Severe Bradycardia Research Articles

The effect on vital signs of concomitant administration of nicardipine and dexmedetomidine sedation after spinal anesthesia: A double-blind, randomized controlled trial.

We evaluated heart rate (HR) and blood pressure (BP) trends when nicardipine (NCD) was co-administered during dexmedetomidine (DEX) sedation after spinal anesthesia. Sixty patients aged 19 to 65 were randomly assigned to the DEX or DEX-NCD groups. Five minutes after infusion of the loading dose of DEX, the NCD was administered intravenously at a rate of 5 μg/kg for 5 minutes in the DEX-NCD group. The study starting point was set at 0 minute when the DEX loading dose was initiated. The primary outcomes were the differences in HR and BP between the 2 groups during the study drug administration. Secondary outcomes included the number of patients whose HR was < 50 beats per minute (bpm) after the DEX loading dose infusion, and associated factors were evaluated. The incidence of hypotension in the postanesthesia care unit, postanesthesia care unit length of stay, postoperative nausea and vomiting, postoperative urinary retention, time to first urination after spinal anesthesia, acute kidney injury, and postoperative hospital length of stay were evaluated. The HR was significantly higher at 14 minutes, and the mean BP was significantly lower at 10 minutes in the DEX-NCD group than in the DEX group. The number of patients with an HR < 50 bpm during surgery was significantly higher in the DEX group than in the DEX-NCD group at 12, 16, 24, 26, and 30 minutes. The DEX group and a low initial HR were independently associated with the occurrence of an HR < 50 bpm after DEX loading dose infusion. Postoperative outcomes were not significantly different between the 2 groups. Simultaneous administration of NCD during the administration of a loading dose of DEX prevented severe bradycardia. Co-administration of NCD may be considered in patients with a low initial HR when severe bradycardia is expected during the DEX loading dose infusion. NCD and DEX may be safely infused simultaneously without affecting postoperative complications (see Figure S1, Supplemental Digital Content, http://links.lww.com/MD/J241 , Graphical abstract).

Sudden cardiac death in myocarditis

According to statistics, myocarditis is one of the leading causes of sudden cardiac death (SCD) in children and young adults. The etiology of myocarditis includes infectious and non-infectious, including autoimmune diseases, as well as toxicities and hypersensitivity to various drugs or bites of insects, spiders, snakes, etc. The risk of myocarditis among patients with COVID-19 is 15.7-fold higher than that in the general population. The most common cause of death in myocarditis is heart arrhythmia, such as ventricular tachyarrhythmia, ventricular fibrillation, or severe bradycardia. Genetic predisposition, ion and metabolic disorders, mechanisms of autoimmune response, and direct cardiotoxic action in viral diseases play a role in the pathophysiology of inflammatory myocardial damage. While the majority of patients with myocarditis, who died suddenly, was asymptomatic or had few symptoms, a timely and accurate diagnosis of myocarditis seems to be an important challenge for prevention or minimization of SCD risk. Nonetheless, at present there is no convincing evidence of an association between laboratory and instrumental parameters and the SCD risk in such patients. Endomyocardial biopsy remains the "golden standard" in the diagnosis of myocarditis. Biomarkers (troponins or creatine phosphokinase) are not highly specific. The most common electrocardiographic findings in myocarditis are sinus tachycardia and nonspecific changes in the ST-T segment. The presence of Q wave, bundle branch block, Brugada syndrome, shortened or prolonged QT interval, and early ventricular repolarization are associated with an increased risk of SCD in myocarditis. Given the absence of specific echocardiographic signs of myocarditis, special attention is paid to the assessment of the size of the cardiac chambers, wall thicknesses, global and regional systolic and diastolic function of both the left and right ventricles, visualization of pericardial effusion and intracardiac thrombi. A combined cardiac magnetic resonance imaging using T2-weighted imaging and early and late gadolinium enhancement provides high diagnostic accuracy and seems to be a useful tool in the stratification of patients with suspected acute myocarditis. With the established etiology of myocarditis, specific therapy is necessary to eliminate the pathogen. It is necessary to take into account the likely arrhythmogenic effects of the drugs used in treatment. Non-steroidal anti-inflammatory drugs are generally not indicated in patients with myocarditis because they cause renal impairment and sodium retention, which can exacerbate left ventricular dysfunction and increase the risk of SCD. In the case of severe conduction disturbances and ventricular tachyarrhythmias, implantation of a pacemaker or cardioverter-defibrillator is necessary.

