Blood Coagulation Normalization Effect of Parkia Biglobosa Seed on Potassium Bromate-induced Coagulopathy.

BACKGROUND: Potassium bromate (KBrO3) has been reported to be toxic, adversely affecting many body tissues and organs. The aim of this study was to determine the blood coagulation effect of Parkia biglobosa (P. biglobosa) seed on potassium bromate induced coagulopathy. METHODOLOGY: P. biglobosa was extracted with soxhlet extractor with ethanol as the solvent. Twenty-four adult male Wistar rats were acclimatized under laboratory conditions and were randomly grouped into A, B, C and D. Group A was given distilled water orally. Animals in groups B, C and D were administered 100 mg/kg body weight of potassium bromate, but groups C and D were also treated with 100 and 200 mg/kg body weight of P. biglobosa respectively. Both potassium bromate and P. biglobosa were freshly prepared on daily basis and administered to rats by oral gavage for 28 days. At the end of the treatment period, blood samples were collected in sodium citrate bottles and were used for analysis of Prothrombin Time (PT), Activated Partial Thromboplastin Time (APTT), Thrombin Time (TT), fibrinogen and vitamin K levels using standard methods. RESULTS: Administration of potassium bromate increased Prothrombin Time (PT) from 11.67±2.15 seconds (in control animals) to 19.53±2.83 seconds. Treatment with 100 and 200 mg/kg body weight of P. biglobosa seed extract neutralized this effect in a dose-dependent manner. Likewise, KBrO 3 was observed to have significantly elevated Activated Partial Thromboplastin Time (APTT) from 29.67±3.93 to 41.10±4.79 seconds and Thrombin Time (TT) from 15.36±2.06 to 25.43±2.83 seconds when compared with those in the control group. The result further showed that exposure of animals to KBrO3 significantly declined the levels of fibrinogen (from 4.05±0.72 to 2.59±0.30 g/dL) and vitamin K (from 3.18±0.73 to 1.84±0.18 ng/mL) when compared with the untreated animals. The effect of KBrO 3 on PT, APTT, TT, Fibrinogen and vitamin k were attenuated by P. biglobosa in a dose-dependent manner. CONCLUSION: The results of this investigation demonstrated that potassium bromate caused prolongation of PT, aPTT and TT and decreased levels of fibrinogen and vitamin K, but P. biglobosa treatment counteracted these effects. Thus, it is recommended that these results be investigated in clinical trials in human volunteers.

CONTEXTE: On a signalé que le bromate de potassium (KBrO3) est toxique et qu'il a des effets néfastes sur de nombreux tissus et organes du corps. Le but de cette étude était de déterminer l'effet de la graine de Parkia biglobosa (P. biglobosa) sur la coagulopathie induite par le bromate de potassium. MÉTHODOLOGIE: P. biglobosa a été extrait à l'aide d'un extracteur soxhlet avec de l'éthanol comme solvant. Vingt-quatre rats Wistar mâles adultes ont été acclimatés dans des conditions de laboratoire et ont été répartis au hasard en groupes A, B, C et D. Le groupe A a reçu de l'eau distillée par voie orale. Les animaux des groupes B, C et D ont reçu 100 mg/kg de poids corporel de bromate de potassium, mais les groupes C et D ont également été traités avec 100 et 200 mg/kg de poids corporel de P. biglobosa respectivement. Le bromate de potassium et P. biglobosa ont été fraîchement préparés quotidiennement et administrés aux rats par gavage oral pendant 28 jours. A la fin de la période de traitement, des échantillons de sang ont été collectés dans des bouteilles de citrate de sodium et ont été utilisés pour l'analyse du temps de prothrombine (PT), du temps de thromboplastine partielle activée (APTT), du temps de thrombine (TT), du fibrinogène et des niveaux de vitamine K en utilisant des méthodes standard. RÉSULTATS: L'administration de bromate de potassium a augmenté le temps de prothrombine (PT) de 11,67±2,15 secondes (chez les animaux témoins) à 19,53±2,83 secondes. Un traitement avec 100 et 200 mg/kg de poids corporel a neutralisé cet effet de manière dose-dépendante. De même, on a observé que le KBrO3 augmentait significativement le temps de thromboplastine partielle activée (TCA) de 29,67±3,93 à 41,10±4,79 secondes et le temps de thrombine (TT) de 15,36±2,06 à 25,43±2,83 secondes par rapport aux animaux du groupe témoin. Le résultat a également montré que l'exposition des animaux au KBrO3 a réduit de manière significative les niveaux de fibrinogène (de 4,05±0,72 à 2,59±0,30 g/dL) et de vitamine K (de 3,18±0,73 à 1,84±0,18 ng/mL) par rapport aux animaux non traités. L'effet du KBrO3 sur le PT, l'aPTT, le TT, le Fibrinogène et la vitamine K a été atténué par P. biglobosa de manière dose-dépendante. CONCLUSION: Les résultats de cette étude ont démontré que le bromate de potassium a provoqué une prolongation du PT, de l'aPTT et du TT et a diminué les niveaux de fibrinogène et de vitamine K, mais le traitement par P. biglobosa a contrecarré cet effet. Il est donc recommandé que ces résultats soient étudiés dans des essais cliniques sur des volontaires humains. Mots-clés: Coagulation sanguine, Coagulopathie, Parkia biglobosa, Bromate de potassium.

Anesthetic Considerations in the Electrophysiology Laboratory: A Comprehensive Review.

