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Saudi Journal of Kidney Diseases and Transplantation
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EDITORIAL Table of Contents   
Year : 2005  |  Volume : 16  |  Issue : 2  |  Page : 129-139
Cardiovascular Disease in Chronic Renal Failure Patients


1 Cardiac Rehabilitation Department, Broussais-HEGP Hospital, Paris, France
2 Chronic Hemodialysis Unit, AURA, Paris, France

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How to cite this article:
Iliou MC, Fumeron C. Cardiovascular Disease in Chronic Renal Failure Patients. Saudi J Kidney Dis Transpl 2005;16:129-39

How to cite this URL:
Iliou MC, Fumeron C. Cardiovascular Disease in Chronic Renal Failure Patients. Saudi J Kidney Dis Transpl [serial online] 2005 [cited 2019 Sep 19];16:129-39. Available from: http://www.sjkdt.org/text.asp?2005/16/2/129/32931

   Introduction Top


A complex inter-relationship exists between the kidney and the heart. This problem has been rather poorly studied in the various cardio­vascular studies, particularly in the past. Many studies have been published concerning hemo­dialysis patients, but little data exist in non end-stage renal disease patients. Moreover, the majority of the studies have been obtained from American registries, making the extrapolations difficult in other countries. However, the management of cardiovascular diseases (CVD) in chronic renal diseases (CRD) represents a true challenge to nephrologists as well as cardiologists.

Obviously, we cannot review in this editorial, all aspects of CVD in CRD; instead we have chosen to focus on some important patho­physiological and clinical points.


   Epidemiology Top


In patients with CRD, CVDs have a high prevalence, high morbidity and mortality; among these, ischemic heart disease is the major cardiac disease.

The high prevalence of CVD in chronic renal insufficiency, even before the occurrence of end-stage renal disease (ESRD), is recognized based mainly on cross-sectional studies. [1] Prolonged survival due to improved health and, increased prevalence of diabetes mellitus, may be contributing factors to the high pre­valence of renal and cardiovascular disease. Renal dysfunction is frequent in older patients (11% in patients over 65-years-old) and represents an independent factor of overall, and cardiac mortality. [2]

In the HDFP study, which included 10,940 patients, the risk of developing cardiac disease increased 2.2 fold in patients with renal dysfunction as compared to patients with normal renal function. This study also shows that cardiovascular mortality (9% per year, a 30-fold increased risk when compared to the overall population) is more frequent among patients with chronic renal insufficiency, than the development of ESRD. [3] Moreover, the pre-dialysis chronic renal disease patients seem have a higher cardiovascular risk than patients with ESRD. [4] This may be due to the death of some patients before reaching ESRD. Nevertheless, in the United States, 40% of incident hemodialysis patients have coronary artery disease.

In the Cardiovascular Health Study, [5] a serum creatinine level > 1.5 mg/dL was associated with a relative risk of cardiovascular death of 1.1 as compared to patients with serum creatinine < 1.5 mg/dL.

Cardiovascular morbidity is three to five times higher in chronic renal disease patients than in the normal population. The risk of a cardio­vascular event is, on average, 20-times higher for dialysis patients than for pre-dialysis ones. Furthermore, there is an even higher mortality rate for young patients. In hemodialysis patients, the overall mortality is estimated at about 25% per year in the US, [6] and ranges from 13.3 to 18.6% in Europe. [7] Mortality increases with age, among male patients, those with diabetes and patients who underwent peritoneal dialysis prior to hemodialysis. Cardiovascular causes account for 0.19 to 0.4 hospitalizations per patient per year. [7] A high mortality rate in hemodialysis patients is not only due to a high prevalence of cardiovascular disease but also due to high case fatality. [8]

Association of CRD and congestive heart failure (CHF), is also very frequent, [9] and is a powerful risk factor for adverse outcome in dialysis patients. [10] For example, mean survival after development of de novo CHF is 18 months. [11]

Many intricate reasons may explain the association of cardiovascular disease and prog­nosis in chronic renal disease. They include presence of cardiovascular risk factors such as anemia, left ventricular hypertrophy and subsequently of coronary artery disease, as well as association of renal diseases with sub­ clinical cardiovascular diseases, all of which share the same causes of renal and cardiac disease progression. [12]

Consequently, patients with CRD are recog­nized as high cardiovascular risk patients (especially for CAD, LVH, and CHF). [13] This is why recent recommendations have targeted this population for specific management strategies.