Hipotensi Berat Intraoperatif Tiba-Tiba saat Kraniotomi Pengangkatan Meningioma

Blood pressure is the multiplication of cardiac output (CO) with systemic vascular resistance (SVR) and CO determined by stroke volume and heart rate frequency. A 61-year-old woman, weight 49 kg, height 154 cm, came to Santosa Hospital Bandung Central in with complaints of a lump on the back of the head that has gotten bigger since 3 years ago and the longer it gets bigger. There were no signs of increased intracranial pressure and other neurological deficits, diagnosed with meningioma with hypertension, tumor removal was carried out in a prone position. Induction with propofol, fentanyl, vecuronium bromide, lidocaine, anesthetic treatment with sevoflurane-oxygen/air and propofol and continuous vecuronium. Intraoperative suddenly occurs 2 times decrease in blood pressure, bradycardia and desaturation. Given liquid with ringerfundin, gelofusin 1 L, blood pack red cells (PRC) 2 units, sulfas atropine, ephedrine and continued with norepinephrine. Post-dissected treated 1 day in the Intensive Care Unit (ICU) and then another 1 day in the High Care Unit (HCU), then moved to the ward and was treated for 3 days before being discharged from the hospital. Severe drops in blood pressure accompanied by severe bradycardia and desaturation are unlikely to be caused by bleeding, but are more likely to be associated with heart disorders. Therapy is carried out by returning these parameters to physiological values as soon as possible. As conclusion, a sudden drop in blood pressure accompanied by bradycardia and desaturation may be due to the occurrence of Bezold-Jarisch Reflexes (BJR).

Comparison of Prophylactic Infusion of Phenylephrine Versus Norepinephrine for the Prevention of Post Spinal Hypotension in Parturients Undergoing Elective Caesarean Section-a Randomized, Double-Blinded, Non-Inferiority Trial.

Postspinal hypotension occurs in nearly 50% of women undergoing cesarean section (CS). Although phenylephrine (PE) is currently the vasopressor of choice, severe maternal bradycardia may adversely affect the fetal status due to the reduction in the maternal cardiac output. Norepinephrine (NE) is not associated with bradycardia and is now being evaluated for the treatment of post-spinal hypotension in obstetric patients. The hypothesis of this study was that the prophylactic NE infusion was non-inferior to PE infusion when used for the prevention of postspinal hypotension. This was a randomized, double-blinded controlled study conducted in 130 parturients scheduled for CS. The participants received either prophylactic NE (5 μg min-1) or PE (25 μg min-1) infusion beginning at the time of spinal injection. The primary outcome was the incidence of hypotension in both groups. Maternal bradycardia, reactive hypertension, nausea and vomiting, requirement of rescue boluses of vasopressor and/or atropine, and neonatal acid base status were also recorded. The incidence of hypotension was 33.80% (22 of 65) in Group PE and 26.10% (17 of 65) in Group NE (P=0.85). The absolute risk difference [90% confidence interval (CI)] in the incidence of hypotension between the groups was -7.7% (-20.9, 5.4). The upper limit of the CI was less than the non-inferiority margin of 20%, indicating that the NE infusion was non-inferior to PE. Prophylactic infusion of NE is not inferior to prophylactic PE infusion in the prevention of postspinal hypotension in patients undergoing CS.

