High-intensity Atorvastatin Research Articles

Comparative Study Between the Effects of High Doses of Rosuvastatin and Atorvastatin on Ventricular Remodeling in Patients with ST-Segment Elevation Myocardial Infarction.

Most studies reported that treating ST-Elevation Myocardial Infarction (STEMI) patients with high doses of rosuvastatin or atorvastatin could improve left ventricular remodeling and cardiac function. The current study compared the impact of high doses of rosuvastatin and atorvastatin on hypertrophy, fibrosis markers, serum inflammatory markers, and left ventricular function in STEMI patients after primary percutaneous coronary intervention (PCI). After primary PCI, eighty STEMI patients were randomized to receive either 20 mg of rosuvastatin (n = 40) or 40 mg of atorvastatin (n = 40) once daily for 3 months. Soluble Suppression of Tumorigenicity-2 (sST2), Matrix Metalloproteinase-9 (MMP9), C-Reactive Protein (CRP), lipid parameters, liver enzymes, and echocardiographic parameters were assessed for the two groups at baseline and after 3 months. After 3 months of treatment, a statistically significant reduction was observed in the rosuvastatin group regarding the levels of CRP (16 ± 6 vs. 20 ± 10 mg/L, P = 0.024) and MMP9 (104 ± 33 vs. 130 ± 42 ng/L, P = 0.003) compared with the atorvastatin group. The median percentage decrease in sST2 level in the rosuvastatin group was higher (6.1%) than in the atorvastatin group (2.3%) after 3 months of treatment. Also, in the rosuvastatin group, LVEF was significantly increased (48.5 ± 9 vs. 43.5 ± 11%, P = 0.029), while LVEDV and LVESV were significantly decreased compared to those of the atorvastatin group (101 [81/135] vs. 134 [100/150] ml, P = 0.041) (53 [37/75] vs. 73 [52/92] ml, P = 0.033), respectively. High-intensity rosuvastatin was superior to high-intensity atorvastatin in reducing the inflammatory response and myocardial fibrosis, thus improving ventricular remodeling and cardiac function better in STEMI patients. This randomized controlled trial was registered on October 11, 2022, on ClinicalTrials.gov under registration number: NCT05895123 "retrospectively registered".

1288-P: Comparison of Moderate Intensity Atorvastatin and Ezetimibe with High Intensity Atorvastatin on Cardiovascular Events and Diabetes in Patients with Angina Pectoris Undergoing Percutaneous Coronary Intervention

1288-P: Comparison of Moderate Intensity Atorvastatin and Ezetimibe with High Intensity Atorvastatin on Cardiovascular Events and Diabetes in Patients with Angina Pectoris Undergoing Percutaneous Coronary Intervention

Combination therapy with moderate-intensity atorvastatin and ezetimibe vs. high-intensity atorvastatin monotherapy in patients treated with percutaneous coronary intervention in practice: assessing RACING generalizability

Abstract Aims Using rosuvastatin, the RACING (randomized comparison of efficacy and safety of lipid-lowering with statin monotherapy versus statin/ezetimibe combination for high-risk cardiovascular diseases) trial showed the beneficial effects of combining moderate-intensity statin with ezetimibe compared with high-intensity statin monotherapy in patients with atherosclerotic cardiovascular disease. This study investigated whether the beneficial effects of combination lipid-lowering therapy extend to patients treated with atorvastatin, not rosuvastatin, in daily clinical practice. Methods and results Using stabilized inverse probability of treatment weighting, a total of 31 993 patients who were prescribed atorvastatin after drug-eluting stent (DES) implantation were identified from a nationwide cohort database: 6215 patients with atorvastatin 20 mg plus ezetimibe 10 mg (combination lipid-lowering therapy) and 25 778 patients with atorvastatin 40–80 mg monotherapy. The primary endpoint was the 3-year composite of cardiovascular death, myocardial infarction, coronary artery revascularization, hospitalization for heart failure treatment, or non-fatal stroke in accordance with the RACING trial design. Combination lipid-lowering therapy was associated with a lower incidence of the primary endpoint (12.9% vs. 15.1% in high-intensity atorvastatin monotherapy; hazard ratio [HR] 0.81, 95% confidence interval [CI] 0.74–0.88, P < 0.001). Compared with high-intensity atorvastatin monotherapy, combination lipid-lowering therapy was also significantly associated with lower rates of statin discontinuation (10.0% vs. 8.4%, HR 0.81, 95% CI 0.73–0.90, P < 0.001) and new-onset diabetes requiring medication (8.8% vs. 7.0%, HR 0.80, 95% CI 0.70–0.92, P = 0.002). Conclusion In clinical practice, a combined lipid-lowering approach utilizing ezetimibe and moderate-intensity atorvastatin was correlated with favourable clinical outcomes, drug compliance, and a reduced incidence of new-onset diabetes requiring medications in patients treated with DES implantation. Trial registration: ClinicalTrial.gov (NCT04715594).

