Impairment In Heart Failure Research Articles

Evaluation of the results of magnetic resonance imaging of the brain for cognitive impairment in patients with heart failure: A review

Cognitive impairment is a very common comorbidity in patients with heart failure (HF). Patients with HF show signs of memory decline, difficulty concentrating, and attention deficits. Cognitive dysfunction in HF is associated with a poor prognosis. However, the diagnosis of cognitive impairment in heart failure has received insufficient attention in routine clinical practice. Neuropsychological screening tests are available to screen for cognitive impairment, but they are used infrequently. Therefore, it is of practical interest to search for magnetic resonance equivalents of cognitive disorders. The use of magnetic resonance imaging as a tool for identifying and quantifying neural correlates of cognitive functions is discussed.

Evaluation of renal circulation in heart failure using superb microvascular imaging, a microvascular flow imaging system.

Renal circulation evaluation is essential in understanding the cardiorenal relationship in heart failure (HF), and there is a growing interest in imaging techniques that visualize renal circulation. This study aimed to assess the effectiveness of superb microvascular imaging (SMI) in evaluating renal circulation in HF patients. The study included 71 HF patients undergoing cardiac catheterization. Prior to catheterization, renal ultrasound examinations were performed. A control group of 18 subjects without HF was also included. SMI was used to measure the vascular index (VI), which was calculated as the percentage of blood flow signal area in the region of interest. The intrarenal perfusion index (IRPI) was determined as a fluctuation index of VI, reflecting variations in the number of blood cells moving through renal tissue during the cardiac cycle. Using the upper 95% confidence interval of IRPI (0.6) from the control group, HF patients were classified into two groups. Patients with IRPI > 0.6 showed a more congestive profile. Right atrial pressure and biphasic or monophasic Doppler intrarenal flow pattern were independent determinants of IRPI > 0.6. In addition, IRPI remained a significant predictor of estimated glomerular filtration rate (eGFR). The parameter IRPI as variations in SMI signal during the cardiac cycle may be a useful evaluation method for renal perfusion impairment in HF.

Decipher Cognitive Impairment in Heart Failure by Text Mining

Decipher Cognitive Impairment in Heart Failure by Text Mining

Cognitive impairment in heart failure patients: association with abnormal circadian blood pressure rhythm: a review from the HOPE Asia Network.

Cognitive impairment (CI) is frequently a comorbid condition in heart failure (HF) patients, and is associated with increased cardiovascular events and death. Numerous factors contribute to CI in HF patients. Decreased cerebral blood flow, inflammation, and activation of neurohumoral factors are all thought to be factors that exacerbate CI. Hypoperfusion of the brain due to decreased systemic blood flow, cerebral venous congestion, and atherosclerosis are the main mechanism of CI in HF patients. Abnormal circadian BP rhythm is one of the other conditions associated with CI. The conditions in which BP does not decrease sufficiently or increases during the night are called non-dipper or riser BP patterns. Abnormal circadian BP rhythm worsens CI in HF patients through cerebral congestion during sleep and atherosclerosis due to pressure overload. Interventions for CI in HF patients include treatment for HF itself using cardiovascular drugs, and treatment for fluid retention, one of the causes of abnormal circadian rhythms. Proposed pathways of cognitive impairment in heart failure through abnormal circadian blood pressure rhythm.

