electrocardiographic findings patients with obstructive...

VOL 58, No 3, SEPTEMBER 1978

left ventricular outflow obstruction in patients with obstructiveasymmetric septal hypertrophy (idiopathic hypertrophic sub-aortic stenosis). Am J Cardiol 35: 337, 1975

45. Gilbert BW, Adelman AG, Buda AJ, MacKenzie GW, CorrigalDM, Wigle ED: Echocardiographic classification of hyper-trophic cardiomyopathy. (abstr) Am J Cardiol 41: 371, 1978

46. Wigle ED, Felderhof CH, Silver MD, Adelman AG: Hyper-trophic obstructive cardiomyopathy (muscular or hypertrophicsubaortic stenosis). In Myocardial Diseases, edited by FowlerNO. New York, Grune and Stratton, 1973, p 297

47. Wigle ED, Trimble AS, Adelman AG, Bigelow WG: Surgery inmuscular subaortic stenosis. Progr Cardiovasc Dis 11: 83, 1968

48. Gilbert BW, Adelman AG, MacKenzie GW, Buda AJ, WigleED: Effect of treatment on echocardiographic findings inmuscular subaortic stenosis. (abstr) Proceedings of the 30th An-nual Meeting of the Canadian Cardiovascular Society, Toron-to. Oct 19-22, 1977, p 130

49. Shah PM, Gramiak R, Adelman AG, Wigle ED: Echo-cardiographic assessment of the effects of surgery andpropranolol on the dynamics of outflow obstruction in hyper-trophic subaortic stenosis. Circulation 45: 516, 1972

50. Wigle ED, Chrysohou A, Bigelow WG: Results of ven-

triculomyotomy in muscular subaortic stenosis. Am J CardiolII: 572, 1963

51. Sutton MG, Tajik AJ, Gibson DG, Brown DJ, Steward JB,Giuliani ER: Echocardiographic assessment of left ventricularfilling and septal and posterior wall dynamics in idiopathichypertrophic subaortic stenosis. Circulation 57: 512, 1978

52. Oakley CM: Hypertrophic obstructive cardiomyopathy -patterns of progression. Hypertrophic Obstructive Car-diomyopathy, CIBA Foundation Study Group No 37, edited byWolstenholme GEW, O'Connor M. London, Churchill, 1971,p 9

53. Criley MJ, Lennon PA, Abbasi AS, Blaufuss AH: Hyper-trophic cardiomyopathy. In Clinical CardiovascularPhysiology, edited by Levine HJ. New York, Grune and Strat-ton, 1976, p 771

54. Liew CC, Sole MJ: Nuclear proteins in the heart of the car-diomyopathic Syrian hamster: fractionation of phenol-solublenonhistone proteins by 2 dimensional polyacrylamide gel elec-trophoresis. Circ Res 42: 628, 1978

55. l iew CC, Sole MJ, Silver MD, Wigle ED: Alterations in non-histone nuclear proteins of human hearts with muscular sub-aortic stenosis. In press

Electrocardiographic Findings in Patientswith Obstructive and Nonobstructive

Hypertrophic CardiomyopathyDANIEL D. SAVAGE, M.D., PH.D., STUART F. SEIDES, M.D., CHESTER E. CLARK, M.D.,WALTER L. HENRY, M.D., BARRY J. MARON, M.D., FELIPE C. ROBINSON, M.D., AND

STEPHEN E. EPSTEIN, M.D.

SI'MMARY One hundred and thirty-four patients with hypertrophic cardiomyopathy were evaluated by standard 12-leadelectrocardiography. Normal electrocardiograms were extremely uncommon, occurring in less than 7% of each subgroup ofpatients (i.e., those with or without either symptoms or obstruction to left ventricular outflow), with the exception of thosewho were both asymptomatic and had no left ventricular outflow obstruction. Even in this subgroup, however, normal elec-trocardiograms occurred in only 27% of patients. Repolarization abnormalities and left ventricular hypertrophy were themost common abnormalities, occurring in 81% and 62%, respectively, of the total population. A broad spectrum of otherelectrocardiographic abnormalities was found, but none was unique to hypertrophic cardiomyopathy.

