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Previous meta-analyses of summary data from randomised controlled trials have shown that statin therapy increases the risk of diabetes, but less is known about the size or timing of this effect, or who is at greatest risk. We aimed to address these gaps in knowledge through analysis of individual participant data from large, long-term, randomised, double-blind trials of statin therapy.

Statin therapy is effective for the prevention of atherosclerotic cardiovascular disease and is widely prescribed, but there are persisting concerns that statin therapy might frequently cause muscle pain or weakness. We aimed to address these through an individual participant data meta-analysis of all recorded adverse muscle events in large, long-term, randomised, double-blind trials of statin therapy.

We describe a patient with torsades de pointes (TdP) who was implanted with cardiac resynchronization therapy defibrillator (CRT-D). At the time of CRT-D implantation, left ventricular (LV) epicardial pacing exacerbated TdPs and developed into electrical storm, which was triggered even by biventricular pacing. We needed to inactivate the LV lead for 2 weeks. At the next device check testing of LV pacing still induced TdPs, whe reas biventricular pacing did not. After starting the continuous biventricular pacing no ventricular arrhythmias happened, and furthermore the QT intervals prolonged by LV pacing were obviously shortened only after 2 weeks as ventricular systolic function recovered. Then even continuous LV alone pacing induced no TdP. These findings indicate novel electrical effects of cardiac resynchronization therapy.

We describe a patient with torsades de pointes (TdP) who was implanted with cardiac resynchronization therapy defibrillator (CRT-D). At the time of CRT-D implantation, left ventricular (LV) epicardial pacing exacerbated TdPs and developed into electrical storm, which was triggered even by biventricular pacing. We needed to inactivate the LV lead for 2 weeks. At the next device check testing of LV pacing still induced TdPs, whe reas biventricular pacing did not. After starting the continuous biventricular pacing no ventricular arrhythmias happened, and furthermore the QT intervals prolonged by LV pacing were obviously shortened only after 2 weeks as ventricular systolic function recovered. Then even continuous LV alone pacing induced no TdP. These findings indicate novel electrical effects of cardiac resynchronization therapy.

Urinary excretion of lipocalin-type prostaglandin D synthase (L-PGDS) has been suggested to be a useful biomarker of early diabetic nephropathy. We studied whether L-PGDS is also a marker of gentamicin (GM)-induced renal damage in the “creatinine-blind” range. A prospective study was conducted in 6 patients who were given long-term intravenous administration of GM (18-42 days in combination with a β-lactam/carbapenem antibiotic or vancomycin) for the treatment of infective endocarditis. Urinary excretions of L-PGDS, β2-microglobulin, and N-acetyl-β-d-glucosaminidase were measured in the early (within 10 days from commencement) and late (thereafter) phases of GM therapy. Systemic clearance of GM (CLGM) and creatinine clearance (CLcr) was also measured concomitantly. CLGMwas reduced significantly (P< 0.05) by 10% from the early to late treatment phase, whereas urinary L-PGDS excretion showed a significant (P< 0.05) increase (from 7.3 ± 4.6 to 8.7 ± 5.0 mg/g creatinine, mean ± SD) concomitantly. In contrast, no significant changes were observed for urinary β2-microglobulin and N-acetyl-β-d-glucosaminidase concentrations. In conclusion, urinary L-PGDS may be a promising biomarker for the early phase of GM-induced renal impairment.

The patient was a 67-year-old female diagnosed with dilated cardiomyopathy. She had chronic atrial fibrillation (AF) with bradycardia and low left ventricular function (left ventricular ejection fraction (LVEF) 40%). She was admitted for congestive heart failure. She remained New York Heart Association (NYHA) functional class III due to AF bradycardia. Pacemaker implantation was necessary for treatment of heart failure and administration of dose intensive ß-blockers. As she had normal His-Purkinje activation, we examined the optimal pacing sites. Hemodynamics of His-bundle pacing and biventricular pacing were compared. Pulmonary capillary wedge pressure (PCWP) was significantly lower on Hisbundle pacing than right ventricular (RV) apical pacing and biventricular pacing (13mmHg, 19mmHg, and 19mmHg, respectively) with an almost equal cardiac index. Based on the examination we implanted a permanent pacemaker for Direct His-bundle pacing (DHBP). After the DHBP implantation, the LVEF immediately improved from 40% to 55%, and BNP level decreased from 422 pg/ml to 42 pg/ml. The number of premature ventricular complex (PVC) was decreased, and non sustained ventricular tachycardia (NSVT) disappeared. Pacing threshold for His-bundle pacing has remained at the same level. His-bundle pacing has been maintained during 27 months and her long-term DHBP can improve cardiac function and the NYHA functional class.

The patient was a 67-year-old female diagnosed with dilated cardiomyopathy. She had chronic atrial fibrillation (AF) with bradycardia and low left ventricular function (left ventricular ejection fraction (LVEF) 40%). She was admitted for congestive heart failure. She remained New York Heart Association (NYHA) functional class III due to AF bradycardia. Pacemaker implantation was necessary for treatment of heart failure and administration of dose intensive β-blockers. As she had normal His-Purkinje activation, we examined the optimal pacing sites. Hemodynamics of His-bundle pacing and biventricular pacing were compared. Pulmonary capillary wedge pressure (PCWP) was significantly lower on Hisbundle pacing than right ventricular (RV) apical pacing and biventricular pacing (13mmHg, 19mmHg, and 19mmHg, respectively) with an almost equal cardiac index. Based on the examination we implanted a permanent pacemaker for Direct His-bundle pacing (DHBP). After the DHBP implantation, the LVEF immediately improved from 40% to 55%, and BNP level decreased from 422 pg/ml to 42 pg/ml. The number of premature ventricular complex (PVC) was decreased, and non sustained ventricular tachycardia (NSVT) disappeared. Pacing threshold for His-bundle pacing has remained at the same level. His-bundle pacing has been maintained during 27 months and her long-term DHBP can improve cardiac function and the NYHA functional class.