Lipoprotein(a): A risk factor for Atherosclerosis and an emerging therapeutic target.

<h2>Key Takeaway</h2>
This review article suggests that assessment of Lipoprotein(a) (Lp[a]) might help to identify individuals with increased risk of ASCVD who might benefit from management of other risk factors.
<ul>
 <li>Understanding of the role of Lp(a)&nbsp;in atherogenesis&nbsp;could help identify targets&nbsp;for treatment aimed at&nbsp;reducing ASCVD risk&nbsp;by lowering Lp(a) levels.</li>
 <li>Lp(a) measurement is&nbsp;suggested to identify individuals with very high levels (&gt;430 nmol/L) of Lp(a),&nbsp;and who have a lifetime ASCVD risk equivalent to that associated with&nbsp;heterozygous familial hypercholesterolemia.</li>
 <li>Patients with high Lp(a)&nbsp;levels should be&nbsp;managed with more intensive approaches&nbsp;to treat other modifiable CV risk factors.</li>
 <li>An effort should be made to&nbsp;increase awareness&nbsp;about the role of Lp(a) as a&nbsp;risk biomarker,&nbsp;and its measurement, and interpretation.</li>
</ul>
Available lipid-lowering agents&nbsp;have moderate effect on Lp(a) levels&nbsp;and newer potent options being developed&nbsp;might lower residual risk and global ASCVD burden.

<h2>Why This Matters</h2>
ASCVD&nbsp;remains the main&nbsp;cause of death&nbsp;despite&nbsp;reducing LDL-C&nbsp;with available lipid-lowering treatments.
The ‘residual risk’ might be attributed to&nbsp;different atherogenic factors, such as triglyceride-rich lipoproteins and their remnants, Lp(a), and inflammation.
This review discussed the pathological mechanisms of Lp(a) in ASCVD, evidence supporting its role in ASCVD risk and emerging approaches to reduce Lp(a).

<h2>Key Highligts</h2>
Lp(a) As a CVD Risk Factor
Causal and independent relationship between high Lp(a) levels and ASCVD risk in individuals with and without previous ASCVD were supported by various studies*
<ul>
 <li>In patients with familial hypercholesterolemia,&nbsp;high ASCVD risk is further heightened with elevated Lp(a).</li>
 <li>Mendelian studies suggest an&nbsp;association between high Lp(a) and risk of peripheral artery disease and HF.</li>
 <li>Lp(a) levels were a&nbsp;determinant of residual ASCVD risk&nbsp;in&nbsp;patients treated with high-efficacy statins&nbsp;who achieved very low LDL-C levels for primary prevention.</li>
 <li>Approximately&nbsp;18 nmol/L&nbsp;increase in Lp(a) was estimated to be&nbsp;associated with a 3.5% increased risk of CHD.</li>
</ul>

