<h2>Key Takeaway</h2>
This systematic review and meta-analysis of randomized clinical trials stratified by follow-up time and degree of LDL-C lowering showed that:
<ul>
 <li>Benefits of LDL-C lowering&nbsp;are not fixed, but&nbsp;increase steadily with longer durations of treatment</li>
 <li>Causal effect of LDL-C&nbsp;on the risk of ASCVD is determined by both the&nbsp;absolute magnitude and the cumulative duration of exposure to LDL-C</li>
 <li>Results from&nbsp;short-term randomized trials&nbsp;were compatible with the very strong associations between LDL-C and cardiovascular events seen in&nbsp;Mendelian randomization (MR) studies</li>
</ul>
Study findings indicate that current guidelines underestimate the benefits of LDL-C lowering interventions that are continued for longer than 5 years, which has particular relevance to intervention in younger people.

<h2>Why This Matters</h2>
<ul>
 <li>Evidence from&nbsp;randomized clinical trials&nbsp;has shown that&nbsp;each mmol/L lower LDL-C*&nbsp;is associated with&nbsp;≈24% lower risk&nbsp;of major vascular events.</li>
 <li>However,&nbsp;MR studies&nbsp;report that&nbsp;each mmol/L lower LDL-C&nbsp;is associated with&nbsp;&gt;50% lower coronary risk, with the LDL cholesterol difference hypothesized to be attributed to the exposure duration.</li>
</ul>
This study evaluated the relationship between lipid-lowering drug exposure time and relative risk reduction of major cardiovascular events in randomized clinical trials, by stratifying the analysis to each year of follow-up, by effect size and LDL-C difference.

<h2>Study Design</h2>
This was a systematic review and meta-analysis of randomized clinical trials of statins, ezetimibe, or PCSK9i that reported LDL-C levels and effect sizes for each year of follow-up Inclusion criteria
<ul>
 <li>Studies with a minimum of 1000 patient-years of follow-up</li>
 <li>Trials that reported the effect size/ summary estimate on clinical events per year of follow-up</li>
 <li>Follow-up LDL-C levels per year of follow-up</li>
 <li>Reporting ≥3 years of data</li>
</ul>
Exclusion criteria
<ul>
 <li>Trials including dietary therapies</li>
 <li>Patients followed up for &lt;6 months or treatment compared with medications other than cholesterol lowering drugs or placebo</li>
</ul>
Primary endpoint
<ul>
 <li>Major vascular events (composite of cardiovascular death, myocardial infarction, stroke, and coronary revascularization).</li>
</ul>
Statistical analysis
<ul>
 <li>Meta-regression comparing duration of treatment to log(HR) was used to examine the relationship between treatment duration and risk of major vascular events.</li>
 <li>Effect estimates from meta-analyses of randomized clinical trials were compared with the expected clinical benefit per unit reduction in LDL-C estimated by&nbsp;<a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC5837225/" target="_blank">Ference et al.</a></li>
</ul>

<h2>Key Results</h2>
Overall, 21 trials of LDL-C lowering were included in the analysis; 4 using ezetimibe and statins; 15 using statin therapy only; and 2 for PCSK9i vs placebo. (N = 184,012 patients; average mean follow-up = 4.4 years) Duration of follow-up and LDL-C reduction
<ul>
 <li>Each subsequent year of follow-up diminished the mean difference in LDL-C between the treatment and control arms.</li>
 <li>Average difference: 
 <ul>
 <li>After one year =&nbsp;1.05 mmol/L</li>
 <li>By 3 years =&nbsp;0.98 mmol/L</li>
 <li>By 7 years =&nbsp;0.54 mmol/L</li>
 </ul></li>
</ul>

<table align="center" border="1" cellpadding="10" cellspacing="1" style="height:100%;width:100%;">
 <tbody>
 <tr>
 <td colspan="4" style="background-color: rgb(244, 242, 246);">
 <h3 style="text-align: center;">LDL-C reduction and relative risk reduction in major CV events</h3></td>
 </tr>
 <tr>
 <td colspan="4" style="text-align: center;">After standardizing for the degree of LDL-C reduction, each mmol/L LDL-C reduction was associated with a relative risk reduction in major vascular events&nbsp;after treatment years</td>
 </tr>
 <tr>
 <td style="text-align: center;">After 1 year of treatment</td>
 <td style="text-align: center;">After 3 years of treatment</td>
 <td style="text-align: center;">After 5 years of treatment</td>
 <td style="text-align: center;">After 7 years of treatment</td>
 </tr>
 <tr>
 <td style="text-align: center;">12% 
 (95% CI: 8%–16%)</td>
 <td style="text-align: center;">20% 
 (95% CI: 16%–24%)</td>
 <td style="text-align: center;">23% 
 (95% CI: 18%–27%)</td>
 <td style="text-align: center;">29% 
 (95% CI: 14%–42%)</td>
 </tr>
 <tr>
 <td colspan="4">
 • No significant heterogeneity for individual meta-analyses was observed (I2&nbsp;between 6% and 39%)</td>
 </tr>
 </tbody>
</table>

<h3 style="text-align: center;">Meta regression and summary estimates</h3>
<table align="center" border="1" cellpadding="10" cellspacing="1">
 <tbody>
 <tr>
 <td style="text-align: center; background-color: rgb(244, 242, 246);">Meta regression</td>
 <td>
 <ul>
 <li>Significantly greater proportional&nbsp;risk reduction of major vascular events per mmol/L LDL-C lowered with each additional year&nbsp;of treatment (P &lt;0.001)</li>
 <li>This observed consistent trend in sensitivity analyses was&nbsp;restricted to only those trials that contributed to the analyses during every year of follow-up</li>
 </ul></td>
 </tr>
 <tr>
 <td style="text-align: center; background-color: rgb(244, 242, 246);">Summary estimates from randomized clinical trials and MR†</td>
 <td>
 <ul>
 <li>Meta-analyses&nbsp;of short-term randomized clinical trials are&nbsp;consistent with those estimates from MR</li>
 <li>Proportional&nbsp;risk reduction&nbsp;in major vascular events&nbsp;increases with longer durations of treatment</li>
 </ul></td>
 </tr>
 </tbody>
</table>

