Transvenous Before Surgical Hybrid Procedure.

BACKGROUND: Historically, persistent atrial fibrillation (PeAF) and long standing persistent atrial fibrillation (LSPeAF) have demonstrated limited clinical success despite hybrid approaches. OBJECTIVE: We describe our experience with the endocardial-before-epicardial approach defined by a comprehensive endovascular approach preceding and guiding the epicardial approach which includes an extensive posterior wall ablation. METHODS: 40 patients were followed over a 12 month period. The procedure was performed in a single center. Patients had a mean duration of atrial fibrillation of 6.0 ± 4.5 years with 22.5% having undergone prior ablations. Mean age was 61.7 ± 7.9 years with a mean left atrial volume of 131.5 ± 46.9 mL. The endovascular procedure remained uniform with antral pulmonary vein isolation, posterior left atrial roof and right atrial cavo-tricuspid isthmus (CTI) linear lesions with mapping and ablation of left atrial complex electrograms (CFAEs) and prior existing atrial arrhythmias. The epicardial procedure included a thorascopic approach with ganglionated plexus (GP) mapping and ablation, left atrial posterior wall ablation, directed CFAE ablation and left atrial appendage ligation. All patients received implantable cardiac monitoring. RESULTS: All 40 patients remained in sinus rhythm at their 12 month follow-up. During the monitoring period, episodes of paroxysmal atrial arrhythmias including fibrillation were documented, without persistence, after discontinuation of oral antiarrhythmic medications. CONCLUSION: The endo-before-epi approach resulted in improved management of persistent and long standing persistent atrial fibrillation over reported results for conventional approaches with no procedural complications, making this a promising option for the management of these arrhythmias.

Racial Differences in Response to Tilt-Table Testing in Patients Refered.

BACKGROUND: Syncope is a common problem in the general population and results in significant societal and patient costs. Several small studies have demonstrated differences in orthostatic response, and possibly tolerance, between blacks and whites. Based on these observations, we retrospectively reviewed results from our tilt table database to identify potential differences in response to tilt-table testing with regards to race, between black and white patients. METHODS: The reports of 446 tilt-table tests performed on adults, older than 18 years of age, at Boston Medical Center, an urban, tertiary-care, academic hospital, were reviewed. Clinical variables were retrieved from the procedure report. Occurrence of syncope was noted and hemodynamic classification was recorded as neurocardiogenic response, with subcategories of mixed, vasodepressor, or cardio-inhibitory. RESULTS: Of records reviewed, 360 patients (80.7%) identified as white and 86 patients as black (19.3%). There was a significantly lower observed frequency of syncope with a neurocardiogenic response in black vs. white patients (45.5% vs. 60.3%, p=0.015). In addition, significantly fewer black patients demonstrated a mixed neuro-cardiogenic response as compared to white patients (7.0% vs. 15.8%, p=0.038) or cardio-inhibitory response (0% vs. 5.3%, p=0.032). There was no difference in frequency of vasodepressor response in black vs. white patients (39.2 vs.38.4%, p=1.000). CONCLUSIONS: We observed a statistically-significant lower incidence of neurocardiogenic syncope among black patients compared to white patients referred for tilt-table testing for evaluation of syncope.

ECG Case of the Month: Unexpected Atrioventricular Conduction in High-Grade Atrioventricular Block. Sinus rhythm; high-grade second degree atrioventricular block with a junctional escape rhythm and three capture complexes, each with right bundle branch block aberration; possible septal myocardial infarct of indeterminate age; ST-T and U wave changes suggesting hypokalemia.

A 90-year-old man with a history of high blood pressure, a cerebrovascular accident without focal residua, dementia, and stage 3 chronic kidney disease went to the emergency department because of dizziness and near syncope. His medications were aspirin 81 mg qd, clopidogrel 75 mg qod, escitalopram oxalate 10 mg qd, Seroquel 25 mg qd, and memantine hydrochloride 10 mg qd. He had orthostatic hypotension with supine blood pressure of 173/77 mm Hg falling to 116/68 on standing, while pulse increased from 66 to 84 beats/ min. He received IV fluid and returned home. Two days later he saw his primary care physician because of episodes of dizziness and confusion. The figure shows an electrocardiogram recorded during that visit.

ECG of the Month. Unexpected Atrioventricular Conduction in High-Grade Atrioventricular Block. DIAGNOSIS: Sinus rhythm; high-grade second-degree atrioventricular block with a junctional escape rhythm and three capture complexes, each with right bundle branch block aberration; possible septal myocardial infarct of indeterminate age; ST-T and U wave changes suggesting hypokalemia.

A 90-year-old man with a history of high blood pressure, a cerebrovascular accident without focal residua, dementia, and stage 3 chronic kidney disease went to the emergency department because of dizziness and near syncope. His medications were aspirin 81 mg qd, clopidogrel 75 mg qod, escitalopram oxalate 10 mg qd, quetiapine fumarate 25 mg qd, and memantine hydrochloride 10 mg qd. He had orthrostatic hypotension with supine blood pressure of 173/77 mmHg falling to 116/68 on standing, while pulse increased from 66 to 84 beats/min. He received IV fluid and returned home. Two days later, he saw his primary care physician because of episodes of dizziness and confusion. The Figure shows an electrocardiogram recorded during that visit.

