On December 31, 2019, several cases of pneumonia-like illness were attributed to a seafood wholesale market in the Wuhan province of China.1 On January 7, 2020, public health officials in China confirmed that these cases were caused by the novel severe acute respiratory syndrome coronavirus 2, SARS-CoV-2, also referred to as COVID-19.2
Recent epidemiologic data has indicated coronavirus to be highly contagious with a high risk of person-to-person transmission.3,4 On March 11, 2020, the World Health Organization (WHO) declared COVID-19 a global pandemic. As of July 1, 2020, there have been a total of 10,512,383 cases and 512,330 deaths reported in at least 215 countries; in addition, 2,751,043 of these cases and 130,390 of these deaths have been reported in the United States.5
Age, male sex, and comorbidity seem to be risk factors for poor outcomes in COVID-19 patients. Despite a low overall case fatality rate of 2.3%, mortality rates among COVID-19 cases are higher among the elderly (14.8% in patients over 80 years) and among patients with cardiovascular disease, hypertension, and diabetes (10.5%, 6.0%, and 7.3%, respectively).6 The most common symptoms associated with COVID-19 are fever (88%) and dry cough (67.7%); less common symptoms include rhinorrhea (4.8%) and gastrointestinal symptoms such as diarrhea (4-14%) and nausea (5%).7 In 14% of patients, severe symptoms occur such as shortness of breath, hypoxia, and respiratory distress. Five percent of patients are critical and require mechanical ventilation in an intensive care unit with clinical presentation of respiratory failure, septic shock, and/or multiorgan failure.8
Radiological investigations including chest x-ray and a CT scan of the chest are characterized by findings of bilateral ground glass interstitial infiltrates indicative of atypical pneumonia. Laboratory workup often shows leukopenia and thrombocytopenia. There can be associated transaminitis as well as elevated ESR, ferritin, LDH, and d-dimer. Complications include acute respiratory distress syndrome (ARDS), acute cardiac injury, and secondary infections.9
With the increasing number of confirmed cases and accumulating clinical data, the cardiac manifestations induced by COVID-19 have generated great concern. A recent study of 138 patients hospitalized with COVID-19 infection showed 16.7% and 7.2% patients later developed arrhythmia and acute cardiac injury, respectively.10 In a separate study, 12.5% of patients with COVID-19 had evidence of myocardial injury with abnormalities similar to myocarditis.9 COVID-19 has also been associated with cardiac arrest, acute-onset heart failure, and acute congestive heart failure. COVID-19 has not been reported as the cause of abnormalities of the cardiac conduction system.
In this article, we present a case that describes the presence of high-grade atrioventricular (AV block) requiring pacemaker support in a patient with COVID-19.
A 77-year-old male with a past medical history of hypertension, vascular dementia, hyperlipidemia, peripheral neuropathy, major depressive disorder, and first-degree AV block was brought from the nursing home to the hospital for bradycardia with a heart rate (HR) of 32 BPM. Per records, the patient sustained a fall at the nursing home two days prior to hospital admission. The patient had no prior history of falls or bradycardia, and no history of taking any medication known to cause AV conduction delay. Physical exam was noted for bradycardia and clear bilateral breath sounds, and the neurological exam showed the patient was alert and oriented to self only. Initial EKG was noted for third-degree AV block with junctional escape rhythm, right bundle branch block with left anterior fascicular block, and HR of 30 BM (Figure 1). Chest x-ray was noted for some bilateral airspace opacities (Figure 2). Initial troponin was 0.018 ng/mL. BUN was 30 mg/dL, and creatinine was 1.42 mg/dL. BNP was 892 pg/mL. Atropine was given, which transiently increased the HR to 50 BPM and then dropped to the high 20s.
Cardiology evaluated the patient, who was later taken to the cardiac catheterization lab for an emergent temporary transvenous pacemaker. It is important to note that we have been testing for COVID-19 in all patients coming to the ER, and we have been treating these patients as COVID-19 positive until proven otherwise. This patient had no typical symptoms of COVID-19 except for atypical third-degree heart block. COVID-19 was discovered after the pacemaker placement test result (ordered in the ER) came back positive.
Full personal protective equipment (PPE) was used during the procedure. The patient was placed in isolation (droplet precautions) and subsequently underwent elective permanent pacemaker implantation. He did well post-operatively and was discharged home the next day in a stable condition.
