The intra-aortic balloon pump (IABP) is the most commonly used temporary cardiac assist device. It has immediate beneficial hemodynamic effects, augmenting coronary perfusion, increasing myocardial oxygen supply and decreasing myocardial oxygen demand. In the setting of acute myocardial infarction, left ventricular unloading by an IABP could prevent early infarct expansion, ventricular remodeling, or both.1
Although used widely in the setting of cardiogenic shock,2–6 the use of aortic counterpulsation in non-shocked, but high-risk, patients remains uncertain. Although it has been shown to be of some benefit in some patients undergoing rescue angioplasty,7,8 other high-risk patients do not appear to have a clear advantage. There remains a debate about which high-risk patient might warrant adjunctive treatment during percutaneous coronary intervention (PCI). Moreover, it remains uncertain whether it is better to use an IABP at the beginning of the procedure, during the procedure, or at the end of the procedure. As well as identifying which patient benefits, it is also necessary to understand the mechanism of benefit.
We wished to investigate the impact of IABP use in a defined group of patients and hypothesized that the use of an IABP following angioplasty may increase coronary blood flow and hence preserve left ventricular function.
Patient selection. The Local Research Ethics Committee, the Radiation Protection Adviser and the Research and Development Committee of our institution approved the study protocol. The study population was drawn from patients undergoing emergency or urgent angiography (ST-elevation and non-ST-elevation myocardial infarction) with a view to angioplasty who fulfilled the randomization criteria. The study was carried out in a tertiary cardiac center. Written consent for participation in the study was obtained from all patients.
Risk assessment and randomization. Following PCI, high-risk patients were defined by one or more of a number of clinical, angiographic and electrocardiographic variables:
1. Patients who were hypotensive with a blood pressure (BP) of < 100 mmHg (but excluding cardiogenic shock);
2. Patients who were tachycardic with a pulse rate > 100 beats per minute;
3. Patients with TIMI 0, 1, or 2 flow post procedure;
4. Persistent ST-elevation post procedure;
5. Evidence of left ventricular failure, i.e., clinical evidence of pulmonary edema, with low oxygen saturation.
Exclusion criteria. The following patients were excluded from the study:
1. Age > 80 years;
2. Cardiogenic shock, defined by hypotension (systolic BP < 90 mmHg); oliguria and poor peripheral perfusion with or without pulmonary edema;
4. Absent peripheral arterial access;
5. Concurrent serious illness (e.g., advanced metastatic disease, end-stage chronic obstructive airways disease or renal or hepatic disease);
6. Inability to comply with the protocol or give informed consent;
7. Aorto-iliac atherosclerotic disease prohibiting IABP use;
8. Patients with known aortic regurgitation;
9. Patients with a history of bleeding diathesis;
10. Stroke within the past 2 years or permanent neurological deficit.
Any patient with coronary anatomy unsuitable for immediate angioplasty in whom an IABP was clinically indicated pending surgical revascularization or deferred PCI (e.g., unstable left main or severe triple-vessel disease requiring coronary artery bypass graft surgery) was also not included.
Intra-aortic balloon pumping. The preferred system was the Datascope 8 Fr sheathless balloon (Datascope® Medical Co. Ltd, Cambridgeshire, United Kingdom) and introducer package. The IABP catheter was inserted percutaneously via the femoral artery. Following insertion of the device, the IABP was used on a 1:1 ratio with full augmentation. Repeat angiography was obtained 10 minutes after the completion of the procedure. The IABP was left in situ for up to 48 hours where possible. If the patient was intolerant of the IABP due to back and groin discomfort, the IABP was removed earlier.
Quantitative coronary angiography and TIMI frame count. Coronary angiography was performed using a Philips DCI-SX Integris Monoplane system (Philips Medical Systems, Andover, Massachusetts). Quantitative coronary angiography was performed using the Philips Inturis Suite R2.2 commercial software by the radiographer in-charge of the case. Angiography was performed at 12.5 frames per second using hand-injection of contrast. Determination of frame counts was carried out by the method described previously.9 TIMI frame counting was measured using a Philips Inturis Suite R2.2 by an independent, experienced observer (KV).