   Pathophysiology Top


Chronic renal disease is a clinical human model of accelerated arteriosclerosis. The classical cardiovascular risk factors are more frequent in CRD patients than in the global population. Some of these risk factors deserve attention: hypertension is present in more than 25% of chronic renal diseases, and 80% of hemodialysis patients. Hypertension is fre­quently severe and requires polytherapy, and is an independent factor of cardiovascular events. [14] On the other hand, hypotension is also a risk factor of mortality in hemodialysis patients, related to occurrence of chronic heart failure. The high prevalence of diabetes may explain in part the occurrence of coronary artery disease even before ESRD. Smoking has been implicated in the progression of renal disease in patients with hypertension, and in increasing the risk of development of atherosclerotic plaques. Low exercise capacities and physical inactivity is common in CRD population especially in hemodialysis patients. [15]

However, one of the key points is the in­sufficient monitoring of these traditional risk factors in CRD patients. [16],[17] In fact, despite their relative high prevalence in CRD, the traditional risk factors fail to entirely account for the progression of atherosclerotic diseases. In chronic renal failure patients, additional specific risk factors have been described as follows. [18],[19],[20],[21]

The lipid disorders in renal diseases have some peculiarities. Indeed, levels of total cholesterol are normal or above the classical threshold, and their effect on mortality is represented by a U curve (low levels of cholesterol may occur in malnutrition). The characteristics are low HDL levels, normal or slightly elevated LDL levels, low Apo A1 and Apo A2, elevated Apo B and Apo C3, high levels of triglycerides, high levels of Lp(a), lipoprotein remnants, and marked oxidation of LDL. [22]

Hyper-homocysteinemia is a cardiovascular risk factor widely accepted in the general population. High levels of homocysteine are almost constant in chronic kidney diseases and correlated with the severity of renal dysfunction (# 90% in ESRD patients) and are not fully corrected by dialysis. Some evidence has been found for a relationship between homocysteine levels and aortic sclerosis. [23],[24] However, even with high doses of folate treatment, the decrease in homocysteine levels is limited (28%), with no evidence of reduced cardio­vascular mortality.

Markers of inflammation (CRP, fibrinogen and cytokines) are frequently increased in CRD and associated with a poor cardiovascular prognosis especially in patients with ESRD. [25] Microalbuminuria, one of the first signs of renal disease in diabetic patients, is associated with a high prevalence of cardiovascular diseases. Proteinuria is frequently associated with other risk factors, which may reflect endothelial dysfunction and anomalies in fibrinolysis. It is frequently associated with inflammatory markers and denotes organic injuries. Even in non-diabetic patients, proteinuria is associated with a high prevalence of cardiovascular risk factors and diseases.

Anemia is a classical risk factor of left ventri­cular hypertrophy, CHF, coronarZ artery disease (CAD) and cardiac mortality. [26] Correction of anemia with erythropoietin has been demon­strated to improve clinical tolerance and to reduce global mortality (the effect in cardio­vascular mortality is still debated). [27]

In CRD patients, phosphate and calcium meta­bolism is disturbed due to secondary hyper­parathyroidism. Hyperphosphatemia seems to be the main deleterious consequence with a 30% increase in cardiovascular mortality for patients who have phosphatemia > 2 mmol/l. [28] Calcium deposits are common in atherosclerotic lesions, in the media of arteries, and in valves. Coronary artery calcification score detected by electron-beam computer tomography is correlated with time spent on dialysis, and significantly associated with ischemic heart disease in adult hemodialyzed patients. [29]

Oxidative stress and inflammation may be the early promoters of arteriosclerosis. Oxidative stress is observed in early stages of renal disease with an increased plasma concentration of products of lipid peroxydation. Oxidated LDL promotes macrophage and monocyte activation, endothelial apoptosis, and cytokine release. [30] In preliminary studies, anti-oxidant agents seem to have a favorable effect on reducing cardiovascular risk, but this point is not entirely definite. [31] These two pathogenic factors are associated with thrombogenic factor abnormalities (increased PAI 1 and decreased fibrinolytic activity).

Hypoalbuminemia and malnutrition are strong predictors of mortality in hemodialysis patients. [32] Increased sympathetic tone is observed in patients with mild to moderate renal insuffi­ciency up to ESRD [33] Sympathetic over­activity results in increased blood pressure which represents a major factor in causing left ventricular hypertrophy and predicts cardiovascular mortality in ESRD patients. [34] Their causes are poorly understood but may directly reflect renal and/or cardiac dysfunction apart from sleep disturbances causing nocturnal hypoxemia.

