CRT teaching day · 36 cases

CRT course sheet

Every case of the CRT day with its device printout. Hover over a blurred cell to show the true diagnosis, the steps of the recording or the clinical pearl; on a touch screen, tap it.

Printouts are the LATITUDE™ reports the cases come from; the patient’s name and full date of birth are covered. Book cases are the tracing pages of the Encyclopédie Boston Scientific (French edition, 2018).

The teaching day

9:00–17:00, 2 h of breaks, 8–15 minutes per case: the 33 cases in bold. Morning: LV lead issues. Afternoon: keeping up the CRT.

  1. 09:00–10:30 1 · LV pacing and threshold (8 × 11.25 min) 1-1 1-2 1-3 1-4 1-5 1-6 1-7 1-8
  2. 10:30–11:00 Coffee break
  3. 11:00–11:50 2 · LV impedance (4 × 12.5 min) 2-1 2-2 2-3 2-4
  4. 11:50–12:30 3 · Sensing (5 × 8 min) 3-1 3-2 3-3 3-4 3-5
  5. 12:30–13:30 Lunch
  6. 13:30–15:30 4 · Keeping up the CRT (10 × 12 min) 4-1 4-2 4-3 4-4 4-5 4-6 4-7 4-8 4-9 4-10
  7. 15:30–16:00 Coffee break
  8. 16:00–16:45 4 · Keeping up the CRT (5 × 9 min) 4-11 4-12 4-13 4-14 4-15
  9. 16:45–17:00 5 · Bonus (1 × 15 min) 5-1
Download .xlsx.csv36 of 36 cases
#CasePDFTrue diagnosisStepsClinical pearl
1-109:00Reading a full LATITUDE CRT-D follow-up reportPDF
Stable CRT-D: no alert, 99% BiV, 1 NSVT, no therapy
RESONATE X4 CRT-D, DDD 60-130, BiV, LV offset −20 ms. p1: no alert → battery 10.5 y, charge 10.1 s → leads (daily): A 3.9 mV/547 Ω/0.6 V, RV 392 Ω/1.3 V, LV 817 Ω/1.7 V, shock 70 Ω → AP 67%, RV 99%, LV 99% → p11 counters/p25 logbook: 1 NonSustV 192 min-1 16 s, 1 ATR 5 s (AT/AF <1%), 0 ATP/shock, 200,481 PVCs → p8-10 trends: LV threshold creeping ~1.2→1.7 V → p19 HF: TI 45.9 Ω, RR 15.5, activity 1.1 h → p3 presenting EGM: AP + LVP/RVP at 1000 ms.
“No alerts” does not mean “nothing to see”: compare each lead value with its implant value and its trend. Here the LV threshold crept up over months without raising any alert
1-209:11Ambulatory PaceSafe LV threshold testPDF b: the same strip, whole, as vectorsPDF a PDF b
Normal PaceSafe LV test: LOC at 0.6 V, LV threshold 0.7 V
RESONATE X4 CRT-D, SR 68 bpm (AS 883-893). LVAT event p1-2 (ambulatory test every 21 h): AS → LVP after 30 ms → backup RVP 80 ms after LVP (LVP interval counted from previous RVP: 803 = 883 - 80) → amplitude ↓ 0.1 V every 3 beats: 1.0 → 0.9 → 0.8 → 0.7 V, same evoked response on ER channel = LV capture → 0.6 V: ER changes, LV activated late by the RVP wavefront ([LVS]) = LOC → 2nd LOC → test ends → LV threshold 0.7 V.
PaceSafe LV measures the LV threshold but does not watch LV capture beat by beat: between two tests, 21 hours apart, only the safety margin keeps the LV captured
1-309:23PaceSafe LV test with an unexpected beatPDF
PVC during PaceSafe LV test: cycle skipped, test continues, threshold 0.7 V
RESONATE CRT-D, SR 96 bpm (AS 618-630). LVAT event p1-2: AS → LVP (~30 ms) → RVP 80 ms later, 3 beats per step: 1.0 → 0.9 V ×3 → RVS 538 ~20 ms after AS, LVS 53 ms later, different RV/LV/ER morphology = PVC → no test pulse on that cycle, no LOC counted → next AS: 0.8 V ×3 → 0.7 V ×3 → 0.6 V: 1st beat captured, then LOC ×2 ([LVS], ER change) → test ends → LV threshold 0.7 V.
An odd beat in an LV threshold test is not always a loss of capture: if its markers show it was sensed (RVS, LVS), it is a PVC that the test simply skips, and the threshold stays valid
1-409:34Non-responder despite 100% BiV pacingBook case: Encyclopédie Boston Scientific (FR 2018), p. 555–557PDF
LV threshold 2.5 V = output: intermittent LV capture, 3.5 V fixes it
COGNIS CRT-D, DCM + LBBB, no response at 6 mo despite 100% BiV pacing. p1 : AS → RVP + LVP 0 ms, constant QRS on Lead I (1). p2 , LV still 2.5 V/0.4 ms: Lead I alternates between QRS (2) = same as 8a and QRS (3) = different, VG EGM alternates too (large sharp vs small deflection) → LV threshold measured at 2.5 V/0.4 ms = output → p3 LV 3.5 V/0.4 ms, same vector: constant QRS (4) = BiV capture → so 8a was RV-only capture.
100% BiV pacing on the counters is not 100% BiV capture: in a non-responder, look at the paced QRS and measure the LV threshold
1-509:45Remote real-time EGM in a dialysis patientBook case: Encyclopédie Boston Scientific (FR 2018), p. 559–565PDF
Loss of BiV capture (RV 6.5 V, LV 4 V) with ventricular escape
AUTOGEN CRT-D, permanent AF + complete AVB, dialysis. p1-2 remote real-time EGM: LVP 0 + RVP every 1000 ms → no paced complex on the Shock (Choc) EGM = non-capture → RVS/LVS 5 ms ~550-650 ms later = regular ventricular escape; the device sees paced/sensed alternation (pseudo-bigeminy) → %BiV drop alert. p3-4 in-office episode: same. p5 RV threshold: LOC at 6.0 V → 6.5 V/0.4 ms (output 3.5 V). p6 LV VGdist>>VGprox: LOC 3.5 V → 4.0 V (output 3.5 V). p7 LV VGdist>>can: 2.2 V → wide margins + LV tip-can vector.
In a dialysis patient, high potassium can raise the RV and LV thresholds together, and the device then paces without capturing. On the real-time EGM of every transmission, check that each pace is followed by a paced complex
1-609:56LV impedance alert and an odd PaceSafe LV testPDF b (report) comes before PDF a (strip, 3 weeks later)PDF a PDF b
LV lead dysfunction: LV-only noise, impedance + threshold jump, unreliable LVAT
