We evaluated the relation between reperfusion indexes and right ventricular (RV) dysfunction in patients with inferior ST-segment elevation myocardial infarction (STEMI). We included patients with inferior STEMI undergoing percutaneous coronary intervention and right coronary artery as infarct-related artery. Myocardial reperfusion was evaluated by Thrombolysis In Myocardial Infarction (TIMI) flow, TIMI frame count, myocardial blush grade, and ST-segment resolution. RV dysfunction was defined as tricuspid annular plane systolic excursion ≤16 mm in M-mode imaging. RV dysfunction was present in 58 of 141 patients (41.1%) and was more frequent in patients achieving suboptimal postprocedural TIMI flow grade (66.7% vs 36.7%, grades 0 to 2 vs 3, p = 0.01), TIMI frame count (63.2% vs 37.7%, ≥40 vs <40 frames, p = 0.04), and myocardial blush grade (33.3% vs 56.2%, grade 0 or 1 vs 2 or 3, p = 0.001). RV dysfunction rates did not differ according to ST-segment resolution. Patients with RV dysfunction had increased rates of cardiac death (13.2% vs 2.6%, p = 0.03), reinfarction (24.5% vs 10.3%, p = 0.03), and stent thrombosis (22.6% vs 6.4%, p = 0.01) at 2-year follow-up. Postprocedural TIMI flow grade 3 (odds ratio 0.25, 95% confidence interval 0.09 to 0.68, p = 0.007) was the only reperfusion correlate of RV dysfunction at multivariate analysis. In an independent cohort of 84 patients with STEMI, postprocedural TIMI flow grade 3 had a limited sensitivity (52%), with a high specificity (74.5%) and negative predictive value (71%) for excluding RV dysfunction. In conclusion, in patients with inferior STEMI undergoing coronary revascularization, RV dysfunction is associated with a worse long-term prognosis. Postprocedural TIMI flow grade may be a useful tool to predict RV dysfunction.
Despite therapeutic advances during the last decades, adverse events still occur in a substantial proportion of patients with ST-segment elevation myocardial infarction (STEMI). Autopsy findings showed that right ventricular (RV) involvement is observed in up to 50% of patients with inferior STEMI. Several studies demonstrated that patients with STEMI experiencing RV dysfunction have a poor prognosis, with increased mortality rates. In patients with inferior STEMI, RV dysfunction has been associated to an infarct-related lesion within the proximal right coronary artery (RCA) segment. However, despite the salutary effects of a successful coronary revascularization on RV function, the influence of reperfusion results achieved with percutaneous coronary intervention (PCI) on the risk of RV dysfunction still remains poorly understood. Therefore, the aim of the present study was to investigate the relation between reperfusion outcomes and RV dysfunction, as assessed by transthoracic echocardiography, in patients with inferior STEMI undergoing primary or rescue PCI, as well as the long-term clinical impact of RV dysfunction.
Methods
This retrospective study was conducted at a single tertiary care center from 2008 to 2013. Patients with STEMI undergoing primary or rescue PCI after failed fibrinolysis were eligible if all inclusion criteria were met: onset of symptoms <12 hours before PCI; ST-segment elevation ≥0.1 mV in 2 contiguous inferior leads II, III, or aVF ; and RCA as the infarct-related artery at baseline coronary angiography. All patients received dual antiplatelet therapy with aspirin and clopidogrel (300 to 600 mg) or prasugrel (60 mg) loading dose. Periprocedural anticoagulation consisted of intravenous unfractionated heparin (70 IU/kg) in all cases. PCI with stent implantation was performed according to guidelines. Clopidogrel (75 mg/day) or prasugrel (10 mg/day) was prescribed for at least 1 year and aspirin (100 mg) indefinitely. Pre- and post-procedural Thrombolysis In Myocardial Infarction (TIMI) flows, TIMI frame counts (TFC), and myocardial blush grade (MBG) were assessed by 2 independent observers. A cut-off value of 40 frames was used for TFC. Major RV branch was defined as the greatest branch (≥1 mm) arising from RCA and pre- and post-procedural TIMI flows were evaluated, as previously described. Complete ST-segment resolution was defined as a reduction of ≥70% in the summed 12-lead extent of ST-segment elevation from baseline to the postprocedural electrocardiogram, which was recorded within 90 minutes after the first balloon inflation. Patients underwent standard 2-dimensional echocardiographic study within 48 hours after PCI and underwent imaging while lying in left lateral decubitus with a digital ultrasonic device system (Vivid 7; General Electric-Vingmed Ultrasound, Horten, Norway). Analysis was performed offline by an independent observer using a dedicated software (EchoPAC PC, version 8.0.0; General Electric-Vingmed). Standard echocardiographic analysis was performed as previously described. RV dysfunction was defined according to American Society of Echocardiography guidelines as tricuspid annular plane systolic excursion (TAPSE) ≤16 mm, using M-mode imaging. Therefore, patients were categorized into 2 groups: patients with (TAPSE ≤16 mm) or without RV dysfunction (TAPSE >16 