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Objective Management of the pandemic caused by the novel coronavirus SARS-CoV-2 challenges both scientists and physicians to rapidly develop, and urgently assess, effective diagnostic tests and therapeutic interventions. The initial presentation of the disease in symptomatic patients is invariably respiratory, with dry cough being the main symptom, but an increasing number of reports reveal multiple-organ involvement. The aim of this review is to summarize the potential role of the renin-angiotensin system activated phagocytes in the pathogenesis of COVID-19 disease. Methods Data for this review were identified by searches of PubMed and references from relevant articles using the search terms “SARS,” “COVID-19,” “renin-angiotensin-system,” “phagocyte,” “reactive free radical,” “antioxidant,” “ARDS,” “thrombosis,” “myocardial,” “ischaemia,” “reperfusion,” “microvascular,” and “ACE2.” Abstracts and reports from meetings were not included in this work. Only articles published in English between 1976 and 2020 were reviewed. Results The cellular target of SARS viruses is the angiotensin-converting enzyme 2, a critical regulating protein in the renin-angiotensin system. The elimination of this enzyme by the viral spike protein results in excessive activation of phagocytes, migration into the tissues via the high endothelial venules, and an oxidative burst. In the case of an overstimulated host immune response, not only devastating respiratory symptoms but even systemic or multiorgan involvement may be observed. Conclusions Early-stage medical interventions may assist in returning the exaggerated immune response to a normal range; however, some therapeutic delay might result in excessive tissue damages, occasionally mimicking a systemic disease with a detrimental outcome.

Coronavirus disease 2019 (COVID-19) arising from Wuhan, China, is currently outbreaking worldwide. The World Health Organization (WHO) has declared COVID-19 to be a global pandemic. COVID-19 could cause a wide range of symptoms ranging from self-limiting fever, sore throat, and cough to more severe symptoms that could lead to acute respiratory distress syndrome. As a result of the lockdown and increased demand, drug shortages could become a growing global issue. This article aims to shed light on the potential impact of drug shortages as a result of this pandemic on patient outcomes and the role of pharmacists and pharmacy policymakers in alleviating this emerging problem.

The rate of venous and arterial thrombotic events among patients infected with severe acute respiratory syndrome coronavirus-2 (SAR-CoV-2) is high. This may be due to a hypercoagulable state induced by the severe inflammation that results from the SAR-CoV-2 infection. We aimed to determine hypercoagulable states’ incidence based on thromboelastography study and its association with thrombotic events in critically ill patients with coronavirus disease 2019 (COVID-19). Fifty-two COVID-19 patients who had thromboelastography study were retrospectively included. All patients received pharmacologic thromboprophylaxis. The hypercoagulable state was observed in 16 patients (30.8%). Among them, maximum amplitude and a-angle were elevated in 75% and 25%, respectively. Reaction time and K were low in only 12.5% for both of them. Inflammatory and coagulation markers, as well as thromboprophylaxis regimens, were not associated with a hypercoagulable state. Fourteen patients (27%) experienced a total of 16 thrombotic events, including 8 (57%) deep venous thrombosis, 6 (43%) pulmonary embolism, and 2 (14.3%) arterial thrombosis. The hypercoagulable state was not significantly associated with thrombotic events. In summary, we observed a lower rate of hypercoagulable state on thromboelastography study in critically ill COVID-19 patients. Also, the hypercoagulable state was not associated with the occurrence of thrombotic events.

Heart failure is a common disease state that can be encountered at different stages in the course of a COVID-19 patient presentation. New or existing heart failure in the setting of COVID-19 can present a set of unique challenges that can complicate presentation, management, and prognosis. A careful understanding of the hemodynamic and diagnostic implications is essential for appropriate triage and management of these patients. Abnormal cardiac biomarkers are common in COVID-19 and can stem from a variety of mechanisms that involve the viral entry itself through the ACE2 receptors, direct cardiac injury, increased thrombotic activity, stress cardiomyopathy, and among others. The cytokine storm observed in this pandemic can be a culprit in many of the observed mechanisms and presentations. A correct understanding of the two-way interaction between heart failure medications and the infection as well as the proposed COVID-19 medications and heart failure can result in optimal management. Guideline-directed medical therapy for heart failure should not be interrupted for theoretical concerns but rather based on tolerance and clinical presentation. Initiating specific cardiac or heart failure medications to prevent the infection or mitigate the disease is also not an evidence-based practice at this time. Heart failure patients on advanced therapies including those with heart transplantation will particularly benefit from involving the advanced heart failure team members in the overall management if they contract the virus.

