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Mechanisms that initiate ventricular tachycardia in the infarcted human heart.

Segal OR, Chow AW, Peters NS, Davies DW - Heart Rhythm (2009)

Bottom Line: The formation of unidirectional or functional lines of block was not identified during identical pacing protocols that failed to initiate VT (n = 14).Initiation of sustained monomorphic VT requires the development of unidirectional block and formation of lines of functional block creating borders for a DP in areas of slow conduction.A transitional stage often exists during the initiation process before a stable VT circuit is established.

View Article: PubMed Central - PubMed

Affiliation: St. Mary's Hospital, London, UK. oliver.segal@uclh.nhs.uk

ABSTRACT

Background: Precise mechanisms that initiate ventricular tachycardia (VT) in the intact infarcted human heart have not been defined.

Objective: The purpose of this study was to investigate the mechanisms that underlie human postinfarct VT initiation.

Methods: Noncontact mapping of the left ventricle was performed in 9 patients (age 67.1 +/- 7.8 years, ejection fraction 34.4% +/- 5%) with previous myocardial infarction and sustained monomorphic VT.

Results: Circuits in which >/=30% of the diastolic pathway (DP) could be defined were identified in 12 VTs (cycle length 357 +/- 60 ms). Eighteen VT episodes were initiated with pacing, and one occurred spontaneously. Ten complete and two partial circuits were mapped (89% +/- 25% of the DP). In all complete circuits, pacing led to the development of unidirectional conduction block at the location of the subsequent VT exit site and the formation of functional block creating a border(s) for subsequent DP. Wavefront velocity in the DP region slowed from 1.22 +/- 0.2 m/s during sinus rhythm to 0.59 +/- 0.14 m/s during VT (P <.005). In 11 initiation episodes, lines of functional block and areas of slow conduction developed progressively over one to six reentrant cycles before a stable DP was established and sustained monomorphic VT ensued. The formation of unidirectional or functional lines of block was not identified during identical pacing protocols that failed to initiate VT (n = 14).

Conclusion: Initiation of sustained monomorphic VT requires the development of unidirectional block and formation of lines of functional block creating borders for a DP in areas of slow conduction. A transitional stage often exists during the initiation process before a stable VT circuit is established.

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Sequence of noncontact left ventricular isochronal maps showing failure of ventricular tachycardia initiation due to formation of only a single line of functional block in patient 7. See text for discussion. Change of isochrones color represents 10-ms intervals in activation, progressing from white to purple.
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fig4: Sequence of noncontact left ventricular isochronal maps showing failure of ventricular tachycardia initiation due to formation of only a single line of functional block in patient 7. See text for discussion. Change of isochrones color represents 10-ms intervals in activation, progressing from white to purple.

Mentions: An example of a failed VT induction due to formation of lines of block extending directly from scar is shown in Figure 4 (patient 7). The first panel shows the last extrastimulus (S3 290 ms following a drive train) originating at the apical LV. Infarct scar is shown in the posterobasal region, and a small line of functional block is associated with the lateral part of the infarct border zone. The second panel shows the first postpacing beat originating from the same area as the pacing site, again with activation spreading basally, but the line of functional block has disappeared. The next point of endocardial activation then occurs at the lateral border of the infarct scar (panel 3). Of note, two lines of block form at the lateral border extending from the scar basally and apically. The final postpacing beat (panel 4) originates from the same site as in panel 3, resulting in some extension of the lines of block, but a protective channel has not formed; therefore, reentry cannot develop (compare Figure 2, panel 5, and Figure 4, panels 3 and 4).


Mechanisms that initiate ventricular tachycardia in the infarcted human heart.

Segal OR, Chow AW, Peters NS, Davies DW - Heart Rhythm (2009)

Sequence of noncontact left ventricular isochronal maps showing failure of ventricular tachycardia initiation due to formation of only a single line of functional block in patient 7. See text for discussion. Change of isochrones color represents 10-ms intervals in activation, progressing from white to purple.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2806968&req=5

fig4: Sequence of noncontact left ventricular isochronal maps showing failure of ventricular tachycardia initiation due to formation of only a single line of functional block in patient 7. See text for discussion. Change of isochrones color represents 10-ms intervals in activation, progressing from white to purple.
Mentions: An example of a failed VT induction due to formation of lines of block extending directly from scar is shown in Figure 4 (patient 7). The first panel shows the last extrastimulus (S3 290 ms following a drive train) originating at the apical LV. Infarct scar is shown in the posterobasal region, and a small line of functional block is associated with the lateral part of the infarct border zone. The second panel shows the first postpacing beat originating from the same area as the pacing site, again with activation spreading basally, but the line of functional block has disappeared. The next point of endocardial activation then occurs at the lateral border of the infarct scar (panel 3). Of note, two lines of block form at the lateral border extending from the scar basally and apically. The final postpacing beat (panel 4) originates from the same site as in panel 3, resulting in some extension of the lines of block, but a protective channel has not formed; therefore, reentry cannot develop (compare Figure 2, panel 5, and Figure 4, panels 3 and 4).

Bottom Line: The formation of unidirectional or functional lines of block was not identified during identical pacing protocols that failed to initiate VT (n = 14).Initiation of sustained monomorphic VT requires the development of unidirectional block and formation of lines of functional block creating borders for a DP in areas of slow conduction.A transitional stage often exists during the initiation process before a stable VT circuit is established.

View Article: PubMed Central - PubMed

Affiliation: St. Mary's Hospital, London, UK. oliver.segal@uclh.nhs.uk

ABSTRACT

Background: Precise mechanisms that initiate ventricular tachycardia (VT) in the intact infarcted human heart have not been defined.

Objective: The purpose of this study was to investigate the mechanisms that underlie human postinfarct VT initiation.

Methods: Noncontact mapping of the left ventricle was performed in 9 patients (age 67.1 +/- 7.8 years, ejection fraction 34.4% +/- 5%) with previous myocardial infarction and sustained monomorphic VT.

Results: Circuits in which >/=30% of the diastolic pathway (DP) could be defined were identified in 12 VTs (cycle length 357 +/- 60 ms). Eighteen VT episodes were initiated with pacing, and one occurred spontaneously. Ten complete and two partial circuits were mapped (89% +/- 25% of the DP). In all complete circuits, pacing led to the development of unidirectional conduction block at the location of the subsequent VT exit site and the formation of functional block creating a border(s) for subsequent DP. Wavefront velocity in the DP region slowed from 1.22 +/- 0.2 m/s during sinus rhythm to 0.59 +/- 0.14 m/s during VT (P <.005). In 11 initiation episodes, lines of functional block and areas of slow conduction developed progressively over one to six reentrant cycles before a stable DP was established and sustained monomorphic VT ensued. The formation of unidirectional or functional lines of block was not identified during identical pacing protocols that failed to initiate VT (n = 14).

Conclusion: Initiation of sustained monomorphic VT requires the development of unidirectional block and formation of lines of functional block creating borders for a DP in areas of slow conduction. A transitional stage often exists during the initiation process before a stable VT circuit is established.

Show MeSH
Related in: MedlinePlus