<h2>Lp(a) lowering treatments</h2>
<ul>
 <li>Lp(a) has emerged as a potential target&nbsp;with evidence supporting role in ASCVD.</li>
 <li>No drugs are approved&nbsp;to reduce Lp(a) levels.</li>
 <li>Life style&nbsp;has&nbsp;little-to-no impact&nbsp;on Lp(a) levels.</li>
</ul>
<table border="1" cellpadding="1" cellspacing="1">
 <tbody>
 <tr>
 <td style="background-color: rgb(244, 242, 246);">Drug/drug class</td>
 <td style="background-color: rgb(244, 242, 246);">
 Effect on Lp(a)</td>
 <td style="background-color: rgb(244, 242, 246);">Additional comments</td>
 </tr>
 <tr>
 <td>
 Statins</td>
 <td>
 Might&nbsp;increase levels&nbsp;by&nbsp;8.5%–19.6%</td>
 <td>
 Inconsistent effects in several studies</td>
 </tr>
 <tr>
 <td>
 Ezetimibe</td>
 <td>
 No effect</td>
 <td>-</td>
 </tr>
 <tr>
 <td>
 Alirocumab and evolocumab</td>
 <td>
 Might decrease by 20%–30%</td>
 <td>
 Smaller percentage reductions in those with higher baseline levels†</td>
 </tr>
 <tr>
 <td>
 Lomitapide</td>
 <td>
 Lowers levels by&nbsp;17%</td>
 <td>
 Reduces hepatic production of lipoproteins by inhibiting microsomal triglyceride transfer protein</td>
 </tr>
 <tr>
 <td>
 Cholesteryl ester transfer protein inhibitors</td>
 <td>
 Lowers levels by 25%–40%</td>
 <td>
 Clinical benefit not demonstrated</td>
 </tr>
 <tr>
 <td>
 Estrogen/progestin replacement therapy</td>
 <td>
 Lowers levels by&nbsp;≈15%</td>
 <td>
 Increases atherothrombotic risk and cannot be used</td>
 </tr>
 <tr>
 <td>
 Thyroid hormone analogues</td>
 <td>
 Found to reduce Lp(a) (up to 43% with eprotirome)</td>
 <td>
 Impact on ASCVD is not known</td>
 </tr>
 <tr>
 <td>
 Aspirin</td>
 <td>
 Lowers levels by&nbsp;20%</td>
 <td>
 Needs confirmation</td>
 </tr>
 <tr>
 <td>
 Inclisiran</td>
 <td>
 Lowers levels by&nbsp;19%–22%</td>
 <td>
 A small interfering RNAs (siRNAs) that acts by inhibiting PCSK9 mRNA translation</td>
 </tr>
 <tr>
 <td>
 Mipomersen</td>
 <td>
 Mean decrease in Lp(a) by 26.4%</td>
 <td>
 Not approved due the adverse effects and no evidence of ASCVD event reduction</td>
 </tr>
 <tr>
 <td>
 Pelacarsen</td>
 <td>
 Might lower levels from 66% to 92%</td>
 <td>
 Dose-dependent reduction in Lp(a) levels</td>
 </tr>
 <tr>
 <td>
 Lipoprotein apheresis</td>
 <td>
 Single treatment has been found to lower Lp(a) levels by&nbsp;~68%</td>
 <td>
 Resulted in a reduction in mean annual incidence of ASCVD events</td>
 </tr>
 <tr>
 <td>
 Niacin</td>
 <td>
 Significant decrease in levels by&nbsp;12%</td>
 <td>
 Magnitude depends on apo(a)-isoform size and baseline Lp(a) levels</td>
 </tr>
 <tr>
 <td>
 Olpasiran and SLN360</td>
 <td>
 Both are siRNAs, and are&nbsp;under development</td>
 </tr>
 </tbody>
</table>

<h2>Measurement of Lp(a) levels</h2>
<table border="1" cellpadding="1" cellspacing="1">
 <tbody>
 <tr>
 <td style="text-align: center; background-color: rgb(244, 242, 246);">Adviced in individuals with</td>
 <td>
 <ul>
 <li>First-degree relatives with premature ASCVD</li>
 <li>Borderline (5%–7.4%) 10-year ASCVD risk</li>
 <li>Intermediate (7.5%–19.9%) 10-year ASCVD risk</li>
 <li>Familial hypercholesterolemia</li>
 </ul></td>
 </tr>
 <tr>
 <td style="text-align: center; background-color: rgb(244, 242, 246);">Suggested in patients on optimal LLT with</td>
 <td>
 <ul>
 <li>Lower-than-expected LDL-C reduction</li>
 <li>Recurrent ASCVD events</li>
 </ul></td>
 </tr>
 <tr>
 <td style="text-align: center; background-color: rgb(244, 242, 246);">Cascade testing suggested in</td>
 <td>
 <ul>
 <li>Relatives of subjects with high Lp(a)</li>
 <li>First-degree relatives of subjects with familial hypercholesterolemia</li>
 </ul></td>
 </tr>
 </tbody>
</table>
*Epidemiological, Mendelian randomization and genome-wide association studies †&nbsp;Post hoc analysis of the pivotal trials of PCSK9-I demonstrate that relationship between Lp(a) reduction and ASCVD risk reduction was dependent on baseline Lp(a) levels

Abbreviations

Reference

Lp(a) as ASCVD risk factor

DYSLIPIDEMIA

CARDIOLOGY

Lp(a) and PCSK9 inhibition in nominally controlled LDL-C patients

Watch the video and learn on how to leverage incremental clinical benefit to patients with recent ACS and LDL-C near 70 mg/dL from optimized statin therapy and PCSK9i.

