Early application of an intra-aortic balloon pump in patients with ST-segment elevation acute myocardial infarction scheduled for elective percutaneous coronary intervention

Abstract

Objective

This study evaluated the effect of early application of intra-aortic balloon pump (IABP) counterpulsation in patients with ST-segment elevation acute myocardial infarction (STEMI), scheduled for elective percutaneous coronary intervention (PCI).

Methods

Patients who had experienced STEMI for 12–72 h received (IABP group) or did not receive (control group) IABP counterpulsation for 3–5 days before PCI.

Results

One hundred patients were included. Frequencies of infarct-related artery thrombolysis in acute myocardial infarction (TIMI) flow rate classes 0, I and II in the IABP group (11.5, 1.9 and 7.7%, respectively) were significantly lower than in the control group (29.1, 14.6 and 22.9%, respectively) before PCI. After PCI, the frequency of TIMI class III flow rate in the IABP group (96.2%) was significantly higher than that in the control group (81.3%). Four weeks after PCI, the left ventricular ejection fraction (LVEF) was significantly higher, and the incidence of major cardiac events was significantly lower, in the IABP group compared with the control group.

Conclusions

Early use of IABP counterpulsation in STEMI patients scheduled for PCI was effective, with a favourable safety profile. IABP counterpulsation reduced the incidence of major adverse cardiac events and improved LVEF. However, IABP devices must be used at an early stage, to obtain optimal results.

Keywords

Intra-aortic balloon pump myocardial infarction transluminal angioplasty percutaneous coronary intervention

Introduction

Intra-aortic balloon pump (IABP) counterpulsation, as a secondary treatment, could improve left ventricular function. IABP counterpulsation is widely used for treating patients with clinically acute myocardial infarction (AMI) complicated by pump and heart failure, or in those experiencing cardiogenic shock.^1,2 IABP counterpulsation can improve diastolic blood pressure and coronary perfusion, and reduce cardiac afterload, thus effectively increasing cardiac output.³ Moreover, this treatment is commonly used as an effective means of support for patients with acute coronary artery disease.

The all-cause hospital mortality rate in AMI was 21.2% in a worldwide survey and the percentage of patients undergoing IABP counterpulsation was 11.6%.⁴ Currently, IABP counterpulsation is used mostly for supportive care, during and after percutaneous coronary intervention (PCI) and coronary artery bypass grafting, in patients with coronary heart disease complicated by cardiogenic shock and complex coronary lesions.⁵ For high-risk AMI patients, using IABP counterpulsation as a preventive treatment before revascularization provides better clinical results than not using this intervention.⁶ Therefore, the application of IABP treatment at an early stage after disease diagnosis and before PCI, in high-risk AMI patients, may provide considerable clinical benefit. The present study included a large number of AMI patients who had missed the opportunity of revascularization at the time of hospitalization. The effect of early application of IABP counterpulsation on the prognosis of AMI patients scheduled for PCI was evaluated by observing the effect of bedside IABP treatment on haemodynamics, coronary blood flow and incidence of major adverse cardiac events (MACEs).

Patients and methods

This study was conducted in accordance with the Declaration of Helsinki, and with the approval of the Ethics Committee of the First Affiliated Hospital of Henan Science and Technology University.

Patient recruitment and treatments

Patients were considered for inclusion in the study if they had ST-segment elevation acute myocardial infarction (STEMI), with no indications for thrombolysis, and were admitted to the Department of Cardiology, First Affiliated Hospital of Henan Science and Technology University, between January 2008 and May 2011.

The inclusion criteria were patient aged between 30 and 80 years and compliant with diagnostic criteria for AMI, with at least two of the following: (i) clinical history of ischaemic chest pain; (ii) dynamic evolution of the ECG; (iii) dynamic changes in myocardial necrosis marker concentrations. Furthermore, the onset of STEMI had to be within the previous 12–72 h, and there should not have been any experience of cardiogenic shock or indication for primary PCI and thrombolytic therapy.

