ASTHMA

RESPIRATORY

Asthma Control Tests (ACT) overview

<p>Dr. Ahmed Abbas, Consultant Pneumologist, Abu Dhabi, UAE and Assistant Professor of Respiratory&nbsp;Medicine, Egypt, provides an overview on ACT scoring.</p>

Asthma Assessment Tools (EPOS)

<p>Dr. Janan Abduwani explains the use of the assessment tools (both subjective and objective tools) and provides an overview on the EPOS guidelines.</p>

ATOPIC-DERMATITIS

DERMATOLOGY

Atopic Dermatitis story

<p>Atopic Dermatitis is a disease with multidimensional burden that affects many Patients. Watch the video to learn more.</p>

<p><strong>Atherosclerotic cardiovascular disease risk assessment: An American Society for Preventive Cardiology clinical practice statement.</strong></p>
<p>The American Society for Preventive Cardiology (ASPC) offers guidance and tools to assess the risk of atherosclerotic cardiovascular disease (ASCVD), with the goal of enabling specialists to provide suitable treatments to prevent ASCVD events.</p>
<h2>Key Takeaway</h2>
<p>For primary prevention of ASCVD, the first step is to assess cardiovascular risk by determining the global risk score, after which the presence of the following factors can be used to further refine risk estimation:</p>
<ul>
 <li>Traditional risk factors: Age, sex, diabetes, systolic blood pressure, antihypertensive treatment, total cholesterol, low-density lipoprotein-cholesterol (LDL-C), high-density lipoprotein-cholesterol, and cigarette smoking</li>
 <li>Risk enhancing factors: Family history of premature ASCVD, sex-specific factors, high-risk ethnicities, primary hypercholesterolemia, metabolic syndrome, chronic inflammatory conditions, and chronic kidney disease</li>
 <li>Female-specific factors: Auto-immune disease, menarche, polycystic ovary syndrome, oral contraceptives, infertility, multiparity, adverse pregnancy outcomes, preeclampsia, gestational diabetes mellitus, early menopause, premature ovarian insufficiency, and vasomotor symptoms</li>
 <li>Inflammatory biomarkers: High sensitivity C-reactive protein (hs-CRP), lipoprotein-associated phospholipase A2, myeloperoxidase, myeloid-related protein 8/14, matrix metalloproteinases, lectin-like oxidized LDL receptor-1, and growth differentiation factor-15</li>
 <li>Other biomarkers: Persistently elevated triglycerides, elevated lipoprotein (a) (Lp[a]) or apolipoprotein B, and low ankle-brachial index (ABI)</li>
 <li>Racial / ethnic factors: Non-Hispanic Black, African American, Asian, etc.</li>
 <li>Social determinants of health: Psychological distress, delayed care due to lack of transport, shortage of food, unemployment, lack of health insurance, inability to pay medical bills, or downward social mobility</li>
 <li>Screening for subclinical atherosclerosis: 
  <ul>
   <li>Carotid intimal-media thickness or established plaque by carotid ultrasound</li>
   <li>Endothelial function by brachial artery reactivity, large vessel (aorta) or small vessel assessment of vascular health</li>
   <li>Provides the largest decrease in LDL-C with clinical benefits in observational studies.</li>
   <li>Enables early decision on introducing PCSK9 inhibitors.</li>
  </ul></li>
 <li>Nutritional factors, physical activity, and cardiorespiratory fitness levels play vital roles in ASCVD risk assessment and should also be considered.</li>
 <li>For secondary prevention, risk stratification (very high, high, moderate, or low), followed by immediate and intensive risk factor management are essential.</li>
</ul>
<h2>Why This Matters</h2>
<ul>
 <li>To reduce the risk of developing ASCVD, an accurate assessment of the risk is crucial to provide patients with appropriately targeted preventive therapies.</li>
 <li>Without doing a formal risk assessment, a clinician’s estimate can be inaccurate, which can underestimate the actual risk; hence, the use of global risk scores can be beneficial to improve the application of guideline-based therapies.</li>
 <li>Cardiovascular risk assessment forms the basis of preventive cardiology to determine the appropriateness or intensification of preventive therapy.</li>
</ul>
<h2>Clinical recommendations</h2>
<ul>
 <li>For primary prevention, global risk scoring provides a calculation of ASCVD risk from a set of standard office-based risk factors for a stipulated period. 
  <ul>
   <li>Clinicians can then determine the best ways to reduce the risk of developing ASCVD and discuss the same with the patient.</li>
  </ul></li>
 <li>The presence, number, and / or extent of risk enhancing factors as well as severity of inflammatory factors such as hs-CRP and laboratory measures such as Lp(a) levels can help to further refine treatment decision.</li>
 <li>In women, it is crucial to obtain a complete and thorough reproductive history from menarche to menopause, including premature menopause, preeclampsia, and autoimmune disease.</li>
 <li>Certain race / ethnic groups have a higher risk of developing ASCVD, which can help to further refine the use of preventive therapy.</li>
 <li>Social determinants of health may exert independent effects and should be part of the clinician-patient discussion to determine appropriate ways to lower risk.</li>
 <li>Among screening tests for subclinical ASCVD, CAC testing provides considerable improvement of risk reclassification over global risk scoring in most primary prevention groups, including diabetes. 
  <ul>
   <li>Additionally, it can be used to refine decisions on preventive therapy, including on the use of statin and aspirin.</li>
  </ul></li>
 <li>If CAC scoring is unavailable, carotid ultrasound imaging together with carotid plaque assessment may be beneficial for risk assessment.</li>
 <li>The use of ABI is valuable for assessment of peripheral artery disease and can improve risk reclassification beyond global risk scoring.</li>
 <li>In patients with pre-existing ASCVD, more aggressive treatment should be considered for those at the highest risk, based on the history of either multiple high-risk conditions and one major ASCVD event or multiple major events.</li>
 <li>Patients with recurrent ASCVD events within a short period of time represent an extreme risk for further events 
  <ul>
   <li>An even more aggressive risk factor management and intensive treatment should be considered</li>
  </ul></li>
 <li>Clinician-patient discussions on lifestyle management and on the benefits and risks of evidence-based pharmacologic therapies that are essential to lower the risk of developing ASCVD is central to preventive cardiology.</li>
</ul>