<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

LLTs Exposure Time and Major Vascular Risk Reduction

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

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<h2>Incident heart failure tied to increased long-term risk for venous thromboembolism</h2>
Findings suggest the need for evidence-based strategies to prevent long-term venous thromboembolism in these patients beyond hospitalisation time.

<h2>Main Takeaway</h2>
<ul>
 <li>Incident heart failure (HF) hospitalisation was associated with more than a 3-fold higher risk for venous thromboembolism (VTE) which persisted through a long-term follow-up.</li>
 <li>The increased risk for VTE persisted in participants with HF with preserved ejection fraction (HFpEF) and HF with reduced ejection fraction (HFrEF).</li>
 <li>In participants without clinical HF, left ventricular (LV) relative wall thickness and mean wall thickness were predictors of VTE.</li>
</ul>
<h2>Why This Matters</h2>
<ul>
 <li>HF not only increases the risk for cardioembolic events and ischaemic stroke but also increases the risk for VTE.</li>
 <li>Hospitalised patients for acute HF are at an increased risk for short-term VTE due to prolonged immobilisation and hypercoagulability</li>
</ul>
<h2>Study Design</h2>
<ul>
 <li>This prospective population-based study included 13,728 participants from the Atherosclerosis Risk In Communities (ARIC) cohort.</li>
 <li>Patients with (mean age, 56.1 years) and without (mean age, 53.5 years) incident HF hospitalisation were included.</li>
 <li>Short- and long-term VTE risks associated with: 
 <ul>
 <li>incident HF during 1987-2015 (n=13,728; design 1);</li>
 <li>HF subtype during 2005-2015 (n=7588; design 2); and</li>
 <li>abnormal echocardiographic measures in the absence of clinical HF during 2011-2015 (n=5438; design 3) were assessed.</li>
 </ul></li>
 <li>Funding: ARIC cohort was funded by the National Heart, Lung, and Blood Institute.</li>
</ul>

<h2>Key Results</h2>
<ul>
 <li>Incident HF occurred in 19.6% of patients included in the design1.</li>
 <li>During a mean follow-up of 22±7 years, incident HF vs no HF was associated with an increased risk for incident total VTE (adjusted HR [aHR], 3.13; 95% CI, 2.58-3.80).</li>
 <li>Incident HF vs no HF was associated with a 2-fold greater risk for all VTE subtypes: 
 <ul>
 <li>Pulmonary embolism: aHR, 2.57; 95% CI, 1.95-3.39;</li>
 <li>Deep venous thrombosis: aHR, 3.90; 95% CI, 2.96-5.13;</li>
 <li>Provoked VTE events: aHR, 2.26; 95% CI, 1.60-3.19; and</li>
 <li>Unprovoked VTE events: aHR, 3.72; 95% CI, 2.94-4.72.</li>
 </ul></li>
 <li>Incident HF occurred in 15.3% of participants allocated to the design2.</li>
 <li>Over a mean follow-up of 9.7±2.6 years, VTE rates in those with vs without HF were 21.8 (95% CI, 16.9-27.6) vs 3.04 (95% CI, 2.64-3.49) per 1000 person-years.</li>
 <li>Compared with no HF, VTE risk was reported in: 
 <ul>
 <li>Any HF: aHR, 5.15; 95% CI, 3.80-6.98;</li>
 <li>HFpEF: aHR, 4.71; 95% CI, 2.94-7.52;</li>
 <li>HFrEF: aHR, 5.53; 95% CI, 3.42-8.94; and</li>
 <li>Undetermined incident HF: aHR, 4.09; 95% CI, 2.60-6.44.</li>
 </ul></li>
 <li>In participants allocated to the design 3, 86 incident VTE events were reported over a mean follow-up of 3.5±0.7 years.</li>
 <li>In the absence of baseline HF, LV relative wall thickness (P=0.002) and mean LV wall thickness (P=0.003) were found to be predictors of incident VTE after additional adjustment for chronic kidney disease and atrial fibrillation</li>
</ul>

<h2>Limitations</h2>
<ul>
 <li>ARIC-based incident HF on hospitalisations.</li>
 <li>VTE validation failed to capture outpatient VTE.</li>
 <li>The number of VTE events for design 3 was small.</li>
 <li>The observed association between HF and VTE may not be causal.</li>
 <li>Incident VTE-related mortality was not assessed.</li>
</ul>

Incident heart failure tied to increased long-term risk for VTE

THROMBOSIS

Discover useful tools and resources which will help diabetic patients with safe fasting during Ramadan.
Looking for more information on Diabetes management during Ramadan, get in touch with Sanofi Medical Scientific Liaison.

