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- Copyright © 2020 Mihaela Ioana Dregoesc et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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Abstract
Hindawi Journal of Interventional Cardiology Volume 2020, Article ID 2863290, 7 pages https://doi.org/10.1155/2020/2863290 Research Article In Acute ST-Segment Elevation Myocardial Infarction, Coronary Wedge Pressure Is Associated with Infarct Size and Reperfusion Injury as Evaluated by Cardiac Magnetic Resonance Imaging 1 2 3 Mihaela Ioana Dregoesc , Raluca Bianca Dumitru , Sorana Daniela Bolboaca˘ , 1 4,5 1 Ma˘da˘lin Constantin Marc , Simona Manole , and Adrian Corneliu Iancu “Iuliu Ha¸tieganu” University of Medicine and Pharmacy, Department of Cardiology, 19-21 Calea Motilor, Cluj-Napoca 400001, Romania Leeds Institute of Rheumatic and Musculoskeletal Medicine, University of Leeds, Woodhouse Lane, Leeds LS2 9JT, UK “Iuliu Ha¸tieganu” University of Medicine and Pharmacy, Department of Medical Informatics and Biostatistics, 6 Louis Pasteur, Cluj-Napoca 400349, Romania “Iuliu Ha¸tieganu” University of Medicine and Pharmacy, Department of Radiology, 3-5 Clinicilor Street Cluj-Napoca 400006, Romania Affidea Diagnostic Imaging Center, 19-21 Calea Mo¸tilor, Cluj-Napoca 400001, Romania Correspondence should be addressed to Adrian Corneliu Iancu; adrianiancu56@gmail.com Received 15 May 2020; Revised 21 July 2020; Accepted 3 August 2020; Published 17 August 2020 Academic Editor: Jochen Wo¨hrle Copyright © 2020 Mihaela Ioana Dregoesc et al. )is is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Background. Coronary collateral flow influences patient prognosis in the setting of acute myocardial infarction. However, few data exist about the relation between coronary collaterals, infarct size, and reperfusion injury. )e angiographic Rentrop score is prone to subjectivism and to the inherent limitations of angiographic images. Its prognostic value is controversial in the setting of acute myocardial infarction. )e invasive measurement of coronary wedge pressure (CWP) represents an alternative to Rentrop score for the evaluation of coronary collateralization. Our study evaluates pre-revascularization CWP as a predictor of infarct size and reperfusion injury as evaluated by cardiac magnetic resonance imaging. Methods. Patients with acute ST-elevation myocardial infarction underwent preprocedural CWP measurement and primary percutaneous coronary intervention. Infarct size, mi- crovascular obstruction, intramyocardial edema, and intramyocardial hemorrhage were evaluated by cardiac magnetic resonance imaging. Results. Mean CWP was inversely associated with infarct size (p � 0.01), microvascular obstruction (p � 0.02), intramyocardial edema (p � 0.05), and intramyocardial hemorrhage (p � 0.01). An excellent association was found between mean CWP and an infarct size≥24% of left ventricular mass (AUC � 0.880, p � 0.007), with an optimal cutoff value≤24.5 mmHg. Both intramyocardial edema (p � 0.02) and hemorrhage (p � 0.03) had a larger extent in patients with coronary wedge pressure ≤24.5 mmHg. Rentrop grade<2 was associated with larger infarct size (p � 0.03), but not with the extent of edema, microvascular obstruction, or intramyocardial hemorrhage. Conclusions. Pre-revascularization CWP was a predictor of infarct size and was significantly associated with a larger extent of intramyocardial edema and intramyocardial hemorrhage. Rentrop grade <2 was associated with a larger infarct size, but had no influence on reperfusion injury. )e clinical trial is registered with NCT03371784. development of microvascular obstruction (MVO) [3, 4]. 