Microvascular impairment in heart failure with preserved ejection fraction

Heart failure with preserved ejection fraction (HFpEF) is a cardiovascular disease characterized by diastolic dysfunction. Main risk factors include advanced age, sex (women being more susceptible), and comorbidities like obesity, type 2 diabetes, and renal dysfunction. The etiology of the disease is poorly known. Our pathophysiological hypothesis is that metabolic disorders and renal dysfunction induced by the risk factors generate a systemic pro-inflammatory state and hemodynamical changes that, accumulating with age, are responsible for endothelial dysfunction and pathological reorganization of the microvascular morphology, leading to diastolic dysfunction. The objective of the study was, using an HFpEF mouse model, to (1) identify the metabolic disorders and the renal dysfunction, (2) evaluate the pro-inflammatory state, (3) quantify the cardiac microvascular morphology, and (4) characterize the cardiac diastolic function. Experiments were done on 14-week-old female C57BL/Ks mice, predisposed to renal dysfunction, deficient for leptin receptors, and hence developing obesity and type 2 diabetes. 8-week-old male C57BL/6J mice, lacking HFpEF risk factors, were used as healthy control. Glycemia, triglyceridemia, cholesterolemia, and % pro-inflammatory cells were analyzed on blood samples. 3D imaging of glomeruli was done by light-sheet microscopy (LSM) on optically cleared kidneys. 3D imaging of the coronary capillary network was done by LSM on optically cleared hearts. Diastolic pressure, developed pressure, and relaxation rate was measured on Langendorff's isolated perfused hearts. Compared to controls, HFpEF mice showed increased plasmatic glucose, triglyceride, and cholesterol concentration, and increased monocyte and granulocyte %. Their kidneys had decreased glomerular volume, and compactness. The coronary capillary network was altered in the left and right ventricles. Isolated hearts showed left ventricle diastolic dysfunction. Our study suggests that risk factors induce diastolic dysfunction related to coronary microvascularisation morphological alteration via a systemic pro-inflammatory state. Further studies are needed to investigate hemodynamic alteration and endothelial dysfunction.

Identification and Characterization of p300-Mediated Lysine Residues in Cardiac SERCA2a.

Impaired calcium uptake resulting from reduced expression and activity of the cardiac sarco-endoplasmic reticulum Ca2+ ATPase (SERCA2a) is a hallmark of heart failure (HF). Recently, new mechanisms of SERCA2a regulation, including post-translational modifications (PTMs), have emerged. Our latest analysis of SERCA2a PTMs has identified lysine acetylation as another PTM which might play a significant role in regulating SERCA2a activity. SERCA2a is acetylated, and that acetylation is more prominent in failing human hearts. In this study, we confirmed that p300 interacts with and acetylates SERCA2a in cardiac tissues. Several lysine residues in SERCA2a modulated by p300 were identified using in vitro acetylation assay. Analysis of in vitro acetylated SERCA2a revealed several lysine residues in SERCA2a susceptible to acetylation by p300. Among them, SERCA2a Lys514 (K514) was confirmed to be essential for SERCA2a activity and stability using an acetylated mimicking mutant. Finally, the reintroduction of an acetyl-mimicking mutant of SERCA2a (K514Q) into SERCA2 knockout cardiomyocytes resulted in deteriorated cardiomyocyte function. Taken together, our data demonstrated that p300-mediated acetylation of SERCA2a is a critical PTM that decreases the pump's function and contributes to cardiac impairment in HF. SERCA2a acetylation can be targeted for therapeutic aims for the treatment of HF.

CMR detects decreased myocardial deformation in asymptomatic patients at risk for heart failure.

The main management strategy of heart failure with preserved ejection fraction (HFpEF) is prevention since HFpEF is associated with many cardiovascular (CV) risk factors, especially since HFpEF is linked to a high risk for both mortality and recurrent heart failure (HF) hospitalizations. Therefore, there is a need for new tools to identify patients with a high risk profile early. Regional strain assessment by CMR seems to be superior in describing deformation impairment in HF. The MyoHealth score is a promising tool to identify cardiac changes early. Heart failure patients irrespective of LVEF and asymptomatic controls were recruited, and CMR based measures were obtained. For this analysis the asymptomatic control group (n = 19) was divided into asymptomatic subjects without CV co-morbidities or evidence of cardiac abnormalities and (n = 12) and asymptomatic subjects with CV co-morbidities or evidence of cardiac abnormalities (n = 7) as well as patients with HFpEF (n = 19). We performed CMR scans at rest and during a stress test using isometric handgrip exercise (HG). Assessing the MyoHealth score at rest revealed preserved regional strain in 85 ± 9% of LV segments in controls, 73 ± 11% in at Risk subjects and 73 ± 8% in HFpEF patients. During stress the MyoHealth score was 84 ± 7% in controls, 83 ± 7 in at risk subjects and 74 ± 11 in HFpEF patients. In summary, we show for the first time that asymptomatic subjects with increased CV risk present with HFpEF like impaired myocardial deformation at rest, while they show results like controls under HG stress. The potential of preventive treatment in this group of patients merits further investigation in future. [https://drks.de/search/de/trial/DRKS00015615], identifier [DRKS00015615].

