ients with hy~~rtro~hi~
Subsequent
FrOlll
thC
studies (8-10)
Dcpartmcnl
car-
from Western countries showed
Of CirdiOlOgicid
Sciences.
St.
George’s
HOSpilill
Medical School. London, England. *Present address: Dcpartamento de Cardiopulmonar. Hospital Univewtario. San Carlos. Madrid. Spaia. Manuscript received August 24. 1989: revised manuscript received November 21, 1989. accepted December 5. 1989’). bb for renri&: William J. McKenna. MD. Department of Cardiological Sciences. St. George’s Hospital Medical School. Cranmcr Terrace. London SW17 ORE, England. 01990 by the American
College of Cardiology
966
JACC Vol. 15. No. 5 April 1990:%5-71
ALFONSO ET AL. T WAVE INVERslON IN HYPERTROPHKCARDlOMYOPATHY
echocardiographic demonstration of unexplained left ventricular hypertrophy (3). Eleven of the 27 patients with giant negative T waves were identified from 73 consecutive patients with hypertrophic cardiomyopathy seen at the Hammersmith Hospital during 1984 (incidence 15%). in whom there were technically adequate echocardiographic recordings for assessment of right ventricular hypertrophy and the distribution of left ventricular hypertrophy. Six of the 73 had repolarization abnormalities secondary to left bundle branch block (n = 2) or ;he Wolff-I’arkinson-White syndrome (n = 4) and were excluded. The remai roup. To increase the nu T waves for analysis, an a hit C~rd~omyoQatby and who were available for reevalunt ovsrall patient cohort. Clink-n1 fenrrm,e ussrssed were: a history of hyQc~ro~hic cardi At the time of the study, chest Qt\i& dysQ~c~ rtnd synco rcnergic blocker, 24 32 patients (38%) were on ne, 6 (7%) on verapamil and 8 (9%) on similar proportion of patients with and ve T waves was receiving these medications. phy. The degree of left ventricular hyluated from a standard 12 lead surface the point score system of 6 ventricular ~y~~~phy wave to the S wave (R/S ratio) in lead V, was >l or if the sum of the R wave in lead I plus the S wave in leads V5 or V6 (RV, + SVs/Vn) WNS I .4 vrtV (I 1~. Q waves were considered ~bflo~~l if they
tip of the mitral valve and at levels). Apical wall thickness and four chamber ssible to the log hs of the left ~t~~~l~r levity and to h the short-axis views ele level were easi
reviewed the video tape in real ti when di~ere~~es ~3 mm existed
and at the onset of the R wave on the IXX, respectively. Systolic ~nte~~r motion of the I valve was graded as complete if there was systolic apposition of the mitral valve and septum, and incomplete if there was no ap Cavity obliteration was assessed from the apical views. In addition, six right ventricular views were employed to assess right ventricular hypertrophy, as previously described (13). T!w r~prodt~ei~ility of measwements of lefi ventricular wnN t~j~~/te~~ at the mitral valve and papillary muscle level ht ventricular wall thickness in our labor has been ~~blisbed (3.5). The re~rodw~ib~~ity of meas ents of left ve~tri~Mlar wall thickness at the apical I was assessed by reanalyzing apical measurements from the al short-axis and apical views of phic recordings of I I patie vious measurements.
(Fig. 2). Left ventrkuhr wall ww me;ilsuredfrom the short-axis views at quad-
a lower intercostal space
Murphy. High temporal resolution left ventricular studies were obtained using red cells labeled with nuclide
967
g al i‘sst or on provoc
variables,
tivity curve was venerated
with a pooled variance ~imate for arate variance estil:wPe fo e chi-square test was u3qg
a? a frame rate of IO to 25
ym The ~e~roduclbi~~ty of the nts was best in the anterior and poster (Table I). The stu Cllnisa patients with by~~rtrophic cardio en), 7 (8%) of whom had a without knowledge ofthe ings. A left ventrisular
Segmcnl *
AAW (9)
LAW (IQ)
PAW r I I b
23.2
23.2
21.0
2 I .(I
Il.5
;!+.H
Mean difference
1.1
1.2
2.2
I.1
0.3
0.0
SD of difference
2.3
4.5
2.9
5.2
3.5
17.1
13.41
Mean (mm)
Coefficient
of varialion
(%)
6.9
13.6
Y.7
_m
MAW
*Segment numbers as in Figure 2. AAW = anterior apical wall: AZCW = apical IWO chamber: AC11 SD/mean x 100; LAW = lateraiapical wall: MAW = medial apical wall; PAW = posterior apical wall.
