<h2>Treatment burden associated with complex insulin regimens in T2D</h2>
<ul>
 <li>Due to the multiple pathophysiological defects and progressive nature of T2D, many individuals will require therapeutic advancement with insulin-based therapies throughout the course of their lives1</li>
 <li>Therapeutic advancement with complex insulin regimens is often associated with an increased burden of disease, contributing to low treatment adherence and reduced quality of life2</li>
</ul>

<h3>Factors impacting adherence to insulin therapy3</h3>

Daily injection 
 frequency

Injection 
 embarrassment

<ul>
 <li>Poor treatment adherence, along with therapeutic inertia, is primarily why people with T2D are experiencing less sustained improvements in a real-world setting compared with RCT data4</li>
 <li>Therapeutic inertia is defined as the failure not only to intensify therapy, but also to de-intensify treatment when people are overtreated5</li>
</ul>

Simple yet effective strategies are required to help overcome these challenges of treatment burden

<ul>
 <li>Treatment simplification offers the opportunity to ease disease burden and may help to reduce polypharmacy and risk of hypoglycemia in adults with T2D2</li>
 <li>Current guidelines support the concept of simplification, but primarily focus on the older adult population and lack clear guidance on how this can be achieved1</li>
</ul>

Treatment simplification with BI + GLP-1 RA FRC

black

The combination of a BI analog and a GLP-1 RA may be a simple and effective way to target the multi-faceted manifestations of T2D and may help reduce the burden and complexity of treatment1

In their main treatment algorithm, the ADA/EASD now recommends BI + GLP-1 RA FRCs as a&nbsp;very high efficacy approach&nbsp;to achieve glycemic goals5

Therapeutic advancement&nbsp;to complex insulin regimens can&nbsp;increase treatment burden&nbsp;for people with T2D, and may be associated with an increased risk of hypoglycemia, reduced treatment adherence and increased body weight
HCPs should regularly assess individual circumstances and needs, and evaluate where it is possible to&nbsp;decrease treatment complexity&nbsp;and the burden of treatment to&nbsp;improve glycemic outcomes&nbsp;on a case-by-case basis
BI + GLP-1 RA FRCs may offer an&nbsp;effective and simple alternative&nbsp;to complex insulin regimens, such as premixed and basal-bolus insulin, to&nbsp;both intensify and simplify treatment

The content of this infographic summarizes key points discussed during an educational video-on-demand with Professor Rory McCrimmon and Dr Alice Cheng. Please note, two FRCs of a basal insulin and a GLP-1 RA are available: iGlarLixi (insulin glargine 100 U/mL + lixisenatide) and IDegLira (insulin degludec + liraglutide).*SoliMix&nbsp;was a multicenter, open-label, randomized study comparing the efficacy and safety of iGlarLixi versus BIAsp 30 in adults with T2D (n=887).&nbsp;DUAL VII&nbsp;was an open-label, two-arm parallel, randomized study comparing the efficacy and safety of IDegLira versus BB in adults with T2D (n=506).&nbsp;SoliComplex&nbsp;was a real-world, retrospective, observational study comparing iGlarLixi and premixed insulin (N=834) or iGlarLixi and BB (N=1070) in adults with T2D advancing on BI. In&nbsp;SoliComplex,&nbsp;data was collected from the US Optum Clinformatics database, therefore the US iGlarLixi pen (Soliqua®&nbsp;100/33) was administered to participants. †For further details and an overview of the supporting data, please refer to the full educational video-on-demand (MAT-GLB-2204912) and the study publications.

Abbreviations

References

Treatment simplification in T2D: A less-is-more approach to help reduce the burden of disease

TYPE-2-DIABETES

DIABETES

<h2>Prognostic impact of achieving guideline-recommended LDL-C target in secondary prevention: A real-world study</h2>
This real-world study of PMI patients emphasizes the importance of achieving guideline-recommended secondary prevention goals of LDL-C &lt;55 mg/dL and ≤50% from baseline to reduce Mace.

<h2>Main Takeaway</h2>
<ul>
 <li>The incidence of Mace&nbsp;was 12.9% and 23.7% in the group attaining the 2019 goals (LDL-C &lt;55 mg/dL) and in the group attaining 2016 goals (LDL-C &lt;70 mg/dL), respectively.</li>
</ul>

<h2>Why This Matters</h2>
<ul>
 <li>The 2019 ESC guidelines recommend a more ambitious target (to achieve LDL-C &lt;55 mg/dL and to reduce it by ≥50% from baseline) than the previous guideline version (LDL-C &lt;70 mg/dL or reduced ≥50% from baseline).</li>
 <li>Data on the reduction of CV events in patients attaining the 2019 ESC goals are lacking in real-world population.</li>
 <li>This study aimed to determine the risk of Mace during follow-up in PMI patients according to the achievement of the guideline-recommended goals in terms of LDL-C reduction.</li>
</ul>

<h2>Study Design</h2>
<ul>
 <li>This was a retrospective analysis of a monocentric observational registry that prospectively enrolled patients hospitalized for ST segment elevation MI and followed-up in PMI ambulatory between January 2011 and February 2019.</li>
 <li>Clinical and demographic data were extracted from digital database, and the clinical events that occurred during follow-up were obtained by telephone interviews or clinical records.</li>
 <li>Endpoints: Mace defined as all-cause death, non-fatal MI, non-fatal stroke, and unplanned revascularization</li>
 <li>LDL-C was collected at baseline and at 1, 6, and 12 months after the events. To define the achievement of target goals, the lower value was collected at follow-up.</li>
 <li>Kaplan-Meier analysis and log-rank test were conducted for comparing patients who achieved LDL-C &lt;55 mg/dL and ≤50% from baseline (group 2019) versus those who achieved LDL-C &lt;70 mg/dL or ≤50% from baseline (group 2016).</li>
 <li>Continuous variables are presented as medians (interquartile ranges).</li>
</ul>