Real-World Attainment of Low-Density Lipoprotein Cholesterol Goals in Patients at High Risk of Cardiovascular Disease Treated with High-Intensity Statins: The TERESA Study.

Despite steady improvements in cardiovascular disease (CVD) prevention, a scarce proportion of patients achieve the recommended LDL-C goals, even under high-intensity lipid-lowering therapy (LLT). Our study aimed to evaluate the attainment rate of LDL-C targets recommended by the 2019 European guidelines, and to characterize potential factors associated with LDL-C goal achievement and change patterns in LLT. We conducted a retrospective, observational study on patients treated with high-intensity atorvastatin or rosuvastatin ± ezetimibe at cardiology and internal medicine clinics across Spain. It included 1570 evaluable patients (median age: 62 years; established CVD: 77.5% [myocardial infarction: 34.3%]; and 85.8% at very high cardiovascular risk). Rosuvastatin ± ezetimibe was the LLT in 52.2% of patients, and atorvastatin ± ezetimibe in 47.8%. LLT had been modified in 36.8% of patients (side effects: 10%), being the most common switch from atorvastatin- to rosuvastatin-based treatment (77.2%). The risk-based LDL-C goal attainment rate was 31.1%, with 78.2% high-risk and 71.7% very high-risk patients not achieving the recommended LDL-C targets. Established CVD and familial hypercholesterolemia were significantly associated with the non-achievement of LDL-C goals. Although having limitations, this study shows that the guideline-recommended LDL-C goal attainment rate is still suboptimal despite using high-intensity statin therapy in a real-world setting in Spain.

Effect of High-Intensity Atorvastatin on the Prevalence of No-Reflow Phenomenon in Patient Undergoing Primary PCI: A Cross-Sectional Study

Introduction: ST-segment elevation myocardial infarction (STEMI) is one of the most common heart problems worldwide. So far percutaneous coronary intervention (PCI) has proved to be the most successful method to restore blood flow after a STEMI attack. However, the breakdown of coronary plaques often results in a failed restoration of blood. The no-reflow phenomenon complicates the treatment and delays the patient’s recovery. Statins have helped reduce cholesterol levels in the blood and have thus been used during primary PCI to enhance the chance of blood reflow. Atorvastatin is a promising candidate drug that reported promising results. Objective: In this study, the effect of high-intensity Atorvastatin has been assessed in preventing the no-reflow phenomenon. Study Design: Cross-sectional study Study Setting: Department of interventional Cardiology Hayatabad Medical Complex, Peshawar from 10-06-2022 to 10-10-2022. Material and Methods: A sample size of 149 was collected using non-probability consecutive sampling and was examined using Chi-Square for independence via the SPSS program. Results: The patients had several comorbidities, with hypertension being the most common. Over half of the patients were given atorvastatin, and over 97% of patients received balloon and stent procedures. 15% of patients experienced a no-reflow phenomenon, while 85% had a successful primary PCI. High-intensity atorvastatin was found to significantly reduce the risk of no-reflow (p < 0.001). Conclusion: The statistical outcome revealed that loading atorvastatin during the primary percutaneous coronary intervention (PCI) significantly reduces the risk of a no-reflow phenomenon. Keywords: ST-segment elevation myocardial infarction (STEMI), Atorvastatin, primary percutaneous coronary intervention (PCI), No-reflow phenomenon

76-Year-Old Woman With Hemoptysis

A 76-year-old woman presented with 2 years of hemoptysis that had been increasing in frequency until it was happening on a daily basis. She had also experienced new hypoxia, exertional dyspnea, fatigue, and weight loss. Her past medical history was pertinent for severe scoliosis, remote myocardial infarction, heart failure with preserved ejection fraction (HFpEF), mild aortic stenosis, hypertension, and chronic kidney disease stage IV. She had no history of atrial fibrillation. Her medications included aspirin, high-intensity atorvastatin, furosemide, metoprolol tartrate, and lisinopril.

