Abstract:The sympathetic nervous system modulates cardiac function by controlling key parameters such as chronotropy and inotropy. Sympathetic control of ventricular function occurs through extrinsic innervation arising from the stellate ganglia and thoracic sympathetic chain. In the healthy heart, sympathetic release of norepinephrine (NE) results in positive modulation of chronotropy, inotropy, and dromotropy, significantly increasing cardiac output. However, in the setting of myocardial infarction or injury, sympath… Show more
“…The composition of the Tris‐buffered saline used to dilute the samples was (in mmol/L): 132 NaCl, 40 Tris, 11.2 glucose, 4.2 KCl, 2 CaCl 2 , 0.7 MgCl 2 , pH 7.0. Norepinephrine was measured using continuous flow, fast scanning cyclic voltammetry by methods we previously reported (Chan et al, 2020 ). Urinary norepinephrine excretion was calculated based on the concentration of norepinephrine in an aliquot of the urine, the aliquot size, the total volume of urine excreted in 24 hrs and rat weight.…”
This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
“…The composition of the Tris‐buffered saline used to dilute the samples was (in mmol/L): 132 NaCl, 40 Tris, 11.2 glucose, 4.2 KCl, 2 CaCl 2 , 0.7 MgCl 2 , pH 7.0. Norepinephrine was measured using continuous flow, fast scanning cyclic voltammetry by methods we previously reported (Chan et al, 2020 ). Urinary norepinephrine excretion was calculated based on the concentration of norepinephrine in an aliquot of the urine, the aliquot size, the total volume of urine excreted in 24 hrs and rat weight.…”
This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
“…Overall, the synergistic neural-myocardial framework we present in this study is vitally important to elucidating the pathophysiology leading to sudden cardiac death. Our approach to structure-function alignment could feasibly incorporate emerging technologies, such as spatial detection of interstitial neurotransmitter levels with fast-scanning cyclic voltammetry ( 54 ) and optical norepinephrine tracers ( 55 ), to generate additional mechanistic insights. Ultimately, a combination of such techniques will be needed to enable the development of more powerful and targeted neuromodulatory therapies for heart disease.…”
Remodeling of injured sympathetic nerves on the heart after myocardial infarction (MI) contributes to adverse outcomes such as sudden arrhythmic death, yet the underlying structural mechanisms are poorly understood. We sought to examine microstructural changes on the heart after MI and to directly link these changes with electrical dysfunction. We developed a high-resolution pipeline for anatomically precise alignment of electrical maps with structural myofiber and nerve-fiber maps created by customized computer vision algorithms. Using this integrative approach in a mouse model, we identified distinct structure-function correlates to objectively delineate the infarct border zone, a known source of arrhythmias after MI. During tyramine-induced sympathetic nerve activation, we demonstrated regional patterns of altered electrical conduction aligned directly with altered neuroeffector junction distribution, pointing to potential neural substrates for cardiac arrhythmia. This study establishes a synergistic framework for examining structure-function relationships after MI with microscopic precision that has potential to advance understanding of arrhythmogenic mechanisms.
“…Both patients also had baseline paced AVD programmed to 250-340ms to avoid unnecessary RV pacing, which in turn, coincided with the PVC T wave downslope when pseudopseudofusion occurred. While R-on-T pacing rarely causes VF, the heart may be significantly more vulnerable after 2 consecutive PVCs due to elevated sympathetic tone and levels of interstitial norepinephrine 6 .…”
Section: Discussionmentioning
confidence: 99%
“…While R-on-T pacing rarely causes VF, the heart may be significantly more vulnerable after 2 consecutive PVCs owing to elevated sympathetic tone and levels of interstitial norepinephrine. 6 Figure 3 Mechanism of masked premature ventricular complex (PVC) leading to ventricular tachycardia (VT) / ventricular fibrillation (VF) in DDD pacing. Following atrial pacing, the post–atrial pacing ventricular blanking (PAVB) period is initiated, followed by a crosstalk detection window (CDW).…”
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