mm). Echocardiographic study of the RV function was completed by the assessment of systolic and diastolic RV diameters, RV fractional area change, and inferior vena cava diameter and its collapse with inspiration. Cardiac biomarkers levels were measured on admission and then every 6 hours for at least 72 hours after PCI. Myocardial infarct size was defined according to peak creatine kinase, creatine kinase-MB, and cardiac troponin T levels. The following clinical end points were evaluated: cardiac death, reinfarction, and stent thrombosis, according to Academic Research Consortium criteria. All deaths were considered cardiac unless an unequivocal noncardiac cause was established. Reinfarction was defined according to the third universal definition of myocardial infarction. Stent thrombosis was reported as the composite of definite, probable, and possible stent thrombosis. In-hospital clinical events were carefully recorded, and postdischarge follow-up included outpatient visit or telephone interview using a standard questionnaire. Continuous variables are presented as mean ± SD whereas categorical variables as counts and percentages. The normality of distribution of continuous variables was evaluated by the Kolmogorov-Smirnov goodness-of-fit test and therefore compared with independent sample Student t or Mann-Whitney U test. Categorical variables were compared with chi-square statistic or Fisher’s exact test as appropriate. Exploratory multivariate analysis was conducted based on the correlates of RV dysfunction at binary logistic regression analysis. The final model included the variables associated with RV dysfunction in univariate analysis. Binary stepwise logistic regression analysis was used to assess independent predictors of RV dysfunction. Kaplan-Meier analysis was performed to assess rates of clinical events in the 2 study groups. A p value of <0.05 was considered statistically significant. Statistical analysis was performed using IBM SPSS 20.0 (IBM Corp., Armonk, New York).
Results
A total of 141 consecutive patients (mean age 60.7 ± 11.4 years, 77.3% men) were enrolled in this study. Two-year clinical follow-up was available in 131 of 141 patients (92.9%). RV dysfunction, defined as TAPSE ≤16 mm, was found in 58 of 141 patients (41.1%). Baseline clinical characteristics were similar between patients with and without RV dysfunction ( Table 1 ). Table 2 summarizes angiographic characteristics. There were no significant differences in baseline angiographic characteristics between the 2 groups, although preprocedural TFC was higher in patients with RV dysfunction than in those without. Table 3 lists echocardiographic findings. Mean TAPSE was 12.7 ± 2.2 mm in patients with RV dysfunction compared with 18.18 ± 2.4 mm in patients without RV dysfunction (p <0.001). Consistently, RV fractional area change was significantly lower in patients with RV dysfunction. Patients with postprocedural TIMI flow grade 3 had lower RV dysfunction rates in comparison with patients with postprocedural TIMI flow grade 0 to 2 ( Figure 1 ). RV dysfunction was observed in 46 patients (37.7%) with TFC <40 compared with 12 of 19 patients (63.2%) with TFC ≥40 (p = 0.04). No significant differences in RV dysfunction rates were noted between patients with postprocedural TIMI flow grade 3 compared with TIMI flow grade 0 to 2 in the major RV branch. Postprocedural MBG 2 or 3 was achieved in 93 patients (66%), and RV dysfunction occurred less frequently in this group than in patients with MBG 0 or 1 (33.3% vs 56.2%, p = 0.001). There was no significant difference in RV dysfunction rates between patients achieving complete (≥70%) versus incomplete (<70%) ST-segment resolution. As shown in Figure 2 , RV dysfunction was associated with a larger infarct size. At 2-year follow-up, RV dysfunction was associated with a higher risk of death (13.2% vs 2.6%, odds ratio 5.6, 95% confidence interval 1.2 to 27.2, p = 0.03), reinfarction (24.5% vs 10.3%, odds ratio 2.7, 95% confidence interval 1.1 to 6.3, p = 0.03), and stent thrombosis (22.6% vs 6.4%, odds ratio 3.7, 95% confidence interval 1.3 to 10.6, p = 0.01; Figure 3 , panels A to C). Follow-up echocardiography was available in 70 patients (49.6%) at a mean follow-up of 59 ± 30 days. Despite a similar rate of RV dysfunction (40%), the difference in RV dysfunction between postprocedural TIMI flow grade 3 versus 0 to 2 groups increased: 20 patients (33.3%) versus 8 patients (80%), respectively (p = 0.008). Using a stepwise forward regression model, the only independent predictor of RV dysfunction was postprocedural TIMI flow grade 3 ( Table 4 ). To evaluate the clinical application of this angiographic tool, the sensitivity, specificity, positive predictive value, and negative predictive value of TIMI flow grade (0 to 2 vs 3) was determined to predict RV dysfunction in an independent cohort of 84 patients with inferior STEMI ( Supplementary Table 1 ). Postprocedural TIMI flow grade 3 had a limited sensitivity (52%), with a high specificity (74.5%) for excluding RV dysfunction. Positive predictive value was 57% and negative predictive value was 71%.