Exercise-induced pulmonary hypertension in HFpEF and HFrEF: Different pathophysiologic mechanism behind similar functional impairment

AimsPathophysiological mechanisms behind cardio-pulmonary impairment in heart failure (HF) with reduced (HFrEF) and preserved (HFpEF) ejection fraction are likely different. We analysed them using combined cardiopulmonary-exercise stress echocardiography (CPET-ESE). MethodsWe matched 1:1 subjects with HFrEF (n = 90) and HFpEF (n = 90) for age, sex, body mass index (BMI), peak oxygen consumption, and minute ventilation/carbon dioxide production slope. All patients underwent a symptom-limited graded ramp bicycle CPET-ESE compared with 40 age-, sex- and BMI-matched healthy controls. ResultsDuring a median follow-up of 25 months, we observed 22 deaths and 80 HF hospitalisations, with similar distribution between HFpEF and HFrEF. Compared with HFrEF, HFpEF had a higher prevalence of metabolic syndrome (p = 0.02) with higher levels of high-sensitivity C-reactive protein and uric acid (p < 0.01). The multipoint mean pulmonary artery pressure/cardiac output (mPAP/CO) slope showed equally increased values in HFrEF and HFpEF (3.5 ± 1.8 and 3.7 ± 1.5 mmHg/L/min) compared with controls (1.8 ± 1.1 mmHg/L/min; p < 0.0001). During exercise, HFpEF displayed more adverse interaction of right ventricle-pulmonary artery (RV-PA; tricuspid annular plane systolic excursion/systolic pulmonary artery pressure: 0.40 ± 0.2 vs 0.47 ± 0.2 mm/mmHg in HFrEF; p < 0.01) and left atrium-left ventricle (LA-LV; LA reservoir strain/LV global longitudinal strain: 1.5 ± 0.8 vs 2.2 ± 1.1 in HFrEF; p < 0.01). The latter were independent predictors of mPAP/CO slope, along with hs-CRP (adjusted R2: 0.21; p < 0.0001). ConclusionDespite similar disease severity, HFpEF and HFrEF show different pathophysiological mechanisms. HFpEF is characterised by a worse LA-LV and RV-PA interaction than HFrEF, with more prevalent low-grade systemic inflammation. In HFpEF, these features may have a role in exercise-induced pulmonary hypertension.

Cognitive Impairment in Heart Failure: Landscape, Challenges, and Future Directions.

Heart failure (HF) is a major global healthcare problem accounting for substantial deterioration of prognosis. As a complex clinical syndrome, HF often coexists with multi-comorbidities of which cognitive impairment (CI) is particularly important. CI is increasing in prevalence among patients with HF and is present in around 40%, even up to 60%, of elderly patients with HF. As a potent and independent prognostic factor, CI significantly increases the hospitalization and mortality and decreases quality of life in patients with HF. There has been a growing awareness of the complex bidirectional interaction between HF and CI as it shares a number of common pathophysiological pathways including reduced cerebral blood flow, inflammation, and neurohumoral activations. Research that focus on the precise mechanism for CI in HF is still ever insufficient. As the tremendous adverse consequences of CI in HF, effective early diagnosis of CI in HF and interventions for these patients may halt disease progression and improve prognosis. The current clinical guidelines in HF have begun to emphasize the importance of CI. However, nearly half of CI in HF is underdiagnosed, and few recommendations are available to guide clinicians about how to approach CI in patients with HF. This review aims to synthesize knowledge about the link between HF and cognitive dysfunction, issues pertaining to screening, diagnosis and management of CI in patients with HF, and emerging therapies for prevention. Based on data from current studies, critical gaps in knowledge of CI in HF are identified, and future research directions to guide the field forward are proposed.

