Skip header and navigation

Refine By

19 records – page 1 of 2.

Absence of protective effect of renin-angiotensin system inhibitors on atrial fibrillation development: insights from the Canadian Trial of Atrial Fibrillation (CTAF).

https://arctichealth.org/en/permalink/ahliterature155217
Source
Can J Cardiol. 2008 Sep;24(9):709-13
Publication Type
Article
Date
Sep-2008
Author
Maryse Palardy
Anique Ducharme
Stanley Nattel
Jean-Claude Tardif
Michel White
Normand Racine
Karine Tétreault
Farida Dabouz
Mario Talajic
Denis Roy
Author Affiliation
Department of Medicine, Montreal Heart Institute, Montreal, Canada.
Source
Can J Cardiol. 2008 Sep;24(9):709-13
Date
Sep-2008
Language
English
Publication Type
Article
Keywords
Aged
Amiodarone - therapeutic use
Anti-Arrhythmia Agents - therapeutic use
Atrial Fibrillation - drug therapy
Canada
Female
Humans
Male
Middle Aged
Multivariate Analysis
Propafenone - therapeutic use
Prospective Studies
Recurrence - prevention & control
Renin - antagonists & inhibitors
Renin-Angiotensin System - drug effects
Sotalol - therapeutic use
Abstract
Antiarrhythmic agents have modest efficacy in preventing atrial fibrillation (AF) recurrence. Although retrospective analyses have suggested a preventive effect of inhibitors of the renin-angiotensin system (RAS) on AF development in patients with congestive heart failure or hypertension, the value of these agents has not been evaluated in patients with AF but without a high prevalence of hypertension or heart failure.
A retrospective analysis of the Canadian Trial of Atrial Fibrillation (CTAF) was conducted. CTAF demonstrated the superiority of amiodarone (A) over sotalol or propafenone (SP) in maintaining sinus rhythm in patients with AF. Of the 403 patients randomly assigned in CTAF, 11.7% of the A group and 12.7% of the SP group were receiving a RAS inhibitor at baseline. By multivariate analysis (including all the risk factors known to be associated with AF available in the database), the use of RAS blockers in addition to antiarrhythmic agents was not associated with additional benefit against AF development. There was a recurrence of AF in 59 patients (38.3%) and 14 patients (29.8%) of groups A and A-RAS, respectively, while 93 patients (61.6%) and 32 patients (62.8%) of the SP and SP-RAS groups, respectively, experienced recurrent AF.
Blocking the RAS did not provide additional benefit against AF recurrence in CTAF patients treated with an antiarrhythmic drug. These results underscore the need for randomized clinical trials to clearly define the role of RAS inhibitors in treating AF.
Notes
Cites: Int J Cardiol. 2005 Dec 7;105(3):315-816274775
Cites: Am Heart J. 2006 Jul;152(1):86-9216838426
Cites: J Am Coll Cardiol. 2005 Jun 7;45(11):1832-915936615
Cites: Am Heart J. 2005 Mar;149(3):548-5715864246
Cites: Heart Rhythm. 2004 Dec;1(6):669-7515851238
Cites: Heart Rhythm. 2004 Nov;1(5):531-715851214
Cites: J Am Coll Cardiol. 2005 Mar 1;45(5):712-915734615
Cites: Circulation. 1999 Jul 27;100(4):376-8010421597
Cites: Circulation. 1999 Jul 6;100(1):87-9510393686
Cites: Circ Res. 1997 Dec;81(6):1045-529400386
Cites: Eur Heart J. 2006 Aug;27(15):1841-616825288
Cites: Cardiovasc Res. 1999 Oct;44(1):121-3110615396
Cites: J Pharmacol Toxicol Methods. 1999 Sep;42(1):11-2010715599
Cites: N Engl J Med. 2000 Mar 30;342(13):913-2010738049
Cites: J Am Coll Cardiol. 2000 May;35(6):1669-7710807475
Cites: Circulation. 2000 Jun 6;101(22):2612-710840013
Cites: Am J Cardiol. 2001 Oct 15;88(8):906-9, A811676961
Cites: Circulation. 2001 Nov 20;104(21):2608-1411714658
Cites: Cardiovasc Res. 2002 May;54(2):230-4612062329
Cites: Circulation. 2002 Jul 16;106(3):331-612119249
Cites: Circulation. 2003 Jun 17;107(23):2926-3112771010
Cites: J Am Coll Cardiol. 2003 Jun 18;41(12):2197-20412821247
Cites: Circulation. 2004 Aug 31;110(9):1042-615313941
Cites: Can J Cardiol. 2004 Oct;20(12):1245-815494777
Cites: Pacing Clin Electrophysiol. 2004 Oct;27(10):1405-1015511250
Cites: Am J Cardiol. 1991 Aug 1;68(4):335-411907089
Cites: JAMA. 1994 Mar 16;271(11):840-48114238
Cites: Circulation. 1995 Mar 1;91(5):1588-957867201
Cites: Circulation. 1995 Oct 1;92(7):1954-687671380
Cites: Circulation. 1996 Oct 1;94(7):1600-68840850
Cites: Circulation. 1996 Dec 1;94(11):2968-748941128
Cites: Circulation. 1997 Aug 19;96(4):1180-49286947
Cites: Circ Res. 1997 Oct;81(4):512-259314832
Cites: Circulation. 1997 Oct 7;96(7):2455-619337224
Cites: Circulation. 1997 Nov 18;96(10):3710-209396475
PubMed ID
18787722 View in PubMed
Less detail

