Statin Group Research Articles

Association between perioperative statin treatment and short-term clinical outcomes following transcatheter aortic valve implantation: a retrospective cohort study

BackgroundStudies have found statin treatment to be associated with improved 1-year survival after transcatheter aortic valve implantation (TAVI), suggesting pleiotropic effects of statins on preventing perioperative complications. Statin treatment is...

Variability in Plasma Lipids Between Intensive Statin Therapy and Conventional-Dose Statins Combined with Ezetimibe Therapy in Patients with Coronary Atherosclerosis Disease.

Dyslipidemia has been widely recognized as a significant risk factor for coronary atherosclerosis disease (CAD). In fact, lipid variability has emerged as a more reliable predictor of cardiovascular events. In this study, we aimed to examine the variability in plasma lipids under two different lipid-lowering regimens (intensive statin therapy versus the combination of conventional-dose statins with ezetimibe). In total, we have retrospectively examined 1275 patients with CAD from January 2009 to April 2019 and divided them into two groups: intensive statin group and conventional-dose statins combined with ezetimibe group. All patients were followed up for at least 1 year. Lipid variability was verified by standard deviation (SD), coefficient of variation (CV), and variability independent of mean (VIM) triple methods. Multiple linear regression and subgroup analyses were performed. In the overall participants, the mean age was 62.3 ± 10.4 years old, and 72.8% were male. Multivariate linear regression analysis indicated that the intensive statin group had lower variability in terms of total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and non-high-density lipoprotein cholesterol (non-HDL-C) in all SD, CV, and VIM triple methods than statins combined with ezetimibe group (P for all <0.05). Similar results were established in the subgroup analyses based on atorvastatin or rosuvastatin, diabetes mellitus or not, and hypertension or not (P for all < 0.05). Thus, we can conclude that intensive statin therapy could contribute in lowering lipid variability than conventional-dose statins combined with ezetimibe therapy among patients with CAD.

Statin dan risiko hiperglikemia: studi praklinis post-market terkontrol

Statin is highly effective in preventing atherosclerosis-cardiovascular disease due to lipid abnormality. However, the current observational study showed statin association with new-onset diabetes mellitus, although the data is still conflicting. Until recently, no controlled study compared all statin drugs with this adverse event. The study aimed to determine the statin effect on blood glucose at a moderate dose for rats within 60 days. The animals were divided into 8 groups, and each group contained three mice, namely negatives (CMC 1%), simvastatin (0.052 mg/20 g BW of mice), atorvastatin (0.104 mg/20 g BW of mice), lovastatin (0.052 mg/20 g BW of mice), pitavastatin (0.010 mg/20 g BW of mice), pravastatin (0.052 mg/20 g BW of mice), rosuvastatin (0.052 mg/20 g BW of mice), and fluvastatin (0.208 mg/20 g BW of mice). The blood glucose test was carried out on days 30th and 60th. The results showed no significant difference in the blood glucose between the negatives group and all statin groups on days 30th and 60th. However, an increase in blood glucose on day 30th for pitavastatin, pravastatin, and rosuvastatin as much as 7.08%, 6.29%, and 6.29%, respectively. Moreover, an increase on day 60th for pravastatin, rosuvastatin, fluvastatin, atorvastatin lovastatin, and simvastatin as much as 36.83%, 27.59%, 26.32%, 18.05%, 17.89% dan 10.97%, respectively. This study failed to prove blood glucose elevation associated with a statin. The longer use of drugs was associated with blood glucose level elevation, except for pitavastatin. Therefore, further studies with a long term of statin administration are necessary.

Randomized trial to assess the potential role of ascorbic acid and statin for post-contrast acute kidney injury prevention

PurposeTo evaluate the effect of using statins and ascorbic acid for the prevention of post-contrast acute kidney injury (PC-AKI) in patients undergoing urologic diagnostic elective contrast-enhanced computed tomography (CECT).MethodsThis registered trial (NCT03391830) was for statin naïve patients underwent elective CECT. Patients were randomized allocated to two groups: the first group received atorvastatin 80-mg the day before the study and atorvastatin 40-mg two hours before the CECT and for continue on atorvastatin 40-mg two days after CECT; plus ascorbic acid 500 mg with atorvastatin. The other group received two tablets of placebo once/daily before the procedure and for another 3 days. The primary outcome was to assess the incidence PC-AKI.ResultsThe baseline parameters were comparable between both groups. The final median (interquartile range “IQR”) serum creatinine were 0.80 (0.60, 1.00) and 0.80 (0.60, 1.00), respectively, with insignificant p-value (p = 0.8). The median (IQR) final estimated GFR were 95.2 (72.8, 108.1) and 88.6 (71.9, 111.0) mL/min in placebo and statin plus ascorbic acid groups, respectively (p = 0.48). The eGFR difference median (IQR) were − 6.46 (− 11.72, − 4.18) and − 6.57 (− 13.38, − 3.82) ml/min in placebo and statin plus ascorbic acid groups, respectively (p = 0.58). PC-AKI occurred in 11 patients (9.8%) in placebo group and in 3 patients (3%) in statin plus ascorbic acid group (p = 0.04).ConclusionsStatin and ascorbic acid did not statistically improve neither serum creatinine nor eGFR values in patient underwent CECT. However, it can decrease the incidence of the clinically insignificant PC-AKI.