A Comparative Study of High-intensity Rosuvastatin Versus Atorvastatin Therapy Post-acute Coronary Syndrome Using Real-world Data.

A high-intensity statin is recommended for the secondary prevention of cardiovascular diseases (CVD). However, real-world evidence of the effectiveness of rosuvastatin following acute coronary syndrome (ACS) is scarce. This retrospective cohort study included patients diagnosed with ACS to compare between the 2 high-intensity statin therapies (rosuvastatin vs atorvastatin) in terms of a primary composite outcome of CVD-associated death, non-fatal ACS, and non-fatal stroke at 1 month and 12 months post discharge. The primary effectiveness outcome did not differ between the 2 groups at 1 month (1.3% vs 1%; aHR = 1.64, 95% CI 0.55-4.94, P= 0.379) and at 12 months (4.8% vs 3.5%; aHR = 1.48, 95% CI 0.82-2.67, P= 0.199). Similarly, the 2 groups had comparable safety outcomes. In conclusion, the use of high-intensity rosuvastatin compared to high-intensity atorvastatin therapy in patients with ACS had resulted in comparable cardiovascular effectiveness and safety outcomes.

Comparative effectiveness of statins on non-high density lipoprotein cholesterol in people with diabetes and at risk of cardiovascular disease: systematic review and network meta-analysis

ObjectiveTo compare the efficacy of different statin treatments by intensity on levels of non-high density lipoprotein cholesterol (non-HDL-C) for the prevention of cardiovascular disease in people with diabetes.DesignSystematic review and...

Is the use of high-intensity atorvastatin associated with memory impairment?

High-intensity statins are the cornerstone of medical management in Acute Coronary Syndromes (ACS). However, their effect on neurocognition are less clear. In this prospective observational study, we gave guideline-directed high-intensity atorvastatin 40 mg to middle-aged statin-naïve ACS patients. Memory assessments were performed before and 6 months after statin therapy using 2 validated scales-the Post-Graduate Institute Memory Scale (PGI-MS), and the Logical Memory Passage Test (LMPT). There was no significant difference in the mean PGI-MS test scores (baseline 75.4 ± 7.9, 6months 76.5 ± 8.2;p = 0.26) or the overall composite scores (baseline 32.02 ± 3.2, 6months 32.8 ± 3.1; p = 0.20), after 6 months of statin use. There was a small improvement in immediate recall (baseline score 8.5 ± 2.5, 6 months 9.04 ± 1.8; p = 0.05), and delayed recall (baseline 6.1 ± 2.6, 6 months 6.9 ± 1.9, p = 0.002). High-intensity atorvastatin use did not affect memory at 6 months among statin-naïve middle-aged patients with ACS.

61-Year-Old Man With Nausea and Vomiting

61-Year-Old Man With Nausea and Vomiting

New onset diabetes mellitus and cardiovascular events in Korean patients with acute myocardial infarction receiving high-intensity statins