The exclusion criteria were: clinically significant aortic insufficiency; aortic sinus aneurysm rupture; aortic dissection; coagulation disorders; cerebral haemorrhage; cardiogenic shock; other diseases (such as severe peripheral vascular disease, severe anaemia, irreversible brain damage and irreversible ventricular failure [terminal stage]).

All participants provided written informed consent to participate. They were randomly divided into two groups: those who received IABP treatment (experimental group); those who did not receive IABP treatment (control group). Both groups received care according to the standardized AMI treatment protocol, as follows. routine oral administration of clopidogrel at 75 mg/day, aspirin at 100 mg/day and atorvastatin at 20 mg/day; benazepril 5 mg/day and metoprolol tartrate (12.5 mg, twice-daily) were given to patients with high blood pressure (i.e. those with blood pressure ≥140/90 mmHg); dopamine (5 µg/kg/min, adjusted to maintain blood pressure at ≥90/60 mmHg) was administered intravenously to those with low blood pressure; coronary angiography and PCI were performed 10–14 days after AMI onset. The experimental group received IABP counterpulsation (described below) for 3–5 days at the bedside, early on during the period of drug therapy; the control group did not receive IABP treatment, or any kind of placebo equivalent.

For IABP counterpulsation, the patient underwent conventional femoral artery puncture using an 8 F sheath, and a 30–50-ml balloon was inserted into the left subclavian artery, reaching as far as the renal arteries. The IABP device was left in situ for 3–5 days according to the patient's condition; most patients received IABP counterpulsation for ≥3 days (but ≤5 days; the treatment period was extended if the blood pressure and heart rate were not stable at 3 days). Coronary angiography and PCI were performed once, 10–14 days after AMI. The left ventricular ejection fraction (LVEF) was measured by cardiac colour ultrasonography during the first week after AMI onset, and again at the end of the 4-week treatment period (Week 1 data are not included in this paper). The following observations were made: (i) infarct-related artery thrombolysis in acute myocardial infarction (TIMI) classification before and after PCI operation;⁷ (ii) LVEF at 4 weeks; (iii) incidence of MACEs 4 weeks after disease onset. MACEs included the following: (i) death from any cause; (ii) recent myocardial infarction, recurrent chest pain for ≥30 min accompanied by new ST–T changes within the previous ≥24 h or new Q waves (≥lead II, >0.03 S) with serum creatine kinase levels at least twice the upper limit of normal (normal creatine kinase levels were defined as 24–170 U/l [males] and 24–150 U/l [females]); (iii) refractory ischaemia with ST–T ischaemic changes (ST segment elevation or depression of 0.1 mV and T-wave inversion).

Statistical analyses

The independent-samples t-test was used to analyse continuous variables and the χ²-test was used to analyse categorical variables. The SPSS® statistical software package, version 17.0 (SPSS Inc., Chicago, IL, USA) was used for statistical analyses. P values <0.05 were considered statistically significant.

Results

One hundred patients met the criteria for study inclusion. Most of the patients had experienced an acute extensive AMI, or an acute inferior wall, posterior wall or right ventricular myocardial infarction. The experimental group comprised 52 patients aged 66.8 ± 5.7 years (28 males and 24 females); the control group comprised 48 patients aged 67.1 ± 5.4 years (25 males and 23 females).General characteristics of the patients in the two groups showed no statistically significant differences (Table 1).

Table 1.

General characteristics of patients with ST-segment elevation acute myocardial infarction (STEMI), treated or not treated with an intra-aortic balloon pump (IABP); IABP treatment and control groups, respectively.

Variable	IABP treatment group n = 52	Control group n = 48
Age, years	66.8 ± 5.7	67.1 ± 5.4
Males/females	28/24	25/23
Risk factors, cases
Smoking	27 (51.9)	25 (52.1)
Hypertension	35 (67.3)	32 (66.7)
Diabetes	20 (38.5)	19 (39.6)
Hyperlipidaemia	20 (38.5)	19 (39.6)
Interval from STEMI onset to hospitalization, h	18.5 ± 2.8	19.1 ± 2.1
Systolic blood pressure, mmHg	98.5 ± 9.1	97.8 ± 9.7
Diastolic blood pressure, mmHg	46.5 ± 7.8	47.6 ± 7.2
Extensive myocardial infarction of anterior wall	28 (53.8)	26 (54.2)
Myocardial infarction under posterior wall of right ventricle	24 (46.2)	22 (45.8)
Left ventricular dysfunction, Killip class⁸
I	5 (9.6)	4 (8.3)
II	29 (55.8)	27 (56.3)
III	18 (34.6)	17 (35.4)
IV	0	0
LVEF, %	37.8 ± 5.2	38.4 ± 4.8

Data presented as n (%) or mean ± standard deviation.