Patients with vs those without electrocardiographic left ventricular hypertrophy or left atrial abnormality had significantly(P < 0.005) greater mean ventricular septal thickness (22 ± 0.6 vs 19 ± 0.6 mm) and left atrial dimension (48 ± I vs 40 ± Imm) measured by echocardiography, and significantly (P < 0.01) higher mean pulmonary capillary wedge pressure (16 ± Iis 10 ± I mm Hg) and left ventricular end-diastolic pressure (20 ± I vs 15 ± I mm Hg). The high prevalence and diversenature of electrocardiographic abnormalities suggest that any patient with an unusual and unexplained electrocardiogramshould be suspected of having hypertrophic cardiomyopathy even if the physical examination is normal, as is often the case inpatients without obstruction.

IN THE DECADE PRIOR TO 1968 there werenumerous reports of electrocardiographic findings inpatients with hypertrophic cardiomyopathy.1-15 Mostof the patients were reported to have obstruction ofleft ventricular outflow, since the resulting murmurheard on physical examination and the gradient

From the Cardiology Branch, National Heart, Lung, and BloodInstitute, National Institutes of Health, Bethesda, Maryland.Address for reprints: Daniel D. Savage, M.D., Cardiology

Branch, National Heart, Lung and Blood Institute, NIH, Building10, Room 7B-15, Bethesda, Maryland 20014.Received March 13, 1978; revision accepted May 16, 1978.

recorded at catheterization were the major criteriaused to establish the diagnosis at that time. In theearly 1970s Henry et al.16 and Abbasi et al.'7 utilizedasymmetric septal hypertrophy, detected by echocar-diography, as a disease marker. This technique led tothe recognition of a broad pathophysiologic spectrumof hypertrophic cardiomyopathy, including patientswith or without either symptoms or left ventricularoutflow obstruction. Little data have subsequentlybeen published regarding the electrocardiographicfindings in this group of patients.

This investigation examined the prevalence anddiagnostic usefulness of electrocardiographic abnor-

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ECG FINDINGS IN HYPERTROPHIC CARDIOMYOPATHY/Savage et al.

malities in 134 patients with hypertrophic car-diomyopathy, and related the electrocardiographicabnormalities to symptomatic status as well asechocardiographic and hemodynamic findings.

MethodsPatient Population

One hundred thirty-four patients with hypertrophiccardiomyopathy were studied. Diagnosis was es-tablished by the echocardiographic demonstration of aventricular septal-to-posterobasal left ventricular free-wall thickness ratio > 1.3.16

Ninety-six of the patients were male and 38 werefemale. We are following several hundred patientswith hypertrophic cardiomyopathy in our clinic, anddecided for this investigation to select and study arepresentative sample of the patients. We examinedour records and entered into the study the first 85patients we found who had hypertrophic car-diomyopathy unequivocably identified by echocar-diography. Another 49 patients were selectedprimarily to provide a more representative cross sec-tion of the clinical and hemodynamic subgroups ofpatients with this disease than was provided by thefirst 85 patients. Of these 49 patients: 1) 16 wereselected because they had large left atrial dimensionon echocardiogram, 2) 19 were studied primarilybecause of a history of syncope, 3) seven came fromfamilies in which premature death (i.e., < 50 years ofage) had occurred in two or more first degree relativeswho had hypertrophic cardiomyopathy'8, and 4) sevenpatients had a history of paroxysmal atrial fibrillation.

Fifty of the 134 patients underwent cardiaccatheterization within one week of the electrocar-diogram. In these 50 patients the resulting hemo-dynamic data were used as the primary method fordetermining the presence of obstruction. Patients wereconsidered to have obstruction if the gradient mea-sured under basal conditions or with provocation (i.e.,isoproterenol infusion or Valsalva maneuver) was 30mm Hg or more. Those with smaller gradients or nogradient were considered not to have obstruction.

