Pathophysiology Of Congestive Heart Failure Research Articles

Congestive Coronary Heart Failure

Congestive heart failure (CHF) is a continual condition characterized by the heart's inability to pump blood efficiently, which is essential for the buildup of fluid within the lungs and distinctive components of the body. It is a critical and regular health problem globally, affecting hundreds of thousands of people, primarily the elderly. CHF can cease owing to several underlying reasons, including coronary artery sickness, excessive blood strain, heart valve troubles, and cardiomyopathy. This summary aims to define CHF together with its pathophysiology, threat elements, clinical manifestations, analysis, and control. The pathophysiology of CHF includes weakening of the coronary heart muscle, which can also occur because of harm from preceding coronary heart attacks, extended high blood pressure, or special elements affecting coronary heart features. Because the pumping ability of the heart diminishes, blood glide in critical organs becomes inadequate, leading to symptoms, shortness of breath, fatigue, and fluid retention. Numerous risk factors contribute to the development of CHF, including age, coronary heart sickness, obesity, diabetes, smoking, and a sedentary lifestyle. Early diagnosis of CHF is critical for saving the patient from improving and decorating consequences. Diagnostic methods may additionally include medical records, physical examinations, imaging checks such as echocardiography, and blood tests to evaluate coronary heart characteristics and discover the underlying functionality. CHF control aims to alleviate signs and symptoms, sluggish sickness development, and enhance the pleasantness of life. Treatment strategies usually involve lifestyle changes such as adopting a coronary heart-wholesome diet, engaging in regular exercise, and quitting smoking. Medicinal pills such as diuretics, ACE inhibitors, beta-blockers, and angiotensin receptor blockers are prescribed to enhance coronary heart characteristics and decrease signs and signs. In severe cases, surgical interventions, such as coronary artery pass grafting or coronary heart transplantation, can be considered. As CHF is a continual condition, affected individual education and regular compliance with healthcare carriers are vital to display the ailment's improvement and regulate remedies. With improvements in scientific treatment plans and early detection, CHF analysis has advanced over the years. However, it remains a vast public health challenge, necessitating continuous research and cognizance efforts to beautify affected person consequences and decrease the load of this situation on affected human beings and healthcare systems.

Breakthrough: a first-in-class virtual simulator for dose optimization of ACE inhibitors in translational cardiovascular medicine

The renin–angiotensin–aldosterone-systems (RAAS) play a central role in the pathophysiology of congestive heart failure (CHF), justifying the use of angiotensin converting enzyme inhibitors (ACEi) in dogs and humans with cardiac diseases. Seminal studies in canine CHF had suggested that the pharmacological action of benazepril was relatively independent of doses greater than 0.25 mg/kg P.O, thereby providing a rationale for the European labeled dose of benazepril in dogs with CHF. However, most of these earlier studies relied on measures of ACE activity, a sub-optimal endpoint to characterize the effect of ACEi on the RAAS. The objectives of this study were (i) to expand on previous mathematical modeling efforts of the dose-exposure–response relationship of benazepril on biomarkers of the RAAS which are relevant to CHF pathophysiology and disease prognosis; and (ii) to develop a software implementation capable of simulating clinical trials in benazepril in dogs bedside dose optimization. Our results suggest that 0.5 mg/kg PO q12h of benazepril produces the most robust reduction in angiotensin II and upregulation of RAAS alternative pathway biomarkers. This model will eventually be expanded to include relevant clinical endpoints, which will be evaluated in an upcoming prospective trial in canine patients with CHF.

