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 Table of Contents  
LETTER TO EDITOR
Year : 2021  |  Volume : 10  |  Issue : 1  |  Page : 45-46

From COVID-19 to CARDEMIC: The tsunami to come


1 Department of Cardiology, Institute of Postgraduate Medical Education and Research, Kolkata, West Bengal, India
2 Department of Reproductive Medicine, Lilavati Hospital and Research Centre, Mumbai, Maharashtra, India

Date of Submission09-Sep-2020
Date of Acceptance30-Sep-2020
Date of Web Publication27-Mar-2021

Correspondence Address:
Dr. Rakesh Agarwal
Department of Cardiology, Institute of Postgraduate Medical Education and Research, Kolkata, West Bengal
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/JCPC.JCPC_57_20

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How to cite this article:
Agarwal R, Baid R. From COVID-19 to CARDEMIC: The tsunami to come. J Clin Prev Cardiol 2021;10:45-6

How to cite this URL:
Agarwal R, Baid R. From COVID-19 to CARDEMIC: The tsunami to come. J Clin Prev Cardiol [serial online] 2021 [cited 2021 Aug 2];10:45-6. Available from: https://www.jcpconline.org/text.asp?2021/10/1/45/312228



The COVID-19 pandemic has taken the world by storm. On the day of writing this article, as many as 21 million people have been affected by the disease worldwide with over 750,000 deaths. As the pandemic stabilizes, however, we must be prepared for a new epidemic to take over the cardemic [Table 1].
Table 1: Cardemic: The components that may contribute to a cardiac crisis

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The long-term outcomes of COVID-19 are unknown but may be akin to those with severe acute respiratory syndrome-coronavirus infection. A 12-year follow-up had shown 40% of patients with cardiovascular abnormalities, 60% with dysgylcemia, and 68% with dyslipidemia.[1] Preliminary evidence suggests that in cities like New York, there has been an increase in cardiac arrests and death rates secondary to cardiac arrests during the COVID-19 pandemic.[2]

Patients have been known to avoid care-seeking behavior due to the perceived risks of acquiring COVID-19 infection. Other contributing factors include unavailability of transport facility including emergency ambulance services due to overwhelmed medical infrastructure, psychological reasons, and the perceived stigma associated with a hospital visit during the COVID-19 era.[3] However, the risk of acquiring COVID-19 infection, or even dying from it, is far less than the mortality due to untreated cardiac disease.[4]

Deferral of elective cardiovascular procedures and cancellation of outpatient visits have been frequent due to disease concerns among both health-care personnel and patients. A mean increase of about 4 h has been reported from Hong Kong from symptom onset to medical contact among patients with ST-elevation myocardial infarction (STEMI).[1],[5] For STEMI patients, there have been reported delay in reperfusion, reduced percutaneous coronary intervention (PCI) activity, reduction in cardiac rhythm monitoring time, reduction in referrals, and increased mechanical ventilations. These can be due to a variety of reasons including but not limited to restricted cath lab activity and lack of personal protective equipment kits.

Cath lab personnel availability has also been affected. These can include physicians, cath lab nurses, or technicians, who were unable to attend cath lab sessions due to being in quarantine or being sick and in isolation. Travel to hospital may be impacted in some places with stringent lockdowns or travel bans. Some cardiologists and cardiac care nurses have been redeployed to support critical care colleagues. A 40% drop in cath lab activation for STEMI has been reported. Elective procedures including PCI, electrophysiology ablations, and coronary artery bypass grafting have been impacted disproportionately.[6],[7]

Use of medications with cardiac side effects is only likely to compound the problem. Azithromycin and hydroxychloroquine (HCQS) have been used extensively in COVID-19 patients, and both drugs have been implicated in QTc prolongation and potential risk for Torsades. While it is unlikely that survivors may exhibit delayed symptoms from such drugs, the prolonged half life of HCQS and the fact that some may be taking it for a long duration of time as a preexposure prophylaxis may aggravate this problem in future. Chloroquine has been implicated in the causation of restrictive and dilated cardiomyopathies.[8],[9]

Corticosteroids have been implicated in causing fluid retention and hypertension and may be associated with long-term cardiac effects. Lopinavir/ritonavir can lead to dyslipidemia apart from cardiac conduction abnormalities. Interferons have been associated with cardiomyopathies and myocardial infarction. Impact of drugs on patients already taking cardiac drugs such as antiplatelets and statins is worrisome.[10]

Microvascular thrombosis with elevated D-dimer levels in COVID-19 patients can lead to deep-venous thrombosis and pulmonary embolism, eventually leading to adverse cardiac remodeling and pulmonary hypertension in the long run. Survivors of acute respiratory distress syndrome and severe parenchymal lung disease can go on to develop right heart failure and pulmonary hypertension.[10],[11]

Cardiac dysfunction secondary to myocarditis may not resolve in all patients and may lead to a greater burden of patients with heart failure and impaired performance. At the same time, increased incidence of stress cardiomyopathy has been reported.[12] Heart transplant patients have been reported to be affected with COVID-19 with the need for omission of immunosuppressive therapy.[1] The impact of the COVID-19 pandemic on heart transplant is uncertain at present, but would likely lead to a deferral of procedures and increased mortality and morbidity in patients awaiting a transplant.