| Variable | Overall Population (n = 141) | Right Ventricular Dysfunction | p Value | |
|---|---|---|---|---|
| Yes (n = 58) | No (n = 83) | |||
| Age (years) | 60.7 ± 11.4 | 62.6 ± 11.9 | 59.3 ± 10.9 | 0.09 |
| Male | 109 (77.3%) | 46 (79.3%) | 63 (75.9%) | 0.63 |
| Hypertension | 80 (56.7%) | 33 (56.9%) | 47 (56.6%) | 0.97 |
| Dyslipidemia | 63 (44.7%) | 23 (39.7%) | 40 (48.2%) | 0.32 |
| Current smoker | 82 (58.2%) | 33 (56.9%) | 49 (59%) | 0.8 |
| Diabetes mellitus | 39 (27.7%) | 17 (29.3%) | 22 (26.5%) | 0.71 |
| Insulin-treated | 17 (12.1%) | 6 (10.3%) | 11 (13.3%) | 0.60 |
| Obesity | 46 (32.6%) | 16 (27.6%) | 30 (36.1%) | 0.29 |
| Previous myocardial infarction | 22 (15.6%) | 9 (15.5%) | 13 (15.7%) | 0.98 |
| Previous percutaneous coronary intervention | 12 (8.5%) | 5 (8.6%) | 7 (8.4%) | 0.97 |
| Previous coronary artery bypass grafting | 3 (2.1%) | 1 (1.7%) | 2 (2.4%) | 0.78 |
| Chronic kidney disease | 9 (6.4%) | 4 (6.9%) | 5 (6%) | 0.83 |
| Heart rate (beats per minute) | 78.1 ± 13.4 | 78.2 ± 13.8 | 78.1 ± 13.2 | 0.95 |
| Time from symptoms onset to percutaneous coronary intervention (hours) | 6.4 ± 6.8 | 5.9 ± 3.35 | 6.8 ± 8.4 | 0.46 |
| Door to balloon time (minutes) | 74 ± 17 | 72 ± 16 | 75 ± 18 | 0.31 |
| Type of percutaneous coronary intervention | 0.62 | |||
| Primary | 67 (47.5%) | 29 (50%) | 38 (45.8%) | |
| Rescue | 74 (52.5%) | 29 (50%) | 45 (54.2%) | |
| Temporary pacemaker | 31 (22%) | 17 (29.3%) | 14 (16.9%) | 0.08 |
| In-hospital therapy | ||||
| Beta-blocker | 89 (63.1%) | 37 (63.8%) | 52 (62.7%) | 0.89 |
| ACE inhibitor/AT-1 antagonist | 86 (61%) | 37 (63.8%) | 49 (59%) | 0.57 |
| Aspirin | 135 (95.7%) | 55 (94.8%) | 80 (96.4%) | 0.65 |
| Clopidogrel | 131 (92.9%) | 53 (91.4%) | 78 (94%) | 0.55 |
| Prasugrel | 10 (7.1%) | 5 (8.6%) | 5 (6.1%) | 0.57 |
| Statin | 124 (87.9%) | 48 (82.8%) | 76 (91.6%) | 0.11 |
| Glycoprotein IIb/IIIa inhibitor | 44 (30%) | 17 (29.3%) | 27 (32.5%) | 0.71 |
| Variable | Overall Population (n = 141) | Right Ventricular Dysfunction | p Value | |
|---|---|---|---|---|
| Yes (n = 58) | No (n = 83) | |||
| Multivessel coronary disease | 87 (61.7%) | 36 (62.1%) | 51 (61.4%) | 0.94 |
| Coronary lesion location | 0.06 | |||
| Proximal | 55 (39%) | 29 (50%) | 26 (31.3%) | |
| Mid | 63 (44.7%) | 23 (39.7%) | 40 (48.2%) | |
| Distal | 23 (16.3%) | 6 (10.3%) | 17 (20.5%) | |
| Reference vessel diameter (mm) | 3.26 ± 0.4 | 3.3 ± 0.4 | 3.24 ± 0.5 | 0.6 |
| Minimal lumen diameter (mm) | 0.09 ± 0.24 | 0.09 ± 0.3 | 0.09 ± 0.2 | 0.67 |
| Lesion length (mm) | 18.7 ± 8.8 | 18.7 ± 7.2 | 18.6 ± 9.8 | 0.23 |
| Calcified lesion | 35 (24.8%) | 15 (25.9%) | 20 (24.1%) | 0.81 |
