CARDIOMETABOLIC SYNDROME The COVID-19 pandemic has highlighted the importance of improving cardiometabolic health. There is a need to devise an all-encompassing prevention program for patients to reduce chronic disease risks and create a healthy culture 46 . Cardiometabolic-based chronic disease results from the interplay between primary and metabolic drivers 47 . Primary drivers include genetic, environmental and behavioral aspects whereas abnormal adiposity, dyslipidemia, dysglycemia and hypertension constitute the secondary drivers 47 . Concerted efforts should be made to decrease the severity of metabolic drivers for primary prevention. Lifestyle changes, diligent use of insulin and antihypertensives in admitted patients and continuation of statins should be emphasized 46 . THROMBOEMBOLIC DISEASE AND DIC COVID-19 predisposes patients to arterial and venous thrombosis due to platelet activation, excessive inflammation, endothelial dysfunction and stasis. Elevated D-dimer levels are a common finding and warrant further investigations for acute venous thromboembolism (VTE) in the presence of other clinical manifestations 11 . In patients with out of proportion hypoxemia, hemodynamic instability and/or unexplained right ventricular dysfunction, VTE should always be considered. Thrombotic complications were reported in 31% of critically ill patients with COVID-19; 25% patients had segmental and subsegmental pulmonary embolism, 3% had ischemic strokes (arterial thrombotic events), 2% had catheter related upper extremity thrombosis and 1% had proximal deep venous thrombosis of leg 48 . Elevated D-dimer levels (>1 g/L) in patients with COVID-19 are strongly associated with in-hospital death with a mortality of 42% and odds ratio of 18.4 (p< 0.005) as reported in one of the retrospective studies 49 . Analysis of 183 patients with COVID-19 also found that non‐survivors had significantly higher D‐dimer levels and fibrin degradation products along with longer prothrombin time at the time of admission. 71.4% patients who died fulfilled the diagnostic criteria of DIC in accordance with International Society on Thrombosis and Haemostasis whereas only 0.6% of the survivors had DIC 50 . These hemostatic changes in COVID-19 reflect coagulopathy that predisposes to thrombotic events.
heart failure patients with COVID-19 is believed to result from exacerbation of the pre-existing comorbid conditions in the setting of an inflammatory surge 37 . COVID-19 patients with heart failure (HF) should be managed as per current HF guidelines including use of angiotensin converting enzyme inhibitors and angiotensin receptor blockers 38 . Optimal fluid and diuretic usage to restore and maintain euvolemia is of primary importance. Management of cardiogenic shock in these patients requires amultidisciplinary approach. The use ofmechanical circulatory support (MCS) should be carefully weighed as the outcomes have not been very promising. In a case series of 52 COVID-19 patients, only 16.7% of the patients who were treated with ECMO survived 39 . MYOCARDITIS The prevalence of myocarditis among COVID-19 patients is unclear 40 . In a case series of 150 COVID-19 patients, 7% of the deaths were attributed to myocarditis 41 . Studies have reported fulminant myocarditis with findings of myocardial inflammatory mononuclear infiltrate during autopsy 9,10 . SARS-CoV-2 particles have been identified in cardiac tissue suggesting direct infection 12,13 . Glucocorticoid therapy and other antiviral agents have been administered to treat myocarditis as more effective treatment strategies are sought. ARRHYTHMIAS AND CARDIAC ARREST Both tachyarrythmias and bradyarrhythmias have been reported in COVID-19 patients. Arrhythmias resulting from inflammatory stress, hypoxia, metabolic derangements and ischemia are more prevalent in critically ill patients. Arrhythmias were reported in 44.4% of ICU patients compared to 6.9% in non-ICU patients, however, the type anddurationof arrhythmiaswerenot reported inthis study 42 . Another study of 700 COVID-19 patients concluded that arrhythmias and cardiac arrest (with an incidence of 7.7%) are consequences of systemic infection and inflammation generally correlating with disease severity 43 . New onset atrial fibrillation was noted in 25 patients, 10 patients had non-sustained ventricular tachycardia and 9 developed clinically significant bradyarrhythmias. All cardiac arrests (in 9 patients) andmost of the arrhythmias occurred in critically ill patients. Only 1 case of torsade de pointes was reported despite many patients being managed with medicines that prolong the QT interval. Other studies have also reported a low incidence (less than 1%) of torsades de pointes in COVID-19 patients 44,45 . As in the general population, QT interval prolonging agents should be avoided in high risk COVID-19 patients who have a baseline QTc of ≥500 ms or with known congenital long QT syndrome and should be discontinued if QTc exceeds to 500 ms during monitoring 45 .
The choice of anticoagulant agent for the treatment of VTE depends on the patient’s comorbidities and admission status. In hospitalized patients, parenteral anticoagulation with unfractionated heparin (UFH) or low molecular weight heparin (LMWH) is recommended as these agents are short acting 51 . UFH has fewer known drug-drug interactions with investigational COVID-19 therapies and can be reversed with protamine. The limitation of UFH is that it takes time to achieve therapeutic aPTT and increases the exposure 26
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