Reference

Atherosclerotic Cardiovascular Disease Risk Assessment

DYSLIPIDEMIA

CARDIOLOGY

<h2>Improve prognosis in patients with type 2 diabetes mellitus<br>
  Regulate low-density lipoprotein cholesterol level for those undergoing coronary revascularisation</h2>
<h3>Main takeaway</h3>
<ul>
 <li>Depending on the revascularisation strategy, LDL-C levels yield a differential influence on cardiovascular (CV) outcomes 
  <ul>
   <li>Compared to patients with 1-year LDL-C &lt;70 mg/dl, patients who had 1-year LDL-C ≥100 mg/dl showed a significant increase in long-term cardiovascular risk</li>
   <li>Patients randomised to coronary artery bypass grafting (CABG) group had lower rates of major adverse cardiac or cerebrovascular events (MACCE) versus the optimal medical therapy (OMT) alone group</li>
  </ul></li>
</ul>

<h3>Why this matters</h3>
<ul>
 <li>Guideline-directed management of patients with coronary heart disease (CHD) and type 2 diabetes mellitus (T2DM) includes intensive lifestyle intervention along with aggressive secondary prevention (OMT) and an appropriate revascularisation strategy 
  <ul>
   <li>This analysis highlights the significance of LDL-C control in the first year post-procedure</li>
  </ul></li>
</ul>

<h3>Study design</h3>
<ul>
 <li>Pooled analysis: combined individual patient-level information from 3 federally funded trials (BARI 2D, COURAGE, and FREEDOM)</li>
 <li>4,050 patients with T2DM (mean age = 62.8 ± 8.8 years; female = 27.0%; median follow-up = 3.9 years [after the index 1-year assessment]) were categorised according to LDL-C levels at 1 year following randomisation 
  <ul>
   <li>Key inclusion criteria: all patients with CHD and T2DM from BARI-2D and FREEDOM trials and only patients with T2DM in the COURAGE trial</li>
   <li>Key exclusion criteria: patients with LDL-C &lt;20 mg/dl and triglycerides &gt;400 mg/dl both at baseline and 1 year</li>
   <li>Primary outcome: 4-year rate of the MACCE composite (all-cause mortality, nonfatal myocardial infarction, and nonfatal stroke)</li>
   <li>Secondary outcomes: subsequent revascularisation</li>
  </ul></li>
</ul>

