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Handgrip-Induced Negative U-Wave in Electrocardiogram of Hypertensive Subjects

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Handgrip-Induced Negative U-Wave in Electrocardiogram of Hypertensive Subjects Handgrip-Induced Negative U-Wave in Electrocardiogram of Hypertensive Subjects Long Tai Fu, M.D., Nobumitsu TAKAHASHI, M.D., Machiko YAMAMOTO, B.S., Masao KUBOKI, M.D., and Shintaro KOYAMA, M.D. SUMMARY To study clinical significance and possible mechanism of negative U- wave observed in hypertensive patients, we applied handgrip test (HG) to 35 patients with hypertension and 20 age-matched normal subjects. HG was sustained for 3min at 50% of maximum voluntary contraction. ECG recording and measurement of blood pressure were made before, during, and after HG. During HG, systolic blood pressure was 188.7•}3.4mmHg (mean•} SE) and diastolic blood pressure was 114.8•}2.1mmHg in hypertensives, while 145.3•}2.6mmHg and 93.8•}1.1mmHg in normals; the difference between hypertensives and normals was statistically significant (p<0.001). Incidence of HG-induced negative U-wave was 0% in normals, while 68.6% in hypertensives. In hypertensive subjects, HG-induced nega- tive U-wave appeared in 24 of the 28 patients (85.7%) with minimum to moderate left ventricular hypertrophy, while it was not seen in all 7 pa- tients (0%) with marked left ventricular hypertrophy shown by ECG and/or UCG findings (QRS-T angle>130•‹ with left high voltage: left ven- tricular wall thickness>12mm). Further we recorded UCG during HG in 14 subjects. In 4 patients, negative U waves appeared simultaneously with increase in left ventricular dimension during diastole. In the re- maining 10 cases that included both normals and hypertensives, however, neither increase in left ventricular end diastolic dimension nor negative U waves were observed. Thus we conclude that HG-induced negative U waves may be caus- ed by stretch of the ventricular wall resulting from acute left ventricular volume overload. Additional Indexing Words: Orthogonal leads Echocardiography LV wall thickness Acute LV dilatation T is generally said that negative U-wave appears in electrocardiogram in 20-30% of hypertensive subjects.1),2) However, with regard to the clinical From the Cardiovascular Institute, 3-10, 7-chome, Roppongi, Minato-ku, Tokyo, Japan. Address for reprint: Long Tai Fu, M.D., the Cardiovascular Institute, 3-10, 7-chome, Rop- pongi, Minato-ku, Tokyo 106, Japan. Received for publication April 15, 1980. 59 Jpn. Heart J. J 60 FU, TAKAHASHI, YAMAMOTO, KUBOKI, AND KOYAMA anuary, 1981 setting in appearance of negative U-wave, there are some controversial results between statistical studies and clinical experiments. Kemp et al,1) as well as Watanabe,2) emphasized that the group of patients with negative U-wave showed a higher incidence of marked cardiomegaly and more advanced con- gestive heart failure, in addition to higher systolic and diastolic pressures than the group of patients without negative U-wave. Meanwhile, Georgopoulos et al3) observed that lowering of arterial pressure with sodium nitroprusside resulted in conversion of negative to positive U-wave in the majority of hy- pertensive patients, and thus they concluded that negativity of U-wave in hy- pertensives correlated only to arterial blood pressure and was not necessarily related to organic myocardial changes. To test the hypothesis proposed by Georgopoulos et al,3) and also to study relationship between negative U-wave and left ventricular hypertrophy we applied isometric handgrip test to hypertensive subjects with and without left ventricular hypertropy, in addition to normal volunteers. Our observa- tions may contribute to the clinical significance and possible mechanism of negative U-wave. MATERIALS AND METHODS Subjects: The material for this study was composed of 35 patients with hypertension (Group H), and 20 age-matched normal subjects (Group C). Hypertension was de- fi ned as blood pressure measured at resting state equal to or greater than 160/95 mmHg at present or in the past history. Patients of Group H were further divided into 3 subgroups based on electro- and vectorcardiographic findings as follows: 10 patients with neither increased voltage of the QRS complexes nor ST•ET changes (Group H0); 18 patients with increased voltage of the QRS complexes (RV5 or V6+ SV1>3.5mV) alone, or coupled either with depression of the ST segment or with lowered or inverted T wave, but with a QRS-T angle in transverse plane vector- cardiogram<130•‹ (Group H1); 7 patients with increased voltage of the QRS com- plexes with a marked ST depression and T inversion, and with a QRS-T angle in transverse plane vectorcardiogram•†130•‹ (Group H2). Patients with asymmetric septal hypertrophy (ventricular septal/left ventricular posterior wall thickness ra- tio>1.3 in eehocardiogram4)) were excluded from this study. There were no patients with complication of acute myocardial infarction, con- gestive heart failure, or cerebral vascular