Occurrence of moderate-to-severe pericardial effusion (PE; ≥10 mm), cardiac tamponade (CT), and sudden electromechanical dissociation (EMD) was investigated in 4,361 patients with ST-elevation myocardial infarction from 1993 to 2011 in 3 different periods: 1993 to 2000 (n: 1,488); 2001 to 2008 (n: 1,844); and 2009 to 2011 (n: 1,014). Their predictors, including the use of no reperfusion therapy (n: 1,186), thrombolysis (n: 1,607), or primary percutaneous coronary intervention (PPCI, n: 1,562), were also evaluated. Incidence of PE (8.7%, 6.8%, and 5.0%), CT (5.0%, 2.9%, and 1.9%), and EMD (3.7%, 1.7%, and 1.0%), declined over the 3 periods as did mortality (12.0% 8.2%, and 5.9%) with different rates of thrombolytic therapy (52%, 37%, and 14%) and PPCI (7%, 38%, and 76%; all p <0.001). In patients treated without reperfusion therapy, thrombolysis, and PPCI, incidence of PE (12.0%, 5.7%, and 4.3%), CT (6.0%, 3.0%, and 2.2%), and EMD (4.1%, 2.2%, and 0.8%) was different as was mortality (14.4%, 8.3%, and 5.9%; all p <0.001). Independent predictors of PE were lateral infarction (odds ratio [OR] 4.09, 95% confidence interval [CI] 2.57 to 6.49), increasing age (OR 1.05, 95% CI 1.04 to 1.07), number of electrocardiographic leads involved (OR 1.34, 95% CI 1.23 to 1.45), and admission delay (OR 1.01, 95% CI 1.01 to 1.02). Increasing ejection fraction (OR 0.97, 95% CI 0.96 to 0.98), thrombolysis (OR 0.53, 95% CI 0.37 to 0.75), and PPCI (OR 0.35, 95% CI 0.25 to 0.50), however, were protectors (all p <0.001). Lateral infarction, age, number of leads involved, ejection fraction, thrombolytic therapy, and PPCI were also predictors/protectors of CT and EMD. In conclusion, PE, CT, and EMD rates in patients with ST-elevation myocardial infarction have objectively fallen in the last 2 decades, and their predictors are lateral site, increasing age, number of leads involved, and lack of reperfusion therapy. Late hospital admission is also a relevant predictor of PE.
Cardiac tamponade (CT) and moderate-to-severe pericardial effusion (PE; ≥10 mm) are life-threatening complications in patients with ST-elevation myocardial infarction (STEMI). Although it has been reported that thrombolysis may reduce the rate of CT due to cardiac rupture, some investigators have disputed this beneficial effect and have claimed that it may increase its occurrence. There are also indications of a lower rate of free wall rupture with primary percutaneous coronary intervention (PPCI) than with thrombolysis. In all these studies, however, the effects of reperfusion therapy on development of PE, CT, or electromechanical dissociation (EMD), as objectively assessed by echocardiography, have not been evaluated. More importantly, predictors of these events have also not been analyzed. Thus, the purpose of this study was to prospectively investigate the incidence of PE, CT, and EMD in patients with STEMI during the last 19 years; their incidence in different reperfusion strategies, namely, no reperfusion therapy, thrombolysis, or PPCI; and their independent predictors.
Methods
We included 4,502 patients with STEMI admitted to our institution from January 1993 to December 2011. Excluded were 29 with PE associated with right ventricular perforation by a pacing catheter or a coronary artery rupture during PPCI, and 112 because of inadequate echocardiogram. Thus, 4,361 patients were finally included. Diagnosis of STEMI was based on concurrence of ST-elevation ≥1 mm in ≥2 leads other than aVR with chest pain or symptoms compatible with acute heart failure or unexplained syncope.
A 2-dimensional transthoracic echocardiagram was performed within 12 hours of admission to the Coronary Care Unit to assess ejection fraction and PE. It was often repeated before discharge and, systematically, in patients who developed hypotension, cardiac arrest, or who had a PE in the initial echocardiogram. Ejection fraction was calculated by the Simpson’s method, and PE was measured at end-diastole at the parasternal long-axis view and graded in millimeters as the summation of anterior and posterior effusions.