Alternative Imaging Modalities in Ischemic Heart Failure (AIMI-HF) IMAGE HF Project I-A: study protocol for a randomized controlled trial.

https://arctichealth.org/en/permalink/ahliterature108622
Source
Trials. 2013;14:218
Publication Type
Article
Date
2013
Author
Eileen O'Meara
Lisa M Mielniczuk
George A Wells
Robert A deKemp
Ran Klein
Doug Coyle
Brian Mc Ardle
Ian Paterson
James A White
Malcolm Arnold
Matthias G Friedrich
Eric Larose
Alexander Dick
Benjamin Chow
Carole Dennie
Haissam Haddad
Terrence Ruddy
Heikki Ukkonen
Gerald Wisenberg
Bernard Cantin
Philippe Pibarot
Michael Freeman
Eric Turcotte
Kim Connelly
James Clarke
Kathryn Williams
Normand Racine
Linda Garrard
Jean-Claude Tardif
Jean DaSilva
Juhani Knuuti
Rob Beanlands
Author Affiliation
Montreal Heart Institute, Montréal, QC, Canada.
Source
Trials. 2013;14:218
Date
2013
Language
English
Publication Type
Article
Keywords
Algorithms
Canada
Clinical Protocols
Diagnostic Imaging - methods
Heart Arrest - etiology
Heart Failure - diagnosis - etiology - mortality - therapy
Humans
Magnetic Resonance Imaging
Myocardial Infarction - etiology
Myocardial Ischemia - complications - diagnosis - mortality - therapy
Patient Readmission
Patient Selection
Positron-Emission Tomography
Predictive value of tests
Prognosis
Registries
Research Design
Time Factors
Tomography, Emission-Computed, Single-Photon
Abstract
Ischemic heart disease (IHD) is the most common cause of heart failure (HF); however, the role of revascularization in these patients is still unclear. Consensus on proper use of cardiac imaging to help determine which candidates should be considered for revascularization has been hindered by the absence of clinical studies that objectively and prospectively compare the prognostic information of each test obtained using both standard and advanced imaging.
This paper describes the design and methods to be used in the Alternative Imaging Modalities in Ischemic Heart Failure (AIMI-HF) multi-center trial. The primary objective is to compare the effect of HF imaging strategies on the composite clinical endpoint of cardiac death, myocardial infarction (MI), cardiac arrest and re-hospitalization for cardiac causes.In AIMI-HF, patients with HF of ischemic etiology (n = 1,261) will follow HF imaging strategy algorithms according to the question(s) asked by the physicians (for example, Is there ischemia and/or viability?), in agreement with local practices. Patients will be randomized to either standard (SPECT, Single photon emission computed tomography) imaging modalities for ischemia and/or viability or advanced imaging modalities: cardiac magnetic resonance imaging (CMR) or positron emission tomography (PET). In addition, eligible and consenting patients who could not be randomized, but were allocated to standard or advanced imaging based on clinical decisions, will be included in a registry.
AIMI-HF will be the largest randomized trial evaluating the role of standard and advanced imaging modalities in the management of ischemic cardiomyopathy and heart failure. This trial will complement the results of the Surgical Treatment for Ischemic Heart Failure (STICH) viability substudy and the PET and Recovery Following Revascularization (PARR-2) trial. The results will provide policy makers with data to support (or not) further investment in and wider dissemination of alternative 'advanced' imaging technologies.
NCT01288560.
Notes
Cites: Am J Cardiol. 2004 May 15;93(10):1275-915135703
Cites: N Engl J Med. 1971 Dec 23;285(26):1441-65122894
Cites: Am J Cardiol. 1974 Oct 3;34(5):520-54278154
Cites: Am J Cardiol. 1983 Mar 1;51(5):831-66681931
Cites: Circulation. 1983 Oct;68(4):785-956352078
Cites: J Thorac Cardiovasc Surg. 1983 Oct;86(4):519-276604845
Cites: N Engl J Med. 1985 Jun 27;312(26):1665-713873614
Cites: N Engl J Med. 1986 Apr 3;314(14):884-83485252
Cites: Ann Surg. 1989 Sep;210(3):348-52; discussion 352-42673084
Cites: Circulation. 1990 Nov;82(5):1629-462225367
Cites: Circulation. 1991 Nov;84(5 Suppl):III290-51934422
Cites: J Am Coll Cardiol. 1993 Oct;22(4):984-978409073
Cites: Am J Cardiol. 1994 Mar 15;73(8):527-338147295
Cites: Circulation. 1994 Dec;90(6):2687-947994809
Cites: Circulation. 1998 Nov 10;98(19 Suppl):II51-69852880
Cites: J Thorac Cardiovasc Surg. 2005 Feb;129(2):246-915678031
Cites: Eur J Heart Fail. 2006 Jan;8(1):63-716084759
Cites: Can J Cardiol. 2006 Jan;22(1):23-4516450016
Cites: Can J Cardiol. 2007 Feb;23(2):107-1917311116
Cites: Curr Probl Cardiol. 2007 Jul;32(7):375-41017560992
Cites: J Nucl Med. 2007 Jul;48(7):1135-4617574986
Cites: J Am Coll Cardiol. 2007 Nov 13;50(20):2002-1217996568
Cites: JACC Cardiovasc Imaging. 2009 Jan;2(1):34-4419356530
Cites: JACC Cardiovasc Imaging. 2009 Sep;2(9):1060-819761983
Cites: J Nucl Med. 2010 Apr;51(4):567-7420237039
Cites: Am J Cardiol. 2010 Jul 15;106(2):187-9220599001
Cites: N Engl J Med. 2011 Apr 28;364(17):1607-1621463150
Cites: N Engl J Med. 2011 Apr 28;364(17):1671-321463151
Cites: N Engl J Med. 2011 Apr 28;364(17):1617-2521463153
Cites: Circ Cardiovasc Imaging. 2012 Mar;5(2):262-70; discussion 27022438424
Cites: J Am Coll Cardiol. 2001 Mar 15;37(4):992-711263626
Cites: Thorac Cardiovasc Surg. 2000 Feb;48(1):9-1410757150
Cites: Ann Intern Med. 2012 Jun 5;156(11):785-95, W-270, W-271, W-272, W-273, W-274, W-275, W-276, W-277, W-27822312131
Cites: J Am Coll Cardiol. 2001 Apr;37(5):1210-311300424
Cites: Am J Kidney Dis. 2002 Feb;39(2 Suppl 1):S1-26611904577
Cites: J Am Coll Cardiol. 2002 Apr 3;39(7):1151-811923039
Cites: Ann Intern Med. 2003 Jul 15;139(2):137-4712859163
PubMed ID
23866673 View in PubMed
Less detail

