+1 Recommend
0 collections
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Mechanically Induced Ectopy via Stretch-Activated Cation-Nonselective Channels Is Caused by Local Tissue Deformation and Results in Ventricular Fibrillation if Triggered on the Repolarization Wave Edge (Commotio Cordis)


      Read this article at

          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.


          Supplemental Digital Content is available in the text.



          External chest impacts (commotio cordis) can cause mechanically induced premature ventricular excitation (PVE M) and, rarely, ventricular fibrillation (VF). Because block of stretch-sensitive ATP-inactivated potassium channels curtailed VF occurrence in a porcine model of commotio cordis, VF has been suggested to arise from abnormal repolarization caused by stretch activation of potassium channels. Alternatively, VF could result from abnormal excitation by PVE M, overlapping with normal repolarization-related electric heterogeneity. Here, we investigate mechanisms and determinants of PVE M induction and its potential role in commotio cordis–induced VF.

          Methods and Results—

          Subcontusional mechanical stimuli were applied to isolated rabbit hearts during optical voltage mapping, combined with pharmacological block of ATP-inactivated potassium or stretch-activated cation-nonselective channels. We demonstrate that local mechanical stimulation reliably triggers PVE M at the contact site, with inducibility predicted by local tissue indentation. PVE M induction is diminished by pharmacological block of stretch-activated cation-nonselective channels. In hearts where electrocardiogram T waves involve a well-defined repolarization edge traversing the epicardium, PVE M can reliably provoke VF if, and only if, the mechanical stimulation site overlaps the repolarization wave edge. In contrast, application of short-lived intraventricular pressure surges neither triggers PVE M nor changes repolarization. ATP-inactivated potassium channel block has no effect on PVE M inducibility per se, but shifts it to later time points by delaying repolarization and prolonging refractoriness.


          Local mechanical tissue deformation determines PVE M induction via stretch-activation of cation-nonselective channels, with VF induction requiring PVE M overlap with the trailing edge of a normal repolarization wave. This defines a narrow, subject-specific vulnerable window for commotio cordis–induced VF that exists both in time and in space.

          Related collections

          Most cited references53

          • Record: found
          • Abstract: found
          • Article: not found

          Prolonged Tpeak-to-tend interval on the resting ECG is associated with increased risk of sudden cardiac death.

          Early studies indicate that prolongation of the interval between the peak and the end of the T wave (Tpeak to Tend [TpTe]) on the 12-lead ECG is a marker of ventricular arrhythmogenesis. However, community-based studies have not been conducted. TpTe and other ECG predictors were evaluated in the ongoing Oregon Sudden Unexpected Death Study based in the Portland, Oregon, metropolitan area using a case-control design. Cases of sudden cardiac death (SCD) (n = 353; mean age, 66.6 years; 95% CI, 65.1 to 68.1 years; 67% men) were compared with living controls with coronary artery disease (n = 342; mean age, 64.7 years; 95% CI, 63.4 to 66.0 years; 69% men) from the same region. Analysis of TpTe and selected ECG intervals was limited to sinus rhythm 12-lead ECGs. For cases, these were obtained before and unrelated to SCD. Independent-samples t tests and multiple logistic regression were used. Mean TpTe was significantly greater in cases (89.4 ms; 95% CI, 87.7 to 91.2 ms; P < 0.0001) than in controls (76.1 ms; 95% CI, 74.8 to 77.4 ms). The other ECG intervals (corrected QT interval [QTc], QRS duration [QRSD], and TpTe/QT ratio) also were significantly prolonged among cases versus controls (P ≤ 0.01). TpTe remained a significant predictor of SCD after adjusting for age, sex, QTc, QRSD, and left ventricular function. Odds of SCD increased more with a 1-SD increase in TpTe (12 ms) among subjects with prolonged QRSD (odds ratio, 3.49; 95% CI, 2.06 to 5.91) than with a 1-SD increase in TpTe among subjects with normal QRSD (odds ratio, 1.96; 95% CI, 1.65 to 2.32). TpTe remained significantly associated with SCD in subjects with normal QTc. Prolongation of the TpTe interval measured in lead V5 was independently associated with SCD, with particular utility when the QTc was normal or not measurable because of prolonged QRSD.
            • Record: found
            • Abstract: not found
            • Article: not found

            ATP-regulated K+ channels in cardiac muscle

            A Noma (1983)
              • Record: found
              • Abstract: not found
              • Article: not found

              Complications of central venous catheterization.


                Author and article information

                Circ Arrhythm Electrophysiol
                Circ Arrhythm Electrophysiol
                Circulation. Arrhythmia and Electrophysiology
                Lippincott Williams & Wilkins
                August 2017
                09 August 2017
                : 10
                : 8
                : e004777
                From the Department of Physiology and Biophysics, Dalhousie University, Halifax, Nova Scotia, Canada (T.A.Q.); Department of Physiology, Anatomy, and Genetics, University of Oxford, United Kingdom (H.J., P.L.); and Institute for Experimental Cardiovascular Medicine, University Heart Centre Freiburg/Bad Krozingen, Medical School of the University of Freiburg, Germany (P.K.).
                Author notes
                Correspondence to T Alexander Quinn, PhD, Department of Physiology and Biophysics, Dalhousie University, 5850 College St, Lab 3F, Halifax, NS B3H 4R2, Canada. E-mail alex.quinn@ 123456dal.ca
                © 2017 The Authors.

                Circulation: Arrhythmia and Electrophysiology is published on behalf of the American Heart Association, Inc., by Wolters Kluwer Health, Inc. This is an open access article under the terms of the Creative Commons Attribution Non-Commercial-NoDerivs License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited, the use is noncommercial, and no modifications or adaptations are made.

                Original Articles
                Custom metadata



                Comment on this article