<h2>Key Results</h2>
<ul>
 <li>A total of 1,201 patients were included in the study (median age: 63 [54–72] years; female: 23%; hypertension: 56%; diabetes: 17%; smokers: 38%).</li>
 <li>Baseline LDL-C was 123 (97–148) mg/dL; at follow-up, median LDL-C was 63 (52–78) mg/dL and was significantly reduced from baseline (P &lt;0.0001).</li>
 <li>Between 6 and 12 months, 83% of patients were treated with statins alone (73% with high intensity) and 17% with the addition of ezetimibe.</li>
 <li>In total, 828 patients (69%) achieved the 2016 target, whereas 270 patients (22.5%) also achieved the 2019 target. Median follow-up was 60 (40–77) months.</li>
 <li>Mace incidence was 12.9% and 23.7% in group 2019 and group 2016, respectively (HR = 0.61, 95% CI: 0.42–0.88; P log rank = 0.0087, number needed to treat = 9).</li>
</ul>

Reference

Prognostic impact of achieving LDL cholesterol guidelines

DYSLIPIDEMIA

CARDIOLOGY

There is a need to understand the burden of cardiovascular diseases (CVDs) in Saudi Arabia (SA) and focus on cardiovascular (CV) risk factors and some proposed solutions. This could pave the way for strategic direction to mitigate CV risks and alleviate CVD burden, by developing policies and practical measures, in compliance to 2030 healthcare and economic vision for SA.

<h2>Key Takeaway</h2>
<ul>
 <li>Risk factors such as unidentified and untreated dyslipidemia, hypertension, diabetes, obesity, sedentary lifestyle, urbanization, and smoking contribute to the high prevalence of CVD in SA. Additionally, globalization, the rise of an aging population, as well as socioeconomic changes and stress, could also contribute to increasing CVD cases.</li>
 <li>Lifestyle modifications such as healthy diets, regular exercise and smoking cessation are among few modifiable risk factors to reduce the risk of CVD.</li>
 <li>Interventions to mitigate CVD should aim at primary prevention level focused on mitigating non-modifiable CV risk factors and preventing CVD onset, as well as on secondary prevention level early screening and diagnosis of CVD.</li>
 <li>Comprehensive awareness campaigns targeting the general population and healthcare professionals, promoting CVD risk factors knowledge, prevention, and early detection can lead to better health outcomes. Inclusion of a CVD prevention program in primary healthcare centers could step up CV health prevention across all SA provinces.</li>
 <li>Collaboration between government entities, healthcare providers, public health organizations, and community stakeholders is vital for a comprehensive approach to tackle CVD. Coordinated efforts can lead to effective policies, better healthcare delivery, and improved outcomes.</li>
 <li>Many interventional national registries have been established for CV care in various countries like USA, Italy, Sweden, Japan, UK based on their population data.</li>
 <li>Current practice in SA relies on latest US and European guidelines. Therefore, there is need for launching a continuous CV health registry for SA population which would help to identify unmet need, improve public health outcomes, and also lead to more specific Saudi-based guidelines.</li>
</ul>

<h2>Why This Matters</h2>
<ul>
 <li>CVD is one of the leading causes of morbidity and mortality across the globe.</li>
 <li>Although some risk factors for CVD are non-modifiable, other determinants such as obesity, hypertension, type 2 diabetes, and dyslipidemia could be mitigated by an array of measures to control CVD.</li>
 <li>This review highlights the current status of CV health and unmet needs in SA, along with focus on the CV risk factors and some proposed solutions.</li>
</ul>