<h2>Science and Innovation in Ramadan</h2>
Learn on how Toujeo and Soliqua can help with safe fasting during Ramadan

Pre-Ramadan Dose Adjustment

Peaceful Ramadan with Soliqua

Peaceful Ramadan with Toujeo

<h2>Events</h2>
Know more about dedicated events on diabetes management during Ramadan

Diabetes Guidelines in Ramadan 
 
 &nbsp;

Nutrition and Insulin management in Ramadan

<h2>Patient Support during Ramadan</h2>
Resources and materials that will help your diabetic patients during Ramadan

Digital Patient Support Program

Diabetes management during Ramadan

INTEGRATED-DIABETES-CARE

DIABETES

<h2>Introduction</h2>
<ul>
 <li>Most Muslim adults with type 2 diabetes (T2D) choose to fast during Ramadan, with &gt;85% fasting for ≥15 days days1-3</li>
 <li>The incidence of hypoglycaemia increases during Ramadan compared with prepre-Ramadan, and adjustments to diabetes treatment must be considered to prevent severe hypoglycaemia3</li>
 <li>Separate administration of basal insulin + the glucagon glucagon-like peptide peptide-1 receptor agonist, lixisenatide, has been shown to demonstrate lower risk of hypoglycaemia during Ramadan versus sulfonylureas + lixisenatide lixisenatide4</li>
 <li>In the SoliRam study, the safety and effectiveness of iGlarLixi (a fixed fixed-ratio combination of insulin glargine 100 U/mL and lixisenatide) were evaluated in adults with T2D during Ramadan</li>
</ul>
<h2>Objective</h2>
To assess the safety and effectiveness of iGlarLixi in people with T2D fasting during Ramadan
<h2>Study design</h2>
SoliRam was a multicentre, multinational, prospective, single-arm, real-world observational study during Ramadan 2020 (Wave 1) and 2021 (Wave 2) (Figure 1)
Figure 1: SoliRam study design and endpoints

<h3>Population</h3>
Adults with T2D treated with iGlarLixi for ≥3 months prior to study start who intended to fast for ≥15 days during Ramadan*

Primary endpoint
<ul>
 <li>Proportion of participants experiencing at least one documented (&lt;70 mg/dL [&lt;3.9 mmol/L]) and/or severe symptomatic hypoglycaemia event during pre pre-Ramadan, Ramadan, post post-Ramadan and the whole study period period‡</li>
</ul>
Secondary endpoints
<ul>
 <li>Changes in HbA HbA1c, FPG and body weight from pre-to post post-Ramadan</li>
 <li>Changes in iGlarLixi and other non-insulin antihyperglycaemic treatment</li>
 <li>AEs and serious AEs</li>
</ul>
*Participants who entered Wave 1 were not included in Wave 2;&nbsp;†Participant follow follow-up was preferably 1 month after the end of Ramadan;&nbsp;‡Whole study period: pre-Ramadan to post-Ramadan.
During the study, iGlarLixi and concomitant treatments were adjusted by physicians as per routine practice AE, adverse event; DAR, Diabetes and Ramadan; FPG, fasting plasma glucose; IDF, International Diabetes Federation; iGlarLixi, a fixed fixed-ratio combination of insulin glargine 100 U/mL and lixisenatide, T2D, type 2 diabetes
<ul>
 <li>Participants were enrolled from Egypt, Indonesia, Israel, Kuwait, Lebanon, Malaysia, Philippines, Saudi Arabia and the United Arab Emirates</li>
 <li>This analysis presents descriptive statistics from the entire SoliRam study</li>
</ul>