1. Introduction )e semiquantitative Rentrop angiographic grade is the )e long-term prognosis after an acute ST-segment eleva- most widely used method for the evaluation of coronary tion myocardial infarction (STEMI) is influenced by the collateralization. However, it is prone to subjectivism and to extent of infarct size and reperfusion injury [1–3]. the inherent limitations of an angiographic image. Its Infarct size depends on total ischemic time, on the prognostic value is controversial in the setting of acute debated presence and extent of collateralization, and on the myocardial infarction [4–7]. An alternative to Rentrop 2 Journal of Interventional Cardiology grading system is represented by the invasive measurement underwent revascularization with drug-eluting stents and of coronary wedge pressure (CWP). CWP represents the received double antiplatelet and anticoagulant therapy according to the most recent guidelines. Secondary pre- distal coronary pressure when the vessel is completely oc- cluded. A CWP value <25 mmHg was found in patients with vention measures were applied in all cases as recommended complete absence of collateral flow, both in clinical and by the current standard of care [12]. animal studies [8–10]. )e absence of angiographic collat- TIMI flow was evaluated at the beginning and at the end eralization was reflected on the prognosis of patients with of the procedure. Angiographic collateralization grade was acute myocardial infarction [11]. Still, literature data is evaluated during the diagnostic injections as originally scarce about the exact relation between coronary collateral described by Rentrop [13]. flow, infarct size, and reperfusion injury, as evaluated by Total ischemic time (TIT) was defined as the time from cardiac magnetic resonance (CMR) imaging [2, 3]. An early, the onset of symptoms to balloon inflation. quantitative, and easily determined predictor of infarct size High-sensitivity cardiac troponin T levels were deter- and reperfusion injury could open a much needed thera- mined at the time of admission and at 24 and 48 hours after reperfusion. peutic window for intracoronary, cardioprotective therapies. CMR, the current gold standard in the evaluation of myocardial necrosis, MVO, intramyocardial edema, and 2.1. CMR Imaging. CMR was performed between three and intramyocardial hemorrhage (IMH) has the major disad- seven days after the index event. Image acquisition was made vantage of being performed only days after the primary on a 1.5 T scanner (Siemens Magnetom Avanto Tim) and percutaneous coronary intervention (PCI), which reduces comprised late gadolinium enhancement for the evaluation the chance for early intracoronary cardioprotection. of infarct size and MVO and T2-weighted imaging for the )e aim of this study was to evaluate pre-revasculari- assessment of edema and IMH. Left ventricular ejection zation CWP as a predictor of infarct size and reperfusion fraction (LVEF), mass, and left ventricular end-systolic injury in patients with acute STEMI undergoing primary volume (LVESV) and left ventricular end-diastolic volume PCI. (LVEDV) were also measured. Complete details regarding CMR protocol are largely 2. Methods described in the Supplementary Materials (available here). )is was a prospective, observational, single-center trial. During six months, consecutive patients referred for a first 2.2. Statistical Methods. Data distribution was assessed using episode of acute STEMI were screened for inclusion. )e Kolmogorov–Smirnov and D’Agostino tests. Quantitative inclusion criteria were typical ongoing ischemic pain ≤12 continuous data were summarized as mean± standard de- hours and ST-segment elevation in two contiguous elec- viation whenever data proved normally distributed; other- trocardiographic leads, according to the Fourth Universal wise, median and interquartile range (Q1–Q3) were used. Definition of Myocardial Infarction [11]. )e exclusion Groups were compared with Student’s t-test, Man- criteria were previous myocardial infarction or coronary n–Whitney, or Wilcoxon rank-sum test, as appropriate. revascularization, left bundle branch block, thrombolysis, Categorical data were presented as percentages. Linear re- Killip class III or IV, active bleeding, or known contrain- gressions were used to model the relation between variables dications for CMR. )e research protocol