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Case Studies in
Clinical Cardiac
Electrophysiology
John M. Miller, MD
Professor of Medicine, Indiana University School of Medicine
Director, Clinical Cardiac Electrophysiology
Indianapolis, Indiana
Mithilesh K. Das, MD
Professor of Clinical Medicine, Indiana University School of Medicine
Indianapolis, Indiana
Douglas P. Zipes, MD
Distinguished Professor Emeritus of Medicine, Pharmacology and Toxicology
Indiana University School of Medicine
Emeritus Director, Krannert Institute of Cardiology
Indianapolis, Indiana
1600 John F. Kennedy Blvd.
Ste 1800
Philadelphia, PA 19103-2899
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Notices
 Knowledge and best practice in this field are constantly changing. As new research and experience broaden
 our understanding, changes in research methods, professional practices, or medical treatment may become
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 material herein.
Names: Miller, John M. (John Michael), 1954- author. | Das, Mithilesh K.,
  author. | Zipes, Douglas P., author.
Title: Case studies in clinical cardiac electrophysiology / John Miller,
  Mithilesh Das, Douglas Zipes.
Description: Philadelphia, PA : Elsevier, [2018] | Includes bibliographical
  references and index.
Identifiers: LCCN 2016053043 | ISBN 9780323187725 (hardcover : alk. paper)
Subjects: | MESH: Heart Diseases--diagnosis | Electrophysiologic
Techniques,
  Cardiac--methods | Case Reports
Classification: LCC RC683.5.E5 | NLM WG 141.5.F9 | DDC 616.1/2075--dc23
LC record available at https://lccn.loc.gov/2016053043
Printed in China
                                                                                      Foreword
The practice of clinical cardiac electrophysiology is one of clinical exploration that starts
with integration of the patient’s symptoms and cardiac evaluation with electrocardio-
graphic interpretation. One of the most gratifying experiences for patient and physician is
when this process culminates in the electrophysiology laboratory with confirmation of the
diagnosis and implementation of effective therapy for the arrhythmia with catheter abla-
tion. Mastery of each component is needed, and the knowledge that is gained from each
step can be applied to the previous step to refine one’s diagnostic acumen. We became
much better electrocardiographers by applying the knowledge gained from the pioneering
work that defined cardiac activation patterns and arrhythmia mechanisms using cardiac
mapping and programmed electrical stimulation. Expertise in the last step, interventional
electrophysiology, is the most challenging to acquire. It requires assimilation of complex
patterns of cardiac activation, interpretation of spontaneous changes in patterns, and ap-
plication of maneuvers to confirm a diagnosis, and this confirmation is critical for guiding
catheter ablation.
   Drs. Miller, Das, and Zipes have assembled a wonderful book that captures the spirit of
clinical exploration leading to effective therapy. They use cases to describe pathophysio-
logic concepts that start with fundamentals and proceed to complex concepts. From the
electrophysiology laboratory they incorporate findings ranging from those that are classic
to those that are only recently described and that require a nuanced interpretation and
understanding, but that are critical to arriving at the correct diagnosis. Examples include
the newest technologies that are now being applied for delineation of arrhythmia mecha-
nisms and substrate.
   The authors are renowned teachers who apply their wealth of experience in communi-
cating complex scenarios and concepts to make the cases accessible for the complete range
of students of clinical electrophysiology, from the trainee to the advanced practitioner.
The cases clarify concepts and provide fundamentals for the new student, but also provide
insights that will expand the knowledge of experienced clinicians. Dr Miller’s hand is
evident throughout in the superb graphics, for which he is widely known among teachers
of cardiology.
   One of the amazing aspects of biology, medicine, and certainly extending to cardiac
electrophysiology, is the variability that one encounters from patient to patient. After
years in the field, one still encounters new arrhythmia problems. A solid basis in under-
standing mapping and diagnostic maneuvers is required for solving new puzzles in the
electrophysiology laboratory, and this learning is acquired from the study of cases. You
can never analyze too many cases. I congratulate the authors of Case Studies in Clinical
Cardiac Electrophysiology on a wonderful book.
