ABSTRACT
RESUMEN La disfunción del nódulo sinusal (DNS) es generalmente secundaria a la senescencia del nodo sinusal y del miocardio auricular circundante. Estamos presentando un paciente de 59 años de edad, hipertenso sin tratamiento y con antecedente de síncope en dos oportunidades en los últimos 4 meses. Ingresa debido a un flutter auricular con conducción auriculoventricular 1:1 con una frecuencia cardiaca de 280 lat/min que cede con goteo de amiodarona. Un Holter de 24 horas demostró un ritmo sinusal predominante, episodios paroxísticos de fibrilación auricular con respuesta ventricular alta, bradicardia sinusal de 47 lat/min. Se realizó el diagnóstico de disfunción del nódulo sinusal, Rubenstein tipo III (Síndrome Bradicardia-Taquicardia). Una coronariografía constató una estenosis del 80% en segmento proximal de la arteria coronaria derecha con componente espástico. La arteria del nódulo sinusal emerge del segmento proximal de la coronaria derecha. Se realizó una angioplastia exitosa con stent medicado. Otro estudio Holter de 24 horas de control pos-angioplastia registró nuevamente episodios paroxísticos de fibrilación auricular con respuesta ventricular alta y episodios de pausas de hasta 3.100 milisegundos por lo que se implantó un marcapasos bicameral. A pesar del restablecimiento de un flujo sanguíneo adecuado a la arteria del nódulo sinusal con la angioplastia de la coronaria derecha no se obtuvo una mejoría de la disfunción del nódulo sinusal.
ABSTRACT Sinus node dysfunction (SND) is generally secondary to senescence of the sinus node and the surrounding atrial myocardium. We are presenting a 59-year-old patient, hypertensive without treatment and with a history of syncope on two occasions in the last 4 months. He was admitted due to a 1: 1 atrioventricular conduction atrial flutter with a heart rate of 280 beats/min that subsides with an amiodarone drip. A 24-hour Holter monitor showed predominant sinus rhythm, paroxysmal episodes of atrial fibrillation with high ventricular response, sinus bradycardia of 47 beats/min. The diagnosis of sinus node dysfunction, Rubenstein type III (Bradycardia-Tachycardia Syndrome) was made. A coronary angiography confirmed an 80% stenosis in the proximal segment of the right coronary artery with a spastic component. The sinus node artery emerges from the proximal segment of the right coronary artery. A successful angioplasty was performed with a medicated stent. Another 24-hour Holter study of post-angioplasty control again recorded paroxysmal atrial fibrillation with high ventricular response episodes and pause episodes of up to 3,100 milliseconds, for which a dual-chamber pacemaker was implanted. Despite the restoration of adequate blood flow to the sinus node artery with right coronary angioplasty, no improvement in sinus node dysfunction was obtained.
ABSTRACT
The mechanism of sudden cardiac death (SCD) in patients with nonischemic dilated cardiomyopathy (NIDCM) is mostly due to sustained ventricular tachycardia and ventricular fibrillation. The clinical guidelines for the therapeutic management of this set of patients are mostly based on left ventricular ejection fraction value which has a low specificity to differentiate the risk of SCD from the risk of mortality associated with heart failure or other comorbidities. Moreover, since SCD can occur in patients with normal or mildly depressed ejection fraction, it is necessary to identify new markers to improve the prognostic stratification of SCD. Several studies that analyzed the ventricular arrhythmia substrate found that myocardial fibrosis plays an important role in the genesis of ventricular arrhythmias in patients with NIDCM. The surrounding zone of the area of fibrosis is a heterogeneous medium, where tissue with different levels of fibrosis coexists, resulting in both viable and nonviable myocardium. This myocardial fibrosis may constitute a substrate for ventricular arrhythmias, where slow and heterogeneous conduction may favor the genesis of reentry mechanism increasing the chance to develop sustained ventricular tachycardia or ventricular fibrillation. Therefore, the evaluation of ventricular fibrosis by late gadolinium enhancement (LGE) cardiac magnetic resonance imaging has been suggested as an indicator for SCD risk stratification. Indeed, LGE in patients with NIDCM is associated with increased risk of all-cause mortality, heart failure hospitalization, and SCD. Detection of myocardial fibrosis as LGE by cardiac magnetic resonance imaging can be considered as a useful pathway of prediction of malignant ventricular arrhythmias since it has excellent prognostic characteristics and may help guide risk stratification and management in patients with NIDCM.
