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OBJECTIVE Beyond lipid lowering, statins have pleiotropic effects with favourable benefits against atherogenesis. Withdrawal of statin therapy has been demonstrated to abrogate vascular protective activity and even increase the incidence of thrombotic vascular events. The purpose of this study is to investigate the serial changes of soluble CD40 ligand (sCD40L) and two adipocytokines, adiponectin and resistin, after short-term atorvastatin therapy and withdrawal in patients with hypercholesterolaemia. METHODS AND RESULTS Thirty-two patients with hypercholesterolaemia received atorvastatin 10 mg/day for 3 months. Serum lipid profiles, and levels of sCD40L, adiponectin and resistin, were assessed before and immediately after 3 months' statin therapy. Serum levels of sCD40L and adiponectin were also measured on the 3 consecutive days after statin withdrawal. After 3 months' statin therapy, levels of sCD40L (1.93 +/- 1.13 vs. 1.30 +/- 0.97 ng/mL), total cholesterol and low-density lipoprotein cholesterol (LDL-C) were all reduced significantly (p < 0.05). However, sCD40L level tended to increase towards baseline on the first and second days after statin withdrawal, but was not significantly elevated until the third day after withdrawal (1.89 +/- 1.28 vs. 1.30 +/- 0.97 ng/mL, p < 0.05). Total cholesterol and LDL-C levels did not increase during the 3 days of statin withdrawal. No significant changes of adiponectin and resistin levels were shown after statin therapy. CONCLUSIONS These results indicate that the effect of statin on sCD40L level was abrogated after therapy withdrawal, and was independent of serum cholesterol level. Statin therapy did not significantly alter levels of adiponectin and resistin.

The Heart Outcomes Prevention Evaluation (HOPE) study demonstrated that the angiotensin-converting enzyme inhibitor, ramipril, significantly reduces mortality, myocardial infarction and stroke in high-risk cardiovascular patients, beyond the benefits from blood pressure lowering. The tolerability of ramipril 10 mg/day has been an important concern when applying these results. Following the same criteria as the HOPE study, we investigated the adverse effects profile and tolerability of 10 mg ramipril in high-risk patients at our institution. In total, 92 patients with high cardiovascular risk were eligible for this study. Initially, ramipril was prescribed 2.5 mg orally once daily, and then titrated up to 5.0, 7.5, and 10.0 mg/day at 1-month intervals. The target maintenance dose was 10 mg/day. All adverse events were recorded during at least 3 months of follow-up. After 4-6 months of the titration protocol, only 18 patients (25.3%) reached and remained on ramipril 10 mg/day; 11 (15.5%), 22 (30.9%), and 20 patients (28.2%) remained on 2.5, 5.0, and 7.5 mg/day, respectively. Twenty-one patients (22.6%) had at least one adverse event. Twelve patients (13.0%) stopped treatment because of adverse effects. A total of 23 episodes of adverse events were reported, including cough (15.1%), dizziness (6.0%), and hypotension (2.4%). Ramipril was relatively well tolerated in our study population. However, only one-quarter of our patients reached the target maintenance dose of 10 mg/day. Dry cough, dizziness, and hypotension were the major side effects. About 15% of our patients discontinued ramipril treatment, which is comparable with previous reports.

In addition to lowering lipid profile, statins have pleiotropic effects on improving vascular function. Changes of these pleiotropic effects and their relationship to lipid profile after withdrawal of statin treatment remained unclear.We investigated the changes of lipid profile and plasma concentrations of human soluble vascular cell adhesion molecule-1 (sVCAM-1) and human tissue type plasminogen activator (tPA) after withdrawal of statin treatment. Twenty-two patients (14 F, 8 M, aged 63+/-13 years) with hypercholesterolemia were treated with atorvastatin (ATOR; 10 mg/day) for 12 weeks. Blood samplings for serum lipid and markers were collected before, after and withdrawal of statin treatment.The total cholesterol, LDL-cholesterol and sVCAM-1 (from 394.4+/-251.7 to 321.0+/-198.9 ng/ml, p0.05) all decreased significantly and the tPA (from 9.47+/-3.57 to 11.62+/-3.99 ng/ml, p0.05) increased significantly after atorvastatin treatment. During the following 3 days after withdrawal of atorvastatin, the total cholesterol and LDL-cholesterol did not show any significant change. However, the plasma sVCAM-1 significantly elevated on day 2 (from 321.0+/-198.9 to 371.2+/-220.4 ng/ml, p0.05) and the plasma tPA significantly decreased on day 1 (from 11.62+/-3.99 to 10.52+/-3.55 ng/ml, p0.05) and day 3 (from 11.62+/-3.99 to 10.27+/-3.69 ng/ml, p0.05). Both the significant elevation of sVCAM-1 and decrease of tPA after withdrawal of atorvastatin treatment occurred within 3 days, while the serum cholesterol and LDL-chol levels did not have any significant change and were still within the therapeutic range.After 12 weeks of atorvastatin treatment, the beneficial pleiotropic effects can be demonstrated simultaneously with lowering the lipid profile. However, after withdrawal of atorvastatin, the beneficial pleiotropic effects are abrogated rapidly within days and are independent on elevation of serum cholesterol.

