BRIEF REPORTS

Sudden Death During Ambulatory

Electrocardiographic

Monitoring

Carl J. Pepine, MD, Joel Morganroth, MD, John T. McDonald, MA, and Sidney 0. Gottlieb, MD lthough a relation betweenambulatory myocardial &hernia and suddencardiac death hasbeen postulated, previous reports suggest that this may be an uncommon occurrence.1-7This suggestion, however,is basedon observationsof a limited number of deaths3-7and data from living patients with chronic stable angina.‘J In the latter patients ventricular arrhythmias related to transient ischemia occur infrequently. But these studies are biased becausethey are conducted in patients who are survivors. Previous suggestionsare also biased by the fact that sudden death occurs rarely during ischemia induced in the exercise laboratory. Therefore, the contribution of ambulatory ischemia to cardiac sudden death is open to question. An examination of the relatively few patients undergoing diagnostic

A

ambulatory electrocardiographic monitoring would not be expectedto provide adequatedata, becausethe occurrence of cardiac death is relatively infrequent. Accordingly, the purpose of this study was to investigate the possiblerelation betweensuddencardiac death and ischemia detectedby ambulatory electrocardiographicmonitoring by examining recordingsof patients who died suddenly while wearing a long-term ambulatory electrocardiographic recorder.

We retrospectively studied the ambulatory electrocardiographic recordings of 35 patients who died suddenly while wearing an ambulatory electrocardiographic recorder. These cases were obtained from the records of our own hospitals and a commercial ambulatory electrocardiographic analysis service (CDS Research, Haddonjield, New Jersey). To be included, From the Division of Cardiology, Department of Medicine, Box J-2777, patients had to have been wearing an operational amUniversity of Florida and VeteransAffairs Medical Center,Gainesville, recorder during the Florida 32610. Manuscript received March 25, 1991; revised manu- bulatory electrocardiographic terminal event and not have been following an experiscript receivedand acceptedMay 20, 1991.

TIME HR

108

RHYTHM COMMENT

TIME HR RHYTHM COMMENT

114

ii3

b

Sinus Start

5.37P 26 Junctional TERMINAL

106

ST+ ONSET

MAX

5.38P 20 Bradycardia ISCHEMIC

60

5:29P 40

Junctional ST+ ONSET

F TERMINAL

ISCHEMIC EPISODE

5.38P

F Asystole

EPISODE CONTINUED

FIGURE 1. Case 1. Example of a patii with ischemia-related bradycardii/asystole. The ambulatory electrocardiographic recorder was applied at 4 P.M. when the ST segment was is&ectric and the patient in sinus rhythm. Appf&mately 11 minutes later an ischsmic episede was detected as 1.0 mm of Slqsegment depression in lead Vs (top fracing), which reacheda maximum (MAX) of 21 mm after 8 mimdes. This episode slow& subsided, but at MS P.M. the patient developed a junctional rhythm assoctated with 1.0 mm ST-segment depression. Eleven minutes later the junctional fiythm slowed to 40 beats/min as ST-segnwmt depression increased and R-wave amplitude diminished. The rate slowed progressivety and asystole occurred. HR = heart rate.

BRIEF REPORTS 785

mental drugprotocol. Recordings had to be technically suitablefor both arrhythmia and ST-segment analysis, and the terminal event had to be clearly recorded. All patients wore Z-channel AM tape recorders adequate for reproduction of ST-segment changes of ischemia. Tapes were analyzed on a CardioData Corporation scanner using version 7.64 software or comparable equipment. Printouts of the electrocardiogram were made at 25 mm/s and baseline recordings at the start of the session; the terminal event and all definite and questionable episodes of ST-segment deviation that suggested ischemia. Strips printed during episodes suggesting ischemia were obtained at the onset of the episode, at the time of maximal ST-segment shift and also at the offset. The strips were then reviewed independently by the investigators for: (1) baseline abnormalities of the QRST, which could limit recognition of ischemia; (2) confirmation of ischemit episode; (3) ischemia-related sudden death; and (4) classification of terminal episode. Only cases in which a consensus agreement on these findings could be reached are included in this report.