Patients with CRD have endothelial dysfun­ction with altered NO/endotheline balance and endothelium dependent vasodilation ab­normalities. [35] This occurs early in some concomitant pathologies (diabetes, hypertension, hyper-cholesterolemia and CAD). [36] Mechanisms which explain the endothelial dysfunction include oxidative stress, hypertension, shear stress, dyslipidemia, inhibition of the production or, of the bioavailability of endothelial NO, or their incapacity to regulate the vascular tone. In CRD patients, even non-end-stage ones, NO production is reduced: [37] studies on nitrates/ nitrites have controversial results, but increased levels of ADMA (inhibitor of NO synthase) have been showed in hemodialysis patients. [38] We recently explored another way leading to endothelial dysfunction: nitrosothiols (endo­thelium NO reserve), which reflect a non-release form of NO, are increased in hemodialysis patients. [39] Furthermore, nitrosothiol levels are associated with increased cardiac mortality in hemodialysis patients. [40]

Finally, for ESRD patients, the quality of dialysis interferes with cardiovascular prognosis: each 0.1 Kt/V gain induces a 9% reduction of mortality by coronary artery disease; [41] but we do not have evidence for the use of any one specific membrane.

Obviously, these different risk factors may jointly play a role in the pathophysiology of cardiovascular abnormalities in chronic renal diseases. Indeed, some markers proposed as surrogates of structural and functional vascular disorders and which have prognostic impli­cations include many of the previous factors cited. Similarly, arterial stiffness and pulse wave velocity reflect complex interrelation­ships between some humoral, hemodynamic and hormonal disorders such as anemia, sympathetic over activity, endotheline, etc. [42] The same goes for left ventricular hypertrophy which produces a mismatch between cardio­myocytes and capillaries and increases the distance through which oxygen must diffuse from the capillary lumen to the myocyte, and results in many myocardial structural and functional abnormalities. [43] Finally, National Kidney Foundation recommendations are applicable for prevention and treatment of cardiovascular risk factors in chronic renal disease.


   Cardiac Diseases Top


Coronary Artery Disease

In chronic renal disease the presentation of coronary artery disease is often atypical: first, chest pain and fluid overload symptoms can be misinterpreted. Second, ST segment modifi­cations may be due to left ventricular hyper­trophy causing ECG interpretation to be most difficult. Last, diagnostic and prognostic value of cardiac markers has been known to be controversial.

Surprisingly, systematic screening to detect coronary artery disease is only recommended by guidelines in a pre-transplant and/or in a symptomatic patient. In our opinion, based on the high prevalence and mortality induced by this disease, CRD patients, even if asympto­matic, might benefit from an evaluation including at least an annual or biannual clinical, ECG, and cardiac marker evaluation.

Exercise stress tests are not helpful in detecting ischemia in patients with chronic renal diseases owing to frequent repolarization abnormalities, presence of left ventricular hypertrophy and also because only 44% of hemodialyzed patients are able to reach 85% of the predicted maximal heart rate. Rest Thallium scintigraphy has a 37% sensitivity and a 73% specificity to detect coronary stenosis. For these reasons, pharmaco­logical tests coupled with echo or radionuclide scintigraphy are preferred. Combined exercise­dipyridamole thallium scintigraphy improves diagnostic and prognostic value in asymptomatic hemodialysis patients: abnormal tests evince 92% sensitivity, 89% specificity and a 9.2 risk ratio. [44],[45] Rest echocardiography may reveal regional or segmental kinetic abnorma­lities, which can be due to ischemic injury or regional fibrosis. Stress echocardiography has similar results to scintigraphy: 95% sensitivity and 86% specificity. [46]

The diagnostic and prognostic value of cardiac markers has been discussed in the last decade. The cardiac troponins T and I are almost accepted as sensitive and specific cardiac bio­markers. Serum levels of cTn I or T seem to be accurate for diagnosing acute coronary syndrome and myocardial infarction. Asympto­matic hemodialysis patients have a high prevalence of cTn T concentrations above the diagnostic threshold of myocardial damage. We suggest that this high prevalence reflects cardiac injury which might be due not only to CAD but also to left ventricular hypertrophy or heart failure. [47] A somewhat high cTnT level in asymptomatic hemodialysis patients is now widely accepted as a prognostic marker for two-year overall mortality (RR: 3.9), [48] and more importantly for cardiac morbidity and mortality (RR: 3.0 and 1.9 respectively). [49] We propose, for hemodialysis patients, serum cTn T assays are to be performed once or twice a year. Unexpected elevation of this marker requires cardiac re-evaluation (clinical and non-invasive test).