<h2>Key Results</h2>
<ul>
 <li>In SA, 201,300 Saudi nationals were living with CVD in 2016 and accounting for over 45% of all deaths. This emphasizes the need to understand CV risk factors and possible solutions.</li>
 <li>Sedentary lifestyle leading to dyslipidemia, hypertension, diabetes, obesity among Saudi Arabians, especially in females and tobacco use have been contributing factors towards increased susceptibility for CVD.</li>
 <li>Economic burden of CVD in SA in year 2016 was estimated to be $3.5 billion ($1.9 billion in direct healthcare costs and $1.6 billion in indirect costs from loss of productivity). This number might triple to $9.8 billion in 2035.</li>
</ul>
Saudi initiatives to reduce modifiable and non-modifiable CV risk factors include:
<table border="1" cellpadding="5" cellspacing="5">
 <tbody>
 <tr>
 <td colspan="2">Modifiable risk factors</td>
 </tr>
 <tr>
 <td>Tobacco use</td>
 <td>Guidelines to improve smoking cessation services, considering global evidence</td>
 </tr>
 <tr>
 <td colspan="1" rowspan="4">Lifestyle modifications</td>
 <td>Obesity Control &amp; Prevention Strategy 2030</td>
 </tr>
 <tr>
 <td>RASHAKA Program for healthy lifestyle</td>
 </tr>
 <tr>
 <td>KSA National Strategy for Diet and Physical Activity</td>
 </tr>
 <tr>
 <td>City humanization and walkability</td>
 </tr>
 <tr>
 <td>Hypertension Guideline</td>
 <td>Updated guidelines on hypertension management</td>
 </tr>
 <tr>
 <td>Dyslipidemia</td>
 <td>2022 Saudi Guidelines for Dyslipidemia Management provide a comprehensive framework for dyslipidemia control and its CV consequences</td>
 </tr>
 <tr>
 <td colspan="2">Non-modifiable risk factors</td>
 </tr>
 <tr>
 <td colspan="1" rowspan="2">Familial hyperlipidemia</td>
 <td>Emphasis on early screening can turn this risk factor into a modifiable one with strict control of risk factors</td>
 </tr>
 <tr>
 <td>There is a need for developing a cardiogenomic database which could help in family mapping, future research, and developing new therapeutics.</td>
 </tr>
 <tr>
 <td>Old age</td>
 <td>Increase exercise and reduce calorie-intake</td>
 </tr>
 <tr>
 <td>Premature early coronary artery disease and sudden cardiac death</td>
 <td>
 Early detection and prompt management of CVD
 Early screening can turn familial hyperlipidemia, which is a non-modifiable risk factor into a modifiable one with strict control of associated risk factors
 Therefore, SA government has considered CVD as a public health priority and allocated one-off $3,000 per patient over 5 years for screening tests, healthcare costs, and lipid-lowering therapies</td>
 </tr>
 </tbody>
</table>
Pillars of healthcare systems in SA:
<ul>
 <li>Free healthcare at primary, secondary or tertiary levels</li>
 <li>Specialized diagnostic and therapeutic services</li>
 <li>Reforms have been started in the primary healthcare system so that primary healthcare centers throughout SA’s 13 regional health directorates could oversee and manage all other healthcare centers and services.</li>
 <li>Decentralization of healthcare services has improved this sector a lot.Access to specialized healthcare services in SA is not limited to physical appointments; “Seha” virtual hospital at the Ministry of Health (MOH) headquarters, with central cardiac imaging and CV information center for cardiac data review and complex cases discussion improved access to healthcare services, patients’ satisfaction along with productivity and efficiency.</li>
</ul>
Gaps still exist in healthcare system of SA:
<ul>
 <li>Some geographical areas of SA still have limited healthcare access.</li>
 <li>There is need to raise more awareness among patients for adherence at the level of primary care offices and about primary prevention and early diagnosis of CVDs.</li>
 <li>There are shortcomings in Saudi health information system such as lack of coordination among medical care levels and challenges in coordination between referral and referring centers. This emphasizes need for a systematic integration of a HIS across the country’s healthcare facilities.</li>
 <li>There is limited access to fitness centers; these warrants need for widely accessible and affordable community fitness centers.</li>
 <li>Manpower shortage emphasizes the need for more physicians, nurses, and nurse practitioners</li>
 <li>Need for leveraging care in primary care centers, for prevention and timely diagnosis of CV risk factors or CVDs and alleviation of CVD burden</li>
 <li>Keeping in consideration the rise in rate of obesity, tools for behavioral changes promoting healthy lifestyle should be widely promoted.</li>
</ul>
Measures/Recommendations that can be undertaken in SA:
<table border="1" cellpadding="5" cellspacing="5">
 <tbody>
 <tr>
 <td>Smoking</td>
 <td>Smoking ban, including electronic cigarettes, and smokeless tobaccos</td>
 </tr>
 <tr>
 <td>Diet</td>
 <td>Rigorous control of salt content and consumption in diet</td>
 </tr>
 <tr>
 <td>Physical activity</td>
 <td>1) Mandatory physical program in schools 2) More community sport centers 3) Improving walkability in big cities</td>
 </tr>
 <tr>
 <td>Screening Programs</td>
 <td>Early detection and treatment of dyslipidemia, with a particular focus on lowdensity lipoprotein cholesterol</td>
 </tr>
 <tr>
 <td>Health check-ups</td>
 <td>Make regular health checks mandatory for all adults of all ages</td>
 </tr>
 <tr>
 <td>Adequate resources</td>
 <td>Provide primary care physicians all the resources they need (time, support, training, etc.) to focus on high quality prevention programs</td>
 </tr>
 <tr>
 <td>Risk management</td>
 <td>Enforce quality measures on CV risk management</td>
 </tr>
 <tr>
 <td>Education and awareness</td>
 <td>
 Health literacy committee at MOH to promote patient and community education, disease prevention, early symptoms reporting, treatment adherence
 Dedicated task force for CV health</td>
 </tr>
 <tr>
 <td>National registries</td>
 <td>
 Many interventional registries in various countries have evolved the field of cardiovascular care
 A continuous CV health registry specific to SA population is needed with multiple tracks focusing on risks, prevention, diagnoses, management, and outcomes of CVDs</td>
 </tr>
 </tbody>
</table>

Cardiovascular Disease in Saudi Arabia: Facts and the Way Forward

Effects of early protein convertase subtilisin/kexin 9 inhibitor therapy after acute coronary syndrome
After acute coronary syndrome (ACS), early use of protein convertase subtilisin/ kexin 9 (PCSK9) inhibitors is strongly recommended to help more rapidly and aggressively prevent major adverse cardiovascular events (MACEs).

<h2>Key Takeaway</h2>
<ul>
 <li>PCSK9 inhibitors significantly reduce Mace in post-ACS patients; this seems to occur directly by modifying plaque composition, with subsequent stabilization, and indirectly by altering lipid metabolism and platelet aggregation. 
 <ul>
 <li>EVACS study:&nbsp;More than 90% patients receiving evolocumab achieved low-density lipoprotein cholesterol (LDL Cholesterol) &lt;55 mg/dL target (European Society of Cardiology [ESC]/European Atherosclerosis Society [EAS] guidelines); 11% patients only receiving statins attained this target.</li>
 <li>EVOPACS study:&nbsp;: Evolocumab reduced&nbsp;LDL Cholesterol&nbsp;levels by 40.7% and helped 95.7% patients achieve LDL Cholesterol &lt;55 mg/dL.</li>
 <li>Odyssey Outcome trial:&nbsp;Alirocumab vs placebo reduced the overall MACE risk, reduced all-cause mortality risk, and caused fewer deaths for coronary heart disease (CHD).</li>
 </ul></li>
 <li>PCSK9 inhibitor resistance may be related to discontinuation of concurrent lipid-lowering therapies after PCSK9 inhibitor initiation.</li>
 <li>Occasionally, a limited&nbsp;LDL Cholesterol&nbsp;lowering response may be noted due to PCSK9 inhibitor hypo-responsiveness.</li>
</ul>

<h2>Why This Matters</h2>
<ul>
 <li>Considering frequency, mortality, and costs, ACS remains one of the most relevant diseases globally. Over time, the approach for treating ACS has changed.</li>
 <li>This review aims to highlight the beneficial effect of early use of PCSK9 inhibitors post-ACS in reducing LDL-C and MACE risk, which is very high in the first year and continues to stay high after the acute event.</li>
</ul>

<h2>Key Highlights</h2>
PCSK9 Inhibitors is implied both directly and indirectly in atherosclerotic plaque formation.
<ul>
 <li>It acts directly via the proinflammatory oxidation of&nbsp;LDL Cholesterol&nbsp;and modification of plaque composition for an inflammatory response.</li>
 <li>It acts indirectly by affecting lipid metabolism (by modulating LDLR, very LDLR, and LDLR-related protein-1 expression) and platelet aggregation.</li>
</ul>

