ORIGINAL PAPER

Relationship and prognostic value of microvascular obstructionand infarct size in ST-elevation myocardial infarctionas visualized by magnetic resonance imaging

Suzanne de Waha • Steffen Desch • Ingo Eitel • Georg Fuernau •

Philipp Lurz • Anja Leuschner • Matthias Grothoff •

Matthias Gutberlet • Gerhard Schuler • Holger Thiele

Received: 9 August 2011 / Accepted: 23 January 2012 / Published online: 8 February 2012

� Springer-Verlag 2012

Abstract

Background Both infarct size and microvascular obstruc-

tion (MO) assessed by cardiac magnetic resonance imaging

(CMR) are known to be predictors for adverse clinical out-

come after ST-elevation myocardial infarction (STEMI). We

hypothesized that a ratio of MO and infarct size (MO/infarct

size) might be an even stronger predictor for outcome after

STEMI, which has not been investigated yet.

Methods STEMI patients reperfused by primary angio-

plasty (n = 438) within 12 h after symptom onset under-

went contrast-enhanced CMR at a median of 3 days

(interquartile range [IQR] 2;4) after the index event. MO

and infarct size were measured 15 min after intravenous

gadolinium injection. Follow-up was conducted after

19 months (IQR 10;27). The primary end point was defined

as a composite of death, non-fatal myocardial reinfarction

and congestive heart failure (major adverse cardiac events

[MACE]).

Results The extent of MO was only weakly correlated

with infarct size (r = 0.21, p \ 0.001). In a first multivar-

iate analysis including extent of MO, infarct size, ejection

fraction, end-systolic and end-diastolic volume, the extent

of MO was independently associated with MACE (hazard

ratio [HR] 1.03, 95%CI 1.02–1.05, p \ 0.001). In a second

multivariate analysis including MO/infarct size on top of

the extent of MO, infarct size, ejection fraction, end-systolic

and end-diastolic volume, MO/infarct size was identified as

the strongest independent predictor for MACE (HR 2.22

[95%CI 1.60–3.08, p \ 0.001]).

Conclusions In contrast to infarct size, MO is associated

with adverse clinical outcome after STEMI even after

adjustment for other CMR parameters. However, MO/

infarct size is a more powerful predictor for long-term

outcome after STEMI than either parameter alone.

Keywords Microvascular obstruction � Infarct size �ST-elevation myocardial infarction � Cardiac magnetic

resonance imaging

Introduction

In acute ST-elevation myocardial infarction (STEMI),

reperfusion has contributed to improved survival due to

limitation of myocardial necrosis. In daily clinical practice,

assessment of reperfusion success is performed using sur-

rogate markers including clinical, angiographic and elec-

trocardiographic parameters [1–4]. In contrast to indirect

markers of myocardial ischemia such as troponin [5–7], with

the introduction of cardiac magnetic resonance imaging

(CMR), direct visualization and quantification of infarct

expansion and microvascular obstruction (MO) have been

made possible [8–10]. Both infarct size and MO have been

shown to be prognostic markers for adverse clinical out-

come after STEMI [11–14]. We could previously demon-

strate that MO is a strong independent prognostic marker for

hard clinical end points, even after adjustment for traditional

outcome measures [15]. However, we observed that some

patients displayed large zones of infarcted myocardium

S. de Waha (&) � S. Desch � I. Eitel � G. Fuernau � P. Lurz �A. Leuschner � G. Schuler � H. Thiele

Department of Internal Medicine, Cardiology,

University of Leipzig-Heart Center,

Strumpellstr. 39, Leipzig 04289, Germany

e-mail: s-dw@gmx.net

M. Grothoff � M. Gutberlet

Department of Diagnostic and Interventional Radiology,

University of Leipzig-Heart Center, Leipzig, German

123

Clin Res Cardiol (2012) 101:487–495

DOI 10.1007/s00392-012-0419-3

constituting of only small areas of MO, whereas others

displayed infarcts mainly constituting of MO. MO reflects

zones of impaired microcirculation and its development is

influenced by factors beyond the actual ischemic damage of

the myocyte, such as reperfusion injury, swelling and pro-

trusion of the endothelial cells, leading to compression of

the capillaries, microvascular plugging by neutrophils, red

blood cells and platelets and even rupture of the microves-

sels [16]. In contrast, the infarcted non-obstructed regions

display intact or less impaired microvasculature and it is

therefore likely that this leads to differing pathophysiolog-

ical consequences [17]. Thus, we hypothesized that a ratio of

MO and infarct size (MO/infarct size) might be a better

predictor for clinical outcome than either parameter on its

own, which has not been investigated so far. Furthermore,

previous studies analyzing the relation of infarct size and

MO led to inconsistent results and are limited due to small

study cohorts, analysis of combined end points including

weak components (including unstable angina, re-hospital-

ization and repeat revascularization) and relatively short

follow-up periods [11, 14, 18].

