Coronary Microvascular Resistance Index Immediately After Primary Percutaneous Coronary Intervention as a Predictor of the Transmural Extent of Infarction in Patients With ST-Segment Elevation Anterior Acute Myocardial Infarction
Hironori Kitabata, MD,
Toshio Imanishi, MD, PhD,
Takashi Kubo, MD, PhD,
Shigeho Takarada, MD, PhD,
Manabu Kashiwagi, MD,
Hiroki Matsumoto, MD,
Hiroto Tsujioka, MD,
Hideyuki Ikejima, MD,
Yu Arita, MD,
Keishi Okochi, MD,
Akio Kuroi, MD,
Satoshi Ueno, MD,
Hideaki Kataiwa, MD,
Takashi Tanimoto, MD,
Takashi Yamano, MD,
Kumiko Hirata, MD, PhD,
Nobuo Nakamura, MD,
Atsushi Tanaka, MD, PhD,
Masato Mizukoshi, MD, PhD,
Takashi Akasaka, MD, PhD*
Department of Cardiovascular Medicine, Wakayama Medical University, Wakayama, Japan
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Abstract
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Objectives: The purpose of this study was to investigate whether microvascular resistance index (MVRI) immediately after primary percutaneous coronary intervention (PCI) can predict the transmural extent of infarction (TEI) defined by contrast-enhanced cardiac magnetic resonance (ce-CMR) in patients with anterior acute myocardial infarction (MI).
Background: The degree of microvascular damage is an important determinant of myocardial viability and clinical outcomes in acute MI. A novel dual-sensor (pressure and Doppler velocity) guidewire has the ability to evaluate microvascular damage. ce-CMR can accurately discriminate transmural from nontransmural MI, and the TEI by ce-CMR can predict future improvement in contractile function.
Methods: In 27 patients immediately after primary PCI for a first anterior acute MI, MVRI, coronary flow reserve (CFR), deceleration time of diastolic velocity (DDT), and zero flow pressure (Pzf) were measured with a dual-sensor guidewire. TEI was graded from 1 to 4 based on the transmural extent of hyperenhanced tissue (1 = 0% to 25% of left ventricular wall thickness, 2 = 26% to 50%, 3 = 51% to 75%, and 4 = 76% to 100%). Infarct size by ce-CMR was also calculated.
Results: Peak creatine kinase-myocardial band values were significantly correlated with MVRI (r = 0.77, p < 0.0001), CFR (r = –0.69, p < 0.0001), DDT (r = –0.75, p = 0.0001), and Pzf (r = 0.75, p < 0.0001). Also, infarct size by ce-CMR was significantly correlated with MVRI (r = 0.78, p < 0.0001), CFR (r = –0.67, p < 0.0001), DDT (r = –0.70, p < 0.0001), and Pzf (r = 0.72, p = 0.0002). Receiver-operating characteristic curve analyses of MVRI, CFR, DDT, and Pzf for predicting transmural MI (TEI-grade 4) demonstrated that the area under the curve tended to be higher for MVRI (0.885) than those for CFR (0.848), DDT (0.862), and Pzf (0.853). The best cut-off value for MVRI was 3.25 mm Hg·cm–1·s (sensitivity 75%, specificity 89%). Moreover, increased MVRI was significantly related to increased TEI-grade (p < 0.0001).
Conclusions: MVRI measured immediately after primary PCI is a useful predictor for the TEI in patients with anterior acute MI.
Key Words: acute myocardial infarction • microcirculation • physiology • cardiac magnetic resonance
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Abbreviations and Acronyms
| | ce-CMR = contrast-enhanced cardiac magnetic resonance | | CFR = coronary flow reserve | | CK-MB = creatine kinase-myocardial band | | DDT = diastolic deceleration time | | FFR = fractional flow reserve | | MI = myocardial infarction | | MVRI = microvascular resistance index | | PCI = percutaneous coronary intervention | | Pzf = zero flow pressure | | TEI = transmural extent of infarction | | TIMI = Thrombolysis In Myocardial Infarction |
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Primary percutaneous coronary intervention (PCI) for ST-segment elevation myocardial infarction is an established reperfusion strategy (1). Primary PCI has been reported to improve clinical outcomes in patients with acute myocardial infarction (MI) (2). However, microvascular perfusion is often impaired after primary PCI, and reperfusion of the epicardial coronary artery will not always guarantee reperfusion at the myocardial tissue level. The aim of current treatment strategies for acute MI is to obtain reperfusion, not only at the level of the epicardial artery but also at the tissue level, but a useful method for assessing coronary microcirculation has not been fully elucidated.
