COPD and Heart Failure: A Report from the ATTEND Registry

COPD and Heart Failure: A Report from the ATTEND Registry

S128 Journal of Cardiac Failure Vol. 18 No. 10S October 2012 Symposium 3 S3-1 COPD and Heart Failure: A Report from the ATTEND Registry DAI YUMINO1,2...

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S128 Journal of Cardiac Failure Vol. 18 No. 10S October 2012

Symposium 3 S3-1 COPD and Heart Failure: A Report from the ATTEND Registry DAI YUMINO1,2, NAOKI SATO2, KATSUYA KAJIMOTO2, YUICHIRO MINAMI2, MASAYUKI MIZUNO2, KUNIYA ASAI2, KOJI MURAI2, RYO MUNAKATA2, TOSHIYUKI AOKAGE2, YASUSHI SAKATA2, ATSUHIKO KEITA2, KEIJI TANAKA2, KYOICHI MIZUNO2, NOBUHISA HAGIWARA2, HIROSHI KASANUKI2, TERUO TAKANO2 1 Department of Cardiology, Tokyo Women’s Medical University, Tokyo, Japan, 2The ATTEND Investigators Drastic progress in treating life-style related diseases and ischemic heart disease along with ageing society, the incidence of heart failure has been growing and is concerned as a social issue due to high readmission rate and mortality. Thus, it is critical to identify “treatable factors” for development and exacerbation of heart failure. COPD (chronic obstructive pulmonary disease) is considered as one of the possible factors. Recent studies have shown not only high rate of COPD comobidity among ischemic heart disease and heart failure patients, but also observed close relationship between prognoses of these patients. In this session, lecturer will introduce sub-analysis result from ongoing study, Decompensated Heart Failure Syndromes Registry in Japan Multicenter prospective observational cohort study ATTEND Registry, and other clinical data to discuss whether COPD should be considered as a risk factor and treatment target.

S3-2 Long-acting Loop Diuretic is Superior to Short-acting One in Treatment of Congestive Heart Failure: The J-MELODIC Study TAKESHI TSUJINO1, TOHRU MASUYAMA2 1 Department of Pharmacy, School of Pharmacy, Hyogo University of Health Sciences, Hyogo, Japan, 2Cardiovascular Division, Department of Internal Medicine, Hyogo College of Medicine, Hyogo, Japan Diuretics are the most frequently prescribed medicine in patients with chronic heart failure (CHF). However, many retrospective analyses of CHF patients have suggested that prognosis is the poorer in CHF patients given the larger dose of loop diuretics. Some experimental studies have demonstrated that furosemide, a short-acting loop diuretic, increases the mortality by activating neurohumoral factors in heart failure models. We hypothesized that the use of the long-acting rather than short-acting loop diuretic might provide the better prognosis in CHF. Thus, we designed a multicenter study, J-MELODIC (Japanese Multicenter Evaluation of LOng- versus short-acting Diuretics In Congestive heart failure) to obtain a clinical evidence about the effects of diuretics in heart failure. In this multicenter, prospective, randomized, open, blinded endpoint trial, we compared effects of azosemide and furosemide in patients with CHF with New York Heart Association class II or III symptoms. 320 patients (160 patients in each group, mean age 71 years) were followed up for a minimum of 2 years. The primary endpoint (a composite of cardiovascular death or unplanned admission to hospital for congestive heart failure) occurred in 23 patients in the azosemide group and 34 patients in the furosemide group (hazard ratio, 0.55, 95% confidence interval, 0.32 to 0.95: P50.03). Azosemide, compared to furosemide, improves the prognosis of patients with chronic heart failure.

S3-3 Imbalance of Placental Growth Factor and Its Endogenous Antagonist Soluble Flt-1, that Exaggerates Atherosclerosis in CKD Patients YUKIJI TAKEDA, SHIRO UEMURA, MASARU MATSUI, TAKAKI MATSUMOTO, AYAKO SENO, KENJI ONOUE, TOMOYA UEDA, HIROYUKI KAWATA, RIKA KAWAKAMI, YOSHIHIKO SAITO The First Department of Internal Medicine, Nara Medical University, Nara, Japan Placental growth factor (PlGF) plays important roles in the development of atherosclerosis, which is antagonized by soluble Flt-1 (sFlt-1). sFlt-1 circulates as well as is stored on endothelial cell surface through binding of heparan sulfate proteogricans. In our study, expression of sFlt-1 mRNA was decreased with progression of CKD stage in human renal biopsy samples, and decreased in the kidney and lung of 5/6 nephrectomized mice. However, plasma level of sFlt-1 was increased in accordance with severity of CKD, suggesting the plasma sFlt-1 level does not represent sFlt-1 production. In contrast, after very small dose of heparin injection (0.4IU/kg), the plasma sFlt-1 level was elevated larger in patients with higher eGFR. Next, we performed in vitro experiments. Heparin stimulated the release of sFlt-1 from ex vivo organ culture model of mouse thoracic aorta and from cultured human endothelial cells, which indicates that heparin releases sFlt-1 from cell surface, and heparin-induced plasma sFlt-1 level is a surrogate marker for total amount of sFlt-1. PlGF/sFlt-1 ratio after heparin injection was positively correlated with eGFR, and associated with higher risk of cardiovascular event. Atherosclerotic plaque area were significantly increased in 5/6 nephrectomized ApoE KO mice.