In addition, TIMI flow grade (TFG)10 and myocardial blush grade (MBG)11 were assessed on the angiograms that were taken pre-PCI, immediately post-PCI and 10 minutes after the end of the procedure. Intracoronary nitrate (200 μg) was used 60 seconds before all angiograms were obtained for analysis.
Other investigations. Blood samples were taken for determination of full blood count, glucose, urea, electrolytes, cholesterol, creatine kinase (CK) and Troponin T (TNT). Subsequently, CK was measured at 6, 12 and 24 hours following the procedure. Troponin T was measured on admission, and at 12 and 24 hours. Twelve-lead electrocardiograms (ECGs) were recorded on arrival, immediately post-angioplasty and subsequently at 3, 6, 12, 24, 48 hours, and just prior to discharge.
Echocardiography. Transthoracic echocardiography was performed the day after angioplasty. Digital cine loops were stored in standard parasternal long-axis, short-axis and apical 2- and 4-chamber views. Repeat echocardiography was undertaken at day 30.
Definitions. Successful PCI was defined as < 50% residual stenosis assessed by quantitative coronary angiography and TIMI grade 3 flow. Re-infarction after PCI for ST-elevation myocardial infarction (STEMI) was defined as chest pain associated with ST-segment re-elevation and an increase in cardiac enzymes (x 3 creatine kinase release). Standardization of medical treatment and follow up.
Standard medical care was offered to all patients following PCI. Medications such as glycoprotein IIb/IIIa inhibitors were used at the discretion of the attending cardiologist. All patients received aspirin and unfractionated heparin prior to PCI. Where possible, patients were loaded with 300 mg of clopidogrel before angioplasty (otherwise, it was given immediately post-PCI). During intervention, the activated clotting time (ACT) was maintained at 250–300 seconds, and following PCI, the ACT was maintained between 175–200 seconds. At 30 days, the New York Heart Association (NYHA) and Canadian Cardiovascular Society (CCS) status were assessed. Clopidogrel was continued for 1 month following the procedure where non-drug-eluting stents were used. When a drugeluting stent was used, clopidogrel therapy was continued for up to 1 year at the discretion of the attending cardiologist.
Primary endpoints. Improvement in the corrected TIMI frame count 10 minutes postprocedure.
a. Improvements in left ventricular wall motion index at day 1 and 30 days postprocedure;
b. Speed and extent of ST-segment recovery (during hospitalization);
c. Ischemic endpoints: recurrent chest pain post-angioplasty, recurrent chest pain with ECG changes, unplanned repeat angiography or PCI within the first 30 days, ventricular tachycardia, ventricular fibrillation or atrial fibrillation and need for emergency coronary artery bypass surgery;
d. Hemodynamic endpoints: heart failure (defined as two out of the following: (i) shortness of breath or low oxygen saturation; (ii) bibasal inspiratory crackles or (iii) typical chest X-ray appearance) and diuretic requirements (expressed as total daily dose of furosemide or equivalent);
e. Bleeding and vascular complications;
f. All-cause mortality.
The SPSS statistical software, version 11 (SPSS, Inc., Chicago, Illinois) was used to perform all statistical calculations. Continuous variables are expressed as mean ± standard deviation, and the categorical variables are expressed as numbers and percentages. Forall tests, a value of p < 0.05 was considered statistically significant.
A chi-square test was used to compare categorical variables. Fisher’s exact test was used where a chisquare test was not applicable. An independent samples t-test was used to compare continuous variables between the two arms. Wilcoxon Signed Ranks test was used to compare nonparametric data. A Kaplan- Meier survival analysis was used to measure 30-day event-free survival in both study arms.
A sample size of 30 patients in each arm would allow demonstration of a 25% reduction in corrected TIMI frame count using the IABP device with a power close to 0.9. We originally planned for 70 patients with an interim analysis after 35 patients were enrolled, but performed the latter after 33 patients. The study was terminated after this analysis, as the primary hypothesis could not be demonstrated by the trial protocol.
