Among patients receiving DES implantation, AF was not rare and was associated with increased ischemic and bleeding risk. In patients with AF, triple therapy was not associated with decreased ischemic events but was associated with increased bleeding risk compared to DAPT.

End-stage heart failure patients with implantable cardioverter-defibrillator (ICD) with/without cardiac resynchronization therapy (CRT-D) often require heart transplantation (HTPL) as a last-resort treatment. We aimed to assess the frequency and clinical impact of retained ICD lead materials in HTPL patients. In this retrospective single center study, we examined the clinical records and chest radiographs of patients with ICD and CRT-D who underwent HTPL between January 1992 and July 2014. Of 40 patients with ICD and CRT-D at HTPL, 19 (47.5%) patients had retained ICD lead materials within the central venous system. Retained ICD lead materials following HTPL were more frequently noted in patients with longer implantation durations until HTPL. None of the patients underwent extraction procedures after HTPL. All patients were asymptomatic and did not exhibit significant complications or death related to the retained ICD lead materials. Seven (7/40, 17.5%) patients without any retained ICD lead materials underwent magnetic resonance imaging (MRI) during the follow-up period (median, 29.5 months); none of the patients with retained lead materials were given MRI. Considering the common use of MRI in HTPL patients, further studies on the prophylactic extraction of retained ICD lead materials and safety of MRI in these patients are needed.

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.

The aim of this study was to describe in more detail the predisposition, natural course, and clinical impact of post-transplantation diabetes mellitus (PTDM) after heart transplantation (HT). The characteristics and clinical outcomes of 54 patients with PTDM were compared with those of 140 patients without PTDM. The mean age of PTDM patients was significantly higher than controls (48.9 ± 9.3 vs 38.6 ± 13.3 yr, respectively, P = 0.001), and ischemic heart disease was a more common indication of HT (20.4% [11/54] vs 7.1% [10/140], respectively, P = 0.008). In multivariate analysis, only recipient age (odds ratio, 1.80; 95% confidence interval, 1.35-2.40; P = 0.001) was associated with PTDM development. In 18 patients (33%), PTDM was reversed during the follow-up period, and the reversal of PTDM was critically dependent on the time taken to develop PTDM (1.9 ± 1.0 months in the reversed group vs 14.5 ± 25.3 months in the maintained group, P = 0.005). The 5-yr incidence of late infection (after 6 months) was higher in the PTDM group than in the control group (30.4% ± 7.1% vs 15.4% ± 3.3%, respectively, P = 0.031). However, the 5-yr overall survival rate was not different (92.9% ± 4.1% vs 85.8% ± 3.2%, respectively, P = 0.220). In conclusion, PTDM after HT is reversible in one-third of patients and is not a critical factor in patient survival after HT.

No abstract

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.

Carbon monoxide is a nonirritant, odorless, colorless gas. Its effects are prominent in organs most sensitive to oxygen deprivation, such as the heart, brain, and kidney. Although less frequently, an association between thromboembolic events and carbon monoxide poisoning has been shown in the literatures. In this case, we report a case of atrial thrombus associated with carbon monoxide poisoning.

evels of B-type natriuretic peptide (BNP) and N-terminal pro BNP (NT-proBNP) help differentiate between cardiac and non-cardiac causes of dyspnea and are useful in predicting prognosis and monitoring treatment efficacy in patients with heart failure (HF). Both BNP and NT-proBNP are affected by demographic characteristics, such as age, sex, obesity, and renal function, 1-4 and their complex inter-relationships leaves uncertainties in the interpretation of the results of these biomarkers.It is well-known that circulating NT-proBNP concentrations are generally higher in females than in males. In addition, circulating NT-proBNP concentrations are reported to increase with age and decrease with obesity. However, in real-world practice, these factors have a complex effect on NT-proBNP levels, making it difficult to identify a uniform relationship. In a recent large-scale general population cohort study, lower NT-proBNP concentrations in Editorial p ????