AUTOGEN X4 CRT-D, VVIR 60 (A lead off, >3000 Ω), 92% BiV. PDF b p1: alert LV impedance out of range; LV 289 → 612 Ω, threshold 0.8 → 2.0 V@0.4 ms; b p6-7: ~430 Ω and 0.6-0.7 V for months, jump on last day. PDF a (3 wk later): LVP → RVP 80 ms, clean capture at 1.3 V → from 1.2 V noise bursts + sharp spikes on LV channel only → [LVS], 'Fusion', LVS 448/445 → Inh-LVP (RVP alone) → 1.1 V LOC ×2 = unreliable test. PDF b p13: LV noise → LVS → Inh-LVP → RV-only pacing.
It is essential to understand the LV channel markers to understand how the LV lead works: an LVS on noise followed by Inh-LVP means that the LV was not paced on that beat
1-710:08BiV Trigger in AF, and the same patient 15 months laterPDF b: the same patient, 15 months laterPDF a PDF b
AF: BiV Trigger (RVP-Tr/LVP-Tr: RV sensed, LV paced, no real RV pacing); 15 months later true BiV ~36%, LV threshold = output
RESONATE X4 CRT-D, DDD 50/155, ATR → VDI. PDF a, new AF (24 h/day, mean V 93 bpm), real-time EGM p4-6: conducted beat sensed in the RV → immediate LVP-Tr + RVP-Tr (BiV Trigger: the RV sense triggers the LV pace; no real RV pacing, the RV is already activated) → the Tr beats keep a native-like shock EGM, unlike the VRR beats (LVP-VR/RVP-VR 703-718 ms) → daily LV pacing 92-96%. PDF b, 15 months later, persistent AF: RV paced ~36% vs LV 83% (Tr paces count as LV only); p4-5 trends: RV auto threshold up to 4.5 V only on AF days (0.4-0.7 V in sinus rhythm, 0.5 V in office); LV threshold 2.2-4.0 V whatever the rhythm (2.9 V @ 0.6 ms in office), 4.0 V @ 0.6 ms = programmed LV output (no margin) → p11-13: VRR, Tr and LV-first beats (LVS → RVP-Tr + Inh-LVP).
The problem here is not the LV lead, even though its high threshold must be watched closely: it is the conducted AF, which leaves most beats without true BiV pacing, whatever the LV counter says
1-810:19CRT-D with a conduction-system lead: the LV trends jumpPDF b: the PowerPoint slides (trends, EGM, X-ray, revision)PDF a PDF b
3830 CSP lead dislodgement: LV threshold 4.0 V, impedance 320 Ω
RESONATE CRT-D, 3830 conduction-system lead on the LV port, LV-only pacing (LVtip>>RV), DDD 50-145. PDF a p1: no alert! LV threshold 1.0 V (implant) → 0.9 V (in office) → 4.0 V (daily), impedance 850 → 413 → 320 Ω, Auto output now 5.0 V; RV 0.5 V, A 0.6 V stable → a p4: LV threshold ~0.5 → 1.1 V, then an abrupt jump > 4 V with an impedance drop → a p10-11: AS-LVP 730-760 ms. PDF b p2: the same LV trends; b p3: AP 1200 ms → the LV channel senses right after the AP (LV 11) → Inh-LVP and an RVP instead; b p4: chest X-ray; b p5-6: venogram and new lead (revision).
No alert does not mean no problem: the automatic LV output simply follows a rising threshold. Read the LV trends in every report: a sudden threshold jump with a fall in impedance means lead dislodgement until proven otherwise
2-111:00LV pacing impedance climbing after implantPDF
Gradual post-implant LV impedance rise within normal range: lead works fine
MOMENTUM X4 CRT-D, first 3 months after implant. LV LVRing2>>Can, fixed 3.5 V @ 0.4 ms. p1 leads: LV impedance 833 Ω in-office → 673 Ω daily; LV threshold 1.9 V @ 0.4 ms. p5 trends: LV impedance ~340 Ω right after the office visit → slow, steady climb to 650-780 Ω; the RV lead does the same (~640 → ~790 Ω), RV auto threshold flat 0.8-1.5 V. p6: LV and RV 96% paced. p11 EGM: AS/AP → LVP 0 + RVP, constant BiV-paced EGM. → maturation profile, values in range → no change.
Read the impedance trend, not two numbers: a slow, steady rise within range in the months after implant does not mean a lead problem; a sudden jump or drop needs an explanation.
2-211:13LV impedance out-of-range alert near battery end of lifePDF a PDF b
Sporadic LV impedance jumps (~1000, then >3000 Ω): probable conductor fracture with intermittent contact; automatic switch to unipolar, kept at the next visit; ERI near
VISIONIST CRT-P, RV and LV 4.0 V @ 0.4 ms. PDF a p1: alert 'LV pacing lead impedance out of range'; LV 323 Ω in-office → >3000 Ω daily on 7 Jun 2025 → automatic safety switch bipolar → unipolar (LVtip>>Can), printed under Leads; kept by programming at the 24 Jun visit; explant in 8 months. a p4 trend: LV 330-400 Ω for months, one spike (~1000 Ω), then >3000 Ω on the last day. PDF b p7 (~6 months later): that single >3000 Ω point, then flat 315-345 Ω on LVtip>>Can. b p1: LV Auto 1.4 V @ 0.4 ms, 100% LV paced, explant < 3 months → decision time at the generator change.
Weigh the clues of LV lead dysfunction (noise, threshold, impedance, phrenic stimulation, ECG) against the risk of adding a new LV lead (or a LBBAP lead), with or without extraction of the old one: a high-risk procedure, with an infection risk above 5%
2-311:25LV impedance jump after an office visitPDF a PDF b
Vector change LVRing4>>Can 4.5 V → LVTip1>>LVRing2 1.6 V: expected impedance jump
VISIONIST X4 CRT-P, 99-100% BiV. PDF a p1: LV LVRing4>>Can, threshold 4.5 V @ 0.8 ms, output 7.5 V @ 0.8 ms; LV 405-589 Ω; a p11: power use 282%, explant in 5 months. a p4: LV impedance flat 540-730 Ω. PDF b (~3 months later) p1: vector LVTip1>>LVRing2, threshold 1.6 V @ 0.8 ms, output 2.5 V @ 0.8 ms; LV 676 Ω in-office → 1625 Ω daily. b p4: step from ~600 to 1600-1870 Ω on the office-visit day, then stable. b p11: power use 92%, explant in 1 year. → jump = new bipolar vector, not a lead fault.
Each LV vector has its own impedance: a jump right after an office visit points first to a new pacing vector, not to a lead fault. Check what was programmed that day before suspecting the lead.
