Nonalcoholic Fatty Liver Disease Is Associated With Higher 1-year All-Cause Rehospitalization Rates in Patients Admitted for Acute Heart Failure

Repeat hospitalization due to acute heart failure (HF) is a global public health problem that markedly impacts on health resource use. Identifying novel predictors of rehospitalization would help physicians to determine the optimal postdischarge plan for preventing HF rehospitalization. Nonalcoholic fatty liver disease (NAFLD) is an emerging risk factor for many heart diseases, including HF. We assessed whether NAFLD at hospital admission predicts 1-year all-cause rehospitalization in patients with acute HF.We enrolled all patients consecutively admitted for acute HF to our General Medicine Division, from January 2013 to April 2014, after excluding patients with acute myocardial infarction, severe heart valve diseases, malignancy, known liver diseases, and those with volume overload related to extracardiac causes. NAFLD was diagnosed by ultrasonography and exclusion of competing etiologies. The primary outcome of the study was the 1-year all-cause rehospitalization rate.Among the 107 patients enrolled in the study, the cumulative rehospitalization rate was 12.1% at 1 month, 25.2% at 3 months, 29.9% at 6 months, and 38.3% at 1 year. Patients with NAFLD had markedly higher 1-year rehospitalization rates than those without NAFLD (58% vs 21% at 1 y; P\u200a<\u200a0.001 by the log-rank test). Cox regression analysis revealed that NAFLD was associated with a 5.5-fold increased risk of rehospitalization (adjusted hazard ratio 5.56, 95% confidence interval 2.46-12.1, P\u200a<\u200a0.001) after adjustment for multiple HF risk factors and potential confounders.In conclusion, NAFLD was independently associated with higher 1-year rehospitalization in patients hospitalized for acute HF

Mitral Regurgitation and Increased Risk of All-Cause and Cardiovascular Mortality in Patients with Type 2 Diabetes

Mitral regurgitation is the most common heart valve disease in the general population, but little is known about the prevalence and prognostic implications of mitral regurgitation in patients with type 2 diabetes

FALCÓN, JOSEFINA [Material gráfico]

Copia digital. Madrid : Ministerio de Educación, Cultura y Deporte, 201

Left ventricular chamber dilation and filling pressure may help to categorise patients with type 2 diabetes

Type 2 diabetes may alter cardiac structure and function. Many patients with type 2 diabetes have diastolic dysfunction with preserved ejection fraction (EF). Recently, this latter measure was criticised. Thus, this research looked at the impact of left ventricular end-diastolic volume and E/e' ratio variations in patients with type 2 diabetes and preserved EF with the aim to recognise different clinical phenotypes

Heart valve calcification in patients with type 2 diabetes and nonalcoholic fatty liver disease

PurposeAortic valve sclerosis (AVS) and mitral annulus calcification (MAC) are two powerful predictors of adverse cardiovascular outcomes in patients with type 2 diabetes, but the aetiology of valvular calcification is uncertain. Nonalcoholic fatty liver disease (NAFLD) is an emerging cardiovascular risk factor and is very common in type 2 diabetes, but whether NAFLD is associated with valvular calcification in this group of patients is presently unknown.MethodsWe undertook a cross-sectional study of 247 consecutive type 2 diabetic outpatients with no previous history of heart failure, valvular heart diseases (aortic stenosis, mitral stenosis, moderate or severe aortic and mitral regurgitation) or hepatic diseases. Presence of MAC and AVS was detected by echocardiography. NAFLD was diagnosed by ultrasonography.ResultsOverall, 139 (56.3%) patients had no heart valve calcification (HVC-0), 65 (26.3%) patients had one valve affected (HVC-1) and 43 (17.4%) patients had both valves affected (HVC-2). 175 (70.8%) patients had NAFLD and the prevalence of this disease markedly increased in patients with HVC-2 compared with either HVC-1 or HVC-0 (86.1% vs. 83.1% vs. 60.4%, respectively; p<0.001). NAFLD was significantly associated with AVS and/or MAC (unadjusted-odds ratio 3.51, 95%CI 1.89–6.51, p<0.001). Adjustments for age, sex, waist circumference, smoking, blood pressure, hemoglobin A1c, LDL-cholesterol, kidney function parameters, medication use and echocardiographic variables did not appreciably weaken this association (adjusted-odds ratio 2.70, 95%CI 1.23-7.38, p<0.01).ConclusionsOur results show that NAFLD is an independent predictor of cardiac calcification in both the aortic and mitral valves in patients with type 2 diabetes

Early impairment in left ventricular longitudinal systolic function is associated with an increased risk of incident atrial fibrillation in patients with type 2 diabetes

It is known that type 2 diabetic patients are at high risk of atrial fibrillation (AF). However, the early echocardiographic determinants of AF vulnerability in this patient population remain poorly known

Nonalcoholic Fatty Liver Disease Is Associated With Ventricular Arrhythmias in Patients With Type 2 Diabetes Referred for Clinically Indicated 24-Hour Holter Monitoring