was approved by of interest. the Local Ethics Committee and all patients gave written Receiver Operating Characteristic (ROC) curves were informed consent. )e study protocol conformed to the constructed to evaluate the association between CWP and principles outlined in the Declaration of Helsinki. CMR parameters. )e area under the curve (AUC) was All patients underwent coronary angiography either reported as a scalar measure of performance. )e ROC curve through radial or femoral access. )e culprit lesion was analyses were performed with SPSS version 25.0 (IBM, crossed with a pressure wire (Verrata Pressure Guide Wire, Chicago, IL, USA). Volcano Corporation, San Diego, CA) and CWP was All other statistical analyses were performed with measured directly, distal to the lesion, if )rombolysis in MedCalc (v. 19.0.3, MedCalc Software, Ostend, Belgium). A Myocardial Infarction (TIMI) flow remained 0. In the sit- two-sided p value <0.05 was considered statistically uation of initial TIMI >0 flow or in case of distal flow significant. restoration following wire crossing, CWP was measured and All authors had full access to all the data in the study. recorded during balloon inflation. )e rationale for the pre- )ey all take responsibility for its integrity and for the data revascularization CWP measurement was the exclusion of analysis. intraprocedural embolism, a process that leads to MVO and increases distal pressure values [5]. 3. Results All the procedures were performed during normal working hours by experienced operators. A mean two- 3.1. Patient Characteristics. A cohort of thirty-five patients minute increase in procedural time was noticed because of was included in the analysis. Baseline patient characteristics CWP measurement. are presented in Table 1. Left anterior descending coronary Following CWP measurement, primary PCI was per- artery was the culprit vessel in 65.71% of patients. Pre- formed according to current practice. All patients procedural TIMI 0 flow was observed in 48.57% of the cases, Journal of Interventional Cardiology 3 Table 1: Clinical and angiographic patient characteristics. with MVO (r � 0.34, p< 0.001), intramyocardial edema 2 2 (r � 0.57, p< 0.001), and IMH (r � 0.35, p � 0.004). Parameter Value (n � 35) ROC curve analysis showed an excellent association Age (years), mean± SD 60.11± 11.97 between mean CWP and an infarct size ≥24% of LV mass Males, n (%) 19 (54.28) (AUC � 0.880, p � 0.007) (Figure 2). A CWP cutoff value Smokers, n (%) 16 (45.71) ≤24.5 mmHg could estimate infarct size with a sensitivity of Arterial hypertension, n (%) 17 (48.57) 80% and a specificity of 89.7%. Diabetes mellitus, n (%) 11 (31.42) Patients with Rentrop grade 0 or 1 had a significantly Dyslipidemia, n (%) 9 (25.71) BMI (kg/m ), median (Q1–Q3) 26.59 (24.97–31.21) lower mean CWP value (p � 0.05) (Figure 3). Infarct size was two times greater in patients with Rentrop score 0 or 1 as Infarct localization, n (%) Anterior 23 (65.71) compared to those with Rentrop score 2 or 3 (15.79 vs. Inferior 8 (22.85) 7.57%, p � 0.03) but the extent of MVO, edema, and IMH Lateral 2 (5.71) did not significantly differ between these two categories Inferolateral 5 (14.28) (p � 0.57, 0.47, and 0.86 resp.). Total ischemic time (min), median (Q1–Q3) 300 (180–480) CWP (mmHg), mean± SD 31.02± 10.29 TIMI flow before the index procedure, n (%) 3.4. Group Comparison. Patients were divided into two 0 17 (48.57) groups based on the 24.5 mmHg mean CWP cutoff for the 1-2 7 (20) prediction of an infarct size ≥24% of LV mass. Infarct size 3 12 (34.28) was two times larger in the group with low CWP TIMI flow at the end of the index procedure, n (%) (22.32± 9.89 vs. 12.17± 7.90 %, p � 0.005), while the extent 0 0 (0) of MVO was more than twice the one measured in patients 1-2 9 (25.71) with CWP >24.5 mmHg (p � 0.21). Both IMH and edema 3 26 (74.28) had a significantly greater extent in patients with CWP Rentrop grade, n (%) ≤24.5 mmHg (p � 0.03 for IMH and 0.02 for edema, resp.) 0 17 (48.57) (Table 3). 