<h2>PCSK9 inhibitors:</h2>
<ul>
 <li>PCSK9 inhibitors reduce circulating&nbsp;LDL Cholesterol&nbsp;levels, and this effect can be potentially increased by a combination with statins.</li>
 <li>The FOURIER trial demonstrated that anti-PCSK9 reduced lipoprotein (a) levels by ≈25%–30%.</li>
 <li>In ORION-1 trial, a single inclisiran injection reduced mean&nbsp;LDL Cholesterol&nbsp;levels by 27.9%–41.9% after 180 days and by 28.2%–36.6% after 240 days (P &lt;0.001). Two doses led to a mean reduction of 35.2% – 52.6% on day 180 (P &lt;0.001).</li>
 <li>Similarly, ORION-10 trial showed that inclisiran reduced&nbsp;LDL Cholesterol&nbsp;levels by 52.3% after 510 days in patients with atherosclerotic cardiovascular disease (CVD).</li>
 <li>In ORION-11 trial, LDL Cholesterol levels reduced by 49.9% in patients with atherosclerotic CVD or an atherosclerotic CVD risk equivalent.</li>
</ul>

<h2>LDL-C management after ACS</h2>
<ul>
 <li>American College of Cardiology/American Heart Association guidelines recommend initiating a more intensive lipid-lowering therapy for patients with LDL-C ≥70 mg/dL (≥1.8 mml/L).</li>
 <li>ESC/EAS guidelines recommend early use of high-intensity statins and addition of ezetimibe and anti- PCSK9 antibodies in ACS patients without both&nbsp;LDL Cholesterol&nbsp;reduction ≥50% from baseline and&nbsp;LDL Cholesterol&nbsp;reduction &gt;1.4 mmol/L (&gt;55 mg/dL).</li>
 <li>Although neither evolocumab nor alirocumab significantly reduced inflammatory markers in patients with ACS, both these PCSK9 inhibitors in combination with high-intensity statins significantly reduced&nbsp;LDL Cholesterol&nbsp;levels after 8 weeks.</li>
 <li>In the EVACS trial, evolocumab helped &gt;90% patients with ACS achieve&nbsp;LDL Cholesterol&nbsp;&lt;55 mg/dL (according to ESC/EAS guidelines) compared with 11% patients receiving only statins.</li>
 <li>In the EVOPACS study, evolocumab on top of a high-intensity statin reduced LDL-C levels by 40.7% and helped 95.7% patients achieve LDL-C &lt;55 mg/dL.</li>
 <li>In Odyssey Outcome study, alirocumab vs placebo reduced overall Mace risk by 15%, and reduced all-cause mortality risk and caused fewer deaths for CHD.</li>
</ul>

<h2>Pitfalls and future perspectives:</h2>
Although most patients receiving PCSK9 inhibitors attain the expected 50%–60% reduction in LDL-C, sporadically, a limited LDL-C-lowering response is noted.
<ul>
 <li>Proposed mechanisms for such PCSK9 inhibitor hypo-responsiveness (&lt;15% of&nbsp;LDL Cholesterol&nbsp;reduction): (1) Impaired monoclonal antibody entry into the systemic circulation and (2) physiological impairment after monoclonal antibody absorption.</li>
</ul>
The most common cause of apparent PCSK9 inhibitor resistance is related to discontinuing concurrent lipid-lowering therapies after initiating PCSK9 inhibitors.
Novel PCSK9 inhibitors that are currently under development: Inclisiran, oral small-molecule inhibitors, vaccines, and clustered regularly interspaced short palindromic repeats.

PCSK9 inhibitors and ACS

PCSK9 inhibitors in cardiovascular disease: A meta-analysis
Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors are generally safe and well tolerated in patients with cardiovascular disease (CVD), with mild and acceptable adverse events.

<h2>Key Takeaway</h2>
In patients with atherosclerotic cardiovascular disease (ASCVD):
<ul>
 <li>PCSK9 inhibitors could ameliorate the lipid profile 
 <ul>
 <li>They could reduce low-density lipoprotein cholesterol (LDL-C) by &gt;50% and increase high-density lipoprotein cholesterol (HDL-C) by &gt;5% as well as markedly reduce total cholesterol (TC) and triglyceride (TG) levels.</li>
 </ul></li>
 <li>Adverse events of PCSK9 inhibitors were mild and acceptable in patients with CVD. However, attention should be paid to injection-site reactions</li>
 <li>PCSK9 inhibitors were generally safe and well tolerated</li>
</ul>

<h2>Why This Matters</h2>
<ul>
 <li>PCSK9 inhibitors are an effective strategy to reduce LDL-C and other lipid parameters, particularly in patients not achieving optimal LDL-C levels or probably having high residual CVD risk despite high-intensity statin therapy.</li>
 <li>However, physicians are still concerned regarding the efficacy and safety of PCSK9 inhibitors; this knowledge gap has been assessed in this study.</li>
</ul>

<h2>Study Design</h2>
<ul>
 <li>This meta-analysis included randomized controlled trials (RCTs) from PubMed, Cochrane Library database, and Clinicaltrials.gov (March 2012–March 2021), with no language, follow-up, or study size restrictions.</li>
 <li>Inclusion criteria (based on the PICOS schema): (P) Patients with hypercholesterolemia or CVD; (I) PCSK9 inhibitors (assessing efficacy and safety of alirocumab, evolocumab, or bococizumab); (C) control (assessing efficacy and safety of control, i.e., placebo, usual care, or ezetimibe); (S) RCTs</li>
 <li>Exclusion criteria: Abstracts, reviews, and case reports; no efficacy and safety data</li>
</ul>

