Percutaneous Device Closure of Congenital Isolated Ventricular Septal Defects:A Single-Center Retrospective Database Study Amongst 412 Cases

To identify suitable cases and reduce failure/complication rates for percutaneous ventricular septal defect (VSD) closure, we aimed to (1) study causes of device failure and (2) compare outcomes with different VSD types and devices in a high-volume single center with limited resources. Retrospective data of 412 elective percutaneous VSD closure of isolated congenital VSDs between 2003 and 2017 were analyzed. Out of 412, 363 were successfully implanted, in 30 device implantation failed, and in 19 the procedure was abandoned. Outcome was assessed using echocardiography, electrocardiography, and catheterization data (before procedure, immediately after and during follow-up). Logistic regression analyses were performed to assess effects of age, VSD type, and device type and size on procedural outcome. Median [interquartile range] age and body surface area were 6.6 [4.1-10.9] years and 0.7 [0.5-1.0] m(2), respectively. Device failure was not associated with age (p = 0.08), type of VSD (p = 0.5), device type (p = 0.2), or device size (p = 0.1). Device failure occurred in 7.6% of patients. As device type is not related to failure rate and device failure and complication risk was not associated with age, it is justifiable to use financially beneficial ductal devices in VSD position and to consider closure of VSD with device in clinically indicated children

Long-term protection and mechanism of pacing-induced postconditioning in the heart

Brief periods of ventricular pacing during the early reperfusion phase (pacing-induced postconditioning, PPC) have been shown to reduce infarct size as measured after 2 h of reperfusion. In this study, we investigated (1) whether PPC leads to maintained reduction in infarct size, (2) whether abnormal mechanical load due to asynchronous activation is the trigger for PPC and (3) the signaling pathways that are involved in PPC. Rabbit hearts were subjected to 30 min of coronary occlusion in vivo, followed by 6 weeks of reperfusion. PPC consisted of ten 30-s intervals of left ventricular (LV) pacing, starting at reperfusion. PPC reduced infarct size (TTC staining) normalized to area at risk, from 49.0 ± 3.3% in control to 22.9 ± 5.7% in PPC rabbits. In isolated ejecting rabbit hearts, replacing LV pacing by biventricular pacing abolished the protective effect of PPC, whereas ten 30-s periods of high preload provided a protective effect similar to PPC. The protective effect of PPC was neither affected by the adenosine receptor blocker 8-SPT nor by the angiotensin II receptor blocker candesartan, but was abrogated by the cytoskeletal microtubule-disrupting agent colchicine. Blockers of the mitochondrial KATP channel (5HD), PKC (chelerythrine) and PI3-kinase (wortmannin) all abrogated the protection provided by PPC. In the in situ pig heart, PPC reduced infarct size from 35 ± 4 to 16 ± 12%, a protection which was abolished by the stretch-activated channel blocker gadolinium. No infarct size reduction was achieved if PPC application was delayed by 5 min or if only five pacing cycles were used. The present study indicates that (1) PPC permanently reduces myocardial injury, (2) abnormal mechanical loading is a more likely trigger for PPC than electrical stimulation or G-coupled receptor stimulation and (3) PPC may share downstream pathways with other modes of cardioprotection

Chronic ventricular pacing in children: toward prevention of pacing-induced heart disease

In children with congenital or acquired complete atrioventricular (AV) block, ventricular pacing is indicated to increase heart rate. Ventricular pacing is highly beneficial in these patients, but an important side effect is that it induces abnormal electrical activation patterns. Traditionally, ventricular pacemaker leads are positioned at the right ventricle (RV). The dyssynchronous pattern of ventricular activation due to RV pacing is associated with an acute and chronic impairment of left ventricular (LV) function, structural remodeling of the LV, and increased risk of heart failure. Since the degree of pacing-induced dyssynchrony varies between the different pacing sites, ‘optimal-site pacing’ should aim at the prevention of mechanical dyssynchrony. Especially in children, generally paced from a very early age and having a perspective of life-long pacing, the preservation of cardiac function during chronic ventricular pacing should take high priority. In the perspective of the (patho)physiology of ventricular pacing and the importance of the sequence of activation, this paper provides an overview of the current knowledge regarding possible alternative sites for chronic ventricular pacing. Furthermore, clinical implications and practical concerns of the various pacing sites are discussed. The review concludes with recommendations for optimal-site pacing in children

Extreme windkessel effect can cause right heart failure early after truncus repair

