Benign Acute Childhood Myositis During Influenza B Outbreak.

Benign acute childhood myositis (BACM) is a syndrome classically occurring in children during the convalescent phase from a febrile upper respiratory tract infection, most commonly after influenza B. BACM can cause difficulty walking due to severe calf pain. Laboratory results show increased serum creatinine kinase and AST. Although alarming, BACM is self-limiting with symptoms disappearing within a week. Herein, we described a case series of BCAM in children in two cities in Poland during the influenza outbreaks in 2012/2013 and 2014/2015. We discussed the presentation and the clinical workup and examinations of the myositic syndrome. In addition, we evaluated the association of BACM with influenza B. We detected specific IgG against influenza B virus in 83% of the children diagnosed with BCAM. Reports from the National Institute of Public Health - National Institute of Hygiene in Warsaw, Poland confirmed a high rate of influenza B cases during both epidemic seasons in question.

Adenosine triphosphate for cardioversion of supraventricular tachycardia in two hydropic fetuses.

OBJECTIVE: We performed a retrospective study to check the effectiveness of adenosine triphosphate (Striadyne) for cardioversion of fetal supraventricular tachycardia (SVT) and to evaluate neonatal outcome after prenatal treatment of severe SVT with fetal hydrops. METHODS: Two hydropic fetuses with SVT were treated with Striadyne injection into the umbilical vein, as an additional treatment to the digoxin given intravenously to the mother. Both fetuses were in severe condition, with ultrasound, Doppler and laboratory signs of fetal distress and congestive heart failure. RESULTS: Sinus rhythm was obtained in both cases for different periods of time, without side effects of Striadyne. The children survived. There were severe cardiac and neurologic problems after delivery. CONCLUSIONS: Striadyne was an effective drug in converting SVT to the sinus rhythm in hydropic fetuses. Digoxin was useless in these fetuses in spite of the therapeutic level which was obtained in both mothers. We suppose that fetal SVT causing fetal hydrops could be the reason of brain damage, and intensive antiarrhythmic treatment seemed to be necessary.

Myocardial perfusion and function of the systemic right ventricle in patients after atrial switch procedure for complete transposition: long-term follow-up.

OBJECTIVES: Our purpose was to assess the right ventricular (RV) function and identify patients with RV impairment long after the Mustard or Senning operation. BACKGROUND: Systemic ventricular failure can cause myocardial perfusion abnormalities in thallium scintigraphy correlating with hemodynamic deterioration. METHODS: Myocardial perfusion at rest and at peak exercise was assessed in 61 patients, aged 7 to 23 years in mean time 10.0 +/- 2.9 years after surgery using technetium-99m methoxyisobutyl isonitrile single-photon emission computed tomography. Ventricular function was assessed by first-pass radionuclide angiography at rest. Exercise capacity was determined with a modified Bruce protocol. RESULTS: The mean RV ejection fraction was 36.1 +/- 7.7%, and left ventricular (LV) ejection fraction was 52.1 +/- 9.4%. Moderate or severe perfusion abnormalities on the rest scan were observed in 20 patients (33%). On exercise perfusion worsened in another 13 patients (21.3%). Patients with perfusion defects on stress scan had significantly lower RV and LV ejection fraction (33.2 vs. 39.4%; p = 0.002 and 49.2 vs. 55.5%; p = 0.01, respectively). They were also older (16.6 vs. 13.0 years; p = 0.002), operated on at an older age (4.0 vs. 2.4 years; p = 0.05) and had longer follow-up (12.5 vs. 10.5 years; p = 0.003). CONCLUSIONS: Myocardial perfusion defects are common findings in patients in long-term follow-up after atrial switch operation. Despite excellent exercise tolerance, the extent of myocardial perfusion abnormalities correlated well with impaired RV and LV function, and greater perfusion defects were seen more frequently in older patients with longer follow-up. It is likely that myocardial perfusion defects could be a sensitive predictor of systemic ventricular impairment.

Middle aortic syndrome treated by stent implantation.

