Reduction of QTc dispersion by the angiotensin II receptor blocker valsartan may be related to its anti-oxidative stress effect in patients with essential hypertension.
QT dispersion has been reported to increase in patients with essential hypertension, and abnormal QT dispersion is associated with arrythmias and sudden cardiac death. However, whether change in QT dispersion is related to oxidative stress is unclear. We examined the effect of the angiotensin II receptor blocker valsartan on QT dispersion and the relationship between oxidative stress and QT dispersion in patients with essential hypertension. Hypertensive patients whose systolic blood pressure (SBP) was more than 140 mmHg and/or diastolic blood pressure (DBP) was more than 90 mmHg were treated with valsartan. Blood pressure was measured once a month for 6 months. The difference between the maximal and minimal QT intervals within a 12-lead surface ECG was measured and QT dispersion and QTc dispersion corrected by heart rate were obtained before and 6 months after treatment. Left ventricular mass (LVM) assessed by echocardiography was obtained at baseline and 6 months after treatment. Venous blood samples were obtained at baseline and 6 months after treatment to measure serum levels of lipoperoxidation (LPO) and type I and III procollagen. Treatment with valsartan significantly decreased SBP and DBP. QTc dispersion decreased significantly 6 months after treatment with valsartan as compared to the baseline values. Valsartan treatment did not affect the LVM. Valsartan significantly decreased the abnormally high LPO levels. The changes in QTc dispersion were positively correlated with changes in the serum levels of LPO and with changes in DBP. The correlation between changes in LPO and QTc dispersion was more close than that between changes in DBP and QTc dispersion. In conclusion, antihypertensive therapy with valsartan reduces QTc dispersion and this may be related to the ability of valsartan to reduce oxidative stress in patients with essential hypertension.
Miyajima
Katsuaki
K
Second Department of Internal Medicine, Gifu University School of Medicine, Gifu, Japan.
Minatoguchi
Shinya
S
Ito
Yoko
Y
Hukunishi
Masanori
M
Matsuno
Yasunari
Y
Kakami
Masao
M
Kawasaki
Masanori
M
Nishigaki
Kazuhiko
K
Takemura
Genzou
G
Fujiwara
Hisayoshi
H
D000368:Aged; D047228:Angiotensin II Type 1 Receptor Blockers / Q000494:pharmacology* / Q000627:therapeutic use; D000959:Antihypertensive Agents / Q000494:pharmacology* / Q000627:therapeutic use; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D024042:Collagen Type I / Q000097:blood; D024061:Collagen Type III / Q000097:blood; D004562:Electrocardiography; D005260:Female; D005500:Follow-Up Studies; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D006801:Humans; D006973:Hypertension / Q000188:drug therapy / Q000503:physiopathology*; D017379:Hypertrophy, Left Ventricular / Q000503:physiopathology; D015227:Lipid Peroxidation / Q000187:drug effects / Q000502:physiology; D008133:Long QT Syndrome / Q000503:physiopathology / Q000517:prevention & control; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects* / Q000502:physiology; D011446:Prospective Studies; D013777:Tetrazoles / Q000494:pharmacology* / Q000627:therapeutic use; D014633:Valine / Q000031:analogs & derivatives* / Q000494:pharmacology / Q000627:therapeutic use; D000068756:Valsartan
D047228:Angiotensin II Type 1 Receptor Blockers; D000959:Antihypertensive Agents; D024042:Collagen Type I; D024061:Collagen Type III; D013777:Tetrazoles; D000068756:Valsartan; D014633:Valine