1 11 (31.42) At the multivariate linear regression analysis, however, 2 5 (14.28) infarct size was associated with intramyocardial edema in- 3 2 (5.71) dependent of mean CWP value (R � 0.53, p< 0.001). An Troponin T (ng/ml), median (Q1–Q3) increase of 1% in infarct size was associated with a 0.9 % Admission value 0.17 (0.08–0.36) increase in edema. )e same observation was made for the Peak value 2.57(1.86–3.88) ∗ association between infarct size and MVO or IMH. Infarct BMI � body mass index; CWP � coronary wedge pressure; n � number; size was associated with MVO and IMH independent of Q1 � 1st quartile; Q3 � 3rd quartile; SD � standard deviation; and 2 2 TIMI � thrombolysis in myocardial infarction. mean CWP value (R � 0.35, p< 0.001 and R � 0.37, p< 0.001, resp.). An increase of 1% in infarct size was as- sociated with a 0.24% increase in MVO, while an increase of while at the end of the procedure, TIMI 3 flow was recorded 1% in infarct size was associated with a 0.07% increase in in 74.28% of the study group. IMH. 3.2. CMR Findings in the Study Population. Evaluable 4. Discussion myocardial edema on T2-weighted acquisitions was present In this study, we investigated the relationship between pre- in all patients, while MVO and IMH were detectable in revascularization CWP, angiographic collateral flow, and the 65.71% and 37.14% of them, respectively. Mean infarct size CMR parameters of postmyocardial infarction prognosis: reached 14.57± 9.34% of LV mass. )e CMR data is pre- infarct size, MVO, intramyocardial edema, and IMH. Sig- sented in Table 2. nificant inverse associations were identified between mean Infarct size, MVO, intramyocardial edema, and IMH CWP on one side and infarct size, MVO, intramyocardial were each positively correlated with peak troponin T value edema, and IMH on the other. What is more, a CWP (r � 0.72, p< 0.001 for infarct size, r � 0.42, p � 0.02 for ≤24.5 mmHg predicted an infarct size≥24% of LV mass with MVO, r � 0.45, p � 0.01 for edema, and r � 0.52, p � 0.004 a sensitivity of 80% and a specificity of 89.7% and could for IMH, resp.). differentiate patients with regard to the presence of intra- myocardial edema and IMH. Both intramyocardial edema 3.3. 8e Association between Mean CWP, CMR Parameters, and IMH represent severe forms of MVO [2]. In a large and Angiographic Collateralization. On univariate linear meta-analysis, a 24% infarct size cutoff was demonstrated as regression analysis, mean CWP was inversely associated a clinically useful parameter for the prediction of post- with infarct size (r � 0.18, p � 0.01) (Figure 1(a)), MVO STEMI mortality [14]. Regarding CWP, the 24.5 mmHg 2 2 (r � 0.14, p � 0.02), intramyocardial edema (r � 0.10, calculated cutoff is close to the 25 mmHg value described by p � 0.05) (Figure 1(b)), and IMH (r � 0.17, p � 0.01), re- former clinical and experimental research as a limit for the spectively. As expected, infarct size was positively associated absence of functional collaterals [8–10]. 4 Journal of Interventional Cardiology Table 2: CMR characteristics, three to seven days after the index procedure. Parameter Value (n � 35) LVESV (ml), mean± SD 75.42± 28.75 LVEDV (ml), mean± SD 144.57± 40.16 LVEF (%), mean± SD 48.69± 10.02 Left ventricular mass/BSA (g/m ), mean± SD 64.69± 14.21 Edema, n (%) 35 (100) Edema (% of left ventricular mass), mean± SD 30.81± 12.12 MVO, n (%) 23 (65.71) MVO (% of left ventricular mass), median (Q1–Q3) 0.36 (0.00–1.57) IMH, n (%) 13 (37.14) IMH (% of left ventricular mass), median (Q1–Q3) 0.00 (0.00–0.57) Necrosis, n (%) 35 (100) Necrosis (% of left ventricular mass), mean± SD 14.57± 9.34 BSA � body surface area; IMH � intramyocardial hemorrhage; LVEF � left ventricular ejection fraction; LVEDV � left ventricular end-diastolic volume; LVESV � left ventricular end-systolic volume; MVO � microvascular obstruction; n � number; Q1 � 1st quartile; Q3 � 3rd quartile; and SD � standard deviation. 