Cognitive Impairment in Heart Failure-A Review.

Simple SummaryCompared to the general population, patients with heart failure have reduced cognition and increased dementia risk. Brain changes have been observed in these individuals, including reduced brain volumes and abnormal areas suggestive of ischaemia (lack of blood and hence oxygen supply to tissues). Patients with heart failure who have cognitive impairment have poorer self-care and are at increased risk of rehospitalisation and death. Causes of cognitive impairment in heart failure have been suggested, including reduced blood supply to the brain, inflammatory processes, protein abnormalities and thromboembolic disease (formation of blood clots which may travel to the brain and impede blood flow). In this article, we discuss these potential causes linking heart failure and cognitive impairment, and discuss the recognition and management of cognitive impairment in patients with heart failure.Cognitive impairment (CI) is common in heart failure (HF). Patients with HF demonstrate reduced global cognition as well as deficits in multiple cognitive domains compared to controls. Degree of CI may be related to HF severity. HF has also been associated with an increased risk of dementia. Anatomical brain changes have been observed in patients with HF, including grey matter atrophy and increased white matter lesions. Patients with HF and CI have poorer functional independence and self-care, more frequent rehospitalisations as well as increased mortality. Pathophysiological pathways linking HF and CI have been proposed, including cerebral hypoperfusion and impaired cerebrovascular autoregulation, systemic inflammation, proteotoxicity and thromboembolic disease. However, these mechanisms are poorly understood. We conducted a search on MEDLINE, Embase and Scopus for original research exploring the connection between HF and CI. We then reviewed the relevant literature and discuss the associations between HF and CI, the patterns of brain injury in HF and their potential mechanisms, as well as the recognition and management of CI in patients with HF.

Skeletal consequences of heart failure.

Heart failure (HF) is a prevalent clinical syndrome that causes significant physical limitations. Osteoporosis is also an important cause of loss of functionality, and it mainly affects women. There are several reports linking HF and osteoporosis, and both share risk factors. Most of the data available so far point to bone fragility as a consequence of HF, and several mechanisms have been identified to explain this relationship. Among the proposed pathophysiological mechanisms are the hyperactivation of the renin-angiotensin-aldosterone system and the increase in parathyroid hormone, functional limitation, production of inflammatory mediators and the use of drugs for HF. The role of osteoprotegerin has gained attention owing to its cardiovascular and skeletal effects, its observed deficiency during the postmenopausal period along with its compensatory increases in HF and severe osteoporosis. The objective of this review was to perform a literature search for the main evidence on skeletal impairment in HF, with emphasis on women. As for epidemiological studies, we selected data from 3 meta-analyses and 20 individual observational studies, which together showed the interrelationship between the two clinical conditions in terms of both decreased bone density and increased fracture risk. In conclusion, HF and osteoporosis are interrelated conditions mediated by complex pathophysiological mechanisms which may be more relevant for postmenopausal women, considered to be a vulnerable population for both cardiovascular diseases and bone fragility.

Cardiomyocyte contractile impairment in heart failure results from reduced BAG3-mediated sarcomeric protein turnover

