Professional Documents
Culture Documents
-, 2019
ª 2019 BY THE AMERICAN COLLEGE OF CARDIOLOGY FOUNDATION
PUBLISHED BY ELSEVIER
ABSTRACT
BACKGROUND A new 5-stage cardiogenic shock (CS) classification scheme was recently proposed by the Society for
Cardiovascular Angiography and Intervention (SCAI) for the purpose of risk stratification.
OBJECTIVES This study sought to apply the SCAI shock classification in a cardiac intensive care unit (CICU) population.
METHODS The study retrospectively analyzed Mayo Clinic CICU patients admitted between 2007 and 2015. SCAI CS
stages A through E were classified retrospectively using CICU admission data based on the presence of hypotension or
tachycardia, hypoperfusion, deterioration, and refractory shock. Hospital mortality in each SCAI shock stage was stratified
by cardiac arrest (CA).
RESULTS Among the 10,004 unique patients, 43.1% had acute coronary syndrome, 46.1% had heart failure, and 12.1%
had CA. The proportion of patients in SCAI CS stages A through E was 46.0%, 30.0%, 15.7%, 7.3%, and 1.0% and
unadjusted hospital mortality in these stages was 3.0%, 7.1%, 12.4%, 40.4%, and 67.0% (p < 0.001), respectively. After
multivariable adjustment, each higher SCAI shock stage was associated with increased hospital mortality (adjusted odds
ratio: 1.53 to 6.80; all p < 0.001) compared with SCAI shock stage A, as was CA (adjusted odds ratio: 3.99; 95%
confidence interval: 3.27 to 4.86; p < 0.001). Results were consistent in the subset of patients with acute coronary
syndrome or heart failure.
CONCLUSIONS When assessed at the time of CICU admission, the SCAI CS classification, including presence or absence
of CA, provided robust hospital mortality risk stratification. This classification system could be implemented as a clinical
and research tool to identify, communicate, and predict the risk of death in patients with, and at risk for, CS.
(J Am Coll Cardiol 2019;-:-–-) © 2019 by the American College of Cardiology Foundation.
From the aDepartment of Cardiovascular Medicine, Mayo Clinic, Rochester, Minnesota; bDivision of Pulmonary and Critical Care
Medicine, Department of Internal Medicine, Mayo Clinic, Rochester, Minnesota; cDepartment of Critical Care Medicine and
Division of Cardiology, Department of Medicine, University of Alberta Hospital, Edmonton, Alberta, Canada; dCarl and Edyth
Lindner Center for Research and Education, Christ Hospital Health Network, Cincinnati, Ohio; eDepartment of Cardiovascular
Medicine, Cleveland Clinic, Cleveland, Ohio; fWestchester Heart and Vascular Institute, Westchester Medical Center and New York
Medical College, Valhalla, New York; and the gSentara Heart Hospital, Advanced Heart Failure Center and Eastern Virginia Medical
School, Norfolk, Virginia. Dr. Baran has served as a consultant for Abiomed, Abbott, Getinge, and LivaNova; and has served as a
speaker for Novartis. All other authors have reported that they have no relationships relevant to the contents of this paper to
disclose.
Manuscript received May 22, 2019; revised manuscript received July 5, 2019, accepted July 7, 2019.
0%
%
10
20
30
40
50
60
70
Cardiac Intensive Care Unit Mortality
Hospital Mortality
Jentzer, J.C. et al. J Am Coll Cardiol. 2019;-(-):-–-.
Cardiac intensive care unit and hospital mortality increased as a function of higher Society for Cardiovascular Angiography and Intervention shock stage.
and treatment biases associated with CICU read- examination data were not available (13–15). All rele-
mission, only data from each patient’s first CICU vant data were extracted electronically from the
admission were analyzed. According to Minnesota medical record using the Multidisciplinary Epidemi-
state law statute 144.295, patients may decline ology and Translational Research in Intensive Care
authorization for inclusion in observational research Data Mart, a repository storing clinical data from all
studies; patients who declined Minnesota Research intensive care unit admissions at the Mayo Clinic
Authorization were excluded from the study. Rochester (16). The admission value of all vital signs,
clinical measurements, and laboratory values was
DATA SOURCES. We recorded demographic, vital defined as either the first value recorded after CICU
sign, laboratory, clinical, and outcome data, as well admission or the value recorded closest to CICU
as procedures and therapies performed during the admission. In addition, vital signs were recorded
CICU and hospital stay, as previously described; every 15 min during the first hour after CICU admis-
radiographic, invasive hemodynamic, and physical sion. Peak vasoactive medication (vasopressor and
T A B L E 2 Definition of CS Stages Used in this Study, Based on the SCAI Consensus Statement Classification
Stage A (“at risk”) Patients without CS who are hemodynamically stable but have acute cardiovascular disease putting them at risk of developing CS
Stage B (“beginning”) Patients without CS who display hemodynamic instability, including hypotension and/or tachycardia, but with normal perfusion
Stage C (“classic”) Patients with CS, manifested by hypoperfusion (lactic acidosis, oliguria, cool/clammy periphery, or altered mentation) requiring
intervention
Stage D (“deteriorating)” Patients with CS whose hemodynamic instability and/or hypoperfusion fails to respond to initial interventions
Stage E (“extremis”) Patients with CS and overt or impending circulatory collapse, including CA with ongoing resuscitation
F I G U R E 1 Study Inclusion and Exclusion Criteria and Distribution of SCAI Shock Stages
The final study population included 10,004 unique patients. CICU ¼ cardiac intensive care unit; SCAI ¼ Society for Cardiovascular Angiography
and Intervention.
