Nonhemodynamic Factors Research Articles

Diastolic function in chronic kidney disease.

Chronic kidney disease (CKD) is characterized by clustered age-independent concentric left ventricular (LV) geometry, geometry-independent systolic dysfunction and age and heart rate-independent diastolic dysfunction. Concentric LV geometry is always associated with echocardiographic markers of abnormal LV relaxation and increased myocardial stiffness, two hallmarks of diastolic dysfunction. Non-haemodynamic mechanisms such as metabolic and electrolyte abnormalities, activation of biological pathways and chronic exposure to cytokine cascade and the myocardial macrophage system also impact myocardial structure and impair the architecture of the myocardial scaffold, producing and increasing reactive fibrosis and altering myocardial distensibility. This review addresses the pathophysiology of diastole in CKD and its relations with cardiac mechanics, haemodynamic loading, structural conditions, non-haemodynamic factors and metabolic characteristics. The three mechanisms of diastole will be examined: elastic recoil, active relaxation and passive distensibility and filling. Based on current evidence, we briefly provide methods for quantification of diastolic function and discuss whether diastolic dysfunction represents a distinct characteristic in CKD or a proxy of the severity of the cardiovascular condition, with the potential to be predicted by the general cardiovascular phenotype. Finally, the review discusses assessment of diastolic function in the context of CKD, with special emphasis on end-stage kidney disease, to indicate whether and when in-depth measurements might be helpful for clinical decision making in this context.

Cardiorenal Syndrome: A Literature Review.

Cardiorenal syndrome (CRS) is a condition characterized by the intricate two-way relationship between the heart and kidneys, which can lead to acute or chronic dysfunction in these organs. The interplay between cardiorenal connectors and both hemodynamic and non-hemodynamic factors is crucial to understanding this syndrome. The clinical importance of these interactions is evident in the changes observed in hemodynamic factors, neurohormonal markers, and inflammatory processes. Identifying and understanding biomarkers associated with CRS is valuable for early detection and enabling intervention before significant organ dysfunction occurs. This comprehensive review focuses on the clinical significance of biomarkers in the diagnosis, prognosis, and management of CRS. Finally, it highlights the necessity for further advancements in managing this condition.

Sirtuin-3-Mediated Cellular Metabolism Links Cardiovascular Remodeling with Hypertension.

Hypertension can cause structural and functional abnormalities in the cardiovascular system, which can be attributed to both hemodynamic and nonhemodynamic factors. These alterations are linked with metabolic changes and are induced by pathological stressors. Sirtuins are enzymes that act as stress sensors and regulate metabolic adaptation by deacetylating proteins. Among them, mitochondrial SIRT3 performs a crucial role in maintaining metabolic homeostasis. Evidence from experimental and clinical studies has shown that hypertension-induced decreases in SIRT3 activity can lead to cellular metabolism reprogramming and, subsequently, increased susceptibility to endothelial dysfunction, myocardial hypertrophy, myocardial fibrosis, and heart failure. This review presents recent research advances in SIRT3-mediated metabolic adaptation in hypertensive cardiovascular remodeling.

Acute Cardiorenal Syndrome: An Update.

The complex dynamic pathophysiological interplay between the heart and kidney causes a vicious cycle of worsening renal and/or cardiovascular function. Acute decompensated heart failure causing worsening renal function defines Type 1 cardiorenal syndrome (CRS). Altered hemodynamics coupled with a multitude of nonhemodynamic factors namely pathological activation of the renin angiotensin aldosterone system and systemic inflammatory pathways mechanistically incite CRS type 1. A multipronged diagnostic approach utilizing laboratory markers, noninvasive and/or invasive modalities must be implemented to enable timely initiation of effective treatment strategies. In this review, we discuss the pathophysiology, diagnosis, and emerging treatment options for CRS type 1.