2-411:38LV threshold and impedance rising in the first weeks after implantPDF a PDF b
Early LV threshold/impedance rise on LV2>>LV3 (3.4 V); LV3>>RV: 1.3 V
RESONATE X4 CRT-D, 2 months after implant (French report). PDF a p1-2: LV LVRing2>>LVRing3 (VGprox2>>VGprox3), LV threshold 2.6 V in-office → 3.4 V @ 0.4 ms daily, impedance 969-996 Ω, LV PaceSafe output Auto 4.4 V. a p10: LV auto threshold 1.3 V just after implant → ~3 V within 2 weeks → 3.4 V; LV impedance 710 → ~1000 Ω in parallel; RV stable. PDF b p1-2 (changed in office): LV LVRing3>>RV (VGprox3>>VD), Auto 1.3 V, daily 1.4 V, 610 Ω, output Auto 2.6 V. b p5: threshold drops to 1.4-1.6 V, impedance to 610-670 Ω.
Watch the LV threshold closely in the first weeks after implant. When it climbs, do not just accept a higher output: test the other vectors of the quadripolar lead, as one may capture at a much lower output.
3-111:50Extra LV sensed events in a CRT-D programmed VVI 40PDF a PDF b
LV oversensing of noise heralding LV lead failure (intermittent impedance >3000 Ω)
MOMENTUM X4 CRT-D, narrow QRS, VVI 40 (8% BiV paced); LV LVRing4>>RV 4.0 V @ 1.0 ms (threshold 2.7 V @ 1.0 ms), LV sense LVRing2>>LVRing3. PDF a p3 EGM: intrinsic RVS/LVS every ~820-980 ms, plus isolated LVS 225 and 570 ms on sharp LV-only spikes, absent on the RV and shock EGM = LV oversensing (noise). PDF b (~8 months later) p1: LV 2532 Ω in-office, LV threshold 3.2 V @ 1.0 ms. b p5: LV impedance 330-450 Ω, then intermittently >3000 Ω (33 of ~60 days) → LV lead failure.
Noise on the LV channel can be the first sign of a failing LV lead, even when it does not disturb pacing: do not dismiss it, follow the LV lead closely
3-211:58Intermittent RV-only paced beats in a RESONATE CRT-DPDF a PDF b
LV noise → Inh-LVP (RV-only beats), then LV lead failure (>3000 Ω)
RESONATE X4 CRT-D, DDD, SAV 70-100 ms; LV LVTip1>>RV, LV sense LVTip1>>LVRing2. PDF a p1: LV 1.2-1.5 V, 839-876 Ω. PDF a p11-12 EGM: AS → LVP 0 + RVP, but bursts of sharp LV-only signals are sensed (LVS 870, 853 ms) → next V pace = RVP + Inh-LVP (LVPP) = RV-only beat. a p5: one LV impedance spike ~1200 Ω, LV threshold up to ~2.2 V. PDF b (~8 months later): vectors changed, VVI 40; p1: LV >3000 Ω, LV threshold 3.3 V @ 0.4 ms, LV amplitude 5.7 → 1.5 mV; p5: LV impedance >3000 Ω nearly every day for months.
Beats paced from the RV alone (Inh-LVP) are lost CRT beats: when noise on the LV channel causes them, suspect the LV lead, even if its impedance and threshold are still normal
3-312:06LV-only pacing with oversensing on the LV and on the RV channelPDF a PDF b
LV oversensing → Inh-LVP + backup RVP; RV oversensing inhibits all pacing
RESONATE CRT-D, LV-only pacing, LVP 855 ms (~70 min-1), A channel flat. PDF a p1: a small signal on LV is sensed (LVS ~700-800 ms) → at 855 ms the LVP falls in the LVPP (Inh-LVP) and an RVP is delivered instead → RV-paced beat, no pause. RVS 620-625 (with LVS) → V timing restarts. PDF b p1: a small signal on RV is sensed (RVS 828, RVS 755) → V escape reset, neither LVP nor RVP → next LVP 855/845 ms later = 1.6-1.7 s pause. → RV sensing drives V timing; LV sensing only blocks the LV output.
Like in most CRT devices, in a Boston CRT the RV channel runs the timing, even when only the LV is paced: noise on the RV channel inhibits all pacing and causes pauses, whereas noise on the LV channel does not inhibit RV pacing
3-412:14Intermittent loss of LV pacing despite 99% RV pacingPDF
Probable oversensing of atrial (far-field) signals on the LV sense vector → LVPP → Inh-LVP
RESONATE X4 CRT-D, DDD 60, SAV 95-110 ms; LV LVTip1>>RV, LV sense LVTip1>>LVRing2 (AGC 1.0 mV). p1: RV 99% paced but LV only 86% (p9 trend ~87%). p3-4 EGM: AS → LVP 0 + RVP ~105 ms later; 6 beats show RVP alone + Inh-LVP: LV pacing is blocked before the RVP by an LV sense during the SAV (small atrial-timed signal on the LV EGM = probable atrial far-field signal) opening the LVPP → wide RV-paced complex, late LV activation marked [LVS] ~220 ms after RVP. Fix (note): shorten the SAV.
If oversensing of atrial (far-field) signals on the LV channel is suspected, get a chest X-ray to confirm the LV lead position and do a threshold test with an ECG. Remember that on a quadripolar lead the distal electrode, number 1, is the furthest from the atrium. If the lead is good, LV sensing may be switched off (on the programmer, under Leads, where the LV sensing vector can also be changed)
3-512:22CRT-D shock: and what about the LV channel?PDF
VT in VF zone, 41 J shock; 2:1 LV sensing from the LV refractory period (nominal 250 ms)
RESONATE X4 CRT-D. p1: V-6 'VF', at detection A 110/V 259 min-1, onset 31% (sudden), stability 9 ms, V>A true. Strips: sinus ~138 min-1 (AS 430-440 ms) with AS-BiV and LV-first beats (Inh-LVP) → sudden regular VT 240-300 ms, then 223-235 ms, A dissociated (AS 413-498 ms) → V-Epsd → LVS only on every other VF beat → V-Detect, charge 11.3 s → 41 J (61 Ω) → 6-8 fast post-shock beats → SR ~145 min-1 with RVS→LVS, Inh-LVP, RVP-MT 428 ms (no full BiV) → end at 49 s.
The LV channel cannot sense two beats closer than its refractory period (nominal 250 ms, i.e. above 240 bpm): in a fast VT, 2:1 LV sensing is expected and harmless, because tachycardia detection relies on the RV channel. It is not a failing LV lead

