Proven Strategies to Reduce Cardiovascular Mortality in Hemodialysis Patients

Abstract

Background: In hemodialysis patients, left ventricular hypertrophy (LVH) correlates with mortality. The reason for LVH in uremics is multifactorial. The primary objective of our study was to investigate the effects of a multi-interventional treatment strategy on LVH. Methods: In 230 ambulatory patients, including patients with coronary artery disease, diabetes, diastolic and systolic dysfunction, we continued optimized cardiac therapy (β-blockers, angiotensin-converting enzyme inhibitors and angiotensin receptor blockers) with full anemia correction by intravenous epoetin-β. The dose of epoetin-β for maintaining target hemoglobin (Hb) was 68 ± 23 IU/kg/week. Serial echocardiograms were recorded every 3–6 months. The mean observation period was 4.8 ± 1.2 years. Results: Mean Hb at baseline was 11.2 ± 2.0 versus 14.1 ± 1.4 g/dl (p < 0.001) at study end. There was a significant reduction in left ventricular mass index (LVMI: 159 ± 50.4 vs. 130.2 ± 42.7 g/m²; p < 0.001). In a subgroup of 2/3 of the patients, LVMI returned to normal (169 ± 33 vs. 114 ± 14 g/m²; p < 0.001). Conclusion: Baseline LVMI (p < 0.001), Hb increase (p < 0.03), and triple cardiac therapy (p < 0.03) were significant and independent prognostic factors for a reduction in LVMI. The annual cardiovascular mortality was 5%. Even anemia correction from 12 to 14 g/dl results in further (p < 0.001) regression of LVMI.

Blood pressure impact on left ventricular geometry in chronic haemodialysis patients

“…Hampl et al (14) confi rmed signifi cant reduction of LVMI, LVEDD and ejection fraction increase, but no left atrial size decrease in a group of 230 patients due to intensifi cated antihypertensive treatment (beta blockers, inhibitors of angiotensin-converting enzyme and AT1 receptors) and correction of anaemia. They suppose that many patients do not get complete antihypertensive treatment to decrease cardiovascular risk.…”

Cardiac Disease in the Dialysis Patient: Good, Better, Best Clinical Practice

“…The main finding of the mentioned studies [32][33][34] is that a multi-interventional approach, which combines optimized cardiac/antihypertensive therapy with ␤ -blockers, ACE inhibitors/ARBs with complete correction of renal anemia by erythropoietin and intravenous iron, resulted in a significant reduction of the LVMI. The metabolic acidosis was optimally corrected, therefore, no potassium problems could be observed with our cardiac/ antihypertensive therapy.…”

“…Since the presence and/or progression of LVH have emerged as an independent prognostic factor, LVH has become accepted as a surrogate parameter for morbidity/mortality outcomes in uremic patients. Hampl et al [32][33][34] found by multivariate analysis that the presence of LVH at baseline, full correction of renal anemia and cardiac/antihypertensive therapy were significant and independent predictors of significant LVH regression.…”

“…renal anemia, cannot be sufficient. The following therapeutic strategies are used [32][33][34] : (1) optimized correction of metabolic acidosis: HCO 3 values 1 22 mmol/l in conservatively treated uremic patients (before onset of dialysis) as well as in patients treated with hemodialysis before hemodialysis after the long dialysis interval; (2) target blood pressure ! 130/80 mm Hg (in hemodialysis patients before dialysis); (3) heart rate 60-70/min; (4) hemoglobin: 13.5 g/dl for women and 14.5 g/dl for men; (5) iron status normal; (6) it is important to check serum values for hypochromic erythrocytes, mean corpuscular hemoglobin concentration, iron, platelet count, and transferrin saturation (TSAT) in relation to the absolute transferrin values as the substrate which is significantly diminished in hemodialysis patients due to malnutrition/inflammation (see below) in order to avoid iron deficiency; (7) low dosages of ESAs for renal anemia correction; (8) adequate high target doses of ␤ -blockers, angiotensinconverting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs); respective targets: 200 mg of metoprolol, 10 mg of ramipril and 32 mg of candesartan.…”

“…These successful therapeutic options were evaluated in multivariate analyses [32][33][34] . Full anemia correction and cardiac triple therapy were independent and significant prognostic factors for LVMI regression.…”