TRH and TRH-like peptide levels covary with caloric restriction and oral metformin in rat heart and testis

BackgroundObesity, type 2 diabetes, and major depression are common comorbidities in aging populations. Metformin (MF) mimics effects of caloric restriction (CR) which increases health and life spans. CR suppresses central TRH activity resulting in bradycardia and suppression of energy expenditure. TRH and TRH-like peptides with sequence pGlu-X-Pro-NH2, (X-TRH) where ‘X’ can be any amino acid residue, have anorectic, antidepressant, anxiolytic, analeptic, anti-epileptic, neuroprotective and anti-aging effects. The present studies compare the effects of CR and oral MF on expression of TRH and TRH-like peptides. CR experiment: Sixteen male Sprague-Dawley rats divided into 4 groups: ad libitum fed (CR-CON), 24 h fasted (CR-AC), fed (ADF1) or fasted (ADF2) 24 h after 10 days of alternate day fasting. MF experiment: Sixteen rats divided into 4 groups: water (MF-CON), 6 mg MF/ml water 24 h (MF-AC), 10 days MF (CHR) or 8 days MF then 48 h water (WD). ResultsComparison of chronic MF and ADF2 treatment effects on TRH and TRH-like peptide levels in testis revealed a consistent pattern for peptide responses observed in the two experiments with Glu-TRH > Val-TRH > TRH > Peak 2 > Trp-TRH > Phe-TRH > Tyr-TRH. TRH levels increased in heart during CR and MF treatment consistent with cardiac responses to congestive heart failure and infarction. ConclusionsBecause TRH reverses aging-induced testicular degeneration and mediates the pathophysiology of congestive heart failure these tripeptides may participate in the therapeutic effects of MF in ameliorating the cardiometabolic risk factors and fertility impairments associated with type 2 diabetes.

Detection of Congestive Heart Failure and Myocardial Dysfunction in Cats With Cardiomyopathy by Using Two-Dimensional Speckle-Tracking Echocardiography.

Congestive heart failure (CHF) is a life-threatening condition in cats with cardiomyopathy. We hypothesized that myocardial dysfunction may induce progression to CHF pathophysiology in cats with cardiomyopathy. However, no previous studies have evaluated the involvement of myocardial dysfunction in cats with CHF. In this study, we aimed to evaluate the relationship between CHF and myocardial function assessed using two-dimensional speckle-tracking echocardiography (2D-STE). Sixteen client-owned healthy cats and 32 cats with cardiomyopathy were enrolled in this study. Cats were classified into three groups: healthy cats, cardiomyopathy without CHF (CM group), and cardiomyopathy with CHF (CHF group). Left ventricular (LV) longitudinal and circumferential strains (SL and SC, respectively), and right ventricular (RV) SL were measured using 2D-STE. Logistic regression analysis was performed to assess the relationship between CHF and echocardiographic variables, including 2D-STE. Results comparing the healthy cats and CM vs. CHF groups showed that increased left atrial to aortic diameter ratio and decreased LV apical SC were significantly associated with the existence of CHF (odds ratio [95% confidence interval]: 1.40 [1.16–1.78] and 1.59 [1.06–2.36], respectively). Results comparing the CM vs. CHF group showed that increased end-diastolic RV internal dimension and decreased RV SL were significantly associated with the existence of CHF (odds ratio: 1.07 [1.00–1.13] and 1.34 [1.07–1.68], respectively). Left atrial enlargement and depressed LV apical myocardial function may be useful tools for predicting the progression to CHF in cats. Furthermore, RV enlargement and dysfunction may lead to the onset of CHF in asymptomatic cats with cardiomyopathy.

Cardiac and pulmonary emergencies: Protocols for effective management and treatment via pharmacists, emergency medical services, and the role of health informatics in future responses

Background: The aging population in the U.S. is rapidly increasing, with those aged 65 and older expected to reach 95 million in the next 40 years. This demographic shift leads to a higher prevalence of cardiopulmonary emergencies, which are commonly encountered in emergency departments (EDs). This paper explores four prevalent conditions—atrial fibrillation (AF), congestive heart failure (CHF), pulmonary embolism (PE), and pneumonia—and their specific considerations in elderly patients. Aim: To review the management protocols for these cardiopulmonary conditions in older adults and to highlight the unique challenges and considerations associated with their treatment and management via pharmacists and ED. The review also focus on the main role of health information system in the future responses to cardiac and pulmonary conditions. Methods: The study involves a comprehensive review of current literature on the epidemiology, pathophysiology, and management of AF, CHF, PE, and pneumonia in elderly patients. The focus is on treatment protocols, diagnostic strategies, and the impact of age-related factors on disease management. Results: Effective management of these conditions requires tailored approaches due to age-related physiological changes. For AF, anticoagulation therapy is crucial but must be carefully balanced against bleeding risks.