Boston CRT: what a sensed event does

On a Boston CRT the RV channel times the ventricles; the LV channel only protects the LV.

RV sense (RVS)

  • An RVS outside refractory restarts the ventricular timing and inhibits both RV and LV pacing: RV noise gives pauses (3-3).
  • With BiV Trigger on, an RVS triggers immediate RVP-Tr + LVP-Tr (no LV offset, up to the BiV Trigger maximum pacing rate). Paradoxically there is no real RV pacing: the RV is already activated, and the RV sense triggers the LV pace, often in fusion or pseudo-fusion; these beats count as RV sensed and LV paced (1-7, 4-1).
  • A ventricular sense with no atrial event before it is a PVC for the device: PVARP is extended (PVP→) and the next P may fall in it (4-2, 4-13, 4-14).

LV sense (LVS)

  • An LVS does not restart the timing: it opens the LV protection period (LVPP: 300-500 ms, nominal 400, shorter than the MTR interval), which also follows every LV pace.
  • An LV pace due inside the LVPP is withheld: Inh-LVP marker, the beat is RV-only (3-2, 3-4, 4-4, 4-9).
  • In LV-only pacing the withheld LVP is replaced by an RVP: no pause (3-3).
  • Usual culprits: far-field P waves, noise from a failing LV lead, the late LVS of LBBB beats at high rates.

Clues and fixes

  • LV % lower than RV % on the counters: look for Inh-LVP on the EGM.
  • Sharp LV-only signals with nothing on the RV or shock EGM = noise: follow LV impedance and threshold (3-1, 3-2).
  • Options: another LV sense vector, a shorter SAV, LV sensing Off; revise the lead if the impedance goes above 3000 Ω.

Draft summary from the cases of the day: check the values against the device manual.

