Search

Apical periodontitis (AP) is an inflammatory dental disease caused by bacterial infections of the endodontic system. The correlation between AP and cardiovascular diseases. (CVD) has been consistently investigated. Statins are a class of drugs that are used to treat hypercholesterolemia and prevent atherosclerotic vascular diseases. They have other beneficial pleiotropic effects such as anti-inflammatory, antithrombotic, and antioxidant activities. The aim of this study was to evaluate the oral health status and prevalence of AP in patients treated with statins (Group S) in comparison with untreated patients (Group C) to understand whether the anti-inflammatory action of these drugs can influence the prevalence of AP. The records of seventy-nine patients (43 men and 36 women, mean age 68 ± 11 years, 1716 teeth) treated with statins and referred to the University clinic for dental evaluation were reviewed. Seventy patients free from systemic diseases and without therapy (39 men and 31 women, mean age 62 ± 9 years, 1720 teeth) constituted the control group. All subjects underwent complete oral, dental, and radiographic examinations to determine the presence and severity of AP. Periapical index (PAI) and decayed, missed, and filled teeth (DMFT) scores were obtained. AP was significantly less common in Group S (22,8%) than in Group C (50%) (P < 0.05). Furthermore, the mean value of the qualitative rank of the severity of AP (PAI score) was higher in Group C than in Group S (P ≤ 0.05). Our results suggest that statins can attenuate the prevalence of AP, which is associated to CVD. [ABSTRACT FROM AUTHOR]

There has been no report about outcome of pitavastatin versus atorvastatin therapy in high-risk patients with hypercholesterolemia. Hypercholesterolemic patients with one or more risk factors for atherosclerotic diseases (n = 664, age = 65, male = 54%, diabetes = 76%, primary prevention = 74%) were randomized to receive pitavastatin 2 mg/day (n = 332) or atorvastatin 10 mg/day (n = 332). Follow-up period was 240 weeks. The primary end point was a composite of cardiovascular death, sudden death of unknown origin, nonfatal myocardial infarction, nonfatal stroke, transient ischemic attack, or heart failure requiring hospitalization. The secondary end point was a composite of the primary end point plus clinically indicated coronary revascularization for stable angina. The mean low-density lipoprotein cholesterol (LDL-C) level at baseline was 149 mg/dL. The mean LDL-C levels at 1 year were 95 mg/dL in the pitavastatin group and 94 mg/dL in the atorvastatin group. There were no differences in LDL-C levels between both groups, however, pitavastatin significantly reduced the risk of the primary end point, compared to atorvastatin (pitavastatin = 2.9% and atorvastatin = 8.1%, HR, 0.366; 95% CI 0.170–0.787; P = 0.01 by multivariate Cox regression) as well as the risk of the secondary end point (pitavastatin = 4.5% and atorvastatin = 12.9%, HR = 0.350; 95%CI = 0.189–0.645, P = 0.001). The results for the primary and secondary end points were consistent across several prespecified subgroups. There were no differences in incidence of adverse events between the statins. Pitavastatin therapy compared with atorvastatin more may prevent cardiovascular events in hypercholesterolemic patients with one or more risk factors for atherosclerotic diseases despite similar effects on LDL-C levels. • The study was a first, randomized, prospective trial of two statins therapy. • Pitavastatin reduced more cardiovascular events compared with atorvastatin. • There were no differences in cholesterol profiles between two statin groups. • This may suggest the action of statin beyond cholesterol-lowering effects. • We may reconsider how to use statins for high-risk patients. [ABSTRACT FROM AUTHOR]

Abstract: Background: The full impact of statins on patients with chronic heart failure (CHF) is unknown. Therefore, we aimed to evaluate the pleiotropic effects of rosuvastatin on vascular and tissue regeneration, its impact on endothelial function and hemodynamics in CHF. Methods: Forty-two patients with CHF (LVEF 30±1%) were randomized to 12weeks of oral rosuvastatin (40mg/d) or placebo. At baseline and at 12weeks, VEGF and oxidized LDL (oxLDL) were assessed by ELISA. Circulating endothelial progenitor cells (CPCs) were quantified using FACS. CPC function was determined by matrigel assay. Number of CD34+ stem cells and capillary density were measured in skeletal muscle (SM). Flow-mediated dilatation (FMD) and left ventricular (LV) function were determined by ultrasound. Results: Rosuvastatin increased VEGF by +43% (p =0.004 vs. placebo) and decreased oxLDL by −27% (p =0.04 vs. placebo). This was associated with an elevation in CPC count by +224% (p =0.04 vs. placebo) and an augmentation of CPC integrative capacity by +91% (p =0.03 vs. placebo). Capillary density increased by +14% (p <0.001 vs. placebo), which was associated with an enhanced homing of CD34+ stem cells. Rosuvastatin improved FMD by +163% (p <0.001 vs. placebo) and enhanced ejection fraction by +27% (p <0.001 vs. placebo). Conclusion: In CHF, rosuvastatin activates CPCs that contribute to neovascularisation and to the enhancement of endothelial function. Correction of vascular abnormalities leads in part to an increase in LV function. Therefore, rosuvastatin''s non-lipid effects may have the potential to promote endogenous tissue regeneration and improve LV performance in CHF. [Copyright &y& Elsevier]