COVID-19 is a global pandemic evolving in real time. Our knowledge of the novel coronavirus and its cardiovascular manifestations is limited and evolving on a daily basis. Thus far, cardiovascular complications have been commonly found in patients with COVID-19, and such patients are at a higher risk of morbidity and mortality. Acute myocardial injury is present in more than 12% of critically ill COVID-19 patients, and acute heart failure can develop as the illness severity intensifies. In this case, we describe a patient without a history of cardiovascular disease who was admitted to the hospital with third-degree heart block and tested positive for COVID-19. Although the exact pathophysiological mechanism underlying the cardiac electrical conduction system is not fully understood, a previous study showed that SARS-CoV-2 viral RNA was detected in the hearts of 35% of patients with SARS-CoV infection.11 This raises the possibility of direct damage of cardiac conduction system and cardiomyocytes by the coronavirus.11 One potential mechanism is angiotensin-converting enzyme 2 (ACE2); coronavirus appears to be affecting cells that express the ACE2 protein, including myocardial and vascular cells.11 Other suggested mechanisms include a cytokine storm, mediated by abnormal T helper cells and hypoxia-induced high intracellular calcium resulting in cardiac myocyte apoptosis. Novel coronavirus is an important differential to consider in patients presenting with symptomatic bradycardia who are diagnosed with AV conduction abnormalities.
Disclosures: The authors have no conflicts of interest to report regarding the content herein.
- Pneumonia of unknown cause — China. World Health Organization. Published January 5, 2020. Available at https://www.who.int/csr/don/05-january-2020-pneumonia-of-unkown-cause-china/en/. Accessed May 4, 2020.
- Novel coronavirus — China. World Health Organization. Published January 12, 2020. Available at https://www.who.int/csr/don/12-january-2020-novel-coronavirus-china/en/. Accessed May 4, 2020.
- Chan JF, Yuan S, Kok KH, et al. A familial cluster of pneumonia associated with the 2019 novel coronavirus indicating person-to-person transmission: a study of a family cluster. Lancet. 2020;395(10223):514-523.
- Phan LT, Nguyen TV, Luong QC, et al. Importation and human-to-human transmission of a novel coronavirus in Vietnam. N Engl J Med. 2020;382:872-874.
- COVID-19 dashboard by the Center for Systems Science and Engineering (CSSE) Johns Hopkins University (JHU). Available at https://gisanddata.maps.arcgis.com/apps/opsdashboard/index.html#/bda7594740fd40299423467b48e9ecf6. Accessed May 4, 2020.
- Novel Coronavirus Pneumonia Emergency Response Epidemiology Team. [The epidemiological characteristics of an outbreak of 2019 novel coronavirus disease (COVID-19)]. Zhonghua Liu Xing Bing Xue Za Zhi. 2020;41(2):45-151. doi: 10.3760/cma.j.issn.0254-6450.2020.02.003
- Report of the WHO-China Joint Mission on Coronavirus Disease 2019 (COVID-19). World Health Organization. Published February 28, 2020. Available at https://www.who.int/publications-detail/report-of-the-who-china-joint-mission-on-coronavirus-disease-2019-(covid-19). Accessed May 4, 2020.
- Zhang H, Penninger JM, Li Y, Zhong N, Slutsky AS. Angiotensin-converting enzyme 2 (ACE2) as a SARS-CoV-2 receptor: molecular mechanisms and potential therapeutic target. Intensive Care Med. 2020;46(4):586-590.
- Deng Q, Hu B, Zhang Y, Wang H, Zhou X, Hu W, Cheng Y, Yan J, Ping H, Zhou Q. Suspected myocardial injury in patients with COVID-19: Evidence from front-line clinical observation in Wuhan, China. Int J Cardiol. 2020 Apr 8.
- Wang D, Hu B, Hu C, et al. Clinical characteristics of 138 hospitalized patients with 2019 novel coronavirus-infected pneumonia in Wuhan, China. JAMA. 2020 Feb 7. [Epub ahead of print]
- Oudit GY, Kassir Z, Jiang C, et al. SARS-coronavirus modulation of myocardial ACE2 expression and inflammation in patients with SARS. Eur J Clin Invest. 2009;39(7):618-625. doi: 10.1111/j.1365-2362.2009.02153