Sex: M
Vaccine: COVID19
Symptoms: Troponin I
Clinical narrative: Complete heart block with ventricular standstill were suspected to be secondary to administration of the Pfizer-BioNTech COVID-19 vaccine; Complete heart block with ventricular standstill were suspected to be secondary to administration of the Pfizer-BioNTech COVID-19 vaccine; lymphocytic myocarditis suspected to be secondary to administration of the Pfizer-BioNTech COVID-19 vaccine; This is a literature report for the following literature source(s).  A 57-year-old male patient received BNT162b2 (BNT162B2), as dose 3 (booster), single (Batch/Lot number: unknown) for covid-19 immunisation. The patient's relevant medical history included: "hypertension" (ongoing). Concomitant medication(s) included: VALSARTAN taken for hypertension. Vaccination history included: Covid-19 vaccine (DOSE 1; MANUFACTURER UNKNOWN), for covid-19 immunization; Covid-19 vaccine (DOSE 2; MANUFACTURER UNKNOWN), for covid-19 immunization. The following information was reported: ATRIOVENTRICULAR BLOCK COMPLETE  (hospitalization, life threatening), CARDIAC ARREST (hospitalization, life threatening), all with latency 1 day after the suspect product(s) administration, outcome "recovered" and all described as "Complete heart block with ventricular standstill were suspected to be secondary to administration of the Pfizer-BioNTech COVID-19 vaccine"; MYOCARDITIS (hospitalization, life threatening), 1 day after the suspect product(s) administration, outcome "unknown", described as "lymphocytic myocarditis suspected to be secondary to administration of the Pfizer-BioNTech COVID-19 vaccine".   Clinical course: A 57-year-old male with a past medical history of hypertension on valsartan and recent COVID-19 booster vaccination presented to the emergency department (ED) by ambulance for evaluation of syncope. The patient had received his third dose of the Pfizer-BioNtech COVID-19 vaccine the previous day. He subsequently experienced multiple syncopal events for which 911 was called. During emergency medical services transport, the patient had another syncopal episode with reported asystole on the cardiac monitor; this episode resolved spontaneously and cardiopulmonary resuscitation (CPR) was not performed. Upon arrival to the ED, the patient was awake and asymptomatic. The patient's initial vital signs were blood pressure: 113/101 mmHg; heart rate: 90 beats per minute; respiratory rate: 26 breaths per minute; peripheral oxygen saturation: 95% on room air; and temperature: 36.1 C degree. He was taken to a resuscitation bay where an ECG was obtained that showed normal sinus rhythm with extreme first degree atrioventricular (AV) block and left bundle branch block (LBBB) (Figure 1). The patient's ECG did not meet Sgarbossa criteria.8 Shortly after being attached to the cardiac monitor, the patient lost consciousness and went into complete heart block with ventricular standstill with loss of pulses (Figure 2). CPR was initiated; however, before completion of the first round of compressions the patient regained consciousness with return of spontaneous circulation and normal sinus rhythm. The decision was made to intubate the patient for airway protection. While being prepared for intubation, the patient again developed complete heart block with ventric ventricular standstill. CPR was restarted and the patient was given 1 mg of intravenous epinephrine. Given that the patient did intermittently regain consciousness, he was administered etomidate and rocuronium before successful first-pass intubation using delayed sequence intubation. Transcutaneous pacing was initiated and mechanical capture was obtained with normalization of hemodynamics. Postintubation analgosedation was managed with intravenous fentanyl as needed and a propofol infusion. Given the patient's recurrent episodes of complete heart block with ventricular standstill, the decision was made to place a transvenous pacemaker (TVP) for sustained pacing. The right internal jugular vein was cannulated under dynamic ultrasound guidance using sterile technique. Using the standard Seldinger technique, a percutaneous sheath introducer was placed. A balloon-tipped transvenous pacing catheter was floated through the sheath to 40 cm with successful electromechanical capture. TVP was programmed to VVI mode with a rate of 90 beats per minute, output of 7 mA, and sensitivity of 3.5 mV. Simultaneously, a radial arterial line was also placed for continuous monitoring of blood pressure and mechanical capture. A chest X-ray was obtained that confirmed appropriate endotracheal tube and TVP placement. The