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A 50-year-old gentleman with old anterior wall myocardial infarction with implantable cardioverter defibrillator (ICD, Abbott Medical, Fortify ST VR 1235-40) presented with recurrent appropriate ICD shock. The ICD stored EGM indicated a possibility of supraventricular tachycardia (SVT) rather than ventricular tachycardia (VT) when the morphology match was found high. Bundle brunch re-entry (BBR) VT was another differential. An EP study conducted on antiarrhythmic drugs (AAD) induced reproducible but only ill-sustained tachycardia too short to perform any SVT maneuvers during tachycardia. However, critical analysis of the tachycardia electrograms suggested atypical AVNRT as the most likely mechanism. The other differentials were atrial tachycardia (AT) and BBR VT. Manoeuvres during sinus rhythm and ventricular pacing excluded other diagnosis. A single point radiofrequency ablation (RFA) near the SP region cured the arrhythmia. The reason for misclassification of SVT as VT was also sought for. It was found that the shocks were received due to fulfilment of 2/3 criteria (sudden onset and regular tachycardia). Hence, he received therapy despite an appropriate morphology match favouring SVT. This is one of the known limitations of ICDs where regular SVTs (AVNRT/AVRT or AT) may receive inappropriate ICD therapies. After slow pathway modification there was no further recurrence of either SVT or VT; hence , a substrate modification was deferred.
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INTRODUCTION: The causes of atrial undersensing in a dual chamber pacemaker include true undersensing (low amplitude electrogram), functional undersensing (related to the effect of special timing cycles in the presence of an adequate signal) and paradoxical undersensing. This case report describes paradoxical atrial undersensing at a higher programmed atrial sensitivity and with the return of normal atrial sensing at a lower programmed sensitivity.
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BACKGROUND: Endless loop tachycardia (ELT) is the commonest pacemaker mediated tachycardia (PMT) encountered among patients with cardiac implantable electronic devices (CIEDs). Despite being enabled with various preventive algorithms, we encountered several cases having recurrent, long, and symptomatic ELT. MATERIALS AND METHODS: We retrospectively analyzed consecutive device checkups at device clinic at a single center of eastern India between January 2019 to March 2023. RESULTS: There were 20 cases of confirmed and sustained ELT among 4520 device checks. Although mostly benign, in two cases ELT led to clinical worsening in patients having left ventricular (LV) systolic dysfunction. Even with good ventricular function, ELT resulted in improper atrioventricular (AV) synchrony leading to disabling symptom in one case. The differentiation of ELT from sinus tachycardia and atrial tachycardia (AT) was not always easy. Magnet application is certainly useful to differentiate. The situations that provoked ELT in this study were-long AV delays, VIP (ventricular intrinsic preferences)/MVP (managed ventricular pacing), atrial non-capture, atrial under/over sensing, premature ventricular contractions (PVCs)/couplets, premature atrial contractions (PAC) and slower ventriculo-atrial (VA) conduction. Rate responsive shortening of post-ventricular atrial refractory period (PVARP) also promoted its occurrence and hindered troubleshooting. When ELT occurred despite post-PVC extension of PVARP, lowering the atrial sensitivity, switching to bipolar sensing and manual setting of longer PVARP after measuring VA conduction time were useful. "Rate responsive PVARP" had to be turned off in a few cases to prevent ELT. On the contrary, an over aggressive prolongation of PVARP led to repetitive non-reentrant ventriculo-atrial synchrony (RNRVAS) in two cases. Checking VA conduction during implantation and noninvasive program stimulation (NIPS) during follow up were useful to check the tendency for ELT. CONCLUSION: Clinically significant ELT is rare but not uncommon among devices having in-built preventive algorithms. Manual adjustments are often useful to troubleshoot the same.
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We report a case of symptomatic supraventricular tachycardia who had absent VA conduction during electrophysiology study. The interesting finding was appearance of VA conduction only at a specific cycle length of ventricular pacing which reproducibly induced a sustained orthodromic re-entrant tachycardia (ORT). We review the literature and conclude that supernormal AP conduction can explain such phenomenon.
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A 13-year-old-girl presented with one episode of pre-syncope while standing in a train. Her ECG was suggestive of preexcitation. Echocardiography revealed structurally normal heart without any ventricular hypertrophy. During electrophysiology study, her ventriculo-atrial (VA) conduction was absent even on isoprenaline. However, a para-Hisian pacing maneuver (PHP) revealed consistent VA conduction with a nodal response. This finding indicated that the VA dissociation at baseline was at infra-Hisian (VH) level and conduction at HA level was intact. In addition, this finding is coherent with a speculation of a fasciculo-ventricular pathway (FVP) resulting in such an ECG pattern in her. Pacing from various atrial sites (right atrium, coronary sinus) exhibited nearly fixed preexcitation and short non-varying HV interval confirmatory of FVP. Testing for a PRKAG mutation was advised for her.
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During ventricular extra stimuli(VES) protocol a VA jump was noted. In upper panel with VES @ 500/270 ms (Fig A) the His signal appeared after the A-EGM, ruling out pure nodal VA conduction and confirming presence of an accessory pathway (AP). The H signal was delayed due to probable retrograde RBBB. The atrium was already depolarised via AP and the VA traversing via left bundle-His-node got blocked with a H signal. In the lower panel with VES of 500/260 ms the retrograde AP conduction reached the effective refractory period and pure nodal VA conduction took place along with retrograde RBBB. The retrograde VA jump was hence due to a jump from AP to AV node.