Efekat metaboličkog sindroma na incidencu i stepen hipertrofije miokarda leve komore kod hipertenzivnih pacijenata

Metabolic syndrome (MetS) is characterized by the simultaneous presence of obesity, hypertension, dyslipidemia and hyperglycemia in an individual, which leads to an increased risk of cardiovascular disease (CVD). Left ventricular hypertrophy (LVH) is thickening of the heart muscle wall -hypertrophy of cardiomyocytes in concentric and/or elongation of cardiomyocytes and hyperplasia of connective tissue in eccentric hypertrophy with the participation of hemodynamic and non-hemodynamic factors (genetics, stress, other external factors). MetS, which essentially includesinsulin resistance, hyperinsulinemia, and hyperglycemia, alters myocardial metabolism and promotes myocardial inflammation, fibrosis, hypertrophy, and left ventricular remodeling. OBJECTIVE: To determine the impact of MetS, that is, obesity to the incidence and degree of severity of LVH in hypertensive patients with metabolic syndrome in comparison with the control group -hypertensive patients without metabolic syndrome. PATIENTS AND METHODS: Consecutive patients of the Office of Internal Medicine "Dr. Bastać" were examined, a total of 55 patients with hypertension, who were divided into two groups: the first group with MetS, 22 people, average age 56±8.5 years with BMI>30kg /m 2 and waist circumference more than 80 cm for women and >94 cm for men, the second control group without MetS-33 people, average age 52±14 years, with BMI<30kg/m 2 . Echocardiography was done for all subjects on a Power Vision 6000 Toshiba echo camera with standard echocardiographic measurements in the M, B and Doppler technique, and the mass of the left ventricular myocardium was determined for them using the Devereux formula. RESULTS: The prevalence of LVH in group 1 with metabolic syndrome (MetS) was 64%, while in the control group without (MetS) it was 36%. There was a statistically significantly higher number of patients with LVH in hypertension with MetS compared to hypertensive patients of the control group without MetS (X2, p=0.027). In the group of hypertensive patients with MetS, the degree of severity of myocardial hypertrophy, that is, the myocardial mass , was statistically significantly higher compared to the control group (respectively 302±84g versus 224±89g, p=0.0002). Arterial pressure values were higher for both systolic and diastolic blood pressure 168/106 mmHg in hypertensive patients with MetS, but did not reach statistical significance in relation to blood pressure values in hypertensive patients without MetS (156/95 mmHg, p=0.16). CONCLUSION. Patients with metabolic syndrome and hypertension have a statistically significantly higher prevalence of left ventricular myocardial hypertrophy and a highly statistically significant degree of left ventricular hypertrophy compared to the control group of hypertensive individuals without MetS. Given that mean values of arterial pressure do not differ between groups, it can be concluded that non-hemodynamic factors for the development of LVH have an important role in the induction of a more severe degree of LVH in hypertensive patients with metabolic syndrome.

Sex, gender, and subclinical hypertensiveorgan damage-heart.

Hypertension-mediated organ damage (HMOD) at cardiac level include a variety of abnormal phenotypes of recognized adverse prognostic value. Although the risk of cardiac HMOD is related with the severity of BP elevation, the interaction of numerous non-hemodynamic factors plays a relevant role in this unfavorable dynamic process. In particular, sex-related differences in cardiovascular (CV) risk factors and HMOD have been increasingly described. The objective of the present review is to provide comprehensive, updated information on sex-related differences in cardiac HMOD, focusing on the most important manifestations of subclinical hypertensive heart disease such as left ventricular hypertrophy (LVH), LV systolic and diastolic dysfunction, left atrial and aortic dilatation. Current evidence, based on cross-sectional and longitudinal observational studies as well as real-world registries and randomized controlled trials, suggests that women are more at risk of developing (and maintaining) LVH, concentric remodeling and subclinical LV dysfunction, namely the morpho-functional features of heart failure with preserved ejection fraction. It should be pointed out, however, that further studies are needed to fill the gap in defining gender-based optimal therapeutic strategies in order to protect women's hearts.