Recently, simultaneous measurement of phasic distal pressure and flow velocity by a single dual-sensor–equipped 0.014-inch guidewire has become possible in daily clinical practice. A previous study reported that using a dual-sensor guidewire, reproducibility of repeated hyperemic resistance parameters derived from distal pressure and velocity measurements in patients with stable angina pectoris was excellent (3). Measurement of distal pressure and flow velocity after reperfusion might provide important information on the state of coronary microvasculature in patients with acute MI. Myocardial necrosis after acute MI progresses as a "wavefront phenomenon" from the endocardium to the epicardium (4). Contrast-enhanced cardiac magnetic resonance (ce-CMR) can accurately discriminate transmural from nontransmural MI at very high spatial resolution (5) and can measure infarct size quantitatively (6–8). The transmural extent of infarction (TEI) defined by ce-CMR allows us to predict future improvement in myocardial contractile function (8,9). The aim of this study was to investigate whether microvascular resistance index (MVRI) measured immediately after primary PCI can predict the TEI in patients with anterior acute MI compared with various indices for assessing coronary microcirculation.
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Methods
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Patient population.
Twenty-seven patients who underwent primary PCI for a first anterior acute MI within 12 h from the onset of symptoms were included. The diagnosis of acute MI was based on chest pain lasting more than 30 min, ST-segment elevation of  2 mm (0.2 mV) in at least 2 contiguous leads on electrocardiography, and Thrombolysis In Myocardial Infarction (TIMI) flow grade of 0 or 1 at the initial coronary angiography. We excluded patients with previous myocardial infarction, left main trunk disease, renal insufficiency (serum creatinine >1.5 mg/dl), and cardiogenic shock. Patients were also excluded if they had absolute or relative contraindications to magnetic resonance examination, such as pacemaker, atrial fibrillation, claustrophobia, and so on. Written informed consent was obtained from all patients for participation in this study. The study was carried out according to the Declaration of Helsinki.
Study protocol.
Cardiac catheterization was performed by a percutaneous femoral approach with a 6-F guiding catheter. All patients received oral aspirin (162 mg) and a bolus of heparin (100 U/kg) before the procedure, and additional heparin was given if the procedure lasted >90 min to maintain an activated clotting time 250 s. An intracoronary bolus injection of isosorbide dinitrate (1 to 2 mg) was administered to obtain a high quality angiogram and before hemodynamic measurements. After thrombectomy by Export catheter (Medtronic Japan, Tokyo, Japan), balloon angioplasty was performed, followed by deployment of a single bare metal stent. Balloon size was determined by the angiographically determined dimension of the target vessel. In all patients, intravascular ultrasound-guided upsizing of the stent was performed according to CLOUT (Clinical Outcomes with Ultrasound Trial) criteria (10). After stenting, all patients received ticlopidine (200 mg/day) and aspirin (100 mg/day) for 30 days followed by aspirin alone indefinitely. Procedural success was defined as  30% residual stenosis of the culprit lesion by visual assessment. TIMI myocardial perfusion grade was determined from the final angiogram by 2 experienced angiographers blinded to the MVRI result, as described previously (11). Blood samples were obtained on admission and serially every 3 h for the first 24 h after primary PCI, and peak values of creatine kinase (CK) and CK-myocardial band (MB) were determined. ce-CMR was performed 13 ± 2 days after the onset of acute MI.
Hemodynamic measurements and data analysis.