Are Canadian guidelines for cholesterol lowering in high-risk patients optimal?

https://arctichealth.org/en/permalink/ahliterature176367
Source
Can J Cardiol. 2005 Jan;21(1):85-90
Publication Type
Article
Date
Jan-2005
Author
David H Fitchett
Lawrence A Leiter
Jean-Claude Tardif
Shaun Goodman
Anatoly Langer
Author Affiliation
Canadian Heart Research Centre, Toronto, Ontario. fitchettd@smh.toronto.on.ca
Source
Can J Cardiol. 2005 Jan;21(1):85-90
Date
Jan-2005
Language
English
Publication Type
Article
Keywords
Dose-Response Relationship, Drug
Drug Administration Schedule
Female
Heptanoic Acids - administration & dosage
Humans
Hypercholesterolemia - diagnosis - drug therapy
Hypolipidemic Agents - administration & dosage
Male
Maximum Tolerated Dose
Practice Guidelines as Topic
Pravastatin - administration & dosage
Prognosis
Pyrroles - administration & dosage
Quebec
Randomized Controlled Trials as Topic
Risk assessment
Sensitivity and specificity
Severity of Illness Index
Treatment Outcome
Abstract
Recent Canadian lipid guidelines recommend that all high-risk patients receive medication to reduce low density lipoprotein cholesterol (LDL-C) below 2.5 mmol/L. The recently published Reversal of Atherosclerosis with Aggressive Lipid Lowering (REVERSAL) and Pravastatin or Atorvastatin Evaluation and Infection Therapy (PROVE IT) studies compared strategies of cholesterol lowering with atorvastatin 80 mg versus pravastatin 40 mg. Atorvastatin halted the progression of atherosclerosis (whereas atherosclerosis progressed in the patients receiving pravastatin), and resulted in a 16% reduction in the primary composite end point (all-cause death, myocardial infarction, unstable angina, revascularization and stroke) compared with the pravastatin-treated group. In the PROVE IT trial, LDL-C was reduced by atorvastatin to 1.6 mmol/L and by pravastatin to 2.46 mmol/L. Although lower LDL-C levels are one explanation for the improved outcomes with atorvastatin, pleiotropic differences of the two statins, such as their effects on inflammation and coagulation, cannot be excluded. Until trials are completed that compare outcomes from LDL-C lowering to different targets with the same statin, it is premature to recommend changes to the current Canadian guidelines. However, future recommendations may suggest much lower LDL-C targets than those currently recommended.
PubMed ID
15685308 View in PubMed
Less detail

