Adenosine Conditioning and Pacing in Conjunction with Early
Intra-Aortic Balloon Pump Use and Glycoprotein IIb/IIIa
Inhibition

Cardiogenic shock complicating myocardial infarction carries a poor prognosis. Data regarding percutaneous intervention in the very elderly with cardiogenic shock is sparse.¹ Age is an independent risk factor for worse outcome with cardiogenic shock.¹ Few studies or registries include the very elderly with cardiogenic shock.^2,3 Improved TIMI (Thrombolysis In Myocardial Infarction) flow post-intervention provides a better outcome in this condition.⁴ Multivessel intervention is also independently prognostic of a worse outcome in cardiogenic shock.⁴ Right ventricular infarction with cardiogenic shock carries a similarly poor prognosis as left ventricular shock.⁵ Renal insufficiency may also have an impact on survival with cardiogenic shock.⁶

High-dose intracoronary adenosine has been demonstrated to precondition human myocardium during coronary angioplasty in an elective setting.^7,8 Adenosine has also improved coronary flow, as evaluated by TIMI frame count post-coronary intervention in an acute coronary syndrome setting, even with “normal” TIMI flow grade post-intervention.⁸ Intracoronary adenosine had also been shown to reduce myocardial reperfusion injury and infarct expansion in the setting of acute myocardial infarction.⁹ In the original AMISTAD trial, a 3-hour infusion of intravenous adenosine attenuated infarct size in anterior infarction, however, clinical outcomes were not significantly altered with this therapy in the AMISTAD-II trial.^10,11

This case describes the first reported use of adenosine and a temporary transvenous pacemaker in conjunction with intra-aortic balloon pump support and glycoprotein IIb/IIIa inhibition to allow for delivery of rapid-bolus intracoronary adenosine prior to each stent insertion in the setting of profound cardiogenic shock in a very elderly woman who underwent successful triple-vessel angioplasty, with salutary effect.

Case Report

An 87-year-old female presented after 3.5 hours of chest pain, rapid atrial fibrillation and an extensive infero-posterior and right ventricular infarction, with a systolic blood pressure of 60 mmHg. She received cardioversion twice without success. Dopamine was initiated, with improvement of systolic blood pressure to 80 mmHg. After a conversation regarding philosophy of care with the patient and family, the decision to proceed with invasive care was made.

Sheaths were inserted in both femoral arteries. Angiography demonstrated a proximally occluded right coronary artery (RCA) with TIMI 0 flow (Figure 1). The circumflex artery had a proximal critical 95–99% lesion with TIMI 2 flow (Figure 2). The left anterior descending artery (LAD) was severely obstructed in its proximal segment (75–80%) with TIMI 3 flow (Figure 2). Left ventricular angiography demonstrated mild mitral regurgitation with no obvious ventricular septal rupture. The patient’s ejection fraction was 24%.

A 7.5 Fr 34 cc intra-aortic balloon pump was inserted via the left femoral artery for stabilization. A JR4 guide was engaged in the right coronary ostium and a Pilot 50 was passed into the distal RCA. A 2.5 x 15 mm balloon was used to “dotter” and dilate the occluded vessel. Restoration of flow was complicated by ventricular tachycardia, which was cardioverted immediately, with return to sinus bradycardia. Although TIMI 3 flow was established, the lesion was extremely long. A temporary transvenous pacemaker was inserted at this point to allow administration of intracoronary adenosine with the hope of preventing slow flow (Figure 3). Two 120 μg boluses of adenosine were delivered rapidly via the guide catheter into the RCA, with the pacemaker as backup. Two bare-metal stents measuring 3.0 x 32 mm and 3.0 x 38 mm were deployed in an overlapping fashion with high-pressure postdilatation using a 3.5 x 15 mm balloon. An excellent result with brisk TIMI 3 flow was achieved (Figure 4). The patient’s mean arterial pressure improved from 54 mmHg to 76 mmHg. By this time, the patient’s available blood work demonstrated a creatine of 173 mmol (weight = 53.6 kg, creatine clearance of 17 ml/minute), further adding to the overall risk profile. At this point, after discussion with the patient and family, we decided to provide complete revascularization with further contrast use, understanding the risk of contrast nephropathy in lieu of further cardiac benefit.