The association between reduced myofilament force-generating capacity (Fmax) and heart failure (HF) is clear, however the underlying molecular mechanisms are poorly understood. Here, we show impaired Fmax arises from reduced BAG3-mediated sarcomere turnover. Myofilament BAG3 expression decreases in human HF and positively correlates with Fmax. We confirm this relationship using BAG3 haploinsufficient mice, which display reduced Fmax and increased myofilament ubiquitination, suggesting impaired protein turnover. We show cardiac BAG3 operates via chaperone-assisted selective autophagy (CASA), conserved from skeletal muscle, and confirm sarcomeric CASA complex localization is BAG3/proteotoxic stress-dependent. Using mass spectrometry, we characterize the myofilament CASA interactome in the human heart and identify eight clients of BAG3-mediated turnover. To determine if increasing BAG3 expression in HF can restore sarcomere proteostasis/Fmax, HF mice were treated with rAAV9-BAG3. Gene therapy fully rescued Fmax and CASA protein turnover after four weeks. Our findings indicate BAG3-mediated sarcomere turnover is fundamental for myofilament functional maintenance.

Cognitive impairment in heart failure: clinical implications, tools of assessment, and therapeutic considerations.

Cognitive impairment (CI) is an important comorbidity in patients with heart failure (HF). Its prevalence parallels the severity of heart failure, while it is an independent prognostic marker of adverse events. Various factors contribute to cognitive decline in HF, influencing self-care. There are no standardized screening methods for the diagnosis and management of these patients. The aim of the present manuscript is to provide an overview of the impact of cognitive impairment in HF, describe the utility of assessment tools and imaging methods for the evaluation of CI, and propose a comprehensive diagnostic and management approach.

Cognitive impairment in myocardial infarction and heart failure

Myocardial infarction (MI) occurs when coronary blood flow is decreased due to an obstruction/occlusion of the vessels, leading to myocardial death and progression to heart failure (HF). Cognitive impairment, anxiety, depression and memory loss are the most frequent mental health problems among patients with HF. The most common cause of cognitive decline is cardiac systolic dysfunction, which leads to reduced cerebral perfusion. Several in vivo and clinical studies provide information regarding the underlying mechanisms of HF in brain pathology. Neurohormonal activation, oxidative stress, inflammation, glial activation, dendritic spine loss and brain programmed cell death are all proposed as contributors of cognitive impairment in HF. Furthermore, several investigations into the effects of various medications on brain pathology utilizing MI models have been reported. In this review, potential mechanisms involving HF-associated cognitive impairment, as well as neuroprotective interventions in HF models, are discussed and summarized. In addition, gaps in the surrounding knowledge, including the types of brain cell death and the effects of cell death inhibitors in HF, are presented and discussed. This review provides valuable information that will suggest the potential therapeutic strategies for cognitive impairment in patients with HF.

Pathophysiology of Cardiorenal Syndrome and Use of Diuretics and Ultrafiltration as Volume Control.

Acute or chronic dysfunction of the heart or kidneys can cause dysfunction of other organs. This interaction between the heart and kidneys is characterized as cardiorenal syndrome (CRS). Recently, a preponderance of data indicated that venous congestion plays an important role in the combination of renal and cardiac diseases. This review aims to focus on the pathophysiology of venous congestion that leads to renal impairment in heart failure and the use of diuretics or ultrafiltration as decongestive therapy in CRS. We found that although clinical studies have confirmed that decongestive therapy has a definite role in decreasing volume overload and the consequent symptom improvement in patients with CRS, the impact of diuretics or ultrafiltration on the improvement of kidney function or mortality remains uncertain. A precise assessment of volume status is required to determine the adequacy of decongestion. Objective measures of renal venous congestion may be a future metric to assess the adequacy of the diuretic response in patients and guide therapeutic decision making.

Chapter 8 - Neurological complications of heart failure

Heart failure (HF) is a major global cause of death with increasing absolute worldwide numbers of HF patients. HF results from the interaction between cardiovascular aging with specific risk factors, comorbidities, and disease modifiers. The failing heart and neuronal injury have a bidirectional interaction requiring specific management strategies. Decreased cardiac output has been associated with lower brain volumes. Cerebral blood flow (CBF) may normalize following heart transplantation among severe HF patients. Stroke and cognitive impairment remain the main neurologic conditions associated with HF. However, HF patients may also suffer from chronic cerebral hypoperfusion. It seems likely that HF-related ischemic strokes are primarily the result of cardiac embolism. Atrial fibrillation (AF) is present in half of stroke patient with HF. The increased risk of hemorrhagic strokes is less well characterized and likely multifactorial, but may in part reflect a higher use of long-term antithrombotic therapy. The steady improvement of neuroimaging techniques has demonstrated an increased prevalence of silent ischemic lesions among HF patients. The populations most likely to benefit from long-term anticoagulant therapy are HF patients with AF. Cognitive impairment in HF can have a variety of clinical manifestations from mild memory problems to dementia.