Treat-to-target versus high-intensity statin treatment in patients with or without diabetes mellitus: a pre-specified analysis from the LODESTAR trial

The impact of titrated versus fixed intensity statin therapy in patients with coronary artery disease (CAD) and diabetes mellitus (DM) remains to be elucidated. This was a pre-specified analysis of patients with and without DM from the LODESTAR trial. Patients with CAD were randomly assigned to receive either a treat-to-target strategy with a target LDL-C level of 50-70mg/dL or a high-intensity statin treatment. Primary outcome was the 3-year composite of all-cause death, myocardial infarction, stroke, or coronary revascularization. Secondary outcomes were safety endpoints. This trial is registered with ClinicalTrials.gov, NCT02579499. Between September 9, 2016 and November 27, 2019, 4400 patients with CAD were enrolled in the LODESTAR trial. The median age was 65 years (interquartile range, 59-73 years), 3172 (72%) were male, and 1468 (33%) had DM at baseline. There was no significant difference in the occurrence of the primary outcome between the treat-to-target group and high-intensity statin group among patients with DM (10.5% versus 11.1%, hazard ratio [HR] 0.94, 95% confidence interval [CI] 0.69-1.29, p=0.70) and those without DM (6.9% versus 7.5%, HR 0.93, 95% CI 0.71-1.21, p=0.58). Among patients without DM, there was a trend towards a lower risk of new-onset DM in the treat-to-target group (8.4% versus 10.4% in the high-intensity statin group, HR 0.79, 95% CI 0.62-1.01; p=0.06). In patients with CAD, a treat-to-target LDL-C strategy of 50-70mg/dL as the goal was comparable to high-intensity statin therapy in terms of 3-year clinical efficacy and safety outcomes regardless of the presence of DM. Sam Jin Pharmaceutical, Seoul, Korea and Chong Kun Dang Pharmaceutical, Seoul, Korea.

The impact of statin use before intensive care unit admission on patients with acute kidney injury after cardiac surgery.

Background: Cardiac surgery-associated acute kidney injury (CSA-AKI) is a common and serious complication after cardiac surgery. The influence of statin use before surgery on the renal outcome of patients undergoing cardiac surgery is controversial. The purpose of this study was to evaluate the effect of statins on postoperative renal outcomes in patients undergoing cardiac surgery. Methods: We included CSA-AKI patients in the Medical Information Mart for Intensive Care (MIMIC)-IV database and were divided into statin group and non-statin group according to whether they used statins before entering intensive care units (ICU). The main outcomes were hospitalization and 30-day mortality, and the secondary outcomes were 60-day mortality and 90-day mortality. We used propensity score matching (PSM) to adjust for confounding factors. The 95% confidence interval (CI) and risk ratio (RO) were calculated by the COX proportional regression model. At the same time, stratified analysis was used to explore whether the relationship between the statins use before intensive care units and mortality was different in each subgroup and whether the relationship between different doses of Atorvastatin and mortality was different. Result: We identified 675 pre-ICU statin users and 2095 non-statin users. In the COX proportional regression model, pre-ICU statin use was associated with decreased in-hospital (HR = 0.407, 95%confidence interval 0.278-0.595, p < 0.001) and 30-day mortality (HR = 0.407, 95%CI 0.279-0.595, p < 0.001). The survival rate of patients who took statins before entering ICU was significantly higher than that of those who did not use statins at 30days, 60days and 90days. There is a significant interaction between patients with aged>65years (HR = 0.373, 95%CI 0.240-0.581, p < 0.001), Acute kidney injury grade I (HR = 0.244, 95%CI 0.118-0.428, p < 0.001), and without post-myocardial infarction syndrome (HR = 0.344, 95%CI 0.218-0.542, p < 0.001). The mortality in hospital and 60days of CSA-AKI patients treated with ≥80mg Atorvastatin before operation was significantly reduced (p < 0.05). Conclusion: The pre-ICU statin use was significantly associated with decreased risk in hospital and 30-day mortality. The preoperative use of ≥80mg Atorvastatin may improve the prognosis of CSA-AKI.