inotrope) doses were used to calculate the vasoactive- creatinine from baseline, increase in serum creatinine
inotropic score and norepinephrine-equivalent vaso- to $4.0 mg/dl, or new dialysis initiation; patients with
pressor dose (17–19). Admission diagnoses included a prior history of dialysis were excluded from this
all International Classification of Diseases-9th analysis (14).
Revision diagnostic codes recorded on the day of
CICU admission and the day before or after CICU DEFINITION OF SHOCK STAGES. We defined hypo-
admission; these admission diagnoses were not tension or tachycardia, hypoperfusion, deterioration,
mutually exclusive, and the primary admission diag- and refractory shock using data from CICU admission
nosis could not be determined. Admission diagnoses through the first 24 h in the CICU (Table 1). Hypo-
of interest included acute coronary syndrome tension and tachycardia were defined within the first
(ACS), heart failure (HF), supraventricular tachy- 1 h of CICU admission. The definition of hypo-
cardia, atrial fibrillation, ventricular fibrillation, perfusion included an elevated lactate level on
ventricular tachycardia, shock, CA, respiratory admission or AKI developing within 24 h after
failure, and sepsis. admission. Deterioration was defined as increasing
The Acute Physiology and Chronic Health Evalua- vasoactive drug requirements after the first hour or a
tion (APACHE)-III score, APACHE-IV predicted hospital rising lactate level after admission. We used prag-
mortality, and Sequential Organ Failure Assessment matic and simplified definitions to divide patients
score were automatically calculated for all patients into the 5 SCAI shock stages with increasing severity
using data from the first 24 h of CICU admission using (A through E) using combinations of these variables
previously validated electronic algorithms, with (Central Illustration). Importantly, the SCAI shock
missing variables imputed as normal as the default classification system (Table 2) involves details such as
(13–15,20–22). The Charlson Comorbidity Index (CCI) rapid escalation of inotropes or addition of temporary
and individual comorbidities were determined from mechanical circulatory support (MCS) devices, which
the medical record using a previously validated elec- were not available in the database (12) Late deterio-
tronic algorithm (23). Severe acute kidney injury (AKI) ration was defined as increasing vasopressor re-
during the CICU stay was defined as doubling of serum quirements after 24 h.
JACC VOL. -, NO. -, 2019 Jentzer et al. 5
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T A B L E 3 Baseline Characteristics, Comorbidities, Admission Diagnoses, and Therapies of Patients According to SCAI Shock Stage
With Data, % Stage A (n ¼ 4,602) Stage B (n ¼ 2,998) Stage C (n ¼ 1,575) Stage D (n ¼ 732) Stage E (n ¼ 97) p Value
Demographics
Age, yrs 100.0 67.1 14.7 66.4 15.7 69.9 16.0 68.7 14.1 68.3 14.7 <0.001
Female 100.0 1,562 (33.9) 1,216 (40.6) 654 (41.5) 278 (38.0) 36 (37.1) <0.001
