Emerging cardiological issues during the COVID‐19 pandemic

Pandemic
DOI: 10.1111/eci.13270 Publication Date: 2020-05-16T19:39:36Z
ABSTRACT
Today the modern world is facing an unprecedented health crisis. The COVID-19 pandemic putting extensive strain on healthcare systems hospitals and medical workers worldwide. Epidemiological data are emerging that patients with cardiac risk factors or pre-existing conditions at increased for complications mortality from COVID-19. As we just begin to understand pathophysiology underlying disease involvement of heart whether through direct myocardial infection damage due already evident. Also current therapy using antiviral agents (hydroxy)chloroquine other off-label used medications not without side effects. Furthermore puts stress organization care both acute chronic in which patient as well physician-related delays treatment could potentially lead harm. Is there a relation between injury COVID-19? Early reports China1 indeed show markedly elevated rates hypertension, diabetes coronary artery (up 10-fold latter) compared conditions. In recent report Shi et al,2 hospitalized Wuhan, China, presenting high-sensitive troponin I levels had higher frequency such ARDS (58.5% vs 14.7%) kidney (8.5% 0.3%), required more invasive mechanical ventilation (22% 4.2%) significant increase in-hospital than (51.2% 4.5%). percentage troponins range 20%-28%2, 3 cardiovascular can be high 69.4%.3 These indicate during this important predictor adverse outcomes. pathophysiological mechanisms by SARS-CoV-2 virus affects seem diverse nature (Figure 1). mentioned, substantial amount signs evident rise biomarkers. This sometimes, but always, accompanied ECG changes LV dysfunction echocardiography (Table viral influenza SARS-CoV,4 form myocarditis (1 SARS Toronto outbreak). Also, release inflammatory cytokines itself also myocarditis, resulting takotsubo-like clinical picture.5, 6 And although present number patients, occlusion vasculature seems relatively uncommon. early Italy, about 60% referred cathlab typical chest pain presented normal arteries. Other groups have reported picture, ST-segment elevation nonobstructive (MINOCA). New York hospitals, only 8 out 18 ST-elevation initial evidence obstructive angiography regional wall-motion abnormalities echocardiography.7 MINOCA microvascular dysfunction, thrombosis embolism, plaque disruption dissection vasospasm. regard, incidence embolism has been reported, probably relates prothrombotic state whom D-dimers commonly seen. arterial thrombotic was recently 3.7% critically ill intensive unit, making strong case for—probably dose—thrombosis prophylaxis these patients.8 On hand, cfr. aforementioned study, true infarctions do occur, many factors. general, median D-dimer noncoronary injury.7 To further complicate forms stress-induced cardiomyopathy, takotsubo, hypoxia-induced injury, MOF pulmonary result troponin. mimic, symptoms baseline ECG, infarction. setting concomitant pericarditis leading pericardial effusion occasionally tamponade. Furthermore, failure, life-threatening arrhythmias ventricular tachycardia sudden death. For instance, some rapidly progressive cases younger fulminant failure cardiogenic shock plays role process. infectious states, worsen condition known decompensation. induces "de novo" atrial fibrillation it destabilize paroxysmal permanent fibrillation. uses ACE2 receptor entry point intracellular invasion, concerns were raised use angiotensin-converting enzyme inhibitors (ACEIs) angiotensin blockers (ARBs). Data supporting derived animal studies. However, human studies did consistent results.9 Nevertheless, clinicians advocated restrictions ACEIs ARBs COVID-19.10 hypothesis premature several international societies warned against withholding ACEIs/ARBs because outcomes, including worsening failure.11 Moreover, SARS-CoV-1 ARDS, ARB (losartan) improved lung injury12, 13 currently active recruiting (NCT04287686 NCT04312009 NCT04311177, respectively). debate going even opposite direction proved significantly lower receiving ACE inhibitors, posing no potential harm.14 another association RAAS susceptibility refuted multivariable analysis, showing ACEI/ARBs prevalence patients.15 Concerning (with azithromycin) first-line option patient, chance QTc prolongation subsequent torsade de pointes fatal arrhythmias. We caution initiate congenital long QT syndrome acquired QT. measurement before initiation (hydroxy)chloroquine, azithromycin drugs lopinavir/ritonavir absolutely necessary, certainly prolonging antiarrhythmic (eg amiodarone, sotalol flecainide), antipsychotics, anticonvulsants, antidepressants, antibiotics, antiemetics, antifungal, antimalarial drugs.16 Regular repeat ECGs therapy, example every 2 days frequently if elevated, continuous monitoring warranted. Hypokalaemia avoided actively corrected. Discontinuation medication when exceeds 500ms tachyarrhythmias occurs. our structures under lot pressure. competing needs non-COVID-19 ICU beds ventilators, staff nurses redeployed dedicated wards witnessing shortages (protective) equipment medications. There personnel transmission co-workers families. leads standard increases physical mental workers. Elective procedures visits postponed, threshold admitting doing procedures. cathlab, staff, urgent PCI restricted most centres infarction (STEMI) highly instable patients. some, revival thrombolysis STEMI. anxious visit doctors, emergency delay, discontinuation serious complications. students fellows, interference education training programmes, will affected, research disturbance ongoing trials. uncertain long-term effects prognosis affected devastating long-lasting function. way, possible witness second wave pandemic, time dilated cardiomyopathy congestive failure. Although still too draw definite conclusions preliminary imaging left function after takotsubo somewhat reassuring general recovery absence scar necrotic foci.5, 17 conclusion, implications affecting way treat All issues great concern stays endemic vaccine effective treatment, continue marked impact daily practice. authors conflicts declare.
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