<h2>Limitations</h2>
<ul>
 <li>Analysis was based on trial-level data; more reliable estimates would have arisen from analyses of individual patient data.</li>
 <li>A significant uncertainty existed about the extrapolation from 7 years of treatment in the included meta-analyses to a lifetime of treatment estimated from the MR studies.</li>
 <li>Some differences existed in the definition of major vascular event between the included randomized trials and the outcome used in the MR study by&nbsp;<a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC5837225/" target="_blank">Ference et al.</a></li>
 <li>Present study was not registered in Prospero.</li>
</ul>
* Lowered through statins, ezetimibe, and PCSK9i 
 † From&nbsp;<a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC5837225/" target="_blank">Ference et al.</a> for increasing durations of treatment, stratified to per 1 mmol/L LDL-C lowered

Abbreviations

Reference

LLTs Exposure Time and Major Vascular Risk Reduction

DYSLIPIDEMIA

CARDIOLOGY

Lipid-lowering therapy in Peripheral arterial disease: European atherosclerosis society/European society of Vascular medicine joint statement
Existing evidence shows that statin-based treatment substantially reduces the risk of major adverse cardiovascular events (MACE) and major adverse limb events (MALE) by about 25% in patients with peripheral arterial disease (PAD) and adding a proprotein convertase subtilisin/kexin type 9 inhibitor (PCSK9i) further decreases this risk.

<h2>Key Takeaway</h2>
This Joint Task Force from the European Atherosclerosis Society (EAS) and the European Society of Vascular Medicine (ESVM) recommends the following:
<ul>
 <li>Statins, at the highest tolerated dose, are indicated in patients with PAD for preventing cardiovascular (CV) events</li>
 <li>Low-density lipoprotein cholesterol (LDL-C) should be lowered to &lt;1.4 mmol/L (&lt;55 mg/dL) and by &gt;50% if pre-treatment levels are 1.8–3.5 mmol/L (70–135 mg/dL)</li>
 <li>A combination of statin and ezetimibe may be considered to improve LDL-C goal attainment</li>
 <li>A PCSK9i should be added if LDL-C levels remain 50% higher than the goal, despite statin treatment, with or without ezetimibe</li>
</ul>

<h2>Why This Matters</h2>
<ul>
 <li>Patients with PAD are at a very high risk of CV events; however, risk factor management is usually suboptimal</li>
 <li>This Joint Task Force from the EAS-ESVM provides updated evidence on the management on dyslipidemia and thrombotic factors in patients with PAD.</li>
</ul>

<h2>Key Highlights</h2>
2019 European Society of Cardiology/EAS dyslipidemia guidelines for PAD
<ul>
 <li>Both LDL-C reduction by ≥50% from baseline and an LDL-C goal of &lt;1.4 mmol/L (&lt;55 mg/dL) recommended in PAD patients (≥10% risk of a fatal CV event).</li>
 <li>Maximally tolerated high-intensity statin is recommended to achieve this goal.</li>
 <li>If patients are unable to attain this goal or report statin intolerance, statin (low dose, if statin intolerant) combined with ezetimibe is recommended, along with PCSK9i if further LDL-C lowering is required.</li>
</ul>
Evidence on statin therapy
<ul>
 <li>Statins are guideline-recommended first-line lipid-lowering therapy for PAD.</li>
 <li>There is evidence on the positive effects of lipid-lowering on MALE and walking performance in patients with PAD.</li>
 <li>In a&nbsp;<a href="https://doi.org/10.1055/s-0040-1709711" target="_blank">meta-analysis</a>&nbsp;of 51 studies in 138,060 PAD patients with stable claudication, critical limb ischemia (CLI), or undergoing lower extremity revascularization, 35% received a statin. 
 <ul>
 <li>Statin treatment reduced all-cause mortality by 39%, CV death by 41%, CV outcomes by 34%, ischemic stroke by 28%, MALE by 30%, and amputations by 35%.</li>
 </ul></li>
 <li>Another&nbsp;<a href="https://journals.sagepub.com/doi/10.1177/1358863X19894055" target="_blank">meta-analysis</a>&nbsp;of 19 studies in 26,985 patients with CLI (about half on statins) showed 25% vs 38% reduction in amputation vs fatal events.</li>
 <li>This Joint Task Force conducted a meta-analysis of randomized controlled trials of statin-based treatment showed that: 
 <ul>
 <li>Statins reduced MACE by 24% (odds ratio [OR] = 0.76, 95% confidence interval [CI]: 0.69–0.83), CV death by 17% (OR = 0.83, 95% CI: 0.26–2.60), and all-cause mortality by 18% (OR = 0.82, 95% CI: 0.69–0.97)</li>
 </ul></li>
 <li>Another meta-analysis conducted by the Joint Task Force showed that 
 <ul>
 <li>Statins improved walking distance by 45 m (95% CI: -64.7 to 154.7) and pain-free walking distance and duration (by 15.3 m [95% CI: -56.8 to 87.5] and 54.9 s [95% CI: 40.4–69.3], respectively).</li>
 </ul></li>
</ul>
Evidence on combination treatment with statin and ezetimibe
<ul>
 <li>In&nbsp;<a href="https://www.nejm.org/doi/10.1056/NEJMoa1410489" target="_blank">Improve-it</a>, adding ezetimibe on top of simvastatin significantly reduced CV events in patients with acute coronary syndrome (ACS) (hazard ratio = 0.936; 95% CI: 0.89–0.99; P = 0.016).</li>
 <li><a href="https://linkinghub.elsevier.com/retrieve/pii/S2213858718302900" target="_blank">Subgroup analysis</a>&nbsp;in polyvascular disease: Absolute benefit was substantially higher, especially those with concomitant type 2 diabetes (absolute risk reductions 4.2% and 9.1% vs 1.7% in those with ACS alone)</li>
</ul>
Evidence on combination treatment with statin and a PCSK9i
<ul>
 <li>The&nbsp;<a href="https://www.nejm.org/doi/10.1056/NEJMoa1615664" target="_blank">Fourier trial</a>&nbsp;assessed the addition of evolocumab to intense statin therapy (with or without ezetimibe) in patients (N = 27,564) with coronary, cerebrovascular, or peripheral arterial atherosclerosis. 
 <ul>
 <li>In a&nbsp;<a href="https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.117.032235" target="_blank">prespecified analysis</a>, the composite of CV death, myocardial infarction, stroke, hospitalization for unstable angina, or coronary revascularization was reduced by 21% and MALE risk by 42%.</li>
 </ul></li>
 <li>In a&nbsp;<a href="https://linkinghub.elsevier.com/retrieve/pii/S073510971933921X" target="_blank">subsequent analysis of the Odyssey outcomes study</a>, patients with recent ACS were randomized to alirocumab on top of maximally tolerated statin or statin alone. 
 <ul>
 <li>In patients who also had PAD (3.2%), a 7% reduction was noted in relative risk for the primary endpoint (composite of coronary heart disease death, nonfatal myocardial infarction, fatal or nonfatal ischemic stroke, or unstable angina requiring hospitalization).</li>
 <li>In a&nbsp;<a href="https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.120.046524" target="_blank">subsequent analysis</a>&nbsp;including all patients with a history of PAD, the risk for PAD events was significantly reduced by 41%, corresponding to an 8.6% absolute reduction in risk at 3 years.</li>
 </ul></li>
 <li>Finally, a combined analysis of both Fourier and Odyssey outcomes studies conducted by this Joint Task Force showed the following: 
 <ul>
 <li>PCSK9i on top of maximally tolerated statin significantly reduced (24%) CV events (OR = 0.76, 95% CI: 0.64–0.91), albeit without significant difference in all-cause mortality (OR = 0.85, 95% CI: 0.67–1.09)</li>
 </ul></li>
</ul>

