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The accuracy of general practitioners' clinical assessment of chest pain patients.

https://arctichealth.org/en/permalink/ahliterature92385
Source
Eur J Gen Pract. 2008;14(2):50-5
Publication Type
Article
Date
2008
Author
Nilsson Staffan
Ortoft Kjell
Mölstad Sigvard
Author Affiliation
General Practice, Department of Medical and Health Sciences, Faculty of Health Sciences, Linkoping, Sweden. staffan.nilsson@lio.se
Source
Eur J Gen Pract. 2008;14(2):50-5
Date
2008
Language
English
Publication Type
Article
Keywords
Adult
Aged
Chest Pain - etiology
Clinical Competence - statistics & numerical data
Family Practice - statistics & numerical data
Female
Health Care Surveys
Humans
Male
Middle Aged
Myocardial Ischemia - complications - diagnosis
Odds Ratio
Physician's Practice Patterns - standards - statistics & numerical data
Risk factors
Sensitivity and specificity
Sweden
Abstract
OBJECTIVE: To study general practitioners' (GP) assessment of the probability of ischaemic heart disease (IHD) and GP action in daily practice regarding chest pain patients. METHODS: All chest pain patients aged 20-79 years, attending three primary health-care centres in south-east Sweden and assessed by the GP to have high, low or very low probability of IHD, were included consecutively over a two year period. The "GP action in daily practice" was classed as "active decisions" (investigation or treatment) or "wait and see". "IHD" or "not IHD" was settled according to the results of acute hospital investigation or exercise testing/myocardial perfusion scintigraphy. RESULTS: 516 patients were included, 93 high, 145 low and 278 very low probability cases. The outcome was "IHD" in 47%, 9% and 1% respectively. The sensitivity and specificity of the "GP assessment of the probability of IHD" were 72% and 89%. The sensitivity and specificity of the "GP action in daily practice" were 88% and 72%, respectively. The negative predictive value was 98%. CONCLUSION: GP assessment, after clinical evaluation, that the probability of IHD was low did not safely rule out IHD. GP action in daily practice however, indicates that general practice is an appropriate level of care for chest pain patients.
PubMed ID
18720273 View in PubMed
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[A comparative study of the hemodynamic and antioxidant effects of Capoten and prazosin in patients with refractory heart failure]

https://arctichealth.org/en/permalink/ahliterature54537
Source
Lik Sprava. 1997 Mar-Apr;(2):72-6
Publication Type
Article
Author
R O Sabadyshyn
B I Rudyk
N H Blinova
O Ia Slipak
Source
Lik Sprava. 1997 Mar-Apr;(2):72-6
Language
Ukrainian
Publication Type
Article
Keywords
Aged
Angiotensin-Converting Enzyme Inhibitors - therapeutic use
Antihypertensive Agents - therapeutic use
Antioxidants - therapeutic use
Captopril - therapeutic use
Cardiomyopathy, Dilated - complications - drug therapy - physiopathology
Comparative Study
Drug Evaluation
English Abstract
Female
Heart Failure, Congestive - drug therapy - etiology - physiopathology
Hemodynamic Processes - drug effects
Humans
Hypertension - complications - drug therapy - physiopathology
Lipid Peroxidation - drug effects
Male
Middle Aged
Myocardial Ischemia - complications - drug therapy - physiopathology
Prazosin - therapeutic use
Abstract
Overall fifty one patients with chronic cardiac insufficiency (ChCI) were studied for changes in parameters characterizing hemodynamics and lipid peroxidation (LPO) under treatment with kapoten and prazosin. Kapoten was found to be capable of exerting an antioxidant effect and working in ways beneficial for the pulmonary circulation, while prazosin is generally indicated to patients with ChCI presenting with increased end diastolic pressure in the left ventricle. Prazosin activates LPO, for which reason its pro-oxidant action needs to be drug-corrected. Because of marked pharmacologic effects of both drugs in dealing with refractory circulatory insufficiency it is advisable that further studies be made in order that we might be able to determine indications for kapoten and prazosin therapy in coronary patients as well as those with arterial hypertension, cardiomyopathies, valvular defects, ChCI with complications more accurately.