patient stayed in a paced rhythm throughout the remainder of his time in the ED. He remained hemodynamically stable while intubated and transvenously paced. He was transferred to the cardiovascular ICU (CVICU) for continued evaluation and treatment ED laboratory testing was notable for elevated initial high sensitivity troponin I of 7959 ng/L (reference: <= 59 ng/L), and mildly elevated aspartate transaminase of 67 U/L. Ultimately, the patient's high-sensitivity troponin I peaked at 14,042 ng/L 5 hours after initial presentation. His magnesium, potassium, renal function, and complete blood cell count were within normal limits. Additionally, testing for infectious etiologies including COVID-19, parvovirus, Lyme disease, influenza A/B, cytomegalovirus, enterovirus, Epstein-Barr virus, adenovirus, human immunodeficiency virus, and respiratory syncytial virus ultimately returned negative. Throughout his CVICU stay, the patient had an extensive cardiac evaluation. On the day of admission, a transthoracic echocardiogram was performed that demonstrated reduced left ventricular ejection fraction (45%-50%) and severe asymmetric left ventricular septal hypertrophy. A coronary angiogram completed that same day showed angiographically normal coronary arteries. He was started on goal-directed medical therapy. Taken together, the patient's constellation of new onset conduction abnormalities, ventricular dysfunction, and absence of ischemic disease raised concern for infiltrative versus inflammatory cardiomyopathy. Subsequent cardiac positron emission tomography scan and nuclear medicine cardiac pyrophosphate scan did not identify evidence of sarcoidosis or transthyretin amyloidosis, respectively. Cardiac magnetic resonance imaging (MRI) was more illuminating with evidence of global left ventricular inflammation and late gadolinium enhancement of the basal septum consistent with myocarditis. This diagnosis was confirmed by endomyocardial biopsy that demonstrated lymphocytic myocarditis with negative immune histochemical staining for amyloid and viral etiologies including parvovirus, adenovirus, herpes simplex virus, and cytomegalovirus. Ultimately, the patient experienced full resolution of his intermittent complete heart block by hospital day 4. An externalized temporary permanent (active fixation of lead) pacemaker was placed by cardiology on the day of admission and was maintained on VVI mode with a rate of 90 beats per minute. The patient remained 100% ventricularly paced until hospital day 2. At that time, the patient's pacemaker rate was decreased to 60 beats per minute with resumption of normal sinus rhythm with intermittent episodes of complete heart block with ventricular standstill requiring ventricular pacing. By the fourth day of hospitalization, the patient's intermittent heart block had resolved and he maintained sinus rhythm for the remainder of the admission. A repeat ECG on hospital day 6 showed normal sinus rhythm with resolution of prior LBBB and first-degree AV block (Figure 3). The patient was discharged home on hospital day 12 without need for long-term pacing. Subsequent 30-day cardiac event monitoring revealed a single 4-beat episode of ventricular tachycardia but no recurrence of heart block. Repeat outpatient cardiac MRI and transthoracic echocardiography showed normalization of left ventricular systolic function and regression of left ventricular concentric hypertrophy. ECG obtained at cardiology follow-up 2 months post discharge again demonstrated sinus rhythm, now with improved R wave progression (Figure 4). Given the temporal association of the patient's pathology with vaccination, rapid resolution of conduction abnormalities and systolic dysfunction, reduction in septal hypertrophy, and results of hospital testing otherwise negative for viral/inflammatory etiologies, the patient's lymphocytic myocarditis and complete heart block with ventricular standstill were suspected to be secondary to administration of the Pfizer-BioNTech COVID-19 vaccine.; Sender's Comments: Based on the information provided, known drug safety profile and plausible temporal association, the causality between the suspect drug and the events cannot be excluded. The impact of this report on the benefit-risk profile of the Pfizer product is evaluated as part of Pfizer procedures for safety evaluation, including the review and analysis of aggregate data for adverse events. Any safety concern identified as part of this review, as well as any appropriate action in response, will be promptly notified to regulatory authorities, ethics committees and investigators, as appropriate.