Previous use of statins does not improve the outcome of bloodstream infection after kidney transplantation.

Previous studies have suggested that exposure to statins confers a protective effect in bloodstream infection (BSI) due to the anti-inflammatory and immunomodulatory properties attributed to these lipid-lowering drugs. Scarce evidence is available for the solid organ transplant population. Therefore, we compared the time to clinical cure (primary outcome) and the time to fever resolution, new requirement of intensive care unit admission or renal replacement therapy, and 30-day all-cause mortality (secondary outcomes) between kidney transplant (KT) recipients with post-transplant BSI that were receiving or not statin therapy for at least the previous 30 days. We included 80 KT recipients that developed 109 BSI episodes (43 [39.4%] and 66 [60.6%] episodes within the statin and non-statin groups, respectively). The median interval since the initial prescription to BSI was 512 days (interquartile range [IQR]: 172-1388). Most episodes were of urinary source and due to Enterobacterales. There were no differences in the median time to clinical cure in the statin and non-statin groups (3.4 [IQR: 3-6.8] versus 4 [IQR: 2-6] days; p-value = .112). The lack of effect was confirmed by multiple linear regression analysis adjusted for confounding factors (standardized β coefficient = 0.040; p-value = .709). No significant differences were observed for any of the secondary outcomes either. Vital signs and laboratory values at BSI onset and after 72-96 h were similar in both groups. In conclusion, previous statin therapy had no apparent protective effect on the outcome of post-transplant BSI among KT recipients.

The anti-inflammatory effects of atorvastatin upon the outcome of traumatic brain injury patients: A randomized-controlled double-blind clinical trial

ABSTRACT Background Traumatic brain injury (TBI) is a quite common health problem. A lot of delayed complications are related to inflammatory responses that occurred within the brain itself. Atorvastatin is related to lipid lowering drugs carrying some anti-inflammatory properties and upon this fact this study hypothesis was built. Methods Twenty adult patients with TBI, Glasgow coma scale (GCS) 9–11. Patients were equally and randomly allocated into two groups (group C as control group and group S received atorvastatin 40 mg once daily for 48 h). After 48 h, participants have undergone magnetic resonance imaging brain spectroscopy examination (MRS). The spectral peaks of N-Acetyl aspartate (NAA), Choline, and Creatinine (Cr) were assessed in brain tissue. The primary outcome was presented as ratios of NAA/Cr), Cho/Cr, and NAA/Cho. Other outcomes included GCS and ICU stay. Results There were insignificant variations between groups were found in the MRS results for metabolite alterations (NAA, Cr, and Cho). Contrasted with the control group, the statin group’s Cho/Cr ratio was significantly lower (P = 0.005), and NAA/Cho was significantly greater in the statin group than control group (P = 0.022). Statin group showed higher GCS the 1st day (P = 0.01), and lesser ICU stay (P = 0.04) Conclusion Atorvastatin can be used safely in mild-to-moderate TBI patients with a favourable outcome in the form of decreased Cho/Cr ratio and increased NAA/Cho ratio, higher GCS, and decreased ICU length of stay.

Impact of previous statin use on first intracerebral hemorrhage in cerebral amyloid angiopathy

ObjectivesStatins have been associated with an increased risk of spontaneous intracerebral hemorrhage (ICH), but without dedicated study in cerebral amyloid angiopathy (CAA). We aimed to evaluate the association between previous statin treatment and radiological hemorrhagic lesions in a CAA population during a first lobar ICH event. Materials and methodsWe retrospectively included all patients meeting the modified Boston criteria for probable CAA and admitted for a first lobar ICH between 2010 and 2021 at Rouen University Hospital. Patients were classified as having previous statin treatment or not. We compared the ICH volume, the number of associated cerebral microbleeds (CMBs), and cortical superficial siderosis (CSS) according to previous statin treatment or not. We also compared functional outcomes and ICH recurrence during the follow-up period between the two groups. ResultsWe included 99 patients, 27 of whom had statin treatment prior to their ICH. The ICH volume and the number of CMBs did not differ between groups. Disseminated CSS was initially more frequent in the statin group (88% versus 57%; P=0.019), but this was no longer significant after adjustment for antiplatelet treatment (P=0.13). The long-term outcome was similar between the two groups with no increased risk of ICH recurrence in the statin-treated group (29.63% versus 23.61%, P=0.54). ConclusionsPrevious statin treatment was not associated with more severe hemorrhagic lesions in CAA in terms of ICH volume or number of microbleeds, but a trend for increased disseminated CSS was highlighted, which will require further larger studies.