Ultrafiltration for management of fluid overload in patients with heart failure.

Heart failure is the number one cause of death in the United States and a significant burden to the healthcare system. One of the primary complications of heart failure is fluid overload, for which current treatments are limited. Medical therapy is first-line; however, rates of diuretic insensitivity are high, medications are not easily titrated, and they do not address the underlying physiologic derangement that leads to hypervolemia. Removal of isotonic fluid via hemofiltration and peritoneal dialysis is an understudied but promising therapy that enables decongestion without maladaptive stimulation of fluid retention pathways. Published studies report conflicting data on long-term outcomes of ultrafiltration but reach consensus on greater and more durable volume reduction with ultrafiltration than conventional medical therapy. These studies are noteworthy for their neglect to standardize both patient selection and fluid removal protocol, which likely contribute to outcome variation. Novel technology in preclinical testing includes implantable ultrafiltration, which has potential to treat volume overload while minimizing the adverse effects associated with conventional hemofiltration. We performed a literature review of English-language studies on hemo- and peritoneal filtration for management of fluid overload in congestive heart failure. Also included is a discussion of the pathophysiology of congestive heart failure and first-line management as well as emerging technologies for ultrafiltration.

Endothelial Progenitor Cells in Heart Failure: an Authentic Expectation for Potential Future Use and a Lack of Universal Definition

Congestive heart failure (CHF) is a prevalent disease (especially among the elderly) with high mortality and morbidity rates. The pathological hallmark of CHF is a loss of cardiomyocytes leading to cardiac fibrosis and dysfunctional cardiac remodeling, which culminates in organ failure. Endothelial progenitor cells (EPCs) are bone marrow-derived cells that contribute to maintenance of the integrity of endothelial wall and protect ischemic myocardium through forming new blood vessels (vasculogenesis) or proliferation of pre-existing vasculature (angiogenesis). Despite its potential, little is known about EPCs and their function in CHF. Here, we define EPC and its role in health and CHF, highlighting their contributions as a cornerstone in the maintenance of a healthy endothelium. Thereafter, we explore the behavior and relevance of EPCs in the pathophysiology of CHF, their prognostic importance, and possible utilization of EPCs as therapy for CHF. Lastly, the restrictions surrounding the use of EPCs in clinical practice will be discussed.

Mortality Prediction in Severe Congestive Heart Failure Patients with Multifractal Point-Process Modeling of Heartbeat Dynamics.

Multifractal analysis of human heartbeat dynamics has been demonstrated to provide promising markers of Congestive Heart Failure (CHF). Yet, it crucially builds on the interpolation of RR intervals series, which has been generically performed with limited links to CHF pathophysiology. We devise a novel methodology estimating multifractal autonomic dynamics from heartbeat-derived series defined in the continuous time. We hypothesize that markers estimated from our novel framework are also effective for mortality prediction in severe CHF. We merge multifractal analysis within a methodological framework based on inhomogeneous point process models of heartbeat dynamics. Specifically, wavelet coefficients and wavelet leaders are computed over measures extracted from instantaneous statistics of probability density functions characterizing and predicting the time until the next heartbeat event occurs. The proposed approach is tested on data from 94 CHF patients, aiming at predicting survivor and non-survivor individuals as determined after a 4 years follow up. Instantaneous markers of vagal and sympatho-vagal dynamics display power-law scaling for a large range of scales, from s to s. Using standard SVM algorithms, the proposed inhomogeneous point-process representation based multifractal analysis achieved the best CHF mortality prediction accuracy of 79.11 % (sensitivity 90.48%, specificity 67.74%). Our results suggest that heartbeat scaling and multifractal properties in CHF patients are not generated at the sinus-node level, but rather by the intrinsic action of vagal short-term control and of sympatho-vagal fluctuations associated with circadian cardiovascular control, especially within the VLF band. These markers might provide critical information in devising a clinical tool for individualized prediction of survivor and non-survivor CHF patients.