Short and midterm outcome of intraprocedural sinus node dysfunction requiring stimulation during ablation of persistent atrial fibrillation

Abstract Funding Acknowledgements Type of funding sources: None. Background Ablation within the superior, antero-lateral portions of the right atrium has been described as a risk for sinus node dysfunction (SND) because of direct damage to the sinus node. The sinoatrial nodal artery arises from the right coronary artery in the majority of people and courses close to the superior posterior aspect of the interatrial septum. Rare cases of SND were observed periprocedurally during atrial fibrillation/flutter ablation. We sought to report on clinical characteristics, ablation set and acute and midterm rhythm outcome of patients who develop acute SND during/immediately after exclusively left atrial ablation. Methods We performed a retrospective analysis of AF/Aflutter ablation patients between January 2017 and December 2019 to characterize those who required temporary pacemaker (TPM) implantation due to acute sinus node dysfunction (sinus arrest, sinus bradycardia &amp;lt;35 beats/min with hemodynamic compromise) following atrial ablation. Results Of 1,072 patients, at nine patients [0,8%] intraprocedural temporary pacemaker implantation was necessary due to severe SND and hemodynamic compromise. The reasons for implantation were identified as sinus arrest (n=6) or severe sinus bradycardia (n=3). Eight of nine patients were male [89%], age 73 +11.2, 6/9 [67%] persistent AF, 2/9 [22%] Aflutter. The ablation set consisted of: pulmonary vein (PV) isolation in all patient (n = 9), left atrium(LA)-substrate modification in 8. In detail: roof line ablation (n = 3), mitral annulus-right superior PV line ablation ( n=8), mitral annulus-left superior PV line (n = 3). No patient had an ablation within the the right atrium. Four of nine [22%] pts. received permanent PM before discharge, performed 5 days postablation (range 3-7 days). At 3-month device interrogation, all patients were atrially paced, with a pacing proportion of &amp;gt;40% in 3/4 [0,3%] patients. Conclusion Acute sinus node dysfunction is a rare complication of sole left atrial ablation outside the pulmonary veins. However, a relevant fraction of these patients requires permanent implantation with substantial pacing proportion during midterm follow up.

AP-452681-2 6 MONTH FOLLOW-UP OF A SUCCESSFUL FLUOROLESS PEDIATRIC GANGLIONATED PLEXI ABLATION

Cardioneuroablation (CNA) has been shown to treat vagally mediated bradyarrhythmias and vasovagal syncope. In this case, an 8-year-old female with Down’s Syndrome, duodenal atresia, and intermittent nocturnal AV block status post pacemaker without significant cardiopathy underwent successful ganglionated plexi ablation. To discuss the novel use of CNA in pediatric patients for symptomatic vasovagal syncope which can significantly reduce the volume of pacemakers implanted and obviate the need for subsequent lifelong generator replacements and lead revisions. CNA and GP locations were described and reviewed by Garcia et al for cardioinhibitory syncope treatment and prevention.1 Guidelines followed for CNA were well defined by Pachon2 and Aksu3. Localized assessments were performed at areas of complex fractionated signals at main ganglionated plexi (GP) locations. GP/cardiac insertion points are defined through high frequency (HF) EGM analysis with fractionation mapping software (NAVX, Abbott), as 3-5 deflections within the atrial cardiac cycle. Higher frequency signals were localized during mapping and correlated with traditional EGM analysis of 30-500Hz. All catheter positions were visualized with vascular ultrasound and NAVX 3-D mapping. Pacing the vagus nerve 50 Hz/50 microseconds provoked sinus slowing on the left and AV block on the right (figure 2). Fluoroscopy was not utilized. Standard RF targets were set at 60°C with maximum power of 50W. RF lesions were applied to previously defined GP1-4, targeting areas of HF signals4 for a maximum of 60 seconds. HR increase was noted with RF at GP1(18%), and this persisted throughout the case. Wenckebach cycle length change was 13%. Post ablation, HR remained unchanged during stimulation of bilateral vagal nerves. Additionally, there was no change in HR with atropine administration. At 6 month follow up, device check shows 0% pacing. Holter monitor demonstrated transient Wenckebach during sleep. Successful fluoroless GP ablation was performed for recurrent severe cardioinhibitory bradycardia. 6 month follow-up device check 0% pacing burden re-demonstrates sustained success of CNA. Future plans include another 6 months of monitoring followed by pacemaker deactivation and extraction discussion.

