Insights in Pediatric Cardiology

Description

Endless His- pack pacing has been gaining fashionability in the adult population taking cardiac resynchronization remedy. Original procedural challenges are being overcome, and this system of pacing has been shown to ameliorate left ventricular function and heart failure symptoms secondary to ventricular dyssynchrony. Though the etiologies of ventricular dyssynchrony may differ in children and those with natural heart complaint than in grown-ups with structurally normal hearts, His- pack pacing may also be a favored option in these groups to restore further physiologic electric conduction and ameliorate ventricular function. We present a review of the current literature and suggested directions involving planting endless His- pack pacing in the pediatric and natural heart complaint population [1].

Atrioventricular

The typical electrical activation of the heart propagates as an electrical impulse that travels from the sinus knot to the Atrioventricular (AV) knot, through the Hisâ??Purkinje system, and to the ventricular myocardium. Conduction through the Hisâ??Purkinje system leads to a narrow QRS complex on the 12-lead Electrocardiogram (ECG), representing coetaneous Left Ventricular (LV) and right ventricular (Caravan) activation [2]. In the setting of AV block, pacing of the ventricle (most generally the Caravan) provides for an acceptable ventricular heart rate. Habitual Caravan apical pacing leads to altered cardiac activation and mechanics with essential Left Bundle Branch (LBB) and ventricular dyssynchrony, performing in reduced systolic function over time due to myocellular redoing. The Caravan septum and exodus tract have been explored as indispensable pacing spots and feel to ameliorate ejection fragments in grown-ups as compared with Caravan apical pacing, although randomized trials haven't shown any differences. With the arrival of biventricular leaders, the resynchronization of ventricular activation has led to clear morbidity and mortality benefits in the adult population. While effective in narrowing the QRS complex by creating a fused ventricular depolarization waveform, biventricular pacing is still unfit to take advantage of the native Hisâ??Purkinje system and profitable ventricular motet exposure for optimal electrical signal transduction. Endless his-pack pacing is an indispensable system that may more restore physiologic ventricular activation [3].

Congenital Heart Disease

In the structurally normal heart, the sinus knot is located in the high right patio at the superior vena cavaâ??right atrial junction and initiates electrical excitation of the myocardium. The electric impulse takes an inferior and leftward course through the right patio until it reaches the AV knot. The AV knot is an atrial structure positioned between the AV faucets posterior to the aortic stopcock at the apex of the triangle of Koch (which is delineated by the coronary sinus perforation, the tendon of todaro, and the septal pamphlet of the tricuspid stopcock). The AV knot exhibits incremental conduction to the pack of His that penetrates the AV plate, allowing for passage of the electric current to the ventricles. The electricity also travels through the pack of His, in the membranous ventricular septum girdled by separating connective towel. The pack of His, though located in the membranous septum, is covered with myocardial filaments that travel through the membranous and muscular septum. This structure exits on the ventricular crest and peregrination to both pack branches to deliver the electrical impulse to the LV and caravan [4]. Trendsetter leads can be placed via a transvenous or epicardial route, which is largely determined by patient size and the presence of natural heart complaint (CHD). Grown-ups with normal cardiac deconstruction can generally accommodate a transvenous pacing system. Babies and youthful children most generally profit from epicardial trendsetter leads as the nameless tone size limits the capability to accommodate a transvenous lead without increased threat of inhibition. Heightened prevalence rates of venous occlusion and thrombosis and the need for reintervention are challenges seen when implanting transvenous pacing systems in youthful children, especially those importing lower than 10 kg. Also, a small subxiphoid approach is frequently sufficient for a binary-chamber epicardial system in an child or youthful child, making this fashion veritably doable. In those with CHD, intracardiac shunts limit the mileage of transvenous pacing systems due to the increased threat of thromboembolism [5].

References

1. Sweeney MO, Hellkamp AS, Ellenbogen KA (2003) Adverse effect of ventricular pacing on heart failure and atrial fibrillation among patients with normal baseline QRS duration in a clinical trial of pacemaker therapy for sinus node dysfunction. Circulation 107: 2932–2937.
2. Little WC, Reeves RC, Arciniegas J, Katholi RE, Rogers EW (1982) Mechanism of abnormal interventricular septal motion during delayed left ventricular activation. Circulation 65:1486–1491.
3. Shimony A (2012) Beneficial effects of RV non-apical vs. apical pacing: a systematic review and meta-analysis or randomized-controlled trials. Europace 14: 81–91.
4. Sharma PS, Ellenbogen KA, Trohman RG (2017) Permanent his bundle pacing: the past, present, and future. J Cardiovasc Electrophysiol 28: 458–465.
5. Zhang XH, Chen H, Siu CW (2008) New-onset heart failure after permanent right ventricular apical pacing in patients with acquired high-grade atrioventricular block and normal left ventricular function. J Cardiovasc Electrophysiol 19: 136–141.