Overview of screening and diagnosis of heart disease in patients on dialysis

INTRODUCTION — Cardiovascular disease is an important cause of morbidity and mortality in patients undergoing maintenance dialysis.

This topic provides an overview of screening and diagnosis of heart disease in patients on dialysis and includes discussion of the diagnosis of heart failure (HF) and asymptomatic left ventricular (LV) dysfunction in this patient population.

The management of heart disease in patients receiving maintenance dialysis is discussed separately:

●HF. (See "Management of heart failure in patients on dialysis".)

●Atrial fibrillation. (See "Atrial fibrillation: Overview and management of new-onset atrial fibrillation" and "Atrial fibrillation in adults: Selection of candidates for anticoagulation", section on 'Chronic kidney disease'.)

PATHOPHYSIOLOGY — Ventricular-vascular remodeling and stiffening contribute to cardiovascular disease in patients on dialysis. Cardiac findings that are common in patients with end-stage kidney disease (ESKD) on dialysis include LV hypertrophy (LVH), diffuse myocardial fibrosis, and hemodialysis-induced myocardial stunning [1].

●Left ventricular hypertrophy – LVH is common among patients with ESKD with a reported prevalence of 75 percent [2-4]. LVH is a major risk factor for cardiovascular morbidity and mortality in patients with ESKD [5]. Among those who have LVH, two-thirds die from HF or sudden death, while one-third die from a noncardiovascular event. Worsening of LVH is a strong predictor of sudden death [6]. LVH is associated with increased QT interval and dispersal [2]. Both concentric and eccentric patterns of LVH (figure 1) are associated with risk of all-cause mortality among patients on dialysis [7,8]. Patients with eccentric LVH may be at higher risk of sudden death than patients with concentric LVH [9,10]. LVH is also associated with LV diastolic dysfunction, and diastolic dysfunction is also observed in some patients on dialysis without LVH [7]. LV systolic dysfunction is less common than LV diastolic dysfunction. Right ventricular (RV) dysfunction has also been observed in patients on dialysis [11,12]. LV diastolic or systolic dysfunction may progress to cause HF [13]. Ventricular stiffening related to LVH can also make the patient more vulnerable to episodes of hypotension during dialysis.

Among patients on dialysis, the major risk factors for LVH are hypertension (particularly systolic blood pressure) and increasing age [14,15]. Chronic volume overload, anemia, Klotho deficiency, increased arterial stiffness with associated loss of aortic distensibility, and possibly an increase in cardiac index induced by the arteriovenous fistula created for hemodialysis access may also contribute. Elevated levels of fibroblast growth factor (FGF) 23 seen with decreased phosphorus renal clearance may directly contribute to an increase in LV mass independent of hypertension [16]. (See "Cardiovascular and renal effects of anemia in chronic kidney disease" and "Evaluation and management of heart failure caused by hemodialysis arteriovenous access".)

●Myocardial fibrosis – Cardiovascular magnetic resonance (CMR) imaging studies have suggested that diffuse myocardial fibrosis is common among patients with ESKD, even in the presence of a normal LV ejection fraction (LVEF), and is associated with LVH [17-19]. A pattern consistent with diffuse fibrosis or infiltration is distinct from a pattern of focal subendocardial fibrosis (likely caused by myocardial infarction) and a pattern of midwall fibrosis or infiltration [19]. Extensive fibrosis has also been identified on biopsy. As an example, endocardial biopsies were performed in a study of 40 patients with ESKD with dilated cardiomyopathy without coronary artery disease and in a control group of 50 patients not on dialysis with idiopathic dilated cardiomyopathy [20]. Severe myocyte hypertrophy and extensive fibrosis were characteristic of the dialysis group. Patients not on dialysis had a similar proportion of fibrosis but, overall, a much smaller proportion of severely hypertrophic myocytes (8 versus 45 percent in patients on dialysis). In the patients on dialysis, increasing fibrosis correlated with a decreased survival rate. CMR spectroscopy in patients with ESKD has identified altered myocardial metabolism with less efficient use of high-energy phosphates [17,21]. (See "Definition and classification of the cardiomyopathies" and "Causes of dilated cardiomyopathy".)