Atherosclerosis imaging and the Canadian Atherosclerosis Imaging Network.

https://arctichealth.org/en/permalink/ahliterature118012
Source
Can J Cardiol. 2013 Mar;29(3):297-303
Publication Type
Article
Date
Mar-2013
Author
Jean-Claude Tardif
J David Spence
Therese M Heinonen
Alan Moody
Josephine Pressacco
Richard Frayne
Philippe L'allier
Benjamin J W Chow
Matthias Friedrich
Sandra E Black
Aaron Fenster
Brian Rutt
Rob Beanlands
Author Affiliation
Montreal Heart Institute, Université de Montréal, Montréal, Québec, Canada. jean-claude.tardif@icm-mhi.org
Source
Can J Cardiol. 2013 Mar;29(3):297-303
Date
Mar-2013
Language
English
Publication Type
Article
Keywords
Algorithms
Angiography - methods
Atherosclerosis - diagnosis - prevention & control - therapy
Canada
Carotid Arteries - pathology - radiography - radionuclide imaging - ultrasonography
Contrast Media - diagnostic use
Diagnostic Imaging - methods
Echocardiography, Three-Dimensional - methods
Evidence-Based Medicine
Humans
Magnetic Resonance Imaging - methods
Multimodal Imaging - methods
Positron-Emission Tomography
Regression Analysis
Research Design
Risk assessment
Risk factors
Tomography, X-Ray Computed - methods
Abstract
Atherosclerosis exacts a large toll on society in the form of cardiovascular morbidity, mortality, and resource use and is exacerbated by the epidemics of obesity and diabetes. Consequently, there is a critical need for more-effective methods of diagnosis, treatment, and prevention of the complications of atherosclerosis. Careful and well-conducted large population studies are needed in order to truly understand the natural history of the disease, its imaging biomarkers, and their links to patient outcomes. The Canadian Atherosclerosis Imaging Network (CAIN) is a unique research network funded by the Canadian Institutes of Health Research and the Canada Foundation for Innovation and designed to address these needs and to enable large population-based imaging studies. The central objective of CAIN is to move innovations in imaging toward their broad application in clinical research and clinical practice for the improved evaluation of cardiac and neurologic vascular disease. CAIN is established as an international resource for studying the natural history, progression, and regression of atherosclerosis, as well as novel therapeutic interventions aimed at atherosclerosis. The network represents Canada's leading atherosclerosis imaging experts, embodying both basic imaging science and clinical imaging research. The network is improving methods of detection and treatment of atherosclerosis and, through a better understanding of the underlying disease itself, improving strategies for disease prevention. The benefits are expected to appear in the next 2 to 3 years. CAIN will drive innovation in imaging technology within the field of cardiology and neurology and improve health outcomes in Canada and worldwide.
PubMed ID
23245557 View in PubMed
Less detail

Canada Acute Coronary Syndrome Risk Score: a new risk score for early prognostication in acute coronary syndromes.

