OBJECTIVE: To examine whether aggressive risk factor modification in chronic kidney disease (CKD) can limit the development of new ischaemia or reduce cardiac events. METHODS:Patients with CKD were randomly assigned to either an aggressive risk factor modification strategy (targeted treatment of hypertension, dyslipidaemia, homocysteine, haemoglobin and phosphate) or standard care. An intention to treat analysis was performed on 152 patients who had baseline dobutamine stress echocardiography (DSE), including 107 who had follow-up DSE. Biochemical parameters, cardiac risk factors and investigations (ECG, two-dimensional echocardiography) were recorded at baseline. New ischaemia was classed as new or worsening stress wall motion abnormality between follow-up and baseline DSE. Patients were followed up for the development of new ischaemia or cardiac death, acute coronary syndrome and non-fatal myocardial infarction over 1.8 years. RESULTS: The development of new ischaemia was common but not different between the standard and aggressively treated groups (15 (21%) v 18 (23%), p = 0.8). Independent predictors of new ischaemia were older age, abnormal ECG, higher systolic blood pressure and lower serum high density lipoprotein cholesterol, but not treatment arm. The standard and aggressively treated groups did not differ in cardiac event rate (10% v 13%, p = 0.6) or all-cause mortality (10% v 19%, p = 0.2). In patients with an abnormal baseline DSE (non-diagnostic, scar or ischaemia), the event rate was similar (22% v 20%, p = 0.9). CONCLUSION:Aggressive risk factor modification in CKD does not limit the development of new ischaemia or reduce cardiac events in patients with an abnormal DSE.
RCT Entities:
OBJECTIVE: To examine whether aggressive risk factor modification in chronic kidney disease (CKD) can limit the development of new ischaemia or reduce cardiac events. METHODS:Patients with CKD were randomly assigned to either an aggressive risk factor modification strategy (targeted treatment of hypertension, dyslipidaemia, homocysteine, haemoglobin and phosphate) or standard care. An intention to treat analysis was performed on 152 patients who had baseline dobutamine stress echocardiography (DSE), including 107 who had follow-up DSE. Biochemical parameters, cardiac risk factors and investigations (ECG, two-dimensional echocardiography) were recorded at baseline. New ischaemia was classed as new or worsening stress wall motion abnormality between follow-up and baseline DSE. Patients were followed up for the development of new ischaemia or cardiac death, acute coronary syndrome and non-fatal myocardial infarction over 1.8 years. RESULTS: The development of new ischaemia was common but not different between the standard and aggressively treated groups (15 (21%) v 18 (23%), p = 0.8). Independent predictors of new ischaemia were older age, abnormal ECG, higher systolic blood pressure and lower serum high density lipoprotein cholesterol, but not treatment arm. The standard and aggressively treated groups did not differ in cardiac event rate (10% v 13%, p = 0.6) or all-cause mortality (10% v 19%, p = 0.2). In patients with an abnormal baseline DSE (non-diagnostic, scar or ischaemia), the event rate was similar (22% v 20%, p = 0.9). CONCLUSION: Aggressive risk factor modification in CKD does not limit the development of new ischaemia or reduce cardiac events in patients with an abnormal DSE.
Authors: J C West; D A Napoliello; J M Costello; L A Nassef; R J Butcher; J E Hartle; T R McConnell; J W Finley; S E Kelley; S Chao; R Latsha Journal: Transpl Int Date: 2000 Impact factor: 3.782
Authors: Carmine Zoccali; Francesco Antonio Benedetto; Francesca Mallamaci; Giovanni Tripepi; Giuseppe Giacone; Alessandro Cataliotti; Giuseppe Seminara; Benedetta Stancanelli; Lorenzo Salvatore Malatino Journal: J Am Soc Nephrol Date: 2001-12 Impact factor: 10.121
Authors: D C Brennan; G Vedala; S B Miller; M E Anstey; G G Singer; A Kovacs; B Barzilai; J A Lowell; S Shenoy; T K Howard; V G Davila-Roman Journal: Transplant Proc Date: 1997 Feb-Mar Impact factor: 1.066
Authors: T H Marwick; C Case; S Sawada; C Rimmerman; P Brenneman; R Kovacs; L Short; M Lauer Journal: J Am Coll Cardiol Date: 2001-03-01 Impact factor: 24.094
Authors: Santhi K Ganesh; Austin G Stack; Nathan W Levin; Tempie Hulbert-Shearon; Friedrich K Port Journal: J Am Soc Nephrol Date: 2001-10 Impact factor: 10.121
Authors: D Poldermans; M Arnese; P M Fioretti; E Boersma; I R Thomson; R Rambaldi; H van Urk Journal: Circulation Date: 1997-01-07 Impact factor: 29.690
Authors: W E Bloembergen; D C Stannard; F K Port; R A Wolfe; J A Pugh; C A Jones; J W Greer; T A Golper; P J Held Journal: Kidney Int Date: 1996-08 Impact factor: 10.612
Authors: R Hoffmann; H Lethen; T Marwick; M Arnese; P Fioretti; A Pingitore; E Picano; T Buck; R Erbel; F A Flachskampf; P Hanrath Journal: J Am Coll Cardiol Date: 1996-02 Impact factor: 24.094
Authors: G Reis; P A Marcovitz; A B Leichtman; R M Merion; W P Fay; S W Werns; W F Armstrong Journal: Am J Cardiol Date: 1995-04-01 Impact factor: 2.778
Authors: D Rosenberger; R Gargoum; N Tyagi; N Metreveli; U Sen; C Maldonado; S Tyagi Journal: Nutr Metab Cardiovasc Dis Date: 2010-03-12 Impact factor: 4.222
Authors: Anuja Shah; Linda F Fried; Shu-Cheng Chen; Yang Qiu; Suying Li; Kerri L Cavanaugh; Keith C Norris; Adam T Whaley-Connell; Peter A McCullough; Rajnish Mehrotra Journal: Am J Kidney Dis Date: 2012-03 Impact factor: 8.860
Authors: Teresa Adragao; Johann Herberth; Marie-Claude Monier-Faugere; Adam J Branscum; Anibal Ferreira; Joao M Frazao; Jose Dias Curto; Hartmut H Malluche Journal: Clin J Am Soc Nephrol Date: 2009-01-21 Impact factor: 8.237
Authors: William G Petchey; Ingrid J Hickman; Emma Duncan; Johannes B Prins; Carmel M Hawley; David W Johnson; Katherine Barraclough; Nicole M Isbel Journal: BMC Nephrol Date: 2009-12-10 Impact factor: 2.388