333 - Predicting Readmission Risk: A Promising Heart Failure Bedside Risk Stratification Tool

Introduction: Although many individual factors have been reported to worsen the prognosis of congestive heart failure (CHF) patients, it is challenging to build an accurate risk stratification tool for physicians and other health care providers to utilize at the point of care to identify patients at risk for readmissions. Limiting factors can include: correlations among reported prognostic factors; healthcare systems' lack of patients' social determinant and behavioral factor data; and difficulty embedding the risk stratification tools into healthcare providers' workflow. Hypothesis: We hypothesized that a model derived from a holistic conceptual framework of readmissions based on CHF's pathophysiology and prognosis would accurately stratify risk for readmissions among CHF patients. In addition, we hypothesized that a simple flowchart developed based on the risk model could suffice to facilitate bedside decisions when operationalizing a full predictive model into workflow was not feasible. Methods: Inpatient admissions with a primary discharge diagnosis of CHF from a large urban academic hospital between May 2013 and April 2016 were studied. A risk stratification model was derived and cross-validated from clinical and nonclinical factors to predict risk of 30-day unplanned all-cause readmission to the same facility. A flowchart was then developed based on the risk model. All data were extracted from electronic medical records and administrative data. Results: The 30-day readmission rate of the CHF study population was 15.23%. The model with 48 predictors demonstrated good discrimination (C statistic 0.77, 95% CI: 0.74 - 0.79) and calibration (Goodness-of-fit P = .8) for readmission. When using 0.15 (the prevalence rate) as the probability threshold for at-risk, the model resulted in a sensitivity of 0.74, specificity of 0.70, positive predictive value of 0.30, and negative predictive value of 0.94. Per the model, by reaching out to the patients with a predicted probability above the threshold (which was 38% of the patients discharged), we could capture 74% of the true readmissions. The flowchart containing only five factors demonstrated a reduced sensitivity, but similar specificity and predictive values as the model. Conclusions: Clinical and non-clinical factors derived from a holistic conceptual framework of readmissions demonstrated promising capability of accurately stratifying risk for readmissions among CHF patients. Risk stratification models may be simplified into a flowchart with acceptable reduction in performance to facilitate use at the point of care.

Implications of Cardiac Resynchronisation Therapy (Crt) on the Pathophysiology of Congestive Heart Failure: Focus on Endothelial Function and Inflammatory Activation

Implications of Cardiac Resynchronisation Therapy (Crt) on the Pathophysiology of Congestive Heart Failure: Focus on Endothelial Function and Inflammatory Activation

Metabolic Syndrome : an Emerging Risk Factor for Congestive Heart Failure

Background : Congestive heart failure (CHF) and metabolic syndrome (MetS) are both current major cardiovascular problems. Until recently, the connection between them has not been well understood yet. Mets is composed by several facets which is closely related with the pathophysiology of CHF. This study will try to discuss the relationship between Mets and CHF.Methods: We conducted an observational analytic study using cross sectional design. Subjects were gathered from January until March 2015. All data are descriptively presented, and analyzed using bivariate and multivariate method.Results: MetS itself does not account as risk factor for CHF (OR 1,49; CI95% 0,67-3,32; p=0,328). Component of Mets which shows significant relationship with CHF are raised blood pressure (OR 6,82; CI95% 1,47-31,53; p=0,014) and impaired glucose tolerance (OR 5,95; CI95% 3,26-10,85; p=0,000)Conclusion: Some elements of Mets, not Mets per se, are strong independent predictor for congestive heart failure.

Advanced Congestive Heart Failure Associated With Disseminated Intravascular Coagulopathy.