Effect of oral premedication of midazolam, ketamine, and dexmedetomidine on pediatric sedation and ease of parental separation in anesthesia induction for elective surgery

Objective: To compare effect of midazolam, dexmedetomidine, and ketamine as oral premedication on pediatric sedation and ease of parental separation anxiety in anesthesia induction. Methods: This multicenter, prospective, randomized, double-blind, clinical trial focused on a pediatric population aged 2-7 years (n=153) with the American Society of Anesthesiologists I-II who required elective surgery. The patients were stratified into three intervention groups: midazolam, ketamine, and dexmedetomidine. Hemodynamic parameters (blood pressure, heart rate, and oxygen saturation) every 5 min until induction of anesthesia along with non-hemodynamic factors, comprised of sedation score before the administration and at the time of being separated from the parents, as well as parental separation anxiety scale, acceptance of anesthesia induction, and side effects were recorded and compared. Results: No statistically significant difference in oxygen saturation, heart rate, blood pressure, duration of surgery, time to achieve an Aldrete score of 9-10, or sedation score was noted in the study groups. More patients in the dexmedetomidine and midazolam groups could better ease parental separation anxiety than the ketamine group (P=0.001). Moreover, fewer patients accept anesthesia induction (P=0.001) and more had side effects in the ketamine group (P=0.047). Conclusions: Our findings indicate that compared to the ketamine group, dexmedetomidine and midazolam are better in easing parental separation anxiety and accepting induction of anesthesia with fewer side effects. Dexmedetomidine and midazolam may be considered better choices. However, the final choice hinges on the patient's specific physical condition and the anesthesiologist's preference. Clinical registarion: This study is registered in the Iranian Registry Clinical Trial center with the clinical trial code of IRCT20211007052693N1.

3D Echocardiography - A Useful Method for Cardiovascular Risk Assessment in End-Stage Renal Disease Patients.

Patients with chronic kidney disease (CKD) have an increased risk of premature mortality, mainly due to cardiovascular causes. The association between hemodialysis and accelerated atherosclerosis has long been described. The ankle-brachial index (ABI) is a surrogate marker of atherosclerosis and recent studies indicate its utility as a predictor of future cardiovascular disease and all-cause mortality. The clinical implications of ABI cut-points are not well defined in patients with CKD. Echocardiography is the most widely used imaging method for cardiac evaluation. Structural and functional myocardial abnormalities are common in patients with CKD due to pressure and volume overload as well as non-hemodynamic factors associated with CKD. Our study aimed to identify markers of subclinical cardiovascular risk assessed using ABI and 2D and 3D echocardiographic parameters evaluating left ventricular (LV) structure and function in patients with end-stage renal disease (ESRD) (patients undergoing dialysis), patients after kidney transplantation and non-ESRD patients (control). In ESRD, particularly in hemodialysis patients, changes in cardiac structure, rather than function, seems to be more pronounced. 3D echocardiography appears to be more sensitive than 2D echocardiography in the assessment of myocardial structure and function in CKD patients. Particularly 3D derived end-diastolic volume and 3D derived LV mass indexed for body surface appears to deteriorate in dialyzed and transplanted patients. In 2D echocardiography, myocardial mass represented by left ventricular mass/body surface area index (LVMI) appears to be a more sensitive marker of cardiac structural changes, compared to relative wall thickness (RWT), left ventricle and diastolic diameter index (LVEDDI) and left atrial volume index (LAVI). We observed a generally favorable impact of kidney transplantation on cardiac structure and function; however, the differences were non-significant. The improvement seems to be more pronounced in cardiac function parameters, peak early diastolic velocity/average peak early diastolic velocity of mitral valve annulus (E/e´), 3D left ventricle ejection fraction (LV EF) and global longitudinal strain (GLS). We conclude that ABI is not an appropriate screening test to determine the cardiovascular risk in patients with ESRD.