We therefore sought to analyze the comparative impact

and relation of (1) MO, (2) infarct size and (3) MO/infarct

size as predictors for long-term clinical outcome after

STEMI in a large prospective cohort.

Methods

Patients and study design

From February 2006 to July 2008, 512 consecutive STEMI

patients underwent primary percutaneous coronary inter-

vention (PCI). Inclusion criteria were the presence of

symptoms \12 h and ST-segment elevation in C2 leads

with C0.2 mV in the precordial leads or C0.1 mV in

extremity leads. Data from the current cohort were previ-

ously analyzed to study the impact of early versus late MO

on clinical outcome after STEMI [15]. Patients with prior

fibrinolysis and contraindications to CMR at study entry

were excluded. All patients received 500 mg of aspirin and

unfractionated heparin (60 IU/kg bodyweight) intrave-

nously prior to PCI. Clopidogrel with a 600-mg loading

dose and subsequently 75 mg for 12 months plus aspirin

indefinitely were mandatory. All other medications

including glycoprotein IIb/IIIa-inhibitors were adminis-

tered according to current guidelines [19, 20].

Primary PCI was performed according to standard

clinical practice. Additional thrombectomy was used

depending on thrombus burden in the infarct-related

artery. Coronary angiography of the target lesion, defined

as an angiographically significant stenosis with significant

ST-elevations in the corresponding ECG-leads, was performed

before and after PCI with the same projections to allow

optimal offline evaluation of the thrombolysis in myocar-

dial infarction (TIMI) flow of the infarct-related artery by

two independent observers [2].

The TIMI-risk score was calculated as described previ-

ously [4]. Early ST-segment resolution, expressed as per-

centage from before to after PCI, was evaluated by

measuring the sum of ST-segment elevation 20 ms after the

end of the QRS complex in the ECG before and after PCI [3].

The study was approved by the University of Leipzig

Ethics Committee and all patients gave written informed

consent.

CMR imaging

All patients were examined at rest in the supine position

with a whole-body 1.5-T MR scanner (Gyroscan Intera CV,

Philips Medical Systems, Best, The Netherlands) equipped

with a five-element cardiac phased-array coil for signal

reception. A vectorcardiogram for gating and triggering

was used. To define the orientation of the heart, a real-time

interactive tool was applied. All images were acquired

during breath-hold at end expiration.

Left ventricular (LV) function was assessed by a stan-

dard steady-state free precession technique acquiring short-

axis slices from base to apex and also horizontal and vertical

long-axis views. Delayed enhancement short-axis images

covering the whole ventricle were acquired at mid-diastole

approximately 15 min after bolus injection (0.2 mmol/kg/

bodyweight) of gadolinium-chelate (Gadovist, Schering,

Germany). A three-dimensional inversion-recovery (IR)

turbo gradient echo sequence (typical spatial resolution

2.0 9 2.0 9 5 mm, prepulse delay 175–300 ms) was used

for image acquisition. The individual IR prepulse delay was

defined to obtain the maximal contrast between viable and

necrotic myocardium. Additionally, myocardial edema

imaging was performed to differentiate between acute and

chronic infarction, acquiring three short-axis slices using a

T2-weighted turbo spin-echo sequence before contrast

administration. Only delayed enhancement displaying the

typical pattern of myocardial infarction with corresponding

myocardial edema was interpreted as the CMR equivalent

for the acute event and thus was further analyzed [21].

CMR measurements were performed off-line in a CMR

core laboratory by observers blinded to clinical, angio-

graphic and electrocardiographic parameters. The perfor-

mance of the CMR core laboratory has been demonstrated

previously [22, 23]. LV ejection fraction (EF), end-diastolic

and end-systolic volumes were calculated from the short-

axes functional views. LV function was graded according to

the corresponding EF: \25, 25–35, 35–45, 45–55 and

[55%. LV mass was assessed for the delayed enhancement

images by tracing the endocardial and epicardial contours

488 Clin Res Cardiol (2012) 101:487–495

123

manually; papillary muscles were included. Once the

myocardial contours were identified, the infarct size was

determined by manual delineation of delayed enhancement

in each of the short-axis images. MO was assessed 1 and

15 min after gadolinium injection (early and persistent

MO). The current analysis was limited to persistent MO due

to its superior prognostic value in comparison to early MO

[13, 24, 25]. The obstructed area within the infarction of the

short-axes slices was manually drawn. MO was analyzed

qualitatively (=presence of MO) and quantitatively (=extent

of MO expressed as percentage of LV mass [%LV]). Infarct

size was expressed as %LV. The MO/infarct size ratio was

calculated for all patients.