None of the differences between groups was statistically significant (P ≥ 0.05).

Statistical analyses undertaken with independent-samples t-test (continuous variables) and χ²-test (categorical variables).

LVEF, left ventricular ejection fraction.

The percentages of patients with TIMI flow classes 0, I and II were lower in the experimental group than in the control group before PCI (P < 0.05, all comparisons; Table 2). The percentages of patients with infarct-related artery TIMI grade III flow class (before and after PCI) in the experimental group was significantly higher than that in the control group (P < 0.05 for both comparisons; Table 2). Four weeks after PCI, the experimental group had significantly higher LVEF, and a significantly lower incidence of MACEs, compared with the control group (P < 0.05 for both variables; Table 2).

Table 2.

Efficacy and safety of reperfusion therapy with an intra-aortic balloon pump (IABP) device, in two groups of patients with ST-segment elevation acute myocardial infarction (STEMI); IABP treatment and control groups, respectively.

Variable	IABP treatment group n = 52	Control group n = 48	Statistical significance
TIMI class before PCI, n, %
0	6 (11.5)	14 (29.1)	P = 0.028
I	1 (1.9)	7 (14.6)	P = 0.020
II	4 (7.7)	11 (22.9)	P = 0.033
III	41 (78.8)	16 (33.3)	P = 0.000
TIMI class after PCI, n, %
I	0	0
II	2 (3.8)	9 (18.8)	P = 0.017
III	50 (96.2)	39 (81.3)	P = 0.017
Major adverse cardiac events 4 weeks after PCI, n, %
Refractory ischaemia	3 (5.8)	9 (18.8)	P = 0.046
Recent STEMI	0	0
Death	0	0
Total	3 (5.8)	9 (18.8)	P = 0.046
LVEF,%, 4 weeks after PCI	56.2 ± 7.6	42.4 ± 5.2	P < 0.01

Data presented as n (%) or mean ± standard deviation.

Statistical analyses undertaken using χ²-test (all variables except LVEF) or independent-samples t-test (LVEF).

TIMI, thrombolysis in acute myocardial infarction;⁷ PCI, percutaneous coronary intervention; LVEF, left ventricular ejection fraction.

Discussion

The use of IABP counterpulsation in AMI patients with severe haemodynamic impairment has increased over the past few years. These devices provide support for a useful period of time after coronary artery revascularization, and constitute an effective complementary measure for treating AMI patients experiencing cardiogenic shock. Accumulating clinical experience and evidence from small-scale studies have extended the indications for IABP counterpulsation,^9.10 and the prophylactic use of an IABP device before revascularization provides better clinical results for high-risk patients, compared with no prophylactic use.^9,10 Therefore, to experience the optimal effect of IABP counterpulsation, the IABP device needs to be used early in the disease process, rather than as the last resort.^9.10

The working principle of IABP counterpulsation is that the balloon inflates rapidly in diastole, causing a small amount of blood to flow into the lower limbs and kidneys. Most of the blood refluxes, which increases blood pressure in the brain and coronary diastolic aortic root, and also increases coronary blood flow and collateral circulation. When the aortic valve opens during left ventricular isovolumic systole, the balloon suddenly deflates and the aortic pressure suddenly drops. This process results in a ‘hole’ effect, resulting in reductions in left ventricular ejection resistance, left ventricular afterload, left ventricular wall tension, and left ventricular work and oxygen consumption. Under conditions of stable myocardial contraction, increases in cardiac output, cardiac index, heart, brain, renal artery and peripheral blood flow perfusion and urine output are observed, whereas myocardial oxygen consumption decreases.¹¹

