Coronavirus disease 2019 is delaying the diagnosis and management of chest pain, acute coronary syndromes, myocarditis and heart failure

Future CardiologyVol. 17, No. 1 EditorialFree AccessCoronavirus disease 2019 is delaying the diagnosis and management of chest pain, acute coronary syndromes, myocarditis heart failureBhurint Siripanthong, Thomas C Hanff, Michael G Levin, Mahesh K Vidula, Mohammed Y Khanji, Saman Nazarian & Choudhary Anwar A ChahalBhurint SiripanthongSchool Clinical Medicine, University Cambridge, CB2 0SP, UKSearch for more papers by this author, HanffDivision Cardiovascular Hospital The Pennsylvania, PA 19104, USASearch LevinDivision VidulaDivision KhanjiDepartment Cardiology, Newham Barts Heart Centre, Health NHS Trust, London, E13 8SL, NazarianDivision author Chahal *Author correspondence: E-mail Address: [email protected]://orcid.org/0000-0001-7825-8827Division USAMayo Clinic Rochester, MN 55905, United StatesRoyal Papworth Hospital, 0AY, authorPublished Online:1 Jul 2020https://doi.org/10.2217/fca-2020-0088AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareShare onFacebookTwitterLinkedInRedditEmail Keywords: syndromemyocardial injurypercutaneous interventionSARS-CoV-2sepsis-related cardiomyopathyST-elevation myocardial infarctionstress-induced cardiomyopathythromboembolismCoronavirus (COVID-19) was first identified in December 2019, yet within months it had spread pandemic levels with critical global health implications clinical practice all specialties. In cardiology, COVID-19 has imposed an unfortunate conundrum: significantly associated death patients pre-existing cardiovascular disease, [1,2] hospital admissions certain cardiac procedures have declined compared prior years [3–5]. This creates a potentially multiplicative problem if its etiologic virus, severe respiratory syndrome coronavirus-2 (SARS-CoV-2), directly or indirectly cause increased damage while are simultaneously undertreated de novo illness. Here, we assess how may influenced apparent decline care. We also consider clinicians can optimize diagnostic process provide appropriate timely patient care setting uncertainty regarding etiology disease. dynamic will necessitate adaptive strategies over time, particularly as many hospitals, states countries transition slowly toward re-escalation standard operations being mindful resurgence.In spite numerous mechanisms that increase likelihood severity COVID-19, centers thus far reported number admitted (ACS). recent report from British Foundation revealed footfall seeking medical attention infarction, which defined cell due prolonged ischemia, essentially halved March 2020, same period year ago England [6]. worrying trend similarly observed other severely affected including USA [5] Spain; [7] latter saw, among 81 centers, numbers percutaneous intervention (PCI) (48% decrease), structural interventions (81% decrease) (56% dropped, significantly. Several societal, system infection-control issues likely contributed decreased frequency diagnoses during pandemic. morbidity mortality understandably begets fear concerns general population. Coupled government public policies recommending avoid unless suffering symptoms emergencies, rates hospitalization overall decreased. While bona fide reduction incidence ACS population lockdown possible, such reduced work-related stress, physical stressors possible environmental factors air pollution reduction, suspect these be minor. Conversely, pandemic-induced stress economic unemployment negatively impact [8].What concerning, however, treatment despite serious nosocomial infection adding overflowing workload at hospitals. Furthermore, way approach infarction ischemic For instance, some advocated measuring enzymes only when exhibit specific dyspnea palpitations [9]. based on observational studies showed elevated biomarkers troponin NT-proBNP common hospitalized up 27.8% raised troponins [1]. However, significant proportion were shown no underlying pathology [9], prompting notion might predispose nonspecific enzyme leak does not necessarily indicate Type 2 [10]. there rationale limiting tests overt symptoms, especially over-burdened resources potential unnecessary staff viral exposure, restricted testing could miss true relatively minor overshadowed symptoms. Some silent infarctions, diabetics elderly [11], delirium present. Recognizing population-prevalence help establish pretest