ABC of clinical electrocardiography: Bradycardias and atrioventricular conduction block

Costa, David da; Brady, William J.; Edhouse, June

doi:10.1136/bmj.324.7336.535

Cited by 61 publications

(26 citation statements)

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“…1 B ). AV blocks indicate defective electrical signal conduction between the atria and ventricles, often at the level of the AV node (Da Costa et al, 2002). We quantified the number of second degree AV blocks in mutants and controls and found that Kv1.1-deficient mice displayed about five AV blocks per hour during interictal periods, a significant five-fold increase compared to wild-type littermates ( P = 0.00034), which exhibited about one second degree AV block per hour (Fig.…”

Section: Resultsmentioning

confidence: 99%

Kv1.1 Potassium Channel Deficiency Reveals Brain-Driven Cardiac Dysfunction as a Candidate Mechanism for Sudden Unexplained Death in Epilepsy

Glasscock¹,

Yoo²,

Chen³

et al. 2010

J. Neurosci.

201

233

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Mice lacking Kv1.1 Shaker-like potassium channels encoded by the Kcna1 gene exhibit severe seizures and die prematurely. The channel is widely expressed in brain but only minimally, if at all, in mouse myocardium. To test whether Kv1.1-potassium deficiency could underlie primary neurogenic cardiac dysfunction, we performed simultaneous video EEG-ECG recordings and found that Kcna1-null mice display potentially malignant interictal cardiac abnormalities, including a fivefold increase in atrioventricular (AV) conduction blocks, as well as bradycardia and premature ventricular contractions. During seizures the occurrence of AV conduction blocks increased, predisposing Kv1.1-deficient mice to sudden unexplained death in epilepsy (SUDEP), which we recorded fortuitously in one animal. To determine whether the interictal AV conduction blocks were of cardiac or neural origin, we examined their response to selective pharmacological blockade of the autonomic nervous system. Simultaneous administration of atropine and propranolol to block parasympathetic and sympathetic branches, respectively, eliminated conduction blocks. When administered separately, only atropine ameliorated AV conduction blocks, indicating that excessive parasympathetic tone contributes to the neurocardiac defect. We found no changes in Kv1.1-deficient cardiac structure, but extensive Kv1.1 expression in juxtaparanodes of the wild-type vagus nerve, the primary source of parasympathetic input to the heart, suggesting a novel site of action leading to Kv1.1-associated cardiac bradyarrhythmias. Together, our data suggest that Kv1.1 deficiency leads to impaired neural control of cardiac rhythmicity due in part to aberrant parasympathetic neurotransmission, making Kcna1 a strong candidate gene for human SUDEP.

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Section: Resultsmentioning

confidence: 99%

Kv1.1 Potassium Channel Deficiency Reveals Brain-Driven Cardiac Dysfunction as a Candidate Mechanism for Sudden Unexplained Death in Epilepsy

Glasscock¹,

Yoo²,

Chen³

et al. 2010

J. Neurosci.

201

233

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“…This hypothesis is supported by the strong resemblance of CMP to the cardiac M pattern in the RBBB, where delayed right ventricular activation produces a secondary R wave (R') in the right precordial EKG leads. 10 Epileptic activities in the cortex or within the subcortical tracks do not propagate in the same way as signals from the heart, although the cardiac M pattern and CMP may have a common pathophysiological mechanism; namely, a conduction defect in projection fibers (Fig. 5).…”

Section: Discussionmentioning

confidence: 99%

EEG spikes resembling cardiac M-shaped waves in the EKG: the cerebral M pattern

Janati¹,

ALGhasab

Aziz

et al. 2017

Ann Clin Neurophysiol

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Interictal epileptiform discharges (IEDs) in the electroencephalogram (EEG) are electroclinical patterns typified by sharp waves and spikes, and defined as waveforms that are distinct from the background activity due to their high amplitude (typically 2.5-fold higher than the background voltage). Their duration may vary from less than 70 ms (classified as spikes) to 70-200 ms (classified as sharp waves). There is a large body of literature on the characteristics of typical IEDs 1-5 but a paucity of data on atypical IEDs.All scalp-recorded electrical activities are generated by postsynaptic potentials in cortical neurons. It is hypothesized that IEDs represent the summation of excitatory postsynaptic potentials (EPSPs) and inhibitory postsynaptic potentials in the cortex. IEDs in scalp recordings typically have a negative polarity that reflects the action of perpendicularly oriented neurons in the cortex. However, it is noteworthy that in certain types of cerebral insult (particularly congenital CNS anomalies), augmentation of the deep cortical EPSPs may Studies of interictal epileptiform discharges are essential for improving the diagnosis, classification, and management of epilepsy. In this case series we sought to identify the clinical and neurophysiological significance of bifid spikes, whose pattern bears a strong resemblance to the cardiac M pattern. We hypothesize that, analogous to the cardiac M pattern, the cerebral M pattern is generated by a conduction defect associated with asynchronous spatiotemporal averaging of electrical signals in the cortex, resulting in the signals reaching the scalp with different latencies. Unlike the cardiac M pattern, the pathology underlying the cerebral M pattern is unknown, although congenital CNS anomalies may be a culprit.

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“…6,7 Additionally, the adverse event of myocarditis is cited in multiple case reports and can clinically manifest as sinus bradycardia. 8 Lastly, two of the four case reports cited by Scrivo However, we highlight to our readership the adverse events of AV block, ventricular dysfunction and myocarditis-all of which can precipitate the downstream effect of bradycardia.…”

mentioning

confidence: 89%