PubMed ID
9333490 View in PubMed
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Adaptation to myocardial ischemia during repeated dynamic exercise in relation to findings at cardiac catheterization.

https://arctichealth.org/en/permalink/ahliterature46459
Source
Am Heart J. 1996 Apr;131(4):689-97
Publication Type
Article
Date
Apr-1996
Author
K. Ylitalo
L. Jama
P. Raatikainen
K. Peuhkurinen
Author Affiliation
Department of Internal Medicine, Division of Cardiology, Oulu University Central Hospital, Finland.
Source
Am Heart J. 1996 Apr;131(4):689-97
Date
Apr-1996
Language
English
Publication Type
Article
Keywords
Angina Pectoris - etiology - physiopathology
Collateral Circulation
Coronary Circulation
Electrocardiography
Exercise Test
Female
Heart Catheterization
Humans
Male
Middle Aged
Myocardial Ischemia - complications - physiopathology
Oxygen consumption
Severity of Illness Index
Survival Analysis
Abstract
It has been suggested that the myocardium is able to recruit endogenous protective mechanisms in response to repeated ischemia and reperfusion. We set out to study whether this is manifested in patients with coronary artery disease in the form of fewer signs of myocardial ischemia during the second of two successive exercise tests and whether any relations exist between ischemia adaptation and findings at cardiac catheterization. Twenty-one patients with typical angina pectoris symptoms underwent two repeated bicycle exercise tests with identical protocols, followed by cardiac catheterization and coronary angiography the next day. The first exercise test was discontinued whenever a 2 mm ST depression in the electrocardiogram (ECG) was achieved or further exercise was limited by symptoms. The second exercise test was performed after disappearance of the symptoms or ST depression or both. Kaplan-Meier survival analysis for the appearance of a 1 mm ST depression demonstrated improved ischemia tolerance during the second test, when the required time for its appearance was significantly longer (6.5 +/- 0.8 min vs 4.5 +/- 0.5 min; p = 0.005). The maximal intensity of anginal pain was lower during the second exercise (2.2 +/- 1.0 min vs 0.7 +/- 0.3 min in Borg's scale; p
PubMed ID
8721640 View in PubMed
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Adherence to antihypertensive agents after ischemic stroke and risk of cardiovascular outcomes.

https://arctichealth.org/en/permalink/ahliterature119300
Source
Neurology. 2012 Nov 13;79(20):2037-43
Publication Type
Article
Date
Nov-13-2012
Author
Sylvie Perreault
Amy Y X Yu
Robert Côté
Alice Dragomir
Brian White-Guay
Stéphanie Dumas
Author Affiliation
Faculty of Pharmacy, University of Montreal, Faculty of Medicine, McGill University, Montreal, Canada. sylvie.perreault@umontreal.ca
Source
Neurology. 2012 Nov 13;79(20):2037-43
Date
Nov-13-2012
Language
English
Publication Type
Article
Keywords
Aged
Aged, 80 and over
Antihypertensive Agents - therapeutic use
Case-Control Studies
Cerebrovascular Disorders - epidemiology - prevention & control
Cohort Studies
Diabetes Complications - prevention & control
Dyslipidemias - drug therapy - epidemiology
Female
Humans
Ischemia - complications - epidemiology
Logistic Models
Male
Medication Adherence
Quebec
Reproducibility of Results
Retrospective Studies
Risk factors
Risk Reduction Behavior
Stroke - epidemiology - etiology - prevention & control
Abstract
To evaluate the relationship between antihypertensive (AH) drug adherence and cardiovascular (CV) outcomes among patients with a recent ischemic stroke and assess the validity of our approach.
A cohort of 14,227 patients diagnosed with an ischemic stroke was assembled from individuals 65 years and older who were treated with AH agents from 1999 to 2007 in Quebec, Canada. A nested case-control design was used to evaluate the occurrence of nonfatal major CV outcomes and mortality. Each case was matched to 15 controls by age and cohort entry time. Medication possession ratio was used for AH agent adherence level. Adjusted conditional logistic regression models were used to estimate the rate ratio of CV events. The validity of the approach was assessed by evaluating the adherence level of CV-protective and non-CV-protective drugs.
