scholarly journals Study of Coronary Atherosclerosis by Modified American Heart Association Classification of Atherosclerosis-An Autopsy Study

2013 ◽  
Author(s):  
Viral M. Bhanvadia
Keyword(s):  
Coronary Atherosclerosis ◽  
American Heart Association ◽  
American Heart ◽  
Heart Association ◽  
Autopsy Study

Classification of cardiomyopathies

2018 ◽  
Author(s):  
Eloisa Arbustini ◽  
Valentina Favalli ◽  
Alessandro Di Toro ◽  
Alessandra Serio ◽  
Jagat Narula
Keyword(s):  
New York ◽  
American Heart Association ◽  
American Heart ◽  
Heart Association ◽  
Genetic Mutation ◽  
Phenotypic Data ◽  
Septal Thickness ◽  
New York Heart Association ◽  
European Society Of Cardiology

For over 50 years, the definition and classification of cardiomyopathies have remained anchored in the concept of ventricular dysfunction and myocardial structural remodelling due to unknown cause. The concept of idiopathic was first challenged in 2006, when the American Heart Association classification subordinated the phenotype to the aetiology. Cardiomyopathies were classified as genetic, acquired, and mixed. In 2008, the European Society of Cardiology proposed a phenotype-driven classification that separated familial (genetic) from non-familial (non-genetic) forms of cardiomyopathy. Both classifications led the way to a precise phenotypic and aetiological description of the disease and moved away from the previously held notion of idiopathic disease. In 2013, the World Heart Federation introduced a descriptive and flexible nosology—the MOGE(S) classification—describing the morphofunctional (M) phenotype of cardiomyopathy, the involvement of additional organs (O), the familial/genetic (G) origin, and the precise description of the (a)etiology including genetic mutation, if applicable (E); reporting of functional status such as American College of Cardiology/American Heart Association stage and New York Heart Association classification (S) was left optional. MOGE(S) is a bridge between the past and the future. It allows description of comprehensive phenotypic data, all genetic and non-genetic causes of cardiomyopathy, and incorporates description of familial clustering in a genetic disease. MOGE(S) is the instrument of precision diagnosis for cardiomyopathies. The addition of the early and unaffected phenotypes to the (M) descriptor outlines the clinical profile of an early affected family member; the examples include non-dilated hypokinetic cardiomyopathy in dilated cardiomyopathy and septal thickness (13–14 mm) in hypertrophic cardiomyopathy classes.

scholarly journals Body of Evidence in Favor of Adopting 130/80 mm Hg as New Blood Pressure Cut-Off for All the Hypertensive Disorders of Pregnancy

Medicina ◽  
2019 ◽  
Vol 55 (10) ◽  
pp. 703 ◽  
Author(s):  
Giovanni Sisti ◽  
Belinda Williams
Keyword(s):  
Blood Pressure ◽  
Systolic Blood Pressure ◽  
Diastolic Blood Pressure ◽  
American Heart Association ◽  
American Heart ◽  
Heart Association ◽  
Hypertensive Disorders Of Pregnancy ◽  
Obstetric Population ◽  
Stage 1

The American College of Cardiology/American Heart Association (ACC/AHA) updated its guideline redefining the classification of hypertension and the blood pressure cut-off in 2017. The current cut-offs for stage 1 hypertension of 130 mm Hg systolic blood pressure or 80 mm Hg diastolic blood pressure replace the previous cut-offs of 140 mm Hg systolic blood pressure or 90 mm Hg diastolic blood pressure which were based on the ACC/AHA guidelines from 1988. However, the blood pressure cut-off for the obstetric population still remains as 140/90 mm Hg despite the scarcity of evidence for it. Recent American College of Obstetricians and Gynecologists (ACOG) bulletins for pregnant women have not reflected the new ACC/AHA change of guideline. We reviewed a mounting body of evidence prompting the implementation of the new ACC/AHA guidelines for the obstetric population. These studies examined maternal and fetal outcomes applying the new ACC/AHA guidelines during antepartum or postpartum care.

scholarly journals Assessing the Requirement for the 6-Hour Interval between Specimens in the American Heart Association Classification of Myocardial Infarction in Epidemiology and Clinical Research Studies