Coronary angiography in CRD patients can compromise the renal function and may precipitate the need for dialysis. Moreover, even in ESRD, angiogram entails cardiac events, hemorrhages and even a risk of death. [50]

In the future, probably cine MRI, which avoids use of iodine-contrast injection, might provide accurate visualization of coronary arteries and replace coronary angiography.

Thus, evolution of ischemic heart disease may be complicated by acute coronary syndrome, myocardial infarction or progressive injury which all lead to ischemic cardiomyopathy. In acute coronary syndromes treated with anti GPIIbIIIa, abnormal renal function is a marker of adverse clinical outcomes. [51] Similarly, renal function is a powerful risk factor of mortality in acute myocardial infar­ction. Recently, analysis of three studies of thrombolysis (TIMI 10, TIMI 14 and InTIME­II trials) found creatinine and creatinine clearance as independent factors of mortality not mediated by CHF at presentation. Interest­ingly, this analysis proves a similar efficacy of thrombolysis in renal failure patients as in non-renal dysfunction patients. [52] Intra­hospital mortality due to acute myocardial infarction, is 6% for patients with mild renal insufficiency, 14% for those with moderate renal failure, 21% in severe renal failure and 30% for patients with ESRD. This is in contrast to 2% mortality in non-renal dys­function patients: [53] the risk ratio is 2.4 to 5.8 depending on the severity of renal dysfunction. During the hospitalization phase, renal dys­function patients have significantly more atrial fibrillation and occurrence of CHF. In studies published on ESRD patients, renal dysfunction is associated with underutilization of reperfusion and/or adjunctive treatments that have witnessed a significant reduction in mortality (-30% for aspirin and beta blockers).

In hemodialysis patients, occurrence of acute myocardial infarction represents a dramatic event with a 59% mortality at one year of follow-up and 73% mortality at two years; [54] these results may be accounted for by under­diagnosis and under-treatment. [55] The optimal medical treatment includes antiplatelet agents, beta-blockers, ACE inhibitors (or ARB), long acting nitrates only for angina, calcium channel antagonists as adjunctive for angina and hypertension, statins and adherence to guide­lines. The optimal method for revascularization is controversial. Coronary angioplasty, especially when stents are used, has low in-hospital and short post-procedure mortality as compared to coronary artery bypass graft (CABG) surgery. However, at long term follow-up, CRD patients display a higher risk of restenosis and poorer survival than normal renal function patients (6 months restenosis: 20-30% vs 15-30%, 1 year cardiac mortality: 15-30 vs 2-5% respectively). In hemodialysis patients, there appears to be a relative survival advantage associated with CABG versus angioplasty (with or without stent). The survival benefit is attributable to the utilization of internal mammary graft, especially for diabetics or multivessel CAD patients. [56]

Congestive Heart Failure

Congestive heart failure is found in around 25% of CRD patients, the main cause being coronary artery disease. The prevalence is correlated with the severity of renal dysfunction. Indeed, a vicious cycle is created early on: renal failure worsens cardiomyopathy and heart failure induces a progression of renal dysfunction, the two failures being aggravated by anemia. Thus, half of congestive heart failure patients have creatinine clearance < 60 ml/min. [57] In hemodialysis patients, the prevalence of heart failure is estimated at 71 per 1000 patients per year, with a 83% mortality at three years of follow-up. [58]

Echocardiography is the right tool for detect­ing and supervising the left ventricular dimen­sions and function. This should be performed for hemodialysis patients on the day without dialysis. In chronic renal disease, echocardio­graphy is normal in only 16% of patients, left ventricular hypertrophy (indexed LV mass > 110 g/m 2 ) is recognized in 65% of patients, ventricular dilation with normal function in 4% and left ventricular dysfunction in 16% of patients. But, it is mandatory to take into account that left ventricular dilation can be due also to anemia, fluid retention or fistulae output.