Abstract: Background: Inflammation and oxidative stress have been associated with atrial fibrillation (AF). On the other hand, accumulating evidence suggests that statins may have antiarrhythmic effects due to pleiotropic properties. However, inconsistent results have been reported with respect to AF. Aims: We conducted a systematic review and meta-analysis of randomized clinical trials (RCTs) and observational studies to examine the association between statin use and development of AF. Methods: PubMed, Cochrane clinical trials database, and EMBASE were searched until November 2006. In addition, a manual search was performed using all review articles on this topic, reference lists of papers, and abstracts from conference reports. Of the 309 initially identified studies, 6 RCTs and 10 observational studies with 7041 patients were finally analyzed. Results: The analysis of RCTs showed no significant effect of statins on AF development (RR=0.76, 95% CI:0.55–1.05, P =0.09), and significant heterogeneity between individual studies (P =0.0008, I 2 =74.0%). Subgroup analysis revealed that differences in AF detection methodology may be the cause of heterogeneity. The analysis of observational studies demonstrated that statin use reduced the relative risk for AF by 23% (95% CI:0.70–0.85, Z =4.95, P <0.00001) without significant differences between the trials (P=0.08, I 2 =41.2%). This favorable effect was greatest in the post-operative patients (RR=0.61, 95% CI:0.49–0.76, Z =4.30, P <0.0001). Conclusion: Our meta-analysis suggests that statins may be effective in AF prevention especially in the post-operative setting. However, there are insufficient data for the widespread use of statins solely for AF prevention. Larger RCTs with long-term follow-up in different clinical settings, and more sensitive methods of arrhythmia detection are needed to clarify the impact of statins on AF. [Copyright &y& Elsevier]

Abstract: The short-term and small-dose pleiotropic effects of atorvastatin and influence on sex steroid production were investigated in 35 premenopausal and 71 postmenopausal hypercholesterolemic, hypertriglyceridemic women, as well as the temporal differences in these pleiotropic effects. Atorvastatin (10 mg daily) was given for 6 months and fasting lipid concentrations, high sensitive CRP, and coagulo-fibrinolytic parameters were measured at baseline and after 3 and 6 months of therapy. Atorvastatin reduced the low-density lipoprotein cholesterol, remnant-like particle lipoprotein cholesterol, and malondialdehyde-modified low-density lipoprotein cholesterol after 3 and 6 months in both pre- and postmenopausal women. Atorvastatin decreased significantly high-sensitivity C-reactive protein concentration (−47.6% and −58.0%, P <0.01) and tissue plasminogen activator/plasminogen activator inhibitor-1 ratio (−31.8% and −40.0%, P <0.001) after 6 months in pre- and postmenopausal women. There was no correlation between the pleiotropic effects and the improvement in the lipid profile. Furthermore, atorvastatin has no influence on sex steroid production in both pre- and postmenopausal period. The results indicate some short-term pleiotropic effects of small-dose atorvastatin therapy without influence of endocrinological status, which may be important with respect to the early benefits of statin therapy in the perimenopausal hyperlipidemic women. [Copyright &y& Elsevier]

Abstract: Background: Oxidative stress contributes to endothelial dysfunction, an important step to the pathogenesis of atherosclerosis and coronary events. Latest studies revealed the existence of pleiotropic and especially antioxidant properties of statins. We sought to examine the effects of pravastatin on lipid peroxidation and endothelial function, independently from lipid-lowering, in patients with unstable angina (UA). Methods: Thirty-seven patients (males), 64.46±9.09 years, suffering from UA enrolled in the study. Patients were not on statin medication before admission and they received after randomization either 40 mg pravastatin daily (group A, n=20), or placebo (group B, n=17). Malondialdehyde (MDA) concentration, an index of lipid peroxidation and plaque instability, flow-mediated dilatation (FMD) of the brachial artery and blood lipids were measured on the second day of hospitalization and 10 days later. Results: MDA decreased significantly in both groups (A, p=0.008; B, p=0.003). FMD increased significantly in group A (p=0.007), whereas in group B it did not change. Serum lipids remained unaltered in all three groups. Conclusions: Pravastatin administration improved FMD within 10 days and this favorable effect occurred before any significant reduction in blood lipids, revealing its pleiotropic effects during the early phase of an acute coronary syndrome. Circulating lipid peroxidation products in patients with UA decreased significantly during the same period independently of endothelial function and pravastatin therapy. [Copyright &y& Elsevier]