Echocardiography was used to estimate themagnitude of obstruction in 78 of the 84 patientswithout recent catheterization. This estimation wasbased on the degree of approximation of the anteriormitral valve leaflet to the ventricular septum.'9 20Patients were classified as having obstruction if thegradient estimated by echocardiography was 30 mmHg or more under basal conditions or with provoca-tion (Valsalva maneuver or amyl nitrite inhalation).Finally, six patients who had not undergone recentcatheterization and in whom mitral valve echocar-diograms were not of sufficiently good quality to es-timate the magnitude of obstruction, were classified aseither obstructed or nonobstructed on the basis of thepresence or absence of a systolic ejection murmur ofgrade III/VI or louder under basal conditions and/orwith provocation (Valsalva maneuver or amyl nitriteinhalation).

Patients were considered symptomatic if they had

one or more of the following symptoms: chest pain,dyspnea on exertion, fatigue, orthopnea, paroxysmalnocturnal dyspnea, lightheadedness, or syncope. Ofthe 55 symptomatic patients with obstruction, 36(65%) were in functional class II (New York HeartAssociation classification), 18 (33%) were in class IIIand one (2%) was in class IV. Of the 40 symptomaticpatients without obstruction, 34 (85%) were in func-tional class II, and six (15%) were in class III. Meanage of the total group of patients was 38 ± 2 years(SEM) (range 9-65 years). Ages of patients in all sub-groups were similar, with the exception of obstructedpatients without symptoms who were significantlyyounger than obstructed patients with symptoms(26 ± 3 years vs 41 ± 2 years, P < 0.001). None ofthe patients had undergone cardiac operation beforethe electrocardiogram.

Electrocardiographic Procedure and Criteria

Patients taking cardioactive medications had thesedrugs discontinued 36-48 hours before the electrocar-diogram, with the exception of four patients who hadchronic atrial fibrillation and continued to take digox-in. Standard 1 2-lead electrocardiograms were per-formed with the patients in the supine position duringquiet respiration. Either a Sanborn heat sensitivepaper or a Marquette ink writer electrocardiographicmachine was used. The electrocardiogram wasrecorded from each patient within one week of themost recent echocardiographic study.

Repolarization abnormalities2' were diagnosed ifany of the following was present: 1) ST segment dis-placement > 1 mV from the isoelectric line in the limbleads, 2) ST segment displacement upward with up-ward convexity in the precordial leads, 3) ST segmentdisplacement downward in the precordial leads, or 4)widening of the angle between the mean spatial QRSvector and the mean spatial T!vector (i.e., > 450 in thefrontal plane, > 60° in the anteroposterior plane inthose over 30 years of age, or > 900 in those under 30years of age). These criteria were supplemented bythose outlined by Friedman21 for abnormal T waves inadults and children.

Left ventricular hypertrophy was diagnosed usingthe point-score system of Romhilt and Estes.22 Four ormore points were considered evidence of left ven-tricular hypertrophy. Point scores were not calculatedfor children less than 16 years of age (N = 8), patientswith QRS duration > 0. 12 seconds (N = 19), patientswith atrial fibrillation (N = 7), or patients with in-determinate axis (N = 2).

Left atrial abnormality23 was diagnosed if theproduct of the depth and duration of the negative por-tion of the P wave in lead V, was greater than -0.03mV-sec.Abnormal Q waves2' were defined by the presence

of any of the following: 1) a Q wave in leads I, II, oraVF > 0.04 seconds wide, > 2 mV deep and > 25% ofthe following R wave, 2) a Q wave in lead aVL > 0.04seconds wide, > 2 mV deep, and > 50% ofthe succeeding R wave, 3) a Q wave in lead III> 0.04 seconds wide and > 6 mV deep or associated

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TABLE 1. Frequency of Common Electrocardiographic Abnormalities inmyopathy