Heart rate turbulence (HRT) has been described as a predictor of high-risk patients with cardiac diseases. The purpose of this study is to determine how the degree of prematurity of a ventricular premature beat (VPB%) and retrograde ventriculoatrial (VA) conduction of VPBs affect HRT. We studied 30 patients without organic heart disease. We calculated turbulent slope (TS) and turbulent onset (TO) from VPBs induced by programmed stimulation from the right ventricular apex. TS was inversely and TO was positively correlated to VPB%. Without retrograde VA conduction of VPBs, TS was inversely and TO was positively correlated to VPB%. In VPBs with retrograde VA conduction, there were no significant correlations between TO and TS with VPB%. In conclusion, TS and TO calculated from VPBs with different degrees of prematurity varied widely. Both VPB% and characteristics of retrograde VA conduction may affect HRT.

Beyond lipid lowering, statins have pleiotropic effects with favourable benefits against atherogenesis. Withdrawal of statin therapy has been demonstrated to abrogate vascular protective activity and even increase the incidence of thrombotic vascular events. The purpose of this study is to investigate the serial changes of soluble CD40 ligand (sCD40L) and two adipocytokines, adiponectin and resistin, after short-term atorvastatin therapy and withdrawal in patients with hypercholesterolaemia.Thirty-two patients with hypercholesterolaemia received atorvastatin 10 mg/day for 3 months. Serum lipid profiles, and levels of sCD40L, adiponectin and resistin, were assessed before and immediately after 3 months' statin therapy. Serum levels of sCD40L and adiponectin were also measured on the 3 consecutive days after statin withdrawal. After 3 months' statin therapy, levels of sCD40L (1.93 +/- 1.13 vs. 1.30 +/- 0.97 ng/mL), total cholesterol and low-density lipoprotein cholesterol (LDL-C) were all reduced significantly (p0.05). However, sCD40L level tended to increase towards baseline on the first and second days after statin withdrawal, but was not significantly elevated until the third day after withdrawal (1.89 +/- 1.28 vs. 1.30 +/- 0.97 ng/mL, p0.05). Total cholesterol and LDL-C levels did not increase during the 3 days of statin withdrawal. No significant changes of adiponectin and resistin levels were shown after statin therapy.These results indicate that the effect of statin on sCD40L level was abrogated after therapy withdrawal, and was independent of serum cholesterol level. Statin therapy did not significantly alter levels of adiponectin and resistin.

Background: C-reactive protein is considered a risk factor for coronary artery disease. In addition to its lipid-lowering properties, statin decreases the level of C-reactive protein. Abrupt cessation of statin therapy during treatment could increase the incidence of cardiac events in patients with atherosclerotic heart disease. The changes of C-reactive protein after withdrawal of statin therapy are still unknown. Methods: Twenty patients with hyperlipidemia received statin (atorvastatin, 10 mg/day) therapy for 3 months. The levels of lipid profiles and C-reactive protein were assessed before receiving the statin therapy, immediately after 3 months of therapy, and on the 3 consecutive days after withdrawal of statin treatment. Results: After 3 months of statin therapy, the total cholesterol, low-density lipoprotein cholesterol (LDL-chol), and C-reactive protein were significantly reduced (264.94 ± 16.23 vs. 183.44 ± 16.34 mg/dl, 183.17 ± 34.56 vs. 122.00 ± 17.66 mg/dl, and 2,309.00 ± 437.85 vs. 1,257.95 ± 207.99 ng/ml, respectively). The level of C-reactive protein increased on the second day after withdrawal of statin therapy (2,590.14 ± 1,045.05 vs. 1,257.95 ± 207.99 ng/ml); however, the total cholesterol and LDL-chol did not increase during the 3-day period after withdrawal of statin therapy. Conclusions: The increase in the level of C-reactive protein after withdrawal of statin therapy may be a contributing factor to the increased incidence of cardiac events in patients who have abruptly stopped statin therapy.

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a rare disease characterized by replacement of myocardium with fibrofatty tissue. It mainly involves the right ventricle (RV) and causes abnormal RV performance. ARVC is the most common cause of sudden cardiac death in young Italian athletes because it induces malignant ventricular tachyarrhythmias. Clinical manifestations of ARVC may be different between Chinese and Western patients. In this paper, we share our experience of the clinical manifestations of ARVC and review previous reports of ARVC.