BackgroundHigh-intensity statin therapy is typically used in patients with acute myocardial infarction (AMI) for secondary prevention. However, there have been consistent concerns regarding its association with diabetes mellitus. We investigated the effect of high-intensity atorvastatin and rosuvastatin on new-onset diabetes mellitus (NODM) and cardiovascular outcomes over a 3-year follow-up period.MethodsData from the Korea Acute Myocardial Infarction Registry were collected from November 2011 to October 2015, and 13,104 patients with AMI were enrolled from major cardiovascular centers. Among them, 2221 patients without diabetes who had been administered with high-intensity atorvastatin (40–80 mg) and rosuvastatin (20 mg) were investigated. The atorvastatin and rosuvastatin groups were evaluated for the incidence of NODM and major adverse cardiac events (MACE) including death, myocardial infarction, and revascularization cases in the following 3 years.ResultsBaseline characteristics were comparable between the two groups. Event-free survival rate of NODM was not significantly different between the atorvastatin and rosuvastatin groups (92.5% vs. 90.8%, respectively; Log-rank P-value = 0.550). The event-free survival rate of MACE was also not significantly different between atorvastatin and rosuvastatin groups (89.0% vs. 89.6%, respectively; Log rank P-value = 0.662). Multivariate Cox analysis revealed that statin type was not a prognostic factor in the development of NODM and MACE.ConclusionsAdministering high-intensity atorvastatin and rosuvastatin in patients with AMI produced comparable effects on NODM and clinical outcomes, suggesting their clinical equivalence in secondary prevention.

Abstract 14986: A Randomized Trial of Statins to Reduce Vascular Endothelial Inflammation in Psoriasis

Introduction: Psoriasis (PsO) is a chronic skin disease associated with increased CV risk. Systemic and vascular endothelial inflammation in PsO is highly prevalent and associated with CVD. Statins reduce LDL-C, systemic inflammation, and CV events. There is minimal data supporting the use of statins in PsO. We, therefore, investigated the effect of statins on circulating and vascular endothelial biomarkers of CV risk in PsO. Methods: We performed blood RNA sequencing, targeted proteomics (n=88), and brachial vein endothelial harvesting in PsO participants (n=45, average age 45 ± 14 years, 49% male, body surface area [BSA] of PsO 8 ± 14%, Framingham Risk Score 6 ± 7%) and age- gender-matched controls (n=18). Next, PsO subjects were randomly assigned to 40 mg atorvastatin (n=15) or no-treatment (n=10). A repeat assessment occurred at week two with the primary end-point change in vascular endothelial inflammation (mean composite of LTB, CCL3, CX3CL1, CCL2, CXCL1, ICAM1, iNOS, IL-8, IL-1B, COX- 2 expression). Results: Blood RNA sequencing with pathway analysis revealed inflammasome signaling as highly upregulated in PsO compared to control with protein expression of IL-6 ( r =0.68, p <0.001) and hs-CRP ( r =0.80, p <0.001) each correlated with PsO severity (psoriasis area and severity index [PASI]). Mean vascular endothelial inflammation was also 3-fold higher ( p =0.02) in PsO compared to control and correlated with both PASI ( r =0.40, p =0.01) and LDL-C ( r =0.29, p =0.05). In PsO patients randomized to two weeks of statin therapy, LDL-C was reduced by ~50% compared to the no-treatment group (60 mg/dL vs. 111 mg/dL, p <0.001 respectively). While no decrease in inflammatory pathways at the whole blood transcriptome and protein levels were noted, vascular endothelial inflammation was 60% lower in the statin vs. no-treatment group ( p =0.02). Change in vascular endothelial inflammation correlated with change in LDL-C ( r =0.53, p <0.05) but not IL-6 ( r =-0.25, p =0.30) or hs-CRP ( r =0.15, p =0.58). Conclusions: Two-weeks of high-intensity atorvastatin reduced vascular endothelial but not systemic inflammation in PsO. These findings suggest that statins may reduce CV risk in PsO either through lipid-mediated or a direct effect of statins on the vascular endothelium.

Clinical outcomes of high-intensity doses of atorvastatin in patients with acute coronary syndrome: A retrospective cohort study using real-world data.