50 75 40 60 30 45 20 30 10 15 0 0 0 15304560 0 15304560 Mean CWP (mmHg) Mean CWP (mmHg) (a) (b) Figure 1: )e association between mean CWP, infarct size, and intramyocardial edema. (a) An inverse, statistically significant association was identified between mean CWP and infarct size, expressed as percentage of left ventricular mass (p � 0.01). (b) An inverse, statistically significant association was identified between mean CWP and intramyocardial edema, expressed as percentage of left ventricular mass (p � 0.05). CWP � coronary wedge pressure and LV � left ventricle. )e extent of infarct size per se was associated with larger In our study, CWP proved to be a more powerful areas of edema and IMH, independent of mean CWP value. predictor of infarct size as compared to Rentrop grade, and it )e most powerful association regarded intramyocardial was also associated with reperfusion injury. A Rentrop grade edema, as each 1% increase in infarct size led to an almost 1% <2 was associated with a larger extent of necrosis, but it had increase in the extent of edema. It has already been dem- no value in the prediction of reperfusion injury as defined by onstrated that infarct size is significantly associated with the the presence of MVO, intramyocardial edema, and IMH. extent of MVO, intramyocardial edema, and IMH [15, 16]. )e utility of Rentrop angiographic grade as a predictor of Necrosis has a centrifuge extension in the myocardium, and post-STEMI prognosis is controversial. In a large meta- its extension is directly associated with the dimensions of the analysis, Rentrop grade was correlated with better outcomes area at risk. )e need for collateral supply to the salvageable only in the setting of stable coronary artery disease, while in acute mechanically reperfused STEMI patients the risk re- borders of the infarcted territory increases with the increase in myocardial edema. )e larger the area of edema, the duction did not reach statistical significance [17]. On the greater the required amount of collateral flow and diffusion contrary, in a recently published study, the presence of a supply from adjacent normally perfused areas. In the setting Rentrop collateralization grade of 1 or 2 was associated with of a large area of edema, the contribution of collateral flow to better in-hospital and 5-year mortality rates following limiting infarct size extension diminishes. STEMI [18]. Another research showed that the presence of Infarct size (% of LV mass) Edema (% of LV mass) Journal of Interventional Cardiology 5 1.0 0.8 0.6 0.4 0.2 0.0 0.0 0.2 0.4 0.6 0.8 1.0 1 – specificity Figure 2: ROC curve analysis. ROC curve analysis for the association between mean CWP and an infarcted area ≥24% of left ventricular mass (AUC � 0.880, p � 0.007). A CWP value≤ 24.5 mmHg was found as the optimal cutoff value to predict an infarct size ≥24% of left ventricular mass. AUC � area under the curve; CWP � coronary wedge pressure; and ROC � receiver operating characteristic. Rentrop <2 Rentrop ≥2 Median 25%–75% Min–Max Figure 3: )e association between mean CWP and Rentrop collateralization grade. Mean CWP was significantly lower in patients with Rentrop collateralization grade <2 (p � 0.05). CWP � coronary wedge pressure. used CMR to demonstrate the importance of Rentrop col- angiographically detectable collaterals had a protective effect on enzymatic infarct size in STEMI patients undergoing lateralization in infarct size and MVO, but the quantitative primary PCI [19]. Literature data is also conflicting with collateral flow evaluation was missing [3]. regard to the correlation between Rentrop angiographic In our study, pre-revascularization CWP emerged as a grade and quantitative assessment of collateral flow through predictor of both infarct size and severe reperfusion injury. invasive physiology indices. Lee et al. found a weak corre- Reperfusion injury is linked to the development of left lation between pressure-derived collateral flow index (CFIp) ventricular adverse remodeling in STEMI survivors. A re- and angiographic collateral grade and observed larger infarct liable pre-revascularization