In this study, we evaluated 160 patients on maintenance hemodialysis at MNH in Dar es Salaam, Tanzania to determine the prevalence of heart failure. Heart failure was noted in 10.6% of the patients. Anemia, the presence of angina, and intradialytic hypertension were independent predictors of HF. Compared to those without, patients with HF had a higher median malnutrition inflammation score, and mean erythropoietin resistance index. A lower prevalence of HF was found in our study when compared to an earlier study done at MNH [4]. This may be explained by better fluid volume control as depicted by a high proportion (76.3%) of HD patients in our study receiving adequate dialysis [13]. Excess fluid (preload) increases the cardiac load that stimulates the renin–angiotensin–aldosterone system (RAAS) subsequently resulting in left ventricular (LV) remodeling [2, 8, 12]. Sympathetic over-stimulation from anemia similarly induces LV hypertrophy that causes diastolic dysfunction [2, 4]. Treatment of anemia using erythropoietin stimulating agents is the mainstay. However, some patients may not respond well especially if concomitant iron deficiency and chronic inflammation are not addressed [14, 15].
Patients with HF were noted to have significantly higher Erythropoietin resistance. The latter has been linked with higher mortality [15]. Erythropoietin-resistant anemia will necessitate higher EPO doses if underlying causes are not adequately treated [14, 16]. Higher EPO doses result in high blood viscosity and elevated blood pressures that increase afterload which can precipitate HF [16].
The presence of HF is significantly associated with having higher MIS. This may be attributed to greater inter-dialytic fluid retention that occurs in patients with MICS [8]. Ongoing weight losses in patients with MICS may limit adequate fluid control. Vlatković et al. found that patients with low BMI are at higher risk of fluid overload [8]. Congestive heart failure is accompanied by increased cytokines like TNF-alpha that propels cardiac cachexia [17]. In addition, MICS is accompanied by hypoalbuminemia that promotes fluid shifts from the intravascular compartment [6,7,8].
High inter-dialytic weight gain is postulated to result in intra-dialytic hypertension [12, 18]. In our study, intra-dialytic hypertension significantly correlated with the occurrence of heart failure. Intra-dialytic hypertension has also been linked with sodium retention, endothelial dysfunction, RAAS, and sympathetic over-stimulation. All these factors propagate LV remodeling increasing the risk of heart failure [12, 18].
Malnutrition and inflammation augment atherosclerosis and is therefore interrelated as Malnutrition–inflammation–atherosclerosis (MIA) syndrome which is linked to poor cardiovascular outcomes [7]. Coronary atherosclerosis in HD patients is widespread and results in gradual myocardial loss causing systolic dysfunction [2, 7]. In our study patients with angina had almost six-fold higher odds of having heart failure. Hypercholesterolemia may not accurately predict coronary atherosclerosis in this population. Instead, patients with low cholesterol levels have advanced CVD. In this study patients with HF had lower cholesterol levels. This is consistent with the concept of reverse epidemiology which is mostly attributed to chronic inflammation, oxidative stress, and resulting endothelial, and myocardial dysfunction [18, 19]. In patients with advanced CKD, traditional risk factors do not strongly relate to CVD unlike the general population [18, 19]. Likewise in our study aging, diabetes, hypertension, and hyperlipidemia did not significantly associate with the occurrence of HF, instead MICS correlated with HF in this population.
Management of heart failure in dialysis patients entails adequate fluid volume control, treatment of hypertension, anemia, and the use of medications like angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and beta-blockers [2]. This class of medications has been shown to reduce cardiovascular events, and mortality in hemodialysis patients [20, 21]. In view of the widespread cardiac impairment in HD patients that is certain to worsen in the setting of MICS, hypertension, and chronic anemia, it is reasonable to consider its use [2,3,4, 20, 21]. The limited use of these drugs by patients in our study demands a collaborative approach by nephrologists, cardiologists, and physicians in updating prescribing practices considering the CVD vulnerability of these patients.
Statins and anti-oxidants may also help curb the inflammatory syndrome that fosters atherosclerosis and myocardial damage [22, 23]. High flux hemodialysis and online hemodiafiltration allow better clearance of middle molecules implicated in inflammation, and erythropoietin refractory anemia [14].
The small number of patients and lack of echocardiography assessment were some limitations of our study. The class of heart failure was not assessed as well. The prevalence of heart failure may be under-estimated as we only included stable dialysis patients attending on an out-patient basis and excluded a few patients with severe respiratory distress.