https://arctichealth.org/en/permalink/ahliterature112576
Source
Am Heart J. 2013 Jul;166(1):58-63
Publication Type
Article
Date
Jul-2013
Author
Thao Huynh
Simon Kouz
Andrew T Yan
Andrew Yan
Nicolas Danchin
Jennifer O'Loughlin
Jennifer O Loughlin
Erick Schampaert
Raymond T Yan
Raymond Yan
Stephane Rinfret
Jean-Claude Tardif
Mark J Eisenberg
Marc Afilalo
Alice Chong
Jean-Pierre Dery
Michel Nguyen
Claude Lauzon
Samer Mansour
Dennis T Ko
Jack V Tu
Shaun Goodman
Author Affiliation
Division of Cardiology, McGill Health University Center, Quebec, Canada. thao.huynhthanh@mail.mcgill.ca
Source
Am Heart J. 2013 Jul;166(1):58-63
Date
Jul-2013
Language
English
Publication Type
Article
Keywords
Acute Coronary Syndrome - epidemiology
Aged
Canada - epidemiology
Electrocardiography
Female
Hospital Mortality - trends
Humans
Male
Middle Aged
Prognosis
Registries
Risk Assessment - methods
Risk factors
Survival Rate - trends
Abstract
Despite the availability of several acute coronary syndrome (ACS) prognostic risk scores, there is no appropriate score for early-risk stratification at the time of the first medical contact with patients with ACS. The primary objective of this study is to develop a simple risk score that can be used for early-risk stratification of patients with ACS.
We derived the risk score from the Acute Myocardial Infarction in Quebec and Canada ACS-1 registries and validated the risk score in 4 other large data sets of patients with ACS (Canada ACS-2 registry, Canada-GRACE, EFFECT-1, and the FAST-MI registries). The final risk score is named the Canada Acute Coronary Syndrome Risk Score (C-ACS) and ranged from 0 to 4, with 1 point assigned for the presence of each of these variables: age =75 years, Killip >1, systolic blood pressure 100 beats/min. The primary end points were short-term (inhospital or 30-day) and long-term (1- or 5-year) all-cause mortality.
The C-ACS has good predictive values for short- and long-term mortality of patients with ST-segment elevation myocardial infarction and non-ST-segment elevation ACS. The negative predictive value of a C-ACS score =1 is excellent at =98% (95% CI 0.97-0.99) for short-term mortality and =93% (95% CI 0.91-0.96) for long-term mortality. In other words, a C-ACS score of 0 can potentially identify correctly =97% short-term survivors and =91% long-term survivors.
The C-ACS risk score permits rapid stratification of patients with ACS. Because this risk score is simple and easy to memorize and calculate, it can be rapidly applied by health care professionals without advanced medical training.
Notes
Erratum In: Am Heart J. 2013 Sep;166(3):604Yan, Andrew [corrected to Yan, Andrew T]; Loughlin, Jennifer O [corrected to O'Loughlin, Jennifer]; Yan, Raymond [corrected to Yan, Raymond T]
PubMed ID
23816022 View in PubMed
Less detail

Cardiometabolic risk in Canada: a detailed analysis and position paper by the cardiometabolic risk working group.

https://arctichealth.org/en/permalink/ahliterature135666
Source
Can J Cardiol. 2011 Mar-Apr;27(2):e1-e33
Publication Type
Article
Author
Lawrence A Leiter
David H Fitchett
Richard E Gilbert
Milan Gupta
G B John Mancini
Philip A McFarlane
Robert Ross
Hwee Teoh
Subodh Verma
Sonia Anand
Kathryn Camelon
Chi-Ming Chow
Jafna L Cox
Jean-Pierre Després
Jacques Genest
Stewart B Harris
David C W Lau
Richard Lewanczuk
Peter P Liu
Eva M Lonn
Ruth McPherson
Paul Poirier
Shafiq Qaadri
Rémi Rabasa-Lhoret
Simon W Rabkin
Arya M Sharma
Andrew W Steele
James A Stone
Jean-Claude Tardif
Sheldon Tobe
Ehud Ur
Author Affiliation
Li Ka Shing Knowledge Institute of St. Michael's Hospital, Toronto, Ontario, Canada.
Source
Can J Cardiol. 2011 Mar-Apr;27(2):e1-e33
Language
English
Publication Type
Article
Keywords
Canada - epidemiology
Cardiovascular Diseases - epidemiology - etiology - therapy
Diabetes Mellitus, Type 2 - epidemiology - etiology - prevention & control
Humans
Metabolic Syndrome X - complications - epidemiology - therapy
Practice Guidelines as Topic
Risk factors
Abstract
The concepts of "cardiometabolic risk," "metabolic syndrome," and "risk stratification" overlap and relate to the atherogenic process and development of type 2 diabetes. There is confusion about what these terms mean and how they can best be used to improve our understanding of cardiovascular disease treatment and prevention. With the objectives of clarifying these concepts and presenting practical strategies to identify and reduce cardiovascular risk in multiethnic patient populations, the Cardiometabolic Working Group reviewed the evidence related to emerging cardiovascular risk factors and Canadian guideline recommendations in order to present a detailed analysis and consolidated approach to the identification and management of cardiometabolic risk. The concepts related to cardiometabolic risk, pathophysiology, and strategies for identification and management (including health behaviours, pharmacotherapy, and surgery) in the multiethnic Canadian population are presented. "Global cardiometabolic risk" is proposed as an umbrella term for a comprehensive list of existing and emerging factors that predict cardiovascular disease and/or type 2 diabetes. Health behaviour interventions (weight loss, physical activity, diet, smoking cessation) in people identified at high cardiometabolic risk are of critical importance given the emerging crisis of obesity and the consequent epidemic of type 2 diabetes. Vascular protective measures (health behaviours for all patients and pharmacotherapy in appropriate patients) are essential to reduce cardiometabolic risk, and there is growing consensus that a multidisciplinary approach is needed to adequately address cardiometabolic risk factors. Health care professionals must also consider risk factors related to ethnicity in order to appropriately evaluate everyone in their diverse patient populations.
PubMed ID
21459257 View in PubMed
Less detail

