Introduction: Heart failure (HF) is a syndrome of epidemic proportions and one of the main reasons for hospitalization worldwide. Different scientific s ocieties have r isen interest in the c reation ...of their own registries to s tudy the characteristics and prognosis of these patients. Each registry covers a part of the spectrum of this heterogeneous syndrome and is useful to address questions that are difficult to answer in clinical trials. The RICA-2 is a national registry created by the Heart Failure Working Group of the Spanish Society of Internal Medicine and offers an Internal Medicine perspective of this pathology. Objectives: The main objective is to assess clinical and epidemiological characteristics and prognostic factors among patients with HF. Secondary objectives include: (1) To determine clinical/epidemiological/phenotypic characteristics and prognosis specifically i n p atients with HF a nd p reserved l eft-ventricle e jection f raction ( LVEF); ( 2) To examine h ow f unctional s tatus, cognition, frailty, and nutrition influence the prognosis of patients with HF; (3) To assess congestion and strategies to achieve decongestion during the acute decompensation phase. Methods: A multicentre, prospective, observational cohort study including patients with HF attended in Spanish Internal Medicine Departments. Patients will be recruited in the acute decompensation phase or in the stable phase in the outpatient setting, including de novo and chronically decompensated patients. Patients will be included regardless of HF aetiology, LVEF values and comorbidities. Conclusions: Our work is a prospective study that aims to improve knowledge regarding epidemiology and prognosis in patients with HF, with focus on functionality, cognition, frailty, nutrition, and congestion phase.
Background Recently, acute kidney injury defined by small changes in serum creatinine levels was associated with worse short-term outcomes; however, the precision and variability of this association ...was not fully explored. Study Design Systematic review and meta-analysis. Setting & Participants Hospitalized patients. Selection Criteria for Studies MEDLINE and EMBASE databases were searched for observational cohort studies and randomized controlled trials published from 1990 through February 2007 that provided information for small changes in serum creatinine levels. Predictor Small acute changes in serum creatinine levels by absolute and percentage of changes in serum creatinine levels (lower threshold for increase in serum creatinine <0.5 mg/dL or <25%). Outcome Short-term mortality (≤30 days). Results Compared with controls, patients with a 10% to 24% increase in creatinine levels had a relative risk (RR) of death of 1.8 (95% confidence interval CI, 1.3 to 2.5). By comparison, subjects with a 25% to 49% acute change in creatinine levels had an RR of death of 3.0 (95% CI, 1.6 to 5.8), and those with the largest change (≥50%) had the greatest RR of death (RR, 6.9; 95% CI, 2.0 to 24.5). Results were similar when absolute changes in creatinine levels were considered and when pooled estimates of adjusted RR were used. Limitations Individual patient data were unavailable; thus, only group-level data were pooled for meta-analysis. Results showed a significant degree of statistical heterogeneity that was only partially ameliorated by separating studies into subsets based on clinical setting. Conclusions Short-term mortality and acute decreases in renal function are associated through a graded relationship such that even mild changes in serum creatinine levels portend worse outcome in a variety of clinical settings and patient-types.
