Early-Onset Cardiomyopathy After Pacemaker Implanted in a Preterm Infant With Congenital Complete Heart Block and Anti-Ro/SSA Antibodies.

Congenital complete heart block is a potentially fatal complication that can occur in neonates whose mothers have autoimmune disorders; it has rarely been reported in the presence of Sjögren syndrome. Pacemaker implantation is recommended to treat rhythm abnormalities in these neonates. We report the case of a late-preterm infant with Sjögren-syndrome-antibody-induced complete heart block who underwent temporary bipolar epicardial pacing as a bridge to permanent pacemaker implantation. Soon after the pacemaker was implanted, takotsubo cardiomyopathy developed. To our knowledge, this is the first report of reversible cardiomyopathy after pacemaker implantation in an infant.

QT Prolongation After Minor Head Trauma in a Pediatric Patient.

We report a case of QTc prolongation associated with mild concussion in a pediatric patient. An 11-year-old male presented to the emergency department after sustaining a head injury during football practice. He complained of headache and blurry vision. Physical examination was within normal apart from an irregular heart rhythm. Electrocardiogram (ECG) showed normal sinus rhythm with QTc (Bazett formula) 460 ms. The patient was diagnosed with concussion and referred for cardiology follow-up of the QTc. ECG the next day showed QTc 462 ms (heart rate 105 bpm) supine and 494 ms after suddenly standing up (heart rate 120 bpm). Family history was negative for sudden cardiac events. Exercise stress testing 1 week later showed a baseline QTc 462 ms and 488 ms at 4 min into recovery. Holter monitoring showed evidence of increased parasympathetic activity manifested by marked sinus arrhythmia. Repeated ECG, exercise stress testing, and Holter monitoring 3 months later showed normalized QTc values. His concussion symptoms were resolved at the time of repeat testing. Mild head trauma/concussion could be associated with prolonged QTc and abnormal cardiac repolarization. While these changes seem to be self-limiting, they remain a possible substrate for malignant arrhythmias. Recognition of these changes would lead to appropriate reassurance and/or precautions in the acute setting, especially in at-risk populations such as long QT syndrome patients.

Utility of Pulmonary Artery Acceleration Time to Estimate Systolic Pulmonary Artery Pressure in Neonates and Young Infants.

Transthoracic echocardiogram (TTE) is commonly used to screen for pulmonary hypertension (PHTN) in neonates and young infants. However, in the absence of sufficient tricuspid regurgitation (TR), a ventricular septal defect (VSD), or a patent ductus arteriosus (PDA), the estimation of systolic pulmonary artery pressure (SPAP) becomes challenging. Pulmonary artery acceleration time (PAAT) is an alternate parameter that is easy to obtain in almost all patients and does not require the presence of tricuspid valvar regurgitation or an anatomical cardiac defect. We sought to examine the correlation of PAAT with estimated SPAP by TTE and create an equation to estimate the SPAP using PAAT. We performed a retrospective review of TTEs performed on neonates and young infants (4 months of age or younger) at our institution between April 2017 and December 2018, along with the corresponding medical records. We included TTEs that provided estimation for SPAP and at least one PAAT measurement. During the study period, 138 TTEs performed on 82 patients met the inclusion criteria. Strong correlation was delineated between PAAT and SPAP estimated by the maximum velocity of tricuspid valve regurgitation Doppler, correlation coefficient (r) = - 0.83. Moderate correlation was detected between PAAT and SPAP estimated by PDA Doppler, r = - 0.66. Utilizing the following equation "SPAP = 82.6 - 0.58 × PAAT + RA mean pressure", PAAT can be used to estimate SPAP in neonates and young infants. PAAT can be used as an alternative to TR jet to assess SPAP when the latter is absent or insufficient. Further studies are needed to verify the accuracy of this equation.

Determination of the Frequency of Right and Left Internal Mammary Artery Embolization in Single Ventricle Patients: A Two-Center Study.