LLTs and Antithrombotic Therapy in PAD

<h2>Lipid-lowering therapy and achievement of prior and new European guideline-recommended lipid targets in post-percutaneous coronary intervention patients: Observational nationwide cohort study</h2>
This retrospective, observational, population study suggests low rate of achievement of the new European Society of Cardiology (ESC)/European Atherosclerosis Society (EAS) lipid targets in post-percutaneous coronary intervention (PCI) population and relatively low rates of prescribing intensive lipid-lowering therapy (LLT) in individuals with uncontrolled lipids.

<h2>Key Takeaway</h2>
<ul>
 <li>Relatively low rate of high-intensity statin (HI statin) prescription ± additional evidence-based LLT agents in a large post-PCI patient population was noted, with a low proportion achieving the 2019 EAS/ESC lipid target. 
 <ul>
 <li>As per 2016 ESC/EAS guidelines, non-high-density lipoprotein cholesterol (non-HDL-C) and low-density lipoprotein cholesterol (LDL-C) targets (&lt;1.8 mmol/l) were achieved in 57% and 48% patients, respectively; as per 2019 guidelines, target (&lt;1.4 mmol/l) was attained in only 37% and 23% of patients, respectively.</li>
 <li>6% of patients undergoing PCI within 2 years of a prior admission for an ACS achieved the new target of &lt;1.0 mmol/l.</li>
 </ul></li>
 <li>There is considerable potential for LLT optimization through statin intensification and appropriate use of novel LLT, which would be expected to improve clinical outcomes at individual and population levels, especially in women.</li>
 <li>Nevertheless, the economic impact of novel management strategies and potential value to healthcare providers and funders requires careful planning and evaluation.</li>
</ul>

<h2>Why This Matters</h2>
<ul>
 <li>The data and treatment of patients with very high cardiovascular disease (CVD) risk who achieve or fail recommended (ESC/EAS) LDL-C (non-HDL-C) and/or triglyceride (TG) levels are limited.</li>
 <li>A better understanding of these relationships will help characterize the therapeutic gap, as well as the potential opportunity to optimize CVD risk management at individual and population levels.</li>
 <li>This study aimed to document (a) LLT and (b) achievement of prior and current ESC/EAS lipid targets in a contemporary national cohort of post-PCI patients.</li>
</ul>

<h2>Study Design</h2>
<ul>
 <li>This was a retrospective, observational cohort study using anonymized electronic health record data of patients undergoing PCI (January 2012–December 2017) in Wales, UK.</li>
 <li>Inclusion criteria: age ≥18 years; ≥90 days of follow-up 
 <ul>
 <li>Date of the first PCI (index date) during the study period for each patient with follow-up for 1 year was recorded.</li>
 </ul></li>
 <li>Time to the first lipid profile and the lowest LDL-C, non-HDL-C, and TG levels between 28–365 days post-discharge were documented.</li>
 <li>Prescriptions were identified during follow-up for LLTs, including statins, ezetimibe, fibrates, and prescription-grade N-3.</li>
 <li>Study evaluated the number and proportion of patients achieving: 
 <ul>
 <li>LDL-C &lt; or ≥: 1.4 and 1.8 mmol/l; non-HDL-C &lt; or ≥: 2.2 and 2.6 mmol/l; TG &lt; or ≥: 1.5 and 2.3 mmol/l; and their respective LLT regimens</li>
 <li>LDL-C &lt; or ≥1.0 mmol/l and non-HDL-C &lt; or ≥1.8 mmol/l and their respective LLT regimens; index PCI was a recurrent event within 2 years of a prior event</li>
 </ul></li>
</ul>