<h3>Key results</h3>
<ul>
 <li>Patients with 1-year LDL-C levels ≥100 mg/dl experienced higher 4-year cumulative risk of MACCE 
  <ul>
   <li>17.2% versus 13.3% (70 to &lt;100 mg/dl) versus 13.1% (&lt;70 mg/dl); p = 0.016</li>
  </ul></li>
 <li>Incidence of CV events following a coronary revascularisation procedure or OMT: 
  <ul>
   <li>When comparing CABG with PCI, CABG led to significantly lower rates of MACCE for those with 1-year LDL-C levels: 
    <ul>
     <li>Between 70 and &lt;100 mg/dl: HR: 0.49; 95% CI, 0.31 to 0.79; p = 0.003</li>
     <li>≥100 mg/dl: HR: 0.53; 95% CI, 0.30 to 0.91; p = 0.022</li>
    </ul></li>
   <li>When compared with both OMT and PCI patients, CABG correlated with lower rates of subsequent revascularisation in all 1-year LDL-C strata 
    <ul>
     <li>No difference in subsequent revascularisation rates were observed when comparing PCI with OMT in any of the 1-year LDL-C strata</li>
    </ul></li>
  </ul></li>
</ul>

<h3>Limitations</h3>
<ul>
 <li>There may be a possibility of additional confounders influencing the association between cardiovascular outcomes and both the choice of revascularisation procedure and the LDL-C control rate</li>
 <li>There is a lack of data for adherence to the prescribed therapy</li>
 <li>A systematic analysis was not pursued for lipid lowering therapy during the first year of follow-up</li>
 <li>There could be an occurrence of immortal time bias</li>
</ul>

Regulate LDL-C level for those undergoing coronary revascularization (Diabetic Patients)

<p>Ulf Landmesser<sup>1</sup>, Jennifer McGinniss<sup>2</sup>, Ph. Gabriel Steg<sup>3,4</sup>, Deepak L. Bhatt<sup>5</sup>, Vera A. Bittner<sup>6</sup>, Rafael Diaz<sup>7</sup>, Mirza Dilic<sup>8</sup>, Shaun G. Goodman<sup>9,10</sup>,&nbsp;J. Wouter Jukema<sup>11,12</sup>, Megan Loy<sup>13</sup>, Ivan Pećin<sup>14</sup>, Robert Pordy<sup>15</sup>, Steen H. Poulsen<sup>16</sup>, Michael Szarek<sup>17,18</sup>, Harvey D. White<sup>19</sup>, Gregory G. Schwartz<sup>20</sup>, for the ODYSSEY OUTCOMES Investigators.</p>
<h2>Background and Objectives</h2>
<ul>
 <li>The 2019 ESC/EAS dyslipidemia guidelines lowered LDL-C treatment goals: 
  <ul>
   <li>In patients considered at very high risk (including those with ACS), LDL-C goal of &lt;1.4 mmol/L is recommended together with &gt;50% LDL-C reduction and a lower goal of &lt;1.0 mmol/L may be considered for those with recurrent CV events within 2 years</li>
  </ul></li>
</ul>
<ul>
 <li>This analysis, using the data of ODYSSEY OUTCOMES trial: 
  <ul>
   <li>Examined how many patients not at goal with high-intensity or MTD statin treatment achieved new LDL-C treatment goals with alirocumab, according to baseline LDL-C values</li>
   <li>Projected how many would have achieved the new treatment goals with the use of ezetimibe when added to MTD statin therapy</li>
  </ul></li>
</ul>
<h2>Methods</h2>
<ul>
 <li>This sub analysis of the ODYSSEY OUTCOMES trial (multicentre, double-blind, randomized placebo-controlled trial in 18,924 patients of ≥40 years of age, hospitalized with an ACS 1–12 months before randomization) comprised of 17,589 patients with LDL-C ≥1.4 mmol/L at baseline who did not receive ezetimibe treatment</li>
</ul>
<h2>Key Findings</h2>
<ul>
 <li>94.6% of patients receiving alirocumab achieved LDL-C goal &lt;1.4 mmol/L at ≥1 post-baseline measurement vs. 17.3% patients receiving placebo</li>
 <li>85.2% of patients with recurrent CV events vs 3.5% receiving placebo, can achieve the lower goal (&lt;1.0 mmol/L)</li>
 <li>In contrast, addition of ezetimibe to optimized statin therapy was projected to achieve LDL-C &lt;1.4 mmol/L in only 10.6% of patients at baseline</li>
 <li>Although the statin/ezetimibe combination is more cost effective than the statin/PCSK9i combination, a substantial number of patients will not achieve the LDL-C goal with this combination</li>
</ul>
<h2>Conclusion</h2>
<p>In post ACS patients with residual dyslipidemia despite intensive or MTD statin, adding alirocumab treatment which has been shown to further reduce the risk of MACE and is associated with a reduction in all-cause mortality after ACS, enabled majority of the patients to reach the 2019 ESC guideline targets for LDL-C &lt;1.4 mmol/L (&lt;55 mg/dL) and &lt;1.0 mmol/L (&lt;40 mg/dL) compared to placebo or ezetimibe</p>

