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Heart 98:893-894 doi:10.1136/heartjnl-2012-301737
  • Images in cardiology

Left ventricular apical mechanics during ectopy in an asymptomatic athlete

  1. Rob Shave
  1. Department of Physiology and Health, Cardiff School of Sport, Cardiff Metropolitan University, Cardiff, UK
  1. Correspondence to Dr Eric J Stöhr, Department of Physiology and Health, Cardiff Metropolitan University, Cyncoed Campus, Cyncoed Road, CF23 6XD Cardiff, UK; estohr{at}cardiffmet.ac.uk
  1. Contributors EJS contributed to the design of the study, data collection, data analysis and drafting of the manuscript. RS contributed to the design of the study and critical revision of the manuscript.

  • Received 27 January 2012
  • Accepted 14 February 2012
  • Published Online First 24 March 2012

The frequent occurrence of ventricular ectopics in athletes is thought to be a part of the physiological adaptation process as a consequence of regular exercise training.1 However, the acute impact of a premature ventricular contraction (PVC) on the mechanical sequence of the myocardium has never been shown. Here, we present data of left ventricular (LV) apical function during a PVC in a 20-year-old healthy, asymptomatic male triathlete (body mass: 76 kg; height: 1.81 m; maximal oxygen uptake (VO2max): 66.4 ml/kg/min). Data were analysed using novel speckle tracking echocardiography (video 1). LV apical rotation and strain were normal prior to the PVC (figure 1). Spontaneous ectopy during repolarisation caused a brief reversal of the normal diastolic mechanics (arrow A). Furthermore, reversed apical rotation was immediately followed by an over-rotation of the apex within the same cardiac cycle (arrow B). The following cardiac cycle was characterised by a markedly enhanced peak systolic rotation and mildly increased circumferential strain (arrows C and D, respectively), potentially reflecting increases in postextrasystolic Ca2+ availability, accumulated storage of kinetic energy in titin molecules and/or altered fibre alignment caused by changes to LV volumes. The second cardiac cycle following the ectopic event, and the two cardiac cycles acquired 30 s thereafter displayed normal mechanical function. Importantly, there was no dyssynchrony between myocardial segments, neither during nor following the ectopic event. The present case shows novel data on the acute coupling of premature ventricular depolarisation and LV mechanics and highlights the importance of examining the impact of frequent ventricular ectopics on LV mechanics in future studies.

Figure 1

(A) During sinus rhythm, apical function was normal as shown by the systolic counter-clockwise and diastolic clockwise rotation as viewed from the apex. (B) The premature ventricular contraction during repolarisation caused a rapid counter-clockwise rotation within diastole, as indicated by the red arrow, and a subsequent increase in clockwise rotation beyond normal. (C) During the following heartbeat, both systolic and diastolic rotations were markedly enhanced, potentially reflecting increases in postextrasystolic Ca2+ availability, accumulated storage of kinetic energy in titin molecules and/or altered fibre alignment caused by changes to left ventricular volumes. (D–F) Subsequent cardiac cycles displayed normal systolic and diastolic function. AVC, aortic valve closure. Vertical red lines represent the time point shown in echocardiographic images.

Footnotes

  • Competing interests None.

  • Patient consent Obtained.

  • Ethics approval Ethics approval was provided by the School of Sport Research Ethics Committee.

  • Provenance and peer review Not commissioned; externally peer reviewed.

Reference