                                                                William G. Stevenson, MD
                                                     Director, Cardiac Arrhythmia Program
                                                                    Cardiovascular Division
                                                            Brigham and Women's Hospital
                                             Professor of Medicine, Harvard Medical School
                                                                      Boston, Massachusetts
                                                                                                           vii
                                                                                                    CONTENTS
                                                                                                Preface
The understanding and care of patients with heart rhythm disturbances (clinical cardiac
electrophysiology [EP]) has evolved in the last three decades from simple diagnostic stud-
ies of the conduction system using a few electrodes, to complex diagnostic and therapeutic
procedures involving recording and stimulation from a large number of electrodes, for the
purpose of finding and ablating arrhythmogenic tissue. With this dramatic change in the
character of EP studies has come the critical need for careful analysis and thorough under-
standing of the meaning of recordings that are made and results of stimulation in order to
achieve optimal results from ablation. At the same time, EP training programs have come
under increasing pressure to perform more procedures in a shorter amount of time, result-
ing in compromising time for careful and methodical study of and learning from these
procedures that are rich with teaching material. Although many excellent texts in our field
explain the principles of recording and stimulation in treatment of arrhythmias, for ex-
ample, Clinical Arrhythmology and Electrophysiology, few are structured to show their
practical application in a case-study format. In light of this, the purpose of this volume is
to take the reader through a representative series of EP procedures from start to finish,
evaluating results of diagnostic pacing maneuvers, sampling and comparing characteristics
of electrograms, and selection of appropriate sites for ablation. It is our hope that readers
will benefit from this mode of presentation, highlighting some of the limitations of tech-
niques that are used on a daily basis, with the aim of improving the efficacy and safety of
procedures they perform on their patients.
Acknowledgments
We gratefully acknowledge the role played by our nursing and technical staff with whom
we performed the procedures reviewed in this work, as well as electrophysiology fellows,
whose patience in keeping catheters in place during long procedures contributed greatly to
the quality of the figures. We also acknowledge our patients, who provide a constant source
for learning.
                                                                                                               ix
PA RT 1               Sinus Node, AV Node, and His-Purkinje System
Baseline ECG
I aVR V1 V4
III aVF V3 V6
II
The ECG in Fig. 1-1 shows sinus rhythm with a prolonged P wave (left atrial abnormality),
slightly prolonged PR interval, RBBB and left anterior fascicular block, and an extensive
anterior infarction. On the basis of this, there are many possible causes of syncope—atrial
arrhythmias (atrial flutter and fibrillation, other reentrant atrial tachycardias), heart block
(either in AV node or His-Purkinje system), or ventricular arrhythmia (ventricular tachy-
cardia or fibrillation). There is nothing in the ECG to favor one cause of syncope over
another, and because treatment strategies are very different depending on the cause
(medications or ablation for atrial arrhythmias; pacemaker for heart block; implantable
defibrillator for ventricular arrhythmias), further investigation is needed.
                                                                                                               1
2   CASE STUDIES IN CLINICAL CARDIAC ELECTROPHYSIOLOGY
    Evaluation
                                                                 Baseline Intracardiac Recordings
                                   1
                                   2
V1
V6
                               HRA
                 Figure 1-2                  A              V
                                                  H
                              Hisprox
Hismid
                              Hisdist
                                                      RBB
                                                                  AH 85 ms            HV 85 ms
                                 RV
                                                                             200 ms
                              Intracardiac recordings during sinus rhythm (Fig. 1-2) show atrial (A), His (H), and
                              ventricular (V) recordings as noted. This confirms the presence of His-Purkinje disease,
                              with an HV interval of 85 ms—prolonged (normal, 40 to 55 ms), but not enough to
                              implicate His-Purkinje dysfunction as a cause of heart block. Surprisingly, though the PR
                              interval is somewhat prolonged, the AH interval is normal (85 ms [normal, 60 to 125 ms]).
                              Usually, prolongation of the PR interval is caused by the AV nodal (AH) component, be-
                              cause to prolong the PR even 60 ms from His-Purkinje disease would require a lengthening
                              of the HV to a degree (that is, from 40 ms to 100 ms) that 1:1 conduction would be unlikely.
                              Note also that there is a delay between the distal His recording and right bundle branch
                              (RBB)—there is usually ,10 ms between these—and that the RBBB is further caused by
                              delay or block between the RBB and RV apical electrogram, with a QRS onset (dashed blue
                              line) to RV electrogram of 75 ms (normal, 10 to 35 ms).