The relationship between statin therapy and adipocytokine/inflammatory mediators in dyslipidemic nondiabetic patients: A comparative study

Background: Statins have emerged as a vital therapeutic option for dyslipidemia, effectively reducing morbidity and mortality in individuals with various medical conditions. Recent research has shed light on the intricate pathophysiology of atherosclerosis, which involves lipid accumulation and inflammatory mediators. This research was conducted to assess the correlation between statin therapy and adipocytokine and inflammatory mediator levels in dyslipidemic nondiabetic patients. Methods: A total of 67 dyslipidemic nondiabetic patients were enrolled, alongside 33 healthy controls. The participants were categorized into three groups: Group (A), comprising patients undergoing statin therapy (n = 34), Group (B), consisting of patients not receiving statin therapy (n = 33); and Group (C), comprising healthy controls (n = 33). Results: Patients not receiving statin therapy exhibited significant dyslipidemic profiles compared to patients undergoing statin therapy and healthy controls. Levels of total cholesterol (TC), triglycerides (TG), very low-density lipoprotein (VLDL), and low-density lipoprotein (LDL) were higher in patients not receiving statin therapy. Serum levels of proprotein convertase subtilisin/kexin type 9 (PCSK9) were higher in the statin group than in the non-statin group and controls. Additionally, PCSK9 levels were higher in patients treated with rosuvastatin than those treated with atorvastatin. Conversely, levels of retinol-binding protein 4 (RBP4) were lower in the statin group compared to the non-statin group and controls. Although no significant difference in RBP4 levels between atorvastatin and rosuvastatin users was found, atorvastatin displayed lower RBP4 values. The study also revealed lower C-reactive protein (CRP) levels in the statin group, primarily in the rosuvastatin subgroup, compared to the non-statin group. Conclusion: Statin therapy increased PCSK9 levels, with a more pronounced rise observed in patients treated with rosuvastatin than atorvastatin. Statin therapy proved protective by reducing RBP4 and CRP levels in dyslipidemic nondiabetic patients.

Association between Serum Oxysterols and Coronary Plaque Regression during Lipid-Lowering Therapy with Statin and Ezetimibe: Insights from the CuVIC Trial.

Several clinical trials using intravascular ultrasound (IVUS) evaluation have demonstrated that intensive lipid-lowering therapy by statin or a combination therapy with statin and ezetimibe results in significant regression of coronary plaque volume. However, it remains unclear whether adding ezetimibe to statin therapy affects coronary plaque composition and the molecular mechanisms of plaque regression. We conducted this prospective IVUS analysis in a subgroup from the CuVIC trial. The CuVIC trial was a prospective randomized, open, blinded-endpoint trial conducted among 11 cardiovascular centers, where 260 patients with coronary artery disease who received coronary stenting were randomly allocated into either the statin group (S) or the combined statin and ezetimibe group (S＋E). We enrolled 79 patients (S group, 39 patients; S＋E group, 40 patients) in this substudy, for whom serial IVUS images of nonculprit lesion were available at both baseline and after 6-8 months of follow-up. After the treatment period, the S＋E group had significantly lower level of low-density lipoprotein cholesterol (LDL-C; 80.9±3.7 vs. 67.7±3.8 mg/dL, p=0.0143). Campesterol, a marker of cholesterol absorption, and oxysterols (β-epoxycholesterol, 4β-hydroxycholesterol, and 27-hydroxycholesterol) were also lower in the S ＋E group. IVUS analyses revealed greater plaque regression in the S＋E group than in the S group (-6.14% vs. -1.18% for each group, p=0.042). It was noteworthy that the lowering of campesterol and 27-hydroxycholesterol, but not LDL-C, had a significant positive correlation with plaque regression. Compared with statin monotherapy, ezetimibe in combination with statin achieved significantly lower LDL-C, campesterol, and 27-hydroxycholesterol, which resulted in greater coronary plaque regression.

The Effectiveness and Safety of Intensive Lipid-Lowering with Different Rosuvastatin-Based Regimens in Patients at High Cardiovascular Disease Risk: A Nonblind, Randomized, Controlled Trial.