End points and definitions

Clinical follow-up was conducted via a structured ques-

tionnaire by telephone. Any clinical event was verified by

hospital charts, or direct contact with the treating physician

or contact with the local government registration. The

follow-up interviewer was not aware of the results of the

CMR studies.

The primary end point was defined as major adverse

cardiac events (MACE) comprising a composite of death,

non-fatal myocardial reinfarction and congestive heart

failure. Death was defined as death from any cause; how-

ever, it was further classified as cardiac and non-cardiac

death. Death was regarded as cardiac in origin unless

obvious non-cardiac causes could be identified. In case of

any doubt, death was counted as cardiac. The diagnosis of

reinfarction during the index hospitalization was based on

clinical symptoms, new ST-segment changes and an

increase in the creatine kinase-MB levels above the refer-

ence limits in patients with normalized values or if there

was an increase of C20% from the last non-normalized

measurement [26]. At follow-up, any new ischemic symp-

toms requiring hospital admission accompanied by troponin

elevation were defined as recurrent myocardial infarction

[26]. New heart failure was defined as any congestive heart

failure (rales, dyspnea, New York Heart Association class

III–IV) leading to medical attention [24 h after the index

event. In patients experiencing[1 event, the first event was

chosen for the combined clinical end point. When C1

events occurred simultaneously, the most severe event was

chosen (death [ myocardial reinfarction [ congestive

heart failure). All outcomes were adjudicated by a clinical

events committee unaware of the CMR results.

Statistical analysis

Each categorical variable is expressed as the number and

percentage of patients. Continuous data are reported as

medians with the corresponding interquartile range (IQR).

For comparison of continuous data, the nonparametric

Wilcoxon rank-sum test was used. Survival curves were

estimated using Kaplan–Meier distributions with log-rank

comparison to illustrate the time-dependent occurrence of

the combined clinical end point in relation to the presence

of MO, as well as to infarct size and MO/infarct size for

Cmedian versus \median.

We fitted univariate Cox proportional-hazards models to

estimate the hazard ratios (HR) for the combined clinical

end point. All parameters with a p value \0.05 entered

multivariate analysis, which was performed using a stepwise

algorithm. A first multivariate Cox regression analysis was

performed including extent of MO, infarct size, EF, end-

systolic and end-diastolic volume. A second multivariate

Cox regression analysis was fitted including MO/infarct size

as well as the extent of MO, infarct size, EF, end-systolic

and end-diastolic volume. In the subgroup of patients dis-

playing extensive myocardial damage defined as an infarct

size Cmedian, a third multivariate analysis including the

parameters of the second multivariate model was per-

formed. In univariate and multivariate Cox regression

analysis, parameters were included as continuous variables.

All statistical tests were performed with SPSS software,

version 17.0 (SPSS Inc., Chicago, Il). All probability val-

ues were two tailed with a = 0.05 and all confidence

intervals (CI) were calculated to the 95th percentile.

Results

Of the 512 STEMI patients referred for primary PCI, 438

underwent CMR 2–7 days (in median 3 days [IQR 2;4])

after the index event with a similar time delay between

patients with and without MO (p = 0.65). In addition,

infarct size did not differ significantly according to the time

of CMR image acquisition (p = 0.73). In total, 74 patients

had to be excluded from CMR due to claustrophobia

(n = 19), death before CMR (n = 18), refusal (n = 15),

prior pacemaker implantation (n = 5), obesity (n = 7),

metallic implant (n = 1), dyspnea (n = 2) or technical

reasons (n = 7). Patient follow-up was performed at a

median of 19 months (IQR 11;27) after index infarction

and was completed for 97% of the patients (n = 423).