To compare the effectiveness and safety of 2 high-intensity atorvastatin doses (40 mg vs 80 mg) among acute coronary syndrome (ACS) patients. This retrospective observational cohort study using real-world data included patients admitted with ACS to the Heart Hospital in Qatar between 1 January 2017 and 31 December 2018. The primary endpoint was a composite of cardiovascular disease-associated death, nonfatal ACS and nonfatal stroke. Cox proportional hazard regression analysis was used to determine the association between the 2 high-intensity atorvastatin dosing regimens and the primary outcome at 1 month and 12 months postdischarge. Of the 626 patients included in the analyses, 475 (75.9%) received atorvastatin 40 mg, while 151 (24.1%) received atorvastatin 80 mg following ACS. Most of the patients were Asian (73%), male (97%) with a mean age of 50 years and presented with ST-elevation myocardial infarction (60%). The incidence of the primary effectiveness outcome did not differ between the atorvastatin 40-and 80-mg groups at 1 month (0.8 vs 1.3%; adjusted hazard ratio = 0.59, 95% confidence interval 0.04-8.13, P = .690) and at 12 months (3.2 vs 4%; adjusted hazard ratio = 0.57, 95% confidence interval 0.18-1.80, P = .340). Similarly, the use of the 2 doses of atorvastatin resulted in comparable safety outcomes, including liver toxicity, myopathy and rhabdomyolysis with an event rate of <1% in both groups. The use of atorvastatin 40 mg in comparison to atorvastatin 80 mg in patients with ACS resulted in similar cardiovascular effectiveness and safety outcomes.

Effect of atorvastatin on lipogenic, inflammatory and thrombogenic markers in women with the metabolic syndrome

Background and aimSpecific drug therapy to target the underlying proinflammatory and prothrombotic state in patients with metabolic syndrome (MS) is lacking. We sought to study the effect of high-intensity atorvastatin on markers of lipogenesis, inflammation and thrombogenesis, in women with MS in the absence of cardiovascular disease or diabetes. Methods and resultsThis randomized double-blinded controlled trial included 88 women with MS (according to National Cholesterol Education Panel Adult Treatment Panel III criteria) and low atherosclerotic cardiovascular risk. Participants were randomized to receive atorvastatin 80 mg or matching placebo. Thrombogenic, lipogenic and inflammatory markers were collected at the time of enrollment, after a 6-week dietary run-in phase (time of randomization), and at 6- and 12-weeks after randomization. At 6 weeks post-randomization, there was significant reduction in total cholesterol, low density lipoprotein cholesterol, triglycerides, apolipoprotein-B (Apo-B) and Apo-B/Apo-A1 ratio in the atorvastatin arm compared to placebo. This difference persisted at 12-weeks post randomization. There was no significant difference in fasting blood glucose, high-density lipoprotein cholesterol, high sensitivity C-reactive protein, serum leptin, Apo-A1, intercellular adhesion molecule 1 and platelet activity. A significant increase in vascular adhesion molecule 1 at 6 and 12 weeks was seen within the atorvastatin arm. No difference was observed in blood pressure and waist circumference. ConclusionsIn conclusion, high-intensity atorvastatin has an early and significant impact on lipoproteins and apolipoproteins but did not lower inflammatory, thrombogenic or biomarkers of platelet activity and aggregation in women with MS. The use of statins for primary prevention in these patients should be further explored.

S2426 Segmental Atrophy Associated With Overestimation of Fibrosis by Transient Elastography

INTRODUCTION: Hepatic atrophy, although rare, may be a potential confounder of transient elastography results. Atrophy can result from tumor or cirrhosis but can also be due to etiologies associated with diversion of portal venous blood flow. We present a case of overestimation of fibrosis by transient elastography in a patient with left hepatic lobe atrophy. CASE DESCRIPTION/METHODS: A 60 year old overweight male with hypertension and hyperlipidemia was referred for evaluation of elevated transaminases. Initial laboratory investigation noted AST 62 U/L, ALT 110 U/L, alkaline phosphatase (ALP) 160 U/L, total bilirubin 0.7 mg/dL, platelet count 172,000/microliter and albumin 4.2 g/dL. He was advised to stop taking high intensity atorvastatin and abstain from alcohol consumption, though alcohol intake was one glass of wine nightly. Repeat testing demonstrated AST 39 U/L, ALT 58 U/L, ALP 98 U/L and total bilirubin 0.9mg/dL. An abdominal ultrasound was obtained and showed cavernous transformation of the portal vein (PV) with gastrosplenic varices. Computed tomography of the abdomen (Image 1) confirmed these findings and also revealed atrophy of the left hepatic lobe. The etiology of chronic PV thrombus was explored. Protein C and S, and antithrombin III were within reference range. Anticardiolipin antibody was negative. JAK2 and Factor V Leiden mutations were negative. Given risk factors for non-alcoholic fatty liver disease, we decided to evaluate the extent of fibrosis with transient elastography during the patient's office visit. FibroScan measured liver stiffness at 21.1 kPa, correlating with F4 fibrosis. No overt confounders were identified. To confirm the diagnosis of cirrhosis, the patient underwent a percutaneous liver biopsy. The sample obtained was from the right liver lobe and was adequate for interpretation, over 2cm in length. It showed minimal macrovesicular steatosis without features of steatohepatitis and no significant portal or lobular inflammation. Trichrome stain revealed stage 1 fibrosis with patchy perisinusoidal fibrosis. DISCUSSION: We concluded that the patient did not have cirrhosis, and that chronic PV thrombus contributed to left hepatic lobe atrophy. The etiology of chronic PV thrombus remains elusive. FibroScan results were likely confounded by the atrophic left hepatic lobe. Our case highlights the importance of confirming cirrhosis with liver biopsy in particular subsets of patients given the many implications in the patient’s monitoring and prognosis with a diagnosis of cirrhosis.Image 1.: Atrophy of the Left Hepatic Lobe.