| Visible thrombus | 133 (94.3%) | 54 (93.1%) | 79 (95.2%) | 0.71 |
| Major right ventricular branch involvement | 71 (50.4%) | 32 (55.2%) | 39 (47%) | 0.34 |
| Thrombectomy | 34 (24.1%) | 16 (27.6%) | 18 (21.7%) | 0.42 |
| Type of stent | 0.13 | |||
| Bare-metal stent | 113 (80.1%) | 50 (86.2%) | 63 (75.9%) | |
| Drug-eluting stent | 28 (19.8%) | 8 (13.8%) | 20 (24.1%) | |
| TIMI flow before percutaneous coronary intervention | 0.13 | |||
| 0 | 88 (62.4%) | 40 (69%) | 48 (57.8%) | |
| 1 | 14 (9.9%) | 7 (12.1%) | 7 (8.4%) | |
| 2 | 5 (3.5%) | 0 (0%) | 5 (6%) | |
| 3 | 34 (24.1%) | 11 (19%) | 23 (27.7%) | |
| TIMI flow in the major right ventricular branch before percutaneous coronary intervention | 0.24 | |||
| 0 | 55 (39%) | 36 (44.8%) | 29 (34.9%) | |
| 1 | 3 (2.1%) | 0 (0%) | 3 (3.6%) | |
| 2 | 5 (3.5%) | 3 (5.2%) | 2 (2.4%) | |
| 3 | 78 (55.3%) | 29 (50%) | 49 (59%) | |
| Variable | Overall Population (n = 141) | Right Ventricular Dysfunction | p Value | |
|---|---|---|---|---|
| Yes (n = 58) | No (n = 83) | |||
| Left ventricular end-systolic volume (ml) | 54.5 ± 19.5 | 56.3 ± 22.7 | 53.3 ± 16.9 | 0.81 |
| Left ventricular end-diastolic volume (ml) | 99.1 ± 26.4 | 98.7 ± 28.8 | 99.4 ± 24.8 | 0.88 |
| Left ventricular ejection fraction (%) | 45.5 ± 6.4 | 43.6 ± 7.4 | 46.8 ± 5.3 | 0.006 |
| Wall motion score index | 1.85 ± 0.4 | 2 ± 0.2 | 1.7 ± 0.5 | <0.001 |
| E/A ratio | 1 ± 0.4 | 1 ± 0.4 | 1.1 ± 0.4 | 0.28 |
| Deceleration time (ms) | 161.1 ± 43.8 | 152.5 ± 35 | 167 ± 48.3 | 0.06 |
| E/E′ | 11.8 ± 6.7 | 12.7 ± 8.8 | 11 ± 3.9 | 0.92 |
| Moderate or severe mitral regurgitation | 12 (8.5) | 6 (10.3) | 6 (7.2) | 0.55 |
| Moderate or severe tricuspidal regurgitation | 27 (20.5) | 13 (22.4) | 16 (19.2) | 0.2 |
| Left atrial volume index (ml/m 2 ) | 16.5 ± 6.2 | 17.1 ± 7.3 | 16.2 ± 5.9 | 0.51 |
| Right ventricular end-systolic volume (ml) | 39.5 ± 15.6 | 42.3 ± 18.5 | 37.7 ± 13.1 | 0.015 |
| Right ventricular end-diastolic volume (ml) | 21.8 ± 10.2 | 25.1 ± 12.3 | 19.6 ± 8 | 0.01 |
| Right ventricular end-systolic area (cm 2 ) | 18.2 ± 5 | 19 ± 5.9 | 17.6 ± 4.2 | 0.03 |
| Right ventricular end-diastolic area (cm 2 ) | 12 ± 3.3 | 13.1 ± 3.9 | 11.2 ± 2.6 | 0.005 |
| Right ventricular fractional area change (%) | 32.9 ± 12 | 29.1 ± 12.9 | 35.5 ± 10.8 | 0.01 |
| Tricuspid annular plane systolic excursion (mm) | 15.1 ± 3.6 | 11.9 ± 2 | 17.4 ± 2.5 | <0.001 |
| Inferior vena cava diameter (mm) | 18.6 ± 4.7 | 20.2 ± 4.8 | 17.4 ± 4.2 | <0.001 |
| Inferior vena cava collapse with inspiration (%) | 23.8 ± 28.2 | 16.2 ± 28.9 | 29.2 ± 26.5 | <0.001 |
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