(12)
= @xl
_-___l__ls
four chamber; c~~i~ie~l
3.N IS.9
of varialion =
968
ALFONSO ET AL. T WAVE INVERSiON
JACC Vol. 1.5.No. 5 :%x-7! April I
IN HYPERTROPHIC CARIXOMYOPATHY
and of hypertrophic cardiomyopathy plus sudden death in 8 (10%).New York Heart Association grade 11 or I11 dyspnea was present in 42 patients (51%). and 24 (29%) were cornplerely asymptomatic. Forty-five patients (54%) reported chest pain, which was exertional in 31 (37%). With the exception of age at diagnosis (patients with giant negative T waves were older; 43 k IS versus 32 9 14 years, p < 0.005). all other clinical features were similar in the two groups. phy. The 27 patients with giant negative re severe ECG signs of left ventricular + RVs 57 & 20 versus 37 zt~ 18 mm, and Estes score (7.4 & 2 versus 5.7 I 2, uced incidence of pathologic Q = 0.01). They also had wide complexes, I more vertical frontal plane axis, a counter&&wise rotation in the horizontal plane and a lower heart rate. The mcrximul ilepth c~gianr negirtive T bkncs was IO to 24 n I6 &I 4) and was located in lead Vz in I patient, V, ients, V, in I6 patients and V6 in 6 patients. The tivc T waves had more e criteria: four leads in o leads in eight and one lead in five. Twenty-one of the 27 patients had serial 12, median 5) recorded over a period of ht patients had a decrease in the amplitude of T wave inversion of I to 7 mm (mean 4) during u mean of I6 years, with loss of giant negative T waves in three patients, In nine patients the m nitude of the T wave inv~rsil~~ increased by 2 to 22 mm (mean 10) during a mean of 8.6 years, with a new development ofgiant negative T waves in
Table 2. Echocardiographic easurements in 83 Patients NO
Giirnt T
Giant
T TOId
Waves
Waves
tn = 27)
tn = 561
(tl = 83)
p Value
I (UAS)
19.8 I 6
20.5 I 5
20.2 9 5
NS
2 (UFW)
15.6 9 4
16.3 f 4
16.1 c 4
NS
3 (UPW)
14.0 * 5
13.1 ?z 3
13.4 ” 4
NS
4 (UPS)
15.7 ” 4
NS
23.7 9 s
16.3 c 4 20.8 2 5
16.1 ” 4
5 (LAS)
21.7 z 5
Subsequent
FrOlll
thC
studies (8-10)
Dcpartmcnl
car-
from Western countries showed
Of CirdiOlOgicid
Sciences.
St.
George’s
HOSpilill
Medical School. London, England. *Present address: Dcpartamento de Cardiopulmonar. Hospital Univewtario. San Carlos. Madrid. Spaia. Manuscript received August 24. 1989: revised manuscript received November 21, 1989. accepted December 5. 1989’). bb for renri&: William J. McKenna. MD. Department of Cardiological Sciences. St. George’s Hospital Medical School. Cranmcr Terrace. London SW17 ORE, England. 01990 by the American
College of Cardiology
966
JACC Vol. 15. No. 5 April 1990:%5-71
ALFONSO ET AL. T WAVE INVERslON IN HYPERTROPHKCARDlOMYOPATHY
echocardiographic demonstration of unexplained left ventricular hypertrophy (3). Eleven of the 27 patients with giant negative T waves were identified from 73 consecutive patients with hypertrophic cardiomyopathy seen at the Hammersmith Hospital during 1984 (incidence 15%). in whom there were technically adequate echocardiographic recordings for assessment of right ventricular hypertrophy and the distribution of left ventricular hypertrophy. Six of the 73 had repolarization abnormalities secondary to left bundle branch block (n = 2) or ;he Wolff-I’arkinson-White syndrome (n = 4) and were excluded. The remai roup. To increase the nu T waves for analysis, an a hit C~rd~omyoQatby and who were available for reevalunt ovsrall patient cohort. Clink-n1 fenrrm,e ussrssed were: a history of hyQc~ro~hic cardi At the time of the study, chest Qt\i& dysQ~c~ rtnd synco rcnergic blocker, 24 32 patients (38%) were on ne, 6 (7%) on verapamil and 8 (9%) on similar proportion of patients with and ve T waves was receiving these medications. phy. The degree of left ventricular hyluated from a standard 12 lead surface the point score system of 6 ventricular ~y~~~phy wave to the S wave (R/S ratio) in lead V, was >l or if the sum of the R wave in lead I plus the S wave in leads V5 or V6 (RV, + SVs/Vn) WNS I .4 vrtV (I 1~. Q waves were considered ~bflo~~l if they
tip of the mitral valve and at levels). Apical wall thickness and four chamber ssible to the log hs of the left ~t~~~l~r levity and to h the short-axis views ele level were easi
reviewed the video tape in real ti when di~ere~~es ~3 mm existed
and at the onset of the R wave on the IXX, respectively. Systolic ~nte~~r motion of the I valve was graded as complete if there was systolic apposition of the mitral valve and septum, and incomplete if there was no ap Cavity obliteration was assessed from the apical views. In addition, six right ventricular views were employed to assess right ventricular hypertrophy, as previously described (13). T!w r~prodt~ei~ility of measwements of lefi ventricular wnN t~j~~/te~~ at the mitral valve and papillary muscle level ht ventricular wall thickness in our labor has been ~~blisbed (3.5). The re~rodw~ib~~ity of meas ents of left ve~tri~Mlar wall thickness at the apical I was assessed by reanalyzing apical measurements from the al short-axis and apical views of phic recordings of I I patie vious measurements.