White 100.0 4,289 (93.2) 2,779 (92.7) 1,430 (90.8) 659 (90.0) 79 (81.4) <0.001
Comorbidities
Charlson Comorbidity Index 99.8 2.1 2.5 2.5 2.6 2.8 2.8 3.0 2.8 2.1 2.6 <0.001
History of MI 99.8 914 (19.9) 581 (19.4) 311 (19.8) 160 (21.9) 14 (14.4) 0.79
History of HF 99.8 746 (16.2) 638 (21.3) 339 (21.6) 212 (29.0) 18 (18.6) <0.001
History of diabetes mellitus 99.8 1,222 (26.6) 851 (28.5) 483 (30.8) 257 (35.2) 24 (24.7) <0.001
History of CKD 99.8 770 (16.8) 604 (20.2) 418 (26.6) 221 (30.2) 18 (20.4) <0.001
Prior dialysis 100.0 131 (2.8) 130 (4.3) 192 (12.2) 107 (14.6) 11 (11.3) <0.001
Admission ICD-9 diagnoses*
ACS 99.0 2,111 (46.4) 1,172 (39.4) 634 (40.7) 300 (41.3) 50 (52.6) <0.001
HF 99.0 1,675 (36.8) 1,562 (52.5) 758 (48.7) 513 (70.7) 56 (59.0) <0.001
Cardiac arrest 99.0 330 (7.3) 311 (10.5) 219 (14.1) 280 (38.6) 53 (55.8) <0.001
Shock 99.0 217 (4.8) 449 (15.1) 166 (10.7) 429 (59.1) 88 (92.6) <0.001
Respiratory failure 99.0 506 (11.1) 660 (22.2) 389 (25.0) 460 (63.4) 64 (67.4) <0.001
Sepsis 99.0 102 (2.2) 205 (6.9) 100 (6.4) 163 (22.4) 35 (36.8) <0.001
AF/SVT 99.0 1,165 (25.6) 1,150 (38.7) 571 (36.7) 304 (41.9) 30 (31.6) <0.001
VT/VF 99.0 665 (14.6) 516 (17.4) 247 (15.9) 158 (21.8) 22 (23.2) <0.001
Therapies and procedures
Vasoactives first 1 h 100.0 126 (2.7) 339 (11.3) 90 (5.7) 249 (34.0) 81 (83.5) <0.001
Number of vasoactives first 1 h 100.0 0.0 0.2 0.1 0.4 0.1 0.3 0.4 0.6 1.4 1.0 <0.001
VIS first 1 h 99.1 0.2 1.6 1.3 10.5 1.4 12.1 5.4 15.3 30.1 46.7 <0.001
NEE first 1 h 100.0 0.00 0.01 0.01 0.10 0.01 0.12 0.05 0.15 0.29 0.47 <0.001
Invasive ventilator first 24 h 100.0 257 (5.6) 419 (14.0) 232 (14.7) 417 (57.0) 73 (75.3) <0.001
Dialysis 100.0 119 (2.6) 138 (4.6) 72 (4.6) 137 (18.7) 21 (21.6) <0.001
CRRT 100.0 9 (0.2) 30 (1.0) 23 (1.5) 94 (12.8) 11 (11.3) <0.001
IABP during hospitalization 100.0 266 (5.8) 330 (11.0) 69 (4.4) 162 (22.1) 38 (39.2) <0.001
Impella 100.0 5 (0.1) 7 (0.2) 4 (0.2) 3 (0.4) 2 (2.1) 0.004
ECMO 100.0 15 (0.3) 28 (0.9) 8 (0.5) 16 (2.2) 5 (5.2) 0.02
PAC 100.0 239 (5.2) 245 (8.2) 49 (3.1) 163 (22.3) 25 (25.8) <0.001
Coronary angiogram 100.0 2,694 (58.5) 1,471 (49.1) 720 (45.7) 349 (47.7) 50 (51.6) <0.001
PCI 100.0 1,834 (39.8) 932 (31.1) 430 (27.3) 205 (28.0) 26 (26.8) <0.001
RBC transfusion 100.0 308 (6.7) 403 (13.4) 197 (12.5) 228 (31.2) 37 (28.1) <0.001
Values are mean SD or n (%), unless otherwise indicated. The p value is for the trend across SCAI shock stages A to E. *Admission diagnoses are not mutually exclusive and sum to >100%.
ACS ¼ acute coronary syndrome; AF ¼ atrial fibrillation; CICU ¼ cardiac intensive care unit; CKD ¼ chronic kidney disease; CRRT ¼ continuous renal-replacement therapy; ECMO ¼ extracorporeal membrane
oxygenation; HF ¼ heart failure; ICD-9 ¼ International Classification of Diseases-9th Revision; MI ¼ myocardial infarction; PAC ¼ pulmonary artery catheter; PCI ¼ percutaneous coronary intervention;
RBC ¼ red blood cell; SVT ¼ supraventricular tachycardia; VF ¼ ventricular fibrillation; VT ¼ ventricular tachycardia; other abbreviations as in Tables 1 and 2.