All patients displayed myocardial edema in the infarct

region indicative of acute myocardial infarction. In addition,

10% of all patients (n = 42) displayed delayed enhance-

ment with a typical post-infarction pattern, but without

corresponding edema in T2-weighted imaging. These

regions were interpreted as chronic or prior myocardial

infarctions and were therefore not further analyzed. The

median infarct size in the overall study cohort was 17.7%LV

(IQR 8.5;28.0) and MO was detected in 68% (n = 296) of

patients involving 1.2%LV (IQR 0.6;3.0). Infarct size and

Clin Res Cardiol (2012) 101:487–495 489

123

MO were only weakly correlated (r = 0.21). The median

value of MO/infarct size was 0.07 (IQR 0.03;0.13) ranging

from 0 to 1. A typical patient example showing infarct size

and the corresponding MO is shown in Fig. 1.

Baseline clinical characteristics as well as electrocar-

diographic, angiographic and CMR data are shown in

Table 1. Importantly, 89.7% of all patients (n = 379)

received glycoprotein IIb/IIIa-inhibitors. However, we

could not observe an association between administration of

glycoprotein IIb/IIIa-inhibitors and MO (presence of MO:

p = 0.38/extent of MO: p = 0.22).

Outcome analysis

Overall, 69 events were recorded throughout the follow-up

period consisting of death in 25 patients (cardiac death

n = 20, stroke n = 4, cancer n = 1), non-fatal myocardial

infarctions in 19 and new congestive heart failure in 25.

Both the extent of MO and infarct size were significantly

greater in patients with MACE compared to patients

without MACE (MO: 1.9%LV [IQR 0.8;3.6] vs. 1.1%LV

[IQR 0.5;2.9], p \ 0.001; infarct size: 24.7%LV [IQR

11.2;34.9], vs. 16.2%LV [IQR 7.9;26.2], p \ 0.001). Fur-

thermore, patients in whom the combined clinical end point

occurred demonstrated a significantly greater value of MO/

infarct size compared to patients who displayed an event-

free survival throughout the follow-up period (0.6 [0.3;0.2]

vs. 0.3 [0;0.1], p = 0.002).

Prognostic evaluation

Kaplan–Meier curves revealed a significant association of

MO, infarct size and MO/infarct size with the occurrence

of MACE (Fig. 2a–d).

Fig. 1 Patient examples. Assessment of microvascular obstruction

(MO) and infarct size using delayed enhancement imaging in two

different patients with anterior myocardial infarction. Patient 1 upper

row without and with infarct size (green) and MO (red) contours (a,

b). Patient 2 lower row without and with infarct size and MO contours

(c, d). Note that the MO/infarct size differs between patients 1 and 2

490 Clin Res Cardiol (2012) 101:487–495

123

In comparison to the extent of MO, infarct size, EF, and

end-systolic and end-diastolic volume, MO/infarct size

demonstrated the strongest unadjusted association with

MACE (Table 2).

In a first multivariate analysis including extent of MO,

infarct size, EF as well as end-systolic and end-diastolic

volume, the extent of MO remained independently associ-

ated with MACE (HR 1.03, 95%CI 1.02–1.05, p \ 0.001;

Table 3).

In a second multivariate analysis including MO/infarct

size on top of the parameters included in the first model, MO/

infarct size was identified as the strongest independent pre-

dictor for MACE (HR 2.22; 95%CI 1.60–3.08, p \ 0.001;

Table 4).

In the subgroup of patients displaying extensive myo-

cardial damage defined as an infarct size Cmedian, a third

multivariate analysis including the parameters of the second

multivariate model, MO/infarct size was the only indepen-

dent predictor for MACE (HR 2.03; 95%CI 1.38–2.98,

p \ 0.001).

Discussion

The main findings of this large outcome analysis in STEMI

patients using CMR parameters can be summarized as

follows: (1) presence and extent of MO, infarct size and

MO/infarct size were associated with adverse clinical

outcome defined by death, reinfarction and congestive

heart failure in univariate analysis; (2) in contrast to infarct

size, the extent of MO was independently associated with

MACE; (3) the newly introduced MO/infarct size ratio is

an even stronger predictor for long-term prognosis after

STEMI than either parameter alone.

With the introduction of CMR, it has been made pos-

sible to directly visualize and quantify regions of acute

myocardial infarction and identify zones of impaired

microperfusion, also referred to as MO. In animal models,

an almost exact relationship between the extent and shape

of MO and infarct size assessed by CMR and histopa-

thological results could be demonstrated [9, 27]. The

results of previous trials examining MO and infarct size as

outcome measures have been ambiguous: Wu et al. [11]

reported a significant association of infarct size with worse

clinical outcome independent of other CMR parameters,

such as MO. In contrast, in other studies, infarct size did

not remain significant in multivariate analysis adjusting for

traditional CMR parameters [12, 13]. Our results could

confirm these findings, which are supported by previous

studies identifying MO as a stronger predictor for LV

remodeling in the post-infarction period than infarct size

[24, 28]. This might be explained in part by altered local

properties in the presence of MO, as well as pre-existing

patient characteristics influencing both the development of

MO and post-infarction outcome, such as endothelial dys-

function [16, 29].

