2011•Circulation JournalOpen access

Retraction:Enhanced Cardiovascular Protective Effects of Valsartan in High-Risk Hypertensive Patients With Left Ventricular Hypertrophy

Jun Shiraishi, Takahisa Sawada, Shinzo Kimura, Hiroyuki Yamada, Hiroaki Matsubara, for the KYOTO HEART Study Group

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Abstract

BACKGROUND: The objective of the present study was to examine whether baseline electrocardiographically diagnosed left ventricular hypertrophy (ECG-LVH) influenced the angiotensin II receptor blocker (ARB) valsartan add-on effects on the cardio-cerebrovascular morbidity and mortality in the high-risk hypertensive patients who participated in the KYOTO HEART Study. METHODS AND RESULTS: The primary endpoint was the same as in the main study: a composite of defined cardiovascular and cerebrovascular events. The median follow-up period was 3.27 years. The study group was divided into 2 groups according to the presence of ECG-LVH: with LVH, n=803; without LVH, n=2,228. The primary endpoint events occurred more frequently in patients with LVH than in patients without LVH (9.3% vs. 7.3%; hazard ratio [HR], 1.33; 95% confidence interval [CI]: 1.01-1.75). Valsartan add-on significantly decreased the occurrence of primary endpoint events in both LVH-positive patients (5.8% vs. 12.9%; HR, 0.45; 95%CI: 0.28-0.72) and LVH-negative patients (5.5% vs. 9.2%; HR, 0.59; 95%CI: 0.44-0.81) compared with non-ARB treatment. The reduction in combined cardiovascular events (composite of acute myocardial infarction, angina pectoris, and heart failure) due to valsartan treatment in patients with LVH was significantly larger than that in patients without LVH (P<0.0001). Changes in blood pressure during the follow-up period did not differ significantly among the study subgroups. CONCLUSIONS: High-risk hypertensive patients with ECG-LVH might gain more cardiovascular benefits from valsartan add-on treatment, compared with patients without ECG-LVH.

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BACKGROUND: The objective of the present study was to examine whether baseline electrocardiographically diagnosed left ventricular hypertrophy (ECG-LVH) influenced the angiotensin II receptor blocker (ARB) valsartan add-on effects on the cardio-cerebrovascular morbidity and mortality in the high-risk hypertensive patients who participated in the KYOTO HEART Study. METHODS AND RESULTS: The primary endpoint was the same as in the main study: a composite of defined cardiovascular and cerebrovascular events. The median follow-up period was 3.27 years. The study group was divided into 2 groups according to the presence of ECG-LVH: with LVH, n=803; without LVH, n=2,228. The primary endpoint events occurred more frequently in patients with LVH than in patients without LVH (9.3% vs. 7.3%; hazard ratio [HR], 1.33; 95% confidence interval [CI]: 1.01-1.75). Valsartan add-on significantly decreased the occurrence of primary endpoint events in both LVH-positive patients (5.8% vs. 12.9%; HR, 0.45; 95%CI: 0.28-0.72) and LVH-negative patients (5.5% vs. 9.2%; HR, 0.59; 95%CI: 0.44-0.81) compared with non-ARB treatment. The reduction in combined cardiovascular events (composite of acute myocardial infarction, angina pectoris, and heart failure) due to valsartan treatment in patients with LVH was significantly larger than that in patients without LVH (P<0.0001). Changes in blood pressure during the follow-up period did not differ significantly among the study subgroups. CONCLUSIONS: High-risk hypertensive patients with ECG-LVH might gain more cardiovascular benefits from valsartan add-on treatment, compared with patients without ECG-LVH.

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Available abstract

BACKGROUND: The objective of the present study was to examine whether baseline electrocardiographically diagnosed left ventricular hypertrophy (ECG-LVH) influenced the angiotensin II receptor blocker (ARB) valsartan add-on effects on the cardio-cerebrovascular morbidity and mortality in the high-risk hypertensive patients who participated in the KYOTO HEART Study. METHODS AND RESULTS: The primary endpoint was the same as in the main study: a composite of defined cardiovascular and cerebrovascular events. The median follow-up period was 3.27 years. The study group was divided into 2 groups according to the presence of ECG-LVH: with LVH, n=803; without LVH, n=2,228. The primary endpoint events occurred more frequently in patients with LVH than in patients without LVH (9.3% vs. 7.3%; hazard ratio [HR], 1.33; 95% confidence interval [CI]: 1.01-1.75). Valsartan add-on significantly decreased the occurrence of primary endpoint events in both LVH-positive patients (5.8% vs. 12.9%; HR, 0.45; 95%CI: 0.28-0.72) and LVH-negative patients (5.5% vs. 9.2%; HR, 0.59; 95%CI: 0.44-0.81) compared with non-ARB treatment. The reduction in combined cardiovascular events (composite of acute myocardial infarction, angina pectoris, and heart failure) due to valsartan treatment in patients with LVH was significantly larger than that in patients without LVH (P<0.0001). Changes in blood pressure during the follow-up period did not differ significantly among the study subgroups. CONCLUSIONS: High-risk hypertensive patients with ECG-LVH might gain more cardiovascular benefits from valsartan add-on treatment, compared with patients without ECG-LVH.

Key concepts: Valsartan, Medicine, Left ventricular hypertrophy, Cardiology, Internal medicine, Hazard ratio, Myocardial infarction, Clinical endpoint

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