                                   1
                                   2
                                   3
                                  V1
                                  V6
                 Figure 1-3
                               HRA       A            V                           V       A
                                             H
                              Hisprox
                                                                                      H
                              Hismid
Hisdist
                                 RV
                                         200 ms                            S                          S
                                             CHAPTER 1 | SINUS NODE AND ATRIOVENTRICULAR CONDUCTION DISEASE 3
The left side of Fig. 1-3 shows a sinus rhythm complex as in the previous figure for refer-
ence, whereas the 2 complexes on the right are during pacing from the right ventricular
apical region. Note that there is retrograde conduction to the atria, with the His bundle
activated from distal to proximal as expected. Usually, the timing of the His potential is
before the local ventricular electrogram in the His recoding, because conduction proceeds
more rapidly up the RBB to the His than does muscle-to-muscle propagation from apex to
base. Because there is RBBB in this case, the impulse cannot ascend the RBB as it normally
would and instead must traverse the interventricular septum, enter the left bundle branch,
and then activate the His retrogradely. These findings just confirm the His-Purkinje disease
but give no further insight as to the cause of syncope.
Normal RBBB
               I                                         I
              II                                        II
              V1                                        V1
                     H                                                     H
             HBp                                       HBp
HBm HBm
             HBd                                       HBd
                                                                                                Figure 1-4
             RVA           V                           RVA           V
LBB LBB
RBB RBB
As illustrated in Fig. 1-4, in patients with normal His-Purkinje function (at left), pacing
from the right ventricular apex (red circle) results in retrograde conduction over the RBB
(white line) that is more rapid than muscle-to-muscle conduction (wavy line in septum),
resulting in a His potential (H) inscribed before the larger local ventricular recording (V).
At right, in the presence of anterograde RBBB, the paced wavefront cannot ascend the
blocked right bundle and instead crosses the interventricular septum (wavy horizontal line)
to engage the left bundle, and then proceeds rapidly to the His that now appears after the
local ventricular recording (that is again generated after muscle-to-muscle spread).
4   CASE STUDIES IN CLINICAL CARDIAC ELECTROPHYSIOLOGY
                                                                          Atrial Pacing
                                   1
V1
V6
                             Hisprox
                                                               A
                                                                HV
                              Hismid
Hisdist
                                                                          HV 85 ms
                                 RV                  400 ms
                             Rapid pacing can often reveal abnormalities of AV conduction that were not very evident
                             at rest. In Fig. 1-5, pacing the atrium (S) slightly faster than the sinus rate shows minimal
                             change in either AH (90 ms) or HV (85 ms) intervals. It is useful to display multiple elec-
                             trode pairs of His recordings because the signal amplitude may vary enough between
                             complexes that the His potential may be poorly visible or even absent in one electrode pair
                             (Hisdist in this case), whereas it is readily visible in other electrode pairs.
Atrial Pacing
V1
                                  V6
                Figure 1-6                  420 ms             400 ms                         380 ms
                               HRA      S        S         S        S          S          S        S           S         S         S
                             AH (ms):        140     145        170     185        230          --       115       130       190       230
                             Hisprox
                                              H       H         H          H         H          ∗        H         H          H          H
                              Hismid
                             HV (ms):        100     110       112      115        115                   90        115       --
                              Hisdist
                                 RV
                                                                                                400 ms
                             More rapid pacing starts to reveal some abnormalities. As the pacing rate increases (cycle
                             length decreases), the AH is expected to prolong but the HV interval usually remains con-
                             stant. In Fig. 1-6, the AH (in blue) does prolong, but so does the HV interval (in green). The
                             asterisk denotes where AV nodal block occurs (no subsequent His potential), but three
                             cycles after this, there is a His potential not followed by a QRS (infra-His block; green dash)
                                            CHAPTER 1 | SINUS NODE AND ATRIOVENTRICULAR CONDUCTION DISEASE 5
and the HV intervals on the prior two cycles had prolonged (thus, infra-His Wenckebach).
This is distinctly abnormal and likely warrants pacemaker implantation. However, this may
not be the reason that syncope had occurred (there may be other abnormalities that have
not yet been uncovered during the study).