PO-04-033 CARDIONEUROABLATION IN A WOMAN WITH ICTAL-INDUCED CARDIAC ASYSTOLE

Ictal-induced cardiac bradyarrhythmia and asystole is a rare phenomenon. The exact mechanism of ictal-induced cardiac bradyarrhythmia and asystole remains unclear. It was postulated that stimulation of central autonomic network during ictal episode may trigger an abrupt burst of hypervagotonia. Prolonged episode of cardiac bradyarrhythmia and asystole may result in syncope or death due to impairment of cerebral perfusion. The role of cardioneuroablation (CNA) in this condition has not been well-described in the literature. To describe a case of successful CNA in a patient with ictal-induced bradyarrhythmia and asystole. n/a A 47-year-old female has a 1.5-year history of intractable focal epilepsy and COVID-19 infection. She started having multiple episodes of seizures following a mild COVID-19 infection. Electroencephalogram (EEG) and brain MRI revealed right temporal onset seizures without structural lesions. Due to ongoing uncontrolled seizures with multiple semiologies despite multiple anti-epileptic drugs, she was admitted to Epilepsy Monitoring Unit for seizure classification. Her ictal EEGs (Figure 1) showed onset of ictal rhythm in the right temporal region with episodes of severe sinus bradycardia (15-30 bpm) and sinus pauses (15-16 seconds). Telemetry tracings demonstrated PP interval slowing with PR interval prolongation prior to the pauses consistent with a vagally-mediated mechanism. Cardiac electrophysiology team recommended CNA for treating the episodes of ictal-induced bradyarrhythmia and asystole. 3D anatomic maps of the right atrium (RA) and left atrium (LA) were created using CARTO system (Biosense Webster). Right superior ganglionated plexus (RSGP) was localized with fractionation mapping and intracardiac echocardiography guidance. RSGP was targeted from the RA using an irrigated radiofrequency catheter with power limit of 25 W. Post-ablations of RSGP, her heart rate increased from 60 - 99 bpm. Additional lesions were delivered from the LA site but no additional heart rate increase was not seen. An implantable loop recorder was implanted post-ablation procedure. During follow-up of 8 months, she had recurrent focal epilepsy, but no bradyarrhythmias or asystole was noted on her loop recorder. Resting heart rates at long-term follow up were between 70 - 100 bpm. This case highlights the utility of CNA in patient with ictal-induced cardiac bradyarrhythmia and asystole. CNA may be an approach to avoid permanent pacemakers in this population.

Genetics of sinoatrial node function and heart rate disorders

The sinoatrial node (SAN) is the primary pacemaker of the mammalian heart, initiating its electrical activation and ensuring that the heart's functional cardiac output meets physiological demand. SAN dysfunction (SND) can cause complex cardiac arrhythmias that can manifest as severe sinus bradycardia, sinus arrest, chronotropic incompetence and increased susceptibility to atrial fibrillation, among other cardiac conditions. SND has a complex aetiology, with both pre-existing disease and heritable genetic variation predisposing individuals to this pathology. In this Review, we summarize the current understanding of the genetic contributions to SND and the insights that they provide into this disorder's underlying molecular mechanisms. With an improved understanding of these molecular mechanisms, we can improve treatment options for SND patients and develop new therapeutics.

Reality of clonidine poisoning in children and adolescents.

We aimed to describe the severity of clonidine poisonings in a paediatric population referred to a tertiary toxicology service. We undertook a retrospective review of all presentations of clonidine poisoning in children or adolescents reported to a tertiary toxicology service from March 2014 to February 2020. Cases were divided into young children (0-6 years), older children (7-11 years) and adolescents (12-17 years). We report clinical effects: bradycardia, hypotension and abnormal Glasgow coma score (GCS), based on standard paediatric observation charts, interventions, length of emergency department stay, proportion admitted to a medical ward or paediatric intensive care unit. We identified 111 clonidine poisonings, 41 young children, 9 older children and 61 adolescents. There were more females in the adolescent group and slightly more males in the younger age groups. The median dose ingested was 13 mcg/kg (interquartile range: 7-38 mcg/kg), which varied across ages. Clonidine alone was ingested in 78 cases (70%) and co-ingestion was more common in adolescents (24/61; 39%). Thirty-seven patients (33%) were admitted and 23 (21%) were admitted to paediatric intensive care unit. Median length of emergency department stay was 16.4 h, longer for adolescents. At least one abnormal observation occurred in 101 of 111 (91%) cases: 76 of 106 (72%) bradycardia, 76 of 110 (69%) hypotension and 4 of 99 (4%) GCS < 9. Thirteen (12%) had severe bradycardia, more common in young children and 23 (21%) had severe hypotension, more common in adolescents. For 27 children (0-11 years) ingesting 5-10 mcg/kg, 3 (11%) had severe bradycardia or severe hypotension and 1 received naloxone (4%). No cases ingesting <5 mcg/kg developed moderate/severe bradycardia or hypotension. Four cases received naloxone with no significant change, two patients got atropine with a transient response. One patient was intubated to facilitate safe inter-hospital transfer. Paediatric clonidine poisoning commonly results in bradycardia, hypotension and decreased GCS, but rarely severe or requiring major interventions. Children ingesting <5 mcg/kg do not require admission.