STATISTICAL ANALYSIS. The primary endpoint was medications, intra-aortic balloon pump, coronary
all-cause hospital mortality; secondary endpoints angiography, percutaneous coronary intervention,
included CICU mortality. Hospital disposition and all- and mechanical ventilation. Discrimination was
cause mortality were determined using electronic re- assessed using the area under the receiver-operating
view of medical records. Categorical variables are re- characteristic curve (C-statistic) value. Two-tailed
ported as number and percentage and the Pearson chi- p values <0.05 were considered statistically signifi-
square test was used to compare groups. Continuous cant. Statistical analyses were performed using JMP
variables are reported as mean SD. Trends across the Pro version 14.1.0 (SAS Institute, Cary, North Carolina).
SCAI shock stages were determined using linear
regression. Logistic regression was used to determine RESULTS
the association between the SCAI shock stages and
hospital mortality before and after adjusting for age, STUDY POPULATION. We screened 12,904 adult ad-
sex, CCI, APACHE-IV predicted hospital mortality, missions to the CICU during the study period and
admission diagnosis of CA, and the use of vasoactive excluded 2,900 patients (1,877 readmissions, 755
6 Jentzer et al. JACC VOL. -, NO. -, 2019
Shock Classification Stratifies Mortality Risk -, 2019:-–-
T A B L E 4 Severity of Illness Scores, Vital Signs, and Laboratory Data of Patients According to SCAI Shock Stage
With Data, % Stage A (n ¼ 4,602) Stage B (n ¼ 2,998) Stage C (n ¼ 1,575) Stage D (n ¼ 732) Stage E (n ¼ 97) p Value
Severity of illness
APACHE-III score 100.0 51.3 18.2 60.8 20.4 69.5 24.4 97.4 31.5 118.5 38.8 <0.001
APACHE-IV predicted hospital mortality, % 100.0 9.9 11.6 15.8 16.7 22.0 20.7 48.4 28.1 64.8 27.8 <0.001
Day 1 SOFA score 99.9 2.3 2.0 3.4 2.7 4.4 2.9 9.1 3.9 11.4 3.9 <0.001
Severe AKI 89.2 257 (6.1) 333 (12.4) 233 (17.8) 269 (44.2) 40 (49.4) <0.001
Late deterioration 100.0 188 (4.1) 190 (6.3) 108 (6.9) 205 (28.0) 17 (17.5) <0.001
Admission vital sign data
Systolic blood pressure, mm Hg 99.4 130.8 22.9 114.4 26.1 123.0 27.7 113.8 27.9 99.8 25.3 <0.001
Diastolic blood pressure, mm Hg 96.2 72.1 14.5 67.1 18.6 68.8 17.8 65.7 19.5 57.6 19.4 <0.001
Mean arterial pressure, mm Hg 96.2 87.2 15.1 79.6 19.6 83.1 18.9 79.9 20.9 70.1 20.9 <0.001
Heart rate, beats/min 99.4 72.4 13.9 93.1 26.8 84.8 25.5 89.4 24.7 95.5 27.9 <0.001
Shock index* 99.4 0.57 0.15 0.84 0.29 0.72 0.28 0.83 0.29 1.04 0.38 <0.001
Respiratory rate, breaths/min 95.9 17.3 5.2 19.1 6.0 19.3 5.9 20.2 5.9 21.8 6.5 <0.001
Pulse oximetry, % 99.4 96.6 4.2 95.6 5.6 95.2 7.3 93.2 9.0 86.5 16.8 <0.001
Glasgow Coma Scale 97.3 14.5 2.0 13.9 2.9 13.6 3.3 9.8 5.1 8.3 5.1 <0.001
Urine output first 24 h, l 97.0 2.16 1.10 2.26 1.42 1.02 1.12 1.25 1.33 1.41 2.41 <0.001
Admission laboratory data
Creatinine, mg/dl 96.3 1.2 0.8 1.3 1.0 1.7 1.7 1.9 1.4 1.9 1.2 <0.001
BUN, mg/dl 96.0 23.5 16.4 27.0 18.9 30.0 20.4 36.0 23.1 34.6 20.5 <0.001
ALT, U/ml 46.5 51.9 139.5 76.2 222.2 127.3 529.8 270.8 675.0 644.5 1211.5 <0.001
Peak troponin T, mg/dl 63.3 1.8 3.3 1.7 3.2 1.8 3.4 3.3 6.9 4.0 6.5 <0.001
Hemoglobin, g/l 96.4 12.5 2.0 11.9 2.2 11.9 2.3 11.8 2.5 11.6 2.5 <0.001
Arterial pH 32.3 7.39 0.08 7.36 0.10 7.36 0.10 7.30 0.11 7.20 0.15 <0.001
Bicarbonate, mEq/l 96.9 24.6 3.7 23.9 4.4 23.4 4.6 21.2 5.3 16.7 6.5 <0.001
Anion gap, mEq/l 89.3 11.0 2.9 11.5 3.2 12.6 3.8 14.4 4.3 20.6 8.7 <0.001
Lactate, mmol/l 21.3 1.2 0.4 1.3 0.4 3.0 2.3 3.6 2.3 10.6 5.1 <0.001
Values are mean SD or n (%), unless otherwise indicated. The p value is for the trend across SCAI shock stages A to E. *Shock index is defined as the ratio of heart rate to systolic blood pressure.
