Our mission is to become a worldwide reference for education in the field for all professionals involved in the process to dissemintate knowledge & skills of Acute Cardiovascular Care
Our mission is to promote excellence in clinical diagnosis, research, technical development, and education in cardiovascular imaging in Europe.
Our mission: To promote excellence in research, practice, education and policy in cardiovascular health, primary and secondary prevention.
Our goal is to reduce the burden in cardiovascular disease in Europe through percutaneous cardiovascular interventions.
Our Mission is "to improve the quality of life of the population by reducing the impact of cardiac rhythm disturbances and reduce sudden cardiac death"
To improve quality of life and logevity, through better prevention, diagnosis and treatment of heart failure, including the establishment of networks for its management, education and research.
Working Groups goals is to stimulate and disseminate scientific knowledge in different fields of cardiology.
ESC Councils goal is to share knowledge among medical professionals practising in specific cardiology domains.
OUR MISSION: TO REDUCE THE BURDEN OF CARDIOVASCULAR DISEASE
List of Authors: Hiroaki Matsubara, Takahisa Sawada, Hiroyuki Yamada, Shinzo Kimura, Jun Shiraishi
Purpose: The KYOTO HEART Study showed an additional beyond BP lowering benefit of Valsartan on cardio- and cerebrovascular (CV) events in high-risk hypertensive patients (Eur Heart J 2009;30:2461). We here report the ancillary analysis regarding primary & secondary prevention, combination therapy with calcium channel blockers (CCB), and CV event prevention. Methods and results: The KYOTO HEART Study is a multicenter, two-arm parallel treatment group comparison study with response-dependent dose titration scheme. High-risk Japanese patients with uncontrolled hypertension (n=3031) were randomized to receive either additional Valsartan or conventional non-ARB therapies. The primary endpoint was a composite of defined CV events such as stroke, myocardial infarction, heart failure, and angina pectoris (AP). Updated analyses were as follows; 1) 915 had previous CV event history and 2116 without CV events. Compared with non-ARB, Valsartan was effective for both primary prevention (3.0% vs 6.7%, HR 0.44, 95%CI:0.29-0.68) in which stroke is significantly inhibited, and secondary prevention (11.5% vs 18.1%, HR 0.63, 95%CI:0.44-0.89) in which AP is significantly inhibited. 2) primary endpoint events in Valsartan plus CCB group (n=773), Valsartan plus non-CCB (744), non-ARB plus CCB (1034), non-ARB plus non-CCB (480) were 5.0%, 6.0%, 9.8% and 11.0%, respectively. Valsartan plus CCB combination showed lower primary events than non-ARB plus CCB (p=0.0003, HR 0.50, 95%CI:0.35-0.73), and Valsartan plus non-CCB vs. non-ARB plus non-CCB (p=0.002, HR 0.55, 95%CI:0.37-0.80). The patient background and BP during follow-up showed no significant differences. 3) AP events were separated into unstable AP and effort AP using clinical information and coronary angiographic findings. Valsartan was significantly effective for effort AP prevention (1.1% vs 2.3%, p=0.01), but was not effective for unstable AP (0.20% vs 0.59%, p=0.10). 4) stroke prevention was mainly due to inhibition in cerebral infarction (18 vs 36 events) but not bleeding (2 vs 5). Conclusions: Valsartan is effective for primary stroke and secondary AP prevention in high-risk hypertensive patients, and Valsartan plus CCB combination therapy provides a more efficient prevention against CV events. Beneficial effects of Valsartan on cardiovascular outcomes were due to prevention of cerebral infarction and effort AP.
In these ancillary analyses of the KYOTO HEART Study, presented at the ESC Congress 2010, Matsubara H. et coll. investigated (a) the effects of valsartan on primary and secondary prevention, (b) the effects of combination therapy with calcium channel blockers (CCB), and (c) performed additional analyses on angina and stroke events. In the main study (Sawada T. et al. Eur Heart J 2009), they previously showed that a valsartan add-on treatment was more effective than a non-ARB regimen for preventing CV events in uncontrolled hypertensive patients with high CV risk. The new finding is that these results are confirmed both for secondary prevention (i.e. in patients with previous CV events, HR=0.63 [0.44-0.89], p=0.0088) and primary prevention (HR=0.44 [0.29-0.68], p=0.0002). Here, the primary end-point is the same as in the main study, i.e. a composite of CV events such as stroke/TIA, MI, worsening HF, angina, dissecting aortic aneurysm, lower limb arterial obstruction, transition to dialysis or doubling of serum creatinin levels. In both secondary and primary prevention, the benefit can be attributed to valsartan, because both “valsartan add-on” and “non-ARB” arms displayed a similar reduction in brachial BP, a similar level of CV risk at baseline, and similar baseline medications. The results concerning primary prevention are particularly important not only for the Japanese/Asian population, but also because in most countries, 1/2 to 2/3 of hypertensives (i.e. no previous CV disease) are at high CV risk; and 2/3 of treated hypertensive patients are currently not controlled. Thus, in those patients, adding valsartan to previous treatment is more effective than a non-ARB regimen for preventing CV events. This ancillary analysis benefits from several strengths: a prespecified analysis, a large number of patients in both primary (n=2116) and secondary (n=915) prevention groups; a similar number of patients in both arms (“valsartan add-on” and “non-ARB”) for primary (1065/1051) and secondary (452/463) prevention; and an incidence of primary end-points close to that expected (10.2% vs 12% in 3 yrs FU), and high enough both in primary (n=102 in 3 yrs FU) and secondary prevention groups (n=146) to correctly size the statistical power. However, a limitation concerns the secondary prevention group: ACE inhibitors were given to 29% of patients at baseline (CHD, CHF), and were continued during FU. Thus, about one third of ARB patients had an AR+ACEI combination, which may have increased the benefit of valsartan. Some remaining issues are: (a) whether the benefit (i.e. prevention of CV events) can be attributed to valsartan, or the ARB pharmacological class, or the RAS blockade (ACE inhibitors were not allowed during the trial); (b) whether these results can be extrapolated to Western populations; and (c) whether valsartan may exert its protective effect, at least in part, through a higher reduction in central BP, for a given fall in brachial BP. An additional ancillary analysis concerned the combination of valsartan with a CCB. The authors’ conclusion that “combination therapy with valsartan+CCB showed lower primary events than non-ARB+CCB” should not be taken in a restrictive way, since the benefit of valsartan over non-ARB has also been shown in patients receiving no CCB. It would be more balanced to state that valsartan add-on treatment lowered the incidence of CV events whether patients received in addition CCB or not. Finally, the authors’ conclusions that “valsartan was significantly effective for prevention of effort angina but not unstable angina” should be taken with caution since only a small number of unstable angina occurred, which may have undersized the statistical power. Thus, it would be more balanced to state that angina prevention by valsartan was rather due to inhibition of effort angina than unstable angina.
711009 - 711010
Clinical Trial Update III
© 2016 European Society of Cardiology. All rights reserved