Atrial Pacing
V1
V6
Hisprox
Hismid
Hisdist
    RV
                                    1 sec
In Fig. 1-7, pacing is repeated for 1 min at the same cycle length as shown in the
prior figure to stress the sinus node. Upon cessation of pacing, a prolonged sinus pause
(4.15 seconds) is observed; a junctional escape complex occurs after 3 seconds. This is
another potential cause of syncope (sinus node dysfunction).
6   CASE STUDIES IN CLINICAL CARDIAC ELECTROPHYSIOLOGY
                                                                         Ventricular Pacing
                                                                                                               ∗
                                   1
V1
                                  V6
                                        Sinus                                                                          Sinus
                Figure 1-8     HRA
                                                                A                 A                    A
Hisprox
                             Hismid
                                                                                                           H
                                                            H                 H                H
                              Hisdist
                                 RV       S            S                 S                 S               S            S
                                                                                  400 ms
                             Turning to the ventricles (Fig. 1-8), slow ventricular pacing again shows that there is retro-
                             grade conduction; the first and last atrial complexes are sinus in origin (HRA before His
                             atrial recordings) but the middle three complexes are retrogradely conducted. The first two
                             of these (blue arrows) are over the fast pathway, but after the fourth ventricular stimulus,
                             the ventriculoatrial interval suddenly increases, signifying a switch to a slow pathway (red
                             arrow). Immediately after this, there is a QRS complex that is not fully paced (asterisk); this
                             is because of fusion between the paced wavefront and one over the normal conduction
                             system (see His potential). This is the result of an atypical AV nodal echo (retrograde slow
                             pathway, anterograde fast—blue arrow). This is a common finding and, unless accompa-
                             nied by sustained atypical AV nodal reentrant SVT, has no relevance for the diagnosis of
                             syncope.
Ventricular Stimulation
V1
V6
                Figure 1-9
                               HRA
                                         SA           SA
Hisprox
Hismid
                                                                                                   H               H           H
                              Hisdist
                                 RV S
                                      1         400 ms S1   S2      S3   S4
                                            CHAPTER 1 | SINUS NODE AND ATRIOVENTRICULAR CONDUCTION DISEASE 7
The last part of the syncope evaluation consists of programmed ventricular stimulation. As
shown in Fig. 1-9, standard stimulation (here, with triple extrastimuli, S2 to S4) initiates a
rapid, hemodynamically unstable ventricular tachycardia (CL 250 ms) that stopped spon-
taneously after 15 seconds. Given the presence of a prior MI and “serious” syncope, this
arrhythmia was deemed a reasonable candidate for the cause of his syncope. He received a
dual-chamber ICD later that day. Note that a His potential is seen on occasion but not with
every complex—excluding bundle branch reentry as a possible cause of the tachycardia
(SA 5 atrial stimulus).
Summary
n   This man had syncope in the presence of structural heart disease—which always needs
    further evaluation.
n   Multiple potential causes of syncope may be present in the same patient; in this case,
    n Sinus node dysfunction
    n His-Purkinje dysfunction
    n Ventricular tachycardia
n   Judgment must be used to determine which possible cause(s) of syncope should be
    treated and how.
PA RT 2              Supraventricular Arrhythmias
                         Typical (“Slow-Fast”)
               Atrioventricular Nodal Reentry                                                      2
Case Presentation
A 48-year-old woman had a history of palpitations for ~5 years. Her episodes started and
stopped suddenly, lasted 1 to 2 minutes, and were associated with lightheadedness. She
came to a local emergency room with a prolonged episode: ECG showed a narrow QRS
tachycardia (by report; no ECG available) that was terminated with adenosine. She was
treated with oral diltiazem and metoprolol but continued to have supraventricular tachy-
cardia (SVT) episodes. She had a normal physical exam; non-invasive evaluation showed
no structural heart disease. She was referred for catheter ablation of her SVT.
aVR
aVL
         aVF
                                                                                           Figure 2-1
          V1
V2
V3
V4
V5
          V6
                    1 sec
Fig. 2-1 demonstrates normal sinus rhythm without delta waves, fractionation, or prolon-
gation of the P wave or QRS and normal QT. ECG is normal.
