Lipoprotein(a)-related cardiovascular and all-cause mortalities in Korean adults.

AIMS: There are inconsistent results on the association between lipoprotein(a) and mortality-related outcomes due to a lack of evidence from large-scale observational studies of Asians. This study aims to evaluate the effects of lipoprotein(a) on mortality-related outcomes in the Korean population. METHODS AND RESULTS: This cohort study included 275 430 individuals (mean age: 38 years; 50.1% men) enrolled in the Kangbuk Samsung Health Study between 2003 and 2016. The median follow-up period was 6.6 years. Cox proportional hazards analysis was used to estimate the adjusted hazard ratios (HRs) for evaluating mortality risk based on lipoprotein(a) levels and specific lipoprotein(a) categories. The median lipoprotein(a) value was 18.5 mg/dL, and the proportion of lipoprotein(a) ≥50 mg/dL was 12.8%. Multivariable Cox regression analysis showed that the group with lipoprotein(a) ≥50 mg/dL had a significantly increased risk of cardiovascular mortality (HR[95% CI]: 1.83[1.26, 2.64]) and all-cause mortality (1.20[1.03, 1.41]) than the group with lipoprotein(a) < 50 mg/dL without increased risk of cancer mortality (1.05[0.81, 1.34]). The relationship between lipoprotein(a) and cardiovascular mortality was significant regardless of low-density lipoprotein cholesterol. Specifically, lipoprotein(a) ≥100 mg/dL was associated with more than twice as increased a risk of cardiovascular mortality (2.45[1.12, 5.34]) than lipoprotein(a) < 10 mg/dL. In subgroup analyses, there was an interaction in the relationships between the two lipoprotein(a) categories and cardiovascular mortality for only high-density lipoprotein cholesterol. CONCLUSIONS: High lipoprotein(a) concentration is an independent predictor of cardiovascular mortality in the Korean population, regardless of low-density lipoprotein cholesterol levels.

Association of environmental tobacco smoke exposure with metabolic syndrome: A longitudinal Cohort Study of 71,055 never smokers.

BACKGROUND AND AIMS: Effects of environmental tobacco smoke (ETS) exposure and a change in ETS exposure status on metabolic syndrome (MetS) remain unknown. Thus, the aim of this study was to evaluate the effect of ETS exposure on MetS in self-reported and cotinine-validated never smokers. METHODS AND RESULTS: From a large longitudinal cohort study, 71,055 cotinine-validated never smokers without MetS at baseline were included. These participants were divided into four groups (no, new, former, and continuous ETS exposure groups) based on their ETS exposure status at baseline and follow-up. The association between ETS exposure and MetS was assessed using multivariable Cox hazard regression analyses. During a median follow-up of 33 months, 15.0 cases/10,000 person-years (PY) developed MetS. Incidence rates per 10,000 PY of MetS in no, new, former, and continuous ETS exposure groups were 14.0, 18.5, 16.5, and 19.0, respectively. In multivariable Cox hazard regression analyses, the new and continuous ETS exposure groups showed increased risk of MetS compared to the no ETS exposure group (hazard ratio [95% confidence interval]: 1.35 [1.16, 1.56], p-value < 0.001 for the new ETS exposure group and 1.19 [1.06, 1.34], p-value = 0.004 for the continuous ETS exposure group). However, the former ETS exposure group did not show an increased risk of MetS (0.96 [0.88, 1.05], p-value = 0.36). CONCLUSION: This study showed that ETS exposure and changes in ETS exposure status over approximately three years could modify the risk of MetS, suggesting that avoidance of ETS may not increase the risk of incidence of MetS.

Clinical Outcomes and Effectiveness of Heart Transplantation in Patients With Systemic Light-chain Cardiac Amyloidosis.