Mean age was 75 years, 54% were male, 38% had coronary artery disease, 23% had diabetes, 47% dyslipidemia, and 14% atrial fibrillation or flutter. High adherence to AH therapy was mirrored by similar adherence to statins and antiplatelet agents and was associated with a lower risk of nonfatal vascular events compared with lower adherence (rate ratio 0.77 [0.70-0.86]). We observed a paradoxic link between adherence to several drugs and all-cause mortality.
Adherence to AH agents is associated with adherence to other secondary preventive therapies and a risk reduction for nonfatal vascular events after an ischemic stroke. Overestimation of all-cause mortality reduction may be related to frailty and comorbidities, which may confound the apparent benefit of different drugs.
Notes
Cites: Lancet Neurol. 2009 Apr;8(4):345-5419233730
Cites: Stroke. 2009 Jan;40(1):213-2019038916
Cites: Circulation. 2009 Oct 20;120(16):1598-60519805653
Cites: Cerebrovasc Dis. 2010 Jan;29(2):146-5319955739
Cites: Am J Med. 2010 Mar;123(3 Suppl):S3-1120206730
Cites: Lancet. 2010 Mar 13;375(9718):906-1520226989
Cites: Lancet. 2010 Mar 13;375(9718):938-4820226991
Cites: Lancet Neurol. 2010 May;9(5):469-8020227347
Cites: J Clin Lipidol. 2010 Nov-Dec;4(6):462-7121122692
Cites: Int J Clin Pract. 2011 Jan;65(1):41-5321091596
Cites: Stroke. 2011 Feb;42(2):517-8421127304
Cites: Value Health. 2011 Jun;14(4):513-2021669377
Cites: Heart. 2011 Nov;97(22):1862-921586421
Cites: Lancet. 2001 Aug 25;358(9282):661-311530175
Cites: Lancet. 2001 Sep 29;358(9287):1033-4111589932
Cites: Epidemiology. 2001 Nov;12(6):682-911679797
Cites: Stroke. 2002 Oct;33(10):2465-7012364739
Cites: Ann Neurol. 2003 Jun;53(6):743-5112783420
Cites: Am Heart J. 2003 Oct;146(4):581-9014564310
Cites: Stroke. 2003 Nov;34(11):2741-814576382
Cites: Stroke. 2004 Apr;35(4):102415053002
Cites: J Clin Epidemiol. 2004 Feb;57(2):131-4115125622
Cites: Hypertension. 2004 Oct;44(4):398-40415326093
Cites: J Clin Epidemiol. 1995 Aug;48(8):999-10097775999
Cites: Med Care. 1999 Sep;37(9):846-5710493464
Cites: JAMA. 2005 Jul 27;294(4):466-7216046653
Cites: N Engl J Med. 2005 Aug 4;353(5):487-9716079372
Cites: J Manag Care Pharm. 2006 Apr;12(3):239-4516623608
Cites: BMJ. 2006 Jul 1;333(7557):1516790458
Cites: J Clin Epidemiol. 2006 Aug;59(8):819-2816828675
Cites: Hypertension. 2006 Aug;48(2):260-516785330
Cites: J Hypertens. 2006 Aug;24(8):1523-916877954
Cites: N Engl J Med. 2006 Aug 10;355(6):549-5916899775
Cites: Ann Pharmacother. 2006 Jul-Aug;40(7-8):1280-8816868217
Cites: Stroke. 2006 Oct;37(10):2493-816931783
Cites: Am J Hypertens. 2006 Nov;19(11):1190-617070434
Cites: Eur Heart J. 2008 Jul;29(13):1605-718523057
Cites: Am J Med. 2009 Jul;122(7):647-5519559167
PubMed ID
23115211 View in PubMed
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Adult height and risk of ischemic heart disease, atrial fibrillation, stroke, venous thromboembolism, and premature death: a population based 36-year follow-up study.

https://arctichealth.org/en/permalink/ahliterature105680
Source
Eur J Epidemiol. 2014 Feb;29(2):111-8
Publication Type
Article
Date
Feb-2014
Author
Morten Schmidt
Hans Erik Bøtker
Lars Pedersen
Henrik Toft Sørensen
Author Affiliation
Department of Clinical Epidemiology, Aarhus University Hospital, Olof Palmes Allé 43-45, 8200, Aarhus, Denmark, morten.schmidt@dadlnet.dk.