BackgroundCongestive heart failure (HF) is a common condition in the intensive care unit (ICU). Cardiomyopathy is an important etiological factor in HF. However, few studies have explored the effect ...of cardiomyopathy on the prognosis of HF. This study explored the association between comorbid cardiomyopathy and the outcomes of critically ill patients with congestive HF. MethodsA retrospective cohort study was performed using data extracted from Medical Information Mart for Intensive Care IV (MIMIC-IV) database. All adult patients with the first ICU admission were enrolled as participants but those diagnosed with cardiomyopathy alone were excluded. The demographics, comorbidities, vital signs, laboratory tests, scoring systems, and treatments of patients were extracted to further analyze. The composite endpoints included in-hospital mortality, cardiac arrest, and re-admission to the ICU. The association between cardiomyopathy comorbidity and the composite endpoints was assessed using propensity-score matching (PSM) and multivariable logistic regression models. ResultsA total of 27,901 critically ill patients were enrolled, including 1,023 patients diagnosed with cardiomyopathy and congestive HF. The average age of the cohort was 64.37±17.36 years, and 58.13% of the patients were men. The ethnicity of patients was mainly white (64.67%). Multivariable logistic regression analyses found the risk of composite endpoints in patients with cardiomyopathy was higher than other groups odds ratio (OR) =1.87; 95% confidence interval (CI): 1.62-2.15; P<0.001. Compared to patients with congestive HF alone (OR =1.43; 95% CI: 1.26-1.62; P<0.001), patients with cardiomyopathy had a similar risk of in-hospital death (OR =1.35; 95% CI: 1.06-1.71; P=0.014). Moreover, the risks of cardiac arrest (OR =1.53; 95% CI: 1.01-2.34; P=0.029) and re-admission to the ICU (OR =1.74; 95% CI: 1.39-2.17; P<0.001) were both higher in patients with cardiomyopathy than other groups. After PSM, the risk of composite endpoints was still higher in patients with cardiomyopathy (OR =1.64; 95% CI: 1.33-2.02; P<0.001). The association was consistent among patients admitted to the coronary care unit (CCU) and medical ICU (MICU)/surgical ICU (SICU). ConclusionsComorbid cardiomyopathy increased the risk of composite endpoints in patients with congestive HF admitted to the ICU. Cardiomyopathy is related to the poor outcomes of critically ill patients with congestive HF.
Matrix metalloproteinases (MMPs) are a family of proteolytic enzymes responsible for myocardial extracellular protein degradation. Several MMP species identified within the human myocardium may be ...dysregulated in congestive heart failure (CHF). For example, MMPs that are expressed at very low levels in normal myocardium, such as collagenase-3 (MMP-13) and the membrane-type-1 MMPs, are substantially upregulated in CHF. However, MMP species are not uniformly increased in patients with end-stage CHF, suggesting that a specific portfolio of MMPs are expressed in the failing myocardium. With the use of animal models of CHF, a mechanistic relationship has been demonstrated with respect to myocardial MMP expression and the left ventricular (LV) remodeling process. The tissue inhibitors of the MMPs (TIMPs) are locally synthesized proteins that bind to active MMPs and thereby regulate net proteolytic activity. However, there does not appear to be a concomitant increase in myocardial TIMPs during the LV remodeling process and progression to CHF. This disparity between MMP and TIMP levels favors a persistent MMP activation state within the myocardium and likely contributes to the LV remodeling process in the setting of developing CHF. The elucidation of upstream signaling mechanisms that contribute to the selective induction of MMP species within the myocardium as well as strategies to normalize the balance between MMPs and TIMPs may yield some therapeutic strategies by which to control myocardial extracellular remodeling and thereby slow the progression of the CHF process.
In the Sudden Cardiac Death in Heart Failure Trial (SCD-HeFT), implantable cardioverter-defibrillator (ICD) therapy significantly reduced all-cause mortality rates compared with medical therapy alone ...in patients with stable, moderately symptomatic heart failure, whereas amiodarone had no benefit on mortality rates. We examined long-term economic implications of these results.
Medical costs were estimated by using hospital billing data and the Medicare Fee Schedule. Our base case cost-effectiveness analysis used empirical clinical and cost data to estimate the lifetime incremental cost of saving an extra life-year with ICD therapy relative to medical therapy alone. At 5 years, the amiodarone arm had a survival rate equivalent to that of the placebo arm and higher costs than the placebo arm. For ICD relative to medical therapy alone, the base case lifetime cost-effectiveness and cost-utility ratios (discounted at 3%) were dollar 38,389 per life-year saved (LYS) and dollar 41,530 per quality-adjusted LYS, respectively. A cost-effectiveness ratio < dollar 100,000 was obtained in 99% of 1000 bootstrap repetitions. The cost-effectiveness ratio was sensitive to the amount of extrapolation beyond the empirical 5-year trial data: dollar 127,503 per LYS at 5 years, dollar 88,657 per LYS at 8 years, and dollar 58,510 per LYS at 12 years. Because of a significant interaction between ICD treatment and New York Heart Association class, the cost-effectiveness ratio was dollar 29,872 per LYS for class II, whereas there was incremental cost but no incremental benefit in class III.
