If you don't remember your password, you can reset it by entering your email address and clicking the Reset Password button. You will then receive an email that contains a secure link for resetting your password
If the address matches a valid account an email will be sent to __email__ with instructions for resetting your password
Correspondence: Young Bin Song, MD, PhD, Department of Medicine, Heart Vascular Stroke Institute, Samsung Medical Center, Sungkyunkwan University School of Medicine, 81 Irwon-ro, Gangnam-gu, Seoul 06351, Republic of Korea.
Department of Radiology, Cardiovascular Imaging Center, Heart Vascular Stroke Institute, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea
Little is known about the association between shock index and myocardial injury in patients with ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PCI).
Methods
We analyzed cardiac magnetic resonance imaging from 306 consecutive patients treated with primary PCI for STEMI. The patients were divided into the following 2 groups: initial shock index >0.7 (n = 88) and ≤0.7 (n = 218). Shock index was calculated as the ratio of heart rate to systolic blood pressure based on the first recorded vital signs upon arrival. The primary end point was myocardial infarct size.
Results
The shock index >0.7 group, exhibited a lower baseline left ventricular ejection fraction (P = 0.01), higher N-terminal prohormone of brain natriuretic peptide level (P = 0.01), higher Killip class (P < 0.01) and higher prevalence of diabetes (P = 0.02) than the shock index ≤0.7 group. There were no significant differences in the angiographic or procedural characteristics between the 2 groups. In cardiac magnetic resonance imaging analysis, the shock index >0.7 group had a larger infarct size than did the shock index ≤0.7 group (22.9 ± 11.2% versus 19.2 ± 11.5%, P < 0.01). According to multivariate analysis, shock index >0.7 was associated with large myocardial infarctions (odds ratio = 3.02; 95% CI: 1.62-5.65; P < 0.01).
Conclusions
Initial shock index is a potentially reliable predictor of myocardial injury in patients with STEMI undergoing primary PCI.
Several recent studies have identified shock index as a simple predictor of clinical outcomes in patients with ST-segment elevation myocardial infarctions (STEMI).
Well-established risk scoring systems such as the Thrombolysis in Myocardial Infarction (TIMI) and Global Registry of Acute Coronary Event tools have been used to estimate prognosis after myocardial infarction (MI). However, these tools are less useful in emergent situations because of their complexity and use of some laboratory results. Shock index, the ratio of heart rate to systolic blood pressure, is a simple parameter for estimating hemodynamic status and predicting clinical outcomes in critically ill patients with various diseases.
Recovery from a psychotropic drug overdose tends to depend on the time from ingestion to arrival, the Glasgow Coma Scale, and a sign of circulatory insufficiency on arrival.
There is little evidence regarding the association between shock index and myocardial injury in patients with STEMI. The evidence that exists is based only on inpatient, short-term outcomes. Late gadolinium enhancement on cardiac magnetic resonance imaging (CMR) is an excellent tool for measuring infarct size in acute MI.
Infarct size by contrast enhanced cardiac magnetic resonance is a stronger predictor of outcomes than left ventricular ejection fraction or end-systolic volume index: prospective cohort study.
Therefore, we used CMR to investigate the association between shock index and myocardial injury in patients with STEMI undergoing primary percutaneous coronary intervention (PCI).
Methods
Study Population
A total of 645 consecutive patients who presented with acute MI and who underwent CMR between December 2007 and July 2014 were enrolled in the Samsung Medical Center Acute Myocardial Infarction—Cardiac Magnetic Resonance Imaging registry (Figure 1). Patients were eligible for CMR unless they had undergone coronary artery bypass graft surgery or thrombolysis for acute MI, or had a history of prior cardiopulmonary resuscitation. Patients who suffered from STEMI were selected for this study. Exclusion criteria for this study were as follows: (1) patients who received reperfusion therapy >12 hours after symptom onset, (2) insufficient information regarding symptom onset time and (3) poor quality of CMR data. A total of 306 patients were finally included in this study.