                                                                                                        9
10   CASE STUDIES IN CLINICAL CARDIAC ELECTROPHYSIOLOGY
                                          1
                                          2
                                          3
                                        V1
                                        V6
                                      HRA
                                     Hisprox
                                                   A
                                     Hisdist
                                                       H   V
                 Figure 2-2          CSprox
CSmid
                                     CSdist
                                        RV
                                                                      200 ms
                              Fig. 2-2 shows normal intracardiac intervals (AH, HV); there is no evidence of preexcita-
                              tion on intracardiac recordings. Normal progression of atrial activation is seen from right
                              atrium to His to coronary sinus proximal to distal.
     Ventricular Pacing
                                                                      Ventricular Pacing (600 ms)
                                         1
                                         2
                                         3
                                        V1
                                        V6
                                    HRA
                                   Hisprox
                                    Hisdist
                                    CSprox
                 Figure 2-3
CSmid
                                    CSdist
                                       RV
                                               S           200 ms              S                      S
                              In Fig. 2-3, with ventricular pacing at 600 ms, retrograde conduction is present with a
                              concentric activation pattern; a retrograde His potential (arrow) is seen between stimulus
                              artifact and local ventricular electrogram.
                                                CHAPTER 2 | TYPICAL (“SLOW-FAST”) ATRIOVENTRICULAR NODAL REENTRY 11
        1
        2
        3
       V1
       V6
    HRA
   Hisprox
   Hisdist
   CSprox
                                                                                                Figure 2-4
CSmid
    CSdist
      RV
             S        200 ms       S                        S                    S
With more rapid ventricular pacing (470–460 ms) the same activation sequence is seen in
Fig. 2-4, with a longer VA interval—most consistent with AV nodal conduction.
             1
              2
              3
             V1
         V6
       HRA
      Hisprox
      Hisdist
      CSprox
                                                                                                Figure 2-5
CSmid
       CSdist
         RV                    S          S      S      S       S        S   S       S
                    400 ms
In Fig. 2-5, with the sudden onset of ventricular pacing (280 ms), a His “out the back”
(arrow) is seen after second stimulus, with atrial activation dependent on His (ie, no bypass
tract). Retrograde block occurs after the third stimulus likely because of block in the
His-Purkinje system, which recovers by the fourth stimulus (after which 1:1 retrograde
conduction resumes).
12   CASE STUDIES IN CLINICAL CARDIAC ELECTROPHYSIOLOGY
ECGs Compared
                                                                        ECGs Compared
                                                              SVT                                 Sinus Rhythm
1 1
                                                                                              2
                                         2
                                                                                              3
                                        3
                                      aVR                                                 aVR
                                       aVL                                                aVL
                                                                                          aVF
                 Figure 2-6           aVF
                                        V1
                                                                                           V1
V2 V2
V3 V3
V4 V4
V5 V5
                                        V6                                                 V6
                                                      1 sec                                       1 sec
                              SVT was induced ((left); sinus rhythm is shown at right in Fig. 2-6. A superimposed sinus
                              complex (red) overlaid on SVT shows no clear difference, implying that the P wave must be
                              hidden within the QRS complex.
                                         1
                                         2
                                         3
                                        V1
                                       V6
                                     HRA
                                    Hisprox
                                                                             A
                                    Hisdist
                 Figure 2-7         CSprox
                                                                         V                V
CSmid
                                     CSdist
                                       RV
                                              S   S       S    S    S            400 ms
                              In Fig. 2-7, ventricular pacing during SVT conducts retrogradely to atrium with the same
                              activation pattern as during SVT. During SVT that resumes on cessation of pacing, atrial
                              activation appears concentric and within (even before) the QRS complex, excluding ortho-
                              dromic SVT. The long pause after pacing suggests conduction down an AV nodal slow
                              pathway. The “VAV” response is consistent with typical atrioventricular nodal reentry
                              (AVNRT), not atrial tachycardia (AT).
                                                     CHAPTER 2 | TYPICAL (“SLOW-FAST”) ATRIOVENTRICULAR NODAL REENTRY 13
Ventricular Pacing
           1
           2
           3
          V1
          V6
     HRA
   Hisprox
   Hisdist
                                               A
   CSprox                                                                                  Figure 2-8
                                       V                                V
CSmid
    CSdist
          RV
                   S               S                      200 ms
Fig. 2-8 is a faster sweep speed of Fig. 2-7, showing the same findings.
