COVID-19-Induced Complete Heart Block: Case Series and Literature Review

Bassi, Raghav; Ismail, Zeeshan; Salabei, Joshua K.; Charles, Kipson; Haider, Asad A; Hussein, Abdullahi; Smock, Andrew

doi:10.7759/cureus.37517

Cited by 2 publications

(2 citation statements)

References 20 publications

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“…Beinart et al [10] noted CHB following influenza A infection in a patient with global cardiac enhancement in cardiac imaging, suggesting underlying myocardial involvement. Such presentation has been observed to a greater extent among severe COVID-19 cases [17].…”

Section: Discussionmentioning

confidence: 88%

Permanent Complete Heart Block: A Rare Complication of Influenza Infection

Badheeb,

Zarich,

Fara

et al. 2023

Cureus

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The cardiovascular complications of viral illnesses are often underestimated in clinical practice. The influenza virus, one of the most prevalent viral infections, has been associated with a wide spectrum of arrhythmias that are typically transient and self-resolving. We present the case of a 60-year-old female with no prior cardiac comorbidities who developed a complete heart block after an influenza infection. She presented to the clinic with flu-like symptoms and was found to have a complete heart block with a junctional escape rhythm. Polymerase chain reaction testing subsequently confirmed an influenza A infection. She was initially placed on a temporary pacemaker. However, a permanent dual-chamber pacemaker was implanted as bradycardia persisted. Later follow-ups in the cardiology clinic showed that the patient remained dependent on the pacemaker. While there are a few descriptions of influenza-induced transient atrioventricular block, cases of influenza-induced permanent complete heart block are extremely rare, particularly in the absence of severe myocardial inflammation.

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Section: Discussionmentioning

confidence: 88%

Permanent Complete Heart Block: A Rare Complication of Influenza Infection

Badheeb,

Zarich,

Fara

et al. 2023

Cureus

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“…This view has given way to the consensus that viral RNA may be present (13), but little direct myocardial infection occurs (21)(22)(23)(24). Nevertheless, evidence of cardiac inflammation is widely reported (15)(16)(17)(18)(19), supporting the systemic cytokine storm as a possible mechanism (19,(78)(79)(80). Consistent with many human studies, we found no evidence of viral protein expression in hearts of hamsters after nasal infection with SARS-CoV-2, which differs from a previous study reporting ~10-15% of myocytes with positive antibody signals for viral spike or N protein (81).…”

Section: Cardiac Innate Immune Responses Underlie Cardiac Arrhythmiasmentioning

confidence: 99%

Innate Immune Activation and Mitochondrial ROS Invoke Persistent Cardiac Conduction System Dysfunction after COVID-19

Ashok,

Liu,

Criscione

et al. 2024

Preprint

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BackgroundCardiac risk rises during acute SARS-CoV-2 infection and in long COVID syndrome in humans, but the mechanisms behind COVID-19-linked arrhythmias are unknown. This study explores the acute and long term effects of SARS-CoV-2 on the cardiac conduction system (CCS) in a hamster model of COVID-19.MethodsRadiotelemetry in conscious animals was used to non-invasively record electrocardiograms and subpleural pressures after intranasal SARS-CoV-2 infection. Cardiac cytokines, interferon-stimulated gene expression, and macrophage infiltration of the CCS, were assessed at 4 days and 4 weeks post-infection. A double-stranded RNA mimetic, polyinosinic:polycytidylic acid (PIC), was used in vivo and in vitro to activate viral pattern recognition receptors in the absence of SARS-CoV-2 infection.ResultsCOVID-19 induced pronounced tachypnea and severe cardiac conduction system (CCS) dysfunction, spanning from bradycardia to persistent atrioventricular block, although no viral protein expression was detected in the heart. Arrhythmias developed rapidly, partially reversed, and then redeveloped after the pulmonary infection was resolved, indicating persistent CCS injury. Increased cardiac cytokines, interferon-stimulated gene expression, and macrophage remodeling in the CCS accompanied the electrophysiological abnormalities. Interestingly, the arrhythmia phenotype was reproduced by cardiac injection of PIC in the absence of virus, indicating that innate immune activation was sufficient to drive the response. PIC also strongly induced cytokine secretion and robust interferon signaling in hearts, human iPSC-derived cardiomyocytes (hiPSC-CMs), and engineered heart tissues, accompanied by alterations in electrical and Ca2+handling properties. Importantly, the pulmonary and cardiac effects of COVID-19 were blunted by in vivo inhibition of JAK/STAT signaling or by a mitochondrially-targeted antioxidant.ConclusionsThe findings indicate that long term dysfunction and immune cell remodeling of the CCS is induced by COVID-19, arising indirectly from oxidative stress and excessive activation of cardiac innate immune responses during infection, with implications for long COVID Syndrome.

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COVID-19-Induced Complete Heart Block: Case Series and Literature Review

Cited by 2 publications

References 20 publications

Permanent Complete Heart Block: A Rare Complication of Influenza Infection

Permanent Complete Heart Block: A Rare Complication of Influenza Infection

Innate Immune Activation and Mitochondrial ROS Invoke Persistent Cardiac Conduction System Dysfunction after COVID-19

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