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PubMed1977

Heart block.

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Heart Block↗
PubMed1996

Acquired left ventricular to right atrial communication and complete heart block following nonpenetrating cardiac trauma.

Intracardiac shunts are uncommon cardiac lesions caused by blunt chest trauma. A very unusual case is reported of a young male with an acquired left ventricular to right atrial communication and complete heart block cause by nonpenetrating chest trauma. The left ventricular to right atrial fistula was diagnosed noninvasively by transthoracic and transesophageal echo-Doppler examination and the findings were confirmed by left ventriculography and by the intraoperative findings.

Adolescent↗
PubMed2001

Complete heart block in an adult with systemic lupus erythematosus and recent onset of hydroxychloroquine therapy.

Complete heart block (CHB) is a rare complication of systemic lupus erythematosus (SLE), mainly seen during an acute flare-up of the disease or after high-dose long-term treatment with antimalarial drugs, although anti-Ro and anti-RNP antibodies have also been implied by some authors. A 40-y-old woman developed CHB in the context of an acute flare-up of SLE, first diagnosed three years ago, having recently commenced hydroxychloroquine (HCQ) treatment. Anti-Ro and anti-RNP antibodies were also positive. No features of myocarditis were found. A temporary pacemaker was required and complete resolution was achieved on steroid therapy with withdrawal of antimalarial therapy. The characteristics of previous cases are well publicised and discussion focuses on the possible aetiology and pathogenesis of the present case.

Adolescent↗
PubMed2004

Autoimmune-associated congenital heart block: dissecting the cascade from immunologic insult to relentless fibrosis.

Few diseases exemplify the integration of research from bench to bedside as well as neonatal lupus, often described as a model of passively acquired autoimmunity. The signature histologic lesion of autoimmune congenital heart block (CHB) is fibrosis of the conducting tissue and, in some cases, the surrounding myocardium. Although anti-SSA/Ro-SSB/La antibodies are detected in > 85% of mothers whose fetuses are identified with conduction abnormalities in a structurally normal heart, the risk for a woman with the candidate antibodies to have a child with CHB is 2%. The mechanism by which maternal anti-SSA/Ro-SSB/La antibodies initiate and finally eventuate in atrioventricular nodal scarring is not yet defined, but it is clear that the antibodies alone are insufficient to cause disease and fetal factors are likely contributory. Previous in vitro and in vivo studies suggest that the pathologic cascade is initiated via apoptosis, resulting in translocation of SSA/Ro-SSB/La antigens to the cell surface where they are bound by maternal autoantibodies. Subsequently, the Fc portion of the bound immunoglobulin engages Fcgamma receptors on tissue macrophages, resulting in release of TGF-beta at a threshold favoring a profibrotic milieu and irreversible scarring. This cascade also involves tissue-specific activation of TGF-beta, which promotes the modulation of fibroblasts into myofibroblasts, a scarring phenotype. Recent findings point to genetic polymorphisms that promote high production of TGF-beta as possible fetal risk factors for CHB. Further elucidation of maternal and fetal contributory factors should provide insight into the pathogenesis of CHB and the rarity of irreversible injury.

Animals↗
PubMed2005

Heart block and empirical therapy after transcatheter closure of perimembranous ventricular septal defect.

Two patients with perimembranous ventricular septal defects (VSDs) and inlet extension have undergone uncomplicated transcatheter device closure using the Amplatzer membranous VSD device. Both patients developed complete heart block 2-4 days from the closure. Both patients responded well to high-dose intravenous therapy with steroids and high-dose oral anti-inflammatory aspirin. Both patients remain in normal sinus rhythm 8 weeks and 10 months, respectively, from the episode.

Aspirin↗
PubMed1979

Non-invasive beat-to-beat analysis of stroke volume and digital pulse volume in patients with complete heart block and artificial pacing.

This study presents a beat-to-beat analysis of digital arterial pulse volume (DAPA), left ventricular end-diastolic diameter (LVEDD), and stroke volume (SV) and their correlation to PQ interval in ten patients with complete heart block and artificial cardiac pacing. DAPA was measured by strain-gauge plethysmography and LVEDD/SV by echocardiography. A close relationship was found between SV and DAPA (R = 0.83-0.97) in seven patients, who all drew considerable benefit from atrial contraction as regards SV and DAPA (increase with 35-94%). The optimal PQ interval was calculated to approximately 240 msec for DAPA and 180 msec for LVEDD and SV. It may be concluded that the present study demonstrates a close relationship between beat-to-beat variations of SV measured by echocardiography and plethysmographically recorded digital arterial pulse volume. These variables may be useful in clinical practice for assessing the hemodynamic effect of atrial contribution in patients with various forms of cardiac conduction disturbances. The two methods may, for instance, be useful for screening in order to pick out patients who may benefit from AV synchronous rather than ventricular pacing.

Adult↗
PubMed2004

Nkx2-5 pathways and congenital heart disease; loss of ventricular myocyte lineage specification leads to progressive cardiomyopathy and complete heart block.

Human mutations in Nkx2-5 lead to progressive cardiomyopathy and conduction defects via unknown mechanisms. To define these pathways, we generated mice with a ventricular-restricted knockout of Nkx2-5, which display no structural defects but have progressive complete heart block, and massive trabecular muscle overgrowth found in some patients with Nkx2-5 mutations. At birth, mutant mice display a hypoplastic atrioventricular (AV) node and then develop selective dropout of these conduction cells. Transcriptional profiling uncovered the aberrant expression of a unique panel of atrial and conduction system-restricted target genes, as well as the ectopic, high level BMP-10 expression in the adult ventricular myocardium. Further, BMP-10 is shown to be necessary and sufficient for a major component of the ventricular muscle defects. Accordingly, loss of ventricular muscle cell lineage specification into trabecular and conduction system myocytes is a new mechanistic pathway for progressive cardiomyopathy and conduction defects in congenital heart disease.

Acetylcholinesterase↗