Since infarct size and MO have both been associated

with adverse clinical outcome after STEMI, we hypothe-

sized that the analysis of a ratio of the two parameters

might add incremental prognostic value, as the extent of

MO can widely differ in infarctions of similar size as

demonstrated in Fig. 1. Indeed, we could demonstrate a

strong prognostic association of MO/infarct size with long-

term clinical outcome after STEMI. The pathophysiologi-

cal consequences and the consecutive impact on functional

recovery after STEMI of an expansion of MO and infarct

size might be slightly different. While MO reflects truly

non-viable regions associated with greater apoptosis and

cellular loss leading to local involution and wall thinning

[30], infarct expansion might also increase wall stress in

adjacent or remote non-infarcted regions [31]. The extent

of infarct size and the development of MO are influenced

by diverging parameters, as MO is known to be associated

with factors beyond the ischemic damage itself, such

as reperfusion injury. Our data emphasize, therefore, the

Table 1 Characteristics of the study cohort

All patients (n = 423)

Age, years 65 (55;73)

Male sex, n (%) 318 (75.4)

Cardiovascular risk factors, n (%)

Hypertension 287 (68.3)

Diabetes mellitus 111 (26.4)

Hyperlipoproteinemia 140 (33.3)

Current smoking 177 (42.1)

BMI, kg/m2 27 (25;30)

Maximal creatine kinase, lmol/l 6.8 (2.8;20.6)

Maximal creatine kinase-MB, lmol/l 1.1 (0.5;2.7)

TIMI-risk score 3.0 (2.0;5.0)

ST-segment resolution, % 73 (50;100)

Angiographic findings, n (%)

TIMI-flow pre-PCI: 0–II 252 (64.8)

TIMI-flow pre-PCI: III 137 (35.2)

TIMI-flow post-PCI: 0–II 20 (5.1)

TIMI-flow post-PCI: III 372 (94.9)

Magnetic resonance imaging

Infarct size, %LV 17.7 (8.5;28.0)

Extent of MO, %LV 1.2 (0.6;3.0)

LV–EF, % 50.1 (40.9;58.4)

LV end-diastolic volume index, mL/m2 143 (121;167)

LV end-systolic volume index, mL/m2 72 (50;93)

Glycoprotein IIb/IIIa-inhibitor use, n (%) 379 (89.7)

Continuous data are presented as median and interquartile range

BMI body mass index (weight in kilograms divided by the square of

the height in meters), TIMI thrombolysis in myocardial infarction,

PCI percutaneous coronary intervention, MO microvascular obstruc-

tion, LV left ventricle, EF ejection fraction

Clin Res Cardiol (2012) 101:487–495 491

123

importance of reperfusion strategies aiming at a reduction

of infarct size while preserving microvascular function,

such as thrombectomy. Therefore, it is conceivable that

MO/infarct size represents a broader reflection of the

degree of injury after STEMI than the separate analysis and

may therefore be considered as an outcome measure for

future reperfusion studies. Focusing solely on infarct size

independent of the microvascular state might not improve

the clinical outcome in patients. As CMR visualizes and

quantifies both infarct size and MO accurately, it may be

judged as a principal imaging technique in studies evalu-

ating reperfusion success in the setting of STEMI.

Some limitations of the current trial need to be addres-

sed. First, we performed CMR in median 3 days (IQR 2;4)

after the index event. Despite previously published data on

animals indicating a stable phase of infarct size and MO

between day 2 and 7 after the acute ischemic event [32],

there is emerging evidence that infarct size assessed by

CMR decreases within the first week after STEMI [33–36].

However, these data are limited due to small study sample

sizes and a selection in patients. In addition, the exact

evolvement of post-infarction CMR parameters within the

first few days after the index event has not been investi-

gated in a large cohort of unselected STEMI patients so far.