●Myocardial stunning due to dialysis – Hemodialysis-induced myocardial stunning is common (eg, prevalences of 27 and 64 percent [22,23]) and is associated with reduced survival rates [22,23]. Hemodialysis-induced myocardial stunning is defined as hemodialysis-induced segmental LV dysfunction in the absence of known heart disease; however, the presence of coronary artery disease has not been excluded in studies of this condition. In support of an ischemic mechanism unrelated to coronary artery disease are observations of similar intradialytic cardiac stunning in 11 of 12 participants in a pediatric population (ages 2 to 17 years) [24]. At one-year follow-up, some patients with hemodialysis-induced myocardial stunning develop worsening LV systolic function with fixed (persistent) regional wall motion abnormalities [22,25].

●Uremic toxins – The retention of a wide variety of solutes in patients with impaired kidney function may adversely affect cardiac structure and function [1]. For example, high phosphate levels can directly damage endothelial cells and are associated with cardiovascular disease among patients on dialysis [26,27]. Compounds such as indoxyl sulfate and asymmetric dimethylarginine (ADMA) induce oxidative stress in vivo [28-30] and are associated with increased mortality and adverse cardiovascular events among patients with advanced chronic kidney disease [31-33]. Uremic retention solutes are discussed in detail elsewhere. (See "Uremic toxins".)

PREVALENCE AND PROGNOSIS

Overview — Cardiovascular events account for over 40 percent of deaths of known etiology in end-stage kidney disease (ESKD) patients (figure 2) [34]. In general, patients with even mild chronic kidney disease have a greater burden of incident cardiovascular disease compared with similar age controls [35,36]. The specific causes of cardiovascular death are the same as in the general population and include ischemic causes, such as coronary heart disease, and nonischemic causes, such as cardiomyopathy, arrhythmias, and valvular heart disease. With declining renal function, there is a progressive shift from ischemic to nonischemic etiologies of cardiac death (figure 3), particularly sudden death in the absence of evidence of an acute myocardial infarction (AMI). (See "Evaluation of sudden cardiac arrest and sudden cardiac death in patients on dialysis".)

Cardiovascular disease is also an important source of morbidity as the annual probability of hospital admission for HF and/or AMI for ESKD patients is greater than 20 percent, with a three- to fivefold greater probability of an admission for HF versus an AMI (figure 4 and figure 5) [34]. (See "Patient survival and maintenance dialysis".)

There are differences in the risk of HF and sudden death between patient groups treated with differing dialysis modalities, with a 34 percent lower rate of HF in patients on peritoneal versus hemodialysis. Furthermore, patients who receive peritoneal dialysis have a markedly lower sudden death rate than patients who receive hemodialysis (2 versus 7 percent) in the 12 months following the initiation of dialysis. This is counterbalanced by a higher unadjusted death rate in patients who receive peritoneal dialysis once diagnosed with HF or a myocardial infarction [34].

Heart failure — HF is more common among patients on dialysis compared with the general population. In an analysis of the United States Renal Data System (USRDS) database in 2018, 43 percent of all patients on dialysis had prevalent HF (17 percent HF with reduced ejection fraction, 14 percent HF with preserved ejection fraction, and 12 percent undifferentiated HF) [37]. By comparison, the prevalence of HF in persons without ESKD is approximately 2.1 percent [38].

The presence of HF independently predicts early mortality in patients on dialysis, as it does in other patients [39-43]. In an analysis of data from the USRDS database, long-term survival was evaluated among 310,456 patients on hemodialysis with a first hospital admission for HF, fluid overload, or pulmonary edema [43]. Five-year survival was only 12.5, 20.2, and 21.3 percent for these three groups, respectively. Increasing clinical severity of HF, as determined by the New York Heart Association (NYHA) classification, is also associated with increased mortality in patients with ESKD [42]. (See "Prognosis of heart failure".)