Thrombolysis with alteplase or tenecteplase within 6 hours from symptom onset was the main reperfusion treatment since 1993, but it was gradually substituted by PPCI within 12 hours. Reasons for no reperfusion therapy were no strict ST-elevation criteria (n: 511, 43%), late hospital arrival (>12 hours, n: 380, 32%), both (n: 154, 13%), or medical contraindications for thrombolysis or PPCI (n: 142, 12%). Aspirin was given to all patients and heparin to those without reperfusion therapy or treated with thrombolysis, whereas thyenopyridines were administered to patients with PPCI. CT was diagnosed in patients who developed EMD or hypotension (≤90 mm Hg) associated with jugular venous distention, pulsus paradoxus ≥15 mm Hg, and PE with compression of the right heart cavities. EMD was defined as sudden cardiac arrest with preserved electrical rhythm, no acute QRS changes, and absence of progressive shock. The cause of death was categorized as (1) cardiogenic shock, when it followed progressive nonarrhythmic hypotension due to hypocontractility; (2) ventricular fibrillation or refractory ventricular tachycardia; (3) EMD, when associated with CT documented echocardiographically or when it occurred in patients with previous PE without a final echo or necropsy study; and (4) noncardiac, when ascribable to other causes. Free wall rupture was diagnosed in 125 patients with PE: 64 dying of EMD with CT by echocardiography, 34 by necropsy, and 27 by thoracotomy.
We compared clinical, electrocardiographic, and echocardiographic variables, the occurrence of PE, CT, or EMD, and the clinical outcome of patients admitted in 3 time periods 1993 to 2000, 2001 to 2008, and 2009 to 2011. The last interval was shorter, but it coincided with a sharp increase in STEMI admissions and the use of PPCI. We also compared patients without reperfusion therapy, thrombolysis and PPCI, and those with and without PE, CT, and EMD. Student t test for continuous variables with normal distribution and the Mann-Whitney U test for variables non-normally distributed were used. The chi-square or the Fisher’s exact test was performed for categorical variables, the analysis of variance with Bonferroni corrections for continuous variables of ≥3 subsets with normal distribution, and the Kruskal-Wallis test for variables non-normally distributed. For comparisons over time, we performed linear regression analysis for continuous variables with normal distribution and the Jonckheere-Tergstra test for those non-normally distributed. A multivariable logistic regression analysis examined the predictive value of variables associated with PE, CT, and EMD in a univariate analysis. The analysis was performed with SPSS 15.0; data are expressed as mean ± SD; and differences considered significant at p <0.05.
Results
Patients admitted during 1993 to 2000 (n: 1,490) showed higher rate of diabetes (28% vs 23% and 23%, p <0.001) and Killip class ≥II (24% vs 17% and 19%, p <0.001) and a lower rate of reperfusion therapy (59% vs 74% and 90%, <0.001) and PPCI (7% vs 38% and 76%, p <0.001) than those admitted during 2001 to 2008 (n: 1,852) or 2009 to 2011 (n: 1,019). Patients without reperfusion therapy showed a higher prevalence of diabetes, peripheral vascular disease, and longer admission delay than those treated with thrombolysis or PPCI. Also, they had lesser ST elevation, number of leads involved, and worse Killip class. Moreover, they were less frequently treated with β blockers and shared rates of treatment with heparin with patients treated with thrombolysis, whereas patients with PPCI were more often treated with thyenopyridines, glycoprotein IIb/IIIa inhibitors, and angiotensin-converting enzyme inhibitors ( Table 1 ). PE, CT, and EMD rates fell through the 3 time intervals ( Figure 1 ) and were higher in patients without reperfusion therapy than in those treated with thrombolysis or PPCI being lowest in the latter ( Figure 2 ). Differences in CT (p = 0.012) and EMD (p = 0.001) between thrombolysis and PPCI groups were also significant but not in PE (p = 0.073).
