Additional file 1 of A nationwide cohort study suggests clarithromycin-based therapy for Helicobacter pylori eradication is safe in patients with stable coronary heart disease and subsequent peptic ulcer disease

Additional file 1. Supplemental Table 1. Risk of study outcomes including arrhythmia events comparing clarithormycin users vs. nonusers

Data_Sheet_1_No dose-response relationship of clarithromycin utilization on cardiovascular outcomes in patients with stable coronary heart disease: Analysis of Taiwan’s national health insurance claims data.pdf

BackgroundClarithromycin is widely used to treat various bacterial infections and has been reported to have potential cardiovascular risk. However, it is uncertain whether this association was dose dependent and confounded by indication bias in patients with stable coronary heart disease (CHD).MethodsThis cohort study retrospectively analyzed a national health insurance claims data from Taiwan’s 2005 Longitudinal Generation Tracking Database. We used a new-user design and 1:1 propensity score matching. A total of 9,631 eligible clarithromycin users and 9,631 non-users in 2004–2015 were subject to final analysis. All patients were followed-up after receiving clarithromycin or on the matched corresponding date until occurrence of cardiovascular morbidity in the presence of competing mortality, all-cause and cause-specific mortality, or through the end of 2015. The effect of cumulative dose, exposure duration, and indications of clarithromycin on cardiovascular outcomes were also addressed.ResultsClarithromycin use, compared with non-use, was associated with higher risk for all-cause [adjusted hazard ratios (aHR), 1.43; 95% confidence interval, 1.29–1.58], cardiovascular (1.35; 1.09–1.67), and non-cardiovascular (1.45; 1.29–1.63) mortality, but not for overall cardiovascular morbidity. Further analysis of individual cardiovascular morbidity demonstrated major risk for heart events (1.25; 1.04–1.51) in clarithromycin users than non-users. However, there was no relationship of cumulative dose, exposure duration, and indications of clarithromycin on cardiovascular outcomes. Analyses of the effects over time showed that clarithromycin increased cardiovascular morbidity (1.21; 1.01–1.45), especially heart events (1.39; 1.10–1.45), all-cause (1.57; 1.38–1.80), cardiovascular (1.58; 1.20–2.08), and non-cardiovascular (1.57; 1.35–1.83) mortality during the first 3 years. Thereafter, clarithromycin effect on all outcomes almost dissipated.ConclusionClarithromycin use was associated with increased risk for short-term cardiovascular morbidity (especially, heart events) and mortality without a dose-response relationship in patients with stable CHD, which was not dose dependent and confounded by indications. Hence, patients with stable CHD while receiving clarithromycin should watch for these short-term potential risks.</p

Well-Controlled Block Polymerization/Copolymerization of Alkenes and/or Carbon Monoxide by Cationic Palladium Methyl Complexes

Cationic palladium imine−phosphine complexes [Pd(P−N)(CH3)(CH3CN)]+ catalyze the living block polymerization and copolymerization of olefins and/or carbon monoxide. The palladium-capped polymers, intermediates of the polymerization, were isolated

Flow diagram of the enrollment process.

We first identified 996,430 patients between 1 January 1996 and 31 December 2012 from the outpatient claim. We excluded patients who had some pre-existing diseases before the index date, had missed data, and could not match well for both cohorts. Finally, a total of 43294 patients with newly diagnosed headache other than migraine were identified as the non-migraine headache cohort. For each patient in the non-migraine headache cohort, 4 control patients were randomly selected, with frequency matching by age and sex.</p

Crude and adjusted hazard ratios for individual tinnitus, sensorineural hearing impairment, and sudden deafness.

Crude and adjusted hazard ratios for individual tinnitus, sensorineural hearing impairment, and sudden deafness.</p

The cumulative incidence of individual tinnitus, sensorineural hearing impairment, and sudden deafness.

The cumulative incidence of tinnitus (a), sensorineural hearing impairment (b), and sudden deafness (c) in the non-migraine headache cohort was significantly higher than that in the control cohort (log rank, p<0.001).</p

Characteristics in non-migraine headache and control cohorts in Taiwan, 1996–2012 (n = 216,470).

Characteristics in non-migraine headache and control cohorts in Taiwan, 1996–2012 (n = 216,470).</p

Pooled and area-specific cumulative 6-day relative risks (RR) of emergency room visit among patients survived with out-of-hospital cardiac arrest associated with 18 and 30°C environment.

Pooled and area-specific cumulative 6-day relative risks (RR) of emergency room visit among patients survived with out-of-hospital cardiac arrest associated with 18 and 30°C environment.</p

Crude and adjusted hazard ratios for combining tinnitus, sensorineural hearing impairment, and sudden deafness.

Crude and adjusted hazard ratios for combining tinnitus, sensorineural hearing impairment, and sudden deafness.</p

Initiation Steps for the Polymerization of Vinyl Ethers Promoted by Cationic Palladium Aqua Complexes

Both deuterium-labeled experimental and NMR spectroscopic analyses of poly(vinyl ether) offer the mechanistic insight into the polymerization, indicating that the cationic palladium aqua imine−phosphine complexes [(P∼N)PdMe(H2O)]BF4 (P∼N = o-C6H4(PPh2)(NCHAr)) promote the reaction via proton-transfer initiation. Insertion of vinyl ether into the Pd−Me bond in [(P∼N)PdMe(H2O)]BF4 does not proceed, but the single insertion of the same substrate into the Pd−acetal bond of [(P∼N)PdCOCH3(L)]BF4 provides the stable inserted product [(P∼N)PdCH(OEt)CH2COCH3]BF4, which has been characterized by an X-ray structural determination. However, these palladium complexes do not catalyze the polymerization or copolymerization of vinyl ether and carbon monoxide