<h2>Key Results</h2>
<ul>
 <li>In total, 15,203 patients met the study inclusion criteria, of which 11,048 (72.7%) patients had a lipid profile documented within the study period.</li>
 <li>Overall, 10,071 of 11,048 patients had an LDL-C documented between 28 days and 1 year (mean [SD] lowest LDL-C = 1.90 [0.79] mmol/l). 
 <ul>
 <li>4,812 (47.8%) achieved LDL-C levels below the 2016 EAS/ESC target (&lt;1.8 mmol/l); only 2,353 (23.4%) patients were below the 2019 target (&lt;1.4 mmol/l).</li>
 </ul></li>
 <li>Of 15,023 patients, 1,020 (6.7%) had experienced an atherosclerotic event within 2 years before the index PCI, of which 627 patients had a documented LDL-C during the study period. Of these, only 33 (5.3%) patients had LDL-C levels below the 2019 target (&lt;1.0 mmol/l).</li>
 <li>Of the patients with recurrent events within 2 years and LDL-C ≥1.0 mmol (n = 594), 52.5% (n = 312) were prescribed HI statins, 36.0% (n = 214) were prescribed standard-intensity statins, 3.1% (n = 19) were prescribed ezetimibe and/or a fibrate in addition to a statin, 2.0% (n = 12) were prescribed either ezetimibe and/or fibrate without a statin, and 6.2% (n = 37) had no LLT prescription.</li>
 <li>Considering patients with documented LDL-C &gt;1.8 mmol/l and 1.4 mmol/l, 2,437 and 4,082 patients, respectively, were prescribed HI statins; only 117 and 146 were prescribed a combination of ezetimibe and/or fibrate plus a statin, with 103 and 109 prescribed ezetimibe and/or fibrate without a statin, respectively.</li>
 <li>Of the 5,340 patients with non-HDL-C levels documented (mean [SD] lowest non-HDL-C = 2.6 [0.97] mmol/l), 42.8% (n = 2,286) had non-HDL-C ≥2.6 mmol/l and 63.0% (n = 3,366) had ≥2.2 mmol; 314 patients had recurrent atherosclerotic events, of whom 12.7% (n = 40) were below the threshold of 1.8 mmol/l.</li>
 <li>Overall, 10,592 patients had TG levels recorded between 28 days and 1 year (mean [SD] lowest TG = 1.54 [1.01] mmol/l); of these, 14.4% (n = 1,524) had TG ≥2.3 mmol/l and 40.7% (n = 4,314) had TG ≥1.5 mmol/l.</li>
</ul>

<h2>Limitations</h2>
<ul>
 <li>The study failed to identify the quantity of medication prescribed.</li>
 <li>No patients with PCSK9 inhibitor prescription were identified in the study dataset.</li>
 <li>Lipid profiles recorded during the index admission were unavailable; moreover, these were not documented for over 25% of patients.</li>
 <li>Acute peripheral vascular events were not included.</li>
</ul>

Lipid-Lowering Therapy and Achievement of Lipid Targets ESC and EAS Guidelines

The role of the patient in Achieving LDL-C Target

Watch Prof. Lale Tokgozoglu, president of the European Atherosclerosis Association providing insights on how to get the patient to the goals that are recommended in the guidelines and the need to keep the patient there.

<h2>Key Takeaway</h2>
This simulation study&nbsp;from Da Vinci&nbsp;identified notable differences&nbsp;between the&nbsp;2019 ESC/EAS&nbsp;and&nbsp;2018 ACC/AHA&nbsp;guidelines in their&nbsp;clinical approach to LLT in patients with ASCVD. The study also identified that:
<ul>
 <li>About&nbsp;80–85%&nbsp;of the patients* were on&nbsp;monotherapy based LLT</li>
 <li>Patients&nbsp;achieving 2018 ACC/AHA&nbsp;(&lt;70 mg/dL) vs&nbsp;2019 ESC/EAS&nbsp;(&lt;55 mg/dL) goals were&nbsp;39% vs 19%</li>
 <li>Achievement&nbsp;of&nbsp;LDL−C&nbsp;&lt;70 mg/dL&nbsp;was&nbsp;more likely in patients&nbsp;receiving&nbsp;combination therapy&nbsp;with either&nbsp;ezetimibe&nbsp;or a&nbsp;PCSK9i&nbsp;vs patients on statin monotherapy</li>
 <li>In patients&nbsp;with&nbsp;LDL−C ≥70 mg/dL, to achieve LDL−C levels of&nbsp;&lt;70 mg/dL, &lt;55 mg/dL&nbsp;and&nbsp;&lt;40 mg/dL, median LDL−C reductions&nbsp;of&nbsp;26%,&nbsp;42%&nbsp;and&nbsp;58%&nbsp;would be needed, respectively</li>
 <li>In patients with&nbsp;LDL–C ≥70 mg/dL&nbsp;vs&nbsp;&lt;70 mg/dL, the estimated&nbsp;10–year risk of CV events&nbsp;were&nbsp;32% vs 35%</li>
 <li>Attaining&nbsp;2018 ACC/AHA or 2019 ESC/EAS goals resulted in&nbsp;simulated ARRs&nbsp;of&nbsp;4%&nbsp;and&nbsp;6%, respectively</li>
 <li>For&nbsp;implementation of the guidelines,&nbsp;greater use&nbsp;of&nbsp;combination therapies&nbsp;would be required</li>
 <li>The&nbsp;residual risk&nbsp;among patients with ASCVD&nbsp;receiving statins&nbsp;could be&nbsp;mitigated&nbsp;if&nbsp;2019 ESC/EAS recommendations&nbsp;were&nbsp;achieved‡</li>
 <li>More stringent 2019 ESC/EAS goals&nbsp;are&nbsp;expected&nbsp;to give&nbsp;better health&nbsp;outcomes&nbsp;vs 2018 ACC/AHA approach</li>
</ul>

