Syncope as the only symptom of SARS-CoV-2 infection / Syncope mint a SARS-CoV-2-fertozés egyedüli tünete

Összefoglaló. Egy 61 éves, SARS-CoV-2-fertozött, traumás syncopés nobeteg rosszullétének hátterében orthostaticus hypotonia igazolódott. A vírusfertozés megszunése után az orthostaticus hypotonia megszunt, de a posturalis tachycardia fennmaradt. A syncopénak egyéb okát kimutatni nem tudtuk. A SARS-CoV-2-fertozésnek egyéb tünete, illetve szervi manifesztációja nem volt. Tudomásunk szerint ez az elso eset, amelyben a SARS-CoV-2-infekció egyedüli tünete a syncope. Orv Hetil. 2021; 162(7): 243-245. Summary. Orthostatic hypotension was demonstrated in the background of malaise in a 61-year-old SARS-CoV-2 infected female traumatic syncope. After cessation of the virus infection, orthostatic hypotension resolved, but postural tachycardia persisted. No other cause of syncope could be detected. There were no other symptoms or organ manifestations of SARS-CoC-2 infection. To our knowledge, this is the first case where the only symptom of SARS-CoV-2 virus infection is syncope. Orv Hetil. 2021; 162(7): 243-245.

Syncope at SARS-CoV-2 onset.

We describe clinical and laboratory findings in 35 patients tested positive for SARS-CoV-2 by reverse transcriptase-polymerase chain reaction on nasopharyngeal swab experiencing one or multiple syncope at disease onset. Clinical neurologic and cardiologic examination, and electrocardiographic findings were normal. Chest computed tomography showed findings consistent with interstitial pneumonia. Arterial blood gas analysis showed low pO2, pCO2, and ratio of arterial oxygen partial pressure to fractional inspired oxygen (PaO2/FiO2) indicating hypocapnic hypoxemia. Patients who presented with syncope showed significantly lower heart rate as compared to 68 SARS-CoV-2 positive that did not. Such poorer than expected compensatory heart rate increase may have led to syncope based on individual susceptibility. We speculate that SARS-CoV-2 could have caused angiotensin-converting enzyme-2 (ACE2) receptor internalization in the nucleus of the solitary tract and other midbrain nuclei, impairing baroreflex and chemoreceptor response, and inhibiting the compensatory tachycardia during acute hypocapnic hypoxemia.

Syncope and presyncope in patients with COVID-19.

INTRODUCTION: Recent studies have described several cardiovascular manifestations of COVID-19 including myocardial ischemia, myocarditis, thromboembolism, and malignant arrhythmias. However, to our knowledge, syncope in COVID-19 patients has not been systematically evaluated. We sought to characterize syncope and/or presyncope in COVID-19. METHODS: This is a retrospective analysis of consecutive patients hospitalized with laboratory-confirmed COVID-19 with either syncope or presyncope. This "study" group (n = 37) was compared with an age and gender-matched cohort of patients without syncope ("control") (n = 40). Syncope was attributed to various categories. We compared telemetry data, treatments received, and clinical outcomes between the two groups. RESULTS: Among 1000 COVID-19 patients admitted to the Mount Sinai Hospital, the incidence of syncope/presyncope was 3.7%. The median age of the entire cohort was 69 years (range 26-89+ years) and 55% were men. Major comorbidities included hypertension, diabetes, and coronary artery disease. Syncopal episodes were categorized as (a) unspecified in 59.4% patients, (b) neurocardiogenic in 15.6% patients, (c) hypotensive in 12.5% patients, and (d) cardiopulmonary in 3.1% patients with fall versus syncope and seizure versus syncope in 2 of 32 (6.3%) and 1 of 33 (3.1%) patients, respectively. Compared with the "control" group, there were no significant differences in both admission and peak blood levels of d-dimer, troponin-I, and CRP in the "study" group. Additionally, there were no differences in arrhythmias or death between both groups. CONCLUSIONS: Syncope/presyncope in patients hospitalized with COVID-19 is uncommon and is infrequently associated with a cardiac etiology or associated with adverse outcomes compared to those who do not present with these symptoms.