Baseline characteristics. The baseline characteristics of the study patients are shown in Table 1. There was no significant difference in the baseline characteristics between the two study arms, except patients in the no-IABP arm were heavier, p = 0.04. In total, 65% of patients received a glycoprotein IIb/IIIa inhibitor (Reopro® [abciximab], Eli Lilly, Hampshire, United Kingdom) in the IABP arm, and 75% in the no-IABP arm, p = 0.7. All patients were taking aspirin and clopidogrel at the time of discharge. The patients with STEMI in this study underwent PCI 426.4 ± 332.5 minutes (IABP arm) and 298.6 ± 159.5 minutes (no-IABP arm), p = 0.2, following the onset of chest pain. The IABP was inserted immediately after the completion of the PCI procedure. The IABP was placed in situ for 39.7 ± 14.9 hours (minimum 24 hours, maximum 72 hours).
There was no significant difference in the heart rate, systolic and diastolic blood pressure (BP) pre-PCI, post-PCI and after randomization between the two arms (Table 2). In patients who received an IABP, the assisted systolic BP was 92.1 ± 16.8 mmHg, and the augmented diastolic BP was 119.2 ± 23.5 mmHg.
Angiographic characteristics. The angiographic characteristics of the culprit arteries are shown in Table 2. All patients underwent stent implantation.
There were no significant differences in the angiographic parameters between the two arms in both the culprit and the nonculprit coronary arteries.
There was a significant improvement in the TFC and MBG post-PCI. There was an improvement in the TFC after randomization in both the arms (IABP arm: 21.8 ± 22 and 19.9 ± 23 post-PCI and post-randomization, respectively; p = 0.03; no-IABP arm: 20 ± 19.3 and 16.9 ± 16.9; p = 0.012). However, the mean difference in the TFC between the two arms was not statistically significant (mean difference 0.38, 95% CI -3.7 to 2.9; p = 0.8). There was significant improvement in the MBG after randomization in the IABP arm (2.29 ± 0.9 and 2.5 ± 0.9; p = 0.046) compared to the no-IABP arm (2.25 ± 0.7 and 2.5 ± 0.7; p = 0.08) post-PCI and post-randomization, respectively. However, the mean difference in the MBG was not significant between the two arms (mean difference 0.021, 95% confidence interval -0.3 to 0.3; p = 0.9 in both arms).
Other tests. The creatine kinase measured at 6, 12 and 24 hours was lower in the IABP arm compared to the no-IABP arm, although these differences were not statistically significant, p = 0.6, 0.2 and 0.5, respectively (Table 3). There was no significant difference in the ECG parameters between the two arms (Table 4). There was no significant difference between the two arms in an analysis of percentage ST-segment resolution post-PCI. In total, 13 (76%) patients had complete resolution of ST-segments in the IABP arm compared to 12 (75%) patients in the no-IABP arm 48 hours after the PCI procedure (p = 1).
Echocardiographic data. There was no significant difference in the wall motion index between the two arms (IABPvs. no-IABP) measured at day 1 and day 30, p = 0.7 and 0.9, respectively (Table 4). The infarct artery segmental score did not differ between the two groups at days 1 and 30, p = 0.6 and 0.07, respectively.
Clinical outcome. There were no significant hemorrhagic complications in either of the study arms. In total, 6 events occurred in 4 patients in the IABP arm and 2 events occurred in 1 patient in the no-IABP arm; p = 0.2. During hospitalization, 2 patients (12%) died in the IABP arm compared to none in the no-IABP arm. One patient in the IABP arm underwent emergency coronary artery revascularization after reinfarction in the same territory. During the PCI procedure, 1 patient in the IABP arm (this patient also subsequently developed heart failure) and another patient in the no- IABP arm (this patient subsequently underwent coronary angiography which showed that the treated vessel was patent) developed ventricular fibrillation requiring cardioversion.