Causes and risk factors for HF in patients on dialysis are discussed below. (See 'Causes and risk factors' below.)

Coronary heart disease — The prevalence of coronary heart disease in patients on dialysis is discussed separately. (See "Risk factors and epidemiology of coronary heart disease in end-stage kidney disease (dialysis)".)

Valvular heart disease — The prevalence of valvular heart disease in patients on dialysis is discussed separately. (See "Valvular heart disease in patients with end-stage kidney disease".)

Arrhythmias — The prevalence of atrial fibrillation and risk of sudden cardiac arrest in patients on dialysis is discussed separately. (See "Evaluation of sudden cardiac arrest and sudden cardiac death in patients on dialysis" and "Atrial fibrillation in adults: Selection of candidates for anticoagulation", section on 'Chronic kidney disease'.)

SCREENING AND DIAGNOSIS OF HEART DISEASE

Approach to screening and diagnosis — As described above, heart disease is highly prevalent among patients on dialysis, and cardiac disease impacts prognosis and management (including dialysis therapies). Thus, as recommended in the 2005 Kidney Disease Outcomes Quality Initiative (KDOQI) guidelines for cardiovascular disease in patients on dialysis, we suggest that patients receiving dialysis undergo screening for heart disease risk factors. In the absence of symptoms of coronary artery disease (CAD), we do not recommend diagnostic testing for CAD unless the patient is under evaluation for kidney transplant [44-46]. In each patient on dialysis, screening is performed to determine the need for additional testing for coronary heart disease, valvular heart disease, ventricular dysfunction, and arrhythmia. Screening of asymptomatic patients is performed in addition to standard diagnostic evaluation of patients with symptoms and signs of heart disease.

Screening includes the following components [44]:

●Assessment for any symptoms or signs of heart disease. (See 'Clinical manifestations' below.)

●Screening for traditional cardiovascular and uremia-related cardiovascular risk factors including diabetes, hypertension, dyslipidemia, smoking, physical activity, anemia, albuminuria, arterial stiffness/vascular calcification, serum phosphorus/parathyroid hormone level, inflammation (C-reactive protein [CRP]), and intradialytic hypotension. Of note, limited data are available on the effects of correction of modifiable traditional risk factors in patients with stage IV or greater chronic kidney disease, making specific recommendations challenging [47].

●A 12-lead electrocardiogram (ECG; at initiation of dialysis and annually) to identify signs of coronary heart disease and arrhythmia and is also helpful to serve as a baseline for comparison.

●A Doppler transthoracic echocardiogram once the patient is at dry weight early after initiation of dialysis (eg, during the first one to three months). Echocardiography is repeated every three years, as clinically appropriate given the patient's clinical condition. Approximately 87 percent of patients initiating dialysis will have abnormalities on echocardiography [12].

The following are key echocardiographic features in patients with end-stage kidney disease (ESKD):

•LV dimensions and wall thickness (to assess LV hypertrophy [LVH] and geometry) (figure 1).

•LV systolic function (LVEF) (see "Tests to evaluate left ventricular systolic function", section on 'Echocardiography'), which has implications for risk of coronary heart disease as well as risk of HF. (See 'For coronary heart disease' below and 'For ventricular dysfunction' below.)

•LV diastolic function. (See "Echocardiographic evaluation of left ventricular diastolic function in adults" and 'For ventricular dysfunction' below.)

•Assessment of valve appearance and function. (See 'For valvular heart disease' below and "Valvular heart disease in patients with end-stage kidney disease".)

•Estimation of right atrial pressure and pulmonary artery systolic pressure, when possible. (See "Echocardiographic assessment of the right heart", section on 'Hemodynamics'.)