4-113:30CRT-P in AF: two different pacing percentagesPDF a PDF b
Rapid AF: CRT loss, LV% inflated by triggered pacing (RVP-Tr)
Octogenarian, VISIONIST X4 CRT-P, DDD 60-150, LV offset 0. PDF a p3: AT/AF burden 23.7 h, RV rate in AF mean 123/max 207 min-1 → daily pacing falls from ~99% to A 1/RV 32/LV 60% (a p5 cumulative counters still 99%). a p10-11 EGM: AF (AS-Fl), ATR fallback → RVS + LVS 113-125 ms later; RVS → RVP-Tr + LVP-Tr 0 (BiV Trigger: the RV sense triggers the LV pace; no real RV pacing, the RV is already activated); RVP-VR/LVP-VR (VRR). RVP-Tr not counted as RV paced, LVP-Tr counted as LV paced → LV% > RV%. HF → bisoprolol 0→10 mg → His ablation → PDF b: DDIR 70, BiV at 855 ms, RV 100/LV 99%.
Conducted AF with a drop in CRT warrants fast clinical action, to avoid a hospitalization for heart failure caused by tachycardia-induced and asynchrony-induced cardiomyopathy combined. Beta-blockers, or other antiarrhythmic drugs, can be a good first step. Some patients are candidates for AF ablation; others are good candidates for His (AV node) ablation, which is 99% effective in fixing this problem
4-213:42CRT-D in sinus rhythm, BiV pacing 89%PDF
Frequent end-diastolic, LV-first PVCs inhibiting BiV pacing (89%)
RESONATE X4 CRT-D, DDD 50-155, SAV 75-120 ms, LV offset 0. p4: daily pacing RV 89/LV 89% (usually 95-100%), mean HR 72, no AF. p6: 4.2 million PVCs since reset. p11-13 EGM: sinus AS + BiV (LVP 0/RVP); PVCs with large RV/LV EGM, LV sensed ~35 ms before RV (LVS 708/RVS 743, 740/778, 710/743), landing on the sinus atrial event → marked AS-LVS-RVS, BiV inhibited; one comes just before the atrial event → PVC + PVP→ (PVARP extension), (AS) not tracked. Each PVC = one beat without CRT.
Each PVC is a beat without CRT, and the PVC counter misses those that fall with the atrial event. When BiV pacing drops in sinus rhythm, look for PVCs on the EGM and treat them
4-313:54CRT pacing alert at 57%, and 2 years laterPDF a PDF b
Ventricular bigeminy → BiV 57%; improved on metoprolol
RESONATE X4 CRT-D, DDD 60-175, SAV 60-100 ms. PDF a p1: alert CRT < 85% (52% in the hours after the in-office reset); p4: BiV drifts from ~95% to RV 59/LV 57%, mean HR 92. p6: 9,531 PVCs in < 1 day. a p12-13 EGM: bigeminy: AS-BiV then PVC (LVS ~25 ms before PVC) + PVP→; sinus atrial event falls in PVARP → (AS) not tracked; couplets (PVC then RVS). Metoprolol 0→100 → PDF b (~2 years later): daily RV 94/LV 93%, regular AS-BiV; cumulative 82/79% since reset keeps the alert on.
Ventricular bigeminy halves CRT: every PVC is a beat without BiV pacing. The answer is to treat the PVCs (here metoprolol) and to judge the result on the daily BiV trend, not on the cumulative counter
4-414:06RV paced 100%, LV only 86%PDF b: chest X-ray 1 week laterPDF a PDF b
Oversensing of atrial (far-field) signals on the LV channel → Inh-LVP: RV and LV leads dislodging into the RA
RESONATE X4 CRT-D, DDD 60-130, SAV 90-130 ms, LV sense LVTip1>>LVRing2. p1: alert CRT 83%; p4: RV 100% but LV 86%. p11-12 EGM: AS → every 2nd-3rd beat RVP + Inh-LVP: an LV sense just before the BiV pace (small atrial far-field signal on the LV EGM, ~90 ms after AS) starts the LVPP → LV pace withheld; the late true LV activation is then marked [LVS] ~250 ms after RVP. p1/p5: RV threshold 0.4→2.6 V, RV impedance 450→300 Ω, R wave 4.0→2.6 mV. LV sensing switched Off. 1 week later (PDF b, X-ray): the RV and LV leads are both in the RA.
Atrial signals on the LV channel mean the LV lead is close to the atrium: think of lead dislodgement and get a chest X-ray, even when the LV numbers look normal. Turning LV sensing off stops the inhibition, not the lead from moving
4-514:18CRT drop in a patient with atrial ectopyPDF c: settings (Ventricular Regulation)PDF a PDF b PDF c
Frequent PACs (in PVARP, conducted) → BiV 69%; 98% on nebivolol
RESONATE X4 CRT-D, DDD 50-130, SAV 120 ms fixed, PVARP 240-280. PDF a p4: BiV 69%, HR mean 104/max 147 (p3: night HR and resp. rate rising); p6: 14.4 million PACs since reset. a p11-12 EGM: PACs tracked up to the MTR (VP-MT 460); PACs in PVARP ((AF), ATR↑) not tracked → conducted RVS-LVS (LVS 5-20 ms) → no BiV; RVS 623 although tracking reaches VP-MT 460: the MTR is only the tracking limit; the RVS comes ~110 ms after the AS, before the 120 ms SAV ends → conducted beat, no BiV (SAV too long). PDF c: BiV Trigger Off in normal mode. Nebivolol, no reprogramming → PDF b (6 months): HR mean 76, BiV 98%, AS-BiV strips.
The problem is not the device but the frequent PACs and the fast heart rate: treat them first. Here beta-blockers alone, with no reprogramming, brought BiV pacing back from 69% to 98%
4-614:30A stored PMT episode at 130 min-1PDF
Sinus tachycardia above MTR 130: CRT loss unmasked by false PMT
RESONATE X4 CRT-D, Event Detail PMT-212, A 130/V 130 min-1. p1 onset: sinus tachycardia, AS 413-440 ms (136-145 min-1) above the MTR → intrinsic RVS-LVS (LVS ~50 ms later), no BiV. Sinus slows to ~460 ms → Inh-LVP (LVPP after the last LVS), then LVP-MT/RVP-MT 460 (130 min-1). p2: 16 VP-MT with stable V-A → PMT-B: PVARP 500 ms for 1 cycle → (AS) not tracked → LVS-RVS → BiV again at the MTR; AS 445 → RVS again. 'PMT' = sinus tachycardia at the MTR; every rise above 130 min-1 = CRT loss → consider raising the MTR.
Loss of CRT during sinus tachycardia is an underappreciated problem in young and active patients. Many CRT candidates have preserved AV conduction and lose their CRT as soon as they cross the MTR (often left at 130 bpm). It is impossible to know: the % of CRT stays high and there are no episodes (unless a false positive PMT, as in this case)
4-714:42Exercise: sinus tachycardia in the VT-1 zoneBook case: Encyclopédie Boston Scientific (FR 2018), p. 576–579PDF
Sinus tachycardia 142 bpm > MTR 130: BiV lost, SVT well discriminated
Autogen CRT-D, DCM + IVCD, MTR 130 (book). p1: V-1 episode in VT-1 zone, A 142 / V 141 min-1 → AS ≈ 425 ms 1:1 with RVS (LVS 23–28 ms later): ST > MTR → AVD stretched to respect MTR → intrinsic conduction, BiV lost → rate stays in VT-1 zone (~140) → 8/10 → V-Epsd (p2), RhythmMatch C96–98 % (threshold 94 %), RhythmID correlated = True, V>A False → V-Detect at end of duration + PVP→ (PVARP extended) → no therapy (“tachy therapy disabled”) → end at 00:01:06. Fix (book): MTR 150, treated VT zone 170.
An MTR set too low takes CRT away on exertion, often without symptoms. In an active patient, raise it (keeping the VT zone above it) and check on an exercise test that BiV pacing holds at peak effort
4-814:54Exercise, anti-PMT algorithm and long PRBook case: Encyclopédie Boston Scientific (FR 2018), p. 581–582PDF
ST at MTR read as PMT → sustained CRT loss (long PR)