Catheter ablation procedures for arrhythmias or implantation and/or extraction of cardiac pacemakers can present many clinical challenges. It is imperative that there is clear communication and understanding between the anesthesiologist and electrophysiologist during the perioperative period regarding the mode of ventilation, hemodynamic considerations, and various procedural complications. This article provides a comprehensive narrative review of the anesthetic techniques and considerations for catheter ablation procedures, ventilatory modes using techniques such as high-frequency jet ventilation, and strategies such as esophageal deviation and luminal temperature monitoring to decrease the risk of esophageal injury during catheter ablation. Various hemodynamic considerations, such as the intraprocedural triaging of cardiac tamponade and fluid administration during catheter ablation, also are discussed. Finally, this review briefly highlights the early research findings on pulse-field ablation, a new and evolving ablation modality.

A case report of deglutition triggered atrial fibrillation in a patient with Laing distal myopathy.

BACKGROUND: Deglutition-induced atrial fibrillation is a rare clinical entity with a reported prevalence of 0.6%. Laing distal myopathy is a rare autosomal dominant muscular dystrophy that is the result of mutations within the slow skeletal muscle fibre myosin heavy chain gene (MYH7). Atrial fibrillation has not been previously reported in patients with Laing distal myopathy. We describe the first reported case of deglutition triggered atrial fibrillation in a female with a history of Laing distal myopathy. CASE SUMMARY: A 44-year-old female with a history of Laing distal myopathy diagnosed at age 32, began experiencing intermittent episodes of pre-syncope and palpitations which occurred after deglutition with food. An ambulatory 30-day patient triggered event monitor recorded episodes of atrial fibrillation with rapid ventricular response. Family history was significant for Laing distal myopathy, atrial fibrillation, as well as sudden cardiac death. Laboratory data, transthoracic echocardiogram, cardiac magnetic resonance imaging, and an exercise treadmill SPECT Imaging stress test were normal. An oesophagram revealed a mild oesophageal dysmotility with no other abnormalities. She was started on flecainide 50 mg p.o. every 8 h and verapamil 40 mg p.o. every 8 h with no further episodes of atrial fibrillation. DISCUSSION: Given the strong genetic component of this myopathy, one could postulate as to a possible genetic component in the development of atrial fibrillation in our patient. Although we cannot make definite correlation between deglutition-induced atrial fibrillation and Laing myopathy, it is important to report this unusual association which has not been described before.

Heart failure as a substrate and trigger for ventricular tachycardia.

Heart failure (HF) is a major cause of morbidity and mortality with more than 5.1 million individuals affected in the USA. Ventricular tachyarrhythmias (VAs) including ventricular tachycardia and ventricular fibrillation are common in patients with heart failure. The pathophysiology of these mechanisms as well as the contribution of heart failure to the genesis of these arrhythmias is complex and multifaceted. Myocardial hypertrophy and stretch with increased preload and afterload lead to shortening of the action potential at early repolarization and lengthening of the action potential at final repolarization which can result in re-entrant ventricular tachycardia. Myocardial fibrosis and scar can create the substrate for re-entrant ventricular tachycardia. Altered calcium handling in the failing heart can lead to the development of proarrhythmic early and delayed after depolarizations. Various medications used in the treatment of HF such as loop diuretics and angiotensin converting enzyme inhibitors have not demonstrated a reduction in sudden cardiac death (SCD); however, beta-blockers (BB) are effective in reducing mortality and SCD. Amongst patients who have HF with reduced ejection fraction, the angiotensin receptor-neprilysin inhibitor (sacubitril/valsartan) has been shown to reduce cardiovascular mortality, specifically by reducing SCD, as well as death due to worsening HF. Implantable cardioverter-defibrillator (ICD) implantation in HF patients reduces the risk of SCD; however, subsequent mortality is increased in those who receive ICD shocks. Prophylactic ICD implantation reduces death from arrhythmia but does not reduce overall mortality during the acute post-myocardial infarction (MI) period (less than 40 days), for those with reduced ejection fraction and impaired autonomic dysfunction. Furthermore, although death from arrhythmias is reduced, this is offset by an increase in the mortality from non-arrhythmic causes. This article provides a review of the aforementioned mechanisms of arrhythmogenesis in heart failure; the role and impact of HF therapy such as cardiac resynchronization therapy (CRT), including the role, if any, of CRT-P and CRT-D in preventing VAs; the utility of both non-invasive parameters as well as multiple implant-based parameters for telemonitoring in HF; and the effect of left ventricular assist device implantation on VAs.

Adherence to the United States Preventative Services Task Force Female Screening Guidelines: An Internal Medicine Residency Program Experience.

Background Various guidelines exist for female preventative screening tests and medical resident physician adherence to the United States Preventive Services Task Force (USPSTF) guidelines varies. National screening rates for breast cancer and osteoporosis have improved but they are still below the expected target. Material and methods Ambulatory medical clinic records of female patients from the period July 2015 to December 2017 were reviewed for breast cancer and osteoporosis screening. Resident performance and commitment with regards to ordering the aforementioned screening tests according to the USPSTF guidelines were compared to the most recent national screening rates for mammograms and dual-energy X-ray absorptiometry (DXA) scans. Results Of the 1327 charts reviewed, 1025 was included in the study. Of the 545 mammograms performed, 93% of them were indicated according to the USPSTF guidelines (P < 0.0001, 95% CI: 125.9-342.0). A total of 480 mammograms were not ordered, of which 6% were indicated and 93.9% were not indicated. Out of a total of 107 DXA scans performed, 88.7% were correctly indicated (P < 0.0001, 95% CI: 37.11-132.9). Conclusion Resident physician adherence to the USPSTF screening guidelines for breast cancer and DXA scans were higher than the national and state screening rates. Our well-structured educational project (strong faculty mentorship, resident to patient continuity of care and the reasonable resident-clinic load) resulted in higher screening rates.