Aortic pressure (Pa) was measured through the guiding catheter. Immediately after primary PCI, pressure (Pd) and flow velocity distal to the culprit site were measured simultaneously with a 0.014-inch dual-sensor (pressure and Doppler velocity) guidewire (ComboWire, Volcano Therapeutics, Rancho Cordova, California) (Fig. 1). After the wire was calibrated, advanced through the catheter, and equaled with the Pa in the catheter, it was placed at least 3 to 4 cm distal to the stented segment of the left anterior descending coronary artery and manipulated until an optimal and stable velocity signal was obtained. The position of the tip of the wire was confirmed by fluoroscopy and angiography. The Pa, Pd, instantaneous peak velocity, and electrocardiogram were obtained online at baseline and after induction of maximal hyperemia with 150 µg/kg/min of intravenous adenosine triphosphate via a central venous catheter (ComboMap Pressure and Flow System, Volcano Therapeutics). Twenty minutes after primary PCI, all signals were digitally recorded on a personal computer for offline analysis by an independent investigator who was unaware of patient data. Fractional flow reserve (FFR) was calculated as the ratio of mean Pd to mean Pa during maximal hyperemia. Coronary blood flow velocity reserve (CFR) was calculated as the ratio of time-averaged peak hyperemic to baseline average flow velocity. In 3 consecutive cardiac cycles, the deceleration time of diastolic velocity (DDT, ms) was measured from phasic coronary flow velocity recording as previously described (12) and averaged for the mean value. MVRI was calculated as the ratio of mean Pd to average peak flow velocity during maximal hyperemia (13). We calculated zero flow pressure (Pzf) using the method previously described (14). During maximal hyperemia, the instantaneous peak coronary flow velocity was plotted against the simultaneous measured distal coronary pressure and a pressure-flow velocity loop was displayed by specially designed software. In the phase of diastolic flow decrease, the diastolic pressure-flow relationship was determined by linear regression analysis. The x-intercept of the slope was calculated as the Pzf.
Protocol and image analysis for CMR.
All patients were examined at rest in the supine position with a whole body 1.5-T MR scanner (Intera Achieva, Philips Medical Systems, Best, the Netherlands) equipped with a 5-element cardiac phased-array coil for signal reception. All images were gated to the electrocardiogram and obtained during repeated breath-holds. ce-CMR was obtained with contiguous short-axis slices and representative long-axis slices of the left ventricle 10 min after intravenous injection of 0.1 mmol/kg gadolinium-diethylenetriamine penta-acetic acid (Magnevist, Schering AG, Berlin, Germany). We optimized the inversion time (200 to 300 ms) to null the normal myocardium. All analyses were performed by the consensus of the 2 blinded observers on an off-line work station (View-Forum, Philips Medical Systems, Best, the Netherlands). Based on a 17-segment model as previously recommended by the American Heart Association (15), representative short-axis slices of the basal (6 segments), mid-ventricular (6 segments), and apical (4 segments) region of the left ventricle were analyzed. The apex was evaluated from long-axis slices. The TEI was graded from 1 to 4 based on the transmural extent of hyperenhanced tissue within each segment: 1 = 0% to 25% of left ventricular wall thickness; 2 = 26% to 50%; 3 = 51% to 75%; and 4 = 76% to 100% (Fig. 2). The highest grade among 16 segments except apex was defined as the TEI-grade of each case. Infarct size was calculated by automatic summation of all slice volumes of delayed enhanced regions and expressed as a percentage of left ventricular volume. Microvascular obstruction was evaluated qualitatively on delayed enhanced images; it was defined as hypodense regions within the hyperenhanced infarcted area, and was included in the calculation of total infarct size.
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Figure 2 Representative Images of Each TEI-Grade in a Short-Axis View
Transmural extent of infarction (TEI) by contrast-enhanced cardiac magnetic resonance (ce-CMR) was graded from 1 to 4 based on the transmural extent of hyperenhanced tissue: 1 = 0% to 25% of left ventricular wall thickness; 2 = 26% to 50%; 3 = 51% to 75%; and 4 = 76% to 100%.
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Statistics.
Data were expressed as mean ± SD or n (%). Continuous variables were compared with the use of an unpaired Student t test. Categorical variables were compared by the chi-square test or Fisher exact test, as appropriate. Pearson's correlation coefficient test was used to assess correlations between the variables, and linear regression analyses were performed to determine the exact relations between the variables. Spearman's rank correlation test was used to analyze the correlation between MVRI and the TEI grade. Receiver-operating characteristic curve analysis was used to compare the diagnostic performance of coronary physiologic parameters to predict transmural MI. The areas under the curve for MVRI, CFR, DDT, and Pzf were compared by using the method of Hanley and McNeil (16). The best cut-off value for MVRI was defined as the value with the highest sum of sensitivity and specificity. Values of p < 0.05 were considered statistically significant. All statistical analyses were performed with SPSS software for Windows version 11.0 (SPSS Inc., Chicago, Illinois).