AKI ¼ acute kidney injury; ALT ¼ alanine aminotransferase; APACHE, Acute Physiology and Chronic Health Evaluation; BUN ¼ blood urea nitrogen; SCAI ¼ Society for Cardiovascular Angiography and
Intervention; SOFA ¼ Sequential Organ Failure Assessment.
patients without Minnesota Research Authorization, Hypotension or tachycardia during the first hour in
and 268 patients whose admission did not occur the CICU was present in 4,367 (43.7%) patients,
entirely within the study period), as demonstrated in including 2,545 (25.4%) who met criteria for hypo-
Figure 1 (13–15). The final study population of 10,004 tension and 2,956 (29.5%) who met criteria for
unique patients had a mean age of 67.4 15.2 years, tachycardia; 1,134 (11.3%) patients met criteria for
including 3,746 (37.4%) women. The mean CCI was both hypotension and tachycardia. Hypoperfusion
2.4 2.6 and the mean APACHE-IV predicted hospital was present in 2,404 (24.0%) patients, including an
mortality was 16.9 20.0% overall. Admission di- admission lactate level >2 mmol/l in 888 (41.6%) of
agnoses (not mutually exclusive) included ACS in 2,135 patients with available data. Deterioration
4,267 (43.1%) patients, HF in 4,564 (46.1%) patients, within 24 h of admission occurred in 2,075 (20.7%)
and CA in 1,193 (12.1%) patients; 2,704 (27.3%) pa- patients, and refractory shock was identified in 153
tients had neither ACS nor HF as an admis- (1.5%) patients. Late deterioration after 24 h occurred
sion diagnosis. in 708 (7.1%) patients.
A total of 2,468 (24.7%) patients received vasoac- The proportion of patients with SCAI shock stages
tive drugs during the CICU stay, including vasopres- A through E were 46.0%, 30.0%, 15.7%, 7.3%, and
sors in 2,090 (20.9%) and inotropes in 928 (9.3%). 1.0%, respectively (Figure 1). Baseline demographics,
Among patients receiving vasoactive drugs, 1,182 comorbidities, admission diagnoses, and critical care
(47.9%) received >1 vasoactive drug. An intra-aortic therapies varied significantly across the SCAI shock
balloon pump was placed during the CICU stay in stages (Table 3). The prevalence of CA increased
865 (8.6%) patients and Impella (Abiomed, Danvers, across the SCAI shock stages, from 7.3% in stage A to
Massachusetts) or ECMO support was used during the 55.8% in stage E. As the SCAI shock stage increased,
hospitalization in 21 (0.2%) and 72 (0.7%) patients, there were more extensive vital sign and laboratory
respectively. abnormalities, higher severity of illness scores, and
JACC VOL. -, NO. -, 2019 Jentzer et al. 7
-, 2019:-–- Shock Classification Stratifies Mortality Risk
F I G U R E 2 Hospital Mortality as a Function of SCAI Shock Stage Among Patients With and Without an Admission Diagnosis of CA
80%
70%
Observed Hospital Mortality (%)
60%
50%
40%
30%
20%
10%
0%
Stage A Stage B Stage C Stage D Stage E
SCAI Shock Stage
Hospital mortality was higher among patients with an admission diagnosis of cardiac arrest (CA) in each Society for Cardiovascular
Angiography and Intervention (SCAI) shock stage (all p < 0.001).
more frequent AKI (Table 4). The use and dosage of shock stages B through E were 2.44, 4.56, 21.80, and
vasoactive medications and supportive therapies 65.22, respectively. The unadjusted OR value for
including mechanical ventilation, MCS, and dialysis hospital mortality was 12.17 (95% confidence interval
increased across the SCAI shock stages (Table 4). The [CI]: 10.34 to 14.31; p < 0.001) in patients meeting
prevalence of late deterioration increased as a func- criteria for SCAI shock stage D or E, compared with
tion of SCAI shock stage, being highest in SCAI shock SCAI shock stages A through C. The SCAI shock clas-
stage D (Table 4). sification itself had an area under the receiver-
operating characteristic curve value of 0.765 for
CICU AND HOSPITAL MORTALITY. There was a step- hospital mortality overall, 0.775 among patients with
wise increase in unadjusted CICU and hospital mor- ACS, and 0.732 among patients with HF.