Prolonged Severe Bradycardia in the Artery of Percheron Infarct.

Prolonged Severe Bradycardia in the Artery of Percheron Infarct.

Managing postoperative atrial fibrillation after open-heart surgery using transdermal β1 blockers

BackgroundPostoperative atrial fibrillation (POAF) after open-heart surgery is a non-negligible complication. We aimed to describe the efficacy of a transdermal patch of bisoprolol for managing POAF and flutter in thoracic surgical procedures.MethodsWe analyzed the data of 384 patients who underwent open-heart surgery at our hospital and received oral bisoprolol to prevent POAF. Among them, 65 patients (16.9%) also received a 4-mg transdermal patch of bisoprolol to control the heart rate due to POAF. We applied the bisoprolol transdermal patch when the heart rate was > 80 bpm and removed it at ≤ 60 bpm; an additional patch was applied when the heart rate was > 140 bpm. Heparin calcium injections were administered twice daily for anticoagulation between 2 and 6 days postoperatively.ResultsThe average number of prescriptions for transdermal patches of bisoprolol during hospitalization was 1.8 ± 1.1 (1–5). The median first prescription date was on postoperative day 2 (range: days 0–37). Sinus rhythm recovered within 24 h in 18 patients (27.7%). Eight patients (12.3%) were switched to continuous landiolol infusion because of persistent tachycardia. In three patients, the transdermal patch was removed owing to severe bradycardia. Fifteen patients experienced persistent atrial fibrillation and were treated with electrical cardioversion during hospitalization. We did not observe any serious complications that could be directly attributed to bisoprolol transdermal patch use.ConclusionsSingle-use bisoprolol transdermal patch may help control the heart rate during the initial treatment of POAF after open-heart surgery.

Massive Venous Air Embolism in a Case of Hysteroscopy: A Rare Grave Complication in a Comparatively Simple Procedure

Hysteroscopic surgery has gained popularity but lethal complication like gas or venous air embolism can occur. It can be recognized by a decrease in oxygen saturation and sudden drop in end-tidal carbon dioxide and may sometimes lead to severe organ failure and death depending on the amount of air embolism. We report the case of a 55-year-old female with no comorbidities posted for evaluation of postmenopausal bleeding by diagnostic hysteroscopy. The procedure was performed under spinal anesthesia using normal saline as distending media. Midway between the procedures, the patient developed severe bradycardia and desaturation. Hence, with the diagnosis of massive pulmonary embolism, the patient was resuscitated but could not be revived. The fatal outcome from a comparatively simple procedure is not uncommon. Complications are to be kept in mind and possible precautionary measures are to be taken at all times. As the eye cannot see what the mind does not know.

A rare case with fetal autoimmune heart block and KNCH2 variant–induced long QT syndrome: a controversial opinion on prenatal management strategy

