Discussion
ICD shock negatively affects patients’ quality of life, causes adverse
outcomes, is associated with higher mortality rates,9and is the most critical cause of rehospitalization in patients with
ICDs. This study revealed a significant increase in hospitalizations due
to ICD shock during the peak period of SARS-CoV-2 infection compared
with the rates in the same period in the past, suggesting a possible
correlation between SARS-CoV-2 infection and ICD shock. Therefore, it is
essential to understand the causes of ICD shock in patients with ICDs
following SARS-CoV-2 infection to provide targeted treatment and prevent
adverse events upon admission.
With the increase in the number of SARS-CoV-2-infected patients and the
accumulation of clinical data, the development of significant
cardiovascular complications after infection has become more
apparent.3,14–19 The current view is that SARS-CoV-2
infection triggers a range of cardiovascular manifestations through
multiple mechanisms.16,20–24 However, owing to the
lack of related reports, the mechanism through which patients with ICDs
become more susceptible to shocks following SARS-CoV-2 infection remains
unknown. A previous multicenter study reported a significant increase in
ICD shock among those with such devices during the COVID-19 outbreak in
the United States.12 Two other single-center studies
reported no increase in ventricular arrhythmic events, although deaths
were observed in patients with ICDs during the peak of the pandemic in
Italy in 2020.25,26 However, these studies evaluated
ICD shocks using continuous remote monitoring systems and did not
determine whether patients experiencing them were infected with
SARS-CoV-2; therefore, the correlation between ICD shock and SARS-CoV-2
infection requires further investigation.
In this study, we analyzed data from seven patients who were admitted to
our hospital for ventricular arrhythmias or ICD shocks within 3–20 days
after SARS-CoV-2 infection. We analyzed their program and clinical data
and observed that they shared specific characteristics that may have
driven the development of ventricular arrhythmias or ICD shocks after
SARS-CoV-2 infection. Most patients exhibited elevated troponin levels,
suggesting the development of myocardial damage post-infection, which
has been suggested to be a cause of ICD-induced
shocks.14,27 A higher incidence of malignant
ventricular arrhythmias has been reported in patients with severe left
ventricular dysfunction and coronary artery
disease.28,29 Among these seven patients, six were
implanted with ICDs or CRT-Ds for ischemic cardiomyopathy and were prone
to malignant arrhythmias. SARS-CoV-2 infection can disrupt the oxygen
supply equilibrium and cause a cytokine storm, further damaging
cardiomyocytes, and the development of malignant arrhythmias increases
the likelihood of ICD shock. In addition, SARS-CoV-2 can directly damage
cardiomyocytes by downregulating angiotensin-converting enzyme 2 (ACE2)
receptors and interfering with ACE2-associated signaling
pathways.30 It should be noted that these six patients
had not experienced sustained VT or recurrent ICD shocks prior to
infection, suggesting that SARS-CoV-2 infection may play a role in ICD
shock as a potential arrhythmia trigger.
Decreased potassium and calcium concentrations may represent another
mechanism underlying ICD shock development after SARS-CoV-2 infection.
Most of the patients developed electrolyte imbalances post-infection,
mainly in the form of reduced potassium and calcium ion levels, possibly
due to a fever-induced increase in sweating post-infection, or
insufficient potassium and calcium ion intake due to decreased appetite.
Decreased calcium ion concentrations can induce arrhythmias by affecting
ion channel functions and the difference in potential between the
interior and exterior of myocardial cells.31Clinically, hypokalemia is a common cause of arrhythmogenesis, and
severe hypokalemia can lead to life-threatening ventricular arrhythmias.
In addition, hypokalemia and hypocalcemia can prolong the QT interval,
inducing the development of malignant arrhythmias. In this study, six
patients exhibited QT interval prolongation (> 440 ms)
(mean QT interval: 460 ± 46 ms; range: 386–536 ms). All patients
exhibited varying degrees of HF symptom exacerbation after SARS-CoV-2
infection, and NT-proBNP levels significantly exceeded the normal range
upon admission. We speculate that the exacerbation of HF due to
SARS-CoV-2 infection may be another important factor leading to ICD
shock. The current view is that an acute increase in cardiac load can
cause cardiomyocyte stretching, altering myocardial electrical activity
and leading to the development of various types of
arrhythmias.32 We believe that myocardial injury and
electrolyte imbalances caused by infection are the leading causes of HF
exacerbation in these patients. Furthermore, most patients did not
continue to take their anti-HF medications regularly after the
infection, out of concern for Safety, which may be another cause of the
acute exacerbation of HF in these patients.
Previous studies have shown that secondary prevention and ICD
implantation are risk factors for the development of malignant
arrhythmias.33 However, the total number of shocks
administered was significantly higher in the patients who received ICDs
for primary prevention than in those who received them for secondary
prevention (68 vs. 12, respectively). This suggests that SARS-CoV-2
infection plays a dominant role in the induction of ICD shock. AF is a
predictor of inappropriate shocks,34,35 and patients
with SARS-CoV-2 infection are more susceptible to AF during the acute
and late recovery phases.36,37 It can be hypothesized
that SARS-CoV-2 infection increases the AF load, serving as another
possible factor contributing to inappropriate shocks in these patients.
Three of the seven patients in this study experienced ventricular
electrical storms post-infection, and these patients did not experience
the reoccurrence of arrhythmias following the administration of
antiarrhythmic drugs and the removal of the triggers. We suggest that
SARS-CoV-2 infection can cause malignant arrhythmias through various
mechanisms such as myocardial damage, electrolyte disturbances, QT
interval prolongation, HF aggravation, and AF induction of AF; most of
these malignant arrhythmias can be terminated by ICD shock, preventing
mortality and demonstrating the value of ICDs in preventing SCD.
Simultaneously, because ICD shock is associated with higher
mortality,9 the frequency of programmed follow-up
should be increased during the COVID-19 pandemic. Post-infection,
follow-up of patients can be conducted by telephone for timely clinical
evaluation and guidance on medications. If necessary, patients should be
admitted to the hospital as early as possible to eliminate the triggers
of arrhythmia and minimize the likelihood of ICD shock. In the present
study, none of the patients experienced further ICD shock after the
removal of the aforementioned triggers.
It is important to note, however, that this study included only seven
patients; therefore, more extensive clinical studies are needed to
confirm these findings.