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Results
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In this study, transmural MI was defined as TEI-grade 4. TEI-grade 4 was observed in 8 (30%) of the 27 patients. These patients were classified as a transmural MI group. The other 19 patients (grade 1, n = 4; grade 2, n = 7; grade 3, n = 8) were classified as a nontransmural MI group.
Patient characteristics are listed in Table 1. There were no differences between the two groups with regard to age, sex, coronary risk factors, history of pre-infarction angina, collaterals, Killip classification, and left ventricular ejection fraction. However, peak CK and peak CK-MB were significantly higher in the transmural MI group than in the nontransmural MI group. Infarct size by CMR was significantly larger in the transmural MI group compared with that in the nontransmural MI group. Microvascular obstruction was present in 5 patients (62%) in the transmural MI group and 3 patients (16%) in the nontransmural MI group (p < 0.03). The average time from onset of symptoms to balloon was not different between the 2 groups. The culprit lesion was successfully treated with stent implantation in all patients without procedure-related complications. After primary PCI, TIMI flow grade 2 reflow was observed in 3 (38%) patients in the transmural MI group, and the other 5 (62%) patients demonstrated TIMI flow grade 3 reflow; almost all patients (95%) in the nontransmural MI group had TIMI flow grade 3 reflow in the final coronary angiography. Normal myocardial perfusion (TIMI myocardial perfusion grade 3) was observed in 2 patients (25%) in the transmural MI group and 8 patients (42%) in the nontransmural MI group.
Pressure-flow velocity loop was obtained appropriately in 5 patients in the transmural MI group and 15 patients in the nontransmural MI group. We calculated Pzf in the 20 patients and used them for analysis. Hemodynamic data are summarized in Table 2. In 24 (89%) of 27 patients, the infarct-related artery was treated without significant residual stenosis remaining (mean of the post-procedural FFR measured after primary PCI was 0.89 ± 0.11). The CFR was significantly lower in the transmural MI group than in the nontransmural MI group (1.14 ± 0.19 vs. 1.75 ± 0.48, p = 0.002). MVRI (3.70 ± 0.98 mm Hg·cm–1·s vs. 2.17 ± 0.84 mm Hg·cm–1·s, p = 0.0004) and Pzf (49.2 ± 11.7 mm Hg vs. 31.9 ± 9.3 mmHg, p = 0.0033) were significantly greater in the transmural MI group than in the nontransmural MI group. DDT was significantly shorter in the transmural MI group than in the nontransmural MI group (336 ± 162 ms vs. 632 ± 244 ms, p = 0.0044).
Peak CK-MB values were significantly correlated with MVRI (r = 0.77, p < 0.0001), CFR (r = –0.69, p < 0.0001), DDT (r = –0.75, p = 0.0001), and Pzf (r = 0.75, p < 0.0001), respectively (Fig. 3). Correlations between infarct size by ce-CMR and indices of coronary microcirculation were as follows: MVRI (r = 0.78, p < 0.0001), CFR (r = –0.67, p < 0.0001), DDT (r = –0.70, p < 0.0001), and Pzf (r = 0.72, p = 0.0002) (Fig. 4).
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Figure 3 Correlations Between Each Index and Enzymatic Infarct Size
Peak creatine kinase-myocardial band (CK-MB) values were significantly correlated with microvascular resistance index (MVRI) (r = 0.77, p < 0.0001), coronary flow reserve (CFR) (r = –0.69, p < 0.0001), diastolic deceleration time (DDT) (r = –0.75, p = 0.0001), and zero flow pressure (Pzf) (r = 0.75, p < 0.0001).
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Figure 4 Correlations Between Each Index and Infarct Size by ce-CMR
Infarct size by contrast-enhanced cardiac magnetic resonance (ce-CMR) was significantly correlated with MVRI (r = 0.78, p < 0.0001), CFR (r = –0.67, p < 0.0001), DDT (r = –0.70, p < 0.0001), and Pzf (r = 0.72, p = 0.0002). LV = left ventricle; other abbreviations as in Figure 3.
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MVRI was significantly correlated with CFR (r = –0.62, p = 0.0004) and DDT (r = –0.68, p < 0.0001). Also, there was a significant positive correlation between MVRI and Pzf (r = 0.75, p < 0.0001) (Fig. 5).
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Figure 5 Correlations Between MVRI and the Other 3 Indices
MVRI was significantly correlated with CFR (r = –0.62, p = 0.0004) and DDT (r = –0.68, p < 0.0001). Also, there was a significant positive correlation between MVRI and Pzf (r = 0.75, p < 0.0001). Abbreviations as in Figure 3.
