INTRODUCTION:This study evaluates dyslipidaemia management in the Arabian Gulf region. METHODS:The multicentre, multinational longitudinal Gulf ACTION registry includes adults (≥18 years old) on lipid-lowering therapy (LLT) recruited from outpatient clinics at 14 tertiary care centres and 9 primary care clinics across five Arabian Gulf countries. RESULTS:A total of 2884 patients were enrolled (mean age 58±12 years); 63% were male. The median first follow-up was 7 (6-11) months, and the median second follow-up was 14 (12-23) months. Among the cohort, 52% of patients were very high risk, 21% of whom achieved their LDL-C target; 40% were high risk, 24% achieved their LDL-C target; 2% were moderate risk, 72% achieved their LDL-C target; and 6% were low risk, 78% achieved their LDL-C target. Only 24% of the overall cohort and 30% of the very high-risk group were treated with combination LLT. DISCUSSION:Similar to international data from the SANTORINI and INTERASPIRE studies, our study showed that only one-fourth of the very high-risk group and one-third of the high-risk group achieved their LDL-C targets. Potential reasons include lower use of combination therapy, poor health behaviors, and psychosocial factors. The variability in practice patterns across the Arabian Gulf and even among study sites is a limitation. CONCLUSION:Very high- and high-risk groups were less likely to achieve their LDL-C target. The low use of combination LLT, unhealthy lifestyle, and social factors in the Gulf region were the main reasons for such poor control. Strategies are needed to achieve current guideline-recommended LDL-C targets.

Growing evidence suggests that lowering non-high-density lipoprotein cholesterol (non-HDL-C) levels is associated with a reduced risk of cardiovascular diseases (CVD) events. However, data on this relationship remain scarce in the Arabian Gulf region. The Gulf TriglyCeride And ResiduaL CardiovascuLar RiSk (Gulf CALLS) study investigated the association between failure to achieve non-HDL-C targets (<2.6 mmol/L) and residual CVD risk in very high-risk patients from the region who were on statin therapy and had well-controlled low-density lipoprotein cholesterol (LDL-C) levels (<1.8 mmol/L [70 mg/dL]). This retrospective study evaluated patients across 5 Arabian Gulf countries, aged > 45 years with established CVD or diabetes, LDL-C levels <1.8 mmol/L (<70 mg/dL), and triglyceride levels <4.5 mmol/L (<400 mg/dL) on lipid-lowering therapy. A total of 22% (521/2344) of the patients did not achieve the non-HDL-C target. In the adjusted Cox regression model, patients who achieved the non-HDL-C goal at baseline had a 25% lower risk of subsequent CVD events than those who did not (hazard ratio, .75; 95% confidence interval: .58-.97; P = .028). In the present study involving very high-risk patients on statin therapy, failure to achieve non-HDL-C targets was associated with a significantly higher residual CVD risk, despite well-controlled LDL-C levels.

Although there are conflicting clinical data on the efficacy of weight reduction in reducing secondary events in patients with comorbid overweight and obesity (OAO) and cardiovascular disease (CVD), there is excellent epidemiological and biological evidence of a cause-effect relationship between OAO, CVD, and other systemic complications. There is also new interventional evidence that pharmacotherapies improve cardiovascular, hepatic, and renal outcomes in individuals with OAO and pre-existing CVD. New trial data confirm that not all weight loss strategies are equal in terms of reducing cardiovascular risk. Using Global Burden of Disease data and a pooled analysis of registry data on ~30,000 patients with CVD, we estimate that about 34 million patients across the Middle East could benefit from secondary prevention of CVD by targeting OAO phenotypes. Implementing secondary prevention in practice will require updating clinical guidelines on both obesity management and CVD secondary prevention, as well as policy changes that allow for reimbursement. Crucially, it will also require a philosophical shift that there exist distinct OAO phenotypes for which treatment success is not solely dictated by weight loss. The cumulative burden of future cardiovascular risk is set to increase, mandating comprehensive strategies to implement secondary prevention in at-risk groups, including children.

Background:Lipoprotein(a) [Lp(a)] is increasingly recognized as an independent and causal risk factor for atherosclerotic cardiovascular (CV) disease including aortic valve stenosis, myocardial infarction, stroke, peripheral arterial disease and CV death. Despite growing global awareness, significant gaps in diagnosis, risk stratification, and management persist in Gulf countries. Objective:To develop regionally tailored consensus statements on the clinical management of elevated Lp(a) in Gulf countries using a modified Delphi-based methodology. Methods:A multidisciplinary panel, mostly of Gulf-based experts in cardiology, lipidology, and endocrinology evaluated 64 evidence-based statements across six thematic domains, including pathophysiology, risk assessment, therapeutic strategies, and implementation challenges. Consensus was defined by ≥ 80% agreement, and relevant literature was reviewed to support each statement. Results:Strong consensus supported the inclusion of Lp(a) in routine CV risk assessment, especially for high-risk individuals. The panel endorsed early detection and aggressive management of modifiable risk factors, including LDL-C, apoB, and non-HDL-C. Areas of partial agreement highlighted practical challenges, including variability in insurance coverage and the need for clearer referral pathways, imaging protocols, and outcome-driven treatment guidance and particularly the current unavailability of specific Lp(a) lowering drugs. Conclusion:These expert recommendations provide a pragmatic framework for integrating Lp(a) into CV care pathways in Gulf countries. By aligning practice with emerging evidence, the consensus has the potential to shape national guidelines, inform payer policies, promote regional research on the epidemiology of Lp(a), and support equitable access to future Lp(a)-targeted therapies, ultimately improving long-term CV outcomes in the region.