biomarker elevations related traditional diseases, represent complications infection, inform strategies. important hitherto evidence suggests comorbidities worse prognosis, they require higher utilization intensive mechanical ventilation [2].In broad differential elevation, remains highly should always considered, given diagnosis. aspects above baseline risk, both via thrombotic events precipitation subclinical artery presence distress hypoxemia exacerbate oxygen demand-supply mismatch leads type infarction. those atherosclerotic plaque, SARS-CoV-2 plaque instability coagulopathy, cytokine storm manifest thromboembolic occlusion [12]. Similar been proposed explain following influenza infections [13]. large vessel pulmonary embolism, microvascular thrombus hypoxic vasoconstriction lead incidences sudden right ventricular dysfunction cor pulmonale, result release. These corroborated autopsy series demonstrating venous thromboembolism embolism frequent often considered immediate [14]. suspected pro-thromboembolic sequela unique etiologies sepsis pneumonia [15], rate appears increased. Compared who died H1N1 influenza, found ninefold alveolar capillary microthrombi (p < 0.001) [16].The elevation broad, even absence further compounded COVID-19. Up 40% ST-elevation (STEMI) taken angiogram identifiable culprit [17]. Thus, majority STEMI remain occlusion, myocarditis, sepsis-related cardiomyopathy, stress-induced (Takotsubo) failure exacerbation wall strain, endotheliitis direct cardiomyocyte [10,12,18]. use multimodality imaging cases eodomyocardial biopsy accurate – utilized part healthcare systems attempts minimize areas hospital. introduces inaccuracies bias, invalidating findings. Recent small necropsy concern two (microvascular damage) identification inclusion bodies endothelial cells, sequestered mononuclear polymorphonuclear cellular infiltration endothelium, apoptosis [19]. relative paucity occasionally enzymes. systematic prone selection underestimates [18].Given importance patients, must able distinguish mimics patients. mainstay (above 99th percentile upper reference range limit) least one sign ECG changes ST-elevation, T-wave changes, left bundle branch block pathological Q waves; pain consistent ischemia; showing new regional abnormalities infarct; angiographic [20]. Patients diagnosed offered PCI or, former promptly available, fibrinolysis. low threshold trigger tests, initiating primary protocol alone less findings overwhelm department’s capacity, infected. Moreover, most mimics, damage, would little benefit, expose professionals procedural risk. cases, refine diagnosis, triaging decision angiography uncertain ACS, illness warranting intervention. Hand-held, point-of-care echocardiography readily deployed walls systolic function undergoing high-resolution computed tomography assessment additional contrast-enhanced add time contamination Cardiac magnetic resonance informative involvement interstitial [21]. tools streamline concomitant At last, acutely depressed contractility just undergone excluding occlusive performing endomyocardial benefit. because suspicion fulminant high, identify active aid initiate immunosuppressive agents [22].Currently, prevalence unclear. Certain initiatives made study epidemiology infection; [23] order recognize them better understand their pathophysiology. It hoped efforts shed light into longer term ensue. valuable insight undoubtedly our manage institutional level future guideline recommendations optimum preparation any waves front-line face.Financial competing interests disclosureTC Hanff supported National Lung Blood Institute NIH grant T32-HL007891, did finance production manuscript. 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Am https://doi.org/10.1016/j.ahj.2020.05.006 ScholarFiguresReferencesRelatedDetailsCited ByCOVID-19 Injury: Manifestations, Biomarkers, Mechanisms, Diagnosis, Treatment14 June 2023 | Reports, Vol. 46The Pathogenesis Long-Term Consequences InjuryJACC: Basic Translational Science, 7, 3Schistosomiasis Focus Africa22 2021 Tropical Medicine Infectious Disease, 6, 3Emergency Department Utilization Patient Outcomes During Pandemic AmericaThe Journal Emergency 60, 6The CardiologyJulia Titova24 2020 STAY CONNECTED Metrics History Received 31 May Accepted 15 Published online July print January Information© LtdKeywordsacute cardiomyopathythromboembolismFinancial manuscript.PDF download