 per 10 mg/dL, respectively). In patients without CAD family history, those with Lp(a) levels ≥30 mg/dL had higher CAD risk than those with Lp(a) levels <30 mg/dL (reference) (OR, 1.33; 95% CI, 1.05–1.61; p<0.001). In patients with CAD family history, those who had Lp(a) levels <30 and ≥30 mg/dL were both highly at risk for CAD (OR, 1.24; 95% CI, 1.04–1.44; p<0.001 and OR, 1.68; 95% CI, 1.34–2.02; p<0.001, respectively). Adding CAD family history and Lp(a) information to other conventional risk factors enhanced CAD risk discrimination (C-statistics: 0.744 [0.704–0.784] to 0.768 [0.730–0.806], and 0.791 [0.751–0.831], respectively; p<0.05 for both). Conclusion Lp(a) level was associated with CAD development regardless of CAD family history status.

Objective: Lipoprotein (a) (Lp[a]), which is a highly heritable trait, is associated with coronary artery disease (CAD). However, the insight into whether the association between Lp(a) and CAD differs according to the family history of CAD remains unclear. Methods: We investigated clinical data of 4,512 participants who underwent serum Lp(a) level measurement at Kanazawa University Hospital between 2008 and 2016. The association between Lp(a) and CAD according to CAD family history was investigated through logistic regression analyses. Results: CAD family history and Lp(a) levels were significantly associated with CAD development (odds ratio [OR], 1.32; 95% confidence interval [CI], 1.12–1.52; p<0.001 and OR, 1.13; 95% CI, 1.03–1.23; p<0.001 per 10 mg/dL, respectively). In patients without CAD family history, those with Lp(a) levels ≥30 mg/dL had higher CAD risk than those with Lp(a) levels <30 mg/dL (reference) (OR, 1.33; 95% CI, 1.05–1.61; p<0.001). In patients with CAD family history, those who had Lp(a) levels <30 and ≥30 mg/dL were both highly at risk for CAD (OR, 1.24; 95% CI, 1.04–1.44; p<0.001 and OR, 1.68; 95% CI, 1.34–2.02; p<0.001, respectively). Adding CAD family history and Lp(a) information to other conventional risk factors enhanced CAD risk discrimination (C-statistics: 0.744 [0.704–0.784] to 0.768 [0.730–0.806], and 0.791 [0.751–0.831], respectively; p<0.05 for both). Conclusion Lp(a) level was associated with CAD development regardless of CAD family history status.

When performing aortic valve replacement in young patients, mechanical valves are recommended due to their durability. However, because mechanical valves require lifelong use of warfarin and carry risks such as easy bleeding, bioprosthetic valve replacement may be performed in some cases even in young patients. In this report, we describe a case of a patient who underwent bioprosthetic aortic valve replacement with aortic annular enlargement in anticipation of TAV in SAV and had a good postoperative course. The patient is a 51-year-old male. He was referred to our hospital for surgical treatment of severe aortic stenosis. The patient strongly preferred a bioprosthetic valve due to the disadvantage of taking warfarin. Therefore, we considered the possibility of TAV in SAV due to his young age, and decided to perform aortic annular enlargement if necessary. Intraoperatively, after resection and decalcification of the valve, a sizer was inserted, but the 19 mm sizer could not pass through, so we decided to perform aortic annular enlargement. Aortic annular enlargement was performed by suturing a Dacron patch and implantation of a 23 mm bioprosthetic valve. The patient had no major postoperative problems and was discharged home on the 14th day after surgery. In order to avoid PPM in the future when TAVI is performed, aortic annular enlargement should be considered in young patients undergoing aortic valve replacement using a bioprosthetic valve if TAV in SAV is considered to be difficult.

Objective: Sitosterolemia is a rare autosomal recessive disease caused by the deleterious variants of adenosine 5'-triphosphate (ATP)-binding cassette sub-family G member 5 (ABCG5) or ATP-binding cassette sub-family G member 8 (ABCG8). There are only few data on the pathogenicity of ABCG5 and ABCG8. This study aimed to propose a scheme for determining variant pathogenicity and to catalog the putative pathogenic variants in sitosterolemia. Methods: This study enrolled 377 consecutive Japanese patients with hyper-low-density lipoprotein cholesterolemia (mean age: 46.5±19.8 years, with 192 men) who have targetedsequenced data on ABCG5 or ABCG8 (among 21 Mendelian lipid genes for any dyslipidemias) and serum sitosterol levels at Kanazawa University Hospital from 2016 to 2021. Serum sitosterol levels were divided by 0.79 in patients treated with ezetimibe, accounting for the average reduction with this drug. ABCG5 or ABCG8 variants were defined as putative pathogenic if associated with serum sitosterol levels ≥5 µg/mL or homozygous if associated with serum sitosterol levels ≥10 µg/mL. Results: Twenty-three ABCG5 or ABCG8 variants (16 missense, 2 nonsense, 2 frameshift, 2 deletion, and 1 splice mutation) were identified. Based on our definition, 11 putative pathogenic variants (median sitosterol level: 10.1 [6.5–17.1] µg/mL) were found in 36 individuals and 12 benign variants (median sitosterol: 3.5 [2.5–4.1] µg/mL) in 14 individuals. Conclusion The scheme proposed for assessing the pathogenicity of genetic variations (ABCG5 and ABCG8) is useful. Using this scheme, 11 putative pathogenic, and 12 benign variants in ABCG5 or ABCG were classified.