Gray matter atrophy, but not vascular brain injury is related to cognitive impairment in patients with heart failure

AbstractBackgroundCognitive impairment in heart failure (HF) interferes with the capacity to self‐care and is associated with adverse health outcomes. This underlines the importance of detecting the extent and nature of cognitive impairment in HF. We report on the presence and mutual association of neuroimaging markers and cognitive impairment in patients with HF.MethodWe included 147 patients with HF (69±10yrs; 32%F; MMSE 29±1) and 121 reference participants (66±8yrs; 46%F; MMSE 29±1) from the Dutch multicenter Heart‐Brain study. Brain MRI scans were rated for (lacunar) infarcts and microbleeds. Total grey and white matter volume, hippocampal volume and white matter hyperintensity (WMH) volume were calculated. We used a standardized neuropsychological test battery to measure cognition and calculated compound z‐scores for each cognitive domain. Associations between neuroimaging markers and cognitive functioning were investigated using linear regression analyses, with separate models for each cognitive domain. We adjusted for participant group, age, sex and education. To investigate whether associations differed according to participant group, interaction terms were included in our analyses.ResultPatients with HF had lower total grey matter volume and more vascular brain injury compared to the reference group, including WMH (median (interquartile range) 1.7(40) versus 0.6(1.8), p&lt;0.001), (sub‐)cortical infarcts (13% versus 3%, p&lt;0.01) and lacunar infarcts (28% versus 10%, p&lt;0.001). Cognitive impairment was found in 18% of HF, most often in the domains of memory and attention/psychomotor speed. Overall, we found associations between smaller total grey matter volume and worse global cognition, more cortical and lacunar infarcts (standardized beta [stβ]=‐0.14‐0.56, p&lt;0.05). Stratification for participant group showed associations between worse global cognition and smaller total (stβ=0.43, p&lt;0.01) and hippocampal (stβ=0.22, p&lt;0.05) grey matter volumes in HF. We found no association between cognition and vascular brain injury.ConclusionPatients with HF exhibit cognitive deficits more pronounced in the domains of memory and attention/psychomotor speed. Grey matter atrophy, but not vascular brain injury seems to be related to cognitive impairment in HF.

Gray matter atrophy but not vascular brain injury is related to cognitive impairment in patients with heart failure

Abstract Background Cognitive impairment in heart failure (HF) interferes with the capacity to self-care and is associated with adverse health outcomes. This underlines the importance of detecting the extent and nature of cognitive impairment in HF. We report on the presence and mutual association of neuroimaging markers and cognitive impairment in patients with HF. Method We included 147 patients with HF (69±10yrs; 32%F; MMSE 29±1) and 121 reference participants (66±8yrs; 46%F; MMSE 29±1) from the Dutch multicenter Heart-Brain study. Brain MRI scans were rated for (lacunar) infarcts and microbleeds. Total grey and white matter volume, hippocampal volume and white matter hyperintensity (WMH) volume were calculated. We used a standardized neuropsychological test battery to measure cognition and calculated compound z-scores for each cognitive domain. Associations between neuroimaging markers and cognitive functioning were investigated using linear regression analyses, with separate models for each cognitive domain. We adjusted for participant group, age, sex and education. To investigate whether associations differed according to participant group, interaction terms were included in our analyses. Result Patients with HF had lower total grey matter volume and more vascular brain injury compared to the reference group, including WMH (median (interquartile range) 1.7 (40) versus 0.6 (1.8), p&amp;lt;0.001), (sub-)cortical infarcts (13% versus 3%, p&amp;lt;0.01) and lacunar infarcts (28% versus 10%, p&amp;lt;0.001). Cognitive impairment was found in 18% of HF, most often in the domains of memory and attention/psychomotor speed. Overall, we found associations between smaller total grey matter volume and worse global cognition, more cortical and lacunar infarcts (standardized beta [stβ] = −0.14–0.56, p&amp;lt;0.05). Stratification for participant group showed associations between worse global cognition and smaller total (stβ=0.43, p&amp;lt;0.01) and hippocampal (stβ=0.22, p&amp;lt;0.05) grey matter volumes in HF. We found no association between cognition and vascular brain injury. Conclusion Patients with HF exhibit cognitive deficits more pronounced in the domains of memory and attention/psychomotor speed. Grey matter atrophy, but not vascular brain injury seems to be related to cognitive impairment in HF. Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): Cardiovasculair Onderzoek Nederland (CVON)

