Background <p>Polymorphic ventricular tachycardia (PMVT) is characterized by a typical change in QRS morphology and amplitude. This study aims to evaluate human PMVT mechanisms through in vivo ECG imaging (ECGI) mapping in patients with a normal QTc.</p> Methods <p>All patients from UZ Brussel and CHU Bordeaux were screened. The inclusion criterion for the study was PMVT mapped with ECGI. Exclusion criteria were as follows: (1) long QT, (2) premature ventricular contractions inducing PMVT, and (3) acute ischemia. Phase mapping was performed for each PMVT episode, and rotational and focal activity was adjudicated.</p> Results <p>A total of five patients were analyzed, and five episodes of PMVT were mapped. PMVT duration was 5.9&#xa0;s, and the cycle length was 242.4&#xa0;ms. The mean number of rotational activities was 2.5 ± 1.2, with a mean of 2.9 rotations on the apex. The mean number of focal activities was 1.4 ± 0.9. PMVT mechanism was consistent with the following. In the first phase of PMVT, a stable rotor was found over the ventricular apex. The reduction of QRS amplitude in PMVT was associated with the appearance of a non-apical activity. The further reduction of QRS amplitude (trough or minimum) was secondary to a fusion between the apical wavefront and the non-apical wavefront. In the second phase of PMVT, a stable rotational or focal activity was found.</p> Conclusion <p>The main mechanism of human PMVT maintenance was rotational activity over the ventricular apex. Changes in QRS morphology and amplitude were secondary to a fusion between apical and non-apical activities.</p> Graphical abstract <p>The main mechanism of human polymorphic ventricular tachycardia maintenance is rotational activity over the ventricular apex. Changes in QRS morphology and amplitude are secondary to a fusion between apical and non-apical activities.</p> <p></p>

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In vivo mapping of human polymorphic ventricular tachycardia

  • Luigi Pannone,
  • Cinzia Monaco,
  • Domenico Giovanni Della Rocca,
  • Pasquale Vergara,
  • Antonio Sorgente,
  • Alvise Del Monte,
  • Giampaolo Vetta,
  • Roberto Menè,
  • Giacomo Talevi,
  • Ivan Eltsov,
  • Ingrid Overeinder,
  • Gezim Bala,
  • Alexandre Almorad,
  • Erwin Ströker,
  • Gudrun Pappaert,
  • Juan Sieira,
  • Ali Gharaviri,
  • Mark La Meir,
  • Pedro Brugada,
  • Gian Battista Chierchia,
  • Andrea Sarkozy,
  • Carlo de Asmundis

摘要

Background

Polymorphic ventricular tachycardia (PMVT) is characterized by a typical change in QRS morphology and amplitude. This study aims to evaluate human PMVT mechanisms through in vivo ECG imaging (ECGI) mapping in patients with a normal QTc.

Methods

All patients from UZ Brussel and CHU Bordeaux were screened. The inclusion criterion for the study was PMVT mapped with ECGI. Exclusion criteria were as follows: (1) long QT, (2) premature ventricular contractions inducing PMVT, and (3) acute ischemia. Phase mapping was performed for each PMVT episode, and rotational and focal activity was adjudicated.

Results

A total of five patients were analyzed, and five episodes of PMVT were mapped. PMVT duration was 5.9 s, and the cycle length was 242.4 ms. The mean number of rotational activities was 2.5 ± 1.2, with a mean of 2.9 rotations on the apex. The mean number of focal activities was 1.4 ± 0.9. PMVT mechanism was consistent with the following. In the first phase of PMVT, a stable rotor was found over the ventricular apex. The reduction of QRS amplitude in PMVT was associated with the appearance of a non-apical activity. The further reduction of QRS amplitude (trough or minimum) was secondary to a fusion between the apical wavefront and the non-apical wavefront. In the second phase of PMVT, a stable rotational or focal activity was found.

Conclusion

The main mechanism of human PMVT maintenance was rotational activity over the ventricular apex. Changes in QRS morphology and amplitude were secondary to a fusion between apical and non-apical activities.

Graphical abstract

The main mechanism of human polymorphic ventricular tachycardia maintenance is rotational activity over the ventricular apex. Changes in QRS morphology and amplitude are secondary to a fusion between apical and non-apical activities.