Pericardial pacing wire placement may occasionally result in intravascular or intratracheal wire migration, infective endocarditis, and sepsis; reportedly, the incidence of complications is approximately 0.09 to 0.4%. We report a case of a retained epicardial pacing wire that migrated into the pulmonary artery. A 66-year-old man underwent coronary artery bypass grafting for angina pectoris, with placement of an epicardial pacing wire on the right ventricular epicardium, 6 years prior to presentation. Some resistance was encountered during wire extraction; therefore, it was cut off at the cutaneous level on postoperative day 8. Computed tomography performed 6 years postoperatively revealed migration of the pacing wire into the pulmonary artery, and it was removed using catheter intervention. Surgeons should be aware of complications associated with retained pacing wires in patients in whom epicardial wires are retained after cardiac surgery.

Background  This study explored the association of residence, caste, social determinants of health (SDH) of parents, and daily junk food intake with the nutritional status of school children living in different residential areas of a district in Nepal. Methods  A survey was conducted from December 2017 to March 2019, including 331 school children aged 6 to 12 years as well as their parents, in the primary village for Japan International Cooperation Agency (JICA) support and the surrounding area in the Machapuchare Administrative Region of Kaski District, Gandagi Province, Nepal. In this study, the body mass index for age z-score (BMIZ), a criterion used by the WHO for assessing malnutrition, was used for determining underweight; BMIZ <−2 SD was defined as underweight.  The children’s anthropometric data were measured to assess their nutritional status, and a survey on children’s daily junk food intake and parents' SDH was conducted among parents. The responses were analyzed by logistic regression analysis.Results  Of the children who participated in the survey, 31 (9.4%) were underweight.   An association between parents’ SDH and children’s underweight was found after adjusting for mothers’ age at marriage, number of siblings, and daily junk food intake, and the results showed that lower caste (OR＝0.241, p＝0.001), lower education of mothers (OR＝3.879, p＝0.011) and non-literacy of fathers (OR＝2.790, p＝0.023) had statistically significant effects on BMIZ.Conclusions  In this study, BMIZ, indicating underweight in Nepalese school children, was associated with higher caste and a mother’s level of educational attainment and father’s of non-literacy. To understand the factors influencing children’s health, it is necessary to evaluate sociodemographic parameters of parents as childcare providers, including culture, education, employment, living conditions, and diet, and to conduct surveys that capture data on the SDH of parents from various perspectives.

We describe a 50-year-old man who was diagnosed with anomalous aortic origin of the right coronary artery (AAORCA) by coronary angiography and coronary computed tomography performed for chest pain on exertion. Exercise-loaded myocardial scintigraphy revealed inferior wall ischemia, and hence surgery was performed. Intraoperatively, the right coronary artery was seen to run in the aortic wall, and hence, right coronary ostioplasty (unroofing) was performed. Postoperatively, coronary computed tomography revealed that the right coronary artery originated from a normal position, and exercise-loaded myocardial scintigraphy indicated no ischemia.

A 42-year-old woman with Turner syndrome was admitted to our hospital due to severe aortic stenosis. Transthoracic echocardiography demonstrated severe aortic stenosis with a bicuspid aortic valve. Enhanced computed tomography revealed that the left upper pulmonary vein connected to the innominate vein, and the ascending aorta was enlarged (maximum diameter of 41 mm). Surgical intervention was performed though median sternotomy with cardiopulmonary bypass. After achieving cardiac arrest by antegrade cardioplegia, we performed an anastomosis to connect the left upper pulmonary vein to the left atrial appendage. Then, aortic valve replacement was performed with an oblique aortotomy in the anterior segment of the ascending aorta. The aortic valve was a unicaspid aortic valve. Following completion of aortic valve replacement with a mechanical valve, reduction aortoplasty was performed on the ascending aorta. The postoperative course was uneventful.