BackgroundAmong all fetal heart block patients, > 50% cases are associated with maternal autoimmune diseases, and such patients should receive treatment. However, nearly half of fetal heart block cases involve a mother with negative results following autoimmune antibody screening. A few studies have reported long QT syndrome (LQTS) can also present as a severe fetal bradycardia, which does not respond to fetal treatment. Herein, we reported a rare case of an infant who presented with high-degree autoimmune-mediated fetal atrioventricular block (AVB) with LQTS induced by a novel KCNH2 variant. This case led us to review our prenatal therapeutic strategy.Case presentationA 1-year-old boy presented to our heart center having experienced syncope 5 times in the past year. He had previously presented with fetal bradycardia during the fetal stage from 27 + 3 gestational weeks. The fetal echocardiography demonstrated AVB (2:1 transmission). As the maternal autoimmune antibody results were positive, his mother had received dexamethasone treatment during pregnancy; subsequently, the fetal AVB had changed from 2:1 to 4:3 transmission with elevated ventricular beating rates. However, this patient was identified to have complete AVB after birth. The initial electrocardiogram and Holter measurements at hospital administration showed complete AVB, pleomorphic ventricular tachycardia, a prolonged QT interval (QT = 602 ms, corrected QT = 538 ms), and wide and deep inverted T-waves. Meanwhile, torsades de pointes could be observed in several transit ventricular tachycardias based on Holter monitoring review. Genetic testing revealed KCNH2 c.2483G > A variant–induced LQTS. An implantable cardioverter defibrillator device and permanent pacemaker were both considered as therapeutic alternations; his parents ultimately accepted the implantation of a permanent pacemaker.ConclusionsFor fetuses with autoimmune-mediated AVB, intrauterine treatment should still be pursued immediately. However, once the treatment outcomes are deemed unacceptable or unexpected, other genetic variant–related channelopathies should be highly suspected. If the fetus lacks a positive family history, fetal genetic testing should be recommended to improve the prognosis of such patients by introducing integrative therapeutic strategies between the prenatal and postnatal phases.

Unexpected cardiorespiratory findings postictally and at rest weeks prior to SUDEP.

Mechanisms underlying sudden unexpected death in epilepsy (SUDEP) are unclear, but autonomic disorders are thought to play a critical role. However, those dysfunctions have mainly been reported in the peri-ictal context of generalized tonic-clonic seizures. Here, we explored whether heart rate variability (HRV), heart rate (HR), and breathing rate (BR) changes could be observed perictally during focal seizures with or without impaired awareness as well as interictally to assess the risk of SUDEP. We report the case of a 33-year-old patient with drug-resistant bilateral temporal lobe epilepsy who died at home probably from an unwitnessed nocturnal seizure ("probable SUDEP"). Ictal and interictal HRV as well as postictal cardiorespiratory analyses were conducted to assess autonomic functions and overall SUDEP risk. The SUDEP patient was compared to two living male patients from our local database matched for age, sex, and location of the epileptic focus. Interictal HRV analysis showed that all sleep HRV parameters and most awake HRV parameters of the SUDEP patient were significantly lower than those of our two control subjects with bitemporal lobe epilepsy without SUDEP (p < 0.01). In two focal with impaired awareness seizures (FIAS) of the SUDEP patient, increased postictal mean HR and reduced preictal mean high frequency signals (HF), known markers of increased seizure severity in convulsive seizures, were seen postictally. Furthermore, important autonomic instability and hypersensitivity were seen through fluctuations in LF/HF ratio following two seizures of the SUDEP patient, with a rapid transition between sympathetic and parasympathetic activity. In addition, a combination of severe hypopnea (202 s) and bradycardia (10 s), illustrating autonomic dysfunction, was found after one of the SUDEP patient's FIAS. The unusual cardiorespiratory and HRV patterns found in this case indicated autonomic abnormalities that were possibly predictive of an increased risk of SUDEP. It will be interesting to perform similar analyses in other SUDEP cases to see whether our findings are anecdotal or instead suggestive of reliable biomarkers of high SUDEP risk in focal epilepsy, in particular focal with or without impaired awareness seizures.

Fetal pulmonary valvuloplasty for pulmonary atresia with intact ventricular septum: a single-center clinical experience.

Fetal pulmonary valvuloplasty for pulmonary atresia with intact ventricular septum: a single-center clinical experience.

