An experiment was carried out to examine the effects of L-carnitine supplementation on growth performance and cardiopulmonary function of broiler chickens reared at high altitude (2100 m above sea level). A total of 96 day-old male chicks (Cobb 500) were randomly assigned into two dietary treatments containing 0 (control group) and 200 mg/kg L-carnitine. The experimental diets were fed for a period of 42 days consisting of the starting (days 1 to 21) and growing periods (days 21 to 42). Nutrient requirements of chickens met the NRC (1994) recommendations. The results showed that dietary L-carnitine had no significant influence on body weight gain, feed intake and feed conversion ratio. L-carnitine reduced plasma concentration of malondialdehyde, packed cell volume (PCV) and abdominal fat deposition compared to the control (P < 0.05). A significant (P < 0.05) decrease was observed in the right to total ventricular weight ratio (RV:TV) in birds receiving L-carnitine when compared to the control. Supplementation of L-carnitine increased plasma nitric oxide and immune responsiveness, which manifested in an increased toe-web thickness index measured at 24 h following the injection of phytohaemagglutinin P. In conclusion, supplementation of Lcarnitine had beneficial effects on preventing lipid peroxidation and pulmonary hypertension in broiler chickens raised at high altitude.

The present study was conducted to examine the effects of L-carnitine on pulmonary hypertensive response in broiler chickens reared at high altitude and exposed to hypobaric hypoxia. A total of 192 day-old male broilers (Cobb 500) were randomly assigned to 4 treatments and 4 replicates of 12 chicks. A basal diet composed of mainly corn and soybean meal was formulated and served as a control. Three additional treatments were made by supplementing graded levels of L-carnitine (50, 100, and 150 mg/kg). Chicks received dietary treatments at free access from 1 to 42 days of age. Results indicated that feeding L-carnitine at 100 mg/kg caused a significant increase in plasma nitric oxide (NO) with concomitant decrease in plasma malonedialdehyde (MDA). The Lead II electrocardiogram indicated reductions of S wave amplitude for all three doses of L-carnitine relative to the control and the difference between the birds that received L-carnitine at 50 mg/kg and the control was significant (P＜0.05). The right ventricular weight ratio (RV/TV) tended to decline when L-carnitine supplemented to diets. In conclusion, L-carnitine reduced ascites mortality in broiler chickens by increased NO production, reduced MDA concentration, and reduced right ventricular hypertrophy.

A 20-year-old man with persistent fifth aortic arch associated with coarctation of the aorta underwent catheterization and stenting of coarctation of the aorta.

Introduction: Pulmonary valve replacement (PVR) is being performed more commonly late after the correction of tetralogy of Fallot. Most valves are replaced with an allograft or xenograft, although reoperations are a common theme. Mechanical prostheses have a less favorable reputation due to the necessity of lifelong anticoagulation therapy and higher risk of thrombosis, but they are also less likely to require reoperation. There is a paucity of data on the use of prosthetic valves in the pulmonary position. We report the midterm outcomes of 38 cases of PVR with mechanical prostheses. Methods: One hundred twenty two patients who underwent PVR were studied. Thirty-eight patients, mean age 25 ± 8.4 years underwent PVR with mechanical prostheses based on the right ventricular function and the preferences of the patients and physicians. Median age of prosthesis was 1 year (range 3 months to 5 years). Results: Seven (18%) patients had malfunctioning pulmonary prostheses and two patients underwent redo PVR. Mean International Normalized Ratio (INR) in these seven patients was 2.1±0.8. Fibrinolytic therapy was tried and five of them responded to it well. There was no significant association between the severity of right ventricular dysfunction, patient’s age, prostheses valve size and age of the prosthesis in the patients with prosthesis malfunction. Conclusion: PVR with mechanical prostheses can be performed with promising midterm outcomes. Thrombosis on mechanical pulmonary valve prostheses remains a serious complication, but most prosthesis malfunction respond to fibrinolytic therapy, underscoring the need for adequate anticoagulation therapy.