Prophylactic use of single-lead, shock-only ICD therapy is economically attractive in patients with stable, moderately symptomatic heart failure with an ejection fraction < or = 35%, particularly those in NYHA class II, as long as the benefits of ICD therapy observed in the SCD-HeFT persist for at least 8 years.
A better understanding of the mechanisms and pathophysiological pathways of heart failure (HF), improved management of associated comorbidities, and advances in identifying genetic cardiac disease ...have led to a near-revolution in the management of patients in terms of pharmacological treatments, surgery and devices. These developments have transformed outcomes and HF-associated mortality, and gene therapies further promise a brighter future for patients who experience the debilitating effects of HF. This new edition of 'Fast Facts: Heart Failure' starts with the definitions of HF (different types of HF require different treatments), then provides the latest thinking on mechanisms and clinical stages, underlying causes and the assessment and management of comorbidities. This is followed by simple diagnostic criteria and a comprehensive overview of investigations. The management chapters focus on the importance of self-care education and healthy lifestyle choices, together with the latest recommendations for pharmacological treatment, device therapy and cardiac surgery from international guidelines. The final chapter on developments is an indication of the ongoing innovation in this rapidly moving field.
The Fontan procedure is a successful palliation for children with single-ventricle physiology; however, many will eventually require heart transplantation. The purpose of this study was to determine ...risk factors for death awaiting transplantation and to examine results after transplantation in Fontan patients.
A retrospective, multi-institutional review was performed of 97 Fontan patients <18 years of age listed at 17 Pediatric Heart Transplant Study centers from 1993 to 2001. Mean age at listing was 9.7 years (0.5 to 17.9 years); 25% were <4 years old; 53% were United Network for Organ Sharing status 1; 18% required ventilator support. Pretransplantation survival was 78% at 6 months and 74% at 12 months and was similar to 243 children with other congenital heart disease (CHD) and 747 children without congenital heart disease (No-CHD), who were also awaiting transplantation. Patients who were younger, status 1, had shorter interval since Fontan, or were on a ventilator were more likely to die while waiting. At 6 months, the probability of receiving a transplant was similar for status 1 and 2 (65% versus 68%); however, the probability of death was higher for status 1 (22% versus 5%). Seventy patients underwent transplantation. Survival was 76% at 1 year, 70% at 3 years, and 68% at 5 years, slightly less than CHD and No-CHD patients. Causes of death included infection (30%), graft failure (17%), rejection (13%), sudden death (13%), and graft coronary artery disease (9%). Protein-losing enteropathy (present in 34 patients) resolved in all who survived >30 days after transplantation.
Heart transplantation is an effective therapy for pediatric patients with a failed Fontan. Although early posttransplantation survival is slightly lower than other patients with CHD, long-term results are encouraging, and protein-losing enteropathy can be expected to resolve.
Aims
Many chronic heart failure (CHF) patients take β-blockers. When such patients are hospitalized for decompensation, it remains unclear how ongoing β-blocker treatment will affect outcomes of ...acute inotrope therapy. We aimed to assess outcomes of SURVIVE patients who were on β-blocker therapy before receiving a single intravenous infusion of levosimendan or dobutamine.