A referral to a cardiologist is suggested in the following settings: suspected HF, suspected coronary heart disease, suspected moderate or greater valve stenosis or regurgitation, new or unexplained pulmonary hypertension (pulmonary artery systolic pressure >35 mmHg), or new-onset arrhythmias (eg, incident atrial fibrillation, marked bradycardia, or ventricular tachycardia).

For coronary heart disease — Additional testing to screen for coronary heart disease may be performed in selected patients on dialysis, including those with LVEF <40 percent as well as in selected potential kidney transplant recipients. Additional criteria for stress testing and considerations in choosing a screening test are discussed separately. (See "Kidney transplantation in adults: Evaluation of the potential kidney transplant recipient", section on 'Coronary artery disease' and "Clinical manifestations and diagnosis of coronary artery disease in end-stage kidney disease (dialysis)", section on 'Evaluation at dialysis initiation'.)

While screening is performed for asymptomatic patients, diagnostic evaluation is performed for patients who develop symptoms of coronary heart disease, and monitoring is performed for patients with known coronary heart disease who have undergone coronary artery bypass graft surgery. (See "Clinical manifestations and diagnosis of coronary artery disease in end-stage kidney disease (dialysis)", section on 'Evaluation of symptomatic patients'.)

For valvular heart disease — Valvular heart disease should be assessed during the screening clinical evaluation and Doppler echocardiography (at baseline dry weight during the first one to three months and repeated every three years). Echocardiography enables assessment of valve appearance, motion, function, pulmonary pressures, as well as changes in ventricular size and function associated with valve disease. (See "Valvular heart disease in patients with end-stage kidney disease", section on 'Evaluation'.)

For asymptomatic patients on dialysis found to have valvular heart disease, recommendations for monitoring are similar to those for the general population except for greater frequency of follow-up for aortic stenosis. Cardiac calcification, including aortic valve calcification, occurs at an accelerated rate in patients on dialysis, and the rate of aortic stenosis progression is greater than that observed in the general population. (See "Medical management of asymptomatic aortic stenosis in adults", section on 'Serial evaluation' and "Valvular heart disease in patients with end-stage kidney disease", section on 'Aortic stenosis'.)

●For patients on dialysis with moderate aortic stenosis, annual echocardiography is recommended.

●For patients on dialysis with severe aortic stenosis, echocardiography is recommended every six months.

In addition, patients who develop signs and symptoms of valvular heart disease should undergo timely diagnostic evaluation including echocardiography. Clinical manifestations and diagnosis of valve disease in patients with ESKD are discussed separately. (See "Valvular heart disease in patients with end-stage kidney disease".)

For ventricular dysfunction — Ventricular dysfunction (eg, LV diastolic and/or systolic dysfunction) and LV remodeling (eg, LVH) should be assessed during the screening clinical evaluation and echocardiography performed at clinically determined dry weight as a baseline early after initiation of dialysis (eg, during the first one to three months) and repeated every three years. Most patients are volume overloaded at the time of initiation of dialysis, and it can take weeks to achieve relative euvolemia. In addition, some small studies have suggested that adjustment of the dry weight targets for patients who receive hemodialysis by echocardiography assessment of inferior vena cava size may improve blood pressure control and the quality of life [48,49]. (See "Tests to evaluate left ventricular systolic function" and "Heart failure with preserved ejection fraction: Clinical manifestations and diagnosis" and "Echocardiographic evaluation of left ventricular diastolic function in adults" and "Management of heart failure in patients on dialysis", section on 'Dialysis prescription'.)

In addition, patients who are being evaluated for kidney transplant generally undergo cardiac evaluation. (See "Kidney transplantation in adults: The kidney transplant waiting list in the United States", section on 'Cardiovascular testing' and "Kidney transplantation in adults: Evaluation of the potential kidney transplant recipient", section on 'Cardiovascular disease'.)

Echocardiography is the test of choice to assess ventricular systolic and diastolic dysfunction and LVH as it is widely available, noninvasive, and provides information on atrial and ventricular volumes, LV mass, biventricular systolic and diastolic function, valve function, and pulmonary pressures. LVH is defined as an LV mass index ≥134 and ≥110 g/m² body surface area in males and females, respectively.