Effect of atorvastatin on muscle symptoms in coronary heart disease patients with self-perceived statin muscle side effects: a randomized, double-blinded crossover trial.

AimsTo estimate the effect of atorvastatin on muscle symptom intensity in coronary heart disease (CHD) patients with self-perceived statin-associated muscle symptoms (SAMS) and to determine the relationship to blood levels of atorvastatin and/or metabolites.Methods and resultsA randomized multi-centre trial consecutively identified 982 patients with previous or ongoing atorvastatin treatment after a CHD event. Of these, 97 (9.9%) reported SAMS and 77 were randomized to 7-week double-blinded treatment with atorvastatin 40 mg/day and placebo in a crossover design. The primary outcome was the individual mean difference in muscle symptom intensity between the treatment periods, measured by visual-analogue scale (VAS) scores. Atorvastatin did not affect the intensity of muscle symptoms among 71 patients who completed the trial. Mean VAS difference (statin-placebo) was 0.31 (95% CI: −0.24 to 0.86). The proportion with more muscle symptoms during placebo than atorvastatin was 17% (n = 12), 55% (n = 39) had the same muscle symptom intensity during both treatment periods whereas 28% (n = 20) had more symptoms during atorvastatin than placebo (confirmed SAMS). There were no differences in clinical or pharmacogenetic characteristics between these groups. The levels of atorvastatin and/or metabolites did not correlate to muscle symptom intensity among patients with confirmed SAMS (Spearman’s rho ≤0.40, for all variables).ConclusionRe-challenge with high-intensity atorvastatin did not affect the intensity of muscle symptoms in CHD patients with self-perceived SAMS during previous atorvastatin therapy. There was no relationship between muscle symptoms and the systemic exposure to atorvastatin and/or its metabolites. The findings encourage an informed discussion to elucidate other causes of muscle complaints and continued statin use.

Abstract 281: A Network Meta-analysis Exploring High-intensity Atorvastatin In Contrast Induced Nephropathy

Introduction: The utility of pre-procedure statins prior to coronary angiography has been utilized as an adjunct in the prevention of contrast-induced nephropathy (CIN). This has been attributed to the pleotropic and anti-inflammatory effects of the statin. Whether there is a dose and intensity dependent effect on the prevention of CIN is unknown. Methods: We performed a hierarchical network meta-analysis on all published randomized-controlled trials up to March 2020 to determine whether high-intensity atorvastatin (40mg or 80mg) was superior to lower intensity atorvastatin (20mg or less) and high-intensity or low-intensity statins. We searched PubMed, MEDLINE, Embase, Web of Science and Cochrane database for randomized-controlled studies without restriction to language. Studies published in Chinese was translated using Google Translate. Network meta-analysis was performed using NetMetaXL version 1.6.1. Results: We analyzed 49 trials, comprised of 13,395 patients, comparing five arms of treatment: Moderate/High intensity atorvastatin, Low intensity atorvastatin, Moderate/High intensity other statin, Low intensity other statin and None. There were 1,029 events for CIN (7.68%). In pairways comparisons, Moderate/High intensity atorvastatin reduced CIN by 0.70 (95% CI: 0.54-0.91) when compared to placebo. When compared to Moderate/High intensity other statins, the difference was not statistically significant (95% CI: 0.50-1.08). Conclusion: Moderate to High Dose Atorvastatin was not superior to other statins in prevention of CIN. Further investigation into the anti-inflammatory properties of statins may be helpful in understanding the role of statins as adjunct treatment to standard of care in preventing CIN.

