Congestive Heart Failure

Mineralocorticoid receptors (MRs) have been identified in the human cardiovascular tissues. We determined MR expression in the failing heart to clarify the mechanism of action of aldosterone antagonist in the treatment of congestive heart failure. MR protein and MR mRNA content were detected by immunohistochemical staining and in situ hybridization in the cardiac tissues. Immunohistochemical staining of the receptor, as well as in situ hybridization of MR mRNA, was dense in cardiomyocytes of the failing left ventricle as compared with the controls. The staining ratio of the cytoplasm to the interstitium showed that MRs were located mainly in the cytoplasm. The cytoplasm to the interstitium in the failing left ventricle was 1.53±0.13, which was significantly higher than that of the controls 1.25±0.19 ( p &lt;0.05). These findings suggest that the efficacy of aldosterone antagonists in treating congestive heart failure may be in part through blocking the MRs, which are upregulated in the failing heart.

Masahiro Yoshida

Jun Ma

Tsutomu Tomita

Norihiro Morikawa

Nobuyoshi Tanaka

Katsuhiko Masamura

Yasuyuki Kawai

Isamu Miyamori

Mineralocorticoid Receptor Is Overexpressed in Cardiomyocytes of Patients With Congestive Heart Failure

盐皮质激素受体在充血性心力衰竭患者心肌细胞中过度表达

Concentrations of both B‐type natriuretic peptide (BNP) and amino‐terminal pro‐BNP (NT‐proBNP) are useful for diagnostic evaluation of patients with acute decompensated heart failure (ADHF), providing important information regarding presence and severity of heart failure. In addition, levels of both BNP and NT‐proBNP are strongly prognostic for adverse outcomes in this setting. While values for BNP and NT‐proBNP at hospital admission predict impending risk for adverse outcome, their measurement following HF treatment provides incremental prognostic information, even more accurately identifying patients at highest risk for death or rehospitalization in the short term. Thus, changes in BNP or NT‐proBNP following treatment should be considered an important part of the pre‐discharge decision making for patients hospitalized with ADHF. ©2012 Wiley Periodicals, Inc.

James L. Januzzi

Alan S. Maisel

Marc Silver

Yang Xue

Christopher DeFilippi

Natriuretic Peptide Testing for Predicting Adverse Events Following Heart Failure Hospitalization

心力衰竭住院后预测不良事件的利钠肽检测

Heart failure is a chronic disease marked by variable acute exacerbations. Once hospitalized the decompensated patient may have signs and symptoms only partially reversed, medical therapy only partially optimized and deranged physiology only partially restored. Therefore, the post‐acute care period is one of unique vulnerability and merits efforts of careful and comprehensive assessment of patients at risk of recurrent decompensation and rehospitalization. Natriuretic peptide (NP) assessment which has the ability to monitor dynamic changes in a patient's physiology, may play an important role as part of a post‐acute care algorithm focused on early detection and prevention of further decompensation and rehospitalization. ©2012 Wiley Periodicals, Inc.

Alan Maisel

James Januzzi

Marc A. Silver

Post-Acute Care: The Role of Natriuretic Peptides

急性后期护理：利钠肽的作用

Assessment of natriuretic peptide (NP) levels has a well‐established role in the diagnosis and prognosis of acute heart failure (AHF) patients. Current guidelines recommend assessment of NPs when the diagnosis is in question, yet multiple studies suggest a broader value of NP assessment. Measurement of NP levels results in more efficient treatment, resource utilization (ie, reduced costs), and possibly improved short‐ and long‐term outcomes. Given the large number of patients hospitalized every year with heart failure, combined with the high post‐discharge mortality, rehospitalization rates, and subsequent large financial costs, improving outcomes for hospitalized HF patients remains an unmet need. In this review, we highlight the value of NP assessment, starting in the emergency department and throughout hospitalization. The contents of this review were generated from a roundtable discussion of AHF and biomarker experts held in Chicago in April 2012 and focused on addressing the burden of AHF and readmission. ©2012 Wiley Periodicals, Inc.

Peter S. Pang

The Role of Natriuretic Peptides: From the Emergency Department Throughout Hospitalization