ECG of the month. Irregular rhythm in a 25-year-old man with three prior cardiac operations. Coarse atrial fibrillation with a rapid ventricular response, left anterior fascicular block, left ventricular hypertrophy with repolarization abnormality.

The patient underwent closure of an atrial septal defect at age 3, had a leaking "mitral" valve repaired at age 9, and at age 13 had a "mitral" valve replacement. He began taking warfarin sodium at that time and remained symptom-free until 10 days before his initial visit here when he presented to another hospital with dyspnea and palpitations. Treatment there consisted of lisinopril 10 mg qd, carvedilol 6.25 mg bid, aldactone 25 mg qd, furosemide 40 mg qd, digoxin 0.25 mg qd, and a continuation of warfarin sodium 7.5 mg qd. An echocardiogram showed a left ventricular ejection fraction of 20%. After diuresis, he was referred to our cardiology clinic. On his initial visit here, his heart rate was an irregular 120 beats/min, his blood pressure was 106/77 mmHg, and closing and opening snaps of a normally functioning mechanical mitral valvular prosthesis were heard. He was obese (height, 5' 9"; weight, 272 lbs). An electrocardiogram was recorded (Figure 1).

Demonstrating new-onset or worsened sudomotor function post-COVID-19 on comparative analysis of autonomic function pre-and post-SARS-CoV-2 infection.

Background: Autonomic dysfunction including sudomotor abnormalities have been reported in association with SARS-CoV-2 infection. Objective: There are no previous studies that have compared autonomic function objectively in patients pre- and post- SARS-CoV-2 infection.We aimed to identify if SARS-CoV-2 virus is triggering and/or worsening dysautonomia by comparing autonomic function tests in a group of patients pre-and post-SARS-CoV-2 infection. Design/methods: Six participants were enrolled and divided into two groups. The first group of 4 participants reported worsened autonomic symptoms post-SARS-CoV-2 infection. These individuals had their first autonomic test prior to COVID-19 pandemic outbreak (July 2019-December 2019). Autonomic function testing was repeated in these participants, 6 months to 1-year post-SARS-CoV-2 infection (June 2021).The second group of 2 participants reported new-onset autonomic symptoms post-COVID-19 infection and were also tested within 6 months post-SARS-CoV-2 infection.All participants had mild COVID-19 infection per WHO criteria. They had no evidence of large fiber neuropathy as demonstrated by normal neurophysiological studies (EMG/NCS). They were all screened for known causes of autonomic dysfunction and without risk factors of hypertension/hyperlipidemia, thyroid dysfunction, diabetes/prediabetes, vitamin deficiencies, history of HIV, hepatitis, or syphilis, prior radiation or chemical exposure or evidence of monoclonal gammopathy, or autoimmune condition. Results: Participants were female (age: 21-37y) and all endorsed orthostatic intolerance (6/6). Gastrointestinal symptoms (⅚), new-onset paresthesias, (3/6), and sexual dysfunction (2/6) were reported. Parasympathetic autonomic function remained stable 6-months to 1-year post-COVID-19 infection and no parasympathetic dysfunction was demonstrated in participants with new-onset dysautonomia symptoms. Postural orthostatic tachycardia was noted in half of the patients, being observed in one patient pre- SARS-CoV-2 infection and persisting post-SARS-CoV-2 infection; while new-onset postural tachycardia was observed in 1/3rd of patients. Sympathetic cholinergic (sudomotor) dysfunction was demonstrated in ALL participants. Worsened, or new-onset, sudomotor dysfunction was demonstrated in those with mild or normal sudomotor function on pre-COVID-19 autonomic testing. Conclusions: Sympathetic adrenergic and cholinergic dysautonomia probably account for some of the symptoms of Long COVID-19. Sudomotor dysfunction was demonstrated as consistently worsened or new-sequelae to COVID-19 infection. COVID-19 may be responsible for triggering new-onset or worsened small-fiber neuropathy in this sample, supporting previously reported studies with similar findings. However, the findings in our study are preliminary, and studies with larger sample size are needed to confirm these observations.

ECG of the month. Bigeminal rhythm VIII. Sinus rhythm with normal antegrade atrioventricular (A-V) conduction and slow retrograde conduction back to the atria, producing atrial reentry or echo complexes and suggesting dual A-V nodal pathways or an accessory A-V pathway that conducts slowly from the ventricles to the atria.

A 55-year-old woman came to the emergency department because of an episode of post-prandial upper abdominal pain radiating to her back and associated with nausea and vomiting. The pain had been recurring intermittently for approximately six months. While in the emergency department, she had another episode of pain and felt lightheaded. Her pulse rate at that point was between 30 and 40 beats per minute, and an electrocardiogram was recorded (Figure).