Background. Disseminated intravascular coagulopathy (DIC) is a complication of an underlying disease and not a primary illness. It is most commonly associated with sepsis, trauma, obstetrical complications, and malignancies. There are very few cases in the literature illustrating the association between DIC and congestive heart failure. Findings. In this report, we present a case of severe congestive heart failure, leading to biventricular thrombi and subsequently DIC. Conclusion. We suggest that the association between congestive heart failure and DIC is an underrecognized one. Congestive heart failure continues to remain a major cause of morbidity and mortality despite advances in medical therapies. Thus far, the precise role of coagulation factors in congestive heart failure is unknown. Further investigations are needed to elucidate the pathophysiology of congestive heart failure and coagulation factors.

Chronobiology and Pharmacologic Modulation of the Renin-Angiotensin-Aldosterone System in Dogs: What Have We Learned?

Congestive heart failure (CHF) is a primary cause of morbidity and mortality with an increasing prevalence in human and canine populations. Recognition of the role of renin-angiotensin-aldosterone system (RAAS) overactivation in the pathophysiology of CHF has led to significant medical advances. By decreasing systemic vascular resistance and angiotensin II (AII) production, angiotensin-converting enzyme (ACE) inhibitors such as benazepril improve cardiac hemodynamics and reduce mortality in human and dog CHF patients. Although several experiments have pointed out that efficacy of ACE inhibitors depends on the time of administration, little attention is paid to the optimum time of dosing of these medications. A thorough characterization of the chronobiology of the renin cascade has the potential to streamline the therapeutic management of RAAS-related diseases and to help determining the optimal time of drug administration that maximizes efficacy of ACE inhibitors, while minimizing the occurrence of adverse effects. We have developed an integrated pharmacokinetic-pharmacodynamic model that adequately captures the disposition kinetics of the paradigm drug benazeprilat, as well as the time-varying changes of systemic renin-angiotensin-aldosterone biomarkers, without and with ACE inhibition therapy. Based on these chronobiological investigations, the optimal efficacy of ACE inhibitors is expected with bedtime dosing. The data further show that benazepril influences the dynamics of the renin-angiotensin-aldosterone cascade, resulting in a profound decrease in AII and aldosterone (ALD), while increasing renin activity for about 24h. From the results of recent investigations in human, it is hypothesized that reduction of AII and ALD is one of the drivers of increased survival and improved quality of life in dogs receiving ACE inhibitors. To support and consolidate this hypothesis, additional efforts should be directed toward the collection of circulating RAAS peptides in spontaneous cases of canine CHF. If such a link could be established, profiling of these biomarkers could support determination of the severity of heart failure, complement clinical and echocardiographic findings, and be used for therapeutic drug monitoring purposes.

PREVALENCE OF VITAMIN D DEFICIENCY IN CANADIAN HEART FAILURE PATIENTS AND INSIGHTS IN TO THE ROLE OF VITAMIN D DEFICIENCY IN THE PATHOPHYSIOLOGY OF HEART FAILURE

Vitamin D has been implicated in the pathophysiology of congestive heart failure (CHF) and vitamin D status has been shown to be inversely associated with increased hospitalization and mortality. The aim of this study was to investigate the prevalence of vitamin D deficiency in a North American heart failure patient population and to investigate potential mechanisms through which Vitamin D deficiency can lead to worse clinical outcomes in patients with CHF. Patients seen in consultation in our heart function clinic were enrolled in this observational study and were randomized to 1 of 3 groups based on their vitamin D levels. The following results are the baseline results of the first 86 patients enrolled. 68.6% (59/86) of patients screened and enrolled, demonstrated Vitamin D insufficiency (<75nmol/L), with 15% (13/86) having severe insufficiency (<35nmol/L). There was no difference in the baseline mean NYHA class, left ventricular ejection fraction (LVEF), brain natureitic peptide (BNP), renal function or inflammatory status, irrespective of the baseline vitamin D status (TABLE). Despite a high prevalence of vitamin D deficiency, amongst our heart failure patients, reduced serum levels of Vitamin D did not correlate with poor baseline characteristics. Vitamin D deficiency was however associated with elevated levels of serum PIIINP, which has been shown to be a poor prognostic marker in patients with ventricular dysfunction. Whether Vitamin D deficiency leads poor clinical outcome in our population remains to be elucidated. Furthermore, the molecular mechanism by which vitamin D deficiency results in increased collagen turnover and it overall cardiac sequeale remains to be elucidated.