ASSOCIATION OF HEMODYNAMIC AND NON-HEMODYNAMIC FACTORS WITH DIASTOLIC DYSFUNCTION IN PATIENTS WITH RESISTANT HYPERTENSION AND TYPE 2 DIABETES MELLITUS

Objective: To identify factors associated with the development of diastolic dysfunction in diabetic patients with resistant hypertension (RHTN). Design and method: The study included 36 patients with RHTN and type 2 diabetes mellitus (DM) (mean age 61,4 ± 6,4 years, 14 men, mean 24-hour (24 h) blood pressure (BP) (systolic/diastolic) 158,6 ± 15,2/79,8 ± 12,7mmHg, mean HbA1c 7,2 ± 1,2%). Office BP, and 24 h ambulatory BP measurements (ABPM), renal Doppler ultrasound, tissue doppler echocardiography, lab tests (24 h urine volume, the plasma levels of metalloproteinases-9 (MMP-9)) were performed in all patients. Results: Average E/e‘ significantly correlated with the duration of diabetes (p = 0.005, R = 0.46), the level of daytime (p = 0.003, R = 0.48), nighttime (p = 0.007, R = 0.44 and average daily (p = 0.037, R = 0.35) pulse BP; the level of MMP- 9 (p = 0.016, R = 0.47), with renal resistive indices (RI) in the main renal arteries: right-sided R = 0.37, p = 0.034, left-sided R = 0.38, p = 0.029; in the segmental arteries - on the right R = 0.41, p = 0.020 and R = 0.35, p = 0.048 on the left. In a multiple regression analysis, average E / e ’ significantly correlated with nighttime pulse BP (b ∗ = 0.42; SE (b) = 0.041; p = 0.004), MMP -9 (b ∗ = - 0.47; SE (b) = 0.001; p = 0.002), 24 h urine volume (b ∗ = - 0.47; SE (b) = 0.001; p = 0.001). Final model R = 0.81, R2 = 0.65, adjusted R2 = 0.61, estimate standard error = 2.56, p = 0.00004. Residuals did not differ from the normal distribution (p = 0.09) Conclusions: Diastolic dysfunction in diabetic patients with RHTN depends from complex of hemodynamic and non-hemodynamic factors, including duration of DM, value both of pulse BP, MMP and 24 h urine volume, as well of renal resistive indexes.

Immunomodulatory Approaches in Diabetes-Induced Cardiorenal Syndromes

Immunomodulatory approaches are defined as all interventions that modulate and curb the immune response of the host rather than targeting the disease itself with the aim of disease prevention or treatment. A better understanding of the immune system continues to offer innovative drug targets and methods for immunomodulatory interventions. Cardiorenal syndrome is a clinical condition that defines disorders of the heart and kidneys, both of which communicate with one another through multiple pathways in an interdependent relationship. Cardiorenal syndrome denotes the confluence of heart-kidney relationships across numerous interfaces. As such, a dysfunctional heart or kidney has the capacity to initiate disease in the other organ via common hemodynamic, neurohormonal, immunological, and/or biochemical feedback pathways. Understanding how immunomodulatory approaches are implemented in diabetes-induced cardiovascular and renal diseases is important for a promising regenerative medicine, which is the process of replacing cells, tissues or organs to establish normal function. In this article, after a brief introduction on the immunomodulatory approaches in diseases, we will be reviewing the epidemiology and classifications of cardiorenal syndrome. We will be emphasizing on the hemodynamic factors and non-hemodynamic factors linking the heart and the kidneys. In addition, we will be elaborating on the immunomodulatory pathways involved in diabetes-induced cardiorenal syndrome namely, RAS, JAK/STAT, and oxidative stress. Moreover, we will be addressing possible therapeutic approaches that target the former pathways in an attempt to modulate the immune system.

Early Vascular Aging in Hypertension.