A Case of Intermittent Left Bundle Branch Block.

An 82-year-old woman with uncontrolled hypertension and occasional exertional dyspnea was found to be in intermittent left bundle branch block (LBBB). Her laboratory results, echocardiogram, and ischemic workup were unremarkable. This case highlights that intermittent LBBB is not always associated with coronary ischemia, vasospasm, blunt cardiac injury, drugs, and high catecholaminergic or inflammatory states.

Cardiac Manifestations in a Case of Severe Hyperkalemia.

Severe hyperkalemia is a life-threatening electrolyte imbalance that may lead to fatal arrhythmias. ECG (electrocardiogram) and serum potassium levels are vital for diagnosing and stratifying the risk. Management involves shifting potassium intracellularly and eliminating it through renal and gastrointestinal routes. Failure to diagnose early and manage severe hyperkalemia requires emergent hemodialysis.

Dynamic ST-Segment Abnormality.

A 37-year-old man came to the emergency department because of several days of intermittent chest pain. An electrocardiogram (ECG) showed sinus rhythm, left atrial and left ventricular enlargement, and an early repolarization pattern. A second ECG recorded 10 minutes later was strikingly different, with ST-segment elevation and large upright T waves in the anterior precordial leads, interpreted as evidence of an ST-segment elevation myocardial infarction, and the cardiac catheterization team was activated. Closer inspection of the ECG, however, disclosed that the changes were because of intermittent ventricular pre-excitation of the Wolff-Parkinson-White type, and no electrocardiographic, echocardiographic, or serum markers of myocardial infarction were found.

Malignant Early Repolarization.

A 27-year-old man presents with successfully resuscitated ventricular fibrillation. Structural and electrical causes of ventricular fibrillation in the young are presented along with a diagnostic strategy. Electrocardiographic features of malignant early repolarization are discussed.

Postinduction Paced Pulseless Electrical Activity in a Patient With a History of Oropharyngeal Instrumentation-Induced Reflex Circulatory Collapse.

BACKGROUND: Reflex hypotension and bradycardia have been reported to occur following administration of several drugs associated with administration of anesthesia and also following a variety of procedural stimuli. CASE REPORT: A 54-year-old postmenopausal female with a history of asystole associated with sedated upper gastrointestinal endoscopy and post-anesthetic-induction tracheal intubation received advanced cardiac resuscitation after insertion of a temporary transvenous pacemaker failed to prevent pulseless electrical activity. The patient's condition stabilized, and she underwent successful cataract extraction, intraocular lens implantation, and pars plana vitrectomy. CONCLUSION: Cardiac pacemaker insertion prior to performance of a procedure historically associated with reflex circulatory collapse can be expected to protect a patient from bradycardia but not necessarily hypotension.

Atrial flutter: Clinical risk factors and adverse outcomes in the Framingham Heart Study.

BACKGROUND: Few epidemiologic cohort studies have evaluated atrial flutter (flutter) as an arrhythmia distinct from atrial fibrillation (AF). OBJECTIVE: The purpose of this study was to examine the clinical correlates of flutter and its associated outcomes to distinguish them from those associated with AF in the Framingham Heart Study. METHODS: We reviewed and adjudicated electrocardiograms (ECGs) previously classified as flutter or AF/flutter and another 100 ECGs randomly selected from AF cases. We examined the clinical correlates of flutter by matching up to 5 AF and 5 referents to each flutter case using a nested case referent design. We determined the 10-year outcomes associated with flutter with Cox models. RESULTS: During mean follow-up of 33.0 ± 12.2 years, 112 participants (mean age 72 ± 10 years, 30% women) developed flutter. In multivariable analyses, smoking (odds ratio [OR] 2.84, 95% confidence interval [CI] 1.54-5.23), increased PR interval (OR 1.28 per SD, 95% CI 1.03-1.60), myocardial infarction (OR 2.25, 95% CI 1.05-4.80) and heart failure (OR 5.22, 95% CI 1.26-21.64) were associated with incident flutter. In age- and sex-adjusted models, flutter (vs referents) was associated with 10-year increased risk of AF (hazard ratio [HR] 5.01, 95% CI 3.14-7.99), myocardial infarction (HR 3.05, 95% CI 1.42-6.59), heart failure (HR 4.14, 95% CI 1.90-8.99), stroke (HR 2.17, 95% CI 1.13-4.17), and mortality (HR 2.00, 95% CI 1.44-2.79). CONCLUSION: We identified the clinical correlates associated with flutter and observed that flutter was associated with multiple adverse outcomes.

Prognostic differences between atrial fibrillation and atrial flutter.

This report presents the outcome of a cohort of 94 patients with atrial fibrillation from the Canadian Registry of Atrial Fibrillation, in which we paid particular attention to the probability of stroke and death. We also evaluated warfarin use over time and compared left atrial dimensions in patients with atrial flutter with those with atrial fibrillation.