If LV systolic function cannot be adequately assessed by echocardiography, alternative methods include radionuclide ventriculography, CMR imaging (for which no exogenous contrast is required for assessment of LV structure and function), cardiac computed tomography (which requires iodinated contrast), and invasive ventriculography (generally performed only if there is a concurrent indication for cardiac catheterization such as an indication for coronary angiography). (See "Tests to evaluate left ventricular systolic function".)

In addition to the above described screening, patients should undergo diagnostic evaluation if they develop symptoms or signs of HF, recurrent hypotension with hemodialysis, or a cardiac event [44]. Diagnostic evaluation of patients with symptoms and signs of HF is discussed below. (See 'Diagnosis of heart failure' below.)

For arrhythmias — Screening for atrial and ventricular arrhythmias in patients on dialysis is generally limited to obtaining a 12-lead ECG at the time of initiation of dialysis and annually. In addition, patients with symptoms and signs of arrhythmias should undergo evaluation as discussed separately. (See "Arrhythmia management for the primary care clinician" and "Narrow QRS complex tachycardias: Clinical manifestations, diagnosis, and evaluation" and "Wide QRS complex tachycardias: Causes, epidemiology, and clinical manifestations" and "Wide QRS complex tachycardias: Approach to the diagnosis".)

For atrial fibrillation — The clinical manifestations and diagnosis of atrial fibrillation are discussed separately. (See "Atrial fibrillation: Overview and management of new-onset atrial fibrillation".)

For ventricular arrhythmias — The clinical manifestations and diagnosis of ventricular arrhythmias and the risk of sudden cardiac arrest in patients with ESKD are discussed separately. (See "Wide QRS complex tachycardias: Approach to the diagnosis" and "Wide QRS complex tachycardias: Causes, epidemiology, and clinical manifestations" and "Evaluation of sudden cardiac arrest and sudden cardiac death in patients on dialysis".)

DIAGNOSIS OF HEART FAILURE

Causes and risk factors — Factors contributing to HF in the patient on dialysis include fluid overload, LV diastolic dysfunction, LV systolic dysfunction, and valvular heart disease (eg, aortic stenosis). A high-output state caused by shunting through hemodialysis arteriovenous access can also precipitate HF, particularly in patients with underlying ventricular dysfunction [50]. (See "Evaluation and management of heart failure caused by hemodialysis arteriovenous access" and "Clinical manifestations, diagnosis, and management of high-output heart failure".)

Risk factors for new-onset HF in end-stage kidney disease (ESKD) patients are similar to the general population and include hypertension, older age, anemia, ischemic heart disease, and baseline systolic dysfunction [13,40]. The prevalence of atheromatous disease in ESKD is high, and this may, in part, be due to the clustering of risk factors and the direct result of kidney function impairment. (See "Clinical manifestations and diagnosis of coronary artery disease in end-stage kidney disease (dialysis)" and "Hypertension in patients on dialysis".)

The pathophysiology of heart disease in patients on dialysis is discussed above. (See 'Pathophysiology' above.)

Clinical manifestations — Symptoms and signs of HF in patients with ESKD are the same as those observed generally. Symptoms include dyspnea, orthopnea, fatigue, and weakness. Signs include elevated jugular venous pressure, an S3 gallop, rales, and peripheral edema. ECG findings (such as LV hypertrophy [LVH] and changes consistent with myocardial infarction or ischemia) are not specific for HF but may suggest a cause of HF. The chest radiograph findings of cardiomegaly, cephalization of pulmonary vessels, Kerley B-lines, and alveolar edema strongly suggest HF but have limited sensitivity. (See "Heart failure: Clinical manifestations and diagnosis in adults" and "Heart failure with preserved ejection fraction: Clinical manifestations and diagnosis", section on 'Clinical manifestations'.)