Embolization of systemic to pulmonary artery collaterals to regulate pulmonary arterial flow or pressure of the cavopulmonary circulation in patients with single ventricle is a common practice. The relative incidence and impact of this practice on future interventions like coronary artery bypass grafting is poorly understood. This study aims to evaluate the frequency and implications of internal mammary artery (IMA) embolization in the single ventricle (SV) population. A retrospective chart review was performed of SV patients who underwent cardiac catheterization before and after Fontan procedure between February 2007 and 2017. Data were collected from two tertiary care centers in the Midwest. Of the 304 SV patients, 62 (20.4%) underwent embolization of one or more IMAs, whereas 242 (79.6%) did not. The rate of embolization of IMA was 40.5% in one center and 14.5% in the second center. Among patients who received IMA embolization, left internal mammary artery (LIMA) embolization was seen in 6 (9.7%) patients. Majority of patients underwent either right internal mammary artery (RIMA) embolization (n = 25; 40.3%) or RIMA and LIMA embolization (n = 27; 43.5%). IMA embolization in SV patients is common. Embolizing IMAs early in life will likely eliminate a valuable graft option for coronary artery bypass grafting should it be required in the future care of these patients. Multi-center, prospective, nation-wide studies are warranted to examine coronary artery disease in the SV population and true frequency of IMA embolization. Delineation of which IMAs were embolized is a necessary in surgical and cardiac intervention national data, such as Society of Thoracic Surgeons (STS) database. All measures should be taken to preserve IMAs patency, if deemed feasible and safe.

Acute Pediatric Colchicine Toxicity is Associated with Marked Bradydysrhythmias.

BACKGROUND: Colchicine ingestion is rare but highly lethal. Patients usually die of multiorgan failure and cardiogenic shock. Colchicine is not only associated with depressed myocardial function but also with fatal heart rhythm disturbances, such as complete heart block, ventricular tachycardia, and asystole. While histologic changes of myocytes are well known, the mechanism by which colchicine affects cardiac impulse generation and conduction is not fully understood. CASE REPORT: We present a case of colchicine ingestion with sinus bradycardia, marked sinus arrhythmia, and first- and second-degree heart block. A 10-year-old previously healthy boy was brought to the emergency department for the sudden onset of dizziness, abdominal pain, and vomiting after ingesting his grandfather's colchicine and furosemide. His symptoms improved with ondansetron and intravenous normal saline. However, because of the colchicine ingestion, he was admitted to the pediatric intensive care unit for observation. He first developed PR prolongation (∼4-30 h postingestion) followed by marked sinus bradycardia and sinus arrhythmia along with second-degree heart block (∼48-60 hours postingestion). The minimum heart rate was 40 beats/min. Marked sinus arrhythmia was observed, suggesting an increase in parasympathetic activity. His heart rhythm improved initially with less sinus arrhythmia followed by resolution of heart block. He was discharged home without any sequelae. Holter monitoring 1 week after discharge showed normal heart rate variability for age. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: This case provides novel insights into how colchicine may affect the heart's electrophysiology. Colchicine may increase the parasympathetic tone enough to cause sinus bradycardia and different degrees of heart block.

Evaluation of tissue factor expression in canine tumor cells.

OBJECTIVE: To determine whether canine tumor cell lines express functional tissue factor and shed tissue factor-containing microparticles. SAMPLE: Cell lines derived from tumors of the canine mammary gland (CMT12 and CMT25), pancreas (P404), lung (BACA), prostate gland (Ace-1), bone (HMPOS, D-17, and OS2.4), and soft tissue (A72); from normal canine renal epithelium (MDCK); and from a malignant human mammary tumor (MDA-MB-231). PROCEDURES: Tissue factor mRNA and antigen expression were evaluated in cells by use of canine-specific primers in a reverse transcriptase PCR assay and a rabbit polyclonal anti-human tissue factor antibody in flow cytometric and immunofluorescent microscopic assays, respectively. Tissue factor procoagulant activity on cell surfaces, in whole cell lysates, and in microparticle pellets was measured by use of an activated factor X-dependent chromogenic assay. RESULTS: Canine tissue factor mRNA was identified in all canine tumor cells. All canine tumor cells expressed intracellular tissue factor; however, the HMPOS and D-17 osteosarcoma cells lacked surface tissue factor expression and activity. The highest tissue factor expression and activity were observed in canine mammary tumor cells and pulmonary carcinoma cells (BACA). These 3 tumors also shed tissue factor-bearing microparticles into tissue culture supernatants. CONCLUSIONS AND CLINICAL RELEVANCE: Tissue factor was constitutively highly expressed in canine tumor cell lines, particularly those derived from epithelial tumors. Because tumor-associated tissue factor can promote tumor growth and metastasis in human patients, high tissue factor expression could affect the in vivo biological behavior of these tumors in dogs.