FIGURE 1Schematic diagram of study enrollment. PCI, percutaneous coronary intervention; STEMI, ST-segment elevation myocardial infarction.
Shock index was calculated as the ratio of heart rate (beats per minute) to systolic blood pressure (mm Hg) based on the first recorded vital signs upon arrival. The best cutoff of shock index for predicting large MI, which was defined as ≥18.7% of the median infarct size measured by CMR, was 0.7 on the receiver operating characteristic curve ([ROC] sensitivity 61%, specificity 74%, area under the curve [AUC] 0.73, P < 0.01) in this study. According to their initial shock index, the patients were divided into 2 groups. A bedside patient monitor was used to measure initial resting heart rate and blood pressure with the patient in the supine position (IntelliVue MX800, Philips Medical Systems, Best, Netherlands). These measurements were made before any medical treatment was initiated, including supplemental oxygen, crystalloid fluids or analgesics.
Data Collection and Definition
Baseline characteristics, angiographic and procedural findings and CMR outcome data were recorded prospectively by research coordinators of the dedicated registry. STEMI was defined as more than 1-mm ST-segment elevation in 2 or more contiguous leads or a presumably new-onset left bundle branch block on electrocardiogram. Before primary PCI, blood was drawn to measure N-terminal prohormone of brain natriuretic peptide and creatine kinase MB isoenzyme (CK-MB) levels. The serum levels of CK-MB were serially measured every 8 hours from the index procedure, until the peak value was confirmed. Transthoracic echocardiography was used to measure baseline LV ejection fraction via Simpson׳s methods before or immediately after primary PCI.
Recommendations for chamber quantification: a report from the American Society of Echocardiography׳s Guidelines and Standards Committee and the Chamber Quantification Writing Group, developed in conjunction with the European Association of Echocardiography, a branch of the European Society of Cardiology.
Association of Killip class on admission and left ventricular dilatation after myocardial infarction: a closer look into an old clinical classification.
Multivessel disease was defined as stenosis ≥50% noted in more than 2 coronary arteries with a diameter ≥2.0 mm. Angiographic no-reflow was defined as impeded blood flow to the ischemic tissue after relief of the occlusion based on the previous description.
Before primary PCI, all the patients were treated with dual oral antiplatelet therapy consisting of 300 mg of aspirin with either 300 or 600 mg of clopidogrel, regardless of previous medication. The anticoagulants were administered during PCI based on the current practice guidelines established by the Korean Society of Interventional Cardiology. Coronary angiography and stent implantation were performed with standard interventional techniques.
Effects of balloon-based distal protection during primary percutaneous coronary intervention on early and late infarct size and left ventricular remodeling: a pilot study using serial contrast-enhanced magnetic resonance imaging.
There were no restrictions regarding implantation of drug-eluting stents. The treatment strategy, use of glycoprotein IIb/IIIa receptor inhibitors and intravascular ultrasound examination, were at the operator׳s discretion. During the final angiogram, TIMI flow grade and myocardial blush grade (MBG) were evaluated, as previously described.
Angiographic assessment of myocardial reperfusion in patients treated with primary angioplasty for acute myocardial infarction: myocardial blush grade. Zwolle Myocardial Infarction Study Group.
All baseline and procedural cine coronary angiograms were reviewed and analyzed at the institution׳s angiographic core laboratory.
CMR Protocol
CMR was performed using a 1.5-T magnetic scanner (Achieva, Philips Medical Systems, Best, Netherlands) with a SENSE cardiac coil based on our laboratory protocol.
A high loading dose of clopidogrel reduces myocardial infarct size in patients undergoing primary percutaneous coronary intervention: a magnetic resonance imaging study.
Comparison of magnetic resonance imaging findings in non-ST-segment elevation versus ST-segment elevation myocardial infarction patients undergoing early invasive intervention.