利钠肽的作用：从急诊科到住院全程

©2012 Wiley Periodicals, Inc. The goal of this study was to determine whether aggressive heart rate (HR) control in patients with both chronic atrial fibrillation (AF) and heart failure (HF) is associated with improved outcomes. HR control is one of the mainstays in management of patients with AF. However, rate control can be challenging in patients with HF. This study was designed as an interventional clinical trial, using patients with chronic AF and left ventricular systolic dysfunction with left ventricular ejection fraction ≤40% (n=20) as their own controls. Intervention consisted of increasing doses of metoprolol succinate to achieve target resting HR &lt;70 beats per minute. Clinical data were collected at baseline and after intervention, with paired t test used to evaluate statistically significant change. After 3 months of intervention, average resting HR decreased from 94±14 beats per minute to 85±12 beats per minute. Average metoprolol succinate dose at the end of the study was 121 mg. None of the outcomes improved significantly after the intervention, including exercise tolerance (meters walked on 6‐minute walk test 326±83 vs 330±86), quality of life (Minnesota Living With Heart Failure Questionnaire score of 42.5±19 vs 38±21), and brain natriuretic peptide (242±306 pg/mL vs 279±395 pg/mL). Aggressive HR control was difficult in this group of patients with chronic AF and HF due to patient intolerance of increasing doses of β‐blockade, and not associated with improved outcomes. Further studies are needed to establish guidelines for target HR in patients with chronic AF who also have significant HF.

Helme Silvet

Lee Ann Hawkins

Alan K. Jacobson

Heart Rate Control in Patients With Chronic Atrial Fibrillation and Heart Failure

慢性心房颤动和心力衰竭患者的心率控制

Diastolic dysfunction of the heart is correlated with cardiac mortality. Serum cystatin C ( CysC ) is an endogenous marker of kidney function. It is not clear whether serum CysC is associated with diastolic dysfunction in patients with varying cardiac conditions with concomitant diastolic abnormalities and preserved ejection fraction ( EF ). The authors measured serum CysC levels in patients with cardiac diseases and examined the relationships between serum CysC levels and diastolic function. Serum CysC was measured and echocardiography was performed in 124 consecutive patients with cardiac diseases. Transmitral flow ( TMF ) patterns surrogating diastolic function were categorized into two groups: a normal group and an abnormal group. Serum CysC and BNP showed a significant positive correlation. There were no significant differences in serum CysC among those cardiac diseases. Seventy‐eight patients with cardiac disease and preserved EF ( left ventricular EF ≥50%) and without renal dysfunction (estimated glomerular filtration rate ≥60 mL/minute/1.73 m 2 ) were examined. Multivariate linear regression analysis demonstrated that left atrium diameter and abnormal TMF patterns were independent determinants of serum CysC . Furthermore, patients with elevated serum CysC levels had poor prognosis. Serum CysC is associated with diastolic dysfunction in patients with various cardiac diseases and preserved EF . Serum CysC might be a biomarker of cardiac diastolic dysfunction in patients with preserved EF .

Kazumasa Nosaka

Kazufumi Nakamura

Kengo Kusano

Norihisa Toh

Takeshi Tada

Toru Miyoshi

Masayuki Doi

Kunihisa Kohno

Hiroshi Morita

Hiroshi Ito

Serum Cystatin C as a Biomarker of Cardiac Diastolic Dysfunction in Patients With Cardiac Disease and Preserved Ejection Fraction