Diagnosis — The clinical syndrome of HF is diagnosed in patients with ESKD based upon identification of a combination of symptoms, signs, and test findings. The evaluation is the same as that for HF generally except that we do not use natriuretic peptides to diagnose HF in patients with ESKD. Similar to the general population, there is a high incidence of HF with preserved ejection fraction (HFpEF). (See "Heart failure: Clinical manifestations and diagnosis in adults" and "Heart failure with preserved ejection fraction: Clinical manifestations and diagnosis", section on 'Evaluation'.)

In addition, signs of diastolic dysfunction are common among asymptomatic patients on dialysis; diastolic dysfunction is a predictor of adverse cardiovascular outcomes including development of HF [51,52]. Some sedentary patients with asymptomatic diastolic dysfunction may develop symptoms and signs of HFpEF with stress.

The role of cardiac tests in the diagnostic evaluation of HF is discussed separately. Since HF is a clinical diagnosis, echocardiography is not used to exclude HF but to identify findings consistent with HF and potential causes of HF (eg, LV systolic dysfunction, LV diastolic dysfunction, and valve dysfunction). Cardiac catheterization is not generally required to diagnose HF, but right heart catheterization may be helpful in selected cases to assess intracardiac pressures and volume status, which may be challenging to assess noninvasively in patients on dialysis.

The use of serial change (either a rise or fall) rather than a static level of cardiac troponin I or T to diagnosis acute myocardial infarction (AMI) in patients with chronic kidney disease (CKD) is discussed separately. (See "Cardiac troponins in patients with kidney disease".)

Identification of the type of heart failure — While most patients with HF (whether HF with reduced ejection fraction [HFrEF], LVEF ≤40 percent; HFpEF, LVEF ≥50 percent; or HF with mid-range ejection fraction [HFmrEF], LVEF 41 to 49 percent) have low or normal cardiac output accompanied by elevated systemic vascular resistance.

A minority of patients with HF present with a high-output state with low systemic vascular resistance. High-output HF should be suspected in patients with predisposing conditions, particularly patients with arteriovenous access for hemodialysis. Patients with high-output HF frequently have concurrent cardiac disease with impaired systolic and/or diastolic function. Diagnosis of high-output HF is discussed separately. (See "Clinical manifestations, diagnosis, and management of high-output heart failure" and "Evaluation and management of heart failure caused by hemodialysis arteriovenous access".)

Limited utility of natriuretic peptides — Neither B-type natriuretic peptide (BNP) nor the amino terminal fragment of the proBNP molecule (NT-proBNP) is sufficiently accurate for diagnosing HF in patients with ESKD. Plasma BNP and NT-proBNP concentrations are elevated in patients with renal failure due to reduced clearance, so thresholds for diagnosis of HF in patients on dialysis have not been established. (See "Natriuretic peptide measurement in heart failure".)

This contrasts with the utility of BNP and NT-proBNP in identifying patients with asymptomatic or symptomatic LV dysfunction among patients with normal renal function or mild to moderate CKD (defined as an estimated glomerular filtration rate [eGFR] >30 mL/min/1.73 m²). (See "Natriuretic peptide measurement in heart failure", section on 'Renal failure'.)

Both BNP and NT-proBNP can provide prognostic information with respect to all-cause mortality, cardiovascular mortality, and cardiovascular events in patients with ESKD, although we generally do not use either for this purpose. In a meta-analysis combining 23 studies and nearly 8000 ESKD patients, an elevated natriuretic peptide level was associated with a 3.85 higher odds ratio for all-cause mortality (95% CI 3.11-4.75) [53]. The odds ratio for cardiovascular death was 4.05 (95% CI 2.53-6.84), but with high heterogeneity, when evaluating 10 studies with 6396 ESKD subjects.

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Dialysis".)

SUMMARY AND RECOMMENDATIONS

●Cardiovascular disease is an important cause of morbidity and mortality in patients with end-stage kidney disease (ESKD). With declining renal function, there is a progressive shift from ischemic to nonischemic etiologies of cardiac death, particularly sudden death in the absence of evidence of an acute myocardial infarction (AMI). (See 'Prevalence and prognosis' above.)