The CMR protocol included cine, T2-weighted, first-pass perfusion and late gadolinium enhancement imaging. CMR was obtained using a fast gradient echo sequence (balance fast-field echo, steady-state free precession) along the long and the short axes, which extended from the apex to the base of the left ventricle. T2-weighted magnetic resonance imaging was obtained in the cardiac short-axis direction using a dark-blood T2-weighted inversion-recovery fast-spin echo sequence. Next, 0.15 mmol/kg gadolinium-diethylenetriamine penta-acetic acid (DTPA-Gd, Magnevist; Bayer Schering Pharma, Berlin, Germany) was injected intravenously at a rate of 3 mL/second, followed by saline flush. The T1-weighted dynamic sequence enabled a first pass of the contrast agent through the myocardium after intravenous bolus injection (turbo field echo with SENSE, repetition time/echo time, 2.6/1.3 milliseconds). The slice thickness was 6 mm, with a field of view of 40 × 40 cm and an image matrix of 128 × 128 for the first-pass perfusion study. Images were obtained for 40 phases at each of the 4 locations for every 2 heart beats. Delayed hyperenhancement and the extent of microvascular obstruction (MVO) were evaluated at 5, 10 and 15 minutes after DTPA-Gd infusion in 10-12 contiguous 6-mm slices. The measurements were made with a 4-mm interslice gap using a multishot turbo field-echo breath-hold sequence, with a nonselective inversion (typical repetition time/time to echo 4.6/1.4 milliseconds). The field of view and image matrix were 35 × 35 cm and 256 × 256, respectively. The inversion delay time ranged between 200 and 300 milliseconds. A Look-Locker sequence was used to determine the optimal inversion time.
CMR Analysis
All measurements were made semiautomatically using validated software (Argus, Siemens Medical System, Erlangen, Germany). Two experienced radiologists who were blinded to patient information made these measurements based on visual assessment (Figure 2). Interobserver variability was 0.95 (P < 0.01) and intraobserver variability was 0.97 (P < 0.01). The infarct size and extent of MVO were assessed on delayed enhanced images, whereas the area at risk (AAR) was measured on T2-weighted images. After acquiring the short-axis images at end-diastole and end-systole, the endocardial borders were traced. The Simpson algorithm was then used to calculate the LV end-diastolic volume, LV end-systolic volume and LV ejection fraction. The infarct size was calculated from the summation of the area with delayed hyperenhancement within each segment of the short-axis images. This value was multiplied by the slice thickness to cover the entire LV. The endocardial and epicardial borders were planimetered to calculate the myocardial area. They were then added to calculate the LV myocardial volume using the same method. The infarct size was expressed as the percentage of affected LV myocardial volume. The T2-weighted images were used to determine the presence of hemorrhagic infarction.
The AAR was quantified on T2-weighted images using a similar algorithm to the one above and was similarly expressed as the percentage of LV myocardial volume affected. The myocardial salvage index (MSI) was calculated using the following formula: MSI = (AAR - infarct size) × 100 / AAR.
Prognostic significance and determinants of myocardial salvage assessed by cardiovascular magnetic resonance in acute reperfused myocardial infarction.
FIGURE 2Representatives of cardiac magnetic resonance imaging analysis. Short-axis slices of a T2-weighted image (A and C) and corresponding late gadolinium enhancement images (B and D) of a patient with shock index >0.7 (A and B) versus shock index ≤0.7 (C and D). The T2-weighted images demonstrate a hemorrhagic infarct (arrow) and late gadolinium enhancement images show a microvascular obstruction (asterisk). The extents of area at risk were 43.2% versus 26.0%. Infarct sizes were 30.2% versus 16.7%. Myocardial salvage indices were 30.1 versus 35.8.
The primary outcome was myocardial infarct size on CMR. The secondary outcomes were AAR, MVO, MSI and the presence of hemorrhagic infarction.
