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      Impact of Postdilation on Intervention Success and Long-Term Major Adverse Cardiovascular Events (MACE) among Patients with Acute Coronary Syndromes



            Postdilation is frequently used during coronary interventions to prevent stent malapposition. Currently there are contradictory findings regarding the benefits of postdilation for both intraprocedural and long-term outcomes. We evaluated the impact of postdilation among patients who presented with acute coronary syndromes (ACS) and underwent percutaneous coronary interventions (PCI). A total of 258 consecutive patients who presented with ACS and underwent PCI were included in the study. The patients were followed up for 25±1.7 months for the occurrence of major adverse cardiovascular events (MACE). During follow-up, 65 patients (25.2%) had MACE. Among patients without MACE, intracoronary nitrate infusion was less frequently used (P=0.005), myocardial blush grade was higher (P<0.001), and a drug-eluting stent was more frequently used (P=0.005). No significant differences were noted between groups regarding the predilation, recurrent dilation, postdilation, and other angiographic characteristics. In multivariate analysis, female sex (P=0.047), myocardial blush grade (P=0.038), previous coronary artery disease (P=0.030), and peak troponin level (P=0.002) were found to be predictors of MACE. In patients who were treated with PCI for ACS, performing postdilation did not predict final Thrombolysis in Myocardial Infarction (TIMI) flow grade, corrected TIMI frame count, myocardial blush grade, or MACE.

            Main article text


            Acute coronary syndromes (ACS) are still a major cause of death worldwide despite recent advances in diagnostic and therapeutic tools. ST-segment elevation myocardial infarction (STEMI) merits particular attention since establishment of coronary perfusion as soon as possible is of utmost importance to prevent adverse cardiovascular events [1, 2]. Coronary angiography and subsequent percutaneous coronary intervention (PCI) if necessary is the method of choice for myocardial revascularization. Stent implantation has replaced balloon angioplasty in most cases as overwhelming evidence suggests that the former reduces the risk of restenosis. Challenges in stent implantation due to the characteristics of coronary arteries and atherosclerotic lesions caused operators to develop feasible strategies depending on the lesion location, diameter, and morphology. Dilation by use of noncompliant balloons after stent implantation is one of the most frequently used techniques to address these challenges [3]. Because incomplete stent expansion is a major cause of stent thrombosis and in-stent restenosis, postdilation has been considered an important technique to help optimal stent implantation [46]. Patients with ACS were found to be particularly prone to stent malapposition because of the presence of an inflammatory milieu and coronary vasoconstriction. These findings suggested that postdilation with high pressures in the context of ACS would reduce stent malapposition and improve outcomes. In contradiction, other studies demonstrated controversial results and some indicated a signal toward harm such that postdilation impaired final Thrombolysis in Myocardial Infarction (TIMI) flow, increased the risk of target vessel revascularization, and predicted adverse clinical outcomes [79]. Myocardial blush grade (MBG) is considered to be a reliable indicator of tissue perfusion and is associated with reduced long-term mortality and morbidity in patients with ACS [10]. Despite several studies evaluating the effect of postdilation on post-PCI angiographic parameters, there are no data to date on the impact of postdilation on MBG. Thus, we aimed to evaluate the effect of postdilation on MBG and long-term major cardiovascular outcomes.


            Study Population

            This study, with a prospective observational cohort study design, was conducted in the cardiology clinic in the Faculty of Medicine of Recep Tayyip Erdoğan University, Rize, Turkey. A total of 258 consecutive patients who presented with ACS (STEMI and non–ST-segment elevation myocardial infraction) and who underwent PCI during hospitalization between February 2017 and August 2017 were included in the study. The study was performed in accordance with the principles stated in the Declaration of Helsinki. The local ethics committee approved the study protocol.

            Exclusion Criteria

            Patients with previous coronary artery bypass graft operation, in-stent restenosis, chronic kidney disease, sepsis, pulmonary embolism, or cardiogenic shock and patients who were being medically treated were excluded from the study.

            Demographic Data

            Clinical characteristics, which consisted of multiple descriptors from each patient’s history and physical examination, of each patient were collected by physicians from cardiology clinics and were stored in the database of the coronary angiography laboratory at Recep Tayyip Erdoğan Education and Research Hospital. We recorded the baseline characteristics, including hypertension, presence of diabetes mellitus, smoking status, family history of premature coronary artery disease, and lipid parameters.