Neurovascular Coupling Impairment in Heart Failure with Reduction Ejection Fraction.

The hemodynamic consequences of a persistent reduced ejection fraction and unknown cardiac output on the brain have not been thoroughly studied. We sought to explore the status of the mechanisms of cerebrovascular regulation in patients with heart failure with reduced (HFrEF) and recovered (HFrecEF) ejection fraction. We monitored cerebral blood flow velocity (CBFV) with transcranial Doppler and blood pressure. Cerebral autoregulation, assessed by transfer function from the spontaneous oscillations of blood pressure to CBFV and neurovascular coupling (NVC) with visual stimulation were compared between groups of HFrEF, HFrecEF and healthy controls. NVC was significantly impaired in HFrEF patients with reduced augmentation of CBFV during stimulation (overshoot systolic CBFV 19.11 ± 6.92 vs. 22.61 ± 7.78 vs. 27.92 ± 6.84, p = 0.04), slower upright of CBFV (rate time to overshoot: 1.19 ± 3.0 vs. 3.06 (4.30) vs. 2.90 ± 3.84, p = 0.02); p = 0.023) and reduced arterial oscillatory properties (natural frequency 0.17 ± 0.06 vs. 0.20 ± 0.09 vs. 0.24 ± 0.07, p = 0.03; attenuation 0.34 ± 0.24 vs. 0.48 ± 0.35 vs. 0.50 ± 0.23, p = 0.05). Cerebral autoregulation was preserved. The neurovascular unit of subjects with chronically reduced heart pumping capability is severely dysfunctional. Dynamic testing with transcranial Doppler could be useful in these patients, but whether it helps in predicting cognitive impairment must be addressed in future prospective studies.

Somatization disorder mediates the association of depression and anxiety with functional impairment in patients with heart failure

ABSTRACT Previous studies have suggested that depression, anxiety, and somatization disorder are strongly associated with diminished functional status. However, research has not tested the mediational models of how depression and anxiety lead to functional impairment. The aim of this study was to examine whether somatization disorder mediates the association of depression and anxiety with functional impairment in heart failure (HF) patients. The self-reported questionnaires were applied to measure depression, anxiety, and somatization disorder. Functional status was evaluated by the NYHA Class. Ordinal logistic regression analysis was performed to examine the association of depression, anxiety, and somatization disorder with functional status. Mediation analysis was conducted to determine indirect effects. Functional impairment was both related to depression (OR = 2.257, 95% CI = 1.534–3.322, P < 0.001) and elevated somatization severity (OR = 1.042, 95% CI = 1.003–1.082, P = 0.032) in HF patients, whereas anxiety was not associated with functional impairment (OR = 0.659, 95% CI = 0.429–1.012, P > 0.05). Mediation analysis indicated that both depression and anxiety have indirect effects on functional impairment as mediated by somatization disorder in HF patients. Additionally, depression has direct effect on functional impairment of the patients.