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Figure 6
shows the receiver operating characteristic curves for the 4 measured hemodynamic parameters. The areas under the curve were 0.885 for MVRI, 0.848 for CFR, 0.862 for DDT, and 0.853 for Pzf. Direct comparison of the receiver operating characteristic analyses by the areas under the curve between MVRI and the other 3 indices did not differ significantly (MVRI vs. CFR, p = 0.68; MVRI vs. DDT, p = 0.80; MVRI vs. Pzf, p = 0.47). The best cut-off value of MVRI for the prediction of transmural MI was determined as 3.25 mm Hg·cm–1·s. The sensitivity, specificity, and predictive accuracy for MVRI were 75%, 89%, and 85%, respectively. In Spearman's rank correlation analysis, a significant positive correlation (p < 0.0001) was also observed between MVRI and TEI-grade (Fig. 7).
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Figure 6 ROC-Analysis for the 4 Measured Hemodynamic Parameters
The areas under the curve (AUC) for predicting transmural extent of infarction grade 4 of MVRI, CFR, DDT, and Pzf were 0.885, 0.848, 0.862, and 0.853, respectively. In direct comparison of the AUCs, there were no significant differences between MVRI and the other 3 hemodynamic variables (MVRI vs. CFR, p = 0.68; MVRI vs. DDT, p = 0.80; MVRI vs. Pzf, p = 0.47). The best cut-off value for MVRI was determined as 3.25 mm Hg·cm–1·s (sensitivity 75%, specificity 89%). Abbreviations as in Figure 3.
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Figure 7 Relationship Between MVRI and TEI-grade
In Spearman's rank correlation analysis, there was a significant positive correlation between MVRI and the transmural extent of infarction grade (p < 0.0001). CMR = cardiac magnetic resonance; other abbreviation as in Figure 3.
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Discussion
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The present study demonstrated that MVRI estimated immediately after primary PCI was strongly correlated with enzymatic infarct size and infarct size as defined by ce-CMR (Figs. 3 and 4), and was able to distinguish between nontransmural and transmural MI immediately after primary PCI at the cardiac catheterization laboratory. Moreover, increased MVRI was significantly related to higher TEI-grade (Fig. 7). These findings may lead us to the concept that MVRI is a useful variable for direct assessment of microcirculatory function.
The distinction between reversible and irreversible injury early after reperfusion is an important and challenging clinical question. However, early after primary PCI, it is difficult to evaluate true infarct size and residual myocardial viability because of stunned myocardium and advancing reperfusion injury. For this purpose, CMR with contrast-enhancement may be more sensitive than echocardiography and single-photon emission computed tomography (5). Using ce-CMR, Choi et al. (8) reported that in patients within 1 week after onset of MI, a decrease in the TEI was associated with greater long-term improvement in contractile function, and only 5% of myocardial segments with 76% to 100% TEI improved in the chronic state. Therefore, in the present study, we used the TEI-grade by ce-CMR to evaluate residual myocardial viability and defined the TEI-grade 4 as transmural MI. We also used various indices, including MVRI, to evaluate microvascular integrity, and we investigated the relations between the TEI and those indices. In this study, the receiver operating characteristic analysis showed that not only MVRI, but also CFR, DDT, and Pzf, were useful hemodynamic variables for predicting transmural MI immediately after primary PCI in patients with anterior acute MI. However, direct comparison of the areas under the curve between MVRI and the other 3 indices did not reveal significant differences. Further investigations will be required to establish which of these measures has the highest clinical relevance for predicting transmural necrosis in the post-infarct setting.
Several previous clinical studies have reported that CFR assessed early after reperfusion is a good predictor of left ventricular wall motion recovery and remodeling (17–19). Several mechanisms, such as distal microembolism during primary PCI, compression by tissue edema, platelet plugging, neutrophil adhesion, damage from oxygen free radicals, thrombus formation in the microvasculature itself, and microvascular vasoconstriction, may contribute to increased microvascular resistance in the infarct area. Because the combination of 2 or more of these mechanisms immediately after primary PCI may result in reduced CFR, CFR measured immediately after primary PCI does not accurately reflect residual myocardial viability. Also, Pzf may reflect microvascular tone and increase after acute MI. In a recent study, Pzf was shown to be a better predictor of residual myocardial viability than CFR (20). These may explain why the correlation between CFR and infarct size was weaker than that with Pzf.