Abbreviations

References

Achievement of ESC/EAS LDL-C Treatment Goals After an ACS with Statin and Alirocumab

<h2>Proprotein convertase subtilisin/kexin type 9 inhibitors for heterozygous familial hypercholesterolemia: A clinical practice experience from the Safeheart registry</h2>

<h2>Key Takeaway</h2>
<p>In clinical practice, PCSK9i (alirocumab or evolocumab) on top of maximum LLT significantly reduced LDL-C levels (by 58%) and improved LDL-C target achievement in patients with heterozygous FH (both in men and women).</p>
<p><strong>LDL-C goals*:</strong></p>
<ul>
 <li>&nbsp;2016 ESC/EAS goals†: Patients with ASCVD = 67%; patients without ASCVD = 80%</li>
 <li>&nbsp;2019 ESC/EAS LDL-C goals‡: VHR patients = 46%; HR patients = 50%</li>
</ul>
<p><strong>Independent predictors for LDL-C goals:</strong>&nbsp;Male gender; smoking; and use of statins + ezetimibe</p>

<h2>Why This Matters</h2>
<ul>
 <li><sup>§</sup>&nbsp;Use of PCSK9i in clinical practice is less frequent (partly due to cost and insurance issues).</li>
 <li>Safeheart&nbsp;registry study assessed the use and efficacy of PCSK9i as well as LDL-C goals attainment in clinical practice setting of FH patients.</li>
</ul>

<h2>Study Design</h2>
<p><strong>Safeheart: Open, Multicenter, Nationwide, Long-term Prospective Study</strong>&nbsp;(N = 433 [Alirocumab = 211; Evolocumab = 222])</p>
<p><strong>Key Inclusion Criteria</strong></p>
<p>Patients with molecular diagnosis of FH (aged ≥20 years) on stable LLT, who received PCSK9i (alirocumab 75/150 mg every 2 or 4 weeks, or evolocumab 140 mg every 2 weeks or 420 mg every 4 weeks) from 2016 to January 2020<sup>¶</sup></p>
<p><strong>Key Exclusion Criteria</strong></p>
<p>Patients who participated in RCTs with PCSK9i before 2016</p>
<p><strong>LDL-C Goals:</strong>&nbsp;Defined and analyzed based on 2016 and 2019 ESC/EAS guidelines</p>

<h2>Key Results</h2>
<p>Overall,&nbsp;<strong>433</strong>&nbsp;patients were included in the analysis</p>
<p>Mean age =&nbsp;<strong>55</strong>&nbsp;years; male =&nbsp;<strong>53%;</strong>&nbsp;history of ASCVD =&nbsp;<strong>39%;</strong>&nbsp;median follow-up =&nbsp;<strong>2.5</strong>&nbsp;years</p>