A statin alone or non-statins as add-ons have been introduced to intensive low-density lipoprotein cholesterol (LDL-C) -lowering therapy in patients at risk for high cardiovascular disease (CVD). The purpose of this study was to evaluate the effectiveness and safety of different rosuvastatin-based regimens for patients at high risk. Three hundred patients at high CVD risk were randomly assigned to the statin group (rosuvastatin, 20 mg/d), statin_EZ group (statin 10 mg/d + ezetimibe 10 mg/d), statin_pcsk group (statin 10 mg/d + alirocumab 75 mg/2 weeks) or combine3 group (statin 10 mg/d + ezetimibe 10 mg/d + alirocumab 75 mg/2 weeks). The primary outcome measure was cholesterol levels after 24 weeks of follow-up. Secondary outcomes included safety markers and the proportion of patients achieving the 70 mg/dL (1.8 mmol/L) target for LDL-C. A logistic regression model was performed to explore the factors affecting lipid target achievement. The total cholesterol (TC) and LDL-C levels in the four groups after treatment were significantly lower than those before treatment. TC and LDL-C levels after treatment were significantly different among the four groups (p 0.05). The levels in both the combine3 and statin_pcsk9 groups were significantly lower than those in the statin and statin_EZ groups (p 0.05), but there was no significant difference between the combine3 and statin_pcsk9 groups. Fifty-one participants (69%) in the statin_pcsk9 group and 56 participants (78%) in the combine3 group achieved the target. Body mass index (BMI) and hypertensive status were related to LDL-C target achievement. The incidence of adverse events in the four groups was low. The combination of a statin and a PCSK9 inhibitor was safe and more effective for the treatment of high-risk CVD patients, while the addition of ezetimibe was unable to significantly lower lipid levels any further. The rate of achieving the target was higher in patients with hypertension and a low BMI. Chinese Clinical Trial Registry, Identifier: ChiCTR2200058389, Date of Registration: 2022-04-08.

Hydrophilic and lipophilic statin use and risk of hearing loss in hyperlipidemia using a Common Data Model: multicenter cohort study

Hearing impairment, the third largest health burden worldwide, currently lacks definitive treatments or preventive drugs. This study compared the effects of hydrophilic and lipophilic statin on hearing loss using a common database model. This retrospective multicenter study was conducted in three hospitals in South Korea (Anam, Guro, Ansan). We enrolled patients with hyperlipidemia with an initial hearing loss diagnosis. Data were collected during January 1, 2022–December 31, 2021 using the Observational Health Data Science and Informatics open-source software and Common Data Model database. The primary outcome was the occurrence of first-time hearing loss following a hyperlipidemia diagnosis, as documented in the Common Data Model cohort database. The measures of interest were hearing loss risk between hydrophilic and lipophilic statin use. Variables were compared using propensity score matching, Cox proportional regression, and meta-analysis. Among 37,322 patients with hyperlipidemia, 13,751 (7669 men and 6082 women) and 23,631 (11,390 men and 12,241 women) were treated with hydrophilic and lipophilic statins, respectively. After propensity score matching, according to the Kaplan–Meier curve, hearing loss risk did not significantly differ among the hospitals. The hazard ratio (HR) of the male patients from Anam (0.29, [95% confidence interval (CI), 0.05–1.51]), Guro (HR, 0.56, [95% CI 0.18–1.71]), and Ansan (hazard ratio, 0.29, [95% CI 0.05–1.51]) hospitals were analyzed using Cox proportional regression. Overall effect size (HR, 0.40, [95% CI 0.18–0.91]) was estimated using meta-analysis, which indicated that hearing loss risk among hydrophilic statin users was less than that among lipophilic statin users and was statistically significant. Men in the hydrophilic statin group had a lower risk of hearing impairment than those in the lipophilic statin group.

Impact of statin treatment and exposure on the risk of chronic allograft dysfunction in Chinese lung transplant recipients

PurposeChronic lung allograft dysfunction (CLAD) was a common complication following lung transplantation that contributed to long-term morbidity and mortality. Statin therapy had been suggested to attenuate recipient inflammation and immune response, potentially reducing the risk and severity of CLAD. This study aimed to evaluate the impact of statin use and in vivo exposure on the incidence of CLAD in lung transplant recipients (LTRs), as well as their effects on immune cells and inflammatory factors. MethodsA retrospective cohort study was conducted on patients who underwent lung transplantation between January 2017 and December 2020. The incidence of CLAD, as per the 2019 ISHLT criteria, was assessed as the clinical outcome. The plasma concentrations of statin were measured using a validated UPLC-MS/MS method, while inflammation marker levels were determined using ELISA kits. ResultsThe statin group exhibited a significantly lower rate of CLAD (P = 0.002). Patients receiving statin therapy showed lower CD4+ T-cell counts, total T-lymphocyte counts, and IL-6 levels (P = 0.017, P = 0.048, and P = 0.038, respectively). Among the CLAD groups, the atorvastatin level (2.51 ± 1.31 ng/ml) was significantly lower than that in the non-CLAD group (OR = 1.438, 95%CI (1.007–2.053), P = 0.046). ConclusionStatin therapy significantly reduced the incidence of CLAD, as well as immune cell counts and inflammatory cytokine levels in LTRs. Although the statin exposure was significantly lower in CLAD patients, it was not associated with the incidence of CLAD.