Cardiac allograft vasculopathy (CAV)-mediated by a heterogeneous myriad of immune and non-immune factors, which contribute to the progressive and diffuse thickening of the arterial allograft's tunica intima in one distinct form of CAV, and the build-up of plaque in another-is a major limiting factor of long-term survival post heart transplantation. Information on the optimal pharmacotherapeutic approaches for the prevention and management of CAV is conflicting, scattered, and inconsistent, with numerous recent studies adding to the literature. In this paper, we present a go-to clinical resource with the most updated and comprehensive information on the topic. Immunosuppressant therapy remains a staple, with mTOR inhibitors and mycophenolate mofetil (MMF) showing direct correlation with CAV prevention. More data is now available with calcineurin inhibitor (CNI) minimizing or sparing regimens. More novel approaches are being investigated for the roles of monoclonal antibodies, anti-thymocyte globulin, and bortezomib in preventing or delaying CAV. On the other hand, statins' established efficacy is attributed to lipid-lowering and lipid-independent immunomodulatory effects, with early initiation associated with improved outcomes. The choice of statin is dependent on drug-drug interactions. Other aiding approaches for the prevention of CAV include antioxidant vitamins, aspirin, vasodilators, folate therapy, and, most pertinently, cytomegalovirus prophylaxis. Larger clinical trials are needed before these options are institutionalised. For management of established CAV, early initiation of augmented immunosuppressive therapies may be effective, as well as CNI conversion to mTOR inhibitors with or without standard MMF and azathioprine therapy. Risk of acute rejection needs to be monitored during conversion. Finally, preclinical investigations highlight novel potential therapies for CAV prevention and attenuation, however robust clinical trials are needed to test their efficacy and safety.

Purpose of review Two major complications compromise the outcomes and quality of life for left ventricular assist device (LVAD) patients. This review aims to discuss the mechanisms of thrombosis and bleeding, recent literature on the optimal approaches for antithrombotic therapy, and novel approaches to prevent bleeding. Recent findings Recent studies with the newly designed LVAD, the fully magnetically levitated rotor, show lower thrombotic risk but sustain similar bleeding risk. Small studies present options for less intense antithrombotic regimens with the newer devices. Bridging anticoagulation when needed in this patient population might require modified regimens and close monitoring to avoid anticoagulation overlap during the bridged periods. The necessity to add an antiplatelet to anticoagulation is particularly being challenged with the recent data. Antiplatelet responsiveness testing is an intriguing approach to customize regimens. In addition, novel approaches that target activation of the angiotensin II receptors and inflammatory responses might offer further protection against bleeding in implanted patients. Summary Close monitoring, novel, and patient-tailored approaches may offer the best antithrombotic strategies for LVAD patients. More clinical and long-term data are needed to establish the potential for less intense regimens particularly with the newly designed devices.