Patients with Hypertrophic Cardio-

Obstructed NonobstructedECG Finding Symptomatic Asymptomatic Symptomatic Asymptomatic

Abnormal ECG 54/55 (98) 13/13 (100) 37/40 (93) 19/26 (73)*Repolarization abnormalities 48/55 (87) 11/13 (85) 34/40 (85) 15/26 (58)t

Left ventricular hypertrophy 31/38 (82) 8/10 (80) 19/33 (58) 7/21 (33)4Left atrial abnormality 37/50 (74) 5/12 (42) 14/38 (37)* 5/26 (19)*

Left axis deviation (0 to -9O0) 25/53 (47) 8/13 (62) 12/40 (30) 5/26 (19)4Abnormal Q waves 23/55 (42) 5/13 (38) 8/40 (20) 8/26 (31)

Right atrial enlargement 9/50 (18) 3/13 (23) 3/38 (8) 1/26 (4)Right atrial enlargement and

left ventricular hypertrophy 7/38 (18) 2/10 (20) 3/33 (9) 0/21 (0)

P-R interval >0.20 sec 5/50 (10) 2/13 (15) 4/38 (11) 1/26 (4)Numbers in parentheses indicate percentages.*Comparison wvith obstructed symptomatic patients (P <0.05).tComparison with obstructed and nonobstructed symptomatic patients (P <0.05).tComparison with obstructed symptomatic and asymptomatic patients (P <0.05).

with Q waves in leads II and aVF, 4) a Q wave in theleft precordial leads (V4-Ve) > 0.04 seconds wide,> 2 mV deep and > 15% of the succeeding Rwave, 5) qR, QR or Qr patterns in the right precordialleads (V1-V3), or 6) a QS pattern in one or more of thefollowing leads: I, II, V3-Vg.

Right atrial enlargement24 was diagnosed if therewere peaked P waves in leads II and III or V, . 2.5mV in amplitude with a mean P axis of more than+ 600.

Left anterior hemiblock25 was defined by: 1) left axisdeviation (mean QRS frontal plane axis of -30° to-90°), 2) a small initial Q in lead I and R in lead III,and 3) a QRS duration < 0.12 seconds if this was anisolated conduction defect.

Left posterior hemiblock25 was diagnosed if therewas: 1) right axis deviation (> + 120°), 2) a small ini-tial R wave in lead I and Q wave in lead III, 3) QRSduration < 0.12 seconds if this was an isolated con-duction defect, and 4) no additional evidence for rightventricular hypertrophy.

Left bundle branch block21 was defined by: 1) aQRS duration > 0.12 seconds in the extremity leads,

2) delayed onset of the intrinsicoid deflection in V5, 3)broad slurred R waves in the left precordial leadswithout a Q wave and 4) ST segment displacementdownward and T wave inversion in the left precordialleads.Right bundle branch block2' was defined by: a QRS

duration > 0.12 seconds and terminal QRS forcesdirected to the right and anteriorly with normal earlyQRS forces.

Intraventricular conduction defect2' was diagnosedif the QRS duration was > 0.12 seconds but did notmeet the additional criteria for either left or right bun-dle branch block.

Preexcitation (Wolff-Parkinson-White pattern)24was defined by: 1) a short P-Q interval (< 0.10 sec), 2)a wide QRS (0.1 1-0. 14 sec) and 3) slurred onset of theQRS (A wave).

Right ventricular hypertrophy2e was defined by: 1)QRS duration of < 0.12 seconds, 2) rightward meanQRS axis in the frontal plane (between +1100 and+ 1800) and an R or R' in lead V, of 5 mV or greaterin amplitude, with an R/S ratio in lead V1 of 1 orgreater.