Statistical Analysis
Continuous variables were presented as mean with standard deviation. Continuous variables were compared using the independent t test or Kolmogorov-Smirnov test. Categorical variables were described as raw numbers (n) with percentages (%). They were compared using the Pearson χ2 or Fisher׳s exact tests. Multivariate binary logistic regression analysis was performed to identify independent predictors of large MI using a stepwise, backward selection process. Covariates were selected based on variables that had P < 0.10 in univariate analysis. The criteria for the inclusion and exclusion of variables in multivariate analysis were 0.05 and 0.10, respectively. The ROC curve analysis of shock index was performed to identify the best cutoff value for prediction of large MI. Finally, we compared each ROC curve of predictors for large MI using the AUC as described by DeLong et al.
All tests were 2-tailed. P < 0.05 were considered statistically significant. Statistical analyses were performed with the SAS 9.2, (SAS Institute Inc., Cary, NC).
Results
Patient Characteristics
The 306 study patients were divided into shock index >0.7 (n = 88) and shock index ≤0.7 groups (n = 218) (Table 1). Baseline LV ejection fraction was significantly lower in the shock index >0.7 group than it was in the shock index ≤0.7 group (P = 0.01). In contrast, the N-terminal prohormone of brain natriuretic peptide at admission was significantly higher in the shock index >0.7 group than it was in the shock index ≤0.7 group (P = 0.01). There were more patients who initially presented with Killip class 3 or 4 in the shock index >0.7 group than there were in the ≤0.7 group. On the contrary, Killip class 1 was more prevalent in the shock index ≤0.7 group (P < 0.01). Diabetes mellitus was more frequent in the shock index >0.7 group than in the shock index ≤0.7 group (P = 0.02). The remaining demographic and clinical characteristics were not significantly different between the 2 groups.
TABLE 1Baseline patient characteristics.
Shock index >0.7
Shock index ≤0.7
P Value
(n = 88)
(n = 218)
Male
72 (81.8)
176 (80.7)
0.83
Age (years)
58.5±12.5
59.7±11.7
0.41
BMI (kg/m²)
24.5±4.0
24.8±3.1
0.23
Current smoking
48 (54.5)
95 (43.6)
0.08
Diabetes mellitus
29 (33.0)
44 (20.2)
0.02
Hypertension
43 (48.9)
96 (44.0)
0.44
Dyslipidemia
18 (20.5)
36 (16.5)
0.41
Previous MI
5 (5.7)
8 (3.7)
0.53
Previous PCI
6 (6.8)
14 (6.4)
0.90
Heart rate (beats/minute)
96.9 ± 19.0
71.9 ± 16.2
<0.01
Systolic blood pressure (mm Hg)
119.3 ± 25.5
139.2 ± 25.3
<0.01
Diastolic blood pressure (mm Hg)
78.7 ± 18.1
87.4 ± 18.5
<0.01
Left ventricular ejection fraction (%)
49.4 ± 10.6
53.9 ± 10.5
0.01
Symptom onset-to-balloon time (minutes)
337.1 ± 325.0
269.7 ± 243.7
0.23
NT-proBNP (pg/mL)
987.3 ± 1731.1
384.3 ± 752.0
0.01
Peak CK-MB (ng/mL)
216.5 ± 179.0
190.8 ± 148.8
0.15
Killip classification
<0.01
Class 1
70 (79.5)
205 (94.0)
Class 2
2 (2.3)
5 (2.3)
Class 3
4 (4.5)
3 (1.4)
Class 4
12 (13.6)
5 (2.3)
Medication after primary PCI
Aspirin
87 (98.9)
215 (98.6)
1.00
Thienopyridine
86 (97.7)
214 (98.2)
1.00
ACEi or ARB
73 (83.0)
182 (83.5)
0.91
Beta blocker
82 (93.2)
201 (92.2)
0.77
Statin
82 (93.2)
210 (96.3)
0.24
Values are described as mean ± standard deviation or n (%).
ACEi or ARB, angiotensin-converting enzyme inhibitor or angiotensin receptor blocker; BMI, body mass index; CK-MB, creatine kinase MB isoenzyme; MI, myocardial infarction; NT-proBNP, N-terminal prohormone brain natriuretic peptide; PCI, percutaneous coronary intervention.
