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Corinna B Brunckhorst

Publications and source records attributed to Corinna B Brunckhorst.

At least 19 recordsLinked to original sources
PubMed2006

[CME-ECG 15].

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Adult↗
PubMed2005

Cardiac contractility modulation by non-excitatory currents: studies in isolated cardiac muscle.

BACKGROUND: Myocardial contractility can be altered using voltage clamp techniques by modulating amplitude and duration of the action potential resulting in enhanced calcium entry in the cell of isolated muscle strips (Non-Excitatory Currents; NEC). Extracellular electrical stimuli delivered during the absolute refractory period (Cardiac Contractility Modulation; CCM) have recently been shown to produce inotropic effects in-vivo. AIM: Understanding the cellular mechanism, underlying the CCM effect, is essential for evaluating its clinical potential. We tested the hypothesis that NEC and CCM modulate contractility via similar cellular mechanisms. METHODS: Square wave electric currents were applied in the organ bath to isometrically contracting rabbit RV papillary muscle and human failing trabecular muscle during the absolute refractory period (ARP). RESULTS: These currents, which did not initiate new action potentials or contractions, modulated action potential duration (shortened or lengthened) and contractility (enhanced or depressed) in a manner that depended upon their amplitude, duration and delay from the pacing stimulus. The contractility modulation effect in the rabbit RV papillary muscle was markedly blunted after exposure to ryanodine, indicating that the sarcoplasmic reticulum plays an important role in the contractility modulation. CONCLUSION: Like voltage clamping, extracellular currents applied during the ARP can similarly modulate action potential duration in-vitro and modulate myocardial contractility by similar intracellular mechanisms. This concept provides the potential of a therapeutic strategy in patients with heart failure to enhance contractility.

Animals↗
PubMed2005

[CME-ECG 5].

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Adult↗
PubMed2005

Impact of changing activation sequence on bipolar electrogram amplitude for voltage mapping of left ventricular infarcts causing ventricular tachycardia.

INTRODUCTION: Wavefront direction is a determinant of bipolar electrogram amplitude that could influence identification of low amplitude regions indicating infarction or scar. METHODS: To assess the importance of activation sequence on electrogram amplitude 11 patients with prior infarction and ventricular tachycardia were studied. At 819 left ventricular sites bipolar electrograms were recorded during atrial pacing and ventricular pacing, followed by unipolar pacing with a stimulus of 10 mA at 2 ms. Sites with a pacing threshold > 10 mA were designated electrically unexcitable scar. RESULTS: Areas of low voltage (< or =1.5 mV) were present in all patients. Atrial paced and ventricular paced electrogram amplitudes were strongly correlated (r = 0.77; P < 0.0001). Changing the activation sequence (from atrial pacing to ventricular pacing) produced a > 50% change in electrogram amplitude at 28% of sites and a > 100% change at 10% of sites, but only 8% of sites had an electrogram amplitude classified as abnormal (< or =1.5 mV) with one activation sequence and normal (> 1.5 mV) with the other activation sequence. Electrically unexcitable scar (6% of sites) was associated with lower electrogram amplitude but could not be reliably identified based on electrogram amplitude alone for either activation sequence. CONCLUSION: Voltage maps created with bipolar recordings using these methods should be relatively robust depictions of abnormal ventricular regions despite variable catheter orientation and activation sequences that might be produced by different rhythms.

Aged↗
PubMed2004

[CME-ECG 2].

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Cardiac Complexes, Premature↗