<h2>LDL-C Levels:</h2>
<ul>
 <li><strong>Before PCSK9i:</strong>&nbsp;Median LDL-C =&nbsp;<strong>145</strong>&nbsp;mg/dL (IQR:&nbsp;<strong>125–173</strong>)</li>
 <li><strong>After addition of PCSK9i:</strong>&nbsp;LDL-C levels reduced by&nbsp;<strong>58%</strong>&nbsp;(IQR:&nbsp;<strong>41–70</strong>&nbsp;<strong>[P &lt;0.001]</strong>) in men and women without differences between both PCSK9i&nbsp;<br>
   Median LDL-C =&nbsp;<strong>62</strong>&nbsp;mg/dL (IQR:&nbsp;<strong>44–87</strong>)</li>
</ul>

<h2>LDL-C Goals*</h2>
<ul>
 <li>2016 ESC/EAS goals†: Patients with ASCVD =&nbsp;<strong>67%</strong>; patients without ASCVD =&nbsp;<strong>80%</strong></li>
 <li>2019 ESC/EAS LDL-C goals‡: VHR patients =&nbsp;<strong>46%</strong>; HR patients =&nbsp;<strong>50%</strong></li>
 <li>Higher LDL-C levels before PCSK9i initiation had a significant inverse relationship with goals attainment</li>
</ul>

<h2>Independent Predictors (2019 ESC/EAS LDL-C GOALS)</h2>
<ul>
 <li>Male gender (P = 0.023); smoking (P = 0.041); and use of statins + ezetimibe (P = 0.008)</li>
</ul>

<h2>Limitations</h2>
<ul>
 <li>Study lacked blinding randomization</li>
 <li>Follow-up analysis was not centralize</li>
 <li>In the follow-up analysis, Lp(a) measurement was not available</li>
</ul>
<p data-font="legal">* Without differences between alirocumab or evolocumab.<br><sup>†</sup>&nbsp;LDL-C target below 70 mg/dL and 100 mg/dL, respectively according to 2016 ESC/EAS guidelines.<br><sup>‡</sup>&nbsp;LDL-C goal according to 2019 ESC/EAS guidelines (for VHR patients &lt;55 mg/dL; for HR patients &lt;70 mg/dL).<br><sup>§</sup>&nbsp;International guidelines recommend PCSK9i for patients with FH with substantially higher LDL-C levels despite maximally tolerated statin ± ezetimibe.<br><sup>¶</sup>&nbsp;Kept a stable dose of PCSK9i at least 3 months before the last analysis. PCSK9i eligibility was based on Spanish National Health System reimbursement regulations in FH patients.</p>

Clinical practice experience in patients with familial hypercholesterolemia (FH) from the Safeheart registry