SARS-CoV-2 infection associated with micturition syncope: Our experience with 4 case reports.

RATIONALE: Syncope is described as the loss of consciousness and postural muscle tone with a short duration and fast onset. Micturition syncope can be caused by abnormal vasovagal response or by the dysfunction of the blood pressure regulating mechanism, which occurs before, during, or immediately after urination. PATIENT CONCERNS: We present 4 cases of COVID-19 hospitalized in the Department of Infectious Diseases of the Academic Emergency Hospital Sibiu, Romania, cases that presented micturition syncope. DIAGNOSES: During hospitalization, patients confirmed with SARS-Cov-2 infection using real time reverse transcriptase-polymerase chain reaction (RT-PCR) assay, presented micturition syncope in different stages of the infection (at the beginning and in the second week of evolution). INTERVENTIONS: Other causes of syncope such as adrenal insufficiency secondary to corticosteroids treatment, cardiac rhythm disorders, neurological impairment, dehydration, vasoactive medication, malignancies, pulmonary hypertension and coughing were excluded. The treatment of SARS-CoV-2 infection was performed following the local and national guidelines. OUTCOMES: The clinical course of all 4 patients diagnosed with COVID-19 and micturition syncope was favorable. To our knowledge, micturition syncope in COVID-19 patients has yet not been reported by other authors. LESSONS: To our knowledge, micturition syncope associated with the evolution of COVID-19, has yet not been reported by other authors.

Acute right ventricular myocarditis presenting with chest pain and syncope.

Myocarditis is assumed to involve both ventricles equally. Right ventricular predominant involvement is rarely described. A case of acute viral right ventricular myocarditis presenting with chest pain and syncope, grade 3 atrioventricular block, right ventricular dilatation and free wall hypokinesia is reported. Cardiac MRI showed late enhancement of the right ventricular free wall without involvement of the left ventricle. Anti-Coxsackie A9 virus neutralising IgM-type antibodies titre was elevated. This case emphasises that manifestations of myocarditis can be limited to the right ventricle and should be considered in the differential diagnosis of right ventricular enlargement.

HIV and Long QT syndrome--cause or coincidence.

The Long QT syndrome is a disorder characterized by abnormalities of cardiac repolarisation, resulting in a propensity to polymorphic ventricular tachycardia (torsades de pointes) and sudden cardiac death. It remains unclear whether cardiac involvement with the HIV virus itself can cause QT prolongation. We report a case of a HIV infected young female presenting with recurrent syncope due to torsades de pointes.

[Syncope in 3rd degree atrioventricular block. Detection of virus genome in the myocardium]. / Synkope bei AV-Block III(o). Nachweis von Virusgenom im Myokard.

HISTORY AND CLINICAL FINDINGS: A 28-year-old woman was admitted after syncope which had been preceded by several flulike episodes. There was no history of any other serious disease. Physical examination was unremarkable. Heart sounds were regular and normal, there were no murmurs. INVESTIGATIONS: White cell count was 9400/microliter, with a normal differential count. Erythrocyte sedimentation rate and C-reactive protein were also normal. Virus serology revealed no abnormality. The electrocardiogram (ECG) showed complete (third degree) atrioventricular (AV) block with an idioventricular rhythm of 38 beats/min and right bundle branch block pattern. TREATMENT AND COURSE: A temporary transvenous pacemaker was inserted on the first hospital day. As myocarditis was suspected a right ventricular endomyocardial biopsy was obtained. Histological and immunohistological examinations demonstrated no unequivocal findings. But molecular-biological tests revealed. Coxsackie-B3 virus genome. The pacemaker was removed on the 6th day, when the ECG had shown intermittent second degree AV block. Regular sinus rhythm with a PR interval of 0.18 s was recorded on day 12, and 24-hour ECG monitoring for several days until her discharge on the 18th day confirmed this rhythm throughout. CONCLUSION: In aetiologically undetermined disease molecular-biological techniques can be indispensable for the exact diagnosis and may be decisive for administering specific treatment.