Some researchers believe that the early use of prophylactic IABP counterpulsation in AMI patients could improve coronary collateral blood circulation, reduce wall tension, improve myocardial oxygen supply and cardiac haemodynamics, prevent myocardial injuries and improve cardiac function.³ IABP counterpulsation can increase aortic diastolic pressure to 100 mm Hg, increase coronary perfusion and increase cardiac output by 20%, without affecting left ventricular low-resistance ejection, thus reducing myocardial oxygen consumption.^12–17

The present study investigated the effect of the timing of IABP application in patients with an onset of STEMI within the previous 12–72 h, who did not have indications for thrombolysis or emergency interventional therapy (which may have affected the patient's prognosis, following AMI). The experimental group had significantly higher infarct-related artery recanalization rates than the control group, based on TIMI class data (Table 2). TIMI flow classifications after PCI also improved significantly in these patients, compared with the flow classifications observed in the control group. Moreover, cardiac function in the experimental group (assessed using LVEF, 4 weeks after early use of IABP counterpulsation) was better than that observed in the control group. The incidence of adverse cardiac events in the experimental group was also lower than that in the control group, and the difference was statistically significant (Table 2).

In the present study, the percentages of patients with TIMI flow classes 0–II were lower, and the percentage with TIMI grade III was higher, in the experimental group compared with the control group, before PCI. This indicates that early application of IABP could increase the recanalization rate of infarcted vessels. The mechanism underlying this phenomenon is that IABP counterpulsation increases diastolic pressure at the aortic root and the perfusion pressure of the coronary artery. This, together with anticoagulation and antiplatelet treatment, increases diastolic pressure at the aortic root and perfusion pressure of the coronary artery. The higher number of patients with TIMI flow grade III in infarct-related vessels in the experimental group, compared with the control group, was presumably attributable to an increased recanalization rate of infarct-related vessels under the action of mechanical force: both groups received the same drug-treatment regimens. Furthermore, the finding that, after PCI, the experimental group had a higher percentage of patients with TIMI class III compared with the control group may be correlated with a lower incidence of microembolization in the experimental group, after PCI.¹⁸ This is presumably because IABP counterpulsation increased the recanalization rate of infarcted vessels, preoperatively. Studies have shown that IABP treatment decreases the incidence of ‘no reflow’ and ‘slow flow’ after PCI. ‘No reflow’ or ‘slow flow’ are very common post-PCI phenomena in patients with large areas of AMI, in whom their incidence is between 0.6% and 2%.¹⁸ However, the mechanism underlying the occurrence of ‘no reflow’ or ‘slow flow’ remains controversial.¹⁸ It is assumed that the obstruction of distal blood capillaries is caused by coronary artery microthrombi, with plaque debris being the major mechanism of ‘no reflow’. Morishima et al.¹⁹ found that a decrease in LVEF, in addition to left ventricular dilatation and reconstruction, led to an increase in MACE events. Experimental research (involving a canine model of coronary artery occlusion) has shown that the use of an IABP device can increase diastolic coronary artery flow, improve myocardial tissue perfusion and reduce the area of no reflow caused by microvascular obstruction, thereby improving heart function.²⁰

With the intensive research on IABP counterpulsation that has been carried out, the application of IABP devices has gone beyond the scope of their original indications.^1,2 The early use of an IABP device, post-AMI, can stabilize haemodynamics, increase coronary perfusion and improve cardiac function in patients.^10,21–24 In cardiogenic shock, high-dose dopamine therapy has to be maintained for blood recirculation; if it is not, the opportunity to save the patient might be lost. Consequently, the authors advocate early application of IABP. The use of IABPs must be regulated, contraindications must be recognized and the rate of operational complications must be reduced, if the optimal effects of early IABP counterpulsation are to be realised. Use of IABP devices must be vigorously promoted for treating patients with AMI, in order to increase their survival rates.

Footnotes

Acknowledgements

This study was supported by the Scientific and Technological Project of Henan Province Health Department, China.

Declaration of conflicting interest

The authors had no conflicts of interest to declare in relation to this article.

Funding

This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.

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