<h2>Achievement of lipid modification goals relating to statins and ezetimibe use for cardiovascular disease prevention in the United Kingdom</h2>
<p>This review emphasized on various reasons for sub-optimal lipid lowering and provided possible strategies for improving lipid management to reduce cardiovascular disease (CVD) risk in practice considering the United Kingdom (UK) clinical guidance.</p>
<h2>Key Takeaway</h2>
<ul>
 <li>This review highlighted that a significant proportion of UK patients with CVD have sub-optimal reductions in cholesterol/non-high-density lipoprotein cholesterol (HDL-C)/ low-density lipoprotein cholesterol (LDL-C) despite the widespread availability of lipid-lowering therapy and guidance.</li>
 <li>Reasons for sub-optimal lipid lowering are multifactorial, including a lack of compliance with guidelines, patient adherence, statin intolerance, and statin reluctance as well as wider genetic factors.</li>
 <li>Possible strategies that improve current lipid management and attainment of lipid-lowering goals include: 
  <ul>
   <li>Improving the patient–healthcare professional partnership; conducting audits of local prescribing versus guidance; implementing plans for the refinement of current services; considering alternative options that improve adherence (cost-effective single-pill combinations)</li>
  </ul></li>
 <li>Additional options are needed in patients at a high risk of CVD events, in whom lipid-lowering goals are not achieved with statins and ezetimibe alone.</li>
</ul>
<h2>Why This Matters</h2>
<ul>
 <li>Despite accepting LDL-C as a causal cardiovascular risk factor and thus a critical component in CVD risk reduction, lipid lowering is not adequately attained in the UK.</li>
 <li>This review was conducted to understand current UK lipid management guidance in relation to treatment with statins and ezetimibe and the corresponding attainment of recommended lipid-lowering goals, with a focus on publications between January 2017 and February 2020.</li>
</ul>
<h2>Key Highlights</h2>
<p>Identified publications were reviewed against lipid management guidelines in relation to CVD risk from National Institute for Health and Care Excellence (NICE, CG181), Scottish Intercollegiate Guidelines Network (SIGN, 149), and European Society of Cardiology (ESC)/European Atherosclerosis Society (EAS).</p>
<p>Lipid management in the UK:</p>
<ul>
 <li>NICE CG181 (updated in 2016) and SIGN 149 (2017) are the main clinical guidelines for lipid management in relation to cardiovascular risk in the UK.</li>
 <li>Current UK guidelines advise that lipid-lowering therapy should be considered for both the primary and secondary prevention of CVD based on CVD risk assessment (10 year) in addition to recommending lifestyle modifications.</li>
 <li>Although a range of lipid-modifying therapies are approved in the UK, statins are the mainstay of initial recommended treatment strategies.</li>
 <li>NICE and SIGN guidance recommend that lipid-lowering therapy should achieve &gt;40% reduction in non-HDL-C at 3 months.</li>
 <li>ESC/EAS guidelines highlight lowering LDL-C and total cholesterol as the primary target of therapy.</li>
 <li>LDL-C measurement remains relevant in routine clinical practice as the guidance for later lines of therapy (post-statin) is predicated on the evaluation of LDL-C levels.</li>
 <li>NICE states that ezetimibe should be considered in combination with statin for primary hypercholesterolemia when total cholesterol or LDL-C is not adequately controlled after initial statin therapy.</li>
 <li>Alternative therapies such as proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors evolocumab or alirocumab may be considered for certain patients with hypercholesterolemia or mixed dyslipidemia who have a high or very high risk of CVD, but only if LDL-C levels are persistently above recommended thresholds.</li>
 <li>Recent ESC/EAS guidelines also state that if patients fail to achieve LDL-C goal within 4–6 weeks despite lifestyle modifications and maximally tolerated highintensity statins, add-on therapy with ezetimibe and subsequently a PCSK9 inhibitor should be considered.</li>
</ul>
<p>Sub-optimal achievement of guideline-derived lipid modification goals:</p>
<ul>
 <li>Several large UK studies highlighted that a significant proportion of patients are not being adequately managed according to best practice guidelines despite widespread availability and supporting evidence on the effectiveness of statins and combination therapy with ezetimibe.</li>
 <li>Variations in individual patient genotypes, statin intolerance, patient adherence, and the potency of statin prescribing might be reasons for sub-optimal LDL-C reductions.</li>
 <li>Limited prescribing of combination therapy may also contribute to sub-optimal lipid lowering.</li>
 <li>Other factors likely to contribute to sub-optimal lipid lowering include late intervention in the disease trajectory, a lack of follow-up and treatment adaptation according to risk factors or fulfillment of therapeutic goals, and statin intolerance.</li>
 <li>Misconceptions about statin intolerance and statin-related adverse events may lead to a reluctance to take statins and early discontinuation and/or non-adherence, which may result in inadequate lipid lowering.</li>
</ul>
<p>Possible strategies that improve current lipid management include*:</p>
<ul>
 <li>Measures for improving the patient–healthcare professional partnership; conducting audits of local prescribing versus guidance; implementing plans for the refinement of current services; follow-up and monitoring procedures for different types of therapy; and considering alternative options that improve treatment adherence (cost-effective single pill)</li>
</ul>
<p>Additional information:</p>
<ul>
 <li>Possible strategies that improve adherence with cholesterol goals*</li>
</ul>