Replacement therapy with recombinant sFlt-1 significantly reduced atherosclerotic plaque formation.In conclusion imbalance of PlGF and sFlt-1 would be involved in the exaggeration of atherosclerosis in CKD.

S3-4 Etiology of Hypertensive Heart Failure: Insight from the CHART-2 Study YASUHIKO SAKATA1, KOTARO NOCHIOKA2, MASANOBU MIURA2, TSUYOSHI TAKADA2, SATOSHI MIYATA1, JUN TAKAHASHI2, YOSHIHIRO FUKUMOTO1, NOBUYUKI SHIBA2, HIROAKI SHIMOKAWA1 1 Department of Evidence-based Cardiovascular Medicine, Tohoku University Graduate School of Medicine, Sendai, Japan, 2Department of Cardiovascular Medicine, Tohoku University Graduate School of Medicine, Sendai, Japan Hypertension is one of the major public health concerns associated with high morbidity and mortality worldwide. Hypertension is involved in the pathogenesis of heart failure, as it causes endothelial dysfunction, left ventricular hypertrophy, and finally systolic and diastolic heart dysfunction. Accordingly, management of hypertension, and consequently hypertensive heart disease (HHD) is highly important to prevent development of de-novo heart failure as well as worsening of stable heart failure. In this symposium, we would like to present analysis data from the Chronic Heart Failure Analysis and Registry in the Tohoku Districrt-2 (CHART-2) Study (ClinicalTrials.gov number NCT 00418041, n510,219). The CHART-2 study is a prospective observational multicenter cohort study to identify the characteristics, mortality and prognostic risks of patients with overt HF and those at high risk for HF. In the CHART-2 study, prevalence of hypertension among stage C/D heart failure patients (N54244) was almost 80%, and prevalence of heart failure due to HHD, namely hypertensive heart failure, was 10%. Hypertensive heart failure was characterized by higher prevalence of female gender and preserved ejection fraction in comparison with heart failure due to other cardiac origins such as ischemic heart diseases or cardiomyopathies, whereas five year mortality was comparable. Comprehensive analysis from the real world practice of hypertensive heart failure will be discussed.

S3-5 The Impact of Left Ventricular Hypertrophy as a Risk of Heart Failure with Preserved Ejection Fraction KAZUHIRO YAMAMOTO Department of Molecular Medicine and Therapeutics, Faculty of Medicine, Tottori University, Yonago, Japan Many epidemiological studies have revealed a close relation between left ventricular (LV) hypertrophy and prognosis of patients with cardiovascular diseases, including heart failure with preserved ejection fraction (HFpEF). Hypertension is a leading cause for HFpEF, and depressor therapy is mandatory and effective in the prevention of LV hypertrophy. However, in some of hypertensive patients, LV hypertrophy progresses even after the reduction of blood pressure or in the absence of hypertension. Our and other experimental studies have suggested that LV hypertrophy is not a homogeneous phenomenon, and that there are at least two types in hypertensive heart disease; adaptive and excessive hypertrophy. Adaptive hypertrophy develops to attenuate LV wall stress in the presence of pressure overload, and is likely independent of renin-angiotensin system. In contrast, excessive hypertrophy is not necessary for the reduction of LV wall stress and is induced at least partly by the activation of reninangiotensin system. This type of hypertrophy may not regress even after the decrease in blood pressure, and early intervention against the development of excessive hypertrophy is desirable. Our experimental study suggests that the blockade of renin-angiotensin system is effective in the prevention of excessive LV hypertrophy and HFpEF. Thus, angiotensin receptor blockers may be effective in the prevention rather than the treatment of HFpEF, and this is consistent with results of clinical studies.