Introduction Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors are transformative lipid-lowering therapies, yet the structure of the research literature is strongly shaped by trial priorities. This study aimed to map global research trends on PCSK9 inhibitors using a bibliometric analysis of Scopus and PubMed. Methods Metadata on publication year, journal, citations, authorship, country, institution, and keywords were extracted. Annual output, mean citations, h-index correlations, and collaboration metrics were calculated, and networks were visualized using Bibliometrix and VOSviewer. Results Approximately 1,390 records published between 1994 and 2024 were identified, involving 7,601 authors and 51,555 citations, with a mean of 37.1 citations per document. Network mapping revealed eight collaboration clusters and an international collaboration index of 1.871. The United States contributed the largest share of corresponding-author articles, with 343 of 1,390 records (24.7%), while the top 10 countries accounted for approximately 65% of outputs. Publication volume increased sharply after 2013, with inclisiran emerging as a highly cited RNA-based therapeutic. However, annual publication volume was not significantly correlated with mean citations (r = 0.059, P = 0.832), indicating no proportional increase in per-article citation influence. Discussion Network analysis identified eight major collaboration clusters. International collaboration was modest, with limited contributions from low- and middle-income countries. Temporal trends showed a notable increase in publications after 2013. Emerging RNA therapeutics were visible in the dataset but had lower citation maturity compared with established monoclonal antibody studies. Conclusion Scopus and PubMed mapping reconstructs the translational progression of PCSK9 research and highlights collaboration patterns, country-level contributions, and the bibliometric visibility of emerging therapeutic modalities.

Objectives:This study aimed to evaluate the screening rate and the prevalence of obstructive sleep apnea syndrome (OSAS) in patients with apparent resistant hypertension (ARH) attending Sultan Qaboos University Hospital, and to assess sex differences. Methods:A cross-sectional retrospective study was conducted using the data from 500 patients with ARH between January 2018 and January 2023. The cohort included 270 women and 230 men. Data extracted from hospital records included demographic and clinical characteristics, antihypertensive medications, results of OSA screening tools (e.g., Epworth Sleepiness Scale and STOP-Bang questionnaire), and polysomnography outcomes. Results:Of the 500 patients with ARH, 54 (10.8%) were diagnosed with OSAS. Only 6.6% (n = 33) were screened for OSA using the Epworth Sleepiness Scale or STOP-Bang questionnaire, while the majority (93.4%, n = 467) were not screened. Women constituted 54.0% of the cohort and had a higher mean body mass index than men (32.7 kg/m2 vs. 30.2 kg/m2, p < 0.001). OSAS prevalence was significantly higher in women than men (14.1% vs. 7.0%, p = 0.013). Conclusions:There was a low rate of screening for OSAS among patients with ARH at Sultan Qaboos University Hospital, which may explain the lower-than-expected prevalence observed. Contrary to published literature, OSAS was more frequently diagnosed in women, who were screened more often, suggesting that OSA may be underdiagnosed in men.

The definition of "Metabolic Associated Fatty Liver Disease - MAFLD" has replaced the previous definition of Nonalcoholic Fatty Liver Disease (NAFLD), because cardiometabolic criteria have been added for the prevention of cardiological risk in these patients. This definition leads to an in-depth study of the bidirectional relationships between hepatic steatosis, Type 2 Diabetes Mellitus (T2DM), Cardiovascular Disease (CVD) and/or their complications. Lifestyle modification, which includes correct nutrition combined with regular physical activity, represents the therapeutic cornerstone of MAFLD. When therapy is required, there is not clear accord on how to proceed in an optimal way with nutraceutical or pharmacological therapy. Numerous studies have attempted to identify nutraceuticals with a significant benefit on metabolic alterations and which contribute to the improvement of hepatic steatosis. Several evidences are supporting the use of silymarin, berberine, curcumin, Nigella sativa, Ascophyllum nodosum, and Fucus vesiculosus, vitamin E, coenzyme Q10 and Omega-3. However, more evidence regarding the long-term efficacy and safety of these compounds are required. There is numerous evidence that highlights the use of therapies such as incretins or the use of Proprotein Convertase Subtilisin/Kexin type 9 (PCSK9) inhibitors or other similar therapies which, by assisting existing therapies for pathologies such as diabetes, hypertension, insulin resistance, have given a breakthrough in prevention and the reduction of cardiometabolic risk. This review gave an overview of the current therapeutic strategies that are expected to aid in the treatment and prevention of MAFLD.

