ABSTRACT
The rate of post-vaccine myocarditis is being studied from the beginning of the massive vaccination campaign against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Although a direct cause-effect relationship has been described, in most cases, the vaccine pathophysiological role is doubtful. Moreover, it is not quite as clear as having had a previous myocarditis could be a risk factor for a post-vaccine disease relapse. A 27-year-old man presented to the emergency department for palpitations and pericardial chest pain radiated to the upper left limb, on the 4th day after the third dose of BNT162b2 vaccine. He experienced a previous myocarditis 3 years before, with full recovery and no other comorbidities. Electrocardiogram showed normal atrioventricular conduction, incomplete right bundle branch block, and diffuse ST-segment elevation. A cardiac echo showed lateral wall hypokinesis with preserved ejection fraction. Troponin-T was elevated (160 ng/L), chest X-ray was normal, and the SARS-CoV-2 molecular buffer was negative. High-dose anti-inflammatory therapy with ibuprofen and colchicine was started; in the 3rd day high-sensitivity Troponin I reached a peak of 23000 ng/L. No heart failure or arrhythmias were observed. A cardiac magnetic resonance was performed showing normal biventricular systolic function and abnormal tissue characterization suggestive for acute non-ischaemic myocardial injury (increased native T1 and T2 values, increased signal intensity at T2-weighted images and late gadolinium enhancement, all findings with matched subepicardial distribution) at the level of mid to apical septal, anterior, and anterolateral walls. A left ventricular electroanatomic voltage mapping was negative (both unipolar and bipolar), while the endomyocardial biopsy showed a picture consistent with active myocarditis. The patient was discharged in good clinical condition, on bisoprolol 1.25 mg, ramipril 2.5 mg, ibuprofen 600 mg three times a day, colchicine 0.5 mg twice a day. We presented the case of a young man with history of previous myocarditis, admitted with a non-complicated acute myopericarditis relapse occurred 4 days after SARS-CoV-2 vaccination (3rd dose). Despite the observed very low incidence of cardiac complications following BNT162b2 administration, and the lack of a clear proof of a direct cause-effect relationship, we think that in our patient this link can be more than likely. In the probable need for additional SARS-CoV-2 vaccine doses in the next future, studies addressing the risk-benefit balance of this subset of patient are warranted. We described a multidisciplinary management of a case of myocarditis recurrence after the third dose of SARS-CoV-2 BNT162b2 vaccine.
ABSTRACT
Introduction: Takayasu's arteritis (TA) is a systemic inflammatory disease that affects aorta and its major branches. There are several cardiac manifestations of TA and an association with Takotsubo syndrome (TTS) - but not coronary vasospasm - has been previously reported. The role of emotional stress in this context is unknown. Case presentation: A 58-year-old Caucasian female elementary school teacher, with a history of generalized anxiety disorder (GAD), severe asymptomatic aortic regurgitation (AR), and TA in remission under corticosteroids, was admitted in the emergency department with worsening chest pain and dyspnea, initiated after a period of intense emotional stress (increased workload during COVID-19 pandemic). Physical examination revealed signs of heart failure (HF) with hemodynamic stability and an early diastolic heart murmur. The electrocardiogram showed sinus tachycardia, T wave inversion in left precordial and lateral leads, and a corrected QT of 487 ms. Laboratorial evaluation presented high values of high-sensitivity troponin I (3494 ng/L) and B-type natriuretic peptide (4759 pg/mL). The transthoracic echocardiogram revealed severe dilation of left ventricle (LV) with moderate systolic dysfunction, due to apical and midventricular akinesia, and severe AR. The coronary angiography showed normal coronary arteries. An acetylcholine provocative test induced spasm of both the left anterior descending and circumflex arteries, accompanied by chest pain and ST depression, completely reverted after intracoronary nitrates administration. The patient was switched to diltiazem and a drug multitherapy for HF was started. A cardiac magnetic resonance revealed severe dilation of the LV, mild apical hypokinesia, improvement of ejection fraction to 53%, signs of myocardial edema and increased extracellular volume in apical and mid-ventricular anterior and anterolateral walls, and absence of myocardial late gadolinium enhancement, compatible with TTS. At discharge, the patient was clinically stable, without signs of HF, and a progressive reduction of troponin and BNP levels was observed. A final diagnosis of TTS and coronary vasospasm in a patient with GAD and TA was done. Discussion: We present the first case of acute HF showing coexistence of TA, TTS and coronary vasospasm. TA is a rare inflammatory disease that can be associated with TTS and coronary vasospasm. Besides that, coronary vasospasm may also be involved in TTS pathophysiology, suggesting a complex interplay between these diseases. Mood disorders and anxiety influence the response to stress, through a gain of the hypothalamic-pituitary-adrenal axis and an increased cardiovascular system sensitivity to catecholamines. Therefore, although the mechanisms behind these three pathologies are not yet fully studied, this case supports the role of inflammatory and psychiatric diseases in TTS and coronary vasospasm.