TABLE 2. Frequency of Less Common Electrocardiographic Abnormalities in Patients with Hypertrophic Cardio-myopathy

ECG Finding Sympt

Atrial fibrillation 5/5zLeft anterior hemiblock 6/5tLeft posterior hemiblock 1/5tLeft bundle branch block 3/5eRight bundle branch block 1/51Intraventricular conduction defect 5/5WPre-excitation (WPW) 0/5'Atrioventricular dissociation 0/5'Right ventricular hypertrophy 0/5ZNumbers in parentheses indicate percentages.Abbreviation: WPW = Wolff-Parkinson-White pattern.

Obstructedtomatic Asymptomatic

5 (9) 0/13 (0)3 (11) 1/13 (8)3 (2) 1/13 (8)5 (5) 0/13 (0)5 (2) 0/13 (0)5 (9) 1/13 (8)5 (0) 0/13 (0)5 (0) 2/13 (15)5 (0) 0/13 (0)

NonobstructedSymptomatic

2/38 (5)4/40 (10)1/40 (3)1/40 (3)2/40 (5)1/40 (3)1/40 (3)0/40 (0)1/40 (3)

Asymptomatic

0/26 (0)1/26 (4)0/26 (0)0/26 (0)1/26 (4)1/26 (4)2/26 (8)0/26 (0)0/26 (0)

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Echocardiographic Measurements

Echocardiographic studies were performed using anAerotech transducer (2.25 MHz, 1.25 cm diameter,unfocused) with a modified Ekoline 20A or a Hoffrel201 ultrasound unit using methods previouslydescribed.16 The ultrasound signal was connected via acustom-built video amplifier to a Honeywell 1856Visicorder and was recorded continuously on lightsensitive paper. Thickness of the ventricular septumwas measured below the tips of the mitral valveleaflets before atrial systole but after rapid ventricularfilling. Posterobasal left ventricular free wall thicknesswas measured at the level of the tips of the mitral valveleaflets during the same phase of the cardiac cycle.One hundred twenty-one of the 134 patients hadechocardiograms of sufficiently good quality tomeasure left atrial transverse dimension. This dimen-sion was taken as the maximal distance between theposterior aortic root wall and the posterior left atrialwall and was measured in the damped portion of therecord when the ultrasonic beam passed through theaortic leaflets.26Where appropriate, the t test or the X-square

test was used to assess statistical significance.

ResultsPrevalence of Electrocardiographic Abnormalities

Abnormal electrocardiograms were found in 123 of134 (92%) patients. Repolarization abnormalities andleft ventricular hypertrophy each occurred in morethan 70% of patients and were the two most common

* PATIENTS WITH OBSTRUCTIONo PATIENTS WITHOUT OBSTRUCTION

-900

+1800°

+900

FIGURE 1. Mean electrical axes in thefrontal plane of 132patients with hypertrophic cardiomyopathy. The arrowfromthe closed circle = overall mean for obstructed patients(N = 66), the arrowfrom the open circle = overall mean fornonobstructed patients (N = 66).

electrocardiographic abnormalities in each subgroupof patients (tables 1 and 2). The left ventricular "strainpattern"25 was present as part of the criteria for leftventricular hypertrophy in 59 of the 65 (91%) patientswith left ventricular hypertrophy. Asymptomaticpatients without left ventricular outflow obstruction(when compared to symptomatic patients with outflowobstruction) had significantly lower frequencies of ab-normal electrocardiograms, repolarization abnor-malities, left ventricular hypertrophy, left atrial ab-normality and left axis deviation. The combination ofright atrial enlargement and left ventricular hyper-trophy, described in a previous report5 of electrocar-diographic findings in patients with hypertrophic car-diomyopathy, was included among the more commonfindings in our patients.More leftward QRS frontal plane axes were found

in patients with left ventricular outflow obstructioncompared with those without obstruction (fig. 1). Twopatients had indeterminate QRS axes, including onewith low QRS voltage (< 5 mV) in all limb leads. Theprevalence of electrocardiographic abnormalities, in-cluding left ventricular hypertrophy and abnormal Qwaves, was similar in younger and older patients (fig.2). In addition, the prevalence of electrocardiographicabnormalities in the 49 patients selected because theywere in specific clinical subgroups was s similar to theprevalence of such abnormalities in the other 85patients.