            Selective Coronary Angiography and PCI Procedure

            Diagnostic coronary angiography and PCI procedures for the study patients were performed by five different experienced interventional cardiologists, who were blinded to the other data. The use and administered dose of nitroglycerin for intracoronary infusion and PCI-related preferences such as predilation, postdilation, stent length, and stent width were left to the discretion of the interventional cardiologist who performed the procedure. Medical treatments of the study patients were according to current guidelines. Three experienced investigators who were blinded to clinical parameters of the patients carefully reviewed the coronary angiograms for the measurements.

            The timing of the selective coronary angiography and PCI were in accordance with current guidelines. Femoral artery puncture and the Judkins technique were performed in all cases. Multiple views were obtained in all patients, with visualization of the left anterior descending artery and left circumflex coronary artery in at least four views and the right coronary artery in at least two views. Coronary angiograms were recorded in digital format for quantitative analysis.

            On the first angiogram, we assessed the basal TIMI flow grade and collateral circulation of the culprit vessel. Variables obtained in the angiographic sequences such as TIMI flow grade, corrected TIMI frame count (cTFC), and TIMI myocardial perfusion grade were acquired immediately after PCI.

            Epicardial blood flow was assessed by use of either TIMI flow grade [11] or cTFC [12], and myocardial perfusion was assessed by use of TIMI myocardial perfusion grade [11]. To allow sufficient filling of the venous system and TIMI myocardial perfusion grading, cine filming was kept sufficiently long (>10 s).

            Thrombus burden was classified by the investigator prior to wire crossing based on the TIMI thrombus grade [13].

            Coronary artery stenoses were classified as lesions of type A, B1, B2, and C [14]. Lesion classification by the American College of Cardiology/American Heart Association system was based on 11 characteristics, including lesion length, lesion eccentricity, lesion tortuosity, lesion angle, lesion contour, calcification, total occlusion for less than 3 months, total occlusion for more than 3 months, ostial lesion, side branch involvement, and presence or absence of thrombus [14].


            All patients were treated medically according to current guidelines [1]. Patients were given loading doses of clopidogrel, ticagrelor, or prasugrel plus a loading dose of acetylsalicylic acid according to the preference of the invasive cardiologist who performed the procedure.

            At the start of each procedure, 10,000 IU heparin was administered intravenously. Coronary stenting directly, or followed by balloon angioplasty, was performed when patients were eligible. Stent and coronary artery diameters and predilation/postdilation details were recorded during PCI. After the procedure, patients were followed up in the coronary care unit until hemodynamic stabilization.

            Laboratory Assays

            Cardiac biomarker levels, including creatine kinaseMB level, troponinI level, admission glucose level, and levels of inflammatory markers, including leukocytes, were analyzed in the emergency department and used in the analyses as admission values. The lipid samples were drawn by venipuncture to perform routine blood chemistry tests after patients had fasted for at least 8 h. Glucose level, creatinine level, and lipid profile were determined by standard methods. White blood cell (leukocyte) counts were obtained with an automated cell counter (Gen-S, Coulter Corporation, Miami, FL, USA). Blood samples were obtained 4 h apart for the determination of peak creatine kinaseMB and troponin levels. Troponin levels reference ranges was 0–0.026.

            Clinical Follow-up Parameters and Identification of Major Cardiac Events

            The follow-up period was 25±1.7 months. Patient clinical data were obtained from physicians, from the data recording system of Recep Tayyip Erdoğan Education and Research Hospital, and by face-to-face and/or telephone interviews.

            Patients were followed up for any occurrence of major cardiac events (MACE), which included cardiovascular death, new heart failure, a cerebrovascular event, recurrent revascularization, reinfarction, and major bleeding.

            Major bleeding was considered to be any intracranial bleeding (excluding microhemorrhages of 10 mm evident only on gradient-echo MRI), clinically overt signs of hemorrhage associated with a drop in hemoglobin level of 5 g/dL, or fatal bleeding (bleeding that directly results in death within 7 days) [15].

            Statistical Analysis

            Continuous variables were expressed as means±standard deviations and categorical variables were presented as percentages. The variables were compared by a two-tailed Student t test for continuous variables with a normal distribution or the Mann-Whitney U test for continuous variables with a nonnormal distribution. A chi-square test was used for the categorical variables. The effects of the various variables on MACE were calculated by Cox regression analysis. All statistical tests were two-tailed, and P<0.05 was considered significant. All analyses were performed with SPSS version 15 (SPSS Inc., Chicago, IL, USA).


            Study patients were followed up for 25±1.7 months. During this period, 65 patients (25.2%) had MACE. Among those patients, 16 (24.6%) were female and the mean age was 67.38 years (standard deviation 11.98 years). Eighteen patients (7.0%) died, two (0.8%) had major bleeding, 24 (9.3%) had decompensated heart failure, two had a cerebrovascular accident, two (0.8%) had a ventricular tachycardia episode, 11 (4.3%) had stent thrombosis, 15 (5.8%) had reinfarction, and 20 (7.8%) had revascularization.