<h2>Key Results</h2>
<ul>
 <li>Of 1,820 studies, 45 RCTs (alirocumab vs evolocumab vs bococizumab: 21 vs 21 vs 3 RCTs) were included (N = 97,297 patients).</li>
</ul>
Lipid profile
<ul>
 <li>In total, 42 RCTs (N = 92,681) reported data on TG, TC, LDL-C, and HDL-C</li>
 <li>PCSK9 inhibitors could significantly reduce LDL-C, TC, and TG and increase HDL-C vs the control.</li>
 <li>Alirocumab vs control: 
 <ul>
 <li>Reduced LDL-C by –51.29% (95% confidence interval [CI]: –55.83 to –46.75, P &lt;0.05), TC by –30.31% (95% CI: –34.26 to –26.36, P &lt;0.05), and TG by –10.31% (95% CI: –13.81 to –6.81, P &lt;0.05)</li>
 <li>Increased HDL-C by 5.63% (95% CI: 4.86–6.40, P &lt;0.05))</li>
 </ul></li>
 <li>Evolocumab vs control: 
 <ul>
 <li>Reduced LDL-C by –53.99% (95% CI: –58.45 to –49.54, P &lt;0.05), TC by –34.2% (95% CI: –36.18 to –32.21, P &lt;0.05), and TG by –8.86% (95% CI: –13.17 to –4.55, P &lt;0.05)</li>
 <li>Increased HDL-C by 7.05% (95% CI: 5.55–8.54, P &lt;0.05)</li>
 </ul></li>
 <li>Bococizumab vs control: 
 <ul>
 <li>Reduced LDL-C by –56.96% (95% CI: –60.69 to –53.23, P &lt;0.05), TC by –38.96% (95% CI: –43.33 to –34.58, P &lt;0.05), and TG by –17.64% (95% CI: –20.79 to –14.48, P &lt;0.05)</li>
 <li>Increased HDL-C by 5.98% (95% CI: 4.86–7.11, P &lt;0.05)</li>
 </ul></li>
</ul>
Cardiac disorders
<ul>
 <li>Unstable angina (UA) was reported in 13 studies (N = 57,717) and myocardial infarction (MI) in 16 studies (N = 90,355). 
 <ul>
 <li>UA was less common in the alirocumab group vs control (odds ratio [OR] = 0.69, 95% CI: 0.48–0.98, P &lt;0.05) as was the frequency of MI (OR = 0.85, 95% CI: 0.76–0.95, P &lt;0.05).</li>
 <li>The risk of UA did not differ significantly between evolocumab and control group (OR = 0.66, 95% CI: 0.42–1.03, P &gt;0.05); however, the risk of MI was lower with evolocumab (OR = 0.73, 95% CI: 0.65–0.82, P &lt;0.05).</li>
 <li>No statistically significant difference in UA (OR = 0.82, 95% CI: 0.67–1.00, P = 0.05) and MI (OR = 0.94, 95% CI: 0.78–1.14, P &gt;0.05) was found between bococizumab and control groups./span&gt;</li>
 </ul></li>
</ul>
Stroke
<ul>
 <li>Incidence of stroke was significantly lower with PCSK9 inhibitors compared with control: Alirocumab (OR = 0.76, 95% CI: 0.60–0.97, P &lt;0.05), evolocumab (OR = 0.79, 95% CI: 0.66–0.95, P &lt;0.05), and bococizumab (OR = 0.60, 95% CI: 0.42–0.84, P &lt;0.05)</li>
</ul>
Safety
<ul>
 <li>Incidence of injection-site reactions was significantly higher with PCSK9 inhibitors vs control: Alirocumab (OR = 1.68, 95% CI: 1.45–1.93, P &lt;0.05), evolocumab (OR = 1.64, 95% CI: 1.41–1.91, P &lt;0.05), and bococizumab (OR = 8.03, 95% CI: 6.85–9.41, P &lt;0.05)</li>
 <li>Incidence of myalgia did not differ significantly between the control and alirocumab (OR = 1.18, 95% CI: 0.92–1.53), evolocumab (OR = 1.09, 95% CI: 0.85–1.38), and bococizumab (OR = 1.05, 95% CI: 0.92–1.20) (all, P &gt;0.05).</li>
</ul>

<h2>Limitations</h2>
<ul>
 <li>PCSK9 inhibitor dose and different follow-up durations may have affected heterogeneity of results.</li>
 <li>Pooling of data in control group was a mixture of placebo or ezetimibe.</li>
 <li>Definitions of efficacy and safety were not uniform in the included studies.</li>
</ul>

PCSK9 Inhibitors in Cardiovascular Disease

The study proved that the addition of PCSK9 inhibitors to traditional lipid-lowering therapies (LLTs) is set to reduce the risk of cardiovascular disease (CVD), including myocardial infarction (MI) and stroke, as well as all-cause mortality.
<h2>Key Takeaway</h2>
<ul>
 <li>This abridged version of a previously published Cochrane review highlighted the effect of adding PCSK9 inhibitors to traditional LLTs in reducing the risk of CVD, including MI and stroke, as well as all-cause mortality.</li>
 <li>High certainty evidence was noted for studies assessing the effect of PCSK9 inhibitors vs placebo when added to background statin or ezetimibe therapy. 
 <ul>
 <li>However, when PCSK9 inhibitors were directly compared with active treatment (either statins, ezetimibe or combination therapy), the evidence base was weaker and it was unclear if there was a protective or harmful effect in these patients.</li>
 </ul></li>
 <li>This review further noted the lack of sufficient data to exclude possible (long-term) safety signals on influenza, hypertension, cancer diagnosis or T2DM.</li>
</ul>

<h2>Why This Matters</h2>
<ul>
 <li>In patients with insufficient response to, or who are unable to tolerate traditional low-density lipoprotein-cholesterol (LDL-C)-lowering therapies (statins or ezetimibe), PCSK9 inhibitors may provide an alternative treatment.</li>
 <li>Present synopsis summarized the findings from a recent update of a Cochrane systematic review with focus on outcomes, safety, and the quality of evidence from the randomized clinical trials (RCTs) evaluating PCSK9 inhibitors.</li>
</ul>