<30 YEARS OF AGEN-41

>30 YEARS OF AGEN=93

ABNORMALEKG

LEFTVENTRICULARHYPERTROPHY

ABNORMALQ WAVES

FIGURE 2. Prevalence of electrocardiographic abnor-malities in younger and older age groups. Frequencies ofab-normalities were not significantly different in the two agegroups.

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TABLE 3. Comparison of ECG Findings with Echocardiographic MeasurementsEchocardiographic measurements - mean Et sEM

Mean age Septal Free wall Left atrialNumber of in years thickness thickness Septal-to-free dimension

ECG Findings patients i SEM (mm) (mm) wall ratio (mm)

Abnormal ECG 123 38 - 1 22 - 0.4* 13 0 .2 1.7 0.03 46 O 0.9t (112)

Normal ECG 11 35 - 4 16 - 0.6* 11 - 0.2 1.5 0.05 34 - 2t (9)

Left ventricular hypertrophyPresent 65 39 + 2 22 - 0.6* 13 - 0.2 1.9 0.1 48 It (59)Not present 37 38 2 19 - 0.6* 12 - 0.3 1.6 0.05 40 It (33)

Left atrial abnormalityPresent 61 39 2 24 0.6* 13 0.2 1.8 - 0.04 49 I t (56)Not present 65 35 2 19 0.5* 12 0.2 1.6 - 0.03 40 0.9t (58)

Repolarization abnormalitiesPresent 108 39 - 1 22 0.5* 13 0.2 1.7 - 0.03 46 0.9t (97)Not present 26 34 - 3 17 0.6* 12 0.3 1.5 - 0.03 40 2t (24)

Numbers in parentheses = number of patients with echocardiograms of sufficiently good quality to measure left atrial dimension.*P <0.005.tP <0.001.

Comparison of Electrocardiographic Findings withEchocardiographic and Hemodynamic Measurements

Patients with abnormal electrocardiograms hadsignificantly greater mean echocardiographic septalthickness and mean left atrial dimension than patientswith normal electrocardiograms (table 3). Similarly,patients with the specific electrocardiographic findingsof left ventricular hypertrophy, left atrial abnormalityor repolarization abnormalities had greater mean sep-tal thickness and left atrial dimension by echocar-diography than patients without these electrocar-diographic findings. In contrast, the presence ofprominent abnormal Q waves, including thosesuggesting prominent septal forces on electrocar-diogram, did not significantly correlate with increasedseptal thickness or septal-to-free wall ratio. Abnormalelectrocardiograms, including abnormal Q waves,were found in 60% (three of five) of the asymptomaticpatients without obstruction who had only slight in-creases in both septal thickness (14-16 mm) andseptal-to-free wall ratio (1.3 to 1.4).

Significantly higher mean pulmonary capillarywedge pressure (or left atrial mean pressure) andhigher mean left ventricular end-diastolic pressurewere found in patients with electrocardiographic leftventricular hypertrophy (table 4). Left atrial abnor-mality on electrocardiogram was also associated withsignificantly higher mean left ventricular end-diastolicpressure.

DiscussionThe prevalence of abnormal electrocardiograms in

patients with hypertrophic cardiomyopathy has beenreported previously as 10%,28 18%,29 and almost100%o.l430 Our study indicates that normal electrocar-diograms are rare in patients with hypertrophic -car-diomyopathy, particularly if they are symptomatic orif they have obstruction to left ventricular outflow.Although patients in our study were not chosen

because of known electrocardiographic abnormalities,it is possible that the observed prevalence of these ab-normalities may have been influenced by selection fac-tors. The prevalence of electrocardiographic abnor-malities in the 49 patients selected because they werein specific clinical subgroups was similar to theprevalence of such abnormalities in the other 85patients. Moreover, even asymptomatic subjectswithout obstruction had a high prevalence of abnor-malities (73%), indicating that selection of patients onthe basis of severe symptoms could not account forour results.A broad spectrum of electrocardiographic abnor-