With increasing age, the cardiovascular risk increases, as does frailty, with negative health consequences such as coronary disease, stroke, and vascular dementia. However, this aging process seems to take a more rapid course in some individuals, as reflected in the Early Vascular Aging (EVA) syndrome that over the recent 10 years has attracted increased attention. The core of the EVA syndrome is arterial stiffness in the media layer of large elastic arteries, a process that can be measured by pulse wave velocity, for example, along the aorta. Hypertension is a well-known cardiovascular risk factor in its own right, but also linked to the EVA process. However, several studies have shown that non-hemodynamic factors also contribute to arterial stiffness and EVA, such as impaired glucose metabolism, chronic inflammation, and oxidative stress. New perspectives have been introduced for linking early life programming affecting new-born babies and birth weight, with a later risk of hypertension, arterial stiffness and EVA. New drugs are being developed to treat EVA when lifestyle intervention and conventional risk factor controlling drugs are not enough. Finally, the opposite phenotype of EVA is Healthy Vascular Aging (HVA) or even Super Normal Vascular Aging (SUPERNOVA). If protective mechanisms can be found and mapped in these fortunate subjects with a slower than expected aging process, there could exist a potential to find new drug targets for preventive therapy.

Association of metabolic syndrome with carotid thickening and plaque in the general population: A meta-analysis.

We performed a meta-analysis of population studies reporting data on carotid intima-media thickness and plaque in patients with and without metabolic syndrome (MetS) to provide a new piece of information on the relationship of MetS with both phenotypes of vascular damage. The Ovid MEDLINE, PubMed, and Cochrane CENTRAL databases were searched without time restriction up to December 31, 2016. Overall, 19696 patients (22.2% with MetS) were included in eight studies. Common carotid intima-media thickness was greater in patients with MetS compared with those without it (788±47μm vs 727±44μm), with a standard means difference of 0.28±0.06 (P=.00003). Increased intima-media thickness in patients with MetS was paralleled by a higher prevalence of plaques. The present meta-analysis shows that MetS is associated with both ultrasonographic phenotypes of carotid damage. This finding is consistent with the view of MetS as a cluster of hemodynamic and nonhemodynamic factors promoting vascular hypertrophy and plaque.

Acute kidney injury in sepsis

Sepsis is life-threatening organ dysfunction resulting from a dysregulated host response to infection. It is one of the commonest causes of acute kidney injury (AKI) and is associated with an increase in both morbidity and mortality. Both haemodynamic and non-haemodynamic factors are involved in the pathogenesis of AKI in sepsis. Newer tests are available for the early diagnosis of AKI in septic patients and may provide an opportunity for prevention. The current mainstay of prevention is adequate fluid resuscitation and maintenance of systemic blood pressure, noradrenaline being the vasopressor of choice. Renal replacement therapy may improve outcomes. Continuous renal replacement modalities are preferred in those who are haemodynamically unstable. There is no consensus on the optimal timing or dose of renal replacement therapy.

Revised definition of predicted left ventricular mass using ambulatory blood pressure in healthy Korean adults

BackgroundLeft ventricular hypertrophy is influenced by both hemodynamic and non-hemodynamic factors. Ambulatory blood pressure is correlated with left ventricular hypertrophy. We established the influences of hemodynamic and non-hemodynamic factors, including ambulatory blood pressure, on variation in left ventricular mass in healthy Korean adults.MethodWe included 172 subjects (male = 71, female = 101), with normal body mass index and blood pressure, in an analysis of data from the Yangpyung and Yeoju cohort studies and a tertiary cardiovascular center. Left ventricular mass was calculated using the equation: [1.04 × (IVSd + LVDd + PWTd) 3-(LDVs3)] × 0.8 + 0.6. Stroke volume was calculated (mL/beat) using Teichholz’s formula. Stroke work (SW in gram-meters/beat [g-m/beat]) was computed as ambulatory systolic BP × stroke volume × 0.0144.ResultsStroke work was the most important determinant associated with left ventricular mass (adjusted R2 = 0.442, p < 0.001), independent of height2.7 and sex. In a regression model including stroke work, height,2.7 and sex, the left ventricular mass was predicted by the equation: 43.11 + 0.61 × SW (g-m/beat) + 9.21 × height2.7-13.99 × sex (male = 1, female = 2) (constant = 43.11 ± 25.88, adjusted R2 = 0.532, p < 0.001).ConclusionWe examined ambulatory blood pressure, as in previous studies, and identified stroke work, height2.7, and sex as important determinants of left ventricular mass in Korean adults of normal weight and normal blood pressure. Ambulatory blood pressure is superior to clinical blood pressure for determining stroke work and predicted left ventricular mass.

