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      Call for Papers: Green Renal Replacement Therapy: Caring for the Environment

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      About Blood Purification: 3.0 Impact Factor I 5.6 CiteScore I 0.83 Scimago Journal & Country Rank (SJR)

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      Haemodialysis-induced myocardial stunning in chronic kidney disease - a new aspect of cardiovascular disease.

      Blood purification
      Arrhythmias, Cardiac, etiology, prevention & control, Baroreflex, physiology, Body Temperature, Coronary Disease, complications, Death, Sudden, Cardiac, Disease Susceptibility, Follow-Up Studies, Heart Failure, Hemodynamics, Humans, Hypertension, physiopathology, Hypotension, Kidney Failure, Chronic, therapy, Myocardial Stunning, Positron-Emission Tomography, Randomized Controlled Trials as Topic, statistics & numerical data, Reflex, Abnormal, Renal Dialysis, adverse effects, methods, Ventricular Dysfunction, Left, radionuclide imaging, ultrasonography

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          Abstract

          Chronic haemodialysis (HD) patients are already primed by a large number of structural and functional peripheral vascular and cardiac abnormalities to experience demand myocardial ischaemia. Transient myocardial ischaemia may lead to left ventricular (LV) dysfunction that can persist after the return of normal perfusion. This prolonged dysfunction is known as myocardial stunning. Repetitive episodes of ischaemia can be cumulative and have been shown to lead to prolonged LV dysfunction (in patients with ischaemic heart disease). Conventional HD itself is a sufficient cardiovascular functional stressor to precipitate such recurrent ischaemic insults, leading to myocardial functional and structural changes, eventually resulting in fixed systolic dysfunction and heart failure (conferring a dismal prognosis for patients undergoing dialysis). Furthermore these same haemodynamic insults may also adversely affect other vascular beds in other vulnerable organ systems, driving an even wider range of pathophysiological processes. A variety of therapeutic manoeuvres aimed at improving the haemodynamic tolerability of treatment have been shown to reduce acute dialysis-induced myocardial ischaemia. This article aims to give an appreciation of the possibility that modification of the dialysis treatment to improve tolerability of therapy may have the potential to provide us with additional therapeutic targets, to reduce currently excessive rates of cardiovascular morbidity and mortality. Copyright (c) 2010 S. Karger AG, Basel.

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          Hemodialysis-induced cardiac injury: determinants and associated outcomes.

          Hemodialysis (HD)-induced myocardial stunning driven by ischemia is a recognized complication of HD, which can be ameliorated by HD techniques that improve hemodynamics. In nondialysis patients, repeated ischemia leads to chronic reduction in left ventricular (LV) function. HD may initiate and drive the same process. In this study, we examined the prevalence and associations of HD-induced repetitive myocardial injury and long-term effects on LV function and patient outcomes. Seventy prevalent HD patients were assessed for evidence of subclinical myocardial injury at baseline using serial echocardiography and followed up after 12 mo. Intradialytic blood pressure, hematologic and biochemical samples, and patient demographics were also collected at both time points. Sixty-four percent of patients had significant myocardial stunning during HD. Age, ultrafiltration volumes, intradialytic hypotension, and cardiac troponin-T (cTnT) levels were independent determinants associated with its presence. Myocardial stunning was associated with increased relative mortality at 12 mo (P = 0.019). Cox regression analysis showed increased hazard of death in patients with myocardial stunning and elevated cTnT than in patients with elevated cTnT alone (P < 0.02). Patients with myocardial stunning who survived 12 mo had significantly lower LV ejection fractions at rest and on HD (P < 0.001). HD-induced myocardial stunning is common, and may contribute to the development of heart failure and increased mortality in HD patients. Enhanced understanding of dialysis-induced cardiac injury may provide novel therapeutic targets to reduce currently excessive rates of cardiovascular morbidity and mortality.
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            The stunned myocardium: prolonged, postischemic ventricular dysfunction.

            Myocardial ischemia has, for many decades, been viewed as an all-or-none process that causes myocardial necrosis when prolonged and severe, but whose effects are transient when it is brief or mild. In view of the evidence that the ischemic process may "hit, run and stun," perhaps our thinking about the consequences of myocardial ischemia should be expanded. According to this formulation, an ischemic insult not of sufficient severity of duration to produce myocardial necrosis may acutely affect myocardial repolarization and cause angina (hit); but these changes wane rapidly (run), when the balance between myocardial oxygen supply and demand has been reestablished. However, the ischemia may interfere with normal myocardial function, biochemical processes and ultrastructure for prolonged periods (stun). The severity and duration of these postischemic changes depend on the length and intensity of the ischemia, as well as on the condition of the myocardium at the onset of the ischemic episode. Furthermore, it is likely that when the myocardium is repeatedly stunned, it may exhibit chronic postischemic left ventricular dysfunction, an ill-defined condition. If prolonged, chronic postischemic left ventricular dysfunction can progress to myocardial scarring and ischemic cardiomyopathy, it may be important to determine how often it can be ameliorated by permanent improvement of myocardial perfusion by surgical treatment.
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              Effects of hemodialysis on cardiac function.

              Hemodialysis (HD) patients are subject to an enormous excess of cardiovascular morbidity and mortality. This appears to be largely driven by factors that are different from those at play in the general population. Chronic HD patients are already primed by a large number of structural and functional peripheral vascular and cardiac abnormalities to experience demand myocardial ischemia. Conventional HD is capable of inducing myocardial ischemia. Recurrent ischemic insults lead to myocardial functional and structural changes, eventually resulting in fixed systolic dysfunction and heart failure (conferring a dismal prognosis for patients undergoing dialysis). Modifications of the HD process to improve the hemodynamic tolerability of the treatment have been shown to reduce the perturbation of myocardial blood flow and functional evidence of dialysis-induced ischemia. Although it is uncomfortable to consider that much of the observed disease burden in HD patients may be an artifact of current dialysis treatment regimes, understanding the role that conventional dialysis plays in the pathophysiology of cardiac injury in HD patients has the potential to provide us with additional dialysis, and non-dialysis, based novel therapeutic targets to reduce currently excessive rates of cardiovascular morbidity and mortality.
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