Sindromul Morgagni-Adams-Stoks indus medicamentos, caz clinic

Abstract

Introducere. Sindromul Morgagni-Adams-Stokes (SMAS), denumit „sincopă cardiacă”, depistat electrocardiografic (ECG) prin bloc atrioventricular paroxistic (BAV), cauzat de boli ale sistemului de conducere sau administrării medicamentelor antiaritmice este diagnosticat la 40% dintre pacienții cu debut recent de BAV. Scopul lucrării. Prezentăm cazul clinic a pacientului cu cardiopatie ischemică (CPI), hipertensiune arterială (HTA) și fibrilație atrială (FA) persistentă la care administrarea incorectă a metoprololului a condus la dezvoltarea SMAS. Material și metode. Bărbat, 64 ani internat cu dureri retrosternale constrictive, cefalee și sincope frecvente. Din anamnestic: hipertensiv de 15 ani, cu angină pectorală (AP) de 8 ani, FA de 1 an. Am efectuat: ECG, ECOCG, radiografia toracelui, ultrasonografia abdominală, marcherii injuriei miocitare, analize hematologice, biochimice, imunologice și consultația neurologului. Rezultate. Acuze: cefalee, dureri retrosternale, periodic stări sincopale. Obiectiv: hiperemia feței, zgomotele cardiace aritmice cu FCC 78 b/min, TA - 181/88 mmHg. Paraclinic: Ureea 13,7 mmol/l; Creatinina 121,2 mmol/l; Glucoza 6,3 mmol/l; Protrombina 114%, Fibrinogen 4,3 g/l; INR 0,95; K 5,44 mmol/l, Na 147,7 mmol/l. ECG: Ritm: Flutter atrial bradisistolic, FCC (25-75 b/min), cu conducere 3:1 11:1. AEC deviată extrem spre stânga. EcoCG: Dilatarea moderată a AS, AD, VD. Hipertrofie ușoara concentrică a m-lui VS. FE - 56%. Insuficiența VM gr.II, VTs gr.II. Afectarea funcției diastolice a VS. Consultația neurologului: BCVC. Microangioencefalopatie de origine mixtă gr. II. Sindrom pseudobulbar ușor exprimat. Tratament după protocol. Concluzii. Pacientul cu FA, pe fond de supradozaj de betablocante, dezvoltă SMAS extrinsec. Evaluat suplimentar prin Holter ECG, tratament conservativ fără efect, a necesitat implantare de electrocardiostimulator.

Introduction: Morgagni-Adams-Stokes syndrome (MASS), also known as „cardiac syncope,” diagnosed by paroxysmal atrioventricular block (AVB) detected on electrocardiogram (ECG), caused by disorders of the conductibility system or the administration of antiarrhythmic drugs is diagnosed in 40% of patients with recent onset of AVB. Aim of the study. Clinical case presentation of a patient with ischemic heart disease (IHD), hypertension (HTN), and persistent atrial fibrillation (AF), in whom incorrect administration of metoprolol led to the development of MASS. Materials and Methods: A 64-year-old man was admitted with constrictive retrosternal pain, headache, and syncope. Patient with HTN for 15 years, angina pectoris (AP) for 8 years, and AF for 1 year. The following examinations were performed: ECG, Eco-CS, chest X-ray, abdominal ultrasound, myocardial injury markers, hematological, biochemical and immunological analyses, neurological consultation. Results. Objective findings: facial flushing, arrhythmic heart sounds, heart rate 78 b/min, blood pressure 181/88 mmHg. Paraclinical Results. urea 13.7 mmol/L, creatinine 121.2 mmol/L, glucose 6.3 mmol/L, prothrombin 114%, fibrinogen 4.3 g/L, INR 0.95, potassium 5.44 mmol/L, sodium 147.7 mmol/L. ECG: atrial flutter with bradysystolic rhythm (25-75 b/min) and 3:1 11:1 conduction, EAH extremely deviated to the left. EcoCG: Moderate dilation of the LA, RA, and RV. Mild concentric hypertrophy of the IVS, with an EF 56%. II degree MV and TV regurgitation. LV diastolic function impairment. The neurological consultation revealed chronic cerebrovascular disease and mild expression of pseudobulbar syndrome. Conclusions. The patient with AF, due to beta-blocker overdose, developed extrinsic MASS. Further evaluation was performed through Holter-ECG monitoring. Conservative treatment yielded no results. The patient required pacemaker implantation.