Combination of Intracardiac Echocardiography and Contact Force Sensing for Left Ventricular Papillary Muscle Arrhythmias

Figures

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  Figure 1. The basic process of the experiment was briefly described, divided into four main stages: data collection, matching, grouping and analysis.

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  Figure 2. (A) An autopsy specimen of a pig heart exhibiting the distribution of the left ventricular papillary muscle; no. ① and ④ show the distal third of the PM (tip); no. ② and ⑤ show the middle portion of the PM (body); no. ③ and ⑥ show the proximal third of the PM (base). (B) APM and PPM were visualized in each 2D plane, including the LV endocardium; both heads of the papillary muscles were marked with different colors and delineated to create a detailed 3D model; two heads were separately described as APM1 (brown, the septal side) and APM2 (yellow, the freewall side), and two heads of the PPM, PPM1 (pink, the septal side) and PPM2 (green, the freewall side) (B,C).

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  Figure 3. (A) Representative PVC body ECG of APM; (B) ECG of sinus rhythm and clinical PVC at ablation site; late potential seen during sinus rhythm (blue arrow) when reversed during PVC (red arrow) and preceded it by 32 ms; (C) pace mapping at the site of blue ball in (D) produced best pace; (D) catheter through retroaortic access was visualized on tip of anterior papillary muscle with ICE, but the CFS showed only 1 g; (E) catheter through trans-septal access gained better CFS, but failed to eliminate PVC completely where the vector was from above to below. (F) Clinical PVC was suppressed with contact orientation adjusted from below to above.

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  Figure 4. Representative ECG, intracadiacechography and 3D electroanatomical mapping at tip, body and base of APM, respectively (A–C).

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  Figure 5. Representative ECG, intracadiacechography and 3D electroanatomical mapping at tip, body and base of PPM, respectively (A–C).

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  Figure 6. Kaplan–Meier survival estimates for recurrence.