BACKGROUND: In systemic light-chain (AL) amyloidosis, cardiac involvement is a major determinant of survival; however, cardiac response is limited even after systemic treatment in a majority of patients, and some require heart transplantation. Additionally, limited information is available on specific indications for heart transplantation. We aimed to explore clinical outcomes of cardiac amyloidosis and its association with heart transplantation, including identifying factors favoring heart transplantation amenability. METHODS: We retrospectively analyzed data from patients diagnosed with AL amyloidosis with cardiac involvement between January 2007 and December 2020 at a tertiary referral center. RESULTS: Among 73 patients, 72 (99%) received systemic treatment, and 12 (16%) underwent heart transplantation. Characteristics at diagnosis were similar between heart transplant recipients and nonrecipients, although left ventricular ejection fraction tended to be lower in recipients (median 48% versus 57%, P = 0.085). Eight weeks after systemic treatment, 67% and 12% of patients achieved hematologic and brain natriuretic peptide responses. Overall survival was longer among heart transplantation recipients than nonrecipients, with 5-y survival rates of 61.1% (95% confidence interval, 25.5%-83.8%) versus 32.0% (95% confidence interval, 20.3%-44.4%; P = 0.022), respectively. Among the 34 with identifiable causes of death out of 51 deaths, 21 nonrecipients (62%) died of cardiac problems compared with none in the heart transplant recipients. Additionally, survival outcomes favored heart transplant recipients in most subgroups, including patients with higher Mayo 2004 European stage at diagnosis and with extracardiac involvement of amyloidosis. CONCLUSIONS: Heart transplantation can achieve long-term survival in appropriately selected patients with AL cardiac amyloidosis.

Severe Cardiomyopathy Due to Arthroprosthetic Cobaltism: Report of Two Cases with Different Outcomes.

Cobalt-induced cardiomyopathy is a well-known but uncommon disease, and the physician must maintain a high index of suspicion in order to make a timely diagnosis. We report two patients with cobalt-induced cardiomyopathy. Both patients developed progressively worsening symptoms of cobalt toxicity following revision of a fractured ceramic-on-ceramic total hip replacement to a metal-on-polyethylene bearing. In both patients, echocardiography showed LV hypertrophy, biventricular systolic dysfunction, and a large amount of pericardial effusion. Due to decompensated heart failure, both patients were initially considered candidates for heart transplantation. One patient was diagnosed with cobalt-induced cardiomyopathy before transplantation. He received cobalt chelation therapy and revision surgery, which led to complete recovery of heart function. In the other patient, the diagnosis was not made until the time of heart transplantation. The gross examination of the explanted heart revealed typical features of cobalt cardiotoxicity, which was then diagnosed as cobalt-induced cardiomyopathy. These cases emphasise the importance of early diagnosis and prompt treatment of cobalt intoxication.

Comparison of aspirin and indobufen in healthy volunteers.

The aim of this study is to quantify the extent and recovery of platelet inhibition after administration of indobufen and aspirin in healthy volunteers. Indobufen inhibits platelet aggregation by reversibly inhibiting the platelet cyclooxygenase enzyme, thereby suppressing thromboxane synthesis. Twenty healthy volunteers completed the study and received aspirin (200 mg/day for 2 weeks) followed by a 4-week washout period and then indobufen (200 mg twice a day for 2 weeks). The percent (%) inhibition of platelet aggregation (IPA) was assessed using arachidonic acid (0.5 mg/ml) and adenosine diphosphate (5 µM) at 4, 12, 24 and 48 hours after last dose of each drug. IPA assessed using arachidonic acid as the agonist was similar at 4 hours after the last dose of indobufen (81.07 ± 9.36%) and aspirin (96.99 ± 0.29%, p = 0.10), but significantly lower at 12 hours (74.04 ± 9.55% vs. 97.94 ± 0.28%, p = 0.02), 24 hours (33.39 ± 11.13% vs. 97.48 ± 0.32%, p < 0.001) and 48 hours (14.12 ± 9.74% vs. 98.22 ± 0.31%, p < 0.001) after indobufen, compared to the relative values for aspirin. IPA assessed using adenosine diphosphate as the agonist was similar in the two groups at 4, 12 and 24 hours after the last dose, but significantly lower 48 hours after the last dose of indobufen, compared to the relative value for aspirin (1.98 ± 3.57% vs. 12.61 ± 2.71%, p = 0.002). Indobufen (200 mg twice a day) caused equivalent initial inhibition of platelet aggregation to aspirin (200 mg daily), and the anti-aggregation effect diminished faster than after aspirin.