The following definitions were used: An ischemic episodewas considered a change in the level of the STsegment compared with the baseline recording, that persistedfor at least I minute and met at least 1 of the following criteria - L 1.O mm horizontal or downsloping depression or 12.0 mm of elevation. Ischemia related sudden death was considered an ambulatory electrocardiographic-documented ischemic episode occurring within 60 minutes of the terminal event. Terminal events were classed as either ventricular tachycardia/‘brillation or bradycardialasystole. When both events werepresent in the same patient the initial episode was considered the terminal event. Uninterpretable for ischemia was taken to mean ST-Twave changes 2 1.Omm or an intraventricular conduction defect (20.12 second) present in the baseline recording. In 12 of the 35 (34%) patients, the electrocardiogram was considered uninterpretable for ischemia. In another 12 (34%) patients, at least 1 or more ischemic episode preceded the terminal event. In 10 of these, there were multiple ischemic episodes. The frequency

: :: :..z?+i/.j/::. :::.I::::. z :,/:. .:: :‘:: :.::::: ‘; ::/:: 7 ii:i” j/j “‘. ,, ,,:: ..& :.! .::. ::::,:::: ” ““. ‘C :: .::: ::.. ;;:;;;; ;s& : : ;:: : :: : :: : : ; : :: :: : : :: j; jjii GJJ ~

TIME 9:05A HR 84 RHYTHM Sinus COMMENTStart

TIME HR

9:OOP 93

RHYTHM Sinus

5:llP

5:17P

5:22P

5:27P

5:31P

5:45P

8:05P

98

85

89

93

80

83

88

8:26P 8:;;P

94 b

ST+ ONSET MAX

9:06P

81 t VPCS ____)

ST+ ONSET

9:13P

81

MAX

ST+ ONSET MAX

9:15P

84 Sinus

+

VTNF

COMMENT ST+ ONSET TERMINAL ISCHEMIC EPISODE

FtQURE 2. Case 2.2xampk oi a patlent wlth multlpk kchemk m temdnatlng In vantrlcular tachycardla (VT)/tlbrlllatlon (VF). Thel mbulaWy ekctrowrdlographk rewrd~ war applkd at 9iO9 A.M.whai~ tha patknt was In slnua rhythm. The ST aegmant ramalrml koekctrk until Ml P.M.and reachad a maxlmum (MAX) of 2.0 mm 6 minutes later In kad V5 (fop tradng) aa Rmwave amplltude and heart rate (HR) IIK#WMI. lids lnltlal 1-k epkode subs&d slowly over tha next S mlnuter. A second kchamk epkode was row&d at 5~27 P.M.wlth a elmllar patkin of increaslnl R-wave amplltude~and ST-segrmmt w. at 8109 P.M.,and a fourth ad temdnal 1-k epkode was mcordad at 9 P.M.During Anathurkclnnnkepkodewasthk eplscde, ST-segment depredon reached 2.0 mm and at 9:09 P.M.was assdated wlth ventrkular premature contractkns (WCs) occurring late In the cyck. At 9:lS P.M.a ventrkular premaWe contraction ocuaved during the T wave folkwed by venWkular tachycardla/flbrlllatlon.