marker of adverse remodeling sizes in the lower CFI group [7]. Meisel et al. demonstrated could open a therapeutic window for an early targeted that both CWP and CFIp values are strongly correlated with cardioprotective strategy. High-risk STEMI patients defined angiographic collateralization in the setting of STEMI [20]. by low CWP could benefit from intracoronary glycoprotein IIb/IIIa inhibitors, intracoronary thrombolytics, or post- Still, none of these studies used the gold standard of CMR for the exact quantification of infarct size, MVO, intra- conditioning. )ere is an increasing interest in the intra- myocardial edema, and IMH. Only recently, Greulich et al. coronary fibrinolytic therapy during primary PCI. Two Sensitivity Mean CWP (mmHg) 6 Journal of Interventional Cardiology Table 3: Patients’ characteristics according to the mean CWP 24.5 mmHg cutoff for infarct size. Parameter CWP ≤24.5 mmHg (n � 8) CWP >24.5 mmHg (n � 27) p value Age (years), mean± SD 54± 18.63 60.11± 9.14 0.39 Males, n (%) 6 (75) 13 (48) 0.18 Smokers, n (%) 4 (50) 12 (44.44) 0.79 BMI (kg/m ), median (Q1–Q3) 25.64 (24.40–29.49) 26.79 (25.25–31.24) 0.51 Arterial hypertension, n (%) 2 (25) 15 (55.55) 0.13 Systolic BP, mean± SD 125.12± 25.35 135.37± 20.37 0.36 Diastolic BP, mean± SD 78.75± 16.42 80.62± 18.04 0.78 Heart rate (beats/min), mean± SD 75± 11.30 78.66± 11.93 0.44 Diabetes mellitus, n (%) 3 (37.50) 8 (29.60) 0.70 Glycaemia (mg/dl), median (Q1–Q3) 140.50 (123.25–206.25) 143.30 (119–223) 0.86 Peak troponin T value (ng/ml), median (Q1–Q3) 3.63 (2.01–5.13) 2.38 (1.56–3.72) 0.19 Total ischemic time (min), median (Q1–Q3) 300 (195–300) 300 (180–540) 0.54 Rentrop grade <2, n (%) 8 (100) 20 (77.14) 0.01 Left ventricular mass/BSA, mean± SD 60.41± 9.24 65.95± 15.28 0.33 Infarct size (% of LV mass), mean± SD 22.32± 9.89 12.17± 7.90 0.005 Edema (% of LV mass), mean± SD 38.92± 13.45 28.41± 10.82 0.02 MVO (% of LV mass), median (Q–Q3) 0.50 (0.01–6.17) 0.19 (0.00–1.36) 0.21 IMH (% of LV mass), median (Q1–Q3) 0.86 (0.00–3.00) 0 (0.00–0.02) 0.03 LVESV (ml), mean± SD 84.82± 28.67 72.63± 28.70 0.31 LVEDV (ml), mean± SD 159.12± 24.43 140.25± 43.16 0.13 LVEF (%), mean± SD 47.51± 12.49 49.03± 9.41 0.75 BMI � body mass index; BP � blood pressure; BSA � body surface area; IMH � intramyocardial hemorrhage; LV � left ventricle; LVEF � left ventricular ejection fraction; LVEDV � left ventricular end-diastolic volume; LVESV � left ventricular end-systolic volume; MVO � microvascular obstruction; n � number; Q1 � 1st quartile; Q3 � 3rd quartile; and SD � standard deviation. ongoing trials will hopefully bring new data with regard to 5. Conclusions low-dose intracoronary thrombolytics administration In this study, coronary collateral flow as assessed by pre- (STRIVE-NCT03335839; RESTORE-MI- revascularization CWP was associated with both infarct size ACTRN12618000778280). )e timely administration of and reperfusion injury. A mean CWP ≤24.5 mmHg pre- dedicated molecules like neprilysin inhibitors could also dicted an infarct size ≥24% of LV mass and was associated be beneficial for the improvement of long-term prognosis with a larger extent of intramyocardial edema and IMH. in this patient subgroup [21, 22]. )e PARADISE-MI trial Angiographic Rentrop grade was associated with infarct size (NCT02924727) is currently investigating the efficacy of but had no influence on the extent of reperfusion injury. sacubitril/valsartan on left ventricular structure and Although larger-scale studies are needed to confirm these function after myocardial infarction. In a recently pub- results, CWP emerges as an early, quantitative, and easily lished review, an area of edema >30% of LV mass was measured predictor of an adverse postmyocardial infarction recommended as criterion for the selection of patients prognosis. Such a parameter could open a much needed who would most likely benefit from cardioprotective window for the timely administration of cardioprotective therapies [23]. In our study, in patients with a mean CWP therapies. ≤24.5 