At 30 day follow up, another patient in the IABP arm died after suffering multiple ventricular fibrillation (VF) arrests, and another patient underwent repeat PCI for reinfarction. There was no significant difference in the CCS and NYHA scores between the two arms. The majority of the patients in both arms were in CCS and NYHA Class I (CCS I: 93% and 88%; NYHA I: 79% and 56%, IABP and no-IABP arms, respectively). There was no significant difference in the cumulative 30- day event-free survival between the two groups, with a trend towards a worse outcome in the IABP group (p = 0.09). A summary of the endpoints is shown in Table 5.
The main finding of this randomized study is that the use of an IABP in this subset of high-risk patients following PCI (virtually all in the setting of STEMI) was not associated with a significant immediate improvement in coronary blood flow in the culprit and the nonculprit coronary arteries immediately following PCI. In addition, there was no demonstrableimprovement in left ventricular function, ST-segment recovery and overall clinical outcome.
There are theoretical benefits of using an IABP in a high-risk population of patients. The augmentation of diastolic aortic pressure during balloon inflation, in theory, should increase coronary arterial blood flow, particularly in subjects with coronary arterial hypoperfusion, because most coronary arterial flow occurs during left ventricular (LV) diastole.12 Several studies in critically ill patients suggest that an IABP may be beneficial in those with impaired coronary arterial autoregulation.13 However, in the setting of a fixed, severe coronary arterial stenosis (> 90% luminal diameter narrowing), the IABP-induced increase in aortic diastolic pressure is not transmitted to the vessel’s poststenotic segment; as a result, poststenotic coronary blood flow is unchanged,13 but can increase flow once the stenosis has been treated by angioplasty. Moreover, an increase in diastolic flow could prevent closure of an intimal flap after coronary angioplasty and could also prevent recurrent thrombus formation.
In a randomized study of prophylactic IABP use in patients undergoing emergency cardiac catheterization during the first 24 hours after acute MI, there was a significantly lower event rate in patients assigned to aortic counterpulsation in terms of a composite clinical endpoint (death, stroke, reinfarction, need for emergency revascularization with angioplasty or bypass surgery, or recurrent ischemia).14 Patients with significant obstruction of the epicardial arteries (% stenosis > 75%) were excluded from the study. In this study, patients were randomized to an IABP or standard therapy at the end of the angioplasty procedure. In the current study utilizing stents, glycoprotein IIb/IIIa inhibitors and thienopyridines, only 1 patient in the IABP arm developed reocclusion in the infarct-related artery and none in the no- IABP arm.
In other studies of so-called high-risk angioplasty, the advantages of an IABP have not been so evident. Studies have determined the impact of prophylactic IABP use after primary percutaneous transluminal coronary angioplasty (PTCA) in acute MI. In contrast to previous studies, Stone et al demonstrated that a strategy of prophylactic IABP use after primary PTCA in hemodynamically stable high-risk patients did not decrease the rates of infarct-related artery reocclusion or reinfarction, neither did it promote myocardialrecovery or improve clinical outcome.15
Brigouri et al, in a nonrandomized study, demonstrated that prophylactic use of IABP support among high-risk patients (in particular, females with LV systolic function, ejection fraction ≤ 30% and high jeopardy score) undergoing PCI was associated with a better early outcome than patients with provisional hemodynamic support.16 The same group recently demonstrated in a nonrandomized study that prophylactic use of IABP in elective, unprotected left main stenting contributes to an uncomplicated and successful outcome, especially in patients with Euroscore > 6 plus bifurcation lesions.17
Mishra et al investigated in a nonrandomized study the outcomes of high-risk patients who received a prophylactic IABP (P-IABP) versus patients who required rescue IABP (RIABP) because of intraprocedural complications. At 6 months, the mortality and major adverse cardiac event rates were lower in the P-IABP group than the R-IABP group (8% vs. 29%; p < 0.01, and 12% vs. 32%; p = 0.02, respectively). Multivariate analysis showed that prophylactic insertion of an IABP was the only independent predictor of survival at 6 months.18 There are a number of differences between their study and the current study. First, their study was not randomized. Criteria for high-risk PCI included one of the following: (1) acute coronary syndrome with hemodynamic stability; (2) clinical congestive heart failure; (3) LV ejection fraction less than (or equal to) 30%; (4) multivessel disease; (5) left main intervention; (6) PCI of one of more saphenous vein graft lesions; and (7) pulmonary capillary wedge pressure > 15 mmHg and/or mean pulmonary artery pressure > 50 mmHg. No-reflow or slow-flow was present in 5–10% of their study population, whereas in the present study, 29% of the study population had slow-flow.