Aims The aim of this study is to evaluate the utilization and success in therapy intensification after initiation of sacubitril/valsartan using a specified protocol within an advanced heart failure and transplant programme in the Middle East Gulf Region. Methods and results We studied a single‐centre, retrospective cohort in a 364‐bedded multi‐speciality hospital located in the United Arab Emirates (February 2016 to July 2017). The advanced heart failure and transplant programme formulated an institutional protocol for initiation of sacubitril/valsartan with defined criteria for switching from angiotensin‐converting enzyme inhibitor (ACEI) and angiotensin II receptor blocker (ARB). Prescribing this drug is intended for patients with heart failure with reduced ejection fraction with left ventricular ejection fraction ≤40%. We excluded patients (i) with age below 18 years or (ii) initiated on sacubitril/valsartan from an outside hospital with or without follow‐up in our outpatient clinic. We included 102 patients with an average initial dose of 78.9 ± 44.2 mg twice daily. Only 17 patients were on target doses of ACEI or ARB prior to switching to sacubitril/valsartan. Up‐titration was successful in 55 patients during the follow‐up period. In addition, 6.9% patients were hospitalized with heart failure exacerbation. In patients with elevated baseline serum potassium prior to initiating this medication, the serum potassium levels decreased post‐initiation by 0.5 ± 0.3 mmol/L (P = 0.0008). Conclusions Initiating sacubitril/valsartan through a defined protocol selects for appropriate candidates and guides starting dose and titration. Overall, significant success can be achieved in replacing ACEI or ARB by sacubitril/valsartan in symptomatic heart failure with reduced ejection fraction patients.

Coronavirus disease 2019 (COVID-19) is the second pandemic of the twenty-first century, with over one-hundred million infections and over two million deaths to date. It is a novel strain from the Coronaviridae family, named Severe Acute Respiratory Distress Syndrome Coronavirus-2 (SARS-CoV-2); the 7th known member of the coronavirus family to cause disease in humans, notably following the Middle East Respiratory syndrome (MERS), and Severe Acute Respiratory Distress Syndrome (SARS). The most characteristic feature of this single-stranded RNA molecule includes the spike glycoprotein on its surface. Most patients with COVID-19, of which the elderly and immunocompromised are most at risk, complain of flu-like symptoms, including dry cough and headache. The most common complications include pneumonia, acute respiratory distress syndrome, septic shock, and cardiovascular manifestations. Transmission of SARS-CoV-2 is mainly via respiratory droplets, either directly from the air when an infected patient coughs or sneezes, or in the form of fomites on surfaces. Maintaining hand-hygiene, social distancing, and personal protective equipment (i.e., masks) remain the most effective precautions. Patient management includes supportive care and anticoagulative measures, with a focus on maintaining respiratory function. Therapy with dexamethasone, remdesivir, and tocilizumab appear to be most promising to date, with hydroxychloroquine, lopinavir, ritonavir, and interferons falling out of favour. Additionally, accelerated vaccination efforts have taken place internationally, with several promising vaccinations being mass deployed. In response to the COVID-19 pandemic, countries and stakeholders have taken varying precautions to combat and contain the spread of the virus and dampen its collateral economic damage. This review paper aims to synthesize the impact of the virus on a global, micro to macro scale.

Summary The reported incidence rate of venous and arterial thrombotic events in critically ill patients with COVID‐19 infections is high, ranging from 20% to 60%. We adopted a patient‐tailored thromboprophylaxis protocol based on clinical and laboratory presentations for these patients in our institution. We hypothesised that patients who received high‐intensity thromboprophylaxis treatment would experience fewer thrombotic events. The aims of our study were to explore the incidence of thrombotic events in this population; to assess independent factors associated with thrombotic events and to evaluate the incidence of haemorrhagic events. A retrospective review of all adult patients with confirmed SARS‐CoV‐2 infection admitted to the intensive care unit (ICU) between 1 March and 29 May 2020 was performed. The primary outcome was a composite of venous and arterial thrombotic events diagnosed during the ICU stay. Multivariable logistic regression was used to identify the independent factors associated with thrombotic events. A total of 188 patients met the inclusion criteria. All received some type of thromboprophylaxis treatment except for six patients who did not receive any prophylaxis. Of the 182 patients who received thromboprophylaxis, 75 (40%) received high‐intensity thromboprophylaxis and 24 (12.8%) were treated with therapeutic anticoagulation. Twenty‐one patients (11.2%) experienced 23 thrombotic events (incidence rate of 12.2% (95%CI 7.9–17.8)), including 12 deep venous thromboses, 9 pulmonary emboli and 2 peripheral arterial thromboses. The multivariable logistic regression analysis showed that only D‐dimer (OR 2.80, p = 0.002) and high‐intensity thromboprophylaxis regimen (OR 0.20, p = 0.01) were independently associated with thrombotic events. Thirty‐one patients (16.5%) experienced haemorrhagic events; among them, 13 were classified as major bleeding according to the International Society on Thrombosis and Haemostasis criteria. Therapeutic anticoagulation, but not the high‐intensity thromboprophylaxis regimen, was associated with major bleeding. A proactive approach to the management of thromboembolism in critically ill COVID‐19 patients utilising a high‐intensity thromboprophylaxis regimen in appropriately selected patients may result in lower thrombotic events without increasing the risk of bleeding.