Recent studies have suggested that nonalcoholic fatty liver disease (NAFLD) is associated with an increased risk of heart rate-corrected QT interval prolongation and atrial fibrillation in patients with type 2 diabetes. Currently, no data exist regarding the relationship between NAFLD and ventricular arrhythmias in this patient population

Health relevance of the modification of low grade inflammation in ageing (inflammageing) and the role of nutrition

Ageing of the global population has become a public health concern with an important socio-economic dimension. Ageing is characterized by an increase in the concentration of inflammatory markers in the bloodstream, a phenomenon that has been termed "inflammageing". The inflammatory response is beneficial as an acute, transient reaction to harmful conditions, facilitating the defense, repair, turnover and adaptation of many tissues. However, chronic and low grade inflammation is likely to be detrimental for many tissues and for normal functions. We provide an overview of low grade inflammation (LGI) and determine the potential drivers and the effects of the "inflamed" phenotype observed in the elderly. We discuss the role of gut microbiota and immune system crosstalk and the gut-brain axis. Then, we focus on major health complications associated with LGI in the elderly, including mental health and wellbeing, metabolic abnormalities and infections. Finally, we discuss the possibility of manipulating LGI in the elderly by nutritional interventions. We provide an overview of the evidence that exists in the elderly for omega-3 fatty acid, probiotic, prebiotic, antioxidant and polyphenol interventions as a means to influence LGI. We conclude that slowing, controlling or reversing LGI is likely to be an important way to prevent, or reduce the severity of, age-related functional decline and the onset of conditions affecting health and well-being; that there is evidence to support specific dietary interventions as a strategy to control LGI; and that a continued research focus on this field is warranted

Does high LDL-cholesterol cause cardiovascular disease?

We read with interest the narrative review article written by Ravnskov et al. (1), who had already reiterated in published letters over the past decade their doubts and claims on both the validity of the \u2018cholesterol hypothesis\u2019 and the beneficial effects of statin treatment on risk of incident cardiovascular disease (CVD) events. The authors claim in the final \u201cKey issues\u201d of their review article that (1) the hypothesis that high LDL-cholesterol levels cause atherosclerosis and CVD has been shown to be false by numerous observations and experiments; (2) the assertion that statin treatment is beneficial has been kept alive by individuals who have ignored the results from trials with negative outcomes and by using deceptive statistics; and (3) clinicians should abandon the use of statins and PCSK-9 inhibitors, and instead identify and target the actual causes of CVD. As with most disagreements in life, there is some truth on both sides. It is well recognized that CVD is a complex and multifactorial disease. So, how much the LDL-cholesterol is increased is important and furthermore increased LDL-cholesterol concentrations per se are not the only important issue. Plasma LDL-cholesterol needs to be incorporated into atherosclerotic plaques and that may happen for different reasons in different people. Some people are more resistant to the negative effects of their high LDL-cholesterol than others. That is why the concept of absolute risk is valuable. As clinicians, we would treat middle-aged patients with diabetes, who were smokers and who were hypertensive with a statin, even if their plasma LDL-cholesterol concentrations were considered fairly \u2018normal\u2019, because their absolute risk of CVD events would be considered high enough to intervene with a treatment (a statin) to attempt to lower that absolute risk. In contrast, most clinicans would not treat a teenager without familial hypercholesterolaemia with a modestly high LDL-cholesterol concentration because their absolute risk of CVD is low. As we say in situations like this \u2026 \u2019the devil is in the detail\u2019! We strongly believe that it is not sufficient to say \u2018a high LDL-cholesterol level always or never causes CVD events and mortality!\u2019. Binary interpretations of the data in biology and medicine are far too simplistic an approach

Troponin I after Cardiac Surgery and 30-Day Mortality

Devereaux et al. corroborate the independent negative prognostic effect of increased levels of cardiac troponin I after cardiac surgery,1 reinforcing the notion derived from a meta-analysis of earlier studies2 that the predictive thresholds of 5670 ng per liter after coronary-artery bypass grafting (CABG) and aortic-valve replacement or repair and of 12,981 ng per liter after other cardiac surgery are much higher than the cut-off points endorsed in guidelines3 and provide sufficient prognostic information for identifying those patients with levels below these thresholds for whom there is a low likelihood of a complicated course. Although the authors were unable to differentiate ischemic myocardial damage from procedural injury, it is well recognized that levels of cardiac troponin I increase almost universally after cardiac surgery, and the magnitude of this increase varies depending on the surgical procedure performed and the anesthesia and cardioplegia used.1,4 We believe that their data beg the question of what is now the truly abnormal value of cardiac troponin I after cardiac surgery, because they have moved the threshold bar to particularly high values, thereby suggesting that caution has to be paid as to the clinical judgment used when integrating the variable elevated cardiac troponin I levels into the complex puzzle of other known powerful independent predictors of worse postoperative outcome.