malities was seen in patients with hypertrophic car-diomyopathy, but no abnormality appeared to beunique to this disease. Furthermore, no electrocar-diographic abnormality that was found frequently oc-curred exclusively in obstructed or nonobstructedpatients. This was consistent with the findings in aprevious study20 of children with obstructed and non-obstructed forms of this disease. In that study theprevalence of abnormal electrocardiograms in asymp-

TABLE 4. ComparisonData

of ECG Findings with Hemodynamic

PCW or LA meanLVEDP in mm Hg pressure in mm Hg

ECG Findings (mean Hsa3M) (mean ± Bsam)Left ventricularhypertrophy

Present 20 i 1 (27)* 16 1 (24)*Not present 15 1 (10)* 10 1 (10)*

Left atrial abnormalityPresent 22 1.5 (26)* 17 1 (29)tNot present 16 1 (19)* 13 1.5 (15)t

Numbers in parentheses = number of patients.*P <0.01.tP = not significant.Abbreviations: LVEDP = left ventricular end-diastolic pressure;

PCW = pulmonary capillary wedge; LA = left atrial.

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tomatic children (average age 10 ± 1 years) withoutleft ventricular outflow obstruction was low (30%),and contrasts with the 73% prevalence found in thesame, but older (average age 38 ± 3 years), sub-group in the present study. This suggests that the fre-quency of abnormal electrocardiograms may increaseas children with hypertrophic cardiomyopathy reachadulthood.The combination of right atrial enlargement and

left ventricular hypertrophy was surprisingly com-mon. Goodwin et al.5 have suggested that identifica-tion of this combination is suggestive of hypertrophiccardiomyopathy, since it is said to be rare in valvularaortic stenosis, which is often included in the differen-tial diagnosis of this disease. Prominent septal forcesin young patients are another helpful diagnostic elec-trocardiographic finding, because they suggest hyper-trophic cardiomyopathy. However, similar to Halpernet al,30 we could not demonstrate a significant rela-tionship between the presence or absence of promi-nent septal forces and the relative thickening of theventricular septum compared with the free wall.

In a recent study3' we reported a high prevalence ofarrhythmias in asymptomatic patients who had onlyslightly increased septal-to-free wall ratios and had noobstruction to left ventricular outflow. The highprevalence of electrocardiographic abnormalities onthe routine electrocardiogram in this subgroup lendsfurther credibility to the concept that such patientshave clinically important disease32 and are not justpart of a normal distribution curve of echocar-diographic findings.33The correlations of electrocardiographic findings

with echocardiographic and hemodynamic measure-ments in our study are generally similar to thosereported by Joye et al,29 who also found that normalelectrocardiograms were associated with less septalthickening and that electrocardiographic left ven-tricular hypertrophy was not associated with higherleft ventricular outflow gradients. However, in con-trast to their study, we did not find that electrocar-diographic left ventricular hypertrophy was accom-panied by increased left ventricular free wallthickness.

This study demonstrates that normal electrocar-diograms are unusual in all subgroups of patients withhypertrophic cardiomyopathy. In addition, significantcorrelations exist between electrocardiographic find-ings and echocardiographic as well as hemodynamicmeasurements. However, the degree of overlap ofelectrocardiographic findings among the subgroups ofpatients limits the usefulness of the electrocardiogramas a predictor of specific echocardiographic or hemo-dynamic abnormalities in the individual patient withthis disease.

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Limitations of Routine Long-TermElectrocardiographic Monitoring

to Assess Ventricular Ectopic FrequencyJOEL MORGANROTH, M.D., ERIC L. MICHELSON, M.D., LEONARD N. HOROWITZ, M.D.,MARK E. JOSEPHSON, M.D., ALAN S. PEARLMAN, M.D., AND W. BRUCE DUNKMAN, M.D.