| Variable | No Reperfusion Therapy (n: 1,187) | Thrombolytic Therapy (n: 1,610) | PPCI (n: 1,564) | p Value |
|---|---|---|---|---|
| Age (yrs) | 64.5 ± 12.4 | 61.0 ± 12.2 | 63.1 ± 13.5 | <0.001 |
| Women | 298 (25) | 290 (18) | 344 (22) | <0.001 |
| Hypertension | 593 (50) | 739 (46) | 812 (52) | 0.003 |
| Diabetes | 367 (31) | 354 (22) | 344 (22) | <0.001 |
| Active smoking | 471 (40) | 817 (51) | 737 (47) | <0.001 |
| PVD | 160 (14) | 174 (11) | 136 (9) | <0.001 |
| Killip class ≥II | 894 (75) | 1,320 (82) | 1,270 (81) | <0.001 |
| Admission delay (h) | 16.0 ± 24.5 | 3.3 ± 2.3 | 5.9 ± 8.9 | <0.001 |
| Infarct site | <0.001 | |||
| Inferior | 640 (54) | 858 (53) | 771 (49) | |
| Anterior | 431 (36) | 697 (43) | 707 (45) | |
| Lateral | 116 (10) | 55 (3) | 86 (6) | |
| Max STE admission (mm) | 1.6 ± 1.3 | 4.2 ± 2.6 | 3.5 ± 2.6 | <0.001 |
| Leads with STE | 4.0 ± 1.7 | 5.1 ± 1.5 | 5.0 ± 1.6 | <0.001 |
| Ejection fraction | (n: 1,078) | (n: 1,485) | (n: 1,516) | |
| 50.4 ± 11.3 | 50.5 ± 10.2 | 50.6 ± 18.8 | 0.975 | |
| Treatment | ||||
| β blockers | 952 (80) | 1,369 (85) | 1,340 (86) | <0.001 |
| Nitrates | 1,161 (98) | 1,597 (99) | 1,543 (99) | 0.019 |
| ACE inhibitors | 460 (39) | 519 (32) | 710 (45) | <0.001 |
| Aspirin | 1,181 (100) | 1,600 (99) | 1,562 (100) | 0.051 |
| Heparin | 1,169 (99) | 1,610 (100) | 42 (3) | <0.001 |
| Thyenopyridines | 21 (2) | 259 (16) | 1,383 (88) | <0.001 |
| Glycoprotein IIb/IIIa inhibitors | 4 (0.3) | 13 (1) | 1,334 (85) | <0.001 |
| Postinfarction angina | 230 (19) | 255 (16) | 39 (3) | <0.001 |
| Reinfarction | 49 (4) | 48 (3) | 9 (1) | <0.001 |
| Pericarditis | 109 (9) | 103 (6) | 69 (4) | <0.001 |
| Cardiac rupture | 116 (10) | 53 (3) | 26 (2) | <0.001 |
| FWR | 65 (6) | 38 (2) | 22 (1) | |
| Septal | 36 (3) | 15 (1) | 2 (0.1) | |
| Papillary muscle | 15 (1) | 0 | 2 (0.1) | |
| Surgery for cardiac rupture | 48 (4) | 13 (1) | 6 (0.4) | <0.001 |
| CABG | 28 (2) | 8 (1) | 12 (1) | <0.001 |
| Hospital mortality, global | 171 (14) | 133 (8) | 92 (6) | <0.001 |
| Cardiac | 151 (13) | 110 (7) | 67 (4) | |
| Shock | 95 (8) | 61 (4) | 50 (3) | |
| VT/VF | 10 (1) | 17 (1) | 4 (0.3) | |
| EMD | 46 (4) | 32 (2) | 13 (1) | |
| Noncardiac | 20 (2) | 23 (1) | 25 (2) | |
Mortality and the proportion of patients dying of EMD also declined over time ( Figure 1 ). Mortality for PE with or without CT or EMD was 40% (124/311), 70% (105/150) for CT, and 88% (96/109) for EMD. Patients without reperfusion therapy showed the highest mortality and patients with PPCI showed the lowest ( Figure 2 ), and differences with thrombolytic therapy or PPCI groups were more significant (p <0.001) than between patients treated with thrombolysis and those treated with PPCI (p = 0.010). Furthermore, mortality associated with EMD was also highest in patients without reperfusion therapy and lowest in those with PPCI. Differences between patients without reperfusion therapy and the thrombolysis group (p = 0.004) and between the latter and the group with PPCI (p = 0.007) were also significant. The rate of cardiac rupture was significantly higher in patients without reperfusion therapy than in the other 2 groups (p <0.001) and were also higher in the thrombolysis than in the group with PPCI (p = 0.003). Similar differences were observed with regard to free wall rupture (p <0.001 and p = 0.051, respectively, Table 1 ).