<h2>Why This Matters</h2>
<ul>
 <li>LDL–C recommendations differ between&nbsp;the 2018 ACC/AHA approach&nbsp;and&nbsp;2019 ESC/EAS guidelines&nbsp;for patients with&nbsp;ASCVD.</li>
 <li>The&nbsp;2018 ACC/AHA guidelines&nbsp;recommend targeted reduction&nbsp;LDL–C &lt;70 mg/dL§, in patients at&nbsp;very–high risk.</li>
 <li>The&nbsp;2019 ESC/EAS guidelines&nbsp;recommend a&nbsp;stricter LDL–C goal of &lt;55 mg/dL.</li>
 <li>Using&nbsp;DA VINCI study cohort, the&nbsp;extent of risk that could be mitigated by adopting 2018 ACC/AHA&nbsp;vs&nbsp;2019 ESC/EAS&nbsp;LDL−C recommended approaches was&nbsp;simulated.</li>
</ul>

<h2>Study Design</h2>
This is a simulation study from Da Vinci.&nbsp;The methods and primary outcomes of Da Vinci study can be obtained from the link:&nbsp;<a href="https://www.sciencedirect.com/science/article/pii/S0021915021013083">Da Vinci.</a>
<ul>
 <li>LLT use across the populations</li>
 <li>LDL–C control in patients with established ASCVD and stratified by ASCVD type¶</li>
 <li>Patients with LDL–C &gt;70 mg/dL vs achievement of LDL–C &lt;55 mg/dL</li>
 <li>Patients achieving LDL–C &lt;40 mg/dL</li>
 <li>Implications of current practice and LDL–C goal achievement in future CV risk</li>
</ul>

<h2>Key Results</h2>
Overall,&nbsp;2,039 patients with ASCVD&nbsp;(23% with CAD; 37% with CBD and 40% with PAD)&nbsp;were on stabilized LLT&nbsp;at the time of&nbsp;LDL–C measurement.

<h3 style="text-align: center;">LLT Use in patients with ASCVD</h3>
<table border="1" cellpadding="10" cellspacing="1" style="width:100%;">
 <tbody>
 <tr>
 <td style="background-color: rgb(244, 242, 246); text-align: center;">Type of&nbsp;LLT</td>
 <td style="background-color: rgb(244, 242, 246); text-align: center;">Patients using LLT (%)</td>
 </tr>
 <tr>
 <td>
 Statin monotherapy</td>
 <td style="text-align: center;">Used most frequently</td>
 </tr>
 <tr>
 <td style="text-align: center;">Moderate–intensity statins#&nbsp;as monotherapy</td>
 <td style="text-align: center;">Ranged from&nbsp;40.4%&nbsp;among patients with CAD to&nbsp;48.7%&nbsp;in patients with CBD</td>
 </tr>
 <tr>
 <td style="text-align: center;">High–intensity statins#</td>
 <td style="text-align: center;">CAD: 51.1%;&nbsp;CBD: 39.7%; PAD: 39.1%</td>
 </tr>
 <tr>
 <td style="text-align: center;">Ezetimibe in combination with statins||</td>
 <td style="text-align: center;">CAD: 15.3%;&nbsp;CBD: 6.7%; PAD: 8.2%</td>
 </tr>
 <tr>
 <td style="text-align: center;">PCSK9i in combination with statins and/or ezetimibe||</td>
 <td style="text-align: center;">CAD: 0.4%; CBD: 1.2%; PAD: 1.6%</td>
 </tr>
 </tbody>
</table>

<h3 style="text-align: center;">Proportion of patients achieving LDL–C Levels</h3>

<ul>
 <li>Achievement of an&nbsp;LDL–C level &lt;70 mg/dL&nbsp;was&nbsp;more likely&nbsp;in patients receiving&nbsp;combination therapy with either ezetimibe or a PCSK9i&nbsp;vs patients on statin monotherapy.</li>
 <li>Despite of using PSCK9i infrequently,&nbsp;58% of patients receiving PSCK9i&nbsp;in combination with other LLT have&nbsp;attained LDL–C level of &lt;55 mg/dL.</li>
</ul>

<h3 style="text-align: center;">Residual risk among the patients</h3>
<table border="1" cellpadding="10" cellspacing="1" style="width:100%;">
 <tbody>
 <tr>
 <td style="background-color: rgb(244, 242, 246); text-align: center;">LDL–C Levels</td>
 <td style="background-color: rgb(244, 242, 246); text-align: center;">Patients&nbsp;(%)</td>
 <td style="background-color: rgb(244, 242, 246); text-align: center;">Median&nbsp;(IQR) LDL–C Level</td>
 <td style="background-color: rgb(244, 242, 246); text-align: center;">Median&nbsp;(IQR) Predicted&nbsp;10–year&nbsp;CV risk</td>
 </tr>
 <tr>
 <td style="text-align: center;">≥70 mg/dL</td>
 <td style="text-align: center;">61%</td>
 <td style="text-align: center;">93 (81–115) mg/dL</td>
 <td style="text-align: center;">32% (25–43%)</td>
 </tr>
 <tr>
 <td style="text-align: center;">&lt;70 mg/dL**</td>
 <td style="text-align: center;">39%</td>
 <td style="text-align: center;">56 (46–63) mg/dL</td>
 <td style="text-align: center;">35% (26–46%)</td>
 </tr>
 </tbody>
</table>
<h3 style="text-align: center;">Simulated risk reduction in patients with established&nbsp;ASCVD (LDL–C Level of ≥70 mg/dL)</h3>
<table border="1" cellpadding="10" cellspacing="1" style="width:100%;">
 <tbody>
 <tr>
 <td style="background-color: rgb(244, 242, 246);">LDL–C Levels</td>
 <td style="background-color: rgb(244, 242, 246);">Median&nbsp;10–year&nbsp;CV risk</td>
 <td style="background-color: rgb(244, 242, 246);">Median&nbsp;RRR of&nbsp;CV events</td>
 <td style="background-color: rgb(244, 242, 246);">Median&nbsp;ARR of CV events</td>
 <td style="background-color: rgb(244, 242, 246);">
 Required&nbsp; 
 median&nbsp; 
 reduction&nbsp;in&nbsp; 
 LDL-C</td>
 <td style="background-color: rgb(244, 242, 246);">AR to lower&nbsp;LDL–C levels&nbsp;to 69 mg/dL</td>
 </tr>
 <tr>
 <td style="text-align: center;">&lt;70 mg/dL</td>
 <td style="text-align: center;">28%</td>
 <td style="text-align: center;">14%</td>
 <td style="text-align: center;">4%</td>
 <td style="text-align: center;">26%</td>
 <td style="text-align: center;">24 mg/dL (12–46)</td>
 </tr>
 <tr>
 <td style="text-align: center;">&lt;55 mg/dL</td>
 <td style="text-align: center;">25%</td>
 <td style="text-align: center;">22%</td>
 <td style="text-align: center;">6%</td>
 <td style="text-align: center;">42%</td>
 <td style="text-align: center;">39 mg/dL (27–91)</td>
 </tr>
 <tr>
 <td style="text-align: center;">&lt;40 mg/dL</td>
 <td style="text-align: center;">23%</td>
 <td style="text-align: center;">29%</td>
 <td style="text-align: center;">8%</td>
 <td style="text-align: center;">58%</td>
 <td style="text-align: center;">54 mg/dL (42–76)</td>
 </tr>
 </tbody>
</table>
For additional information about simulated risk reduction, please click on the&nbsp;<a href="http://${link:{uuid:{e3579e13-0af7-4531-bdf0-88d2e3d87092},repository:{dam},path:{/Portal/KSA/Articles/recommendations-for-residual-risk-reduction-in-ascvd/STRATIFIED-BY-ASCVD-TYPE.pdf}}}">hyperlink.</a>