Methods and results
Cox proportional hazard regression revealed all-cause mortality benefits of levosimendan treatment over dobutamine when the SURVIVE population was stratified according to baseline presence/absence of CHF history and use/non-use of β-blocker treatment at baseline. All-cause mortality was lower in the CHF/levosimendan group than in the CHF/dobutamine group, showing treatment differences by hazard ratio (HR) at days 5 (3.4 vs. 5.8%; HR, 0.58, CI 0.33-1.01, P = 0.05) and 14 (7.0 vs. 10.3%; HR, 0.67, CI 0.45-0.99, P = 0.045). For patients who used β-blockers (n = 669), mortality was significantly lower for levosimendan than dobutamine at day 5 (1.5 vs. 5.1% deaths; HR, 0.29; CI 0.11-0.78, P = 0.01).
Conclusion
Levosimendan may be better than dobutamine for treating patients with a history of CHF or those on β-blocker therapy when they are hospitalized with acute decompensations. These findings are preliminary but important for planning future studies.
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BFBNIB, FZAB, GIS, IJS, IZUM, KILJ, NLZOH, NUK, OILJ, PILJ, PNG, SAZU, SBCE, SBMB, UL, UM, UPUK
Subarachnoid hemorrhage (SAH) frequently results in myocardial necrosis with release of cardiac enzymes. Historically, this necrosis has been attributed to coronary artery disease, coronary ...vasospasm, or oxygen supply-demand mismatch. Experimental evidence, however, indicates that excessive release of norepinephrine from the myocardial sympathetic nerves is the most likely cause. We hypothesized that myocardial necrosis after SAH is a neurally mediated process that is dependent on the severity of neurological injury.
Consecutive patients admitted with SAH were enrolled prospectively. Predictor variables reflecting demographic (age, sex, body surface area), hemodynamic (heart rate, systolic blood pressure), treatment (phenylephrine dose), and neurological (Hunt-Hess score) factors were recorded. Serial cardiac troponin I measurements and echocardiography were performed on days 1, 3, and 6 after enrollment. Troponin level was treated as a dichotomous outcome variable. We performed univariate and multivariate analyses on the relationships between the predictor variables and troponin level.
The study included 223 patients with an average age of 54 years. Twenty percent of the subjects had troponin I levels >1.0 microg/L (range, 0.3 to 50 microg/L). By multivariate logistic regression, a Hunt-Hess score >2, female sex, larger body surface area and left ventricular mass, lower systolic blood pressure, and higher heart rate and phenylephrine dose were independent predictors of troponin elevation.
The degree of neurological injury as measured by the Hunt-Hess grade is a strong, independent predictor of myocardial necrosis after SAH. This finding supports the hypothesis that cardiac injury after SAH is a neurally mediated process.
ABSTRACT—Increased activity of matrix metalloproteinases (MMPs) has been implicated in numerous disease processes, including tumor growth and metastasis, arthritis, and periodontal disease. It is now ...becoming increasingly clear that extracellular matrix degradation by MMPs is also involved in the pathogenesis of cardiovascular disease, including atherosclerosis, restenosis, dilated cardiomyopathy, and myocardial infarction. Administration of synthetic MMP inhibitors in experimental animal models of these cardiovascular diseases significantly inhibits the progression of, respectively, atherosclerotic lesion formation, neointima formation, left ventricular remodeling, pump dysfunction, and infarct healing. This review focuses on the role of MMPs in cardiovascular disease, in particular myocardial infarction and the subsequent progression to heart failure. MMPs, which are present in the myocardium and capable of degrading all the matrix components of the heart, are the driving force behind myocardial matrix remodeling. The recent finding that acute pharmacological inhibition of MMPs or deficiency in MMP-9 attenuates left ventricular dilatation in the infarcted mouse heart led to the proposal that MMP inhibitors could be used as a potential therapy for patients at risk for the development of heart failure after myocardial infarction. Although these promising results encourage the design of clinical trials with MMP inhibitors, there are still several unresolved issues. This review describes the biology of MMPs and discusses new insights into the role of MMPs in several cardiovascular diseases. Attention will be paid to the central role of the plasminogen system as an important activator of MMPs in the remodeling process after myocardial infarction. Finally, we speculate on the use of MMP inhibitors as potential therapy for heart failure.
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