Patients with PE were older than those without, were more frequently women, and presented higher incidence of diabetes, peripheral vascular disease, lateral infarction, longer admission delay, higher ST elevation and number of leads involved, and lower ejection fraction. They also showed higher rate of adverse events. However, they were less frequently treated with β blockers, nitrates, thyenopyridines, and glycogen IIb/IIIa inhibitors and received more frequently heparin. Similar differences in clinical features, treatment, and outcomes were observed between patients with and without CT and between those with and without EMD ( Table 2 ). Among patients with coronary angiography, isolated lateral infarctions (n: 136) were more often associated with the left circumflex as a culprit artery than the anterior (n: 1,057) or inferior (n: 1,158) sites (54% vs 1% and 22%, respectively). In the multivariable analysis, independent predictors of PE were age, lateral infarction, number of leads involved, and admission delay, whereas increasing ejection fraction, thrombolysis, and PPCI were protectors. The same variables were predictors of CT and EMD, although admission delay showed lesser degree of significance for CT and was not predictor of EMD ( Table 3 ).
| Variable | PE ≥10 mm | p Value | Cardiac Tamponade | p Value | Electromechanical Dissociation | p Value | |||
|---|---|---|---|---|---|---|---|---|---|
| No (n: 4,050) | Yes (n: 311) | No (n: 4,211) | Yes (150) | No (n: 4,252) | Yes (109) | ||||
| Age (yrs) | 62.1 ± 12.8 | 70.5 ± 10.1 | <0.001 | 62.4 ± 12.8 | 71.6 ± 8.7 | <0.001 | 62.5 ± 12.8 | 73.3 ± 7.9 | <0.001 |
| Women | 826 (20) | 107 (35) | <0.001 | 881 (21) | 51 (34) | <0.001 | 891 (21) | 41 (38) | <0.001 |
| Hypertension | 1,984 (49) | 159 (53) | 0.135 | 2,074 (49) | 70 (49) | 0.956 | 2,099 (49) | 45 (49) | 0.959 |
| Diabetes | 976 (24) | 93 (30) | 0.020 | 1,019 (24) | 47 (31) | 0.049 | 1,034 (24) | 31 (32) | 0.086 |
| Active smoking | 1,932 (48) | 90 (29) | <0.001 | 1,979 (47) | 46 (31) | <0.001 | 1997 (47) | 25 (26) | <0.001 |
| PVD | 423 (10) | 47 (15) | 0.009 | 448 (11) | 23 (16) | 0.057 | 454 (11) | 17 (18) | 0.024 |
| Killip class ≥II | 3,303 (82) | 182 (55) | <0.001 | 3,407 (81) | 77 (51) | <0.001 | 3,430 (81) | 54 (56) | <0.001 |
| Admission delay (h) | 7.0 ± 13.6 | 16.1 ± 24.2 | <0.001 | 7.3 ± 14.2 | 16.6 ± 24.4 | <0.001 | 7.5 ± 14.5 | 14.8 ± 21.1 | <0.001 |
| Infarct site | <0.001 | <0.001 | <0.001 | ||||||
| Inferior | 2,150 (53) | 119 (39) | 2,209 (53) | 60 (40) | 2,226 (52) | 43 (44) | |||