The IABP is associated with risks of its own and inconvenience for the patient. If an IABP is to be used in specific situations, it is important to understand the actual, rather than theoretical, mechanisms of benefit, and define a high-risk population for which one can demonstrate that the additional expense and inconvenience of an IABP is associated with an improved clinical outcome. Defining a high-risk group is difficult, especially as stenting and a greater use of glycoprotein IIb/IIIa inhibitors and thienopyridines have improved the efficacy and safety of PCI. It is possible that these adjuncts may provide a greater benefit to the patients than an IABP, and thus previous studies of the use of an IABP in the setting of balloon angioplasty showing a lower incidence of reocclusion after infarct angioplasty may have no relevance in the stent era.
Previous studies have shown that stenting significantly improves the TFC compared to balloon angioplasty alone.19 As all patients in this study received stents, it is possible that the IABP would not make a further impact on this measure, at least in the short term. However, some patients were enrolled in the setting of slow-flow, even in the presence of a stent, and using the TFC has the advantage of demonstrating improvement in flow, even when it appears normal. In other studies, including a previous study from our group, minor and subtle changes in coronary flow can be identified using the TFC method in the setting of an acute coronary syndrome, even when there is angiographic evidence of TIMI flow grade 3.20
Our patient group was clearly high risk, but they were not in cardiogenic shock, a group in whom there is a general consensus that an IABP should be used (although there are no randomized trials in this context). However, even in such high-risk groups, the potential benefits of stenting may outweigh any benefit of an IABP. Although our protocol was not intended to be specifically a study of patients with STEMI, that is what it has in effect turned out to be, although patients were undergoing a variety of procedures including primary PCI, rescue PCI and PCI for reinfarction.
The mechanism and magnitude of benefit (if there is any) of an IABP in these patients have not yet been established. Our study was specifically designed to demonstrate early improvement in flow, and that this improvement would be reflected in LV recovery. Our results would suggest that either there is no benefit of an IABP in these patients, or that the timing of insertion of an IABP is an issue, or that our primary outcome measure was not the best means of demonstrating benefit, if it exists. The ultimate study would be based on clinical endpoints, but would almost certainly require a large number of patients to show benefit.
It is worth noting that our study did not demonstrate improvement in other parameters or other surrogates. However, it was not powered for these, and there are some slight trends that could help design a study to look at this in more detail, perhaps concentrating on ST-resolution, total ST scores over time, area under the curves (AUC) of enzyme or biomarker profiles and imaging techniques to establish perfusion and LV function over time.
In trying to determine the impact of an IABP, clinical benefit should be demonstrated, but the mechanism of achieving benefit should also be understood. Given that an IABP changes a number of hemodynamic parameters, it is possible that the use of the TFC 10 minutes after the procedure is not the ideal way of demonstrating how such benefit is achieved. However, the changes that occur with an IABP should lead to improved coronary flow (in the absence of a stenosis). Our study was always designed as a mechanistic study, not an outcomes study. The hypothesis was that in the high-risk patients we enrolled, an IABP would lead to a clinically meaningful increase in coronary flow early after PCI, and that this would influence LV recovery.
Many interventionists believe that an IABP improves coronary flow immediately after PCI, even with stenting, and it was on the basis of this belief that we powered and performed the study. We accept the view that perhaps coronary flow does improve, but later, and that the current study could not evaluate the latter possibility. To evaluate this would have required additional follow-up angiography or possibly the useof noninvasive means such as Doppler contrast echocardiographic studies (suitable only for patients with left anterior descending artery lesions). Nevertheless, we can conclude that in the population tested, the use of an IABP does not lead to a significant increase in early flow, probably because of issues relating to the microcirculation.