It has been long known that respiratory infections can subsequently increase the risk for acute coronary syndromes, and we may see the same in adult survivors of COVID-19, particularly those with cardiac risk factors. Further, with the virus moving on to infect those with established risk factors, and deeper into the pandemic, we may see more cases of acute coronary syndromes as time passes on.[10],[11],[12]

Sooner or later, the ongoing pandemic will stabilize and abate, as is the rule for all pandemics. But, another public health crisis is in the making, and we as health-care professionals must be ready for it. Like the US Coast Guards say – Semper paratus!

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Tam CC, Cheung KS, Lam S, Wong A, Yung A, Sze M, et al. Impact of Coronavirus Disease 2019 (COVID-19) outbreak on ST-segment–elevation myocardial infarction care in Hong Kong, China. Circ Cardiovasc Qual Outcomes 2020;13:E006631.  Back to cited text no. 1
    
2.
Lai PH, Lancet EA, Weiden MD, Webber MP, Zeig-Owens R, Hall CB, Prezant DJ. Characteristics Associated With Out-of-Hospital Cardiac Arrests and Resuscitations During the Novel Coronavirus Disease 2019 Pandemic in New York City. JAMA Cardiol. 2020;5:1154–63. doi: 10.1001/jamacardio.2020.2488. Epub ahead of print. PMID: 32558876; PMCID: PMC7305567.  Back to cited text no. 2
    
3.
Madanelo M, Ferreira C, Nunes-Carneiro D, Pinto A, Rocha MA, Correia J, et al. The impact of the coronavirus disease 2019 pandemic on the utilisation of emergency urological services. BJU Int 2020;126:256-8.  Back to cited text no. 3
    
4.
Wessler BS, Kent DM, Konstam MA. Fear of Coronavirus Disease 2019-An Emerging Cardiac Risk. JAMA Cardiol. 2020;5:981-2. doi: 10.1001/jamacardio.2020.2890. PMID: 32936280.  Back to cited text no. 4
    
5.
Mahmud E, Dauerman HL, Welt FG, Messenger JC, Rao SV, Grines C, et al. Management of acute myocardial infarction during the COVID-19 pandemic: A Consensus Statement from the Society for Cardiovascular Angiography and Interventions (SCAI), the American College of Cardiology (ACC), and the American College of Emergency Physicians (ACEP). Catheter Cardiovasc Interv 2020;96:336-45.  Back to cited text no. 5
    
6.
Piccolo R, Bruzzese D, Mauro C. Population trends in rates of percutaneous coronary revascularization for acute coronary syndromes associated with the COVID-19 outbreak. Circulation 2020;141:2035-7.  Back to cited text no. 6
    
7.
Roffi M, Capodanno D, Windecker S, Baumbach A, Dudek D. Impact of the COVID-19 pandemic on interventional cardiology practice: Results of the EAPCI survey. EuroIntervention 2020;16:247-50.  Back to cited text no. 7
    
8.
Joyce E, Fabre A, Mahon N. Hydroxychloroquine cardiotoxicity presenting as a rapidly evolving biventricular cardiomyopathy: Key diagnostic features and literature review. Eur Heart J Acute Cardiovasc Care 2013;2:77-83.  Back to cited text no. 8
    
9.
Galvis V, Spinelli FR, Tello A, Sossa CL, Higuera JD, Gomez ED, et al. Hydroxychloroquine as Prophylaxis for Coronavirus SARS-CoV-2 Infection: Review of the Ongoing Clinical Trials [Hidroxicloroquina como profilaxis para la infección por coronavirus SARS-CoV-2: revisión de los ensayos clínicos en curso]. Arch Bronconeumol. 2020;56:606-8. doi:10.1016/j.arbres.2020.05.008.  Back to cited text no. 9
    
10.
Driggin E, Madhavan MV, Bikdeli B, Chuich T, Laracy J, Biondi-Zoccai G, et al. Cardiovascular considerations for patients, health care workers, and health systems during the COVID-19 pandemic. J Am Coll Cardiol 2020;75:2352-71.  Back to cited text no. 10
    
11.
Sipmann FS, Santos A, Tusman G. Heart-lung interactions in acute respiratory distress syndrome: Pathophysiology, detection and management strategies. Ann Transl Med 2018;6:27.  Back to cited text no. 11
    
12.
Jabri A, Kalra A, Kumar A, Alameh A, Adroja S, Bashir H, et al. Incidence of stress cardiomyopathy during the coronavirus disease 2019 pandemic. JAMA Netw Open 2020;3:e2014780.  Back to cited text no. 12
    



 
 
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