            Univariate analysis among patients who had undergone postdilation (n=52, 20.2%) and patients who had not undergone postdilation (n=206, 79.8%) revealed that stent length was longer (P<0.001) and diabetes was more frequent (P=0.089) among patients who had undergone postdilation, although the latter did not reach statistical significance (Table 1).

            Table 1

            Characteristics of Study Patients According to Postdilation Status.

            Without postdilation (n=206)With postdilation (n=52)P-value
            Demographic characteristics
             Female sex33 (16.0%)9 (17.3%)0.345
             Dyslipidemia64 (31.1%)19 (36.5%)0.276
             Hypertension90 (43.7%)21 (40.4%)0.376
             Diabetes91 (44.2%)17 (32.7%)0.089
             Family history of CAD82 (39.8%)22 (42.3%)0.430
             Age (years)61.3±11.0463.27±12.60.574
             Prior CAD20 (9.7%)5 (9.6%)0.611
            Killip class
             I132 (95.0%)33 (97.1%)0.873
             II–IV7 (5.0%)1 (2.9%)
             LVEF (%)53.6±9.352.13±9.50.770
            Laboratory data
             Peak creatine kinase MB (ng/mL)78.33±98.986.6±106.70.595
             Peak troponin I (ng/mL)22.62±21.223.15±21.70.575
             Blood glucose (mg/dL)152.2±69.6143.1±69.90.862
             Creatinine (mg/dL)1.00±0.371.05±0.3230.876
             WBC (103/μL)10.04±3.39.67±3.050.549
             CRP (mg/dL)0.89±1.390.97±1.600.430
             HbA1c (%)6.7±1.616.56±1.70.841
             Clopidogrel115 (55.8%)23 (44.2%)0.355
             Prasugrel17 (8.3%)6 (11.5%)0.213
             Ticagrelor74 (35.9%)23 (44.2%)0.513
            Angiographic data
             Stent type
             BMS28 (13.8%)11 (21.2%)0.334
             DES156 (76.8%)38 (73.1%)
             BMS and DES19 (9.4%)3 (5.8%)
             USAP/NSTEMI123 (59.7%)29 (55.8%)0.873
             STEMI83 (40.3%)23 (44.2%)
            Culprit artery
             LAD artery and branches79 (39.3%)31 (59.6%)
             RCA and branches71 (35.3%)14 (26.9%)
             LCX artery and branches51 (25.4%)7 (13.5%)0.025
            Lesion type
             A3 (1.5%)0 (0%)
             B164 (32.7%)10 (20.4%)
             B2111 (56.6%)31 (63.3%)
             C18 (9.2%)8 (16.3%)0.141
             Intracoronary nitrate infusion138 (70.0%)33 (63.5%)0.372
            MBG after dilation
             08 (3.9%)4 (7.7%)
             148 (23.3%)15 (28.8%)
             257 (27.7%)13 (25.0%)0.503
             393 (45.1%)20 (38.5%)
             cTFC after PCI14.61±10.515.43±7.340.340
            TIMI flow grade, final
             01 (0.5%)0 (0%)
             14 (2.0%)3 (5.8%)
             211 (5.4%)4 (7.7%)
             3187 (92.1%)45 (86.5%)
             Deployed stent diameter (mm)23.62±9.8933.25±15.60.240
             Deployed stent length (mm)2.94±0.352.97± 0.4<0.001
            MACE data
             MACE48 (23.3%)17 (32.7%)0.113
             Death13 (6.3%)5 (9.6%)0.285
             Major bleeding2 (1%)0 (0%)0.637
             Heart failure19 (9.2%)5 (9.6%)0.554
             CVA1 (0.5%)1 (1.9%)0.363
             Ventricular arrhythmias2 (1%)0 (0%)0.637
             Stent thrombosis8 (3.9%)3 (5.8%)0.388
            Revascularization15 (7.3%)5 (9.6%)0.330
             Reinfection10 (4.9%)5 (9.6%)0.162

            BMS, Bare metal stent; CAD, coronary artery disease; CRP, C-reactive protein; CVA, cerebrovascular accident; DES, drug-eluting stent; HbA1c, hemoglobin A1c; LAD, left anterior descending; LCX, left circumflex; LVEF, left ventricular ejection fraction; MACE, major adverse cardiovascular event; MBG, myocardial blush grade; NSTEMI, non–ST-segment elevation myocardial infarction; PCI, percutaneous coronary intervention; RCA, right coronary artery, STEMI, ST-segment elevation myocardial infarction; TFC, Thrombolysis in Myocardial Infarction frame count; TIMI, Thrombolysis in Myocardial Infarction; USAP, unstable angina pectoris, WBC, white blood cells.

