WITHDRAWN: Cardiac Troponin T: An Early Molecule Marker of Normalization of Left Ventricular Ejection Fraction in Patients with Peripartum Cardiomyopathy.

The article entitled, "Cardiac Troponin T: An Early Molecule Marker of Normalization of Left Ventricular Ejection Fraction in Patients with Peripartum Cardiomyopathy", by Li et al, which originally was published in this space, has been removed because an article by the same authors and reporting very similar work already has been published in HEART [Published Online First: 25 October 2006], entitled, "Troponin T measurement can predict persistent left ventricular dysfunction in peripartum cardiomyopathy", by Hu et al. The printed version of the article in HEART can be found at Heart 2007;93:488-490.

Atrial fibrillation: rhythm control offers no advantage over rate control for some, but not all.

Atrial fibrillation (AF) is not a benign condition. Although AF is the most common sustained cardiac arrhythmia, the management of AF remains controversial. In recent years, several clinical trials comparing rhythm control with rate control for AF management found that rhythm control offers no advantage over rate control, but the findings may not apply equally to all patients. The main point is the high risk of AF recurrence in these trials and the toxic effects and poor efficacy of presently available antiarrhythmic drugs negate the benefit of rhythm control. Rhythm control should be considered as the preferred initial therapy if sinus rhythm had been maintained in a higher proportion of patients. For the moment, the optimal strategy to treat AF should be individualized, with a bias towards rate control if patients are at high risk for arrhythmias or can be kept asymptomatic. Rhythm control may still be justified in younger patients or patients who still have symptoms despite adequate rate control. In addition, patients with new or first-episode AF often warrant at least an initial trial of rhythm control.

Effects of withdrawal of Xuezhikang, an extract of cholestin, on lipid profile and C-reactive protein: a short-term time course study in patients with coronary artery disease.

OBJECTIVE: C-reactive protein (CRP) is considered a risk factor for coronary artery disease. In addition to its lipid-lowering properties, statin decreases the level of CRP. Abrupt cessation of statin therapy during treatment could increase CRP level independently of the elevation of serum lipids and the incidence of cardiac events in patients with atherosclerotic heart disease. Xuezhikang (XZK), an extract of cholestin, has a marked modulating effect on lipid and CRP concentrations in different study time course. However, no attention has been paid to the changes of lipid profile and CRP concentrations after withdrawal of XZK treatment. This study was designed to explore short-term time course effects on lipid profile and CRP concentrations after withdrawal of XZK treatment in coronary heart disease patients. MATERIALS AND METHODS: Seventy-five consecutive patients with documented coronary heart disease were randomly divided into three groups: 1. Pretreatment with XZK 1,200 mg daily for 6 weeks and then replaced by placebo (XZK discontinued group; n = 25); 2. Treatment with XZK 1,200 mg daily throughout the study (XZK continued group; n = 25); or 3. Placebo (no XZK group; n = 25). Lipid levels (total cholesterol, HDL-C, LDL-C and triglycerides) and CRP were assessed before receiving the XZK therapy, 1 day before discontinuation of XZK, and on days 1, 2, 3, 7 and 14 after discontinuation of XZK, respectively. RESULTS: After 6-week XZK treatment, the fasting total cholesterol, LDL-C, triglyceride and median hs-CRP concentrations decreased, whereas HDL-C concentration increased significantly (p < 0.001, respectively). At day 14 after discontinuation of XZK therapy, total cholesterol (15%), LDL-C (17%) and triglyceride (20%) significantly increased (p < 0.001, respectively), whereas HDL-C level (15%) significantly decreased (p < 0.05). The median level of CRP increased by 11, 65, 128, 103 and 101% on the first, second, third, seventh, and fourteenth day after withdrawal of XZK therapy (p > 0.05, <0.05, <0.001, <0.001, <0.001, compared with 1 day before withdrawal of XZK therapy, respectively). There was a prominent rebound of CRP concentration 3 days after discontinuation of XZK therapy. At this time point, hs-CRP concentration was higher than in the placebo group (p < 0.05). Seven to 14 days after discontinuation of XZK therapy, the hs-CRP concentration declined to a similar level as in the placebo group. No significant correlation was seen between the changes in hs-CRP and lipid profile at all time points. CONCLUSIONS: The level of hs-CRP increases on the second day after withdrawal of XZK and there is a prominent rebound 3 days after discontinuation of XZK therapy. The increase of CRP ends within 7 days, where lipids increase at 14 days after discontinuation of XZK therapy. The results may be clinically important for patients with coronary artery disease.