Association of white blood cell counts with left ventricular mass index in hypertensive patients undergoing anti-hypertensive drug therapy.

Although studies using animal models have demonstrated that nonhemodynamic factors, including inflammatory cells and cytokines, contribute to left ventricular hypertrophy (LVH), there is little clinical data to confirm this association. Therefore in the present study, levels of circulating specific types of leukocyte were measured to determine the association between white blood cells and left ventricular mass index (LVMI) in hypertensive patients undergoing anti-hypertensive drug therapy. A total of 144 consecutive hypertensive patients taking anti-hypertensive drug therapy were enrolled in the current study. Subjects were divided into two groups: Those with normal geometry and those with left LVH. Total white blood cells and differentiated subtypes (neutrophils, lymphocytes, monocytes) were counted, and left ventricular end-diastolic diameter, left ventricular posterior wall thickness in diastole and inter-ventricular septal wall thickness in diastole were all measured. Analysis revealed a significant correlation between LVMI and total white blood cell levels (P=0.013). The percentage of LVH in the highest tertile of WBC was increased compared with the middle tertile (P=0.008). Furthermore, a significant correlation between the highest tertile of neutrophil counts and LVH was observed (P=0.039). However, no significant associations between LVMI and monocyte or lymphocyte counts were detected. Therefore, the current study determined that increased total white blood cell and neutrophil subtype counts were associated with LVMI in hypertensive patients undergoing anti-hypertensive drug therapy. They may provide convenient and useful markers for further risk appraisal of LVH caused by nonhemodynamic factors of hypertension.

Role of imaging in the evaluation of renal dysfunction in heart failure patients

Heart failure and kidney disease share common pathophysiological pathways which can lead to mutual dysfunction, known as cardiorenal syndrome. In heart failure patients, renal impairment is related to hemodynamic and non-hemodynamic factors. Both decreased renal blood flow and renal venous congestion due to heart failure could lead to impaired renal function. Kidney disease and worsening renal function are independently associated with poor prognosis in heart failure patients, both in acute and chronic clinical settings. The aim of this review is to assess the role of renal imaging modalities in the evaluation and management of heart failure patients. Renal imaging techniques could complete laboratory data, as estimated glomerular filtration rate, exploring different pathophysiological factors involved in kidney disease and adding valuable information about renal structure and function. In particular, Doppler examination of arterial and venous hemodynamics is a feasible and non invasive technique, which has proven to be a reliable method for prognostic stratification in patients with cardiorenal syndrome. The renal resistance index, a measure related to renal hemodynamics, can be calculated from the Doppler evaluation of arterial flow. Moreover, the analysis of Doppler venous flow patterns can integrate information from the arterial study and evaluate renal congestion. Other imaging modalities are promising, but still confined to research purposes.