            We performed multivariate analysis to identify predictors of MACE during follow-up. Male sex (P=0.047), MBG (P=0.038), previous coronary artery disease (P=0.030), and peak troponin level (P=0.002) were found to be predictors of MACE (Table 2).

            Table 2

            Independent Predictors of Major Adverse Cardiovascular Events.

            VariableUnivariate analysis
            Multivariate analysis
            HR95% CIP-valueHR95% CIP-value
            Sex (male)0.6150.237–0.9600.0380.5420.297–0.9910.047
            Prior CAD2.1580.917–5.0750.0782.2001.080–4.4810.030
            Killip class8.0651.621–40.1350.011
            HbA1c fraction1.1550.982–1.3580.081
            Blood glucose level1.0041.001–1.0080.023
            Serum creatinine level2.7931.321–5.9030.007
            Stent type1.2250.680–2.2060.500
            Intracoronary nitrate infusion0.4480.252–0.7990.006
            Peak creatine kinase MB level1.0051.002–1.008<0.001
            Peak troponin I level1.0231.009–1.0370.0011.0191.007–1.0320.002
            WBC count1.0901.002–1.1860.046
            Neutrophil count1.0991.004–1.2030.041
            CRP level1.2231.020–1.4460.030

            ACE, Angiotensin-converting enzyme; ARB, angiotensin receptor blocker; CAD, coronary artery disease; CI, confidence interval; CRP, C-reactive protein; HbA1c, hemoglobin A1c; HR, hazard ratio; LVEF, left ventricular fraction; MBG, myocardial blush grade; WBC, white blood cell.

            No significant difference was noted between patients in whom postdilation had been performed and patients in whom postdilation had not been performed. There was no difference regarding MBG (P=0.305), final TIMI flow grade (P=0.218), and cTFC (P=0.118) with use of clopidogrel, ticagrelor, or prasugrel in patients in whom postdilation had been performed. Postdilation was found to be neutral in predicting procedural success and long-term MACE.


            In the present study, we found that among patients who presented with ACS and had PCI during hospitalization, postdilation predicted neither short-term PCI success as assessed by final TIMI flow grade, cTFC, and MBG nor MACE during follow-up. In addition, clopidogrel, ticagrelor, and prasugrel did not affect outcomes in patients in whom postdilation had been performed.

            In a previous study that included 405 patients with STEMI and treated by primary PCI, Tasal et al. [7] showed that postdilation did not reduce final TIMI flow and improved outcomes at 6 months. Compared with the present study, the number of patients in whom postdilation was performed was significantly higher (52 vs. 20%) and only patients with STEMI were included. Similarly to our findings, no significant differences were noted between patients with postdilation and patients without postdilation regarding acute PCI success as assessed by final TIMI flow, cTFC, and MBG. However, they found that postdilation reduced the incidence of stent thrombosis and target vessel revascularization. No significant difference was noted between groups regarding the markers reflecting myocardial damage and left ventricular ejection fraction, which was in accordance with our findings. In their study demonstrating that postdilation increased mortality, Zhang et al. [9] showed that postdilation did not increase the risk of coronary no reflow. Importantly, postdilation was performed in a higher proportion of patients (43.1%) than in our study. Furthermore, postdilation did not predict worse outcomes in the non–acute myocardial infarction subgroup.

            Although Zhang et al. [9] demonstrated worse outcomes associated with postdilation, the causative mechanisms remained unknown. Other studies proposed that stent overexpansion secondary to balloon inflation at very high pressures could be the underlying reason for adverse outcomes [16]. Accordingly, Maekawa et al. [16] showed that although stent overexpansion reduced the risk of target vessel revascularization, but the incidence of heart failure in the overexpansion group was higher than that in the nonoverexpansion patients during intravascular ultrasound evaluation. Maekawa et al. suggested that distal microembolisms of thrombogenic material from the plaque that were stented with overexpansion were the possible cause. Similarly, Soylu et al. [8] showed that in patients with STEMI and treated by primary PCI, postdilation reduced final coronary flow evaluated by cTFC and TIMI score in patients who did not have stent overexpansion. In contradiction to our results, in their retrospective study, which included 9000 STEMI patients, Fobert et al. [17] found that postdilation increased stent restenosis only in those patients in whom ticagrelor and prasugrel were not administered. On the other hand, a subsequent prospective study that included patients using ticagrelor and prasugrel showed the beneficial effect of postdilation on stent thrombosis and restenosis [18].