Background: It is unclear whether there are temporal differences for the pleiotropic effects for different members of the statin class. The present study investigated differences in the short- and intermediate-term pleiotropic effects of statins in hypercholesterolemic patients. Methods: Thirty-five hypercholesterolemic patients were randomly treated with either atorvastatin or cerivastatin for 3 months. We measured fasting lipid concentrations, thiobarbituric acid reactive substances (TBARS), fibrinolytic parameters, and flow-mediated dilation of the brachial artery (FMD) at baseline and after 2 weeks and 3 months of therapy. Results: After 2 weeks of therapy, atorvastatin decreased the low density lipoprotein (LDL) cholesterol, small, dense LDL cholesterol (34±22 vs. 18±20%, P<0.01), remnant-like particles (RLP) cholesterol (8.8±6.0 vs. 5.1±2.6 mg/ml, P<0.01), and TBARS (3.3±1.0 vs. 3.1±0.9 nmol/ml, P<0.05), and cerivastatin decreased LDL cholesterol. After 3 months of therapy, atorvastatin decreased small dense LDL cholesterol (8±13%, P<0.0001) additionally, and cerivastatin decreased small, dense LDL cholesterol (51±11 vs. 12±22%, P<0.0001) and plasminogen activator inhibitor type 1 (68±32 vs. 51±21 ng/ml, P<0.05). FMD increased significantly in both groups after 2 weeks, although the relative change in FMD was greater with cerivastatin therapy after 2 weeks than atorvastatin therapy (60±78 vs. 23±26%, P<0.05). However, FMD was the same for both groups after 3 months (58±65 vs. 66±61%, NS), because atorvastatin additionally increased FMD. There was no correlation between these pleiotropic effects and the improvement in the lipid profile for either group. Conclusions: These findings suggest that the degree of pleiotropic effect as well as the time course for the effect are different among members of the statin class of drugs. [Copyright &y& Elsevier]

Abstract: We analyzed 6317 patients with a baseline LDL-cholesterol level of 70 to 130 mg/dL among 13,812 patients of the Japanese Coronary Artery Disease (JCAD) study. We divided the patients into 2 groups according to statin treatment and its lipophilicity. We compared the incidence of all-cause events between 2000 statin-treated patients and 4317 patients without statins during a median follow-up period of 1092 days (range 0 to 1676 days). After propensity score matching (n =1641, for each group), Kaplan–Meier analysis showed 25% reduction in the incidence of all-cause events with statin treatment (p =0.0016). The incidence of all-cause events was also compared between 1139 patients with hydrophilic statin and 861 patients with lipophilic statin. After propensity score matching (n =778, for each group), Kaplan–Meier analysis showed no significant difference in the incidence of all-cause events with respect to lipophilicity. Subgroup analysis of the JCAD study suggested a lipid-independent beneficial treatment effect of statins on all-cause events, and these favorable effects were comparable between the hydrophilic and lipophilic statins. [Copyright &y& Elsevier]

Abstract: We compared short- and intermediate-term effects on lipid profiles, fibrinolytic parameter, and endothelial function between pitavastatin and atorvastatin. Short-term improvement of endothelial function was superior with pitavastatin compared to atorvastatin therapy. Pitavastatin could be a potentially better therapeutic choice for lipid-lowering and early alterations in endothelial function. Our study provides an important basis on which further trials involving larger numbers of patients may be studied prospectively. [Copyright &y& Elsevier]

Abstract: Statins appear to play a role in preventing atherosclerosis. Here, we compared the effects of two statins, fluvastatin, a lipid-soluble “vascular statin”, and rosuvastatin, a water-soluble “superstatin” with potent LDL-lowering potency, on endothelial function, as evaluated by flow-mediated vasodilatation (FMD) of the brachial artery following forearm ischemia in ultrasound studies of patients with type 2 diabetes. For this, we treated 30 hypercholesterolemic diabetic patients with 30 mg fluvastatin or 2.5 mg rosuvastain for 3 months, and measured FMD, LDL-cholesterol, HDL-cholesterol, high-sensitive C-reactive protein, oxidized LDL, and urine isoprostane. We found that fluvastatin improved FMD (%) from 3.85±1.43 to 5.61±2.48, while rosuvastatin improved FMD from 3.63±1.76 to 4.97±2.70 (change in FMD: fluvastatin 1.76±1.59 vs. rosuvastatin 1.34±1.56). On the other hand, fluvastatin lowered LDL-cholesterol (mg/dl) from 152±62.9 to 120±43.9, while rosuvastatin lowered LDL-cholesterol from 153±29.4 to 91.9±18.8, which was a more potent change. Thus, we conclude that fluvastatin exerts a protective action on vascular endothelial cells despite being a less potent cholesterol-lowering agent, while rosuvastatin exerts similar effects and has a potent cholesterol-lowering effect, in diabetic patients. [ABSTRACT FROM AUTHOR]

Abstract: Thiazolidinediones (TZDs) represent insulin-sensitizing agents that have several pleiotropic properties, possibly related to their favorable effects on cardiovascular remodeling. We briefly describe 2 diabetic patients who experienced a remarkable improvement in their paroxysmal atrial fibrillation (AF) after treatment with rosiglitazone. Current evidence suggests that atrial remodeling represents a prominent mechanism of AF development and perpetuation while inflammation and oxidative stress are possibly implicated in this process. It could therefore be speculated that the pleiotropic effects of TZDs favorably affect atrial remodeling reducing the arrhythmia burden. Further studies are needed in order to elucidate the merit of this pharmacological approach in AF. [Copyright &y& Elsevier]