Characteristics and evidence-based management of stable coronary artery disease patients in Canada compared with the rest of the world: insights from the CLARIFY registry.

https://arctichealth.org/en/permalink/ahliterature106123
Source
Can J Cardiol. 2014 Jan;30(1):132-7
Publication Type
Article
Date
Jan-2014
Author
Sumeet Gandhi
Paul Dorian
Nicola Greenlaw
Jean-Claude Tardif
P Gabriel Steg
Thao Huynh
Graham C Wong
Michael P Love
Paul Poirier
Shaun G Goodman
Author Affiliation
Terrence Donnelly Heart Centre, St Michael's Hospital, University of Toronto, Toronto, Ontario, Canada.
Source
Can J Cardiol. 2014 Jan;30(1):132-7
Date
Jan-2014
Language
English
Publication Type
Article
Keywords
Aged
Canada - epidemiology
Coronary Artery Disease - epidemiology - therapy
Evidence-Based Medicine - methods
Female
Follow-Up Studies
Guideline Adherence
Humans
Male
Prognosis
Prospective Studies
Registries
Risk Assessment - methods
Risk factors
Secondary Prevention - methods
World Health
Abstract
Previous Canadian high vascular risk registries have demonstrated suboptimal goal-directed reductions in cardiovascular risk factors and underutilization of guideline-recommended therapies in part because of physician underestimation of cardiovascular risk.
The Prospective Observational Longitudinal Registry of Patients With Stable Coronary Artery Disease (CLARIFY) registry enrolled 33,438 stable coronary artery disease patients in 45 countries. In Canada, supplemental information was obtained specifying reasons that patients were not taking guideline-recommended medications.
In Canada, 1232 patients (9 provinces, 110 physicians) were enrolled and in comparison with the rest of the world, there were several differences in cardiovascular risk factors and medical history; in addition, the Canadian cohort had undergone less percutaneous coronary intervention, but more coronary artery bypass grafting. Among the Canadian cohort, many still continue to smoke (13%) and many do not meet secondary prevention targets for waist circumference (54%), body mass index (81%), physical activity (71%), cholesterol (43%), and systolic blood pressure (20%). Nevertheless, the use of guideline-recommended cardiovascular therapy was high and >90% reported partial/full financial coverage for medications. The number of patients not receiving guideline-recommended therapies because of apparent underestimation of risk was particularly low for antiplatelet agents (2%), ß-blockers (11%), and lipid-lowering therapies (1%).
Canadian patients with stable coronary artery disease did not meet several guideline-recommended secondary prevention targets, despite high use of evidence-based therapy, extensive financial coverage for these medications, and low physician underestimation of risk. Additional work is needed to identify and address the remaining barriers to effective risk factor control.
PubMed ID
24238756 View in PubMed
Less detail

Effects of pyridoxal-5'-phosphate (MC-1) in patients undergoing high-risk coronary artery bypass surgery: results of the MEND-CABG randomized study.

