第46回日本集中治療医学会学術集会

講演情報

パネルディスカッション

[PD7] パネルディスカッション7
集中治療における多臓器機能とバイオマーカー

2019年3月2日(土) 14:00 〜 15:30 第5会場 (国立京都国際会館1F Room D)

座長:佐藤 直樹(日本医科大学武蔵小杉病院内科・循環器内科・集中治療室), 松田 兼一(山梨大学医学部附属病院集中治療部)

[PD7-1] Differentiating type 1 from type 2 acute myocardial infarction is necessary but can be difficult to do. A biomarker profile may be the answer.

Richard Michael Nowak (Henry Ford Hospital, USA)

同時通訳付き】

EDUCATION:

Michael Power High School1961 - 1966
Toronto, Ontario
Senior Matriculation (Grade 13)

University of Toronto1966 - 1968
Pre-Medicine
Toronto, Ontario, Canada

University of Toronto1968 - 1972
Medical School
Medical Doctor
Toronto, Ontario, Canada

Executive MBA Program1988 - 1990
Michigan State University
Business School
Broad Graduate School of Management
East Lansing, Michigan
Masters Business Administration
Member, Beta Gamma Sigma


GRADUATE TRAINING:

Montreal General Hospital1972 - 1973
Montreal, Quebec
Straight Medicine

Research Fellow1974 - 1975
Clinical Science Division
University of Toronto



LICENSURE AND CERTIFICATION:

National Board of Medicine Examinations1972


College of Physicians and Surgeons of Ontario1972 - 1976
1985 - 2013

California State Medical Licensure1973 - present

Michigan State Medical Licensure1975 - present

Diplomate of the American Board of Emergency Medicine1981 - 1991

Recertification - American Board of Emergency Medicine1991 - 2001
2001 - 2011
2011 - 2021

Fellow, American College of Emergency Physician1982 - present

Fellow, American Academy of Emergency Medicine2000 - present


HOSPITAL AND STAFF APPOINTMENTS:

Staff Physician1973 - 1974
Emergency Department
Belleville General Hospital
Belleville, Ontario

Staff Physician1974 - 1975
(East York Medical Emergency Group)
Emergency Department
Toronto East General Hospital
Toronto, Ontario

Senior Staff1975 - present
Division/Department of Emergency Medicine
Henry Ford Hospital
Detroit, Michigan

Associate Head 1981 - 1983
Division of Emergency Medicine
Henry Ford Hospital
Detroit, Michigan

Vice Chairperson1983 - 1988
Department of Emergency Medicine
Henry Ford Hospital
Detroit, Michigan



Associate Staff1989 - 1994
Emergency Medicine 2007 - present
Cottage Hospital
Grosse Pointe Farms, Michigan

Chairperson1988 - 1992
Department of Emergency Medicine
Henry Ford Hospital
Detroit, Michigan

Vice Chairperson1992 - 2006
Department of Emergency Medicine
Henry Ford Hospital
Detroit, Michigan

Past Chairperson 2006 - present
Department of Emergency Medicine
Henry Ford Hospital
Detroit, Michigan
The fourth universal definition of acute myocardial infarction (AMI) describes 2 types of AMI that are commonly seen in the Emergency Department (ED). Each diagnostic type requires a typical rise and/or fall of cardiac troponin (cTn) with at least one value above the 99th percentile reference range of a normal population. Type 1 (T1MI) is related to atherosclerotic plaque rupture or erosion with resulting occlusive or non-occlusive thrombus. Type 2 (T2MI) is caused by an imbalance between oxygen supply and demand related to a condition unrelated to coronary thrombosis that results in myocardial injury with necrosis. Examples are tachycardia/bradycardia, acute anemia or hypovolemia, exacerbations of congestive heart failure, renal failure, sepsis and pulmonary embolus and is often seen in the setting of stable coronary artery disease.
It is important to accurately distinguish between these 2 AMI types as most clinicians would agree that therapy for T2MI should be directed to the underlying etiology and to correct the altered variable within the existing supply/demand imbalance. However the presenting symptoms in the ED are similar for each type of AMI making accurate distinctions difficult. We hypothesized that T2MI patients had preexisting non AMI conditions present that caused the supply/demand mismatch before the eventual rise and/or fall of cTn resulting in the diagnosis of AMI. These patients would have more and earlier cardiac wall stress resulting in higher levels of natriuretic peptide release than those with T1MI, resulting in an increase in the natriuretic/cTn ratio.
In the REACTION-US single center study we found that the T1MI and T2MI patient demographics, clinical characteristics, comorbidities and presenting vital signs were very similar and thus did not allow reliable differentiation between these 2 AMI types. However the N-terminal pro-B type natriuretic peptide (NT-proBNP)/generation 5 cardiac troponin T (cTnT Gen 5) median ratios measured at baseline, 30, 60 and 180 minutes later were always significantly higher in patients with T2MI. The cTnT Gen 5 and creatinine levels were not significantly different between patients with these 2 different AMI types at any of these time points.
As the recommended treatments and inpatient dispositions of patients with non-segment elevation T1MI and T2MI are currently different accurate diagnosis of the AMI type is important. The NT-pro BNP/cTnT Gen 5 ratio can aid in the differentiation of these conditions. Future multicenter trials in different parts of the world are needed to determine how naturietic peptide/cTn ratios can be best clinically used to accurately diagnose T1MI and T2MI.