Background Hospitals in the Middle East Gulf region have experienced an influx of COVID-19 patients to their medical wards and intensive care units. The hypercoagulability of these patients has been widely reported on a global scale. However, many of the experimental treatments used to manage the various complications of COVID-19 have not been widely studied in this context. The effect of the current treatment protocols on patients’ diagnostic and prognostic biomarkers may thus impact the validity of the algorithms adopted. Case presentation In this case series, we report four cases of venous thromboembolism and 1 case of arterial thrombotic event, in patients treated with standard or intensified prophylactic doses of unfractionated heparin or low molecular weight heparin at our institution. Tocilizumab has been utilized as an add-on therapy to the standard of care to treat patients with SARS-CoV-2 associated acute respiratory distress syndrome, in order to dampen the hyperinflammatory response. It is imperative to be aware that this drug may be masking the inflammatory markers (e.g. IL6, CRP, fibrinogen, and ferritin), without reducing the risk of thrombotic events in this population, creating instead a façade of an improved prognostic outcome. However, the D-dimer levels remained prognostically reliable in these cases, as they were not affected by the drug and continued to be at the highest level until event occurrence. Conclusions In the setting of tocilizumab therapy, traditional prognostic markers of worsening infection and inflammation, and thus potential risk of acute thrombosis, should be weighed carefully as they may not be reliable for prognosis and may create a façade of an improved prognostic outcome instead. Additionally, the fact that thrombotic events continued to be observed despite decrease in inflammatory markers and the proactive anticoagulative approach adopted, raises more questions about the coagulative mechanisms at play in COVID-19, and the appropriate management strategy.

Background and aims Familial hypercholesterolemia (FH) is a common autosomal dominant disorder that can result in premature atherosclerotic cardiovascular disease (ASCVD). Limited data are available worldwide about the prevalence and management of FH. Here, we aimed to estimate the prevalence and management of patients with FH in five Arabian Gulf countries (Saudi Arabia, Oman, United Arab Emirates, Kuwait, and Bahrain). Methods The multicentre, multinational Gulf FH registry included adults (≥18 years old) recruited from outpatient clinics in 14 tertiary-care centres across five Arabian Gulf countries over the last five years. The Gulf FH registry had four phases: 1- screening, 2- classification based on the Dutch Lipid Clinic Network, 3- genetic testing, and 4- follow-up. Results Among 34,366 screened patient records, 3713 patients had suspected FH (mean age: 49±15 years; 52% women) and 306 patients had definite or probable FH. Thus, the estimated FH prevalence was 0.9% (1:112). Treatments included high-intensity statin therapy (34%), ezetimibe (10%), and proprotein convertase subtilisin/kexin type 9 inhibitors (0.4%). Targets for low-density lipoprotein cholesterol (LDL-C) and non-high-density lipoprotein cholesterol were achieved by 12% and 30%, respectively, of patients at high ASCVD risk, and by 3% and 6%, respectively, of patients at very high ASCVD risk (p Conclusions This snap-shot study was the first to show the high estimated prevalence of FH in the Arabian Gulf region (about 3-fold the estimated prevalence worldwide), and is a “call-to-action” for further confirmation in future population studies. The small proportions of patients that achieved target LDL-C values implied that health care policies need to implement nation-wide screening, raise FH awareness, and improve management strategies for FH.