<h2>Limitations</h2>
<ul>
 <li>Over 90% of patients were white (homogenous ethnicity).</li>
 <li>Simulation might have underestimated CV risk and ARR in very high-risk patients.</li>
 <li>Use of LLT may vary across countries and might not necessarily reflect practice in other regions.</li>
 <li>The study sites might have focused on lipid management and prevention of CV events. Hence, the study findings are likely to present better than average management scenario.</li>
</ul>
For additional details, please refer the source publication&nbsp;<a href="https://link.springer.com/article/10.1007/s10557-022-07343-x#Abs1">Vallejo-Vaz AJ, et al.</a> 
 * Most of the patients with major manifestations of ASCVD 
 † Probably due to additional comorbidities like diabetes, history of smoking and increased use of more potent LLTs including combination therapies. 
 ‡ In a population like Da Vinci cohort § Using 70 mg/dL as a limit to guide additional LLT 
 ¶ As per 2019 ESC/EAS guidelines, all patients are at very–high risk 
 # With or without other LLT || High/moderate/unknown intensity 
 ** Had slightly higher prevalence of risk factors such as a history of smoking and diabetes (50.7%)

ACC/AHA vs ESC/EAS LDL–C recommendations for residual risk reduction in ASCVD: A simulation study from Da Vinci

CAD is defined as the pathological process characterised by atherosclerotic plaque accumulation in the epicardial arteries. It covers different conditions, including:1
<ul>
 <li>Patients with stable angina</li>
 <li>Patients after elective coronary revascularisation procedures, such as percutaneous coronary intervention (PCI) or coronary artery bypass graft (CABG)</li>
 <li>Patients with significant coronary disease without prior revascularisation as evidenced by either: 
 <ul>
 <li>≥70% stenosis of at least one coronary artery</li>
 <li>≥50% stenosis of the left main coronary artery</li>
 <li>Three-vessel obstructive (&gt;70%) disease</li>
 </ul></li>
</ul>

Ischaemic heart disease accounts for 16% of all deaths worldwide.2*

The presence of T2DM alongside CAD was shown to increase the risk of a CV event by 28% vs those without diabetes in the CLARIFY study.3 
 Diabetes is a well-established risk factor for ischaemic heart disease, and CAD accounts for 40–80% of deaths in patients with T2DM.1

New 2024 ESC guidelines for the management of chronic coronary syndromes have been published recently and can be downloaded by clicking the button

These guidelines present the following steps for management of chronic coronary syndrome (CCS), including CAD4

Adapted from 2024 ESC CCS Guidelines.4
a&nbsp;High–risk CAD: obstructive CAD at high risk of adverse events by CCTA: ≥50% stenosis of the left main stem; three–vessel disease with severe stenoses (≥70% diameter stenosis); single- or two– vessel disease including the proximal LAD with severe stenoses. Consider functional imaging or invasive investigation.
Patients with CAD, with or without T2DM, are at&nbsp;very high CV risk.5&nbsp;These patients require a&nbsp;holistic multifactorial approach&nbsp;to prevention and management.

Patients with PAD,&nbsp;with or without T2DM, are at very&nbsp;high CV risk.1 
 These patients require a&nbsp;holistic multifactorial approach&nbsp;to prevention and management.
Reduce increased levels of causal CV risk factors, such as:5

Target: see below

Target: SBP 120–129 mmHg†

Target is &lt;7.0% (53 mmol/mol)

Reducing LDL-C levels represents the primary target for reducing CV risk5
According to the 2019 ESC/EAS dyslipidemia guidelines, and 2024 ESC chronic coronary syndromes guidelines, all patients with CAD have the following LDL-C goals.4,5
An LDL-C reduction of ≥50% from baseline‡&nbsp;and an&nbsp;LDL-C goal of &lt;55 mg/dL (&lt;1.4 mmol/L)&nbsp;are recommended
For patients at&nbsp;very high CV risk&nbsp;(including those with CAD) not achieving their LDL-C goal on a maximum tolerated dose of statin and ezetimibe, combination&nbsp;with a PCSK9i is recommended.5

Recommendations for pharmacological LDL-C lowering5

It is recommended that a high-intensity statin is prescribed up to the highest tolerated dose to reach the goals set for the specific level of risk.

Step 1

If the goals are not achieved with the maximum tolerated dose of a statin, combination with ezetimibe is recommended.

Step 2

For secondary prevention, patients at very high risk not achieving their goal on a maximum tolerated dose of a statin and ezetimibe, combination with a PCSK9i is recommended.

