Christina F Kneip

Publications (2)7.19 Total impact

• Article: Vagal modulation of heart rate variability during atrial fibrillation in pigs.

  Christina F Kneip, Robert T Mallet, Arthur G Williams, Mohamed H Hamdan, Michael L Smith
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  ABSTRACT: Atrial fibrillation (AF) is the most common sustained cardiac dysrhythmia and is associated with an increased risk for sudden cardiac death. The ventricular rhythm is irregular and displays both non-linear and linear patterns; however, it has not been determined whether vagally derived patterns are manifest within the irregular rhythm. Moreover, indices of increased vagal control are associated with reduced risk of sudden cardiac death. In this study, we sought to determine whether the ventricular rhythm pattern during AF is, in part, modulated by vagal activity. Vagal oscillations were forced at 0.15 Hz by neck suction in 12 pigs with sustained AF with and without glycopyrrolate (0.15 microg/kg, intravenously) vagal blockade. Vagal activity was evaluated using time- and frequency-domain heart rate variability measures. The standard deviation of RR intervals (SDRRI) was significantly increased during vagal activation compared with baseline (P = 0.006). Moreover, SDRRI correlated significantly with spectral power at 0.15 Hz during baseline (r = 0.90, P < .001) and vagal activation (r = 0.86, P < 0.05). Glycopyrrolate blocked the increase in SDRRI (P < 0.001) and blunted spectral power at 0.15 Hz (P < 0.05). These results indicate that: (1) power spectral analysis may be used to assess parasympathetic regulation during AF, and (2) vagal oscillations produce an entrainment of the ventricular rhythm during AF in pigs.
  Experimental Biology and Medicine 08/2010; 235(8):1007-14. · 2.64 Impact Factor
• Article: High-frequency ventricular ectopy can increase sympathetic neural activity in humans.

  Michael L Smith, Mohamed H Hamdan, Stephen L Wasmund, Christina F Kneip, Jose A Joglar, Richard L Page
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  ABSTRACT: Sudden cardiac death is usually caused by ventricular arrhythmias and in many cases, is preceded by frequent ventricular ectopy. It is known that ectopic beats cause transient increases in sympathetic nerve activity (SNA). Because high SNA is known to be arrhythmogenic, we hypothesized that high rates of ectopy increase SNA, thereby creating a milieu that favors development of ventricular tachycardia and/or fibrillation. This study measured muscle SNA, coronary sinus catecholamine, and arterial pressure during graded rates of ventricular ectopy (from 4:1 to 1:1, sinus to ectopic beat ratio) in a total of 21 patients referred for electrophysiologic testing. Both muscle SNA and coronary sinus norepinephrine increased significantly with increased ectopy frequency (P < .05). Moreover, the change in muscle SNA correlated significantly with the change in coronary sinus norepinephrine levels (r = .72, P < .001). These data demonstrate that sympathoexcitation evoked by high rates of ventricular ectopy can contribute to a state of elevated SNA both in peripheral tissues and within the heart. This altered autonomic state may contribute to an increased susceptibility to life-threatening tachyarrhythmias in patients with high rates of ectopy.
  Heart rhythm: the official journal of the Heart Rhythm Society 01/2010; 7(4):497-503. · 4.56 Impact Factor