accident. Ischemic heart disease was com- plicated in 2 patients of Group H2, and none of other hypertensive groups. There was no patient with bundle branch block, ventricular preexcitation, or atrial fibril lation in studied cases. Handgrip exercise test: The maximum voluntary contraction (MVC) for the left hand of each subject was determined in Kg's as described by Lind et al5),6) and others.7),8) Each subject was then asked to sustain a constant effort by keeping the indicator needle on the Vol.22 No.1 HANDGRIP-INDUCED NEGATIVE U 61 dynamometer at 50% of his or her MVC for a period of 3min. A normal venti- latory pattern was observed in each subject throughout the test period. Before, dur- ing, and after handgrip corrected orthogonal leads X, Y, and Z (Frank lead system) were recorded simultaneously at a paperspeed of 50mm/sec and a gain of 20-30 mm/mV. In addition, in most cases unipolar chest leads V1 or V2 and V5 were also recorded. Blood pressure was measured with a mercury sphygmomanometer. Handgrip-induced NegativeU-wave: Handgrip-induced negative U-wave generally appeared in left-sided chest leads and lead X, and it was judged present when preexisted positive or biphasic, or neg- ative U-wave became absolute negative, or more negative in the same leads dur- ing handgrip. The negative U-wave was usually identified as a distinct negative deflection relative to the base line (P-P) between T and P waves. To avoid misac- cepting a negative terminal T-wave as a negative U-wave, we confirmed the timing of at least 2 out of the starting, peak, and end points of the negative U wave to be almost coincident with those of the positive U wave on the simultaneously recorded vertical lead (Y), where the morphology of U-wave was little affected by handgrip. We discarded the cases with tachycardia of 100 beats per minute or more from this study, in which the terminal portion of U-wave often fused with the initial portion of P-wave and the correct observation of change in U-wave morphology was dis- turbed. Echocardiography: M-mode echocardiographic studies were performed in the supine or left Table I. Heart Rate, Blood Pressure Before and During Handgrip, and Incidence of Handgrip-Induced Negative U-Wave in Hypertensive Patients and Age-Matched Control Subjects (mean•}SE) BP=blood pressure; p=probability; *p<0.001, before vs during handgrip; NS=not significant. Jpn. Heart J. J 62 FU, TAKAHASHI, YAMAMOTO, KUBOKI, AND KOYAMA anuary, 1981 Vol.22 No.1 HANDGRIP-INDUCED NEGATIVE U 63 64 FU, TAKAHASHI, YAMAMOTO, KUBOKI, AND KOYAMA Jpn. Heart J. January, 1981 lateral decubitus position using an Aloka ultrasonoscope with a 2.25 megaherz me- dium (7.5cm) internally focused transducer. Permanent recordings were obtained with a Honeywell Recorder. Statistical analysis: Results were expressed as mean•}SE. A paired-samples t-test was used to as- sess changes for each group, and for comparison between groups an independent- samples t-test, or chi square test with Yates' correction was applied. RESULTS Summarized data of Groups C and H, detailed tabulation of data of Groups H0, H1, and H2 and statistical significance of differences in measure- ments are listed in Tables I, II, and III. Heart rate and blood pressure: With the handgrip, all of Groups C, H0, H1, and H2 showed a significant increase in heart rate with no difference between groups. There was a signi- fi cant rise in both systolic and diastolic blood pressures in each group during the third minute of sustained handgrip. Between Group C and Group H there was significant difference in degree of pressure rise induced by handgrip, and the attained pressure levels in Group H were significantly higher than those in Group C. Among subgroups of hypertension mean values of systolic Table III. Statistical Significance of Measurements in Table II Abbreviations: HG=handgrip; HR=heart rate; SBP=systolic blood pressure; DBP=diastolic blood pressure; HG-NU=incidence of HG-induced negative U-wave; NS=no statistically signi- fi cant difference. Vol.22 No.1 HANDGRIP-INDUCED NEGATIVE U 65 and diastolic blood pressures at rest, and also during handgrip were the hi- ghest in Group H2, intermediate in Group H1 and the lowest in Group H0, and the differences were significant in a great majority (Table III). How- ever, there was no difference in degree of pressure rise induced by handgrip in each hypertensive group. NegativeU-wave: In about two thirds of hypertensive subjects electrocardiographic U-wave became negative or increased its negativity during handgrip. As mentioned earlier, this change of U-wave morphology was most prominent in the left- sided chest leads, especially V4 and V5, and orthogonal lead X, while there were only minimal changes of U waves in other leads. Sequential changes during the grip test are illustrated in Fig. 1. A preexisted tiny negative U- wave increased in its negativity with the progression of time during handgrip, and returned to the control within 60sec after release of the handgrip.
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