https://arctichealth.org/en/permalink/ahliterature163308
Source
J Thorac Cardiovasc Surg. 2007 Jun;133(6):1604-11
Publication Type
Article
Date
Jun-2007
Author
Jean-Claude Tardif
Michel Carrier
David E Kandzari
Robert Emery
Robert Cote
Therese Heinonen
Marjorie Zettler
Vic Hasselblad
Marie-Claude Guertin
Robert A Harrington
Author Affiliation
Montreal Heart Institute, Montreal, Canada. jean-claude.tardif@icm-mhi.org
Source
J Thorac Cardiovasc Surg. 2007 Jun;133(6):1604-11
Date
Jun-2007
Language
English
Publication Type
Article
Keywords
Administration, Oral
Adult
Aged
Aged, 80 and over
Area Under Curve
Canada
Cardiopulmonary Bypass
Cardiovascular Diseases - mortality - surgery
Chi-Square Distribution
Coronary Artery Bypass - adverse effects
Creatine Kinase, MB Form - blood
Double-Blind Method
Female
Humans
Male
Middle Aged
Myocardial Infarction - etiology - prevention & control
Pyridoxal Phosphate - administration & dosage - therapeutic use
Stroke - etiology - prevention & control
Treatment Outcome
United States
Abstract
Coronary artery bypass graft surgery remains associated with significant postoperative cardiovascular morbidity and mortality in high-risk patients. MC-1 (pyridoxal-5'-phosphate monohydrate) inhibits purinergic receptors and intracellular influx of Ca2+, thereby reducing cellular injury during experimental ischemia and reperfusion. The MEND-CABG trial tested the hypothesis that MC-1 reduces cardiovascular morbidity and mortality after coronary artery bypass graft.
In a phase 2, double-blinded, placebo-controlled study, 901 patients scheduled for coronary artery bypass graft surgery with cardiopulmonary bypass and at high risk for subsequent cardiac or neurologic complications were randomly assigned to receive oral MC-1 (250 mg or 750 mg/d once daily) or placebo beginning 3 to 10 hours prior to surgery and continued to postoperative day 30.
At 30 days, MC-1 250 mg (compared with placebo) reduced the composite of death, nonfatal cerebral infarction, and nonfatal myocardial infarction by 14.0% (P = .3124) with peak creatinine kinase-myocardial band > or =50 ng/mL (prespecified primary end point); 32.3% (P = .0349) with peak creatinine kinase-myocardial band > or =70 ng/mL; and 37.2% (P = .0283) with peak creatinine kinase-myocardial band > or =100 ng/mL. Myocardial infarctions with peak creatinine kinase-myocardial band> or =100 ng/mL were reduced by 47.2% in the MC-1 250-mg group versus placebo (P = .0083). Greater efficacy was demonstrated with 250 mg than with the 750-mg dose of MC-1.
In high-risk patients undergoing coronary artery bypass graft, treatment with MC-1 did not significantly affect the prespecified primary end point but was associated with a significant reduction in perioperative myocardial infarction with creatinine kinase-myocardial band > or =100 ng/mL. A larger, well-powered trial is needed to evaluate the cardioprotective effects of MC-1.
Notes
Comment In: J Thorac Cardiovasc Surg. 2007 Jun;133(6):1409-1117532929
PubMed ID
17532963 View in PubMed
Less detail

Enalapril decreases the incidence of atrial fibrillation in patients with left ventricular dysfunction: insight from the Studies Of Left Ventricular Dysfunction (SOLVD) trials.

https://arctichealth.org/en/permalink/ahliterature185213
Source
Circulation. 2003 Jun 17;107(23):2926-31
Publication Type
Article
Date
Jun-17-2003
Author
Emmanuelle Vermes
Jean-Claude Tardif
Martial G Bourassa
Normand Racine
Sylvie Levesque
Michel White
Peter G Guerra
Anique Ducharme
Author Affiliation
Department of Medicine, Montreal Heart Institute, Montreal, Canada.
Source
Circulation. 2003 Jun 17;107(23):2926-31
Date
Jun-17-2003
Language
English
Publication Type
Article
Keywords
Angiotensin-Converting Enzyme Inhibitors - therapeutic use
Atrial Fibrillation - diagnosis - epidemiology - prevention & control
Canada - epidemiology
Comorbidity
Disease-Free Survival
Electrocardiography
Enalapril - therapeutic use
Female
Follow-Up Studies
Humans
Incidence
Male
Middle Aged
Multivariate Analysis
Proportional Hazards Models
Randomized Controlled Trials as Topic - statistics & numerical data
Retrospective Studies
Ventricular Dysfunction, Left - diagnosis - drug therapy - epidemiology
Abstract
Atrial fibrillation (AF) is frequently encountered in patients with heart failure (HF) and is also a predictor of morbidity and mortality in this population. Recent experimental studies have shown electrical and structural atrial remodeling with increased fibrosis in animals with HF and have suggested a preventive effect of ACE inhibitors (ACEi) on the development of AF. To verify the hypothesis that ACEi prevent the development of AF in patients with HF, we conducted a retrospective analysis of the patients from the Montreal Heart Institute (MHI) included in the Studies Of Left Ventricular Dysfunction (SOLVD).
Clinical charts were reviewed and serial ECGs interpreted by a single cardiologist blinded to drug allocation. Patients with AF or flutter on the baseline ECG were excluded. Baseline characteristics were obtained from the SOLVD databases. The mean follow-up was 2.9+/-1.0 years. Of the 391 patients randomly assigned at MHI, 374 were in sinus rhythm at the time of random assignment, with 186 taking enalapril and 188 taking placebo. Baseline characteristics were similar in the two groups except for a higher incidence of previous myocardial infarction in the enalapril group. Fifty-five patients had AF during the follow-up: 10 (5.4%) in the enalapril group and 45 (24%) in the placebo group (P
Notes
Comment In: Circulation. 2004 Jan 20;109(2):e1114734513
PubMed ID
12771010 View in PubMed
Less detail

