The pathophysiology of narrow complex dilated cardiomyopathy is not defined, so therapeutic options are limited. By utilising the velocity equation, the pathophysiology of narrow complex cardiomyopathy allows above normal conduction propagation velocities. There are two pathophysiological theories that allow above normal conduction velocities and failure to capture the myocardium: (1)insulating fibres of the conduction system extending beyond the apex and (2) reduction of axon branching. A patient with narrow complex cardiomyopathy was subjected to graded increase in amplitude and pulse width pacing to overcome the failure of native conduction to capture the myocardium. Peak systolic strain maps demonstrated a progressive increase in apical contractility with increasing pulse width and amplitude. Ejection fraction improved from 17% to 31%. Understanding the pathophysiology of narrow complex cardiomyopathy leads to proposed therapies. One potential pacing therapy is multi-lead pacing at high amplitude and pulse width to capture myocardial cells not captured by native conduction.
- cardiovascular medicine
- heart failure
- pacing and electrophysiology
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PDH, BJ, RP and GO contributed equally.
Contributors All authors have contributed in design, execution and writing of this report. PDH made the observation that conduction velocity is increased in narrow complex cardiomyopathy and designed the study protocol. GO is the electrophysiologist who implanted the defibrillator. RP is the cardiology fellow who managed the research protocol. BJ is a cardiologist who provided insight and review. PDH is the first author who conceived the notion after losing a patient with narrow complex cardiomyopathy.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests None declared.
Provenance and peer review Not commissioned; externally peer reviewed.
Patient consent for publication Obtained.
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