Fig. 2 a Major adverse cardiovascular events with and without

microvascular obstruction. Kaplan–Meier curve for the cumulative

incidence of major adverse cardiac events in patients with and without

microvascular obstruction (MO). b Major adverse cardiovascular

events depending on median infarct size. Kaplan–Meier curve for the

cumulative incidence of major adverse cardiac events in patients with

an infarct size \median versus Cmedian. c Major adverse cardio-

vascular events depending on median ratio of microvascular obstruc-

tion/infarct size. Kaplan–Meier curve for the cumulative incidence of

major adverse cardiac events in patients with a ratio of microvascular

obstruction and infarct size (MO/infarct size) \median versus

Cmedian. d Major adverse cardiovascular events depending on the

presence of microvascular obstruction and the median ratio of

microvascular obstruction/infarct size. Kaplan–Meier curve for the

cumulative incidence of major adverse cardiac events in patients

without microvascular obstruction (MO) versus with MO, and a ratio

of MO and infarct size (MO/infarct size) \median versus with MO

and a MO/infarct size Cmedian

492 Clin Res Cardiol (2012) 101:487–495

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In the current study, CMR image acquisition was per-

formed in a relatively narrow period of time in comparison

to many previously published studies (in median 3 days

after STEMI, IQR 2;4). However, we cannot definitely rule

out potential changes of infarct size and MO within the first

days after myocardial ischemia, although it is unlikely that

these changes would substantially influence the current

results. Indeed, neither infarct size nor MO was signifi-

cantly influenced by the timing of CMR assessment fol-

lowing infarction. Second, CMR image analysis was

performed by manual delineation. Recently, an alternative

method using automatic planimetry for quantification of

infarct size and MO has been suggested to achieve higher

reproducibility. However, the optimal method for automatic

analysis has not been fully established [37–39] and notably

our CMR core laboratory has proven excellent reproduc-

ibility and low interobserver and intraobserver variability

for manual analysis of infarct size [22, 23]. Given these

issues, we prefer to planimeter the infarct manually in our

core laboratory using experienced readers who can care-

fully segment myocardial borders and can account for

artifacts, no-reflow regions and areas with intermediate

image intensity. Third, the study sample size is still limited

to draw definitive conclusions on clinical outcome. Finally,

all patients were treated at a single high-volume tertiary

referral center. As a consequence, the results may not be

generalized to the entire STEMI population.

In conclusion, in contrast to infarct size, the extent of

MO is associated with adverse clinical outcome after

STEMI even after adjustment for other CMR parameters.

However, MO/infarct size is an even more powerful pre-

dictor for long-term outcome after STEMI.

Conflict of interest The authors have nothing to disclose.

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Table 3 Multivariate Cox regression models for major adverse car-

diac events and traditional CMR parameters including infarct size and

microvascular obstruction

MACE (n = 69)

HR (95%CI) p value

Extent of MO, %LV 1.03 (1.02–1.05) \0.001

LV-EF, % 1.66 (1.34–2.04) \0.001

Infarct size, %LV – –

LV end-diastolic volume

index, mL/m2– –

LV end-systolic volume

index, mL/m2– –

MACE major adverse cardiac event, MO microvascular obstruction,

LV left ventricle, EF ejection fraction

Table 4 Multivariate Cox regression models for major adverse car-

diac events and traditional CMR parameters, and the ratio of micro-

vascular obstruction and infarct size

MACE (n = 69)

HR (95%CI) p value

MO/infarct size 2.22 (1.60–3.08) \0.001

LV–EF, % 1.74 (1.40–2.15) \0.001

Extent of MO, %LV – –

Infarct size, %LV – –

LV end-diastolic volume

index, mL/m2– –

LV end-systolic volume

index, mL/m2– –

MACE major adverse cardiac event, MO/infarct size ratio of micro-

vascular obstruction and infarct size, EF ejection fraction, MOmicrovascular obstruction, LV left ventricle

Table 2 Unadjusted hazard ratios for major adverse cardiac events

MACE (n = 69)

HR (95%CI) p value

MO/infarct size 1.83 (1.34–2.50) \0.001

Extent of MO, %LV 1.03 (1.01–1.04) \0.001

Infarct size, %LV 1.03 (1.01–1.05) \0.001

LV-EF, % 1.04 (1.02–1.06) \0.001

LV end-diastolic volume

index, mL/m21.00 (0.99–1.01) 0.28

LV end-systolic volume

index, mL/m21.02 (1.01–1.03) 0.001

MACE major adverse cardiac event, MO/infarct size ratio of micro-

vascular obstruction and infarct size, MO microvascular obstruction,

LV left ventricle, EF ejection fraction

Clin Res Cardiol (2012) 101:487–495 493

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