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THE AMERICAN JOURNAL OF CARDIOLQGY VOLUME 68

SEPTEMBER 15, 1991

the same manner that they would be in a prospective study directed specifically at ambulatory electrocardiographic monitoring. Third, a large number of patients irk this study had ST segmentsthat were considered uninterpretable for &hernia when reviewedby the authors and were excluded as ischemia-related sudden deaths. This should result in an underestimation of the frequency of ischemia-related sudden death. Fourth, this is a sample representativeof only adult patients dying suddenly. Despite these limitations, evidencefor ischemia was present in about half of the patients with interpretable electrocardiograms.These results suggestthat ischemia may be found more often than previously anticipated in patients with sudden cardiac death. Also, the similarity in frequenciesof ventricular tachycardia/fibrillation and bradycardia/asystole is a deviation from the commonly held notion that asystoleis a relatively infrequent terminal event.4,7This conclusion, however, would remain to be establishedin a larger prospectivecohort study of this kind. Such a study would be able to supply the important denominator data neededto assessthe actual frequencies

ranged from 1 to 4 episodesper patient and the duration ranged from 2 minutes to 8 hours. Finally, in the remaining 11 patients (31%), no definite evidencefor ischemia was detected before the terminal episode in the leads monitored. But 2 of these latter 11 patients had evidencefor ischemia after a period of ventricular tachycardialfibrillation. These latter 2 patients were not considered to have ischemia-related sudden deaths. There was no signijcant association between STsegment elevation, depression or the presence of both types of shifts and either a bradycardia/asystole terminal event or a ventricular tachycardialfibrillation terminal event. Ischemia preceded the terminal event in most of the 23 patients with interpretable ST segments (12 of 23 or 52%). Representative examples of these patients appear in Figures 1 to 3. This study has several limitations. First, becauseof the retrospective analysis, carried out long after the patients had died, limited clinical information was available. Second, the technical aspectsof the ambulatory electrocardiographic recordings were not controlled in

9:13A HR 77 RHYTHM Sinus TIME

3:02P 130 S.Tach

COMMENT

Start

OST

TIME HR RHYTHM

4:45P

4347P

COMMENT

52 50 Junctional +VPCs ST+

STf

4:17P 100 Sinus ST + ONSET

4:19P 76 + Junctional

4:39P 6%

83 -+

Act. Vent. +

ST t

4:49P

4:54P

5:06P

52 b

43

32 -

Junctional

4:44P 53 Junctional ST) ONSET

Asystole

TERMINAL ISCHEMIC EPISODE

FIGURE 3. Case 3. Example of a patient with epkdes of ST-segment elevation preceding bradycardii/asystete. In this patient the ST segment was isoekctk and the hythm was sinus at 9:13 A.M. when ths amlnhtory ekbcardiographie receder was applied. At 3ti2 P.M. the patient had an episode of sinus tachycardii (S. Tech) to 130 beats/min, but no ST-segment shift eccurred during tachycardia. Abwt 1 hou and 15 minutes later, at a heart rate (HR) of 100 beats/min, 2.0 mm of ST-segment et(Act. evatii was recoded in Vs (fop tracing) to mark enset of terminal isdwmii episode. An episods of accelerated ventridar Vent.) tachycardia at 93 beats/min was noted that terminated at 439 P.M. with a junctienal rhythm at 68 beats/min. ST-segmerit elevation was again de&ted at 4:44 P.M. at a rate of 53 beatshnin and reached 2.0 mm at 4:4S P.M. The ST-segment elevation progreesivety increased and was assobted with ventriah pmnatum contractlens (VPCs) several times over the next 2 to 3 minutes as shown in the example at 4:47 P.M. The terminal episode, however, was pmgredve bradycardii leading to asystote.

BRIEF REPORTS

787

of ischemia-related cardiac sudden death and provide insight into its mechanism. 1. Hausmann D, Nikutta P, Trappe HJ, Daniel WG, Wenzlaff P, Lichtlen PR. Incidenceof ventricular arrhythmias during transient myocardial ischemiainpatients with stable coronary artery disease.J Am CONCardiol 1990;16:49-54. 2. Stern S, Banai S, Keren A, Tzivoni D. Ventricular ectopic activity during myocardial ischemic episodesin ambulatory patients. Am / Cardiol 1990; t&412-416. 3. Leclercq JF, Maisonblanche F, CanchemezB, Coumel P. Respectiverole of