            There is overwhelming evidence that stent underexpansion is one of the major causes of stent thrombosis [19]. The underlying factors that can be associated with stent underexpansion include the techniques used during stent implantation, coronary vasospasm, and lesion characteristics [20]. Patients with ACS are particularly susceptible to coronary vasospasm because of increased local inflammation, and thus stent deployment without use of intracoronary nitrate infusion is traditionally thought to increase stent underexpansion. In addition, the operator’s own experience can also impact the development or prevention of stent underexpansion. There are several strategies to reduce the risk of stent underexpansion, including determining the optimal stent length and size, dilation before stent deployment, and inflation of the stent balloon with maximal pressure. Incomplete stent apposition (ISA) is another important factor for optimal stent implantation, and is classified as early and late. Procedural factors are primarily responsible for early ISA, while degenerations in the lesion and stent are responsible for late ISA. The incidence of ISA was found to be as low as 4% and as high as 20% in studies conducted with intravascular ultrasonography [21]. The discrepant results were considered to be due to different stent deployment techniques, distinct stent structures, and different clinical conditions [22]. Adverse events associated with ISA were milder than those associated with incomplete stent expansion, and the risk of stent thrombosis was lower [20]. In the TAXUS study, the incidence of MACE was not increased in patients with acute ISA during 12–24 months of follow-up [23].

            Despite favorable outcomes of postdilation with regard to stent malapposition, the same is not applicable to clinical outcomes. Moreover, adverse cardiovascular outcomes were reported as were favorable outcomes with postdilation. In the SIRUS study, stent restenosis was significantly higher at the edges of the stent in patients to whom postdilation had been performed [24]. Similarly, it was shown that postdilation increased neointimal hyperplasia and subsequent restenosis in studies conducted in both animals and humans [25]. However, these data should be interpreted with caution as postdilation was most commonly used in long and calcific lesions, which could neutralize potential favorable outcomes.

            A possible explanation for the controversial results regarding the effect of postdilation on cardiovascular outcomes is the lack of the standardization of the technique and of patient selection. When (in which case) and how (at what pressure) to perform postdilation is decided arbitrarily by operators in accordance with their clinical experiences. Performing unnecessary and/or high-pressure postdilation causes adverse outcomes. On the other hand, withholding postdilation when deemed necessary could also cause adverse events. Further research is needed to define in which patients and for which lesions postdilation is needed and at what pressures noncompliant balloons should be inflated. In the present study, the current coronary lesion classification was used but it fell short for guidance to identify patients who would benefit most from postdilation. Moreover, it is reasonable to suggest not performing postdilation because of lack of standardization of the technique and of patient/lesion selection and lack of clinical evidence.


            The present study was a nonrandomized, single-center study with a limited number of patients.


            In patients who were treated by PCI for ACS, performing postdilation did not predict final TIMI flow grade, cTFC, MBG, or MACE.

            Conflicts of interest

            The authors declare that they have no conflicts of interest.


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            Author and article information

            Cardiovascular Innovations and Applications
            Compuscript (Ireland )
            January 2020
            March 2020
            : 4
            : 3
            : 185-193
            [1] 1Department of Cardiology, Faculty of Medicine, Recep Tayyip Erdoğan University, Rize, Turkey
            [2] 2Department of Cardiology, Recep Tayyip Erdoğan Education and Research Hospital, Rize, Turkey
            [3] 3Department of Cardiology, Kaçkar State Hospital, Rize, Turkey
            [4] 4Department of Cardiology, Atatürk Education and Research Hospital, İzmir Katip Çelebi University, İzmir, Turkey
            Author notes
            Correspondence: Hakan Duman, MD, Department of Cardiology, Faculty of Medicine, Recep Tayyip Erdoğan University, 53100 Rize, Turkey, Business Tel.: +90 464 2130491, Fax: +90 464 2170364, E-mail: drhakanduman@ 123456hotmail.com
            Copyright © 2020 Cardiovascular Innovations and Applications

            This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 Unported License (CC BY-NC 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. See https://creativecommons.org/licenses/by-nc/4.0/.

            : 28 September 2019
            : 12 November 2019
            : 18 November 2019

            General medicine,Medicine,Geriatric medicine,Transplantation,Cardiovascular Medicine,Anesthesiology & Pain management
            postdilation,percutaneous coronary intervention,acute coronary syndromes


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