Background: Data on patient characteristics and provider practices in the management of lipids per the new guidelines in specific secondary prevention patients in the Middle East is limited.Objective: To explore patient characteristics and lipid management practices according to the new cholesterol guidelines in secondary prevention patients, up to one year following discharge for coronary artery bypass graft surgery (CABG).Methods: A retrospective chart review of patients discharged post CABG between February 2017 and February 2018 at a quaternary care centre in the Middle East. Patients were characterized by baseline demographics, comorbidities, and use of lipid lowering medications.Results: 189 patients were included in the analysis. Most were diabetic (70.9%) and classified as very high risk per the ACC/AHA guidelines (84.1%) and as extremely high risk per the AACE guidelines (85.2%). Most patients (93.1%) were discharged on high intensity statin. About one third (28.6%) were never seen or only followed once within the first 2 weeks post discharge. Of those who continued to follow up beyond 3 months and within 1 year of discharge (44.4%), about half (51.2%) had follow-up lipid panels performed. Patients who followed up and were seen by a cardiologist were five times more likely to have lipid panels ordered than those seen solely by a CT surgeon. Of those with follow-up lipid panels beyond 3 months: 59.3% achieved LDL goal of

Heart failure readmissions are associated with significant morbidity and mortality. Adequate education on adherence and self-care behaviours can affect readmission rates positively and nurses are at the frontline of patient education. Such education is valuable when establishing heart failure programmes in developing countries, in light of the challenging socioeconomic circumstances in these. This study aimed to evaluate nurses' heart failure knowledge, to assess patients' baseline knowledge, and to evaluate the effectiveness of structured nurse-driven education. Methods: a total of 131 cardiac centre-based nurses and 30 chronic heart failure patients participated in the study in Kuwait. Patients were surveyed a second time 3 to 6 months later, while being followed at an advanced heart failure clinic by dedicated heart failure nurses. Results: the majority of the nurses (80%) had not received heart failure education previously, although they were able to recognise most heart failure symptoms. Significant improvement in patients' knowledge was noted between the initial and follow-up surveys. Conclusion: establishing a dedicated advanced heart failure programme to care for patients in a developing country can result in significant improvement in disease awareness and self-care behaviours when led by well-trained heart failure nurses. More research is needed to determine if these findings are shared by other countries in the Middle-East and other developing countries.

Background The 2017 ACC expert consensus decision pathway for optimization of heart failure (HF) treatment emphasizes the fact that target doses of medications are associated with the best outcomes. It has been reported that a significant portion of HFrEF patients are not on optimal doses of medical therapy, and gaps exist in longitudinal medication titration. The objective of this retrospective study is to describe medical therapy after 12 months of follow up in a newly established multidisciplinary HF program in the Middle East Gulf region. Methods A retrospective outpatient chart review was conducted on HF patients after initial outpatient clinic enrollment between October 2015 and July 2017. All patients with EF ≤ 40 were included. We documented baseline and follow-up evidence based HF medications including beta blockers, RAAS inhibitors, and MRA. Results Out of 305 enrolled patients, only 186 had a 12 month follow up appointment, out of which 139 had HFrEF and were included in this analysis. At baseline, 25.2%, 13.7%, and 42.4% of patients were receiving target doses of beta-blocker, ACEI/ARB/ARNI, and MRA, respectively. Only 2.9% were on target doses of all 3 classes of evidence based therapies. At 12 months, percentage of patients on target doses significantly increased to 51.8% for beta blockers and 31.7% for ACEI/ARB/ARNI, while there was no significant change in patients on target dose MRA (36.7%). More patients (10.1%) were on target doses of all 3 evidence based therapies (table 1). A significant increase was observed in the rate of adoption of ARNI from baseline to follow-up (10.1% vs 48.9%, p Conclusion Close follow up of patients with HFrEF was associated with statistically significant increase in those on target doses of both beta blockers and ACE/ARB/ARNI and patients on simultaneous target doses of all evidence based medications. Compared to recent western outpatient registries, our study shows that the success of longitudinal titration of evidence based medications and adoption of new ones can be enhanced when patients are followed by a specialized multidisciplinary program.