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Treatment of prosthetic heart valve thrombosis using intravenous thrombolytics, although an acceptable alternative to surgery, is not complication free, and the literature has a dearth of data on the subject. This study analyzed the results of fibrinolytic treatment (FT) among a single-center group of patients with mechanical pulmonary valve thrombosis. Between 2000 and 2013, 23 consecutive patients with 25 episodes of pulmonary valve thrombosis received FT. The diagnosis of mechanical pulmonary valve thrombosis was established by fluoroscopy and echocardiography. Streptokinase (SK) was used in 24 cases and alteplase in 1 case. The FT was continued a second day for 14 patients (58.3%), a third day for 1 patient, and a fourth day for 1 patient. Echocardiography and fluoroscopy were performed every day until improvement of malfunction was achieved. Of the 23 patients, 19 had complete resolution of hemodynamic abnormalities after FT, 1 had partial resolution, and 2 showed no change. No patient had major complications. Five minor complications were detected, namely, fever, nausea, thrombophlebitis, epistaxi, and pain. Seven patients (30%) experienced recurrence of thrombosis, whereas four patients had surgery (biological pulmonary valve replacement) without re-thrombolytic therapy, one patient was treated with Alteplase, one patient received SK, and one patient received intense anticoagulation using heparin and warfarin. Overall, FT had a success rate of 84%. The results indicate that regardless of the time to pulmonary valve replacement and echocardiographic and fluoroscopic findings, FT was effective in most cases of mechanical pulmonary valve thrombosis. The efficacy increased with second-day thrombolytic therapy. Major complications were not common after lytic therapy for mechanical pulmonary valve thrombosis.

BackgroundWomen with congenital heart disease (CHD) may experience menstrual disturbances secondary to hemodynamic instability during the mensturation phase.ObjectivesWe investigated the menstrual bleeding pattern and its relationship with certain clinical findings in adult women with CHD.Patients and MethodsClinical data and menstrual bleeding pattern of adult women ≥15 years old who were referred to adult CHD clinic between March and September 2014 were recorded. Patients with syndromic congenital anomalies were excluded.ResultsData of 304 women (151 and 153 with simple and complex CHD groups, respectively) were recorded. Their mean (SD) age was 25.2 (1) years (range, 15 - 46 years). The median (IQR) age at menarche was 13 (12 - 14.25) years. Menarche was later in patients with CHD than in the normal population. Furthermore, the simple group showed earlier menarche than the complex group. The most common menstrual abnormality was menorrhagia in both groups (14.5% and 20.5% in the simple and complex groups, respectively). The incidence of menstrual abnormality was higher, though not significantly, in the complex group (40% vs. 25% in the simple group; P = 0.2). Menorrhagia was associated with the severity of oxygen desaturation (P = 0.007).ConclusionsMenstrual abnormalities are common in women with CHD, and therefore this group of patients should be aware of the menstrual function and its abnormalities.

Familial hypercholesterolemia (FH) is a common, yet underdiagnosed, genetic disorder characterized by lifelong elevated low-density lipoprotein cholesterol levels, which can increase the risk of early-onset coronary artery disease (CAD). In the present study, we screened the nucleotide variations of the LDLR and PCSK9 genes, as well as a part of the APOB gene, in Iranian patients with FH and premature CAD to find the genetic cause of the disorder. Fifteen unrelated individuals with a clinical diagnosis of FH and premature CAD were recruited. Direct DNA sequencing was applied to screen the whole coding exons and exon–intron boundaries of the LDLR and PCSK9 genes and the main parts of their introns, together with exon 26 of the APOB gene. The pathogenicity of the identified mutations was investigated via either segregation analyses in the family or in silico predictive software. Six different point mutations (p.Cys148Tyr, p.Cys216Tyr, p.Cys302Trp, p.Cys338Trp, p.Leu479Gln, and p.G593Afs∗72) in LDLR and a double mutation (p.Asp172His and p.Ala53Val) in both LDLR and PCSK9 genes were identified in seven families with clinically diagnosed FH (43%), whereas no pathogenic mutations were found in eight families with clinically diagnosed FH. This study is the first to identify 1 pathogenic mutation in the LDLR gene (c.1014C &gt; G [p.Cys338Trp]) and to cosegregate it from the affected individual in the family. No mutations were found in the APOB gene, whereas several silent mutations/polymorphisms were identified in the LDLR and PCSK9 genes. Genetic testing and reports on nucleotide alterations in the Iranian population are still limited. Our findings not only further confirm the significant role of FH in the incidence of premature CAD but also enlarge the spectrum of LDLR and PCSK9 variations and exhibit the heterogeneity of FH in Iranians. In patients with no mutation in the examined genes, the disease could be begotten either by a polygenic cause or by gene defects occurring in other related genes and regions not targeted in this study.