Evaluation of links between high-density lipoprotein genetics, functionality, and aortic valve stenosis risk in humans.

https://arctichealth.org/en/permalink/ahliterature105693
Source
Arterioscler Thromb Vasc Biol. 2014 Feb;34(2):457-62
Publication Type
Article
Date
Feb-2014
Author
Benoit J Arsenault
Marie-Pierre Dubé
Mathieu R Brodeur
Adriana Benjamin de Oliveira Moraes
Véronique Lavoie
Anne-Elen Kernaleguen
Sandra Guauque-Olarte
Patrick Mathieu
Philippe Pibarot
David Messika-Zeitoun
Yohan Bossé
David Rhainds
Eric Rhéaume
Jean-Claude Tardif
Author Affiliation
From the Montreal Heart Institute, Montreal, Canada (B.J.A., M.-P.D., M.R.B., A.B.d.O.M., V.L., A.-E.K., D.R., É.R., J.-C.T.); Department of Medicine, Faculty of Medicine, Université de Montréal, Montreal, Canada (B.J.A., M.-P.D., M.R.B., A.B.d.O.M., É.R., J.-C.T.); Beaulieu-Saucier Université de Montréal Pharmacogenomics Centre, Montreal, Canada (M.-P.D., J.-C.T.); Centre de Recherche, Institut Universitaire de Cardiologie et de Pneumologie de Québec (S.G.-O., P.M., P.P., Y.B.) and Department of Molecular Medicine (Y.B.), Laval University, Québec, Canada; Cardiology Department, AP-HP, Bichat Hospital, Paris, France (D.M.-Z.); and INSERM U698, University Paris 7, Paris, France (D.M.-Z.).
Source
Arterioscler Thromb Vasc Biol. 2014 Feb;34(2):457-62
Date
Feb-2014
Language
English
Publication Type
Article
Keywords
Aged
Animals
Aortic Valve - physiopathology - ultrasonography
Aortic Valve Stenosis - blood - genetics - physiopathology - ultrasonography
Case-Control Studies
Chi-Square Distribution
Cholesterol, HDL - blood - genetics
Coronary Artery Disease - blood - genetics
Female
Genetic markers
Genetic Predisposition to Disease
Hep G2 Cells
Hepatocytes - metabolism
Humans
Lipoproteins, HDL - blood - genetics
Logistic Models
Macrophages - metabolism
Male
Mice
Middle Aged
Paris
Phenotype
Polymorphism, Single Nucleotide
Prospective Studies
Quebec
Risk factors
Abstract
Studies have shown that high-density lipoprotein (HDL)-raising compounds induce regression of aortic valve stenosis (AVS) in animal models. However, whether patients with AVS have an impaired HDL metabolism is unknown.
A total of 1435 single nucleotide polymorphisms in genes associated with HDL cholesterol levels (in or around GALNT2, LPL, ABCA1, APOA5, SCARB1, LIPC, CETP, LCAT, LIPG, APOC4, and PLTP) were genotyped in 382 patients with echocardiography-confirmed AVS (aortic jet velocity =2.5 m/s) and 401 controls. After control for multiple testing, none of the genetic variants showed a positive association with case/control status (adjusted P=0.05 for all single nucleotide polymorphisms tested). In a subsample of this cohort, HDL cholesterol levels, apolipoprotein AI levels, lecithin-cholesterol acyltransferase activity, pre-?-HDL, HDL size, and 4 parameters of cholesterol efflux capacity were measured in apolipoprotein B-depleted serum samples from 86 patients with and 86 patients without AVS. Cholesterol efflux capacity was measured using J774 macrophages with and without stimulation of ATP-binding cassette A-1 expression by cAMP, and HepG2 hepatocytes for scavenger receptor class B type 1-mediated efflux. None of these parameters were different between cases and controls. However, compared with patients without coronary artery disease, sera from patients with coronary artery disease had lower HDL cholesterol levels, scavenger receptor class B type 1-mediated efflux, and HDL size (P=0.003), independently of the presence or absence of AVS.
Results of the present study suggest that, based on HDL genetics and HDL functionality, HDL metabolism does not seem to predict the risk of AVS. Because of our limited sample size, additional studies are needed to confirm these findings.
PubMed ID
24334872 View in PubMed
Less detail

19 records – page 1 of 2.