血清胱抑素C作为心脏疾病伴保留射血分数患者心脏舒张功能障碍的生物标志物

There are many confusing things in life, and many things that may not obviously appear so are in fact a paradox.—Vittorio Gassman1 Since overweightness and obesity have adverse effects on cardiac structure and systolic and especially diastolic left ventricular (LV) function, as well as on cardiovascular (CV) diseases, including coronary heart disease (CHD) and hypertension (HTN), which are the leading causes of heart failure (HF), it really is no surprise that the prevalence of HF markedly increases with increasing severity of obesity.2 In a study of 5881 Framingham Heart Study participants, Kenchaiah and colleagues3 demonstrated that for every 1-kg/m2 increase in body mass index (BMI), the risk of HF increases by 5% in men and 7% in women during a 14-year follow-up, with graded increases in the risk of HF across the entire spectrum of BMI. In addition, in a study by Alpert and colleagues4 of 74 morbidly obese patients, nearly one third had clinical evidence of HF, and the prevalence of HF increased dramatically with the increasing duration of morbid obesity. Despite this evidence, numerous large studies5, 6 and meta-analyses7 have demonstrated an obesity paradox in HF, ie, overweight and obese patients with HF have a better prognosis than do their leaner counterparts, with overall similar HF severity at baseline. More than a decade ago, we demonstrated this paradox with both BMI and percentage of body fat (BF); thus, in our study, for every 1% increase in BF there was a 13% reduction in major CV events.8, 9 The mechanisms of the obesity paradox in HF remain unclear, and we have recently discussed the potential reasons for this puzzling paradox.2 Certainly, very few studies of the obesity paradox in HF have addressed the potential role of nonpurposeful weight loss prior to study entry, and in almost every condition, including HF, nonpurposeful weight loss, especially with cachexia, is associated with a poor prognosis. Many overweight and obese patients may have developed HF secondary to HTN and CHD and as a result of the abnormalities in left ventricular diastolic and systolic function that often develops in these patients. Conversely, lean patients who develop HF do so from other mechanisms that may result in a more negative prognosis. Obese patients present with HF at younger ages, have a higher LV ejection fraction (EF) and higher blood pressure, thus allowing obese patients to tolerate more cardioprotective medications and at higher doses and to have a lower expression of brain natriuretic peptides. All these factors and others may lead to an earlier presentation with less severe disease, which could lead to a better prognosis in obese patients with HF compared with lean patients. In the present and final issue of Congestive Heart Failure, Nagarajan and colleagues10 from the Cleveland Clinic HF program confirmed the obesity paradox in 501 patients in an advanced HF clinic, but their data suggest that there may be a “limit to this madness” by demonstrating a poor prognosis and, therefore, no obesity paradox in very obese patients (BMI ≥40 kg/m2) with HF. Although their data are statistically significant, it must be recognized that this relatively “new” finding is based on a very small number of only 21 morbidly obese HF patients, as the authors acknowledge. Nevertheless, considering the progressive decline that has occurred during the past 5 decades in total energy expenditure, the marked increases in obesity prevalence during this period, and the fact that “morbid” obesity is increasing even more so than is obesity per se,2, 11, 12 these results reported herein are still noteworthy and are also in line with other recent studies demonstrating a worse prognosis among the very obese. Although substantial evidence suggests that the obesity paradox in CV diseases, especially CHD, represents as much as a “lean” paradox (the leaner patients by BMI, BF, and lean body mass doing particularly poorly13, 14) or an “overweight” paradox (the overweight patients, or those with BMI 25 to 30 kg/m2, doing particularly well15-17), the results from Nagarajan and colleagues and others support that the paradox may not apply to the most obese, where prevention of morbid obesity and weight loss strategies (nonpharmacologic, pharmacologic, and surgical) are desperately needed. It is important to point out that the major clinical guidelines from various societies have differed regarding levels where weight loss is recommended (currently none recommend weight loss for patients with BMI <30 kg/m2, with various cutpoints between BMI 30–40 kg/m2), but all of the guidelines advocate weight loss for BMI ≥40 kg/m2.2 Greater efforts are needed to better define the exact role of weight reduction in many CV diseases, including CHD and HF, as well as to determine ideal body composition in both primary and secondary CV prevention. However, there is no question that there is a limit to the madness regarding more morbid obesity, where there are no longer questions regarding the adverse impact of this level of obesity in primary and secondary prevention of CV diseases. In any discussion of the obesity paradox in CV diseases, some attention directed at the critical role of cardiorespiratory fitness (CRF) is needed. As in primary prevention18 and CHD,19 CRF has a major role in impacting prognosis that also applies to HF. We have recently demonstrated that patients with high levels of CRF in both CHD20 and HF21 have a more favorable prognosis, and an obesity paradox may not be present in patients with higher CRF, whereas a strong obesity paradox is present in patients with low CRF. Thus, leaner HF patients with low CRF (eg, peak oxygen consumption <14 cc/kg/min) have a particularly poor prognosis.21 Since higher BF in HF patients correlates with muscular strength,22 which may be a very important predictor of prognosis,23 total fitness (CRF and muscular fitness/strength) may be especially important for HF, supporting exercising training and cardiac rehabilitation for these patients. Although it is certainly possible for morbidly obese individuals, even an occasional one with HF, to maintain a preserved level of CRF, even our large recent study of more than 2000 HF patients could not assess the impact of CRF in this level of obesity, due to the limitations of CRF assessment in the morbidly obese patients.21 In our experience, very few morbidly obese HF patients can adequately perform a typical fitness test, much less achieve high CRF levels, again supporting the critical role of prevention and treatment of this level of obesity in the primary and secondary prevention of HF. In summary, very similar to other CV diseases, the obesity paradox is present in patients with HF with one notable exception being very obese patients, as demonstrated by the preliminary results of this study. In these patients, clinical measures to reduce body weight may be needed to improve the prognosis and outcomes in HF.

Carl J. Lavie

Hector O. Ventura

Analyzing the Weight of Evidence on the Obesity Paradox and Heart Failure—Is There a Limit to the Madness?

分析肥胖悖论与心力衰竭的证据权重——疯狂是否有极限？

Persistent atrial flutter ( AFL ) in left ventricular assist device ( LVAD ) recipients can result in loss of AV synchrony, impaired ventricular filling and right heart failure ( RHF ). The authors report the largest series of HeartMate II ( HMII ) patients who developed AFL with decompensated RHF, which successfully resolved with AFL ablation. Eight patients with HMII LVAD (mean age, 57±12 years) had medically refractory AFL , with 7 developing de novo AFL after LVAD implant (onset range, 2 days–22 months post‐implant). Three patients developed recurrent syncope, 2 had inappropriate implantable cardioverter‐defibrillator shocks, and 6 had new or escalating need for inotropes. All had features of decompensated RHF . Seven patients underwent electrophysiology testing where mapping confirmed typical counterclockwise AFL (mean AFL cycle length, 252±49 ms) and radiofrequency ablation of cavotricuspid isthmus restored sinus rhythm in all patients. Complete resolution of symptoms and signs of RHF with improved quality of life were noted in all. No procedural complications were noted. During a mean follow‐up of 9±5 months, all patients remained free of atrial flutter. Catheter ablation of AFL in LVAD patients is safe and highly effective, resulting in immediate and significant improvement in symptoms of RHF , and should be considered first‐line therapy for AFL in these patients.