Source
Eur J Epidemiol. 2014 Feb;29(2):111-8
Date
Feb-2014
Language
English
Publication Type
Article
Keywords
Adult
Atrial Fibrillation - complications - diagnosis - epidemiology
Body Height
Body mass index
Denmark - epidemiology
Follow-Up Studies
Humans
Incidence
Life expectancy
Male
Middle Aged
Mortality, Premature
Myocardial Ischemia - complications - diagnosis - mortality
Population Surveillance
Proportional Hazards Models
Risk factors
Stroke - complications - diagnosis - epidemiology
Venous Thromboembolism - complications - diagnosis - epidemiology
Abstract
Few studies have associated height with cardiovascular diseases other than myocardial infarction. We conducted a population-based 36-year cohort study of 12,859 men born in 1955 or 1965 whose fitness for military service was assessed by Draft Boards in Northern Denmark. Hospital diagnoses for ischemic heart diseases, atrial fibrillation, stroke, and venous thromboembolism were obtained from the Danish National Patient Registry, covering all Danish hospitals since 1977. Mortality data were obtained from the Danish Civil Registration System. We began follow-up on the 22nd birthday of each subject and continued until occurrence of an outcome, emigration, death, or 31 December 2012, whichever came first. We used Cox regression to compute hazard ratios (HRs) with 95 % confidence intervals (CIs). Compared with short stature, the education-adjusted HR among tall men was 0.67 (95 % CI 0.54-0.84) for ischemic heart disease (similar for myocardial infarction, angina pectoris, and heart failure), 1.60 (95 % CI 1.11-2.33) for atrial fibrillation, 1.05 (95 % CI 0.75-1.46) for stroke, 1.04 (95 % CI 0.67-1.64) for venous thromboembolism, and 0.70 (95 % CI 0.58-0.86) for death. In conclusion, short stature was a risk factor for ischemic heart disease and premature death, but a protective factor for atrial fibrillation. Stature was not substantially associated with stroke or venous thromboembolism.
PubMed ID
24337942 View in PubMed
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Age- and gender-specific prevalence of cardiovascular risk factors in 40,102 patients with first-ever ischemic stroke: a Nationwide Danish Study.

https://arctichealth.org/en/permalink/ahliterature139905
Source
Stroke. 2010 Dec;41(12):2768-74
Publication Type
Article
Date
Dec-2010
Author
Klaus Kaae Andersen
Zorana Jovanovic Andersen
Tom Skyhøj Olsen
Author Affiliation
Institute of Informatics and Mathematical Modelling, Section for Statistics, Technical University of Denmark, Lyngby, Denmark.
Source
Stroke. 2010 Dec;41(12):2768-74
Date
Dec-2010
Language
English
Publication Type
Article
Keywords
Adult
Age Factors
Age of Onset
Aged
Brain Ischemia - complications - epidemiology
Cardiovascular Diseases - complications - epidemiology
Denmark - epidemiology
Female
Humans
Life Style
Magnetic Resonance Imaging
Male
Middle Aged
Risk factors
Sex Factors
Smoking - epidemiology
Stroke - epidemiology - etiology
Tomography, X-Ray Computed
Abstract
We describe the prevalence of cardiovascular risk factors at stroke onset in men and women of all ages.
A registry started in 2001, designed to register all hospitalized stroke patients in Denmark, now holds 40,102 patients with first-ever ischemic stroke. Patients underwent evaluation including stroke severity (Scandinavian Stroke Scale), CT, and cardiovascular risk factors: hypertension, atrial fibrillation, diabetes mellitus, intermittent arterial claudication, previous myocardial infarction, body mass index, smoking, and alcohol consumption. We estimated the independent effect of gender and age on prevalence of cardiovascular risk factors and calculated age and gender-specific prevalence rates for each risk factor.
