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1.
Europace ; 23(2): 305-312, 2021 02 05.
Article in English | MEDLINE | ID: mdl-33083839

ABSTRACT

AIMS: Rate adaptation of the action potential ensures spatial heterogeneities in conduction across the myocardium are minimized at different heart rates providing a protective mechanism against ventricular fibrillation (VF) and sudden cardiac death (SCD), which can be quantified by the ventricular conduction stability (V-CoS) test previously described. We tested the hypothesis that patients with a history of aborted SCD due to an underlying channelopathy or cardiomyopathy have a reduced capacity to maintain uniform activation following exercise. METHODS AND RESULTS: Sixty individuals, with (n = 28) and without (n = 32) previous aborted-SCD event underwent electro-cardiographic imaging recordings following exercise treadmill test. These included 25 Brugada syndrome, 13 hypertrophic cardiomyopathy, 12 idiopathic VF, and 10 healthy controls. Data were inputted into the V-CoS programme to calculate a V-CoS score that indicate the percentage of ventricle that showed no significant change in ventricular activation, with a lower score indicating the development of greater conduction heterogeneity. The SCD group, compared to those without, had a lower median (interquartile range) V-CoS score at peak exertion [92.8% (89.8-96.3%) vs. 97.3% (94.9-99.1%); P < 0.01] and 2 min into recovery [95.2% (91.1-97.2%) vs. 98.9% (96.9-99.5%); P < 0.01]. No significant difference was observable later into recovery at 5 or 10 min. Using the lowest median V-CoS scores obtained during the entire recovery period post-exertion, SCD survivors had a significantly lower score than those without for each of the different underlying aetiologies. CONCLUSION: Data from this pilot study demonstrate the potential use of this technique in risk stratification for the inherited cardiac conditions.


Subject(s)
Death, Sudden, Cardiac , Ventricular Fibrillation , Death, Sudden, Cardiac/etiology , Heart , Humans , Pilot Projects , Risk Factors , Survivors , Ventricular Fibrillation/diagnosis
2.
Emerg Med J ; 39(12): 887-917, 2022 12.
Article in English | MEDLINE | ID: mdl-36414321
4.
J Stroke Cerebrovasc Dis ; 20(1): 10-15, 2011.
Article in English | MEDLINE | ID: mdl-20538485

ABSTRACT

Blood pressure (BP) in healthy individuals exhibits a diurnal variation, with a nighttime dip of 10%-20%. A persistently high nighttime BP is associated with increased cardiovascular morbidity. The effects of diurnal BP variations on the neurologic deficit in acute stroke at presentation and in the first few weeks poststroke are unclear. We hypothesized that persistently elevated BP results in poor outcome. Patients with an acute ischemic stroke presenting within 48 hours of onset underwent 24-hour ambulatory monitoring of systolic, diastolic, and mean BP. There were a total of 35 patients (16 males; mean age, 74 ± 14 years). The percentage change between mean day and night BP classified patients into dippers (> 10% change), nondippers (0-10% change), or reverse-dippers (< 0% change). The Scandinavian Stroke Scale (SSS) and the National Institute of Health Stroke Scale (NIHSS) were assessed on admission, at week 1, and at week 3. The relationship between neurologic score and dipping classification was analyzed using analysis of variance and analysis of covariance, with age and baseline score as covariates. Based on both the SSS and NIHSS, the reverse-dippers had the lowest neurologic scores at baseline, week 1, and week 3, followed by the nondippers. The dippers performed the best in comparison. No significant differences in demographics and/or other BP characteristics among the groups that could account for these differences in outcome were noted. A reverse-dipping profile in diastolic BP was associated with poor neurologic state at baseline and weeks 1 and 3 compared with both dippers and nondippers.


Subject(s)
Blood Pressure/physiology , Brain Ischemia/complications , Brain Ischemia/physiopathology , Circadian Rhythm/physiology , Nervous System Diseases/etiology , Stroke/complications , Stroke/physiopathology , Adult , Aged , Aged, 80 and over , Female , Humans , Male , Middle Aged , Neurologic Examination
5.
J Invasive Cardiol ; 29(8): E92-E93, 2017 Aug.
Article in English | MEDLINE | ID: mdl-28756424

ABSTRACT

A 52-year-old man with previous mitral valve replacement, cavotricuspid isthmus, and left-sided roof-line ablation for previous typical atrial flutter and tachycardia presented with recurrence of symptoms with an atrial tachycardia measuring 260 ms cycle length on electrocardiogram. Rhythmia electroanatomical mapping (Boston Scientific) was performed to understand the mechanism of arrhythmia and to guide ablative treatment.


Subject(s)
Atrial Flutter , Catheter Ablation , Heart Atria , Atrial Flutter/etiology , Atrial Flutter/pathology , Atrial Flutter/physiopathology , Atrial Flutter/surgery , Body Surface Potential Mapping/methods , Catheter Ablation/adverse effects , Catheter Ablation/methods , Heart Atria/diagnostic imaging , Heart Atria/pathology , Humans , Male , Middle Aged , Recurrence , Reoperation , Treatment Outcome
6.
Card Electrophysiol Clin ; 7(1): 71-8, 2015 Mar.
Article in English | MEDLINE | ID: mdl-25784023

ABSTRACT

The clinical utility of noninvasive electrocardiographic imaging has been demonstrated in a variety of conditions. It has recently been shown to have superior predictive accuracy and higher clinical value than validated 12-lead electrogram algorithms in the localization of arrhythmias arising from the ventricular outflow tract, and displays similar potential in other conditions.


Subject(s)
Electrocardiography , Electrophysiologic Techniques, Cardiac , Heart Ventricles/physiopathology , Imaging, Three-Dimensional/methods , Adolescent , Child , Child, Preschool , Electrocardiography/instrumentation , Electrocardiography/methods , Electrophysiologic Techniques, Cardiac/instrumentation , Electrophysiologic Techniques, Cardiac/methods , Humans , Tachycardia, Ventricular/diagnosis , Tachycardia, Ventricular/physiopathology , Ventricular Premature Complexes/diagnosis , Ventricular Premature Complexes/physiopathology
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