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L-Asparaginase owes considerable significance in food and pharmaceutical applications. L-Asparaginase is an antineoplastic enzyme that finds application in the treatment of Acute Lymphoblastic Leukemia (ALL) and in mitigating acrylamide (a potent carcinogen) production during baking. In this study, we aimed to optimize nutritional parameters that are significant in initiating and regulating a bioprocess system in order to maximize enzyme production from a novel isolated bacterial species Brevibacillus borstelensis ML12 so the high-yielding enzyme producers can be selected and utilized for better efficacy of this commercially viable enzyme in pharmaceutical field, food industry, in biosensors and as an antioxidant growth kinetics study of the organism was performed and the maximum specific growth rate µo (min-1) and Monod half saturation constant Ks for L-Asparagine came out to be µo = 0.0189 min-1 and Ks = 2.44 mM, respectively at 0.04 M asparagine concentration and 37 °C. Effect of different nutritional parameters like carbohydrates, organic and inorganic nitrogen sources, L-Asparagine, minerals, surfactants and bile were performed. Maximum L-Asparaginase production occurred at 0.01% dextrose, 20 g L-1 L-Asparagine, 10 mM cobalt chloride, 0.1% Tween 80 and 1% bile concentrations (237.319 IU mL-1).
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Antineoplásicos , Asparaginasa , Asparagina , Antineoplásicos/farmacología , Preparaciones FarmacéuticasRESUMEN
Newer devices incorporate advanced algorithms to have more accurate delivery of implantable cardioverter-defibrillator (ICD) therapy. Newer models of Abbott Implantable cardioverter-defibrillators like Gallant and Entrant have a new ventricular fibrillation (VF) therapy assurance algorithm. This algorithm has a proven role in avoiding under-detection of VF where some of the smaller electrograms are under-sensed. We report a case of ventricular fibrillation therapy assurance (VFTA) algorithm malfunction in a 48-year-old lady having single chamber Entrant Implantable cardioverter-defibrillator, where the patient received inappropriate therapies. The VFTA algorithm eventually had to be turned off.
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Desfibriladores Implantables , Taquicardia Ventricular , Femenino , Humanos , Persona de Mediana Edad , Fibrilación Ventricular/terapia , Fibrilación Ventricular/diagnóstico , Alta del Paciente , Arritmias Cardíacas/terapia , AlgoritmosRESUMEN
Ventricular fibrillation induced by short-coupled premature ventricular complex is an uncommon cause of cardiac arrest in young individuals with no structural heart disease. The genetic substrate of this condition is heterogeneous and remains incompletely defined. We describe a case of short-coupled premature ventricular complex-triggered ventricular fibrillation with a likely pathogenic variant in the titin (TTN) gene. (Level of Difficulty: Advanced.).
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A 63-year-old lady with a high-grade atrioventricular (AV) block and a structurally normal heart underwent permanent pacemaker implantation (dual chamber, Medtronic Ltd) 8 years back. On follow up, she had a recurrence of syncope after 3 years. The device interrogation at that time had revealed ventricular tachycardia (VT) for which she underwent implantable cardioverter defibrillator (ICD, Medtronic Ltd, Egida DR, DF1) upgradation at another center (electrograms not available). Now, she presents with episodes of presyncope after another 5 years. The Echocardiography was unremarkable. The ICD was interrogated & there was a stored ventricular fibrillation (VF) episode. But the electrograms suggested noise over a true VF electrogram noted in both near and far-field. In all probability, the VF was not a true one which might have arisen from some lead noise or from an electromagnetic interference (EMI). Fluoroscopy revealed an evident lead fracture near the superior vena cava (SVC) coil. The stored electrogram (EGM) characteristics also suggested possible lead noise rather than a true VF. She was advised for lead revision. Interestingly, all pacing parameters were normal along with normal impedance despite the evident lead fracture. This happened due to the ICD lead arrangements as there are separate electrodes for the SVC/RV coil and pacing. While the SVC coil was damaged, the pacing electrodes remained unaffected. Since the patient has no episode of true VT/NSVT and the echocardiography was normal, she was managed temporarily by changing the pacemaker to asynchronous (DOO) mode.
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The present study has been aimed at evaluating the antiobesity, antihyperglycemic, and antidepressive potentials of Asparagus racemosus starter-based rice fermented foods. High-throughput NGS technology has revealed a number of bacterial genera in the prepared fermented rice, such as Lactobacillus (29.44%), Brevundimonas (16.21%), Stenotrophomonas (6.18%), Pseudomonas (3.11%), Bacillus (2.88%), and others (<2%). Eight-week administration of rice fermented food has increased food intake, whole-body weight, organ weight, different fat masses, serum lipid profiles, and histology of liver and adipose tissues in HFD-induced obese mice. In addition, upregulation of fatty acid oxidation and downregulation of adipocytogenesis- and lypogenesis-related genes along with the expression of their regulatory nuclear factors such as PPARα, PPARγ, PPARδ, and SREBP-1c have also been noted. Moreover, fermented food decreases fasting blood glucose level and improves glucose and insulin tolerance as well as the expression of GLUT4 receptor. Antiobesity and antihyperglycemic effects are also supported by the changes in insulin, leptin, and adiponectin hormone levels. The real-time polymerase chain reaction (RT-PCR) and denaturing gradient gel electrophoresis (DGGE) analyses have clearly demonstrated the intense colonization of Bacteroides, Lactobacillus, and Bifidobacterium, as well as the suppressed growth rate of γ- and δ-Proteobacteria and Firmicutes in the gut after fermented food intake. In the intestine, the latter group of microorganisms possibly modulate short-chain fatty acid (SCFA) levels such as acetate, butyrate, and propionate more than twofold. The impairment of memory-learning and anxiety-like obesity-associated cognitive phenotypes is mitigated significantly (p < 0.01) by fermented food as well. Thus, the formulated fermented food could be used as a natural therapeutic to alleviate obesity and its associated psychological and pathophysiological ailments.