Brain natriuretic peptide, which is elevated in increased cardiac filling pressure, might be helpful in following volume status. [59]

CHF is one of the main predictors for starting dialysis in 11,912 male veterans. [60] After myo­cardial infarction, glomerular filtration rate decreases by 5.5 ml/min/year in patients with­out CHF, and by 0.5 ml/min/year if they are treated with ACE inhibitors. The decrease in glomerular filtration rate is 15.7 ml/min/year in patients who develop congestive heart failure and who have not had ACE inhibitor treatment, and is 11.2 ml/min/year with ACE inhibitors. [61] However, in the SOLVD trial, they have shown that if ACEi acting alone worsens renal function, the latter seems to be preserved with beta blockers co-prescription. [62] Furthermore, treatment by carvedilol in heart-renal failure patients has been shown to cause an improve­ment in functional status with a reduction of left ventricular volumes and an improvement of cardiac function. [63]

Rhythm Disorders

Chronic renal disease patients have a high susceptibility to arrhythmias. This finding can be explained by variations in serum potassium, left ventricular hypertrophy, myocyte ultra­structure and function abnormalities, inter­stitial fibrosis, endothelial dysfunction and decreased myocardial perfusion with diminished ischemia tolerance. In hemodialysis patients, prolonged signal-averaged QRS is known to precipitate arrythmias, but a link between increased arrythmias and sudden death has not been established. [64],[65] Sudden cardiac death (SCD) may be implicated in 60% of all cardiac deaths in dialysis patients: in the USRDS database, 47% of all cardiac deaths are reported as "cardiac arrest, cause unknown", 13% attributed to arrhythmias. [66] The pre­valence is 93 events per 1000 patients per year at one year, 164 per 1000 at four years, 1.5 times higher for diabetic than for non­diabetic patients. The risk factors for sudden death in patients with renal disease are: high serum troponins levels, prolonged QT dispersion, [67] heart rate variability abnormal­ities, [68] and a low potassium level in dialysis bath. Premature ventricular beats are very frequent in hemodialysis patients, but their presence has not got any prognostic value. In the three sessions per week dialysis protocols, sudden cardiac death occurs more frequently on Monday and Thursday. [69] The prognosis after SCD is very poor: 60% mortality after 48 hours if sudden death occurs during the dialysis session and > 95% outside a medical center. [70]

Valvular Diseases

Valvular diseases are a frequent co-morbidity, given the increasing elderly population. They are mainly due to degenerative lesions, chara­cterized by the massive calcifications pre­dominant in aortic and mitral positions with or without hemodynamic compromise. [71],[72] Valvular calcifications are found in 30-50% of hemodialyzed patients among whom 25­30% have valvular stenosis (aortic stenosis is frequent, mitral calcifications are often free of hemodynamic effect). The progression of valve calcification is accelerated in CRD patients. [73] Features of chronic renal failure such as increased cardiac output by fistulae, fluid overload, anemia, and magnitude of left ventricular hypertrophy can influence the left ventricular function. Functional and clinical evaluation is difficult in patients with limited physical activity; furthermore, ejection systolic murmur is very common in this population. Doppler echocardiography is the key to diagnosis. However, trans-valvular gradient evaluation by Doppler echocardiography may result in some misinterpretations; overesti­mation in the case of high cardiac output and underestimation in the case of left ventricular dysfunction and the importance of calcifi­cations may induce errors in valvular area assessment. Two echocardiographies per year are required in patients with non-significant or mild valvular disease, while the test is required every three months in moderate and severe aortic stenosis.

The prognosis of valvular disease is better than that for coronary artery disease and has a mortality rate of 1.5 per 1000 patients per year. [74] The annual incidence of valvular diseases requiring surgery is evaluated at 1.5 to 1.9 per 1000 hemodialysis patients in France. [75] Decision in favor of surgical treat­ment requires caution because renal dysfunction is an independent factor for mortality after valve replacement (20% mortality in valve replacement alone, and 30% mortality if surgery combines valve replacement and CABG). [76],[77],[78] Usually, mechanical valves are proposed, the suggested reason being the potential risk of degradation of bioprosthesis, but the retro­spective study conducted by Herzog and colleagues (> 5000 patients) did not find any survival differences between mechanical or bioprosthesis at 1.5 years of follow-up. [79] Further studies are needed before changing current practices.


   Conclusion Top


CVD is a frequent and serious cause in CRD patients. It calls for early and inten­sive treatment. This is difficult and requires close co-operation between nephrologists and cardiologists.

 
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Correspondence Address:
Marie Christine Iliou
Service de Readaptation Cardiaque – Hospital Broussais, 96 rue Didot - 75014, Paris
France
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PMID: 18202488

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    Introduction
    Epidemiology
    Pathophysiology
    Cardiac Diseases
    Conclusion
    References
 

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