tality with each higher SCAI shock stage in the overall After multivariable adjustment, each higher SCAI
population, with hospital mortality rising from 3.0% shock stage was associated with increased hospital
in SCAI shock stage A to 67.0% in SCAI shock stage E mortality compared with SCAI shock stage A (all
(p < 0.001) (Central Illustration). Unadjusted hospital p < 0.001), as was CA (adjusted OR: 3.99; 95% CI: 3.27
mortality was higher among patients with CA at each to 4.86, 95% CI; p < 0.001); the final multivariable
SCAI shock stage (Figure 2) (all p < 0.001). The same model area under the receiver-operating character-
stepwise increase in hospital mortality was seen in istic curve value was 0.883 in the overall population.
patients with ACS and HF and in patients without a Compared with SCAI shock stage A, the adjusted OR
diagnosis of either ACS or HF (Figure 3). Patients with values for hospital mortality in SCAI shock stages B
late deterioration had higher mortality overall (31.4% through E were 1.53, 2.62, 3.07, and 6.80, respectively
vs. 7.4%; p < 0.001), and in each SCAI shock stage (Figure 5). Each higher SCAI shock stage was associ-
except stage E (Figure 4). ated with higher adjusted hospital mortality
Compared with SCAI shock stage A, the unadjusted compared with SCAI shock stage A among patients
odds ratio (OR) values for hospital mortality in SCAI with ACS (all p < 0.001), HF (all p < 0.001), and
8 Jentzer et al. JACC VOL. -, NO. -, 2019
Shock Classification Stratifies Mortality Risk -, 2019:-–-
80%
70%
50%
40%
30%
20%
10%
0%
ACS HF Neither ACS nor HF
(n = 4,267) (n = 4,564) (n = 2,704)
Stage A Stage B Stage C Stage D Stage E
Hospital mortality as a function of Society for Cardiovascular Angiography and Intervention (SCAI) shock stage among patients with acute
coronary syndrome (ACS) (left), heart failure (HF) (middle), or neither ACS nor HF (right). Hospital mortality increased as a function of higher
SCAI shock stage in patients with ACS or HF.
neither ACS nor HF (all p < 0.001). Likewise, CA was diagnosis of CA increased the risk of hospital mor-
associated with higher adjusted hospital mortality in tality among patients with each SCAI shock stage,
each of these subgroups (all p < 0.001). supporting its inclusion as an effect modifier in the
SCAI shock classification schema. These data support
DISCUSSION the validity of the recent SCAI classification of CS
stages for mortality risk stratification as a framework
Using a large cohort of unselected CICU patients, we for future CS clinical practice and research. Our ex-
validated the association between the recently amination of a mixed CICU cohort allowed us to
described SCAI shock classification and hospital demonstrate the predictive ability of this classifica-
mortality. We stratified patients into 5 SCAI shock tion system in patients with diagnoses of ACS and HF,
stages at the time of CICU admission, reflecting a which are the dominant causes of CS, as well as in
continuum of increasing shock severity using a patients without these diagnoses. The strong associ-
simplified definition based on hypotension or tachy- ation between SCAI shock stages and mortality in a
cardia, hypoperfusion, deterioration, and refractory heterogeneous CICU population, even after adjust-
shock, which can be easily applied in clinical practice. ment for known predictors of mortality, emphasizes
This functional SCAI shock stages classification the robustness of this classification system and its
effectively stratified mortality risk and performed potential to be applied in other critically ill patient
similarly in patients with admission diagnoses of ACS cohorts.
and HF, even when adjusting for the higher illness The SCAI shock classification was developed using
severity and greater use of hemodynamic support at expert consensus for the purpose of describing CS
higher shock stages. Patients with refractory shock severity to clarify communication of patient status
(SCAI shock stage E) had >20-fold higher crude hos- between providers in different care settings to facili-
pital mortality than hemodynamically stable patients tate patient triage and selection for advanced thera-
without shock (SCAI shock stage A). An admission pies (12). In addition, the SCAI classification of CS
JACC VOL. -, NO. -, 2019 Jentzer et al. 9
-, 2019:-–- Shock Classification Stratifies Mortality Risk
Stage A
(Referent)
Stage B
SCAI Shock Stage
Stage C
Stage D
Stage E
0 1 2 3 4 5 6 7 8 9 10 11 12
Adjusted OR for Hospital Mortality
Adjusted odds ratios (ORs) and 95% confidence intervals for hospital mortality with each Society for Cardiovascular Angiography and
Intervention (SCAI) shock stage derived from multivariable logistic regression, using stage A as referent. Higher SCAI shock stages had
incrementally higher adjusted odds for hospital mortality.
future studies should address whether brief CA epi- or clinical deterioration, to highlight their escalating
sodes have any prognostic importance and whether mortality risk in real time and facilitate early
the presence of brain injury from CA modifies the transfer or involvement of palliative care services if
response to CS therapies (26). indicated (1).