Incepta CRT-D, active 71-y/o woman, IVCD. p1: “PMT” episode, A/V 136 min-1 → AS + RVP/LVP (adaptive AVD) → AS at MTR: RVP-MT/LVP-MT 443 ms → p2: 16 VP-MT cycles, stable VP-AS → PMT-B → PVARP 500 ms for 1 cycle → (AS) not tracked → intrinsic conduction RVS 575 (LVS just before), taken as a PVC → PVARP stays long → every atrial event (PR ≈ 240 ms, V-A ≈ 200 ms) falls in PVARP: (AS) → LVS-RVS 405–450 ms → CRT lost, even below the MTR. Fix (book): short dynamic PVARP at peak rate, Tracking Preference.
With a long PR, a single anti-PMT intervention on exertion can switch CRT off for many beats: each following atrial event falls in the PVARP. Consider a dynamic PVARP, short at high rates, and Tracking Preference
4-915:06Exercise, anti-PMT algorithm and LV sensingBook case: Encyclopédie Boston Scientific (FR 2018), p. 584–585PDF
Anti-PMT PVARP extension on ST → RV-only pacing, Inh-LVP (LVPP)
Autogen CRT-D, 73-y/o, DCM + LBBB. p1: “PMT” episode, A 131 / V 130 min-1 → AS + RVP/LVP, then AS-RVP-MT/LVP-MT 460 ms (MTR) → p2: 16 VP-MT → PMT-B → PVARP 500 ms → (AS) → intrinsic LBBB beat: RVS 500, LVS 120 ms later → next AS tracked, RVP-MT at 460 ms but the LV pulse would come ≈ 340 ms after LVS → Inh-LVP (LV protection period) → next AS conducted (RVS-LVS 118–123) → alternation RVS-LVS / RVP-MT + Inh-LVP: no BiV beat left. Fix (book): raise MTR; LV sensing off or shorter LV refractory.
LV sensing has a cost: on exertion in left bundle branch block, the late LV sense of each conducted beat inhibits the next LV pace, and CRT can stay lost while the RV is still paced
4-1015:18Sinus tachycardia, Wenckebach and pro-arrhythmiaBook case: Encyclopédie Boston Scientific (FR 2018), p. 587–592PDF
False PMT at the MTR: one beat in 16 without BiV pacing; Wenckebach → long-short → VT, shock
Cognis CRT-D, ischemic CM + LBBB, shock felt on exertion. p1–4 (PMT episode, A 121 / V 120): AS → RVP-MT/LVP-MT 500 ms (MTR 120) → 16 stable cycles → PMT-B → PVARP 500 ms → (AS) not tracked → AP-Sr, then RVP-Sr/LVP-Sr at 838 ms on a conducted beat (different RV EGM): BiV pacing lost for that beat → back to VP-MT → PMT-B again 16 cycles later, and so on. p5–6 (VT episode, A 125 / V 234): ST > MTR → AVD stretched, (AS) in PVARP (Wenckebach) → AP-Sr, RVP-Sr 750 → long-short → VT 250–295 ms in VF zone → V-Epsd → Quick Convert: 8 BiV pulses at 230 ms fail → charge 9.5 s → 41 J shock.
A too-low MTR is not always harmless: on exertion, each blocked atrial event (Wenckebach, or a sinus tachycardia taken for a PMT) gives a long-short sequence that can, rarely, set off a fast VT, as in this ischaemic heart
4-1116:00Ventricular episodes in a CRT-P: what started them?PDF Simulator Simulator
VT/NSVT started by pacing at a too high MTR (185) on tracked atrial noise (interference from a PC)
VISIONIST CRT-P, DDD 45-185 min-1, PVARP 150 ms, RV-only pacing (LV 0%). p1-2: no alert but 1 VT (V>A) 288 min-1, 1 NSVT 267 min-1, 9 ATR. p3/p7: A channel = continuous ~50 Hz comb, interference from a PC (AN markers on p8) → sensed as PAC/[AS] → tracked at MTR: RVP-MT 323 ms → long-short: RVP 950/1055 → RVP-MT 323 → VT 273/285 then ~190-250 ms (avg 267-288 min-1, RV before LV) → spontaneous end (17 s / 21 s) → ATR fallback, RVP-VR → noise stops → AS-RVP 600-900 ms.
A stored VT may have been started by the pacing itself: look at the beats just before it. Here the device tracked interference from a PC up to the maximum tracking rate, and the long-short sequence it made started each VT
4-1216:09RA lead impedance alert in a paced CRT patientPDF
Complete RA loss of capture without loss of CRT (AV block)
Autogen CRT-D, DDD 70/MTR 100, AP 98 %, RV/LV paced 99 %. p1: alert “Atrial pacing lead impedance out of range”: daily 2399 Ω (1304 Ω in office); A threshold 2.5 V @ 0.4 ms = A output 2.5 V @ 0.4 ms (no margin); p4: RA auto threshold ~0.6 V, then “no data” in the last weeks. p10–11 presenting EGM: AP with no atrial capture; native A rhythm regular ≈ 1310–1380 ms (~45 bpm), not reset by AP → AS/PAC tracked (RVP-MT 600 = MTR) or (PAC) in PVARP → every V event still LVP + RVP (815/855, LV offset −40) → CRT kept (AVB), only AV synchrony lost.
In AV block, losing atrial capture does not stop CRT: each atrial pulse still starts the AV delay and both ventricles are paced. The counters cannot show it (98% atrial pacing); the atrial EGM can
4-1316:18BiV markers with changing far-field morphologyPDF
Fusion with intrinsic conduction (PR ≈ SAV): CRT lost behind BiV markers
RESONATE X4 CRT-D, DDD 50/130, SAV 120 / PAV 150 ms (fixed), LV offset 0, BiV 98 %. p11–13 real-time EGM: every AS → LVP/RVP at 120 ms, but the far-field (shock) EGM switches between a large biphasic paced complex and a smaller, different complex (fusion), e.g. p11A beats 7–9 at A–A 755–770 ms. p11B: AS 740 → RVS ≈ 110 ms later and PAC 383 → RVS 455 (before the MTR-delayed pace), LVS 13 ms: intrinsic PR ≈ SAV → paced beats fuse → CRT lost while still counted as BiV.
A BiV marker is not BiV capture: fused beats carry the same LVP and RVP markers and count as paced, so 98% BiV pacing can hide a partial loss of CRT. The far-field (shock) EGM shows the difference. Here the sensed AV delay needs to be shortened, so that the pacing comes before the patient’s own conduction
4-1416:27CRT drop and low-amplitude atrial eventsPDF a PDF b
Intermittent atrial undersensing (atrial amplitude 0.2–0.3 mV) → intrinsic conduction, BiV 74 %
MOMENTUM X4 CRT-D, DDDR 60/130, PAV 180–280 ms, A sens. AGC 0.15 mV. p1 alerts: BiV < 85 % (74 %/24 h) + A amplitude out of range (0.3 mV). p3–5: low-amplitude native atrial events not sensed → AP-Sr falls just after them (no capture) → the atrial event conducts: RVS then LVS 125–130 ms (LBBB), or [RVS] + RVP-Sr with Inh-LVP (pseudo-fusion) → V event with no A event = PVC → PVP→ (PVARP extension) → more atrial events missed; when an atrial event is sensed: AS → BiV. PDF b (Autogen, atrial amplitude 0.4 mV, BiV 76 %): same AP/[RVS]/Inh-LVP–PVC loop.
When BiV pacing falls in sinus rhythm, think of the atrial lead, not only of the LV lead. An atrial event that is not sensed is not tracked: it conducts, and that beat gets no CRT, even when pacing markers follow it
4-1516:36CRT loss at rest with sinus bradycardiaPDF b: after DDD 70PDF a PDF b
V escape > sinus, functional AUS: CRT lost; DDD 70 fixes
RESONATE X4 CRT-D, DDD 50/130, SAV 95–120 ms, A amplitude 2–3.3 mV (good). p8–9: LV paced 99–100 %, then within days 60 → 17–22 %; mean HR 52–55 → 70. p3–5 real-time EGM: sinus ≈ 1280–1310 ms (~46 bpm) slower than an escape rhythm (RVS, LVS +128 ms) at 920–1050 ms → escape after a BiV beat has no A before it → “PVC” → PVP→ (PVARP extended) → next atrial event falls in PVARP ~120 ms later: (AS) (functional AUS) → RVS 920 → next AS tracked → 1 BiV beat in 3. PDF b: DDD 70 → AP-LVP/RVP 855 ms, rare sensed beats.
A sinus rate slower than the patient’s own escape rhythm costs CRT: the ventricles beat before the next atrial event can be tracked. Pacing the atrium faster than the escape rhythm (here DDD 70) brings BiV pacing back