There were no significant differences between the 2 groups with regard to angiographic and procedural findings (Table 2). The most common baseline TIMI flow grade was 0. The baseline TIMI flows were not different between the 2 groups. The prevalence of each culprit vessel was also not significantly different between the 2 groups, with the most common vessel being the left anterior descending coronary artery. The presence of multivessel disease and collateral flow were similar between the 2 groups. Stent implantation was performed equally in the 2 groups. There were no significant differences between the groups with regard to angiographic no-reflow, final TIMI grade 3 and final MBG grade 3.
TABLE 2Angiographic and procedural findings.
Shock index >0.7
Shock index ≤0.7
P Value
(n = 88)
(n = 218)
Baseline TIMI
0.36
Grade 0
67 (76.1)
165 (75.7)
Grade 1
6 (6.8)
14 (6.4)
Grade 2
11 (12.5)
18 (8.3)
Grade 3
4 (4.5)
21 (9.6)
Culprit vessel
0.65
LAD
44 (50.0)
110 (50.5)
LCX
12 (13.6)
22 (10.1)
RCA
32 (36.4)
86 (39.4)
Multivessel disease
44 (50.0)
94 (43.1)
0.27
Presence of collateral flow
45 (51.1)
119 (54.6)
0.58
Aspiration thrombectomy during PCI
59 (67.0)
139 (63.8)
0.59
GPIIb/IIIa inhibitor IC injection
22 (25.0)
38 (17.4)
0.13
Stent implantation
80 (90.9)
201 (92.2)
0.71
Number of stents
1.0 ± 0.69
1.0 ± 0.60
1.00
Drug-eluting stents
78 (97.5)
198 (98.5)
0.63
Bare-metal stents
2 (2.5)
3 (1.5)
0.63
Stent diameter (mm)
3.2 ± 0.5
3.2 ± 0.6
0.77
Stent length (mm)
30.7 ± 16.5
30.2 ± 16.0
1.00
Angiographic no-reflow
8 (9.1)
11 (5.0)
0.18
Final TIMI grade 3
82 (93.2)
204 (93.6)
0.90
Final MBG grade 3
82 (93.2)
198 (90.8)
0.50
Values are described as mean ± standard deviation or n (%).
CK-MB, creatine kinase MB isoenzyme; LAD, left anterior descending coronary artery; LCX, left circumflex coronary artery; MBG, myocardial blush grade; PCI, percutaneous coronary intervention; RCA, right coronary artery; TIMI, thrombolysis in myocardial infarction.
CMR was performed a median of 3.4 days (interquartile range: 2.8-4.5 days) after the index procedure. The interval from primary PCI to CMR was not different between the 2 groups (Table 3). The size of the infarcted myocardium was significantly larger in the >0.7 group than it was in the ≤0.7 group (22.9 ± 11.2% versus 19.2 ± 11.5%, P < 0.01). The AAR was greater in the >0.7 group than in the ≤0.7 group (45.9 ± 14.5% versus 42.0 ± 13.9%, P < 0.01). The extent of MVO area was 10.1 ± 7.2% in the >0.7 group and 6.9 ± 6.0% in the ≤0.7 group (P = 0.01). In the shock index >0.7 group, MSI was significantly lower compared with that in the ≤0.7 group (38.7 ± 13.9% versus 41.7 ± 17.4%, P = 0.02). Multivariate analysis suggested that shock index >0.7 was an independent predictor of large MI (Table 4). Based on the difference among the AUCs, shock index was more predictive of a large MI than Killip class or final MBG, and the prognostic ability was significantly improved with peak CK-MB level (Figure 3 and Supplementary Table 1).
TABLE 3Cardiac magnetic resonance analysis.