Para-Hisian Pacing
Para-Hisian Pacing
     1
     2
     3
   V1
   V6                                                     HA 90 ms
 HRA
Hisprox
Hisdist        S                             S      H
CSprox                                                                                     Figure 2-9
                       SA 90 ms                          SA 210 ms
CSmid
CSdist
 RV
                                  200 ms
The complex at right of Fig. 2-9 shows a normal sinus complex. The complex in middle
has a wide QRS suggesting pure ventricular capture. Retrograde conduction is evident.
The complex at left is relatively narrow, indicating some element of His capture, though
not pure His capture (His 1 V capture); retrograde conduction is evident with the same
pattern as during the wider complex and S-A interval is 90 ms; in the wide complex
(V capture only), the S-A interval is 210 ms, indicating conduction only over AV node.
The retrograde His is visible (H), with HA still 90 ms.
14   CASE STUDIES IN CLINICAL CARDIAC ELECTROPHYSIOLOGY
                                         1
                                         2
                                         3
                                        V1
                                       V6
                                     HRA
                                    Hisprox
                                    Hisdist
                Figure 2-10         CSprox
CSmid
                                     CSdist
                                       RV
                                              S1          200 ms           S1                  S2
                                       1
                                       2
                                       3
                                      V1
                                     V6
                                                      370 ms            370 ms          350 ms         370 ms          370 ms
                                   HRA
                                  Hisprox
                                  Hisdist
                Figure 2-11       CSprox
CSmid
                                   CSdist
                                     RV
                                                    200 ms                                S2
                              In Fig. 2-11, a ventricular extrastimulus is given during SVT. The A-A interval surrounding the
                              extrastimulus is shorter than the rest of the A-A intervals, but the His was not refractory (blue arrow
                                               CHAPTER 2 | TYPICAL (“SLOW-FAST”) ATRIOVENTRICULAR NODAL REENTRY 15
shows where it would be expected if not for the extrastimulus). Advancement of the timing of
atrial activation surrounding a His-refractory ventricular extrastimulus demonstrates the existence
of a path of conduction extrinsic to the normal conduction system (bypass tract). If the extra-
stimulus occurs at a time when the His is not refractory (as here), it is feasible that conduction
could occur through the His to the AV node and atrium, and would not implicate a bypass tract.
                                                         350 ms           370 ms
       1
      2
      3
     V1
     V6
   HRA S                 S                S
  Hisprox
  Hisdist
  CSprox                                                                                               Figure 2-12
PCL 350 ms
CSmid
  CSdist
     RV
                        200 ms
Overdrive atrial pacing during SVT is shown in Fig. 2-12. At first glance, the third QRS complex
appears to result from the third stimulus. On closer inspection, it is clear that the third stimulus
causes the fourth QRS complex because the V-V interval there is the same as the paced cycle
length (350 ms). This indicates the presence of slow AV nodal conduction (no surprise, because
this type of AV nodal reentry uses an anterograde slowly conducting pathway).
16   CASE STUDIES IN CLINICAL CARDIAC ELECTROPHYSIOLOGY
                                    1
                                   2
                                   3
                                  V1
                                  V6
                                                                                  S2
                               HRA
                              Hisprox
                              Hisdist
                Figure 2-13                 H-H 370 ms         370 ms        370 ms          370 ms           370 ms
                              CSprox
CSmid
                               CSdist
                                 RV           200 ms
                              In Fig. 2-13, a single atrial extrastimulus is given during SVT. His-His intervals are as indi-
                              cated; the His immediately after the extrastimulus (blue arrow) is on time and unaffected
                              by the stimulus. Thus, if this were a focal junctional tachycardia, it would have already
                              “fired” for that complex and its next occurrence should be right on time. Although this is
                              exactly what happens—the next His (red arrow) occurs on time—this finding is also con-
                              sistent with AV nodal reentry or even AT conducting over a slow AV nodal pathway (the
                              impulse is already on its way down the slow pathway and is unaffected by the atrial extra-
                              stimulus). Thus this finding by itself is not diagnostic of focal junctional tachycardia.