Synergy between Membrane Currents Prevents Severe Bradycardia in Mouse Sinoatrial Node Tissue

Bradycardia is initiated by the sinoatrial node (SAN), which is regulated by a coupled-clock system. Due to the clock coupling, reduction in the 'funny' current (If), which affects SAN automaticity, can be compensated, thus preventing severe bradycardia. We hypothesize that this fail-safe system is an inherent feature of SAN pacemaker cells and is driven by synergy between If and other ion channels. This work aimed to characterize the connection between membrane currents and their underlying mechanisms in SAN cells. SAN tissues were isolated from C57BL mice and Ca2+ signaling was measured in pacemaker cells within them. A computational model of SAN cells was used to understand the interactions between cell components. Beat interval (BI) was prolonged by 54 ± 18% (N = 16) and 30 ± 9% (N = 21) in response to If blockade, by ivabradine, or sodium current (INa) blockade, by tetrodotoxin, respectively. Combined drug application had a synergistic effect, manifested by a BI prolonged by 143 ± 25% (N = 18). A prolongation in the local Ca2+ release period, which reports on the level of crosstalk within the coupled-clock system, was measured and correlated with the prolongation in BI. The computational model predicted that INa increases in response to If blockade and that this connection is mediated by changes in T and L-type Ca2+ channels.

Collapse of inferior vena cava during complex filter retrieval with consequent intra-procedural systemic hypotension and bradycardia: a case report

BackgroundProlonged dwelling time of inferior vena cava (IVC) filters has been shown to increase the need for the use of complex IVC filter retrieval techniques. In this report, we describe a case of complex retrieval of an IVC filter with prolonged dwelling time, which was temporarily accompanied by severe bradycardia and hypotension.Case presentationFifty-nine-year-old male patient past medical history of morbid obesity, atrial fibrillation status post-ablation, obstructive sleep apnea, and end-stage renal disease presented for IVC filter retrieval 16 years after placement. When the IVC filter was covered by sheaths, and the IVC was temporarily collapsed and occluded, the patient developed severe bradycardia and hypotension without compensatory tachycardia. Contrast injection through the common femoral vein sheath showed complete occlusion of IVC while the IVC filter was covered by both sheaths, likely due to the embedment of the IVC filter in the wall by extensive fibrinous tissues. IVC filter was successfully retrieved, and the blood pressure and heart rate were improved immediately afterward. A large non-occlusive IVC thrombus was identified on the final venogram, which was aspirated using a mechanical thrombectomy device.ConclusionComplex retrieval of IVC filters with prolonged dwelled time can result in acute severe bradycardia and hypotension due to vasovagal reaction, acute collapse, and occlusion of IVC in the setting of IVC filter embedment in the wall by extensive fibrinous tissues.

Rate of decline of fetal base excess after neuraxial anesthesia for scheduled cesarean delivery

In scheduled cesarean deliveries, the rate of decrease in the umbilical artery pH is related to the severity of maternal hypotension and the interval from spinal placement to delivery. Base excess values have greater use than umbilical artery pH values to time the duration of fetal acidemia because they demonstrate a linear rather than logarithmic correlation with the degree of acidosis. This study aimed to evaluate the rate of decline in the fetal base excess in scheduled cesarean deliveries that were converted to emergency cesarean delivery owing to fetal bradycardia following spinal anesthesia. All cases of scheduled cesarean deliveries in gestations at >34 weeks' gestation under spinal anesthesia that were converted to emergency cesarean deliveries owing to fetal bradycardia in the period May 2019 to May 2021 were reviewed. Included were those with (1) a preoperative reactive nonstress test and (2) fetal acidemia (umbilical artery pH <7.20). Excluded were those with anesthesia other than spinal and a birthweight below the 10th percentile for gestational age. Time intervals between the completion of spinal anesthesia and delivery were calculated and related to umbilical cord gas analytes. From a cohort of 1064 scheduled cesarean deliveries, 7 fulfilled the study criteria yielding 8 neonates. Mean ± standard error of the mean interval of spinal anesthesia to delivery was 15.0±1.9 minutes, and the decrease in mean blood pressure after spinal anesthesia was 39.1±3.0 mm Hg. Umbilical artery base excess ranged from -5.2 to -16.6 mmol/L (median, -8.0). Based on published normative data of prelabor fetal umbilical artery base excess (-2±0.6 mmol/L), the mean rate of base excess decrease was 0.38±0.25 mmol/minute. The rate of decrease in base excess when scheduled cesarean deliveries are converted to emergency cesarean deliveries owing to fetal bradycardia related to spinal anesthesia (1 mmol/2.6 min) matches the estimated rate of loss of base excess (1 mmol/2-3 minutes) reported in cases of severe bradycardia or sentinel events during labor.