Van Diepen et al. (1) have proposed a “hub-and- We propose that the relative efficacy of various
spoke” care model involving transfer to tertiary cen- therapeutic interventions at each CS stage should be
ters for patients with CS, as has been instituted for further explored, as CS severity might determine the
other high-acuity medical conditions such as trauma. need for and clinical response to specific therapies.
Uncertainty remains regarding when transfer to a For example, temporary MCS devices can effectively
higher level of care is warranted, and ideally this increase cardiac output in CS, yet none of these
should be determined early in the course if a patient temporary MCS devices has resulted in a proven
is not responding as expected to initial therapy. improvement in survival in published randomized
Based on the high risk of mortality after the onset of clinical trials of CS patients (1,8,9,27). Notwith-
hemodynamic deterioration (SCAI shock stage D), we standing their established hemodynamic benefits, the
propose that patients with hypoperfusion (SCAI shock invasive nature and acquisition costs of temporary
stage C) who do not rapidly stabilize (i.e., progression MCS devices emphasize the need to evaluate when
to SCAI shock stage D) should be considered for and in whom these devices may be most effective for
transfer to a higher level of care before development improving patient-centered outcomes (1,8,27). We
of overt deterioration. The simple functional defini- suspect that each temporary MCS device will have a
tions used in this study could be leveraged by an different risk-benefit profile at a given CS stage, but
electronic medical record system to identify patients this hypothesis will need to be tested in future
with new onset or increasing severity of shock studies.
JACC VOL. -, NO. -, 2019 Jentzer et al. 11
-, 2019:-–- Shock Classification Stratifies Mortality Risk
REFERENCES
1. van Diepen S, Katz JN, Albert NM, et al. Classification of Cardiogenic Shock: this document 22. Harrison AM, Yadav H, Pickering BW, Cartin-
Contemporary management of cardiogenic shock: was endorsed by the American College of Cardi- Ceba R, Herasevich V. Validation of computerized
a scientific statement from the American Heart ology (ACC), the American Heart Association automatic calculation of the sequential organ
Association. Circulation 2017;136:e232–68. (AHA), the Society of Critical Care Medicine failure assessment score. Crit Care Res Pract 2013;
(SCCM), and the Society of Thoracic Surgeons in 2013:975672.
2. Kolte D, Khera S, Aronow WS, et al. Trends in
April 2019. Catheter Cardiovasc Interv 2019;94:
incidence, management, and outcomes of cardio- 23. Singh B, Singh A, Ahmed A, et al. Derivation
29–37.
genic shock complicating ST-elevation myocardial and validation of automated electronic search
infarction in the United States. J Am Heart Assoc 13. Jentzer JC, Bennett C, Wiley BM, et al. Pre- strategies to extract Charlson comorbidities from
2014;3:e000590. dictive value of the sequential organ failure electronic medical records. Mayo Clin Proc 2012;
assessment score for mortality in a contemporary 87:817–24.
3. Hunziker L, Radovanovic D, Jeger R, et al.
Twenty-year trends in the incidence and outcome cardiac intensive care unit population. J Am Heart 24. Stevenson LW, Pagani FD, Young JB, et al.
of cardiogenic shock in AMIS Plus registry. Circ Assoc 2018;7:e008169. INTERMACS profiles of advanced heart failure: the
Cardiovasc Interv 2019;12:e007293. 14. Jentzer JC, Murphree DH, Wiley B, et al. current picture. J Heart Lung Transplant 2009;28:
Comparison of mortality risk prediction among 535–41.
4. Berg DD, Bohula EA, van Diepen S, et al.
Epidemiology of shock in contemporary cardiac patients >/¼70 versus <70 years of age in a 25. Gupta N, Kontos MC, Gupta A, et al. Charac-
intensive care units. Circ Cardiovasc Qual Out- cardiac intensive care unit. Am J Cardiol 2018;122: teristics and outcomes in patients undergoing
comes 2019;12:e005618. 1773–8. percutaneous coronary intervention following
15. Bennett CE, Wright RS, Jentzer J, et al. cardiac arrest (from the NCDR). Am J Cardiol 2014;
5. Hochman JS, Sleeper LA, Webb JG, et al. Early
Severity of illness assessment with application of 113:1087–92.