<h2>Study Design</h2>
<ul>
 <li>Systematic review of 24 RCTs evaluating PCSK9 monoclonal antibodies for the primary and secondary prevention of CVDs: 
 <ul>
 <li>Databases: Cochrane Central Register of Controlled Trials, Medline, Embase, Web of Science, ClinicalTrials.gov and the International Clinical Trials Registry Platform</li>
 <li>Eligibility criteria: Parallel-group and factorial RCTs with at least 24 weeks of follow-up were eligible</li>
 <li>Exclusion criteria: Studies evaluating bococizumab and RG7652 (as these were discontinued)</li>
 <li>Primary outcomes: (1) Composite endpoint of CVD (defined as urgent coronary revascularization, unstable angina pectoris, non-fatal and fatal MI, non-fatal and fatal stroke, and coronary heart disease death); (2) all-cause mortality; (3) MI; and (4) stroke</li>
 <li>Secondary outcomes: (1) Influenza; (2) T2DM; (3) cancer; and (4) hypertension</li>
 </ul></li>
</ul>

<h2>Key Results</h2>
Predominantly high-risk patients were included in the RCTs evaluated in the Cochrane review (patients with non-optimal LDL-C concentration despite treatment with statins or ezetimibe, or with a history of CVD): Patient characteristics
<ul>
 <li>Overall participants: N = 60,997 ([for whom this was reported: men = 71%; women = 29%; race/ethnicity = 83% Caucasian]; age = 61.57 vs 57.93 years)</li>
 <li>The study sample included: 
 <ul>
 <li>A total of 1,879 participants who had familial hypercholesterolemia (FH)</li>
 <li>18,908 (31%) with a diagnosis of T2DM at baseline</li>
 <li>No prior history of CVD (n = 4,590)</li>
 </ul></li>
</ul>
Trial characteristics
<ul>
 <li>Alirocumab was evaluated in 18 trials, while evolocumab in 6 trials 
 <ul>
 <li>Comparator: Placebo in 18 trials, while ezetimibe and/or statins in 6 trials; study period: 2011–2018; setting: outpatient and home settings; countries: international</li>
 </ul></li>
 <li>PCSK9 inhibitors studied (randomization): Alirocumab = 43.5% participants; evolocumab = 56.5% participants</li>
</ul>
Key outcomes*
<ul>
 <li>PCSK9 inhibitors vs placebo (+background LLT [either statin, ezetimibe or a combination of these]): High certainty of evidence 
 <ul>
 <li>Composite endpoint of CVD (relative effect — odds ratio [OR {95% confidence interval; CI}]): Alirocumab vs placebo = 0.87 (0.80–0.94); evolocumab vs placebo = 0.84 (0.78–0.91)</li>
 <li>All-cause mortality (relative effect — OR [CI]): Alirocumab vs placebo = 0.83 (0.72–0.96); evolocumab vs placebo = 1.04 (0.91–1.19)</li>
 <li>MI (relative effect — OR [CI]): Alirocumab vs placebo = 0.86 (0.79–0.94); evolocumab vs placebo = 0.72 (0.64–0.82)</li>
 <li>Any stroke (relative effect — OR [CI]): Alirocumab vs placebo = 0.73 (0.58–0.91); evolocumab vs placebo = 0.79 (0.65–0.94)</li>
 </ul></li>
</ul>

<h2>Limitations</h2>
<ul>
 <li>Low/very low quality of evidence for studies directly comparing PCSK9 inhibitor efficacy with statins and/or ezetimibe (alirocumab: low; evolocumab: very low)</li>
 <li>Limited information was available regarding potential safety issues of either evolocumab or alirocumab</li>
</ul>
*Please refer the source publication&nbsp;<a href="https://heart.bmj.com/content/108/1/14" target="_blank">(Carter et al.)</a>&nbsp;for more details of the reported outcomes (including risk difference and certainty of evidence [Tables 1 and 2]).

The synopsis of a Cochrane Systematic review on PCSK9 monoclonal antibodies for the primary and secondary prevention of cardiovascular disease.

PCSK9i and Prevention of CVD

Effectiveness and safety of PCSK9 inhibitors in Czech real-world practice. 
 Proprotein convertase subtilisin/kexin type 9 inhibitors (PCSK9i) were effective and well-tolerated, with sustained effects, comparable to those in randomized studies.

<h2>Key Takeaway</h2>
<ul>
 <li>PCSK9i were effective in statin-intolerant patients, as significantly lower levels of low-density lipoprotein-cholesterol (LDL-C) were seen within 12 weeks.</li>
 <li>Target LDL-C levels were attained by 35.9% of patients in primary atherosclerotic cardiovascular disease (ASCVD) prevention and 65.7% of those in secondary ASCVD prevention at 1 year after therapy initiation.</li>
</ul>

<h2>Why This Matters</h2>
<ul>
 <li>In patients with ASCVD with insufficient response or intolerant to traditional LDL-C-lowering therapies, PCSK9i can be beneficial.</li>
 <li>The extent to which the outcomes of therapy with PCSK9i in Czech real-world practice was comparable with those reported by large, randomized studies involving Czech patients was unknown.</li>
</ul>

<h2>Study Design</h2>
<ul>
 <li>The effect of PCSK9i therapy was assessed in the entire study population (N = 314; men = 44%; mean age = 63 years) in a Prague-based center of preventive cardiology between 31 July 2018 and 30 September 2020, including in the following subgroups of patients: 
 <ul>
 <li>With familial hypercholesterolemia (FH, 65%) vs. without FH, with LDL-C levels ≥4 mmol/L despite maximum tolerated dose (MTD) of statin 
 <ul>
 <li>Ezetimibe was given as an add-on, except if LDL-C levels were &gt;50% than target if statin-naïve, or &gt;20% if on statin at MTD</li>
 </ul></li>
 <li>With FH in primary (69%) or secondary (31%) ASCVD prevention, with LDL-C levels ≥3 mmol/L, despite lipid-lowering therapy at MTD 
 <ul>
 <li>Without FH in secondary ASCVD prevention (n = 107)</li>
 </ul></li>
 <li>On PCSK9i monotherapy alone vs. PCSK9i in combination with a statin</li>
 </ul></li>
 <li>Potential differences in the effect and tolerability of alirocumab (75 mg or 150 mg; n = 113) and evolocumab (140 mg; n = 156) were also assessed.</li>
 <li>Primary endpoints: Change in LDL-C, total cholesterol (TC), lipoprotein (a) Lp(a), apolipoprotein B (apoB), high-density lipoprotein-cholesterol (HDL-C), and triglycerides (Tg) at 12 and 24 weeks, and 1 and 2 years after initiation of therapy with PCSK9i</li>
 <li>Secondary endpoints: Impact on glucose metabolism</li>
</ul>