The register contained 47.9% women and 52.1% men. Men had more often diabetes mellitus, previous myocardial infarction, intermittent arterial claudication, and over the limit alcohol consumption. Women had more often hypertension and obesity. Atrial fibrillation and smoking were equally frequent in both genders. Age stratification revealed that the lifestyle cardiovascular risk factors smoking, alcohol, and obesity were more common in the younger patients with stroke ( 70 to 80 years), the decrease being generally more pronounced in men than in women.
Cardiovascular risk factors were generally more prevalent in men. Lifestyle cardiovascular risk factors were more common in the young. Prevalence of hypertension, diabetes mellitus, coronary heart disease, and, in men, also atrial fibrillation go down after the age of 70 to 80 years.
PubMed ID
20966413 View in PubMed
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Age and mental health predict early device-specific quality of life in patients receiving prophylactic implantable defibrillators.

https://arctichealth.org/en/permalink/ahliterature126084
Source
Can J Cardiol. 2012 Jul-Aug;28(4):502-7
Publication Type
Article
Author
Sandra L Carroll
Maureen Markle-Reid
Donna Ciliska
Stuart J Connolly
Heather M Arthur
Author Affiliation
School of Nursing, Faculty of Health Sciences, McMaster University, Hamilton, Ontario, Canada. carroll@mcmaster.ca
Source
Can J Cardiol. 2012 Jul-Aug;28(4):502-7
Language
English
Publication Type
Article
Keywords
Age Factors
Aged
Character
Cohort Studies
Defibrillators, Implantable - psychology
Depressive Disorder - psychology
Female
Heart Failure - complications - psychology
Humans
Male
Middle Aged
Multivariate Analysis
Myocardial Ischemia - complications - psychology
Ontario
Patient Acceptance of Health Care - psychology
Prospective Studies
Quality of Life - psychology
Socioeconomic Factors
Treatment Outcome
Ventricular Fibrillation - prevention & control - psychology
Abstract
Ventricular arrhythmia is a significant cause of sudden death. Implantable cardioverter-defibrillators (ICDs) offer at-risk patients a prophylactic treatment option. This prophylaxis is largely responsible for growth in utilization of ICDs. Identification of factors that may impact device-specific quality of life (QOL) is warranted. The influence of preimplant patient variables on postimplant device-specific QOL is unknown. The study aimed to determine whether preimplant psychosocial, generic health-related quality of life (HRQOL), personality disposition, or demographic factors predicted early postimplant device-specific QOL.
A prospective cohort study design was employed in 70 adults receiving an ICD for primary prevention. Preimplant, we measured generic HRQOL, personality disposition, depressive symptoms, age, and sex. The primary outcome was 3-month ICD device-specific QOL as measured by the Florida Patient Acceptance Scale (FPAS). We applied hierarchical multivariate regression analysis.
Mean age was 64.8 ± 9.4 years; 12.9% were women. Most had ischemic heart disease (77%) and a heart failure history (54.3%). Preimplant prevalence of elevated depressive symptoms was 30%. Three months post implant, the mean adjusted FPAS score was 76.8 ± 12.98. Of the variance in FPAS scores, 37% was explained by the independent variables. Younger age and poor preimplant mental HRQOL contributed most to lower FPAS scores.
Patient support and psychosocial interventions should target younger ICD candidates and those reporting poor preimplant mental HRQOL; these patients may be at risk for poor postimplant device-specific QOL.
PubMed ID
22425267 View in PubMed
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Age dependency of ischaemic stroke subtypes and vascular risk factors in western Norway: the Bergen Norwegian Stroke Cooperation Study.

https://arctichealth.org/en/permalink/ahliterature275818
Source
Acta Neurol Scand. 2016 Mar;133(3):202-7
Publication Type
Article
Date
Mar-2016
Author
A. Nacu
A. Fromm
K M Sand
U. Waje-Andreassen
L. Thomassen
H. Naess
Source
Acta Neurol Scand. 2016 Mar;133(3):202-7
Date
Mar-2016
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Age Factors
Aged
Aged, 80 and over
Atherosclerosis - complications - epidemiology
Brain Ischemia - complications - epidemiology
Cerebral Infarction - epidemiology - etiology
Cerebral Small Vessel Diseases - complications - epidemiology
Embolism - epidemiology
Female
Humans
Magnetic Resonance Imaging
Male
Middle Aged
Norway - epidemiology
Registries
Risk factors
Socioeconomic Factors
Stroke - epidemiology
Young Adult
Abstract
Age dependency of acute ischaemic stroke aetiology and vascular risk factors have not been adequately evaluated in stroke patients in Norway. Aims of this study were to evaluate how stroke subtypes and vascular risk factors vary with age in a western Norway stroke population.