2006 ◽  
Vol 52 (5) ◽  
pp. 812-818 ◽  
Author(s):  
Andrew R MacRae ◽  
Peter A Kavsak ◽  
Viliam Lustig ◽  
Rakesh Bhargava ◽  
Rudy Vandersluis ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
American Heart Association ◽  
Troponin I ◽  
American Heart ◽  
Heart Association ◽  
Case Definition ◽  
Time Interval ◽  
Time Intervals ◽  
Additional Specimen

Abstract Background: The American Heart Association (AHA) case definition for acute myocardial infarction (AMI) requires an “adequate set” of biomarkers: 2 measurements of the same marker at least 6 h apart. A sensitive troponin assay might detect significant changes in concentration earlier. We determined AMI prevalence, using protocols with shorter intervals between measurements, with and without incorporating the time from onset of symptoms. Methods: The AHA case definition was used to retrospectively assign a diagnosis in 258 patients presenting to the emergency department with symptoms of cardiac ischemia. AMI was diagnosed if either specimen in an adequate set had a cardiac troponin I (cTnI) above the 99th percentile (AccuTnI® >0.04 μg/L; Beckman Coulter) with a ≥20% change in concentration between specimens. We assessed positivity for AMI after progressively decreasing the time interval between specimens in specimen sets. In addition, for each patient, 2 additional specimen pairs were selected: pairs collected at least 1 h apart with 1 specimen being either ≥3 h after onset or ≥6 h after onset. Results: When we used the AHA definition, the AMI prevalence was 35.7%. Prevalence was not significantly diminished when the interval between specimens was ≥5, ≥4, or ≥3 h (36.4%, 34.5%, and 33.7%, respectively) compared with the AHA ≥6 h interval. When the time from onset of symptoms was included in the specimen selection algorithm, a 1-h interval was sufficient provided that at least one specimen was collected ≥6 h after onset (prevalence, 34.1%; P = 0.48 vs AHA definition). Conclusion: A sensitive cTnI assay in specimen sets with time intervals ≥3 h, or having one specimen ≥6 h after onset, gave an AMI prevalence equivalent to the AHA definition.

Classification of cardiomyopathies

ESC CardioMed ◽  
2018 ◽  
pp. 1432-1437
Author(s):  
Eloisa Arbustini ◽  
Valentina Favalli ◽  
Alessandro Di Toro ◽  
Alessandra Serio ◽  
Jagat Narula
Keyword(s):  
New York ◽  
American Heart Association ◽  
American Heart ◽  
Heart Association ◽  
Genetic Mutation ◽  
Phenotypic Data ◽  
Septal Thickness ◽  
New York Heart Association ◽  
European Society Of Cardiology

For over 50 years, the definition and classification of cardiomyopathies have remained anchored in the concept of ventricular dysfunction and myocardial structural remodelling due to unknown cause. The concept of idiopathic was first challenged in 2006, when the American Heart Association classification subordinated the phenotype to the aetiology. Cardiomyopathies were classified as genetic, acquired, and mixed. In 2008, the European Society of Cardiology proposed a phenotype-driven classification that separated familial (genetic) from non-familial (non-genetic) forms of cardiomyopathy. Both classifications led the way to a precise phenotypic and aetiological description of the disease and moved away from the previously held notion of idiopathic disease. In 2013, the World Heart Federation introduced a descriptive and flexible nosology—the MOGE(S) classification—describing the morpho-functional (M) phenotype of cardiomyopathy, the involvement of additional organs (O), the familial/genetic (G) origin, and the precise description of the (a)etiology including genetic mutation, if applicable (E); reporting of functional status such as American College of Cardiology/American Heart Association stage and New York Heart Association classification (S) was left optional. MOGE(S) is a bridge between the past and the future. It allows description of comprehensive phenotypic data, all genetic and non-genetic causes of cardiomyopathy, and incorporates description of familial clustering in a genetic disease. MOGE(S) is the instrument of precision diagnosis for cardiomyopathies. The addition of the early and unaffected phenotypes to the (M) descriptor outlines the clinical profile of an early affected family member; the examples include non-dilated hypokinetic cardiomyopathy in dilated cardiomyopathy and septal thickness (13–14 mm) in hypertrophic cardiomyopathy classes. Finally, in the recently released scientific statement of the American Heart Association on the classification and diagnosis of cardiomyopathy in children the consensus was to use a classification system based on a hierarchy incorporating the required elements of the MOGE(S) classification.

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