OBJECTIVES: To determine outcome of stent implantation in patients with middle aortic syndrome. DESIGN: Prospective study, case series. SETTING: A tertiary paediatric cardiology centre in a children's hospital. PATIENTS: Five patients, aged 4 to 17 years (mean 11.4 years), with upper limb hypertension due to middle aortic syndrome. INTERVENTION: Stents were implanted in the mid/lower thoracic/upper abdominal aorta. MAIN OUTCOME MEASURE: Satisfactory deployment of stents and blood pressure control. RESULTS: In all patients, angiocardiography showed long segment stenosis in the mid or lower thoracic/upper abdominal aorta. The pressure gradient was between 40 and 90 mm Hg (mean 63.2 mm Hg). Seven Palmaz stents were implanted. Immediately after implantation, the gradient decreased to between 0 and 35 mm Hg (mean 13.6 mm Hg). Angiography showed a satisfactory result with widely patent stents in all. In one patient, thrombosis of the stent occurred six days after implantation. This was successfully treated with infusion of alteplase, further balloon dilatation, and implantation of a second stent overlapping the first, both dilated to 10 mm diameter. One patient had elective redilatation of the stent six months after implantation, with further reduction of the gradient from 35 mm Hg to 10 mm Hg. At the latest follow up between three and 20 months (mean 12.2 months) after stent implantation, in four patients blood pressure was better controlled with antihypertensive drugs. One patient was normotensive without drugs. Computed tomography showed no aneurysm formation in the region of the stents. CONCLUSIONS: Stent implantation is a preferable alternative to surgery in the treatment of patients with middle aortic syndrome and merits further evaluation.

[Indications for emergency surgical treatment of ectopic atrial tachycardia]. / Chirurgiczne leczenie ektopowego czestoskurczu przedsionkowego--ze wskazan pilnych.

Recurrent automatic atrial tachycardia can induce dilated cardiomyopathy. We present clinical and therapeutic problems of 16 years old male with ectopic left atrial tachycardia refractory to pharmacological therapy. In this patient long periods of atrial tachycardia 200-240/min due to lack of effective medication caused cardiac failure. Uncontrolled taking of various antiarrhythmic drugs and persistent tachycardia led to cardiogenic shock. The electrophysiologic study revealed focus of the tachycardia localized in the area of left cardiac auricle. The rate of the tachycardia was changing from 84 to 240/min, with periods of Mobitz I block in the AV node. In periods of 1:1 AV conduction the tachycardia had sometimes LBBB QRS morphology. The atrial tachycardia provoked unsustained ventricular one. The patient was operated. Resection of left auricle and mitral valvuloplasty were performed. After the operation the patient regained undisturbed sinus rhythm and symptoms of heart failure disappeared.

[Transesophageal stimulation of the left atrium in children with arrhythmia (preliminary report)]. / Stymulacja przezprzelykowa przedsionka lewego w zaburzeniach rytmu serca u dzieci (doniesienie wstepne).

The conduction system of the heart was studied in 41 patients with cardiac arrhythmias by oesophageal stimulation of the left atrium. 31 children had a history of paroxysmal supraventricular tachycardia, 5 supraventricular or/and ventricular premature beats and 5 were studied because of suspected bradycardia-tachycardia syndrome. In all patients stimulation of the left atrium was well tolerated. There were no side effects or complications. The results showed that oesophageal stimulation of the left atrium was a faithful noninvasive method in diagnostic studies of the conduction system of the heart. This method was effective in studying the mechanism of supraventricular arrhythmias.

[Cyanosis in children caused by inherited methemoglobinemia due to deficiency of NADH-dependent methemoglobin reductase in erythrocytes]. / Sinica u dzieci spowodowana wrodzona methemoglobinemia na tle niedoboru reduktazy methemoglobiny NADH-zaleznej krwinek czerwonych.

Two cases of the congenital methemoglobinemia in children due to the deficiency of NADH-dependent methemoglobin reductase in erythrocytes. These children were referred to the Cardiological Ward at the Child Health Centre with suspected cyanotic heart defect. Cardiological examinations excluded heart defect but an increased blood methemoglobin level and decreased activity of NADH-dependent methemoglobin reductase were found, that caused methemoglobinemia. Methylene blue and vitamin C diminished cyanosis. These cases advocate inclusion of methemoglobinemia into differential diagnosis of cyanotic disorders especially if there is no evident pathology in cardio-vascular system.