                                      1
                                      2
                                      3
                                     V1
                                     V6                              S2           S3
                                  HRA
                                 Hisprox
                                 Hisdist      H-H 370 ms       370 ms        370 ms           350 ms         370 ms
                Figure 2-14      CSprox
CSmid
                                 CSdist
                                    RV           200 ms
                              Double atrial extrastimuli are now given during SVT (Fig. 2-14). The His potential after second
                              extrastimulus (blue arrow) is on time (370 ms), unaffected by the first atrial stimulus (S2). How-
                              ever, the next His (red arrow), driven by the second atrial stimulus (S3) is advanced by 20 ms. This
                              shows that focal junctional tachycardia cannot be the diagnosis, because a focal discharge from
                              the His at the red arrow cannot be advanced by an atrial stimulus that did not affect the prior His.
                                              CHAPTER 2 | TYPICAL (“SLOW-FAST”) ATRIOVENTRICULAR NODAL REENTRY 17
       1
       2
       3
      V1
       V6
    HRA S               S                 S
   Hisprox
  Hisdist
  CSprox                                                                                     Figure 2-15
                                     AH 362 ms                      AH 330 ms
CSmid
   CSdist
     RV
                        200 ms
Atrial overdrive pacing during SVT is performed again, as shown in Fig. 2-15; the AH in-
terval with pacing (362 ms) exceeds the AH in SVT (330 ms); this is consistent with AV
nodal reentry and inconsistent with right AT (in which case the AH intervals should be
similar between pacing and SVT).
              1
              2
              3
             V1
             V6
         HRA
        Hisprox
       Hisdist
       CSprox          HA 92 ms                                 HA 80 ms
                                                                                             Figure 2-16
CSmid
        CSdist
            RV
                  S   200 ms     S
The HA interval with ventricular pacing at the SVT cycle length (92 ms) is always the same
as or longer than HA in SVT (80 ms), when measured as shown in Fig. 2-16 (end of His to
A during pacing, onset of His to A during SVT, with standard 5-mm interelectrode record-
ing catheters). This is not found with very closely spaced, very proximal His recordings,
however, where the difference between HA intervals with pacing and SVT narrows as the
point of turnaround between anterograde slow and retrograde fast pathways occurs.
18   CASE STUDIES IN CLINICAL CARDIAC ELECTROPHYSIOLOGY
                                       1
                                       2
                                       3
                                      V1
                                      V6
                                    HRA
                                   Hisprox
                                   Hisdist
                Figure 2-17        CSprox
CSmid
                                                                SA 166 ms               VA 46 ms
                                   CSdist
                                      RV                                PPI 544 ms
                                             S   PCL 320 ms S                200 ms                             TCL 344 ms
                              Ventricular overdrive pacing during SVT is shown in Fig. 2-17, with intervals as indicated;
                              the SA-VA difference (120 ms) exceeds 85 ms, and the postpacing interval (PPI)–tachycardia
                              cycle length (TCL) difference (200 ms) exceeds 115 ms; both indices indicate AV nodal
                              reentry rather than orthodromic SVT.
Atrium
AV node
Ventricle
Atrium
AV node
Ventricle
                                                                                                          PPI             TCL
                                                                                              SAVpacing - VASVT > 85 ms
                              Fig. 2-18 displays entrained ventricular pacing during orthodromic SVT; the bypass tract
                              shown here (connecting left atrium and left ventricle) is indicated in the ladder diagrams
                              as a dotted line.
                                               CHAPTER 2 | TYPICAL (“SLOW-FAST”) ATRIOVENTRICULAR NODAL REENTRY 19
                                                                AV nodal reentry
                                                                      SVT
Atrium
AV node
Ventricle
Atrium
AV node
Ventricle
                                                                     PPI              TCL
                                                        SAVpacing - VASVT > 85 ms
Atrium Atrium
AV Node AV node
Ventricle Ventricle
Fig. 2-20 is a comparison of SVT and responses to overdrive ventricular pacing in ortho-
dromic reentry with a bypass tract versus AV nodal reentry. In each case, the paced wavefront
must travel from the pacing site to the circuit (stimulus-atrial interval, SA) and back to the
pacing site (PPI). Fundamentally, because a right ventricular pacing site is relatively near an
orthodromic tachycardia circuit, the SA-VA and PPI-TCL differences are shorter than similar
indices in cases of AV nodal reentry, in which the ventricular pacing site is remote from the
circuit.
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5.
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 Ovi oli lukossa, juuri niinkuin olin sen sulkenutkin, kun panin
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6.
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7.
8.
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Nainen naurahti.
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10.