Keeping up the CRT: why BiV pacing is lost

Aim for 98% or more true BiV capture. The counters count pulses, not capture or fusion: read the daily trend, compare RV % and LV %, and look at the EGM.

Rhythm

  • AF: conducted beats are sensed; BiV Trigger and Ventricular Rate Regulation keep the counters up but often fuse. Rate control, then AV node ablation (1-7, 4-1).
  • PVCs: each one is a beat without CRT, and its PVARP extension can hide the next P (4-2, 4-3).
  • PACs: those in PVARP are not tracked and conduct (4-5).
  • Sinus rate above the MTR: Wenckebach or 2:1 with intrinsic conduction; a stored “PMT” is often sinus tachycardia at the MTR (4-6 to 4-10).

Timing

  • PMT termination: 16 consecutive VP at the MTR after AS with a stable V-A (within 32 ms) → PVARP 500 ms for one cycle: one untracked P, a sustained loss with a long PR (4-8), or a long-short sequence (4-10).
  • An AV delay longer than the intrinsic PR gives conducted or fused beats behind BiV markers (4-5, 4-12).
  • Atrial undersensing, true or functional: an RV sense with no atrial event before it is a “PVC” and extends PVARP for one cycle, so the next P may fall in it (4-13, 4-14).
  • LV protection period: LVS, then Inh-LVP and RV-only beats (3-4, 4-4, 4-9).

What to do on a Boston device

  • Treat the rhythm first: beta-blocker, antiarrhythmic, ablation; reset the counters after a change.
  • Raise the MTR (and the VT zone above it); shorter PVARP; Tracking Preference (after 2 cycles with the P in PVARP before an RV sense, PVARP is shortened until tracking resumes); PMT termination Off when there is no true PMT.
  • A shorter or rate-adaptive SAV to stay ahead of intrinsic conduction; a higher lower rate to overdrive a slow escape (4-14: DDD 70).
  • BiV paced is not BiV captured: check the threshold and the paced QRS (1-4, 1-5, 4-11).

Draft summary from the cases of the day: check the settings against the device manual.

Key article Oravský 2026
5-116:45CRT with a dual chamber pacemaker using LBBAPPDF: LATITUDE report 8 months after the implant (slides of the implant: local PowerPoint)PDF
LBBB, LVEF 30%: LBBAP with a DDD pacemaker; V paced 99% = 99% CRT, RYTHMIQ off
ACCOLADE MRI EL dual chamber pacemaker, INGEVITY+ lead in the LBB area, instead of a CRT-P (76 years, LBBB, LVEF 30%, HF symptoms). Slide 6: INGEVITY+ (models 7840/7841/7842: 45/52/59 cm) and SSPC NXT guiding catheters (curves 2.5 and Y; 42 cm, 9 Fr outer / 7 Fr inner, radiopaque tip). Slides 7-9: mapping (II positive, III negative, slurring in V1) → fixation beats while screwing → bipolar pacing: narrow QRS with R’ in V1, LV activation time < 80 ms; slide 11: 12-lead ECG with LBBAP. PDF p6 (8 months later): NSVT 174 min-1 alert; V threshold 0.5/0.7 V, 375/345 Ω; DDD 60-130, RYTHMIQ off, PAV 80-180, SAV 65-150 ms; V output Trend 3.5 V @ 0.4 ms (auto threshold off), unipolar pace/bipolar sense → p9: V paced 99% (= % CRT) → p7: V paced ~100% every day → p13: presenting EGM AP-VP 60 min-1. Slide 12: the automatic threshold test works on the LBBAP lead (LOC at 0.6 V, threshold 0.7 V). Slide 13: PMT at 130 min-1 = sinus tachycardia 132 min-1 tracked at the MTR, PMT-B drops one beat (VS).
After LBBAP for resynchronization, read the % of ventricular pacing as the % of CRT, and keep RYTHMIQ and AV Search+ off: every conducted beat brings the left bundle branch block back
5-2Tachycardia while dancing: what the CRT-P and the S-ICD sawPDF a: CRT-P · PDF b: S-ICDPDF a PDF b
ST → PVC run → 1:1 AT → VT → S-ICD shock → VF → 2nd shock → ST
CRT-P (V-47 ‘SVT (V<=A)’, A 196/V 198 min-1, 1 min 48 s) + S-ICD (episode 001, treated, 2 shocks, 133 Ω), same evening. CRT-P p1: ST, AS 450-463 ms, V sensed (LVS/RVS, no BiV) + isolated PVCs (VT 330) → p2: PVC run 315→223 ms while A stays 453-458 ms (the trap) → pause → 1:1 tachycardia at 310-320 ms, the A leading at onset (A cycle changes first, AS-Fl 30-60 ms before each RV) = AT conducted 1:1 → V-Epsd → gap (‖) → VF (VT 145-180 ms) → shock artefact → pause → AP/BiV 1500 ms. S-ICD: the AT at ~192 min-1, all ‘S’, sinus morphology (< 200 zone) → ~35.5 s smaller, faster ‘T’ ~240 min-1 = VT → charge → shock 1 → VF → shock 2 → ST ~120 min-1 (S markers, p3-4).
Sometimes devices can live together: for example a leadless pacemaker as a backup for a malfunctioning pacemaker, an S-ICD on top of a CRT because of venous access problems, or a CRT on top of an S-ICD when LBBB or AV block develops
5-3LOT-CRT with a Boston CRT-P
LOT-CRT: LBBAP lead on RV port, CS lead paced 30 ms later
Case from Université Laval (Quebec). CRT-P (magnet rate 100 min-1): 3830 in the LBB area on the IS-1 RV port, RA on IS-1, quadripolar CS lead on IS-4 (slide notes). Slide 3: baseline ECG, SR + LBBB → slides 4-5: CS venogram, 3830 in the septum + quadripolar lead in a lateral branch → slide 6: CXR → slide 7: 'RV' (= LBBAP) 13.2 mV, 384 Ω, 1.1 V; LV 476 Ω, 0.3 V; DDD 50-170, PAVD 90-140, SAVD 50-80 ms, BiV, LV offset 30 ms → slide 8 RT-EGM: AS → RVP → LVP 30 ms later (880-935 ms) → slide 9: paced QRS clearly narrower than baseline.
LOT-CRT on a standard CRT device: the LBBAP lead goes into the RV port and the CS lead into the LV port, so 'RV' measurements belong to the LBBAP lead and the LV offset (here CS 30 ms after LBBAP) is tuned on the ECG for the narrowest QRS.
5-4CRT AV delay: reading fusion on the ECGPDF a: programmer EGM · PDF b: 12-lead ECGPDF a PDF b
AV-delay optimisation guided by ECG fusion
MOMENTUM X4 CRT-D, real-time log (leadless ECG, A, RV, shock EGM) + separate 12-lead ECG (same morning). Strip 1: AP-Sr 820-910 ms (sensor-driven) → RVP-Sr + LVP-Sr (BiV) after the paced AVD → 2 LV-first beats: AS → LVS 665/RVS 748 and (AS) → LVS 603/PVC 678, PVP→, with a different leadless-ECG QRS → strip 2: AS 810-863 ms → RVP/LVP (sensed AVD), then AP-Sr → BiV: QRS shape differs between AS- and AP-driven beats. 12-lead: BiV-paced QRS (spike artefacts), QS V2-V6, negative I, 2 beats of other morphology.
Optimise the CRT AV delay on the 12-lead ECG: shorten it until the paced QRS stops changing (no fusion with intrinsic conduction) or aim for the narrowest QRS; check sensed (AS) and paced (AP) AV delays separately, AP lengthens AV conduction.