A previous study showed that using a Doppler guidewire offers a better quantitative assessment of coronary flow velocity and microvascular damage in patients with reperfused MI (21). It has been demonstrated that the coronary flow velocity pattern, including DDT, immediately after primary PCI can predict in-hospital complications and mortality after acute MI, left ventricular functional recovery, and long-term cardiac events (22–25). In this study, the DDT correlated well with infarct size by CMR and peak CK-MB values. This finding may provide new support for clarifying the correlation between DDT and microvascular integrity as well.
In the present study, MVRI correlated well with CFR (r = –0.62, p < 0.0004), DDT (r = –0.68, p < 0.0001), and Pzf (r = 0.75, p < 0.0001) (Fig. 5). All correlations between MVRI and other indices of myocardial tissue level perfusion may suggest that microvascular malperfusion after primary PCI is likely due to increased microvascular resistance.
Study limitations.
Several limitations of our study must be considered. First, our study population was limited to only 27 patients with anterior acute MI undergoing primary PCI to the left anterior descending artery. A large number of examinations including other coronary arteries will be required to determine the clinical usefulness of our results. Second, although the analysis of hemodynamic measurements was blinded, measurements were performed by an angiographer, so it is not possible to exclude entirely the influence of investigator bias in our results. Third, MVRI, CFR, and Pzf are limited by their reliance on the achievement of maximal hyperemia. Failure to achieve peak hyperemia, by not achieving maximal reduction in microvascular resistance, may result in overestimation of MVRI and Pzf and underestimation of CFR. For these reasons, we used intravenous adenosine triphosphate to induce steady-state maximal hyperemia. Finally, coronary flow velocity measured within a few minutes after reperfusion may reflect a hyperemic reaction after direct angioplasty. In this study we performed all hemodynamic measurements 20 min after primary PCI to obtain a standardized value, as described previously (25).
Clinical implications.
Despite early successful reperfusion, some patients with acute MI have inadequate myocardial perfusion in the absence of angiographic evidence of mechanical epicardial artery obstruction. This inadequate myocardial perfusion may be associated with higher microvascular resistance and larger myocardial infarcts than in patients with adequate perfusion. Some therapeutic agents have shown improvement in coronary microcirculatory perfusion. One pilot trial reported that administration of low-dose intracoronary streptokinase immediately after primary PCI improved myocardial reperfusion (26). In a randomized trial of intracoronary verapamil in patients with acute MI, there was improvement of perfusion at the tissue level, using myocardial contrast echocardiography, compared with placebo (27). The agent nicorandil, an adenosine triphosphate-sensitive K+ channel opener with vasodilating action, was also shown to improve coronary microcirculatory perfusion in the infarct area (28). Therefore, in patients with high microvascular resistance immediately after primary PCI, it may be necessary to think about pharmacologic strategies such as intracoronary streptokinase, verapamil, nicorandil, or a combination of these agents as an adjunct to primary PCI. Measuring MVRI, given its simplicity and high reproducibility of measurement (3), may allow us to determine the efficacy of those therapeutic strategies for microvascular protection in patients with acute MI.
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Conclusions
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Simultaneous measurement of distal pressure and flow velocity immediately after reperfusion may provide additional insight into the management of patients with acute MI. Coronary microvascular resistance index measured immediately after primary PCI is a useful coronary physiologic parameter for predicting the TEI in patients with anterior acute MI.
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Reprint requests and correspondence: Dr. Takashi Akasaka, Department of Cardiovascular Medicine, Wakayama Medical University, 811-1 Kimiidera, Wakayama 641-8509, Japan (Email: akasat{at}wakayama-med.ac.jp).
Manuscript received August 7, 2008;
revised manuscript received October 27, 2008,
accepted November 5, 2008.
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R. McGeoch, S. Watkins, C. Berry, T. Steedman, A. Davie, J. Byrne, S. Hillis, M. Lindsay, S. Robb, H. Dargie, et al.
The Index of Microcirculatory Resistance Measured Acutely Predicts the Extent and Severity of Myocardial Infarction in Patients With ST-Segment Elevation Myocardial Infarction
J. Am. Coll. Cardiol. Intv.,
July 1, 2010;
3(7):
715 - 722.
[Abstract]
[Full Text]
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