Is carotid body denervation the silver bullet for heart failure?

The carotid body chemoreceptors are traditionally viewed as the body's primary oxygen sensors. Activation of the carotid body chemoreceptors in response to a fall in arterial oxygen levels results in reflex increases in both ventilation and sympathetic nervous system activity. Additionally, a growing body of experimental evidence in both animals and humans supports a role for the carotid body chemoreceptors in the pathophysiology of several sympathoexcitatory conditions such as hypertension, sleep apnoea and congestive heart failure (CHF). Consistent with this idea, in a recent issue of The Journal Physiology, Marcus and colleagues (Marcus et al. 2013) confirmed that the carotid body chemoreceptors play a central role in CHF pathophysiology. Expanding on their previous experiments in rats (Del Rio et al. 2013), Marcus et al. induced CHF in a group of rabbits through ventricular pacing and examined the effect of carotid body denervation on ventilation, autonomic nervous system activity and markers of cardiac function. Remarkably, only 9 days after denervation, a number of ventilatory, autonomic and cardiac function variables commonly impaired in CHF were improved. These results raise several important questions regarding the contribution of the carotid body chemoreceptors to CHF pathophysiology: how does carotid body denervation initiate improvements in CHF; what is the link between the carotid body chemoreceptors and cardiac function in CHF; could carotid body denervation replace traditional therapeutic strategies for CHF?

The Indian Consensus Document on cardiac biomarker

Despite recent advances, the diagnosis and management of heart failure evades the clinicians. The etiology of congestive heart failure (CHF) in the Indian scenario comprises of coronary artery disease, diabetes mellitus and hypertension. With better insights into the pathophysiology of CHF, biomarkers have evolved rapidly and received diagnostic and prognostic value. In CHF biomarkers prove as measures of the extent of pathophysiological derangement; examples include biomarkers of myocyte necrosis, myocardial remodeling, neurohormonal activation, etc. In CHF biomarkers act as indicators for the presence, degree of severity and prognosis of the disease, they may be employed in combination with the present conventional clinical assessments. These make the biomarkers feasible options against the present expensive measurements and may provide clinical benefits.

Recent Patents on Biomarkers for Cardiorenal Syndrome

Congestive heart failure (CHF) is an increasingly common and severe condition that confers substantial morbidity and mortality. In advanced CHF, progressive functional impairment of renal function and structural renal disease may eventually develop. This condition has been recognized and is increasingly referred to as one manifestation of the cardiorenal syndromes (CRS), particularly its subtypes 1 and 2. These are defined by either acute or chronic deterioration in renal function depending on the rate of progression of CHF. This review first briefly highlights important features of the epidemiology, pathophysiology and treatment of CHF, then defines and briefly describes the various cardiorenal syndromes and their unique features. Recent patents for diagnosis and treatment of the cardiorenal syndromes 1 and 2 are then presented in the patent review coverage section and summarized in a table. Patents and patent applications on pharmacotherapeutics including novel diuretic agents, natriuretic peptides, endothelin antagonists, vasodilators and renal drug delivery systems, vasopressin receptor antagonists, among other compounds are presented. In addition, device-based patents for renal sympathoadrenergic denervation or modulation, isolated transluminal renal perfusion, bio-artificial cellbased therapies and implantable fluid removal devices, among others, are a special focus of this review. Potential future developments are also touched upon in conclusion. Keywords: Biomarkers, cardiorenal, cardiorenal syndrome, patents, renocardiac sydrome.