<h2>Key Results</h2>
Effect on lipid parameters
<ul>
 <li>Changes in LDL-C levels: There was a significant reduction at 12 weeks (−59.4%) that continued to persist at 2 years (−62.6%)</li>
 <li>Changes in TC levels: There was a significant reduction at 12 weeks (decrease by 41.7%) and at 2 years (decrease by 43.9%)</li>
 <li>Changes in Lp(a) levels: There was a reduction at 12 weeks (−25.4%) and a further reduction at 24 weeks (−35.5%)</li>
 <li>Changes in apoB levels: There was a significant reduction at 12 weeks (54.2%) and at 2 years (58.1%)</li>
 <li>Changes in HDL-C levels: There was a slight increase at 12 weeks (4%) and at 2 years (5.6%)</li>
 <li>Changes in Tg levels: There was a significant reduction at 2 years (−30.3%), with levels reaching targets set by the 2019 ESC/EAS guidelines</li>
</ul>
Effect on glucose parameters
<ul>
 <li>Glucose metabolism was not affected by PCSK9i therapy</li>
</ul>
Effect on patients with and without FH
<ul>
 <li>Dynamics of decrease after therapy initiation were similar, with a decrease in LDL-C levels by 56.7% and 61.8% at 12 and 24 weeks in patients with FH compared to 67.4% and 68.8% in patients without FH, respectively</li>
 <li>At 2 years, significantly lower LDL-C levels were observed in both patients with FH (−63.5%) and those without FH (−62.3%)</li>
</ul>
Effect on patients with primary and secondary ASCVD prevention
<ul>
 <li>Dynamics of decrease after therapy initiation were similar, with a decrease in LDL-C levels by 55.7% and 61.5% at 12 and 24 weeks in patients in primary prevention, and by 63.9% and 66.3% in those in secondary prevention</li>
 <li>At 2 years, significantly lower LDL-C levels were observed in both patients in primary (−61.7%) and secondary (−64.2%) prevention</li>
</ul>
Effect on patients tolerant vs intolerant to statins
<ul>
 <li>By week 12, LDL-C levels in patients on maximum statin dose decreased by 65.2% compared to 55% in those not on statin therapy</li>
 <li>At 2 years, significant differences in LDL-C levels were seen between patients on maximum statin dose vs those who were statin-intolerant (64% vs 59.3%)</li>
</ul>
Effect on patients treated with alirocumab vs evolocumab
<ul>
 <li>By week 12, LDL-C levels in patients on alirocumab decreased by 55.5% compared to 66.1% in patients on evolocumab</li>
 <li>At 2 years, significant differences in LDL-C levels were seen (64.7% vs 61%) Correlation between baseline LDL-C levels and their decrease relative to therapy</li>
</ul>
Correlation between baseline LDL-C levels and their decrease relative to therapy
<ul>
 <li>Moderately strong inverse correlation (Pearson’s r = −0.7147) was seen</li>
</ul>
Effect on safety
<ul>
 <li>Side effects were reported by 9% of patients (alirocumab-related: 14; evolocumab-related: 16); 15 patients withdrew due to side effects</li>
 <li>Flu-like syndrome was more frequent (n = 13), followed by pain at injection site (n = 5), myalgia (n = 5), and gastrointestinal intolerance (n = 3)</li>
</ul>

<h2>Limitations</h2>
<ul>
 <li>Patients were enrolled only from a single center and those not meeting the reimbursement criteria and self-payers were not included.</li>
 <li>Cardiovascular effects of PCSK9i were not assessed</li>
 <li>Patients were enrolled only if diagnosed with FH or statin intolerance, two indications for which reimbursement for treatment is permitted.</li>
</ul>

PCSK9 Inhibitors in Real World Practice

<h2>Key Takeaway</h2>
In this retrospective cohort analysis of patients with an AMI hospitalization:
<ul>
 <li>42%&nbsp;of patients who initiated a PCSK9i during the first year after hospital discharge did so within 89 days</li>
 <li>Statin&nbsp;use was associated with a&nbsp;lower possibility,&nbsp;whereas&nbsp;ezetimibe&nbsp;use, with a&nbsp;higher possibility of initiating a PCSK9i&nbsp;within 89 days following hospital discharge</li>
 <li>Many patients had a&nbsp;recurrent ASCVD&nbsp;event prior to PCSK9i initiation–Cumulative incidence for&nbsp;recurrent ASCVD&nbsp;events: 
 <ul>
 <li>8.0%&nbsp;at 90 days*</li>
 <li>10.5%&nbsp;at 180 days*</li>
 <li>12.5%&nbsp;at 365 days*</li>
 </ul></li>
</ul>

<h2>Why This Matters</h2>
<ul>
 <li>Risk for recurrent ASCVD events is high following hospital discharge of patients with AMI. 
 <ul>
 <li>In-hospital initiation of a PCSK9i in these patients has lowered the levels of LDL-C following discharge</li>
 </ul></li>
 <li>Determining characteristics of patients with AMI, who initiate PCSK9i following hospital discharge may help to identify unmet treatment needs in this population, which has high risk for recurrent events.</li>
</ul>

<h2>Study Design</h2>
A retrospective cohort study utilizing data from patients who had an AMI hospitalization with government health insurance through Medicare or with commercial health insurance in the MarketScan database.
Inclusion Criteria
<ul>
 <li>Patients aged ≥21 and &lt;65</li>
 <li>Medicare beneficiaries ≥66 years of age who had an AMI hospitalization†&nbsp;and initiated a PCSK9i‡, within 365 days following their hospital discharge</li>
</ul>
Patient Categorization
Patients were categorized into three groups based on time of initiation of PCSK9i following hospital discharge for AMI:
<ul>
 <li>0–89 days</li>
 <li>90–179 days</li>
 <li>180–365 days</li>
</ul>
Occurrence of ASCVD events§&nbsp;was assessed between hospital discharge for each patient’s index AMI¶and their first fill for a PCSK9i.