Cardiac Toxicity of Alectinib in PatientsWith ALK+ Lung Cancer: Outcomes of Cardio-Oncology Follow-Up.

Anaplastic lymphoma kinase (ALK) translocations in metastatic non-small cell lung cancer (3% to 7%) predict for response to ALK-inhibitors (eg, alectinib, first line), resulting in a 5-year survival rate of ∼60% and median progression-free survival of 34.8months. Although the overall toxicity rate of alectinib is acceptable, unexplained adverse events, including edema and bradycardia, may indicate potential cardiac toxicity. This study's aim was to investigate the cardiotoxicity profile and exposure-toxicity relationship of alectinib. Between April 2020 and September 2021, 53 patients with ALK-positive non-small cell lung cancer treated with alectinib were included. Patients starting with alectinib after April 2020 underwent a cardiac work-up at start, at6months and at 1 year at the cardio-oncology outpatients' clinic. Patients already receiving alectinib >6months underwent 1 cardiac evaluation. Bradycardia, edema, and severe alectinib toxicity (grade≥3 and grade≥2 adverse eventsleading to dose modifications) data were collected. Alectinib steady-state trough concentrations were used for exposure-toxicity analyses. Left ventricular ejection fraction remained stable in all patients who underwent an on-treatment cardiac evaluation (n=34; median 62%; IQR: 58%-64%). Twenty-two patients (42%) developed alectinib-related bradycardia (6 symptomatic bradycardia). One patient underwent a pacemaker implantation for severe symptomatic bradycardia. Severe toxicity was significantly associated with a 35% higher alectinib mean Ctrough (728 vs 539ng/mL, SD=83ng/mL; 1-sided P=0.015). No patients showed signs of a diminished left ventricular ejection fraction. Alectinib caused more bradycardia than previously reported (42%) with some instances of severe symptomatic bradycardia. Patients with severe toxicity generally had an elevated exposure above the therapeutic threshold.

Incidence and potential risk factors for remdesivir-associated bradycardia in hospitalized patients with COVID-19: A retrospective cohort study.

Background: Remdesivir is widely used for the management of COVID-19 and several studies have reported bradycardia as a potential side effect associated with this agent. The aim of the present study was to evaluate the incidence rate, severity, and potential risk factors of remdesivir-associated bradycardia. Methods: We performed a retrospective cohort study among hospitalized adult patients with COVID-19 who were treated with remdesivir from March 2020 to October 2021. Our primary outcome of interest was the incidence rate and severity of bradycardia after remdesivir administration. We defined mild bradycardia as a heart rate of 51-59 beats per minute, moderate bradycardia as a heart rate of 41-50 beats per minute, and severe bradycardia as a heart rate of ≤40 beats per minute. We also performed univariable and multivariable regression analyses to determine potential bradycardia risk factors. Baseline characteristics were reported as means with standard deviations or medians with interquartile ranges (IQRs). All the statistical tests are shown as odds ratios (ORs) with 95% confidence intervals (CIs). Results: In total, 1,635 patients were included in this study. The median age with IQR was 68 (57-79) years and 51.7% of the patients were male. In total, 606 (37.1%) patients developed bradycardia. Among them, 437 patients (26.7%) developed mild bradycardia, 158 patients (9.7%) moderate bradycardia, while 11 patients (0.7%) experienced severe bradycardia. In our adjusted multivariate logistic regression, the odds of bradycardia development after remdesivir administration were higher among patients with age ≥65years (OR 1.76, 95% CI: 1.04-2.99, p = 0.04), those with hypertension (OR 1.37, 95% CI: 1.07-1.75, p = 0.01), and obesity (OR 1.32, 95% CI: 1.02-1.68, p = 0.03). Conclusion: More than 1 out of 3 patients (37%) who received remdesivir for COVID-19 developed bradycardia with the majority of these patients developing mild or moderate bradycardia that is usually a benign manifestation not needing treatment in most cases. Age ≥65years, hypertension, and obesity were potential risk factors for remdesivir-associated bradycardia among hospitalized COVID-19 patients. Clinicians should be aware of this adverse event and consider close clinical monitoring for patients at high risk for this adverse event.