Rashmi U. Hottigoudar

Allen G. Deam

Emma J. Birks

Kelly C. McCants

Mark S. Slaughter

Rakesh Gopinathannair

Catheter <scp>A</scp>blation of <scp>A</scp>trial <scp>F</scp>lutter in <scp>P</scp>atients With <scp>L</scp>eft <scp>V</scp>entricular <scp>A</scp>ssist <scp>D</scp>evice <scp>I</scp>mproves <scp>S</scp>ymptoms of <scp>R</scp>ight <scp>H</scp>eart <scp>F</scp>ailure

左心室辅助装置患者心房扑动导管消融改善右心衰竭症状

Obese patients have been noted to have better prognosis in many conditions including heart failure. We hypothesize that this favorable prognosis for obesity may not be seen in patients with morbid obesity and advanced heart failure. A total of 501 consecutive patients with advanced heart failure referred for heart transplant evaluation to the Cleveland Clinic were studied. Patients were categorized into 3 groups based on their body mass index score as nonobese (≤30 kg/m 2 ), obese (30.1–40 kg/m 2 ), and morbidly obese (≥40 kg/m 2 ). There were fewer cardiovascular risk factors in the morbidly obese group. Unadjusted event‐free survival rates were 48.4%, 57.4%, and 28.6% in the nonobese, obese, and morbidly obese groups, respectively ( P =.02). In univariate analysis, both the nonobese group (hazard ratio [ HR ], 1.44; 95% confidence interval [ CI ], 1.09–1.91; P =.01) and the morbidly obese group ( HR, 2.46; 95% CI, 1.40–4.30; P =.002) had significantly higher risk of all‐cause mortality/transplantation compared with the obese group. This difference persisted in multivariate analysis after adjustment for confounding factors. Our study re‐emphasizes the presence of an obesity paradox even in patients with very advanced heart failure. This favorable prognosis, however, may not be relevant in patients with morbidly obesity. Cardiovascular risk factors may not contribute to this phenomenon

Vijaiganesh Nagarajan

Clay A. Cauthen

Randall C. Starling

Wai Hong Wilson Tang

Prognosis of Morbid Obesity Patients With Advanced Heart Failure

病态肥胖合并晚期心力衰竭患者的预后

Providing effective discharge instructions, appropriate dose uptitration, education regarding heart failure ( HF ) monitoring, and strict follow‐up have all been shown to decrease readmissions for HF but are all underutilized. The authors developed and evaluated the impact of a quality‐improvement HF checklist as a tool to remind physicians to improve quality of care in HF patients. The checklist was used in randomly selected patients admitted with a primary diagnosis of acute decompensated HF . It included documentation regarding medications and dose uptitration, relevant counseling, and follow‐up instructions at discharge. The checklist was used in 48 patients, and this checklist group was compared with 48 patients as a randomly selected control group. Higher proportions of patients were taking angiotensin‐converting enzyme ( ACE) inhibitors or angiotensin receptor blockers ( ARBs ) in the checklist group compared with the control group (40 of 48 vs 23 of 48, P &lt;.001). Compared with the controls, the rate of dose uptitration for β‐blockers and/or ACE inhibitors / ARBs was more common in the checklist group (4 of 48 vs 21 of 48, P &lt;.001). Both 30‐day (19% to 6%) and 6‐month (42% to 23%) readmissions were lower in the checklist group. The use of an HF checklist was associated with better quality of care and decreased readmission rates for patients admitted with HF .

Abhijeet Basoor

Nitin C. Doshi

John F. Cotant

Tarek Saleh

Mina Todorov

Nishit Choksi

Kiritkumar C. Patel

Michele DeGregorio

Rajendra H. Mehta

Abdul R. Halabi

Decreased Readmissions and Improved Quality of Care With the Use of an Inexpensive Checklist in Heart Failure

使用廉价清单降低再入院率并提高心力衰竭护理质量

Publication Information	Publisher: Wiley-Blackwell Publishing Ltd，Publishing cycle: ，Journal Type: journal，Open Access Journals: No
Basic data	Year of publication: 1996，Proportion of original research papers: ，Self Citation Rate:， Gold OA Rate:

Congestive Heart Failure

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