(Fig. 2). Left ventrkuhr wall ww me;ilsuredfrom the short-axis views at quad-
a lower intercostal space
Murphy. High temporal resolution left ventricular studies were obtained using red cells labeled with nuclide
967
g al i‘sst or on provoc
variables,
tivity curve was venerated
with a pooled variance ~imate for arate variance estil:wPe fo e chi-square test was u3qg
a? a frame rate of IO to 25
ym The ~e~roduclbi~~ty of the nts was best in the anterior and poster (Table I). The stu Cllnisa patients with by~~rtrophic cardio en), 7 (8%) of whom had a without knowledge ofthe ings. A left ventrisular
Segmcnl *
AAW (9)
LAW (IQ)
PAW r I I b
23.2
23.2
21.0
2 I .(I
Il.5
;!+.H
Mean difference
1.1
1.2
2.2
I.1
0.3
0.0
SD of difference
2.3
4.5
2.9
5.2
3.5
17.1
13.41
Mean (mm)
Coefficient
of varialion
(%)
6.9
13.6
Y.7
_m
MAW
*Segment numbers as in Figure 2. AAW = anterior apical wall: AZCW = apical IWO chamber: AC11 SD/mean x 100; LAW = lateraiapical wall: MAW = medial apical wall; PAW = posterior apical wall.
(12)
= @xl
_-___l__ls
four chamber; c~~i~ie~l
3.N IS.9
of varialion =
968
ALFONSO ET AL. T WAVE INVERSiON
JACC Vol. 1.5.No. 5 :%x-7! April I
IN HYPERTROPHIC CARIXOMYOPATHY
and of hypertrophic cardiomyopathy plus sudden death in 8 (10%).New York Heart Association grade 11 or I11 dyspnea was present in 42 patients (51%). and 24 (29%) were cornplerely asymptomatic. Forty-five patients (54%) reported chest pain, which was exertional in 31 (37%). With the exception of age at diagnosis (patients with giant negative T waves were older; 43 k IS versus 32 9 14 years, p < 0.005). all other clinical features were similar in the two groups. phy. The 27 patients with giant negative re severe ECG signs of left ventricular + RVs 57 & 20 versus 37 zt~ 18 mm, and Estes score (7.4 & 2 versus 5.7 I 2, uced incidence of pathologic Q = 0.01). They also had wide complexes, I more vertical frontal plane axis, a counter&&wise rotation in the horizontal plane and a lower heart rate. The mcrximul ilepth c~gianr negirtive T bkncs was IO to 24 n I6 &I 4) and was located in lead Vz in I patient, V, ients, V, in I6 patients and V6 in 6 patients. The tivc T waves had more e criteria: four leads in o leads in eight and one lead in five. Twenty-one of the 27 patients had serial 12, median 5) recorded over a period of ht patients had a decrease in the amplitude of T wave inversion of I to 7 mm (mean 4) during u mean of I6 years, with loss of giant negative T waves in three patients, In nine patients the m nitude of the T wave inv~rsil~~ increased by 2 to 22 mm (mean 10) during a mean of 8.6 years, with a new development ofgiant negative T waves in
Table 2. Echocardiographic easurements in 83 Patients NO
Giirnt T
Giant
T TOId
Waves
Waves
tn = 27)
tn = 561
(tl = 83)
p Value
I (UAS)
19.8 I 6
20.5 I 5
20.2 9 5
NS
2 (UFW)
15.6 9 4
16.3 f 4
16.1 c 4
NS
3 (UPW)
14.0 * 5
13.1 ?z 3
13.4 ” 4
NS
4 (UPS)
15.7 ” 4
NS
23.7 9 s
16.3 c 4 20.8 2 5
16.1 ” 4
5 (LAS)
21.7 z 5