| Anterior | 1,685 (42) | 150 (48) | 1,773 (42) | 62 (42) | 1,798 (42) | 37 (38) | |||
| Lateral | 215 (5) | 42 (14) | 230 (5) | 27 (18) | 240 (6) | 17 (18) | |||
| Max STE admission (mm) | 3.0 ± 2.5 | 3.6 ± 2.6 | 0.027 | 3.0 ± 2.5 | 3.5 ± 2.6 | 0.017 | 3.0 ± 2.5 | 3.5 ± 2.4 | 0.536 |
| Leads with ST elevation | 4.7 ± 1.7 | 5.3 ± 1.9 | <0.001 | 4.7 ± 1.7 | 5.4 ± 2.0 | <0.001 | 4.7 ± 1.7 | 5.3 ± 2.0 | 0.021 |
| Ejection fraction | (n: 3,797) | (n: 282) | (n: 3,956) | (n: 123) | (n: 4,009) | (n: 70) | |||
| 50.8 ± 10.6 | 45.4 ± 10.7 | <0.001 | 50.6 ± 10.7 | 44.5 ± 10.8 | <0.001 | 50.5 ± 10.7 | 46.3 ± 10.0 | 0.001 | |
| Treatment | |||||||||
| β blockers | 3,435 (85) | 222 (72) | <0.001 | 3,558 (85) | 101 (67) | <0.001 | 3,589 (84) | 72 (74) | 0.008 |
| Nitrates | 4,005 (99) | 296 (96) | <0.001 | 4,161 (99) | 140 (94) | <0.001 | 4,211 (99) | 89 (92) | <0.001 |
| ACE inhibitors | 1,582 (39) | 104 (36) | 0.255 | 1,647 (39) | 41 (29) | 0.017 | 1,667 (39) | 22 (24) | 0.005 |
| Aspirin | 4,033 (100) | 310 (100) | 0.795 | 4,194 (100) | 149 (99) | 0.622 | 4,247 (100) | 96 (99) | 0.337 |
| Heparin | 2,591 (64) | 231 (74) | <0.001 | 2,708 (64) | 114 (76) | 0.003 | 2,741 (64) | 80 (83) | <0.001 |
| Thyenopyridines | 1,586 (39) | 77 (25) | <0.001 | 1,638 (39) | 24 (16) | <0.001 | 1,651 (39) | 12 (12) | <0.001 |
| Glycoprotein IIb/IIIa inhibitors | 1,289 (32) | 61 (20) | <0.001 | 1,326 (32) | 25 (16) | <0.001 | 1,339 (31) | 11 (11) | <0.001 |
| Reperfusion | |||||||||
| NRT | 1,041 (26) | 145 (47) | <0.001 | 1,110 (26) | 76 (51) | <0.001 | 1,137 (27) | 49 (51) | <0.001 |
| Thrombolytic therapy | 1,515 (37) | 97 (31) | 0.033 | 1,561 (37) | 49 (33) | 0.302 | 1,574 (37) | 36 (37) | 0.934 |
| PPCI | 1,495 (37) | 69 (22) | <0.001 | 1,539 (37) | 25 (17) | <0.001 | 1,552 (36) | 12 (12) | <0.001 |
| Postinfarction angina | 433 (11) | 70 (24) | <0.001 | 462 (11) | 44 (30) | <0.001 | 480 (11) | 25 (26) | <0.001 |
| Reinfarction | 77 (2) | 22 (8) | <0.001 | 83 (2) | 17 (12) | <0.001 | 89 (2) | 11 (12) | <0.001 |
| Pericarditis | 191 (5) | 88 (30) | <0.001 | 233 (6) | 48 (34) | <0.001 | 262 (6) | 18 (20) | <0.001 |
| Cardiac rupture | 66 (2) | 129 (42) | <0.001 | 75 (1.8) | 120 (80.0) | <0.001 | 97 (2.3) | 98 (90) | <0.001 |
| FWR | 0 (0) | 125 (40) | 7 (0.2) | 118 (79) | 31 (0.7) | 94 (86) | |||
| Septal | 49 (1.2) | 4 (1.3) | 51 (1.2) | 2 (1.3) | 49 (1.2) | 4 (3.7) | |||
| Papillary muscle | 17 (0.4) | 0 (0) | 17 (0.4) | 0 (0) | 17 (0.4) | 0 (0) | |||
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