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(Stroke. 2002;33:1167.)
© 2002 American Heart Association, Inc.

Letters to the Editor

Laterality of Ruptured Aneurysm Has No Influence on QT Prolongation After Subarachnoid Hemorrhage

Shinji Fukui, MD; Naoki Otani, MD; Nobusuke Tsuzuki, MD, DMSc; Hiroshi Nawashiro, MD, DMSc Katsuji Shima, MD, DMSc

Department of Neurosurgery, National Defense Medical College, Tokorozawa, Japan

To the Editor:

We write in response to the recent interesting article of Hirashima et al, entitled "Right Sylvian Fissure Subarachnoid Hemorrhage Has Electrocardiographic Consequences."¹ Although in this article the authors concluded that cardiac consequences are possible in patients with massive right sylvian fissure subarachnoid hemorrhage (SAH), we have some reservations about the methodology in this study, especially about the assessment of ECG.

The authors mentioned that 26 patients had changes on admission ECG [ECG(+) group], while 92 patients did not [ECG(-) group]. The inclusion criteria for the ECG(+) group in this study were any ECG changes on admission, including T-wave inversion, QT prolongation, or ST-segment elevation or depression. However, the authors did not quantitatively assess these ECG changes. In addition, it is unclear that T-wave inversion or ST-segment changes increase susceptibility to sudden death associated with SAH. On the other hand, QT prolongation is commonly believed to cause life-threatening ventricular arrhythmias such as torsades de pointes, thus leading to sudden death associated with SAH.^2,3

We herein assessed the corrected QT (QTc) intervals on admission in 57 SAH patients and 57 controls (age-matched hospitalized patients) to determine whether there was any difference on the basis of the laterality of ruptured aneurysm in their QTc intervals on the first days of SAH. The SAH patients who were included in our study were admitted within 24 hours after onset of SAH to the National Defense Medical College Hospital and had a ruptured aneurysm that was located in the anterior circulation, namely, right or left middle cerebral artery (MCA), right or left internal carotid artery (ICA), or anterior communicating artery (ACoA). These 5 subgroups of the SAH group were matched for patient age, Hunt and Kosnik grade, and Fisher’s classification for CT. The exclusion criteria in our study included heart disease, previous SAH or intracerebral hemorrhaging, a young age (<19 years), pregnancy, pacemaker rhythm, or use of the following drugs: digitalis, quinidine, procainamide, or disopyramide. Measurements of 12 leads of a standard ECG were done on the first days of SAH. Two consecutive QT intervals were manually measured in all 12 leads of a standard ECG with the assessor blinded to the name and group of the patient. The QT intervals were measured from the beginning of the QRS complex to the visual return of the T wave to the isoelectric line and were corrected for heart rate with the Bazett formula: QTc=QT/square root of RR interval. The mean QTc interval was calculated from all QTc intervals measured. The intraobserver coefficients of variation were 1.6%, and the interobserver coefficients of variation were 1.9%. All data were compared by Student’s t test or ANOVA with the post hoc test of Scheffé F.

The mean QTc interval of the SAH group was significantly longer (466 [SD 51] ms; P<0.0001, Student’s t test) than that of the control group (395 [SD 24] ms). However, the individual subgroup comparison showed no significant difference on the basis of the laterality of the ruptured aneurysm in the mean QTc interval (right MCA: n=5, 452 [SD 47]; right ICA: n=12, 468 [SD 73]; ACoA: n=19, 450 [SD 45]; left ICA: n=12, 498 [SD 37]; left MCA: n=9, 462 [SD 36] ms). In addition, there was no particular prolongation of QTc intervals in the 2 patients with right-sided massive sylvian hematoma.

These findings suggested that there was no difference on the basis of the laterality of the ruptured aneurysm in the degree of QT prolongation on the first days of SAH. However, the amount of SAH in each of the cisterns and fissures was not measured quantitatively in our study, and therefore there are limitations to the conclusions that can be drawn. Further studies are required to assess whether there is any right-sided dominance in cardiovascular effects, especially QT prolongation, during the acute phase of SAH.

References

1. Hirashima Y, Takashima S, Matsumura N, Kurimoto M, Origasa H, Endo S. Right sylvian fissure subarachnoid hemorrhage has electrocardiographic consequences. Stroke. 2001; 32: 2278–2281.[Abstract/Free Full Text]

2. Andreoli A, di Pasquale G, Pinelli G, Grazi P, Tognetti F, Testa C. Subarachnoid hemorrhage: frequency and severity of cardiac arrhythmias: a survey of 70 cases studied in the acute phase. Stroke. 1987; 18: 558–564.[Abstract/Free Full Text]

3. Lanzino G, Kongable GL, Kassell NF. Electrocardiographic abnormalities after nontraumatic subarachnoid hemorrhage. J Neurosurg Anesthesiol. 1994; 6: 156–162.[Medline] [Order article via Infotrieve]

Yutaka Hirashima, MD; Nobuhisa Matsumura, MD; Masanori Kurimoto, MD Shunro Endo, MD

Department of Neurosurgery

Shutaro Takashima, MD

Second Department of Internal Medicine

Hideki Origasa, PhD

Division of Biostatistics, Toyama Medical and Pharmaceutical University, Toyama, Japan

Response

We appreciate the interesting comments of Dr Fukui and colleagues regarding our recent article.¹ First, they did not measure the amount of subarachnoid hemorrhage (SAH) in each cistern and fissure, as they pointed out. Therefore, it is difficult to discuss our results according to their data, although their study is very interesting. They have reservations about the assessment of ECG in our study. We think that the changes of ECG by sympathetic cardiovascular effects at the acute stage of SAH include not only QT prolongation but also other findings such as T-wave inversion or ST-segment elevation or depression. We also calculated QTc in this study and defined QT prolongation as QTc >0.44 in men and QTc >0.46 in women. We evaluated the changes in ECG at admission and 1 month later. When abnormal findings disappeared on subsequent ECG, we defined them as abnormality due to SAH. Although they stressed quantitative assessment of ECG changes, they did not evaluate ECG 1 month later. Therefore, we have some apprehensions, such as that QT prolongation in their study is not always due to SAH. Systolic blood pressure >160 mm Hg and the amount of SAH in the right sylvian fissure on admission were independently associated with ECG changes due to sympathetic cardiovascular effects, and we suggested that these phenomena may be via the stimulation of the right insular cortex.

References

1. Hirashima Y, Takashima S, Matsumura N, Kurimoto M, Origasa H, Endo S. Right sylvian fissure subarachnoid hemorrhage has electrocardiographic consequences. Stroke. 2001; 32: 2278–2281.

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