sympathetic tone and of cardiac pausesin the genesisof 62 casesof ventricular

fibrillation recordedduring Holter monitoring. Eur Heart J 1988;9:1276-1283. 4. Bayesde Luna A, Coumel P, Leclercq JF. Ambulatory suddencardiac death: mechanismsof productionof fatal arrhythmia on the basisof data from 157cases. Am Hearl J 1989;117:151-159. 5. Panidis JP, Morganroth J. Sudden death in hospitalized patients: cardiac rhythm disturbancesdetectedby ambulatory electrocardiographicmonitoring. J Am Coil Cardiol 1983;2:798-805. 6. Pratt CM, Francis MJ, Luck JC, Wyndham CR, Miller RR, QuinonesMA. Analysis of ambulatory electrocardiogramsin 15 patients during spontaneous ventricular fibrillation with special reference to precedingarrhythmic events.J Am CON Cardiol 1983;2:789-797. 7. OlshausenKV, Witt T, PopT, TreeseN, BethgeKP, Meyer J. Suddencardiac death while wearing a Holter monitor. Am J Cardiol 1991;67:381-386.

Prevalence of Non-Q-Wave Acute Myocardial Infarction with Total Angiographic Occlusion of the Left Circumflex Coronary Artery Within Eight Weeks of Infarction Joel S. Landzberg, MD, and W. Barton Campbell, MD he genesisof Q wavesin acute myocardial infarction (AMI) has been associatedwith complete occlusion of the infarct-related coronary artery by coronary arteriography and autopsy studies.l In contrast, subtotal coronary stenosisis describedin association with non-Q-wave AMI. Mapping studiesof depolarization sequencesin the isolated human heart show late activation of the lateral and posterobasalwalls (170 ms after the earliest ventricular sites of excitation).3 Transmural AM1 involving these regions may result in no Q-wave genesisowing to this late activation sequence. Earlier studies that relate Q wavesto transmural lateral AM1 involved necropsy data. These studies are more likely biasedtoward large infarctions than clinical studies in living patients. This report evaluatesthe incidence of Q-wave AM1 in patients with acute complete occlusion of the left circumflex coronary artery. All cardiac catheterizations performed over a I year period at St. Thomas Hospital, a tertiary care, university-affiliated referral center, were reviewed. Cardiac catheterization was routinely performed in all patients after AMI. The criteria for inclusion were: (1) an AMI defined by typical symptoms and creatinine-phosphokinase levels >3.50 n/; (2) no history of percutaneous transluminal coronary angioplasty, thrombolytic therapy or previous AMI; and (3) coronary arteriography within 8 weeks of AMI showing complete occlusion of the left circumflex coronary artery or its obtuse marginal branch, without >90%diameter stenosis of other arteries. All 12-lead electrocardiograms obtained throughout the patients’ admissions were read blindly by 2

T

From the Cardiovascular Division of the Department of Medicine, Vanderbilt University, and St. Thomas Hospital, P.O. Box 380, Nashville, Tennessee 37202. Manuscript received January 23, 1991; revised manuscript received and accepted May 23,199l.

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THE AMERICAN JOURNAL OF CARDIOLOGY VOLUME 68

independent reviewers. Abnormal Q waves were defined as those of 230 ms duration. Q-wave AMI was defined by the presence of pathologic Q waves in 22 contiguous electrocardiographic leads. A patient was considered to have had a Q-wave AMI if either reviewer read any electrocardiogram as a Q-wave AMI. Total coronary occlusion was defined as the total absence of anterograde flow of contrast material in the involved coronary artery. All catheterization films were interpreted by a blinded reviewer. The distribution of the occluded portion of the circumflex artery was classified as anterolateral, midlateral or inferolateral (Figure 1). Of 4,481 coronary angiograms reviewed, 51 patients (38 men and 13 women, mean age f standard deviation 58 f 9 years) met inclusion criteria. Mean time to catheterization after infarction was 2 f 2 weeks.* *Time to catheterization: 12 patients