Non-hemodynamic factors associated to the risk of developing hypertensive cardiopathy

Non-hemodynamic factors associated to the risk of developing hypertensive cardiopathy

PP.16.23] REVISED DEFINITION OF PREDICTED LEFT VENTRICULAR MASS USING AMBULATORY BLOOD PRESSURE IN HEALTHY KOREAN ADULTS

Objective: The left ventricular is known to be influenced by both hemodynamic and non-hemodynamic factors. Body size and gender are the most representative non-hemodynamic factors. This study was performed to establish the influences of these variables including ambulatory BP on the variation of the left ventricular mass in healthy Korean adults. Design and method: 627 subjects (male = 270, female = 357), with a normal body mass index and blood pressure, were included in the analysis form database of the Yangpyung Epidemiologic cohort. The left ventricular mass was calculated using the equation: [1.04 × (IVSd + LVDd + PWTd)3-(LDVs3)] × 0.8 + 0.6. The stroke volume was calculated (mL/beat) using Teichholz's formula. The stroke work (SW in gram-meters/beat [g-m/beat]) was computed as ambulatory systolic BP × stroke volume × 0.0144. Results: The stroke work (SW) was the most important factor associated with the LV mass (adjusted R2 = 0.422, p < 0.001), and body weight, age and gender were independent factors (adjusted R2 = 0.524). In a regression model, including stroke work, gender and height2.7, the LV mass was predicted by the equation: 79.4 + 6.35 × height (m2.7) + 0.45 × SW (g-m/beat)-15.6 × gender (male = 1, female = 2)(constant = 79.3 ± 14.7 g, adjusted R2 = 0.517, p = 0.001).Conclusions: In this study using ambulatory BP, as with the previous studies, the stroke work, gender and height2.7 were important determinants of the left ventricular mass in Korean adults with a normal weight and normal blood pressure.

An Update on Intradialytic Cardiac Dysfunction.

Cardiac dysfunction is a key factor in the high morbidity and mortality rates seen in hemodialysis (HD) patients. Much of the dysfunction is manifest as adverse changes in cardiac and vascular structure prior to commencing dialysis. This adverse vascular remodeling arises as a dysregulation between pro- and antiproliferative signaling pathways in response to hemodynamic and nonhemodynamic factors. The HD procedure itself further promotes cardiomyopathy by inducing hypotension and episodic regional cardiac ischemia that precedes global dysfunction, fibrosis, worsening symptoms, and increased mortality. Drug-based therapies have been largely ineffective in reversing HD-associated cardiomyopathy, in part due to targeting single pathways of low yield. Few studies have sought to establish natural history and there is no framework of priorities for future clinical trials. Targeting intradialytic cardiac dysfunction by altering dialysate temperature, composition, or ultrafiltration rate might prevent the development of global cardiomyopathy, heart failure, and mortality through multiple pathways. Novel imaging techniques show promise in characterizing the physiological response to HD that is a unique model of repetitive ischemia-reperfusion injury. Reducing HD-associated cardiomyopathy may need a paradigm shift from empirical delivery of solute clearance to a personalized therapy balancing solute and fluid removal with microvascular protection. This review describes the evidence for intradialytic cardiac dysfunction outlining cardioprotective strategies that extend to multiple organs with potential impacts on exercise tolerance, sleep, cognitive function, and quality of life.

Cardiorenal Syndrome

Although combined cardiac and renal dysfunction is common in hospitalized patients and portends a poor prognosis, lack of understanding of the pathogenesis and classification of the condition has hampered the development of therapeutic strategies. Interactions between the heart and kidney involve multiple hemodynamic and nonhemodynamic factors and are usually bidirectional, as acute or chronic dysfunction of the cardiac or renal systems can negatively affect one another. This review introduces a new definition and classification system of cardiorenal syndrome advocated by a consensus conference of the Acute Dialysis Quality Initiative and summarizes the current understanding of cardiorenal syndrome. Keywords: Cardio-renal syndrome; Heart failure; Acute kidney injury; Chronic kidney disease; Cardiovascular disease 중심 단어: ì‹¬ì‹ ì¦í›„êµ°; ì‹¬ë¶€ì „; 급성 ì‹ ì†ìƒ; 만성 ì‹ ìž¥ë³‘; 심혈관계 질환