●Left ventricular hypertrophy (LVH) is a major risk factor for cardiovascular morbidity and mortality in patients on dialysis. Major risk factors for LVH include hypertension (particularly systolic blood pressure) and increasing age; chronic volume overload, anemia, and increased cardiac index may be contributing factors. (See 'Pathophysiology' above.)

●Heart failure (HF) is common among patients on dialysis and predicts early mortality. Risk factors for HF include hypertension, older age, anemia, ischemic heart disease, and baseline systolic dysfunction. (See 'Pathophysiology' above and 'Causes and risk factors' above.)

●Given the high burden of heart disease among patients on dialysis, we suggest that patients receiving maintenance dialysis undergo screening for heart disease including assessment of any symptoms and signs of heart disease, screening for cardiovascular risk factors, a 12-lead ECG (at initiation of dialysis and annually), and a Doppler transthoracic echocardiogram (once the patient is at dry weight within the first one to three months after initiation of dialysis and repeated every three years). In each patient on dialysis, this screening is performed to determine the presence of and need for additional testing for coronary heart disease, valvular heart disease, ventricular dysfunction, and arrhythmia. Screening of asymptomatic patients is performed in addition to standard diagnostic evaluation of patients with symptoms and signs of heart disease. (See 'Approach to screening and diagnosis' above.)

•Additional testing to screen for coronary heart disease is performed in selected patients on dialysis including those with LV ejection fraction (LVEF) <40 percent as well as in selected potential renal transplant recipients. Screening is performed by noninvasive stress imaging (nuclear or echocardiographic) and/or coronary angiography. Additional criteria for stress testing and considerations in choosing a screening test are discussed separately. (See 'For coronary heart disease' above and "Kidney transplantation in adults: Evaluation of the potential kidney transplant recipient", section on 'Coronary artery disease' and "Clinical manifestations and diagnosis of coronary artery disease in end-stage kidney disease (dialysis)", section on 'Evaluation at dialysis initiation'.)

•Valvular heart disease should be assessed during the screening clinical evaluation and Doppler echocardiography. For asymptomatic patients on dialysis found to have valvular heart disease, recommendations for monitoring are similar to those for the general population except for greater frequency of follow-up for aortic stenosis. (See 'For valvular heart disease' above and "Valvular heart disease in patients with end-stage kidney disease" and "Medical management of asymptomatic aortic stenosis in adults", section on 'Serial evaluation'.)

•Ventricular dysfunction (eg, LV diastolic and/or systolic dysfunction) and LV remodeling (eg, LVH) should be assessed during the screening clinical evaluation and echocardiography. (See 'For ventricular dysfunction' above and "Tests to evaluate left ventricular systolic function" and "Heart failure with preserved ejection fraction: Clinical manifestations and diagnosis" and "Echocardiographic evaluation of left ventricular diastolic function in adults".)

•Screening for atrial and ventricular arrhythmias in patients on dialysis is generally limited to obtaining a 12-lead electrocardiogram at the time of initiation of dialysis and annually. (See "Arrhythmia management for the primary care clinician" and "Narrow QRS complex tachycardias: Clinical manifestations, diagnosis, and evaluation" and "Wide QRS complex tachycardias: Causes, epidemiology, and clinical manifestations" and "Wide QRS complex tachycardias: Approach to the diagnosis".)

●The clinical syndrome of HF is diagnosed in patients with ESKD based upon identification of a combination of symptoms, signs, and test findings. The evaluation as the same as that for HF generally except that we do not use natriuretic peptides to diagnose HF in patients with ESKD. (See "Heart failure: Clinical manifestations and diagnosis in adults" and "Heart failure with preserved ejection fraction: Clinical manifestations and diagnosis", section on 'Evaluation' and "Natriuretic peptide measurement in heart failure", section on 'Renal failure'.)