Step 3

Adapted from Vrints et al. 2024 and Mach et al. 20204,5

You should aim to assess your patients response to therapy&nbsp;6–8 weeks from initiation.5

Prevent The 1st&nbsp;Event&nbsp;for your CAD&nbsp;patients with&nbsp;PAD + T2DM¥
*The term stable ischaemic heart disease often is used synonymously with chronic CAD and encompasses a variety of conditions that result in a mismatch between myocardial oxygen supply and demand.6
†Provided the antihypertensive treatment is well tolerated.
‡The term ‘baseline’ refers to the LDL-C level in a person not taking any LDL-C-lowering medication. In people who are taking LDL-C-lowering medication(s), the projected baseline (untreated) LDL-C levels should be estimated, based on the average LDL-C-lowering efficacy of the given medication or combination of medications.5
¥Prevent the first major CV event for your CAD and T2DM patients without prior major CV event. CLARIFY is an observational registry of patients with chronic coronary syndromes, taking place across 45 countries from 2009 to 2010; follow-up was 5 years. Chronic coronary syndromes were defined by ≥1 of the following criteria: prior myocardial infarction, evidence of coronary stenosis &gt;50%, proven symptomatic myocardial ischaemia, or prior revascularisation procedure.3
ANOCA&nbsp;= angina with non-obstructive coronary arteries;&nbsp;CABG&nbsp;= coronary artery bypass graft;&nbsp;CAD&nbsp;= coronary artery disease;&nbsp;CCS&nbsp;= chronic coronary syndromes;&nbsp;CCTA&nbsp;= coronary computed tomography angiography;&nbsp;CMR&nbsp;= cardiac magnetic resonance;&nbsp;CV&nbsp;= cardiovascular;&nbsp;EAS&nbsp;= European Atherosclerosis Society;&nbsp;ECHO&nbsp;= echocardiography;&nbsp;ESC&nbsp;= European Society of Cardiology;&nbsp;FFR&nbsp;= fractional flow reserve;&nbsp;HbA1c&nbsp;= glycated haemoglobin;&nbsp;ICFT&nbsp;= invasive coronary functional testing;&nbsp;iFR&nbsp;= instantaneous wave-free ratio;&nbsp;INOCA&nbsp;= ischaemia with non-obstructed coronary arteries;&nbsp;LAD&nbsp;= left anterior descending artery;&nbsp;LDL-C&nbsp;= low-density lipoprotein cholesterol;&nbsp;LV&nbsp;= left ventricular;&nbsp;PCI&nbsp;= percutaneous coronary intervention;&nbsp;PCSK9i&nbsp;= proprotein convertase subtilisin/kexin type 9 inhibitor;&nbsp;PET&nbsp;= positron emission tomography;&nbsp;SBP&nbsp;= systolic blood pressure;&nbsp;SPECT&nbsp;= single-photon emission computed tomography;&nbsp;T2DM&nbsp;= type 2 diabetes mellitus.

References

Approach for Patients with CAD: Focus on LDL-C Control

PAD is a common manifestation of atherosclerosis and encompasses all vascular sites, including:1
<ul>
 <li>
 Lower extremity arteries</li>
 <li>
 Carotid artery</li>
 <li>
 Vertebral artery</li>
 <li>
 Upper extremity arteries</li>
 <li>
 Mesenteric artery</li>
 <li>
 Renal artery</li>
 <li>
 Aorta</li>
</ul>
New 2024 ESC&nbsp;guidelines for the management of peripheral arterial and aortic diseases (PAAD) show:2

Increased risk of CV events in patients with PAD compared with those without PAD2

Patients with both PAD and T2DM are at a ‘very high’ risk of cardiovascular events2

In a prospective cohort study in Europe, patients with PAD and T2DM had...

Higher risk of CV events* compared to those with neither PAD nor T2DM3

Screening for lower-extremity arterial disease (LEAD) is recommended on a regular basis, with clinical assessment and/or ankle-brachial index (ABI) measurement.2,4

Adapted from Marx N et al. 2023 and Mazzolai L et al. 2024.2,4
a&nbsp;TBI when ABI &gt;1.4. b&nbsp;Further information regarding wound management and exercise training can be found in the 2017 ESC guidelines on the diagnosis and treatment of peripheral arterial diseases. c&nbsp;MRA or CTA when duplex sonography is not sufficient for planning revascularisation.

Patients with PAD,&nbsp;with or without T2DM, are at very&nbsp;high CV risk.1 
 These patients require a&nbsp;holistic multifactorial approach&nbsp;to prevention and management.
Reduce increased levels of causal CV risk factors, such as:1

Reducing LDL-C levels represents the primary target for reducing CV risk1
According to the 2019 ESC/EAS dyslipidaemia guidelines, and 2024 ESC chronic coronary syndromes guidelines, all patients with PAD have the following LDL-C goals.1,2
An LDL-C reduction of ≥50% from baseline‡&nbsp;and an&nbsp;LDL-C goal of &lt;55 mg/dL (&lt;1.4 mmol/L)&nbsp;are recommended
For patients at&nbsp;very high CV risk&nbsp;(including those with PAD and T2DM) not achieving their LDL-C goal on a maximum tolerated dose of statin and ezetimibe, combination&nbsp;with a PCSK9i is recommended.1

Recommendations for pharmacological LDL-C lowering1

Adapted from Mach F et al. 2019 and Mazzolai L et al. 2024.1,2

You should aim to assess your patients response to therapy&nbsp;6–8 weeks from initiation.1