Patients aged 15-100 years consecutively admitted to our neurovascular centre with acute ischaemic stroke between 2006 and 2012 were included. The study population was categorized as young (15-49 years), middle-aged (50-74 years) or elderly (= 75 years). Stroke aetiology was defined by TOAST criteria. Risk factors and history of cardiovascular disease were recorded.
In total, 2484 patients with acute cerebral infarction were included: 1418 were males (57.3%). Mean age was 70.8 years (SD ± 14.9), 228 patients were young, 1126 middle-aged, and 1130 were elderly. The proportion of large-artery atherosclerosis and of small-vessel occlusion was highest among middle-aged patients. The proportion of cardioembolism was high at all ages, especially among the elderly. The proportion of stroke of other determined cause was highest among young patients. Some risk factors (diabetes mellitus, active smoking, angina pectoris, prior stroke and peripheral artery disease) decreased among the elderly. The proportions of several potential causes increased with age.
The proportion of stroke subtypes and vascular risk factors are age dependent. Age 50-74 years constitutes the period in life where cardiovascular risk factors become manifest and stroke subtypes change.
Notes
Cites: Stroke. 2009 Apr;40(4):1195-20319246709
Cites: Stroke. 2009 May;40(5):1557-6319325154
Cites: Cerebrovasc Dis. 2009;27(5):493-50119342825
Cites: Curr Neurol Neurosci Rep. 2010 Jan;10(1):14-2020425221
Cites: J Neurol. 2010 Nov;257(11):1777-8720623300
Cites: Stroke. 2010 Dec;41(12):2768-7420966413
Cites: Stroke. 2001 Dec 1;32(12):2735-4011739965
Cites: Lancet. 2003 Jan 11;361(9352):107-1612531577
Cites: Stroke. 1999 Dec;30(12):2644-5010582991
Cites: Circulation. 2001 May 1;103(17):2171-511331258
Cites: Stroke. 2001 Nov;32(11):2559-6611692017
Cites: Stroke. 2011 Feb;42(2):517-8421127304
Cites: Neurology. 2011 Sep 20;77(12):1174-8121900632
Cites: N Engl J Med. 2012 Jan 26;366(4):321-922276822
Cites: Cerebrovasc Dis. 2012;33(1):69-7522133999
Cites: Eur Neurol. 2012;68(3):162-522906845
Cites: Stroke. 2013 Jan;44(1):119-2523150649
Cites: Stroke. 2013 Feb;44(2):340-923306324
Cites: Eur J Neurol. 2013 Nov;20(11):1431-923837733
Cites: J Stroke Cerebrovasc Dis. 2014 Jan;23(1):140-723352689
Cites: BMC Res Notes. 2014;7:17624669965
Cites: Neurol Sci. 2014 Apr;35(4):577-8224122024
Cites: Acta Neurol Scand. 2016 Mar;133(3):202-726032994
Cites: Stroke. 2004 Jul;35(7):1779-8015166382
Cites: Stroke. 2004 Jul;35(7):1778-915166384
Cites: Cerebrovasc Dis. 2004;18(2):154-915256790
Cites: Stroke. 1993 Jan;24(1):35-417678184
Cites: Stroke. 1999 Apr;30(4):736-4310187871
Cites: Stroke. 2006 Oct;37(10):2493-816931783
Cites: Eur Neurol. 2007;57(4):212-817268202
Cites: Tidsskr Nor Laegeforen. 2007 Oct 4;127(19):2532-617925822
Cites: Pract Neurol. 2008 Aug;8(4):222-818644908
Cites: Expert Rev Neurother. 2009 Feb;9(2):179-9619210194
Cites: J Neurol Sci. 2009 Apr 15;279(1-2):1-819185319
PubMed ID
26032994 View in PubMed
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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
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