SI)IMMARY Variations in the frequency of ventricular premature depolarizations (VPDs) were evaluated with three con-

secutive 24-hour long-term electrocardiograph monitor recordings from 15 clinically stable patients with various cardiac dis-orders. Mean hourly VPD frequencies ranged from 37-1,801 per hour. Data were subjected to 4 and 5 factor nested analysesof variance. The extent of spontaneous variation in arrhythmia frequency that occurred in individual patients from day to daywas 23%, between 8-hour periods within days was 29%, and from hour to hour was 48%. In addition, the variability betweenrepeated three-day monitoring periods over time was quantified in five patients and found to be 37%. This analysis deter-mined that to distinguish a reduction in VPD frequency attributable to therapeutic intervention rather than biologic or spon-

taneous variation alone required a greater than 83% reduction in VPD frequency if only two 24-hour monitoring periodswere compared, and greater than 65% reduction if two 72-hour periods were compared. The limitations of routine 24-hourelectrocardiographic monitoring must be considered in diagnostic and therapeutic decision-making.

THE EFFECTIVE MANAGEMENT of ventriculararrhythmias is a difficult therapeutic challenge.Sudden death is usually due to ventricular fibrillation,and ventricular ectopy has been considered as a majorrisk factor.1-7 Identification of ventricular ectopy inthe ambulatory patient is not easy, however, sincearrhythmias often occur sporadically, and patients arenot always aware of their presence.6 810 Theavailability of recorders that can monitor the elec-trocardiogram continuously in ambulatory patientshas greatly enhanced our ability to detect and under-stand the nature of ventricular arrhythmias beyondthat possible with standard resting electrocar-diography (45 seconds) or electrocardiographic

From the Cardiovascular Section, Hospital of the University ofPennsylvania, and the Department of Medicine, University of Penn-sylvania School of Medicine, Philadelphia, Pennsylvania.

Supported by a grant from El. du Pont de Nemours & Companyand grant #NIH 5 MO 1 PROO040.

Dr. Michelson is recipient of a Research Fellowship Award of theSoutheastern Pennsylvania Chapter of the American HeartAssociation.

Address for reprints: Joel Morganroth, M.D., 937 West GatesBuilding, Hospital of the University of Pennsylvania, 3400 SpruceStreet, Philadelphia, Pennsylvania 19104.

Received March 15, 1978; revision accepted May 16, 1978.

rhythm strips (several minutes to 1 hour).8-10 Twenty-four-hour long-term electrocardiographic monitoringhas further documented cardiac arrhythmias as acause of disability and death and has foundwidespread application as a means of quantitatingventricular ectopy and guiding antiarrhythmictherapy.6, 11

The evaluation of antiarrhythmic agents has led toincreased awareness of the limitations of presentmethods of arrhythmia detection.'2 13 Previous studieshave noted the inconstant relation of ventricular ec-topy to patient physical activity, diurnal, neural andpsychological factors, and current monitoring recom-mendations have increased from 8-24 hours to betteraccount for these physiologic variables.5 6, 9, 10, 14-17The use of exercise testing has been considered com-

plementary to 24-hour ambulatory electrocar-diographic monitoring.'8 19 Recently, however, thereproducibility of arrhythmia detection by thistechnique has been questioned by Sheps et al.20 Theydemonstrated that, in two successive exercise testsperformed only 45 minutes apart, there was a markedvariability of arrhythmia frequency, thus limiting theusefulness of paired exercise tests in evaluating an-tiarrhythmic therapy.

CIRCULATION408



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D D Savage, S F Seides, C E Clark, W L Henry, B J Maron, F C Robinson and S E Epsteinhypertrophic cardiomyopathy.

Electrocardiographic findings in patients with obstructive and nonobstructive

Print ISSN: 0009-7322. Online ISSN: 1524-4539 Copyright © 1978 American Heart Association, Inc. All rights reserved.

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