Acute Coronary Syndrome and Myocardial Ischemia in Hypertrophic Cardiomyopathy

47 years old male smoker with no co morbidities, presented with history of chest pain in the retrosternal area for the 3 days. The Pain was described as sharp, non-exertional and intermittent. Patient did not have any family history of known cardiac disease or sudden cardiac death. A Clinical examination failed to reveal any abnormalities. An ECG revealed deep T wave inversion in the anterolateral chest leads with left ventricular hypertrophy (LVH). Bloods analysis showed normal Complete blood count, liver function and mildly increased cardiac troponins. The Patient was admitted to the CoronaryCare Unit with a diagnosis of acute coronary syndrome. Patient was initiated dual antiplatelets, fondaparinux and high intensity atorvastatin. Following this, an echocardiogram revealed severe Left ventricular hypertrophy and reduced LV (left ventricular) cavity dimensions. Good LV systolic function with grade 3 diastolic dysfunction was noted. Coronary angiogram showed a normal right and left coronary system. Patient was diagnosed with hypertrophic cardiomyopathy. Cardiac MRI Showed severe Left ventricular hypertrophy with interventricular septum thickness 3.7 cm with rest of the walls hypertrophied. There was evidence of severe fibrosis of the septum, anterior and lateral wall. On the basis of severe left ventricular hypertrophy (especially septal thickness >3.5 cm) and myocardial fibrosis, Patient was started on beta blockers and ICD was inserted for primary prevention of arrhythmias.

Safety of High-Intensity Statins in the Veteran Population: Atorvastatin 40 to 80 mg Compared With Rosuvastatin 20 to 40 mg.

Background: High-intensity statin therapy is recommended in patients with clinical atherosclerotic cardiovascular disease (ASCVD) or at high risk of ASCVD. Current evidence demonstrates efficacy of high-intensity statin therapy in reducing major adverse cardiovascular events; yet the comparative safety profile between high-intensity statin agents remains unknown. In 2011, when atorvastatin became generic, the Veteran's Health Administration made the formulary switch from rosuvastatin to atorvastatin. Currently, rosuvastatin is generic; however, at the time of this study, it was still under patent. Objective: The primary objective was to determine if high-intensity atorvastatin compared with rosuvastatin is associated with an increased incidence of adverse drug reactions (ADRs) in the veteran population. Methods: A retrospective cohort study at James A. Haley Veterans' Hospital compared patients receiving rosuvastatin 20 to 40mg from January 2009 to November 2011 (n = 4,165) and atorvastatin 40 to 80mg from May 2012 to June 2016 (n = 5,852). Patients were excluded if they were nonadherent to statin therapy or had a documented ADR to atorvastatin prior to formulary switch. Results: A difference in overall ADR rates was found between atorvastatin and rosuvastatin groups (4.59% vs 2.91%; odds ratio [OR], 1.61; 95% CI, 1.29 to 2.00; P < 0.05). Statistically significant differences in abnormal liver transaminases (3.99% vs 1.39%; OR, 2.95; 95% CI, 2.21 to 3.94; P < 0.05) and statin-associated muscle symptoms (1.14% vs 0.5%; OR, 2.29; 95% CI, 1.39 to 3.74; P < 0.05) were identified between groups. Patients receiving rosuvastatin were on therapy 2.5 times longer before developing an ADR. Conclusion and Relevance: High-intensity atorvastatin compared with rosuvastatin is associated with an increased incidence of ADRs.

Adverse events with high-intensity atorvastatin vs rosuvastatin

Adverse events with high-intensity atorvastatin vs rosuvastatin