Prognostic impact of systemic inflammatory diseases in elderly patients with congestive heart failure

Inflammation is part of the pathophysiology of congestive heart failure (CHF). However, little is known about the impact of the presence of systemic inflammatory disease (SID), defined as inflammatory syndrome with constitutional symptoms and involvement of at least two organs as co-morbidity on the clinical course and prognosis of patients with CHF. This is an analysis of all 622 patients included in TIME-CHF. After an 18 months follow-up, outcomes of patients with and without SID were compared. Primary endpoint was all-cause hospitalization free survival. Secondary endpoints were overall survival and CHF hospitalization free survival. At baseline, 38 patients had history of SID (6.1%). These patients had higher N-terminal pro brain natriuretic peptide and worse renal function than patients without SID. SID was a risk factor for adverse outcome [primary endpoint: hazard ratio (HR) = 1.73 (95% confidence interval: 1.18-2.55, P = 0.005); survival: HR = 2.60 (1.49-4.55, P = 0.001); CHF hospitalization free survival: HR = 2.3 (1.45-3.65, P < 0.001)]. In multivariate models, SID remained the strongest independent risk factor for survival and CHF hospitalization free survival. In elderly patients with CHF, SID is independently accompanied with adverse outcome. Given the increasing prevalence of SID in the elderly population, these findings are clinically important for both risk stratification and patient management.

Diagnosis and Treatment of Depression in Patients With Congestive Heart Failure

Major depressive disorder (MDD) can be challenging to diagnose in patients with congestive heart failure, who often suffer from fatigue, insomnia, weight changes, and other neurovegetative symptoms that overlap with those of depression. Pathophysiologic mechanisms (eg, inflammation, autonomic nervous system dysfunction, cardiac arrhythmias, and altered platelet function) connect depression and congestive heart failure. We sought to review the prevalence, diagnosis, neurobiology, and treatment of depression associated with congestive heart failure. A search of all English-language articles between January 2003 and January 2013 was conducted using the search terms congestive heart failure and depression. We found 1,498 article abstracts and 19 articles (meta-analyses, systematic reviews, and original research articles) that were selected for inclusion, as they contained information about our focus on diagnosis, treatment, and pathophysiology of depression associated with congestive heart failure. The search was augmented with manual review of reference lists of articles from the initial search. Articles selected for review were determined by author consensus. The prevalence, diagnosis, neurobiology, and treatment of depression associated with congestive heart failure were reviewed. Particular attention was paid to the safety, efficacy, and tolerability of antidepressant medications commonly used to treat depression and how their side-effect profiles impact the pathophysiology of congestive heart failure. Drug-drug interactions between antidepressant medications and medications used to treat congestive heart failure were examined. MDD is highly prevalent in patients with congestive heart failure. Moreover, the prevalence and severity of depression correlate with the degree of cardiac dysfunction and development of congestive heart failure. Depression increases the risk of congestive heart failure, particularly in those patients with coronary artery disease , and is associated with a poorer quality of life, increased use of health care resources, more frequent adverse clinical events and hospitalizations, and twice the risk of mortality. At present, limited empirical data exist with regard to treatment of depression in the increasingly large population of patients with congestive heart failure. Evidence reveals that both psychotherapeutic treatment (eg, cognitive-behavioral therapy) and pharmacologic treatment (eg, use of the selective serotonin reuptake inhibitor sertraline) are safe and effective in reducing depression severity in patients with cardiovascular disease. Collaborative care programs featuring interventions that work to improve adherence to medical and psychiatric treatments improve both cardiovascular disease and depression outcomes. Depression rating scales such as the 9-item Patient Health Questionnaire should be used to monitor therapeutic efficacy.

研究会 第34回河口湖心臓討論会 メインテーマ : 「心不全と神経体液因子」 心不全における神経体液因子間のクロストーク

研究会 第34回河口湖心臓討論会 メインテーマ : 「心不全と神経体液因子」 心不全における神経体液因子間のクロストーク