<h2>Results</h2>
Participant baseline characteristics
<ul>
 <li>Overall, 420 people with T2D were eligible. Baseline characteristics are presented in Table 1</li>
 <li>In total, 409 participants were assessed during the Ramadan period</li>
</ul>
<h3>Table 1: Participant baseline characteristics</h3>
<table border="1" cellpadding="10" cellspacing="1" style="width:100%;">
 <tbody>
 <tr>
 <td style="width: 70%; background-color: rgb(244, 242, 246);">Baseline characteristics</td>
 <td style="width: 30%; background-color: rgb(244, 242, 246);">N=420*</td>
 </tr>
 <tr>
 <td style="width: 70%;">Age (years) 
 ≥65 years</td>
 <td style="width: 30%;">57.1 ± 9.8 
 101 (24.0)</td>
 </tr>
 <tr>
 <td style="width: 70%;">Female</td>
 <td style="width: 30%;">188 (44.8)</td>
 </tr>
 <tr>
 <td style="width: 70%;">BMI (kg/m2) 
 Body weight (kg)</td>
 <td style="width: 30%;">30.9 ± 5.3 
 86.5 ± 14.9</td>
 </tr>
 <tr>
 <td style="width: 70%;">Diabetes duration (years) 
 ≥10 years</td>
 <td style="width: 30%;">12.1 ± 6.4 
 246 (58.6)</td>
 </tr>
 <tr>
 <td style="width: 70%;">HbA1c(%) pre-Ramadan period</td>
 <td style="width: 30%;">8.2 ± 1.2</td>
 </tr>
 <tr>
 <td style="width: 70%;">FPG (mg/dL) pre-Ramadan period</td>
 <td style="width: 30%;">140 ± 38</td>
 </tr>
 <tr>
 <td style="width: 70%;">Duration of iGlarLixi treatment (months months†) 
 iGlarLixi started in insulin-naïve ve participants 
 iGlarLixi started after previous insulin treatment</td>
 <td style="width: 30%;">6.2 ± 4.2 
 174 (41.9) 
 241 (58.1)</td>
 </tr>
 <tr>
 <td style="width: 70%;">Concomitant non-insulin antihyperglycaemic treatment pre-Ramadan period period&nbsp;‡ 
 Biguanides 
 Sulfonylureas 
 SGLT-2 inhibitors 
 Thiazolidinedione 
 Glinides 
 DPP-4 inhibitors</td>
 <td style="width: 30%;">359 (85.5) 
 234 (55.7) 
 188 (44.8) 
 173 (41.2) 
 18 (4.3) 
 7 (1.7) 
 1 (0.2)</td>
 </tr>
 </tbody>
</table>

*Eligible population; †Up to signing of informed consent form;&nbsp;‡A participant can be included in several categories Data are mean ±&nbsp;SD&nbsp;or n (%)

Antihyperglycaemic therapies during Ramadan
<ul>
 <li>At the selection visit (n=420), iGlarLixi injection time was at breakfast, lunch or dinner for 41.2%, 36.2% and 22.6% of participants, respectively</li>
 <li>During Ramadan most participants (88.8%) took iGlarLixi at Iftar</li>
 <li>iGlarLixi mean&nbsp;± standard deviation (SD) daily dose was 25.8&nbsp;±&nbsp;11.0 U pre-Ramadan and 24.8&nbsp;± 9.9 U during Ramadan</li>
 <li>Minimal adjustments were made to antihyperglycaemic therapies from pre-Ramadan to during Ramadan. Oral antihyperglycaemic drugs were used by 83.8% of participants during Ramadan (54.5% biguanides, 43.8% sulfonylureas and 40.5% sodium sodium-glucose co-transporter-2 [SGLT SGLT-2] inhibitors)</li>
</ul>
Fasting during Ramadan
<ul>
 <li>Most participants (96.9%) were able to fast for ≥25 days (mean&nbsp;± SD, 28.8&nbsp;± 2.7 days), with 92.4% not breaking their fast during the whole Ramadan period</li>
 <li>Of the 31 (7.6%) participants who did break their fast, four (12.9%) reported hypoglycaemia as the reason</li>
</ul>
Hypoglycaemia during Ramadan
<ul>
 <li>Primary endpoint:&nbsp;The number of participants reporting ≥1 severe and/or documented symptomatic hypoglycaemia events &lt;70 mg/dL (&lt;3.9 mmol/L) was low throughout the whole study (&nbsp;Figure 2A)</li>
 <li>The number of participants reporting ≥1 severe and/or documented symptomatic hypoglycaemia events &lt;54 mg/dL (&lt;3.0 mmol/L) was also low throughout the study (&nbsp;Figure 2B)</li>
 <li>No severe hypoglycaemia events occurred during the whole study period</li>
</ul>