Shock index >0.7
Shock index ≤0.7
P Value
(n = 88)
(n = 218)
LV end-diastolic volume (mL)
155.0 ± 43.8
146.5 ± 34.5
0.07
LV end-systolic volume (mL)
84.4 ± 42.8
74.1 ± 28.3
0.02
LV mass (g)
116.0 ± 25.1
114.1 ± 27.8
0.88
LV ejection fraction (%)
47.5 ± 9.9
50.5 ± 9.8
0.01
LV stroke volume (mL)
70.6 ± 14.5
72.5 ± 16.4
0.16
LV cardiac output (L/minute)
5.2 ± 1.0
5.1 ± 1.1
0.54
Infarct size (% of LV)
22.9 ± 11.2
19.2 ± 11.5
<0.01
Area at risk (% of LV)
45.9 ± 14.5
42.0 ± 13.9
<0.01
Myocardial salvage index
38.7 ± 13.9
41.7 ± 17.4
0.02
MVO area (% of LV)
10.1 ± 7.2
6.9 ± 6.0
0.01
Hemorrhagic infarction
48 (54.5)
88 (40.4)
0.02
Values are described as mean ± standard deviation or n (%).
LV, left ventricle; MVO, microvascular obstruction.
Adjusted odds ratio with male, LAD infarction, LV ejection fraction <40%, initial shock index >0.7, initial Killip class: 3 or 4, final MBG grade <3 and level of peak CK-MB.
95% CI
P Value
Male
248 (81.0)
2.18
1.20-3.93
0.01
2.32
1.13-4.77
0.02
LAD infarction
154 (50.3)
2.28
1.44-3.60
<0.01
2.48
1.45-4.24
<0.01
Initial shock index >0.7
88 (28.8)
2.45
1.46-4.11
<0.01
3.02
1.62-5.65
<0.01
Initial Killip class: 3 or 4
24 (7.8)
2.43
0.98-6.04
0.06
–
–
–
Final MBG grade <3
26 (8.5)
2.25
0.95-5.35
0.07
3.32
1.22-8.98
0.02
Peak CK-MB
198.2 ± 158.2
1.01
1.01-1.01
<0.01
1.01
1.01-1.01
<0.01
BMI, body mass index; CK-MB, creatine kinase MB isoenzyme; LAD, left anterior descending coronary artery; LV, left ventricle; MBG, myocardial blush grade; OR, odds ratio; TIMI, thrombolysis in myocardial infarction.
Adjusted odds ratio with male, LAD infarction, LV ejection fraction <40%, initial shock index >0.7, initial Killip class: 3 or 4, final MBG grade <3 and level of peak CK-MB.
To the best of our knowledge, this is the first study to investigate the association between initial shock index and myocardial infarct size using CMR in patients with STEMI undergoing primary PCI. Myocardial infarct size was found to be significantly larger in the shock index >0.7 group than it was in the shock index ≤0.7 group. In addition, a shock index >0.7 was associated with greater MVO area extension and lower MSI than a shock index ≤0.7. Shock index >0.7 was a strong independent predictor for large MI.
Bilkova et al found shock index to be a strong independent predictor of in-hospital mortality in patients with STEMI.
found that admission shock index values were predictive of 7- and 30-day all-cause mortality. Although these studies demonstrated the prognostic value of shock index in patients with STEMI, they were based on short-term inpatient outcomes. Furthermore, no prior studies determined the association between shock index and myocardial infarct size. The present study found that shock index was positively correlated with larger myocardial injuries in patients with STEMI undergoing primary PCI. Many previous studies have reported associations between long-term clinical outcomes of STEMI and CMR parameters. Myocardial infarct size, as assessed by CMR, is related to LV remodeling and is strongly associated with long-term major adverse cardiovascular events.
Infarct size by contrast enhanced cardiac magnetic resonance is a stronger predictor of outcomes than left ventricular ejection fraction or end-systolic volume index: prospective cohort study.
Hemorrhagic infarcts, which are a sign of severe microvascular injury, are also independent predictors of adverse LV remodeling irrespective of infarct size.
Cardiovascular magnetic resonance-derived intramyocardial hemorrhage after STEMI: influence on long-term prognosis, adverse left ventricular remodeling and relationship with microvascular obstruction.
as a parameter for estimating hypovolemic shock. Since then, many studies have demonstrated its usage for assessing systemic oxygenation and cardiac function during the initial treatment of shock.