revascularization in acute myocardial infarction
complicated by cardiogenic shock. SHOCK In- the APACHE IV predicted mortality and outcome 26. Jentzer JC, Herrmann J, Prasad A,
vestigators. Should We Emergently Revascularize trends analysis in an academic cardiac intensive Barsness GW, Bell MR. Utility and challenges of an
Occluded Coronaries for Cardiogenic Shock. N Engl care unit. J Crit Care 2018;50:242–6. early invasive strategy in patients resuscitated
J Med 1999;341:625–34. from out-of-hospital cardiac arrest. J Am Coll
16. Herasevich V, Pickering BW, Dong Y,
Cardiol Intv 2019;12:697–708.
6. Investigators T, Alexander JH, Reynolds HR, Peters SG, Gajic O. Informatics infrastructure for
et al. Effect of tilarginine acetate in patients with syndrome surveillance, decision support, report- 27. Rihal CS, Naidu SS, Givertz MM, et al. 2015
acute myocardial infarction and cardiogenic shock: ing, and modeling of critical illness. Mayo Clin Proc SCAI/ACC/HFSA/STS Clinical Expert Consensus
the TRIUMPH randomized controlled trial. JAMA 2010;85:247–54. Statement on the Use of Percutaneous Mechanical
2007;297:1657–66. Circulatory Support Devices in Cardiovascular
17. Nguyen HV, Havalad V, Aponte-Patel L, et al.
Care: Endorsed by the American Heart Assocation,
7. Thiele H, Akin I, Sandri M, et al. PCI strategies in Temporary biventricular pacing decreases the
the Cardiological Society of India, and Sociedad
patients with acute myocardial infarction and vasoactive-inotropic score after cardiac surgery: a
Latino Americana de Cardiologia Intervencion;
cardiogenic shock. N Engl J Med 2017;377:2419–32. substudy of a randomized clinical trial. J Thorac
Affirmation of Value by the Canadian Association
Cardiovasc Surg 2013;146:296–301.
8. Thiele H, Jobs A, Ouweneel DM, et al. Percu- of Interventional Cardiology-Association Cana-
taneous short-term active mechanical support 18. Jentzer JC, Vallabhajosyula S, Khanna AK, dienne de Cardiologie d’intervention. J Am Coll
devices in cardiogenic shock: a systematic review Chawla LS, Busse LW, Kashani KB. Management of Cardiol 2015;65:e7–26.
and collaborative meta-analysis of randomized refractory vasodilatory shock. Chest 2018;154:
28. Hasdai D, Holmes DR Jr., Califf RM, et al.
trials. Eur Heart J 2017;38:3523–31. 416–26.
Cardiogenic shock complicating acute myocardial
9. Thiele H, Zeymer U, Neumann FJ, et al. Intra- 19. Jentzer JC, Wiley B, Bennett C, et al. Temporal infarction: predictors of death. GUSTO In-
aortic balloon support for myocardial infarction trends and clinical outcomes associated with vestigators. Global Utilization of Streptokinase
with cardiogenic shock. N Engl J Med 2012;367: vasopressor and inotrope use in the cardiac and Tissue-Plasminogen Activator for Occluded
1287–96. intensive care unit. Shock 2019 Jun 4 [E-pub Coronary Arteries. Am Heart J 1999;138:21–31.
10. Harjola VP, Lassus J, Sionis A, et al. Clinical ahead of print].
29. Stretch R, Sauer CM, Yuh DD, Bonde P. Na-
picture and risk prediction of short-term mortality 20. Chandra S, Kashyap R, Trillo-Alvarez CA, et al. tional trends in the utilization of short-term me-
in cardiogenic shock. Eur J Heart Fail 2015;17: Mapping physicians’ admission diagnoses to chanical circulatory support: incidence, outcomes,
501–9. structured concepts towards fully automatic and cost analysis. J Am Coll Cardiol 2014;64:
11. Poss J, Koster J, Fuernau G, et al. Risk strati- calculation of acute physiology and chronic health 1407–15.
fication for patients in cardiogenic shock after evaluation score. BMJ Open 2011;1:e000216.
acute myocardial infarction. J Am Coll Cardiol
21. Aakre C, Franco PM, Ferreyra M, Kitson J, Li M,
2017;69:1913–20.
Herasevich V. Prospective validation of a near KEY WORDS cardiac intensive care unit,
12. Baran DA, Grines CL, Bailey S, et al. SCAI real-time EHR-integrated automated SOFA score cardiogenic shock, critical care, mortality,
Clinical Expert Consensus Statement on the calculator. Int J Med Inform 2017;103:1–6. shock