<h3>Figure 2: Incidence of documented symptomatic and/or severe hypoglycaemia (A) &lt;70 mg/dL (&lt;3.9 mmol/L), (B) &lt;54 mg/dL (&lt;3.0 mmol/L)</h3>

Eligible population. Last month pre-Ramadan and first month post-Ramadan

Secondary endpoints
<ul>
 <li>HbA1c&nbsp;, FPG and body weight all improved from pre-to post-Ramadan&nbsp;(Figure3)</li>
 <li>The proportion of participants reaching HbA1c&nbsp;&lt;7 % increased from 7.9% pre-Ramadan to 28.6% post-Ramadan (evaluable population, n=343)</li>
</ul>

<h3>Figure 3: Changes in (A) HbA1c, (B) FPG and (C) body weight between pre-and post-Ramadan periods</h3>

Evaluable population: HbA1c, N=343; FPG, N=334; Eligible population: body weight, N=356 (post-Ramadan observed data)

Adverse events
<ul>
 <li>Overall, 4.7% of participants (n=20) reported adverse events (AEs) of any cause ( Table 2)</li>
</ul>
<h3>Table 2: Adverse events</h3>
<table border="1" cellpadding="10" cellspacing="1" style="width:100%;">
 <tbody>
 <tr>
 <td style="width: 70%; background-color: rgb(244, 242, 246);">Adverse events</td>
 <td style="width: 30%; background-color: rgb(244, 242, 246);">N=428*</td>
 </tr>
 <tr>
 <td style="width: 70%;">Any</td>
 <td style="width: 30%;">20 (4.7)</td>
 </tr>
 <tr>
 <td style="width: 70%;">Any serious AE</td>
 <td style="width: 30%;">0 (0.0)</td>
 </tr>
 <tr>
 <td style="width: 70%;">Any treatment treatment-related AE</td>
 <td style="width: 30%;">0 (0.0)</td>
 </tr>
 <tr>
 <td style="width: 70%;">Any AE leading to permanent treatment discontinuation</td>
 <td style="width: 30%;">1 (0.2)</td>
 </tr>
 <tr>
 <td style="width: 70%;">Any AE leading to death</td>
 <td style="width: 30%;">0 (0.0)</td>
 </tr>
 </tbody>
</table>
*Included population. Data are n (%)&nbsp;AE, adverse event
<ul>
 <li>Gastrointestinal&nbsp;AEs&nbsp;were reported by four (0.9%) participants</li>
 <li>The&nbsp;AE&nbsp;leading to discontinuation was asthenia, and treatment was stopped by the participant without physician advice</li>
</ul>

<h2>Incidence of other Hypoglycaemia events</h2>
Incidence of documented (&lt;54 mg/dL [&lt;3.0 mmol/L]) symptomatic and/or severe hypoglycaemia events

Eligible population. n=410 Last month Pre-Ramadan, n=394 Ramadan and n=380 First month Post-Ramadan Poster presentation&nbsp;EDEC&nbsp;2022, Mohamed Hassanein et al,&nbsp;EDEC2022&nbsp;(edec-uae.com) last accessed 27th February 2022.

Improvements were also observed in FPG
FPG n=334 for both Pre- and post-Ramadan; Body weight n=406 (Pre-Ramadan), n=356 (Post-Ramadan) CI, confidence interval; FPG, fasting plasma glucose; SD, standard deviation.

<h2>Discussion</h2>
<ul>
 <li>In this real real-world study of adults with T2D from diverse regions fasting during Ramadan, over 90% of participants treated with iGlarLixi were able to fast for the entire month of Ramadan, with few participants experiencing severe and/or documented (&lt;70 mg/dL [&lt;3.9 mmol/L]) symptomatic hypoglycaemia</li>
 <li>Adjustments to antihyperglycaemic regimens were minimal and HbA1c&nbsp;levels did not increase over Ramadan</li>
 <li>No participants experienced severe hypoglycaemia</li>
</ul>
<h2>Conclusion</h2>
iGlarLixi may be a suitable and effective treatment option for people with T2D who intend to fast during Ramadan

References

iGlarLixi Enables Safe Ramadan Fasting for Most T2D Patients


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