mmHg, the mean extent of intramyocardial edema reached 38.9% of LV mass. Data Availability Data supporting the conclusions of the study will be made 4.1. Study Limitations. )e main limitation of this study is represented by the small sample size. )e exclusion of pa- available on request. tients with primary pharmacological reperfusion, the most frequently applied strategy in the geographical region the Conflicts of Interest center covers, led to a reduced number of study participants. Despite the relatively small cohort, the study did show )e authors declare that there are no conflicts of interest several significant associations between CWP, infarct size, regarding the publication of this article. and reperfusion injury. Larger cohort studies are needed to confirm these results. Acknowledgments )e analysis is also limited by the lack of a six-month CMR follow-up examination for the evaluation of left )e authors would like to acknowledge the Affidea Diag- ventricular adverse remodeling. However, the strong asso- nostic Imaging Center for the contribution to this study. ciation between CWP and infarct size is an indirect argu- )is research was supported by the Executive Unit for the ment in favor of CWP’s value as a potential marker of Financing of Higher Education, Research, Development, adverse remodeling. and Innovation (UEFISCDI) (Grant no. PN-III-P4-ID-PCE- Journal of Interventional Cardiology 7 electrocardiographic and hemodynamic variables,” Journal of 2016-0393, no. 171/2017], by )e Romanian Academy of the American College of Cardiology, vol. 33, no. 3, pp. 670–677, Medical Sciences, and by )e European Regional Devel- opment Fund (Grant no. 2/Axa 1/31.07.2017/107124 SMIS). [11] M. Hara, Y. Sakata, D. Nakatani et al., “Impact of coronary )e funding sources had no role in the study design, in the collaterals on in-hospital and 5-year mortality after ST-ele- collection, analysis, and interpretation of data, in the writing vation myocardial infarction in the contemporary percuta- of the report, and in the decision to submit the article for neous coronary intervention era: a prospective observational publication. study,” BMJ Open, vol. 6, no. 7, Article ID e011105, 2016. [12] K. )ygesen, J. S. Alpert, A. S Jaffe et al., “Fourth universal definition of myocardial infarction (2018),” 8e European Supplementary Materials Heart Journal, vol. 40, pp. 237–269, 2019. [13] M. Valgimigli, H. Bueno, R. A. Byrne et al., “ESC scientific Detailed cardiac magnetic resonance imaging protocol and document group; ESC committee for practice guidelines STROBE checklist. (Supplementary Materials) (CPG); ESC national cardiac societies. 2017 ESC focused update on dual antiplatelet therapy in coronary artery disease References developed in collaboration with EACTS: the task force for dual antiplatelet therapy in coronary artery disease of the [1] S. De Waha, M. R. Patel, C. B. Granger et al., “Relationship European society of cardiology (ESC) and of the European between microvascular obstruction and adverse events fol- association for cardio-thoracic surgery (EACTS),” 8e Eu- lowing primary percutaneous coronary intervention for ST- ropean Heart Journal, vol. 39, pp. 213–260, 2018. segment elevation myocardial infarction: an individual pa- [14] K. P. Rentrop, F. Feit, W. Sherman, and J. C. )ornton, “Serial tient data pooled analysis from seven randomized trials,” angiographic assessment of coronary artery obstruction and European Heart Journal, vol. 38, no. 47, pp. 3502–3510, 2017. collateral flow in acute myocardial infarction. report from the [2] Y. S. Hamirani, A. Wong, C. M. Kramer, and M. Salerno, second Mount Sinai-New York University reperfusion trial,” “Effect of microvascular obstruction and intramyocardial Circulation, vol. 80, no. 5, pp. 1166–1175, 1989. hemorrhage by CMR on LV remodeling and outcomes after [15] G. W. Stone, H. P. Selker, H. )iele et al., “Relationship myocardial infarction,” JACC: Cardiovascular Imaging, vol. 7, between infarct size and outcomes following primary PCI,” no. 