Prevent The 1st&nbsp;Event&nbsp;for your 
 patients with&nbsp;PAD + T2DM¥
*When compared to those with neither PAD nor T2DM, HRs adjusted for age, gender, BMI, smoking, hypertension, LDL-C, and HDL-C were 1.26 (95% Cl 0.84, 1.91); P=0.267, HR 4.17 (95% Cl 2.97, 5.85); P&lt;0.001, and HR 7.82 (95% Cl 5.49, 11.12); P&lt;0.001 for those with T2DM only, for those with PAD only and for those with the combination of PAD plus T2DM, respectively.3
†Provided the antihypertensive treatment is well tolerated.
‡The term ‘baseline’ refers to the LDL-C level in a person not taking any LDL-C-lowering medication. In people who are taking LDL-C-lowering medication(s), the projected baseline (untreated) LDL-C levels should be estimated, based on the average LDL-C-lowering efficacy of the given medication or combination of medications.1
¥Prevent the first major CV event for your ASCVD patients without prior major CV event.
In a prospective cohort study, cardiovascular events were prospectively recorded over a mean follow-up period of 7.2 ± 2.6 years in 1,049 subjects, encompassing 4 groups: 558 with neither PAD nor diabetes, 153 with T2DM but without PAD, 192 with PAD but without T2DM, and 146 with the combination of PAD and T2DM. 4 PAD patients were defined as those with an ankle brachial index &lt;0.9 or with previous revascularisation of peripheral arteries who underwent routine duplex sonography and in whom PAD was sonographically verified.3
ABI&nbsp;=&nbsp;ankle–brachial index;&nbsp;ASCVD&nbsp;= atherosclerotic cardiovascular disease;&nbsp;BMI&nbsp;= body mass index;&nbsp;CI&nbsp;= confidence interval;&nbsp;CTA&nbsp;= computed tomography angiography;&nbsp;CV&nbsp;= cardiovascular;&nbsp;EAS&nbsp;= European Atherosclerosis Society;&nbsp;ESC&nbsp;= European Society of Cardiology;&nbsp;HbA1c&nbsp;= glycated haemoglobin;&nbsp;HDL-C&nbsp;= high-density lipoprotein cholesterol;&nbsp;HR&nbsp;= hazard ratio;&nbsp;LEAD&nbsp;= lower- extremity artery disease;&nbsp;LDL-C&nbsp;= low-density lipoprotein cholesterol;&nbsp;MRA&nbsp;= magnetic resonance angiography;&nbsp;PAAD&nbsp;= peripheral arterial and aortic disease;&nbsp;PAD&nbsp;= peripheral artery disease;&nbsp;PCSK9i&nbsp;= proprotein convertase subtilisin/kexin type 9 inhibitor;&nbsp;SBP&nbsp;= systolic blood pressure;&nbsp;TBI&nbsp;= toe-brachial index;&nbsp;TcPO2&nbsp;= transcutaneous oxygen pressure;&nbsp;T2DM&nbsp;= type 2 diabetes mellitus;&nbsp;WlfI&nbsp;= Wound, Ischaemia, foot Infection.

Approach for Patients with PAD and T2D: Focus on LDL-C Control

Act Now for Your ACS Patients: Optimize Your ACS Pathway

Watch Professor Kausik Ray, a Cardiologist and Professor of Public Health, Imperial College London, presenting ACS initiatives while providing ways to easily implement such methods into clinical practice with the objective to help adopting the 2019 guidelines of ESC/EAS major direction of: Treat aggressively, use combination and start early.

<h2>Advancing therapy with iGlarLixi*</h2>
<h3>Differentiation from complex insulin regimens, including the premixed insulin IDegAsp</h3>

<h3 style="text-align: center;">Current unmet needs in T2D</h3>

<ul>
 <li>Despite advances in technology and therapeutics, many people with&nbsp;T2D across the globe fail to meet their glycemic goals1–5</li>
 <li>This may be attributed to&nbsp;therapeutic inertia&nbsp;due to several patient-and physician-related barriers to treatment advancement, including perceived treatment complexity, fear of hypoglycemia, weight gain and stepwise treatment approaches6,7</li>
 <li>Long-term insufficient glycemic control leads to a&nbsp;“dysglycemic legacy”&nbsp;and is associated with an increased risk of complications;7&nbsp;achieving blood glucose targets may play an important role in reducing the risk of MACE8,9</li>
 <li>Due to the progressive nature of T2D,&nbsp;treatment advancement to insulin-based therapiesis&nbsp;often needed to maintain glycemic control</li>
 <li>In order to overcome therapeutic inertia and the resulting dysglycemic legacy, there is a&nbsp;clinical need for the timely therapeutic advancement of injectable therapy&nbsp;in people with inadequate glycemic control</li>
 <li>Several insulin advancement options are available following insufficient control with basal insulin, including the progressive addition of a rapid-acting insulin to basal insulin, premixed insulin, addition of a GLP-1 RA, or FRCs</li>
</ul>

<h3 style="text-align: center;">iGlarLixi versus other insulin advancement options</h3>

<ul>
 <li>Both direct (RCTs) and indirect treatment comparisons of insulin advancement options play an important role in identifying potential, clinically-relevant treatment options for people with T2D insufficiently controlled on basal insulin10–12</li>
 <li>In a NMA of RCTs,&nbsp;it was shown that iGlarLixi is associated with an improved HbA1c reduction from baseline versus premixed insulin&nbsp;(with a similar or improved safety profile compared with other intensification options)†10</li>
 <li>In the SoliMix RCT,&nbsp;iGlarLixi was found to provide improved HbA1c control with better weight change and less hypoglycemia than twice-daily BIAsp3011</li>
 <li>In a recent ITCcomparing iGlarLixi and IDegAsp, it was shown that iGlarLixi may offer clinical benefit in glucose control and bodyweight change in people who require both basal and meal-time intervention†12</li>
 <li>Based on the benefits observed in a RCT and ITC, FRCs, such as iGlarLixi, may offer a&nbsp;&nbsp;suitable alternative to other intensification options&nbsp;in adults with T2D, demonstrating benefits in HbA1c control and body weight change11,12</li>
</ul>

The content of this infographic summarizes key points discussed during an educational video-on-demand with Professor Philip Homeand Dr Khadija Hafidh. *iGlarLixi is a fixed-ratio combination of insulin glargine 100 U/mL and lixisenatide. †Note, this study was an indirect comparison of products across different studies and, as such, definitive conclusionscannot be drawn.

Advancing Therapy with iGlarLixi

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