Background-Functional reentry in the heart takes the form of spiral waves. Drifting spiral waves can become pinned to anatomic obstacles and thus attain stability and persistence. Lidocaine is an antiarrhythmic agent commonly used to treat ventricular tachycardia clinically. We examined the ability of small obstacles to anchor spiral waves and the effect of lidocaine on their attachment. Methods and Results-Spiral waves were electrically induced in confluent monolayers of cultured, neonatal rat cardiomyocytes. Small, circular anatomic obstacles (0.6 to 2.6 mm in diameter) were situated in the center of the monolayers to provide an anchoring site. Eighty reentry episodes consisting of at least 4 revolutions were studied. In 36 episodes, the spiral wave attached to the obstacle and became stationary and sustained, with a shorter reentry cycle length and higher rate. Spiral waves could attach to obstacles as small as 0.6 mm, with a likelihood for attachment that increased with obstacle size. After attachment, both conduction velocity of the wave-front tip and wavelength near the obstacle adapted from their pre-reentry values and increased linearly with obstacle size. In contrast, reentry cycle length did not correlate significantly with obstacle size. Addition of lidocaine 90 mol/L depressed conduction velocity, increased reentry cycle length, and caused attached spiral waves to become quasiattached to the obstacle or terminate. Conclusions-Anchored spiral waves exhibit properties of both unattached spiral waves and anatomic reentry. Their behavior may be representative of functional reentry dynamics in cardiac tissue, particularly in the setting of monomorphic tachyarrhythmias.
Compared with the best of the currently available device nominal AV and VV delays, 23-45% of CRT patients can yield additional acute haemodynamic effect by individual optimization of the delays. A new nominal VV delay of 40 ms LV pre-activation is recommended. Male gender, ischaemic aetiology, and longer PR interval are associated with a larger effect of individual optimization.
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