9, pp. 940–952, 2014. Journal of the American College of Cardiology, vol. 67, no. 14, [3] S. Greulich, A. Mayr, S. Gloekler et al., “Time-dependent pp. 1674–1683, 2016. myocardial necrosis in patients with ST-segment–elevation [16] D. J. Hausenloy, W. Chilian, F. Crea et al., “)e coronary myocardial infarction without angiographic collateral flow circulation in acute myocardial ischaemia reperfusion injury- visualized by cardiac magnetic resonance imaging: results a target for cardioprotection,” Cardiovascular Research, from the multicenter STEMI-SCAR project,” Journal of the vol. 115, pp. 1143–1155, 2019. American Heart Association, vol. 8, no. 12, Article ID e012429, [17] H. Bulluck, M. Hammond-Haley, S. Weinmann, R. Martinez- Macias, and D. J. Hausenloy, “Myocardial infarct size by CMR [4] S. Schumacher, H. Everaars, W. Stuijfzand et al., “Association in clinical cardioprotection studies,” JACC: Cardiovascular between coronary collaterals and myocardial viability in Imaging, vol. 10, no. 3, pp. 230–240, 2017. patients with a chronic total occlusion,” Eurointervention, [18] P. Meier, H. Hemingway, A. J. Lansky, G. Knapp, B. Pitt, and vol. 16, pp. 453–461, 2020. C. Seiler, “)e impact of the coronary collateral circulation on [5] K. Yamamoto, H. Ito, K. Iwakura et al., “Pressure-derived mortality: a meta-analysis,” European Heart Journal, vol. 33, collateral flow index as a parameter of microvascular dys- no. 5, pp. 614–621, 2012. function in acute myocardial infarction,” Journal of the [19] P. Elsman, A. V. J. Van `t Hof, M. J De Boer et al., “Role of American College of Cardiology, vol. 38, no. 5, pp. 1383–1389, collateral circulation in the acute phase of ST-segment-ele- vation myocardial infarction treated with primary coronary [6] M. Sezer, Y. Nisanci, B. Umman et al., “Pressure-derived intervention,” European Heart Journal, vol. 25, no. 10, collateral flow index: a strong predictor of late left ventricular pp. 854–858, 2004. remodeling after thrombolysis for acute myocardial infarc- [20] S. R. Meisel, M. Shochat, A. Frimerman et al., “Collateral tion,” Coronary Artery Disease, vol. 17, no. 2, pp. 139–144, pressure and flow in acute myocardial infarction with total coronary occlusion correlate with angiographic collateral [7] C. W. Lee, S. W. Park, G. Y Cho et al., “Pressure-derived grade and creatine kinase levels,” American Heart Journal, fractional collateral blood flow: a primary determinant of left vol. 159, no. 5, pp. 764–771, 2010. ventricular recovery after reperfused acute myocardial in- [21] M. Kitakaze, M. Asakura, J. Kim et al., “Human atrial na- farction,” Journal of the American College of Cardiology, triuretic peptide and nicorandil as adjuncts to reperfusion vol. 35, no. 4, pp. 949–955, 2000. treatment for acute myocardial infarction (J-WIND): two [8] M. Sezer, Y. Nisanci, B. Umman, E. Yilmaz, F. Erzengin, and randomised trials,” 8e Lancet, vol. 370, no. 9597, O. Ozsaruhan, “Relationship between collateral blood flow pp. 1483–1493, 2007. and microvascular perfusion after reperfused acute myocar- [22] J. H. Traverse, C. M. Swingen, T. D. Henry et al., “NHLBI- dial infarction,” Japanese Heart Journal, vol. 44, no. 6, Sponsored randomized trial of postconditioning during pp. 855–863, 2003. primary percutaneous coronary intervention for ST-elevation [9] J. A. E. Spaan, J. J. Piek, J. I. E. Hoffman, and M. Siebes, myocardial infarction,” Circulation Research, vol. 124, no. 5, “Physiological basis of clinically used coronary hemodynamic pp. 769–778, 2019. indices,” Circulation, vol. 113, no. 3, pp. 446–455, 2006. [23] G. Niccoli, R. A. Montone, B. Ibanez et al., “Optimized [10] R. A. M. Van Liebergen, J. J. Piek, K. T. Koch, R. J. De Winter, treatment of ST-elevation myocardial infarction,” Circulation C. E. Schotborgh, and K. I. Lie, “Quantification of collateral Research, vol. 125, no. 2, pp. 245–258, 2019. flow in humans: a comparison of angiographic,
Journal
Journal of Interventional Cardiology – Hindawi Publishing Corporation
Published: Aug 17, 2020