No case matches.

Abbreviations
(AF)
atrial sense in refractory, classified fast (counted by ATR)
(AS)
atrial sense in a refractory period (not tracked)
[AS]
atrial sense in a blanking/noise window (not used)
[LVS]
LV sensed event in a refractory period (no action)
[RVS]
RV sense in a refractory/blanking window (bracketed)
A
atrial (lead/channel)
AF
atrial fibrillation
AGC
automatic gain control (sensing)
AN
atrial noise marker
AP
atrial paced event / % atrial pacing
AP-Sr
atrial pace at sensor rate
AS
atrial sensed event
AS-Fl
atrial sense in the Atrial Flutter Response window (not tracked)
AS-LVP
atrial sensed → LV paced
AS-RVP
atrial sensed → RV paced
AT / AF
atrial tachycardia / atrial fibrillation
ATP
antitachycardia pacing
ATR
Atrial Tachy Response (mode switch episode)
ATR↑
ATR entry counter up
AUS
atrial undersensing
AV
atrioventricular
AVB
atrioventricular block
AVD
atrioventricular delay
BiV
biventricular pacing
bpm
beats per minute
Can
device housing used as the anode
CM
cardiomyopathy
CRT
cardiac resynchronization therapy
CRT-D
cardiac resynchronisation therapy defibrillator
CRT-P
cardiac resynchronization therapy pacemaker
CS
coronary sinus
CSP
conduction-system pacing (His / left bundle branch area)
CXR
chest X-ray
DCM
dilated cardiomyopathy
DDD
dual-chamber pacing mode, tracking
DDDR
rate-responsive dual-chamber mode
DDIR
dual-chamber non-tracking, rate-responsive pacing mode
ECG
electrocardiogram
EGM
intracardiac electrogram
ER
evoked response channel (used to confirm capture)
ERI
elective replacement indicator (battery)
HF
heart failure
HR
heart rate
Inh-LVP
LV pace inhibited (LV protection period after an LV sense)
IVCD
intraventricular conduction delay (nonspecific bundle branch block)
LBBAP
left bundle branch area pacing
LBBB
left bundle branch block
LOC
loss of capture
LRL
lower rate limit
LV
left ventricle/left ventricular
LVAT
LV automatic threshold test (PaceSafe LV)
LVP
LV paced event (marker); 'LVP 0' = LV paced simultaneously with the RV (0 ms)
LVP-MT / RVP-MT
LV / RV pace at the MTR
LVP-Sr
LV paced event at the sensor-driven rate (marker)
LVPP
LV protection period: after an LV sensed event, no LV pacing for a set time
LVS
LV sensed event
min-1
beats per minute
MTR
maximum tracking rate
NonSustV
non-sustained ventricular episode (NSVT) in the logbook
NSVT
non-sustained ventricular tachycardia
PAC
premature atrial contraction (also the Boston marker)
PaceSafe
Boston automatic capture threshold algorithm ('Auto' output)
PAV
paced AV delay
PMT
pacemaker-mediated tachycardia
PMT-B
Boston marker: PMT detected, PVARP extended to 500 ms for one cycle
PVARP
post-ventricular atrial refractory period
PVC
premature ventricular contraction
PVP→
PVARP extension after a PVC
QRS
ventricular depolarization complex
QS
entirely negative QRS
Quick Convert
Boston ATP in the VF zone before/while charging
RA
right atrium
RhythmID
Boston SVT/VT discrimination algorithm
RhythmMatch
morphology correlation with the stored sinus template (C%)
RR
respiratory rate
RV
right ventricle/right ventricular
RVP
RV paced event (marker)
RVP-MT
RV pace at the MTR
RVP-Sr
RV pace at sensor rate
RVP-Tr / LVP-Tr
BiV Trigger markers: an RV sensed event triggers the LV pace (no real RV pacing: the RV is already activated)
RVP-VR
RV paced by Ventricular Rate Regulation during ATR fallback
RVP-VR / LVP-VR
RV / LV pace delivered by Ventricular Rate Regulation
RVS
RV sensed event (marker)
RYTHMIQ
Boston mode switching AAI(R) with VVI backup, to limit ventricular pacing
S / T
S-ICD markers: sensed beat / tachycardia-detected beat
S-ICD
subcutaneous implantable cardioverter-defibrillator
SAV
sensed AV delay
SR
sinus rhythm
ST
sinus tachycardia
SVT
supraventricular tachycardia
TI
thoracic impedance
V-A
ventriculo-atrial interval
V-Detect
ventricular detection met (end of duration)
V-Epsd
ventricular episode onset (8/10 met)
V>A
ventricular rate greater than atrial rate
VA
ventriculo-atrial (conduction)
VDI
fallback mode (no atrial tracking)
VF
ventricular fibrillation (zone)
VG
French label of the LV EGM channel on the printout (ventricule gauche)
VGdist / VGprox
LV distal / proximal electrode (French printout labels)
VGprox2 / VGprox3
French printout names of LV electrodes = LVRing2/LVRing3
VP-BP
ventricular backup pace after a test pulse (automatic threshold test)
VP-MT
ventricular pace at the MTR (RVP-MT/LVP-MT)
VRR
Ventricular Rate Regulation
VT
ventricular tachycardia
VT-1
lowest VT zone
VVI
ventricular pacing, ventricular sensing, inhibited mode
VVIR
ventricular inhibited pacing, rate responsive

Course sheet of the Boston Scientific CRT teaching day by M. Strik. Book cases from Encyclopédie Boston Scientific by P. Bordachar, R. Eschalier, S. Ploux, M. Strik. Published by Cardiocases.