<h2>Key Results</h2>
<ul>
 <li>In total,&nbsp;1,352&nbsp;patients with government health insurance through the Medicare program and&nbsp;353&nbsp;patients with commercial health insurance in the MarketScan database were included.</li>
 <li>
 Overall,&nbsp;42%,&nbsp;25%,&nbsp;and&nbsp;33%&nbsp;of patients initiated a PCSK9i 0–89 days, 90–179 days, and 180–365 days following AMI hospital discharge, respectively.</li>
 <li>
 114 days&nbsp;median time to PCSK9i initiation following hospital discharge for AMI 
 &nbsp;
 <table align="center" border="1" cellpadding="10" cellspacing="1" style="height:100%;width:100%;">
 <tbody>
 <tr>
 <td colspan="2" style="text-align: center; background-color: rgb(235, 235, 235);">Patient Characteristics</td>
 </tr>
 <tr>
 <td style="text-align: center;">Patients&nbsp;in&nbsp;0–89 days group vs 
 180–365 days&nbsp;group&nbsp;were&nbsp;less likely&nbsp;to:</td>
 <td style="text-align: center;">Patients&nbsp;in 0–89 days group vs 
 180–365 days group were more likely to:</td>
 </tr>
 <tr>
 <td>
 <ul>
 <li>Be female</li>
 <li>Hava a history of HF or diabetes</li>
 <li>Initiate a statin within 30 days folllowing discharge</li>
 </ul></td>
 <td>
 <ul>
 <li>Have had a CABG/PCI during their index AMI</li>
 <li>Have been taking ezetimibe within 365 days prior to their index AMI</li>
 <li>Initiate ezetimibe within 30 days following hospital discharge after AMI</li>
 </ul></td>
 </tr>
 </tbody>
 </table></li>
</ul>

<table border="1" cellpadding="20" cellspacing="1" style="height:100%;width:100%;">
 <tbody>
 <tr>
 <td colspan="2" style="background-color: rgb(235, 235, 235);">
 Factors Associated With Possibility of Initiating a&nbsp;PCSK9i 0–89 Days vs&nbsp;180–365 Days*</td>
 </tr>
 <tr>
 <td style="text-align: center;">Lower Possibility</td>
 <td style="text-align: center;">Higher Possibility</td>
 </tr>
 <tr>
 <td>
 <ul>
 <li>Being 55–64 vs 65–79 years of age(OR =&nbsp;0.66;&nbsp;95% CI: 0.44–0.99)</li>
 <li>Being female (OR =0.79; 95% CI: 0.62–1.00)</li>
 <li>Taking a statin within 365 days prior to indexAMI (OR =0.64;95% CI: 0.49–0.84)</li>
 <li>Initiating a statin within 30 days afterdischarge for AMI(OR =0.39; 95% CI: 0.28–0.54)</li>
 </ul></td>
 <td>
 <ul>
 <li>Having a CABG/PCI during the index AMIhospitalization(OR =&nbsp;1.44; 95% CI: 1.07–1.95)</li>
 <li>Taking ezetimibe within 365 days prior to index AMI (OR =&nbsp;1.83; 95% CI: 1.35–2.49)</li>
 <li>Initiating ezetimibe within 30 days after discharge (OR =&nbsp;1.76; 95% CI: 1.11–2.80)</li>
 </ul></td>
 </tr>
 </tbody>
</table>

<table align="center" border="1" cellpadding="10" cellspacing="1" style="height:100%;width:100%;">
 <tbody>
 <tr>
 <td colspan="2" style="text-align: center; background-color: rgb(235, 235, 235);">Cumulative incidence of recurrent ascvd events prior to pcsk9i initiation</td>
 </tr>
 <tr>
 <td>
 • 8.0%&nbsp;at 90 days* • 10.5%&nbsp;at 180 days* • 12.5%&nbsp;at 365 days*</td>
 <td>
 At&nbsp;356&nbsp;days*:
 •&nbsp;AMI:8.4% 
 •&nbsp;CHD:12.0% 
 •&nbsp;PAD:0.5% 
 •&nbsp;Ischemic stroke: None</td>
 </tr>
 </tbody>
</table>

<h2>Limitations</h2>
<ul>
 <li>
 Owing to the lack of data on LDL-C levels, it was not possible to determine whether patients initiated a PCSK9i in accordance with the 2018 AHA/ACC cholesterol guideline recommendations.</li>
 <li>
 Data were only available for prescriptions filled, but not for written prescriptions.</li>
 <li>
 It was not possible to determine whether prescriptions required a prior authorization, which may have delayed the time to fill a PCSK9i.</li>
 <li>
 Most of the claims were filed before the current AHA/ACC blood cholesterol guidelines were published.</li>
</ul>
*Following hospital discharge for AMI. †Between 1 July 2015 – 31 December 2018. ‡Evolocumab or alirocumab. §Recurrent AMI, CHD (i.e., AMI or coronary revascularization), ischemic stroke, and PAD. ¶Date of discharge for the earliest AMI hospitalization closest to and after July 1, 2015.

Factors associated with time to PCSK9i initiation following hospital discharge for acute myocardial infarction.

PCSK9i after hospital discharge for acute MI

SOLIQUA®, a combination of basal insulin and GLP-1 receptor agonists, has been jointly recommended by the ADA and EASD as an effective strategy for achieving and maintaining glycemic control in type 2 diabetes.
SOLIQUA®&nbsp;distinguishes itself from intensified insulin regimens by offering robust glucose-lowering benefits while minimizing weight gain and reducing the risk of hypoglycemia. Furthermore, SOLIQUA®&nbsp;streamlines the administration of insulin regimens, providing individuals with an easier and more efficient approach to diabetes management.

ADA/EASD recommend considering combination injectables therapy of basal insulin/GLP-1 RA (Such as Soliqua®) as valuable treatment option to provide adequate efficacy for achieving and maintaining glycemic goals.

New 2022 ADA/EASD Guidelines: GLPP-1 RA/Insulin Combination Is Recommended

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