Statin Therapy Induces Gut Leakage and Neuromuscular Disjunction in Patients With Chronic Heart Failure.

Statins are commonly used to limit the risk of cardiovascular diseases, including ischemic heart attack and stroke. However, treatment often leads to myopathy and muscle weakness. Therefore, a better understanding of underlying pathomechanism is needed to improve the clinical outcomes. Here, we assessed the physical performance, including handgrip strength (HGS), gait speed (GS), and short physical performance battery, in 172 patients diagnosed with chronic heart failure (CHF) treated with (n = 50) or without (n = 122) statin and 59 controls. The plasma biomarkers, including sarcopenia marker C-terminal agrin fragment-22 (CAF22), intestinal barrier integrity marker zonulin, and C-reactive protein (CRP), were measured and correlated with the physical performance of patients. The HGS, short physical performance battery scores, and GS were significantly compromised in patients with CHF versus controls. Irrespective of etiology, significant elevation of plasma CAF22, zonulin, and CRP was observed in patients with CHF. There were strong inverse correlations of CAF22 with HGS (r 2 = 0.34, P < 0.0001), short physical performance battery scores (r 2 = 0.08, P = 0.0001), and GS (r 2 = 0.143, P < 0.0001). Strikingly, CAF22 and zonulin were positively correlated with each other (r 2 = 0.10, P = 0.0002) and with the level of CRP in patients with CHF. Further investigations revealed a significant induction of CAF22, zonulin, and CRP in patients with CHF taking statin versus nonstatin group. Consistently, HGS and GS were significantly lower in the statin versus nonstatin CHF patients' group. Collectively, statin therapy adversely affects the neuromuscular junction and intestinal barrier, which potentially induces systemic inflammation and physical disability in patients with CHF. Further prospective confirmation of the findings is required in a well-controlled study.

The effect of statins on mortality and cardiovascular disease in primary care hypertensive patients without other cardiovascular disease or diabetes.

Studies in primary healthcare (PHC) assessing the effect of primary prevention with statins on mortality and cardiovascular disease (CVD) are scarce. This study aimed to estimate the effect of statins on all-cause mortality, cardiovascular mortality, myocardial infarction (MI), and stroke in individuals in PHC with hypertension without CVD or diabetes. Using the Swedish PHC quality assurance register QregPV, the study included 13 193 individuals with hypertension without CVD or diabetes, who had filled a first statin prescription between 2010 and 2016, and 13 193 matched controls without a filled statin prescription at the index date. Controls were matched on sex and propensity score using clinical data and data from national registers on comorbidities, prescriptions, and socioeconomic status. The effect of statins was estimated in Cox regression models. During a median of 4.2 years of follow-up, 395 individuals in the statin group vs. 475 in the control group died, 197 vs. 232 died of cardiovascular disease, 171 vs. 191 had an MI, and 161 vs. 181 had a stroke. The treatment effect of statins was significant for all-cause mortality [hazard ratio (HR) 0.83, 95% confidence interval (CI) 0.74-0.93] and cardiovascular mortality (HR 0.85, 95% CI 0.72-0.998). Overall, no significant treatment effect of statins was seen for MI (HR 0.89, 95% CI 0.74-1.07), but there was a significant interaction with sex (P = 0.008) with decreased risk of MI for women but not for men (HR 0.66, 95% CI 0.49-0.88 vs. HR 1.09, 95% CI 0.86-1.38). Primary prevention with statins in PHC was associated with reduced risk of all-cause mortality, cardiovascular mortality, and in women, lower risk of MI.