Objectives: We sought to estimate the percentage achievements of non-high-density lipoprotein cholesterol (non-HDL-C) target in patients with very high atherosclerotic cardiovascular diseases (ASCVD) risk stratified by triglyceride (TG) levels despite statin-controlled low-density lipoprotein cholesterol (LDL-C) in the Centralized Pan-Middle East Survey on the under treatment of hypercholesterolemia. Methods: The non-HDL-C target achievement in patients with diabetes mellites (DM) and patients with established ASCVD was defined according to European Society of Cardiology and European Atherosclerosis Society 2019 guidelines for managing dyslipidemia. Patients were stratified to controlled LDL-C defined as < 70 mg/dL (< 1.8 mmol/L) with normal TG < 150 mg/dL (< 1.7 mmol/L) and high TG between 150–400 mg/dL (1.7–4.5 mmol/L). Results: The mean age of our cohort was 58.0±11.0 years, 6.8% (n = 717) were male, 9.7% (104) were smokers, and 48.4% (n = 518) had body mass index of ≥ 30 kg/m2. Those with high TG levels male (76.5% vs. 63.8%; p < 0.001), smokers (16.1% vs. 7.7%; p < 0.001), have metabolic syndrome (77.6% vs. 17.1%; p < 0.001), and low HDL-C levels (79.2% vs. 49.4%; p < 0.001). The majority (93.9%, n = 1008) were on statins (atorvastatin and rosuvastatin) with only 2.2% (n = 24) on the combined statins plus fenofibrate/gemfibrozil. Only 27.4% (n = 294) of patients had non-HDL-C goal attainment. Goal attainment rates in patients with diabetes (3.1% vs. 34,4%; p < 0.001), coronary artery disease (CAD) (2.4% vs. 37.9%; p < 0.001), diabetes plus CAD (0% vs. 40.0%; p < 0.001), and CVD (0% vs. 30.0%; p =0.048) were significantly lower in those with higher TG levels. Conclusions: A large proportion of statin-controlled LDL-C diabetic patients and patients with established ASCVD with high TGs did not achieve the non-HDL-C target. Our study did not demonstrate an association between ASCVD and high TG levels; and therefore, a follow-up study is highly required to assess long-term ASCVD outcomes in this cohort.

Familial hypertriglyceridemia (F-HTG) is an autosomal disorder that causes severe elevation of serum triglyceride levels. It is caused by genetic alterations in LPL, APOC2, APOA5, LMF1, and GPIHBP1 genes. The mutation spectrum of F-HTG in Arabic populations is limited. Here, we report the genetic spectrum of six families of F-HTG of Arab ancestry in Oman. Methods: six Omani families affected with triglyceride levels >11.2 mmol/L were included in this study. Ampli-Seq sequencing of the selected gene panels was performed. Whole-exome sequencing and copy number variant analysis were also performed in cases with negative exome results. Three novel pathogenic missense variants in the LPL gene were identified, p.M328T, p.H229L, and p.S286G, along with a novel splice variant c.1322+15T > G. The LPL p.H229L variant existed in double heterozygous mutation with the APOA5 gene p.V153M variant. One family had a homozygous mutation in the LMF1 gene (c.G107A; p.G36D) and a heterozygous mutation in the LPL gene (c.G106A; p.D36N). All affected subjects did not have a serum deficiency of LPL protein. Genetic analysis in one family did not show any pathogenic variants even after whole-exome sequencing. These novel LPL and APOA5 mutations are not reported in other ethnic groups. This suggests that patients with F-HTG in Oman have a founder effect and are genetically unique. This warrants further analysis of patients of F-HTG in the Middle East for preventative and counseling purposes to limit the spread of the disease in a population of high consanguinity.

We evaluated the impact of olanzapine on metabolic changes in patients with psychotic disorders. This was a retrospective cohort study involving patients prescribed olanzapine and attending Sultan Qaboos University Hospital (Muscat, Oman). Patients were followed up retrospectively from March 2006 until April 2021. Cardiovascular treatment targets were evaluated as per the 2019 European Society of Cardiology guidelines. We enrolled 253 patients (mean age: 40±17 years). Olanzapine monotherapy was associated with increased body weight (+8 kg; 95% confidence interval (CI): 6–9; P < .001), body mass index (+3 kg/m2; 95% CI: 2–4; P < .001), total cholesterol (+.4 mmol/L; 95% CI: .3–.5; P < .001), low-density lipoprotein cholesterol (LDL-C) (+.3 mmol/L; 95% CI: .1–.4; P < .001), fasting triglycerides (+.2 mmol/L; 95% CI: .1–.3; P<.001), fasting glucose (+.6 mmol/L; 95% CI: .4–.7; P< .001), HbA1c (+.3%; 95% CI: .2–.4; P < .001), systolic blood pressure (BP) (+9 mmHg; 95% CI: 6–12; P < .001) and diastolic BP (+4 mmHg; 95% CI: 2–6; P < .001) levels. Cardiovascular therapeutic goals were attained in 38% (n = 97), 61% (n = 154), 71% (n = 180), and 59% (n = 150) for LDL-C, non–high-density lipoprotein cholesterol, triglycerides, and BP, respectively. Olanzapine was associated with adverse metabolic changes. Therefore, many patients were not at their target cardiovascular treatment goals.