Angiography in our study was performed after the administration of intracoronary nitrate. We have previously shown that intracoronary nitrate increases the reference diameter and increases the TFC.21 In the current study, we did not see an improvement in coronary flow. This might be because any theoretical benefit of IABP is nullified by either the use of intracoronary nitrates or, more likely, by high downstream intravascular pressures (secondary to nitrate-resistant distal vasoconstriction, vascular edema, embolization, etc). We did not routinely measure the end diastolic pressures in our patient population. It is possible that these patients had a high end-diastolic intraventricular pressure that was not influenced significantly in the early phase by an IABP.
In addition to identifying which patients might best be treated with an IABP, the best timing of the use of the device also has to be determined. In our study, as with others, we randomized after PCI. We found no benefit and terminated the study when the interim analysis demonstrated that we would not be able to prove the primary hypothesis. It would be of interest to repeat the study using the IABP prior to PCI. We performed repeat angiography 10 minutes after randomization. Although we might have seen benefits if we had performed repeat angiography at other time intervals after randomization, we saw no benefits in terms of LV recovery, nor in ECG changes over the first 30 days. The definite time period and the duration of insertion of IABP that provides maximum benefit to patients are not known. Previous studies have used IABP pre-PCI, during PCI or after the completion of the PCI procedure. We might have seen some benefit if we had randomized the patients prior to PCI. There might be theoretical advantages by allowing distal vasodilatation and improving ventricular performance during the PCI itself. We also removed the IABP after 24–48 hours, and it is possible that a longer period might be needed to gain clinical benefits, although longer duration of use increases the risk of bleeding and other arterial complications.22
The fact that we did not see an improvement in early coronary flow does not mean that an IABP would not benefit some patients, as it might have an influence on ventricular remodeling, but this has not yet been satisfactorily proven, and the duration of IABP therapy that would influence this is not known. The overall results, however, do question the potential benefits of the IABP in these circumstances and stress the importance of further research. A large cohort of patients involving a large multicenter trial would be required to demonstrate a clinical effect, but other mechanistic studies using other surrogates might allow us to tease out some of these issues with smaller cohorts of patients. To date, there are no randomized trials involving this cohort of patients in the modern PCI era. However, there are retrospective studies showing some benefit in terms of clinical endpoints with the use of an IABP. These studies have a number of limitations as described above.
Currently, a multicenter study (the Balloon pump assisted Coronary Intervention Study [BCIS-1] study) is underway in the United Kingdom to determine the benefit of an IABP prior to the start of PCI in patients with poor LV function and those with a large area of myocardium at risk. This trial however, is different from that of the present study in that it does not include patients with STEMI. The BCIS study includes patients with an ejection fraction < 35%, patients undergoing multivessel angioplasty and those patients who have a large area of myocardium at risk in an elective setting. Therefore, the results of the BCIS-1 trial would not be applicable to patients undergoing PCI in the setting of an acute MI.
An experienced, independent observer measured the angiographic parameters including the TFG, TFC and MBG. One could argue that the observer could tell whether the patient received an IABP or not on the angiograms. However, we do not believe this would have significantly altered our findings. We have previously demonstrated the reproducibility of TFC (intra- and interobserver variability) in our laboratory.9 We also demonstrated the reproducibility of the wall motion index between observers in a previous study.20
Our results do not mean that intracoronary flow does not improve at a later stage of recovery. Nor do our results imply that an IABP does not have clinical utility in this context. The small size of the study makes it impossible to make meaningful comments regarding clinical outcomes, especially as early termination of the study resulted in numerical differences in some of the clinical parameters that might be important. Our results simply mean that if an IABP does have a therapeutic role in these circumstances, it does not achieve benefit by an early increase in coronary flow.
Whether an IABP is of any benefit in non-shocked, but high-risk, patients undergoing PCI remains to be established, but any potential benefit does not appear to be associated with early improvement in coronary flow. Whether insertion of an IABP improves coronary flow beyond 10 minutes is not known. An IABP did not significantly affect subsequent LV wall motion index or ECG ST-segment resolution in this study.
Acknowledgments. We are grateful to the staff in the cardiac catheterization laboratory and coronary care unit at the James Cook University Hospital for their efforts in the undertaking of this study.
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