Differential prediction of high-sensitivity cardiac troponin-I, but not N-terminal pro-brain natriuretic peptide, in different pitavastatin doses on cardiovascular events in stable coronary artery disease

BackgroundThis study aimed to examine whether high-sensitivity cardiac troponin-I (hsTnI) and N-terminal pro-brain natriuretic peptide (NT-proBNP) could predict future major adverse cardiovascular events (MACE) in stable coronary artery disease (CAD) patients with high- or low-dose of pitavastatin. MethodsThis was a case-cohort analysis of the REAL-CAD study, a randomized trial of high- or low-dose (4 or 1 mg/day) pitavastatin therapy in patients with stable CAD. We examined the MACE risk according to the quartile of hsTnI and NT-proBNP at baseline. ResultsA total of 1336 and 1396 patients including 582 MACE cases were randomly examined into the hsTnI and NT-proBNP cohort, respectively. Both higher levels of hsTnI and NT-proBNP at baseline were significantly associated with increased risk of MACE (p < 0.001, respectively). When separately analyzed in statin dose, the higher marker levels were significantly associated with higher MACE risk in all cohorts (p < 0.001 in all cohorts). After multivariable adjustment, hsTnI levels were significantly associated with MACE risk in low-dose statin group (HR 2.54, p = 0.0001); however, in high-dose pitavastatin therapy, a significant association was diminished in MACE risk among the quartiles of baseline hsTnI levels (p = 0.154). Conversely in the NT-proBNP cohort, the association between NT-proBNP levels and MACE risk was constantly observed regardless of pitavastatin dose even after multivariable adjustment (both p < 0.0001). ConclusionsPatients with high hsTnI levels had high risk of MACE in low-dose statin group, but not in high-dose, suggesting that high-dose statin treatment might decrease MACE risk in stable CAD patients with high hsTnI levels.

#5848 ROLE OF STATINS IN THE CONTRAST-INDUCED ACUTE KIDNEY INJURY PREVENTION AFTER COMPUTED TOMOGRAPHY WITH CONTRAST MEDIA

Abstract Background and Aims Contrast-induced acute kidney injury (CI-AKI) is a serious complication of the use of iodinated contrast media (CM). A number of researches have shown that statins have a protective role in the prevention of CI-AKI due to their pleiotropic effects. The aim of the study was to assess the influence of statins on the incidence of CI-AKI after intravenous CM administration. Method A randomized controlled open-label prospective study was conducted. Statin naive patients with cardiovascular diseases referred for contrast-enhanced computed tomography (CT) were included. Exclusion criteria were the use of statins and chronic kidney disease (CKD) stages 4-5. Acute kidney injury was defined as an increase in serum creatinine level by more than 44 μmol/L (0.5 mg/dL) or 25% from baseline within 48 hours after CM administration according to KDIGO guidelines. Glomerular filtration rate was calculated using the CKD-EPI formula. Overall, 181 patients were included in the study and divided into two groups. The first group (120 people) received high doses of atorvastatin (80mg or 40mg) 24 hours after and before the CM administration, while the second group (61 people), the control group, did not receive any statin therapy. Low-osmolar solutions in an amount of 100 ml were used. All patients were given intravenous hydration with saline before the study and 24 hours later. The statistical analysis was done using IBM SPSS Statistics v26.0. Results The patients in both groups did not significantly differ in age, BMI, coexisting conditions, and medications taken (Table 1). Both groups showed an increase in average creatinine levels after CT with intravenous CM administration, however, in the group of patients receiving high doses of statins, the average level increased less, p = 0.092 (Table 2). AKI developed in 12 individuals (6.7%), 9 of them were in the control group, and 3 were in the group receiving high doses of statins, p = 0.003. The chances of AKI development in the group receiving high doses of statins were 6.95 times lower compared to the control group (OR = 6.05, 95% CI: 1.7-21.5). Most of the patients had preserved kidney function and did not suffer from diabetes mellitus. There were statistically significantly more patients with preserved kidney function in the statin group, p = 0,007, OR: 2,374 (CI 95% 1,258 - 4,479), and fewer patients with CKD 3a stage, p = 0,05, OR: 0,406 (CI 95% 0,195 – 0,844). Conclusion Despite the presence of patients at risk, the incidence of CI-AKI was 6.7%, possibly due to additional prevention of this complication with intravenous saline before and after administration of the CM. In this trial, we observed that periprocedural administration of atorvastatin in high doses for a short duration, reduced the incidence of CI-AKI.