Achievement of lipid modification goals with Statins & Ezetimibe

<h2>Safety and Efficacy of Ezetimibe Added on to Rosuvastatin 5 or 10 mg Versus Up-Titration of Rosuvastatin in Patients with Hypercholesterolemia (the ACTE Study)</h2>
<p>Harold E Bays, Michael H Davidson, Rachid Massaad, Doreen Flaim, Robert S Lowe, Andrew M Tershakovec, Charlotte Jones-Burton</p>
<h2>Objective</h2>
<p>The primary objective of the present study was to compare the low-density lipoprotein (LDL) cholesterol-lowering efficacy of ezetimibe added to stable rosuvastatin therapy (5 or 10 mg/day) versus doubling the rosuvastatin dose (from 5 to 10 mg/day or 10 to 20 mg/ day, pooled across doses).</p>
<h2>Endpoints</h2>
<p>The primary efficacy endpoint was the percentage of change from baseline in LDL cholesterol evaluated in the overall population (pooled across doses). The evaluation of this endpoint for each stratum separately, and the percentage of subjects reaching the National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) recommended LDL cholesterol targets in the overall population (pooled across doses) constituted the key secondary efficacy endpoints. Other secondary efficacy endpoints included the percentage of subjects reaching the NCEP ATP III recommended LDL cholesterol targets evaluated in each stratum separately; the percentage of subjects achieving an LDL cholesterol level of &lt;70 mg/dl in the overall population and in each stratum separately; and the percentage of change from baseline in other lipids, lipoproteins, and high-sensitivity C-reactive protein evaluated in the overall population and in each stratum separately. Safety and tolerability were assessed by review of all safety parameters, including adverse experiences and laboratory values.</p>
<h2>Methods</h2>
<p>The 6-week, randomized, double-blind, parallel-arm study included patients who were hypercholesterolemic, aged 18 to 79 years with a moderately high risk (subjects with ≥2 risk factors conferring a 10-year risk of CHD of 10% to 20%, as estimated from the Framingham risk scores), high risk without AVD (subjects with CHD risk equivalents such as diabetes mellitus or ≥2 risk factors conferring a 10-year risk of CHD ≥20%, as estimated from the Framingham risk scores), or high risk with AVD (subjects with established CHD or patients with CHD risk equivalents and other AVD [peripheral arterial disease, atherosclerotic aortic disease, or carotid artery disease]).</p>
<p>Once eligible, patients were assigned to receive run-in open-label rosuvastatin 5 or 10 mg/day for 4 weeks (5 weeks for those switching medication or treatment naïve) according to their cardiovascular risk, current use of lipid lowering therapy, and LDL level at screening. Patients were stratified according to their runin treatment (stratum I, rosuvastatin 5 mg; stratum II, rosuvastatin 10 mg). The subjects receiving rosuvastatin 5 mg during the run-in period (stratum I) were randomized to rosuvastatin 5 mg plus ezetimibe 10 mg add-on or rosuvastatin up-titration to 10 mg. Those receiving rosuvastatin 10 mg (stratum II) were randomized to rosuvastatin 10 mg plus ezetimibe 10 mg add-on or rosuvastatin up-titration to 20 mg.</p>
<h2>Results</h2>
<p>440 patients were administered the study drug, with 197 (44.8%) receiving rosuvastatin 5 mg and 243 (55.2%) receiving rosuvastatin 10 mg during the 4- to 5-week open label run-in period. Pooled data demonstrated that ezetimibe added to stable rosuvastatin 5 mg or 10 mg reduced LDL cholesterol by 21%. In contrast, doubling rosuvastatin to 10 mg or 20 mg reduced LDL cholesterol by 5.7% (between-group difference of 15.2%, p &lt;0.001). Individually, ezetimibe plus rosuvastatin 5 mg reduced LDL cholesterol more than did rosuvastatin 10 mg (12.3% difference, p &lt;0.001), and ezetimibe plus rosuvastatin 10 mg reduced LDL cholesterol more than did rosuvastatin 20 mg (17.5% difference, p &lt;0.001). Compared to rosuvastatin up-titration, ezetimibe add-on achieved significantly greater attainment of LDL cholesterol levels of &lt;70 or &lt;100 mg/dl (59.4% vs 30.9%, p &lt;0.001), and &lt;70 mg/dl in all subjects (43.8% vs 17.5%, p &lt;0.001); produced significantly greater reductions in total cholesterol, non–high-density lipoprotein cholesterol, and apolipoprotein B (p &lt;0.001); and resulted in similar effects on other lipid parameters. Adverse experiences were generally comparable among the groups.</p>
<h2>Conclusions</h2>
<p>compared to up-titration doubling of the rosuvastatin dose, ezetimibe 10 mg added to stable rosuvastatin 5 mg or 10 mg produced greater improvements in many lipids’ parameters and achieved greater attainment of recommended LDL cholesterol targets in subjects with elevated LDL cholesterol and at moderately high/high coronary heart disease risk.</p>

The ACTE Study

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