An infant developed severe right heart failure early after truncal repair with a pulmonary homograft. A mechanical obstruction by narrowing could not be identified at the homograft or pulmonary arteries. However, functional obstruction was caused by an extreme windkessel effect in a massively dilated homograft that absorbed rather than transmitted the pulse wave. Effective treatment consisted of replacing the dilated homograft by a rigid aortic homograft of equal size as the initial homograft. When confronted with circulatory failure after allograft placement, the clinician should not only look for obstruction by narrowing, but also consider the windkessel phenomenon.status: publishe

Pacing Postconditioning: Impact of Pacing Algorithm, Gender, and Diabetes on Its Myocardial Protective Effects

Pacing postconditioning (PPC) induces cardioprotection. The aim of this study was to determine the optimal pacing algorithm and possible influence of gender and diabetes on PPC. Unprotected regional ischemia for 30 min served as negative control and classical PPC (ten cycles of 30 s left ventricular pacing alternated with 30 s right atrial pacing) as positive control. Area at risk and infarct size were determined by blue dye and triphenyltetrazolium chloride staining. For achieving protection, the minimal number of PPC cycles was seven and the minimal duration of a PPC protocol was 200 s. The protective effect of PPC was comparable in male and female hearts, but no protection could be induced by PPC in diabetic hearts. PPC can provide myocardial protection when using at least seven cycles of ventricular pacing. PPC protection is independent of gender, but sensitive to experimental diabetes

Late recovery of atrioventricular conduction after postsurgical chronic atrioventricular block is not exceptional

OBJECTIVE: Postsurgical atrioventricular block may complicate surgery for congenital heart defects and is generally considered permanent when persisting longer than 14 days after surgery. In this study, we evaluate the occurrence of spontaneous late recovery of atrioventricular conduction in postsurgical chronic atrioventricular block and discuss its clinical implications. METHODS: We retrospectively reviewed all cardiac surgical procedures on cardiopulmonary bypass between January 1993 and November 2010 in subjects younger than 18 years. Patients with postsurgical advanced second- or third-degree atrioventricular block persisting longer than 14 days after surgery were included. RESULTS: Of a total of 2850 cardiac surgical procedures on cardiopulmonary bypass, 59 (2.1%) were immediately complicated by chronic postsurgical atrioventricular block of advanced second (n = 4) or third degree (n = 55). In another 6 patients (0.2%), late occurrence of chronic advanced second- (n = 3) or third-degree (n = 3) atrioventricular block, without signs of any etiology other than previous surgery, was seen 0.4 to 10 years after surgery (median, 5.7 years). Late (>2 weeks) regression to either completely normal atrioventricular conduction or asymptomatic first-degree atrioventricular block occurred 3 weeks to 7 years (median, 3.1 years) after surgery in 7 (12%) patients with immediate postsurgical chronic atrioventricular block. CONCLUSIONS: Complete recovery of atrioventricular conduction or regression to asymptomatic first-degree atrioventricular block occurred in 12% of patients with postsurgical chronic second- or third-degree atrioventricular block. To prevent unnecessary adverse side effects of chronic ventricular pacing and to prolong battery longevity, ventricular pacing should be minimized in patients with recovered normal atrioventricular conduction.status: publishe

Late recovery of atrioventricular conduction after postsurgical chronic atrioventricular block is not exceptional

ObjectivePostsurgical atrioventricular block may complicate surgery for congenital heart defects and is generally considered permanent when persisting longer than 14 days after surgery. In this study, we evaluate the occurrence of spontaneous late recovery of atrioventricular conduction in postsurgical chronic atrioventricular block and discuss its clinical implications.MethodsWe retrospectively reviewed all cardiac surgical procedures on cardiopulmonary bypass between January 1993 and November 2010 in subjects younger than 18 years. Patients with postsurgical advanced second- or third-degree atrioventricular block persisting longer than 14 days after surgery were included.ResultsOf a total of 2850 cardiac surgical procedures on cardiopulmonary bypass, 59 (2.1%) were immediately complicated by chronic postsurgical atrioventricular block of advanced second (n = 4) or third degree (n = 55). In another 6 patients (0.2%), late occurrence of chronic advanced second- (n = 3) or third-degree (n = 3) atrioventricular block, without signs of any etiology other than previous surgery, was seen 0.4 to 10 years after surgery (median, 5.7 years). Late (>2 weeks) regression to either completely normal atrioventricular conduction or asymptomatic first-degree atrioventricular block occurred 3 weeks to 7 years (median, 3.1 years) after surgery in 7 (12%) patients with immediate postsurgical chronic atrioventricular block.ConclusionsComplete recovery of atrioventricular conduction or regression to asymptomatic first-degree atrioventricular block occurred in 12% of patients with postsurgical chronic second- or third-degree atrioventricular block. To prevent unnecessary adverse side effects of chronic ventricular pacing and to prolong battery longevity, ventricular pacing should be minimized in patients with recovered normal atrioventricular conduction