Cardiologists Do Advise Hyperlipidemic Patients to Maintain or Follow Prophylactic Measures in Scenario of Genetic Susceptibility of Hyperlipidemic Patients

Biotransformation in human body results accumulation of free radicals (reactive oxygen species or ROS). If patients LDL particles are more than normal in systemic circulation, get interacted with free radicals and form foamy cells; initial stage of coronary artery disease (CAD). Hyperlipidemia may be primary (genetic reason) or secondary which is acquired type of dyslipidemia. Free radicle formation in human body is very much normal phenomenon. Just reducing LDL or raising HDL may prevent interaction of LDL with reactive oxygen species (free radicals), escaping patient to develop CAD. Commonly used drugs in prophylaxis or treatment of dyslipidemia include statins (HMGCo-A reductase inhibitors), niacin, bile resins and fibric acids. There are alternative therapies for dyslipidemia including use of fibers, fruits, and vegetables. In Pakistan there are huge number of fruits and herbs which are getting popularity as hypolipidemic agents. One of the important fruit in Pakistan having hypolipidemic potential is JUJUBES (in urdu called Bair). In this study we have compared hypolipidemic effects of Bair with statin in hyperlipidemic patients. This study was conducted at Begum Jan hospital, Islamabad-Pakistan. Sixty hyperlipidemic patients were selected and divided in two groups. Their lipid profile (LP) was determined in the hospital and blood pressure (BP) was recorded at start of treatment. Group-1 was advised to take 10 mg tablet Rosuvastatin in divided doses, and group-2 was advised to use 500 mg Bair (JUJUBES) in divided times per day for the period of 2 months. RESULTS: after two months therapy their lipid profile and BP was re-determined and analyzed statistically by using SPSS version 22.00.01. It was observed that Rosuvastatin decreased systolic BP and LDL-c highly significantly (p-value &lt; 0.001), while diastolic BP was reduced significantly (p-value &lt;0.01) and HLD-c was increased significantly with p-value &lt;0.01. In group-2 JUJUBES (Bair) reduced systolic BP and LDL-c significantly (p-value &lt;0.01) but no significant changes were observed in diastolic BP and HDL-c in this group. CONCLUSION: It was concluded from the research study that Jujubes reduce LDL-c and systolic BP in hyperlipidemic patients, but lesser than statin group of antihyperlipidemic agents.

“The impact of statins addind to the fixed combination antihypertensive therapy on the arterial stiffness in patients with moderate and severe hypertension"

AimThe objective of this study was the evaluation of the arterial stiffness, which changed after adding statins to the guidelines recommended dual or triple fixed combination antihypertensive therapy in patients with moderate to severe arterial hypertension. Materials and methodsIt was included 99 patients in total being diagnosed with moderate and severe arterial hypertension (2nd and 3rd stages of arterial hypertension) without diabetes. Those patients were divided into 2 groups. The first group (n = 59) was assigned to the dual or triple fixed combination antihypertensive therapy plus including statins.Patients in the second group (n = 40) received only the dual or triple fixed combination antihypertensive treatment following the recommended guidelines without any statins. The CAVI index was performed in order to measure in all participants before and at the end of the follow-up period. Furthermore, the Office (Clinic BP) Blood Pressure (BP) was monitored in assigned participants as well as the Ambulatory Blood Pressure Monitoring (ABPM). The laboratory investigations also took place such as the standard blood test, the urine and biochemistry analysis and the estimated Carotid Intima-Media Thicknesses with Ultrasound. The study-duration was 6 months. ResultsOffice BP and ABPM had decreased significantly and equally in both treatment groups. The total cholesterol (TC) and LDL cholesterol had decreased significantly in the statin group on 1,76 mmol/l (30%, p < 0,05) and 1,51 mmol/l (41%, p < 0,05) respectively. In the group without statin therapy, there was no changes in the level of TC and LDL cholesterol. In the group without statins, it was noted a significant decrease in the level of BP, however, the CAVI index level was shown the growth to +0,9 units on the right side and +1,0 units on the left.In the group without statin's treatment, the CAVI index was changed from 7.73 ± 0.17/7.62 ± 0.19 units to 8.63 ± 0.22/8.62 ± 0.12 units on the right/left site after treatment (p < 0,05). It means there was an increase in the stiffness of the arterial wall in terms of cardio-vascular index CAVI in the group without added statin after 6 months of the therapy. In the group with added statin after 6 months of the therapy, the CAVI had not have any changes. It can be seen from the observed figures: the CAVI on the right/left site was 8.32 ± 0.16/8.33 ± 0.19 initially and 8.44 ± 0.16/8.24 ± 0.15 units treatment (p > 0,05) afterwards.We did not note any impact of statin therapy on the BP level. However, a significant correlations was found between the CAVI index with age and the serum level of blood Triglycerides before treatment, including LDL Cholesterol and HDL Cholesterol, duration of hypertension, the blood glucose level, the Potassium level and the Maximum Thickness of Intima-Media of Carotid Arteries in the statins group. ConclusionThe adding of the statin to the current fixed dual or triple combination of the antihypertensive therapy could prevent the progression of arterial stiffness in patients with 2nd and 3rd stages of arterial hypertension.