Clinical meaning
Brugada Syndrome involves specific alterations in brugada syndrome physiology. The pathophysiology of Brugada Syndrome encompasses changes in myocardial contractility, cardiac conduction, vascular resistance, endothelial function, or structural integrity depending on the primary mechanism involved. Key cellular processes include ion channel dysfunction, inflammatory mediator activation, oxidative stress, fibrotic remodeling, and neurohormonal dysregulation that drive the clinical manifestations of brugada syndrome.
Diagnosis & workup
Diagnostics & workup: - BNP >100 pg/mL or NT-proBNP >300 pg/mL for volume overload assessment - Coagulation studies: PT/INR, aPTT, D-dimer - Cardiac catheterization: coronary anatomy, hemodynamic measurements - Holter or event monitor for intermittent arrhythmia detection - CRP and ESR for inflammatory/infectious cardiac conditions - Thyroid function tests (hyperthyroidism causes high-output states) - Chest X-ray: cardiac silhouette, pulmonary vascularity, effusions
Risk factors: - Diabetes mellitus type 2 with HbA1c >7% - Heavy alcohol use (>14 drinks/week males, >7 females) - Obstructive sleep apnea (AHI >15 events/hr) - Prior stroke or TIA with residual neurological deficit - Left ventricular hypertrophy on ECG or echo - Cocaine or amphetamine use causing coronary vasospasm - Chronic inflammatory conditions (RA, SLE, psoriasis)