Shock index is the ratio of heart rate to systolic blood pressure. Even in patients with normal vital signs, elevated shock index has been associated with clinically ill status.
Most patients in this study were Killip class 1 upon admission. In spite of the relative stability of patients, increased shock indices reflected coronary hemodynamic status and adverse CMR outcomes in this study. It is not completely understood why shock index represents myocardial infarct size and clinical outcomes in acute MI; however, several possible mechanisms should be considered. In acute MI, there is a disturbance of coronary blood flow. In response to decreased blood flow, sympathetic stimulation increases heart rate and cardiac contractility, which further increases blood pressure and coronary perfusion.
These changes increase the extravascular compressive force and decrease the length of diastole, leading to a rise in myocardial oxygen demand and a reduction in subendocardial blood flow.
Contractility of an infarcted territory is initially enhanced by this; however, shortly after, it declines because of an imbalance in the oxygen demand supply.
Therefore, shock index in MI is an integrated measure of the cardiovascular system and hemodynamic status. An increase in the shock index may reflect extension of the myocardial infarct, AAR or hemorrhagic infarction, as assessed by CMR.
Study Limitations
This study has several limitations. The results may have been affected by confounding owing to the nonrandomized, retrospective and observational design. In addition, only patients who were available for CMR were included in this study. This resulted in a small sample size that may have limited the results in patients with relatively stable vital signs and modest myocardial injuries. This limited study population may have underestimated the true association between shock index and infarct size.
Conclusions
In patients with STEMI undergoing primary PCI, shock index >0.7 is associated with a larger myocardial infarct size, higher AAR and a higher hemorrhagic infarction rate compared to shock index ≤0.7. Based on our results, initial shock index may reflect myocardial injury in patients with STEMI undergoing primary PCI. Therefore, shock index may facilitate assessment of prognosis in such patients. Future, large-scale studies are needed to confirm these findings.
Recovery from a psychotropic drug overdose tends to depend on the time from ingestion to arrival, the Glasgow Coma Scale, and a sign of circulatory insufficiency on arrival.
Infarct size by contrast enhanced cardiac magnetic resonance is a stronger predictor of outcomes than left ventricular ejection fraction or end-systolic volume index: prospective cohort study.
Recommendations for chamber quantification: a report from the American Society of Echocardiography׳s Guidelines and Standards Committee and the Chamber Quantification Writing Group, developed in conjunction with the European Association of Echocardiography, a branch of the European Society of Cardiology.
Association of Killip class on admission and left ventricular dilatation after myocardial infarction: a closer look into an old clinical classification.
Effects of balloon-based distal protection during primary percutaneous coronary intervention on early and late infarct size and left ventricular remodeling: a pilot study using serial contrast-enhanced magnetic resonance imaging.
Angiographic assessment of myocardial reperfusion in patients treated with primary angioplasty for acute myocardial infarction: myocardial blush grade. Zwolle Myocardial Infarction Study Group.
A high loading dose of clopidogrel reduces myocardial infarct size in patients undergoing primary percutaneous coronary intervention: a magnetic resonance imaging study.
Comparison of magnetic resonance imaging findings in non-ST-segment elevation versus ST-segment elevation myocardial infarction patients undergoing early invasive intervention.
Prognostic significance and determinants of myocardial salvage assessed by cardiovascular magnetic resonance in acute reperfused myocardial infarction.
Cardiovascular magnetic resonance-derived intramyocardial hemorrhage after STEMI: influence on long-term prognosis, adverse left ventricular remodeling and relationship with microvascular obstruction.
☆The authors have no financial or other conflicts of interest to disclose.The first 2 authors (JKH, WJJ) contributed equally to this work as first authors.
Adjusted odds ratio with male, LAD infarction, LV ejection fraction <40%, initial shock index >0.7, initial Killip class: 3 or 4, final MBG grade <3 and level of peak CK-MB.
30454-2&id=gr1.jpg){kind=link}
30454-2&id=gr2.jpg){kind=link}
30454-2&id=gr3.jpg){kind=link}