The left main artery was engaged with a GL 3.5 6 Fr guide catheter, and the circumflex artery was dilated first with a 2.5 x 12 mm balloon. Next, a rapid 120 μg bolus of adenosine was administered via the guide catheter before placement of a 2.5 x 15 mm Vision stent at 20 atm. This resulted in excellent TIMI 3 flow in the circumflex artery (Figure 5). The LAD was then predilated using the same 2.5 x 12 mm balloon. After administration of another 120 μg of adenosine as a rapid intracoronary bolus, a 3.0 x 18 mm Vision stent was placed in the proximal LAD. This was further postdilated with a noncompliant Quantum 3.25 mm balloon at high pressure. Brisk TIMI 3 flow and an optimal angiographic result were achieved in the LAD as well (Figure 6).

The mean arterial pressure by the end of the procedure was 96 mmHg. The patient was weaned off dopamine and changed to dobutamine over the next 24 hours. Over the next 48 hours, the patient was also weaned off the intra-aortic balloon pump, transvenous pacemaker and inotropes. The patient recovered inhospital for another week, tolerating afterload reduction and ambulating well. Fortunately, her renal function remained stable and her creatine clearance was 19.4 ml/minute at discharge. An echocardiogram obtained 24 hours post-intervention demonstrated an ejection fraction of 30–40%. The right ventricle was moderately-to-severely hypokinetic with mild mitral regurgitation. At 1-month follow up, the patient was clinically symptomfree and living independently.

Discussion

This case demonstrates that complete multivessel revascularization can be accomplished with good effect on selected very elderly patients who have good pre-event function and desire aggressive care. We risk-stratified our patient according to the Hasdai et al risk prediction model, and the patient accumulated 202 points, which approximated an 80% risk of 30-day mortality.¹ This model, however, does not account for her significant renal dysfunction, which may add further to her morbidity and mortality risk.

Favorable characteristics for survival in our patient included an early presentation at 3.5 hours and efficient primary angioplasty. Early insertion of an intra-aortic balloon pump likely helped stabilize her hemodynamics. Previously reported literature indicates the benefit in outcomes of glycoprotein IIb/IIIa inhibitor use in the setting of cardiogenic shock.^13,14 Therefore, the early use of a glycoprotein IIb/IIIa inhibitor may have possibly improved our patient’s outcome as well. Although the need for multivessel angioplasty generally portends a worse prognosis, in our case, the completeness of revascularization may have improved left and right ventricular function sufficiently to achieve 30-day survival. The ability to successfully deliver sents in this setting may improve mortality and improve TIMI flow.¹⁴ The achievement of brisk TIMI 3 flow in interventionally treated vessels remains one of most critical factors in the prediction of survival to discharge and medium-term survival in patients with cardiogenic shock.⁴

There is some evidence demonstrating that the use of rapid-bolus or high-dose intracoronary adenosine improves flow characteristics in the setting of elective percutaneous intervention and acute coronary syndromes.^7,8 The use of an intracoronary bolus of adenosine has never been described on a prophylactic basis in the setting of cardiogenic shock. In the present case, we describe the insertion of a temporary transvenous pacemaker in the setting of an inferior and right ventricular infarction to allow us to deliver rapid-bolus adenosine to all 3 vessels. Adenosine has also been shown to inhibit neutrophil activity and accumulation and to improve microvascular function.¹² In animal and human studies, reduction in infarct size and improvement in coronary blood flow have been demonstrated with the use of bolus-infusion or intracoronary adenosine.^7–9

In this scenario, the likely determinants of survival were early presentation, the ability to perform complete revascularization in an expeditious manner, the early use of an intra-aortic balloon pump and the early use of glycoprotein IIb/IIIa inhibition. Although adenosine is clearly not the major reason for recovery in our patient, it may play a role in selected patients as an adjunctive agent for further improvement in microvascular perfusion in this critically ill population.

References

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2. Dzavik V, Sleeper LA, Picard MH, et al. Outcome of patients aged ≥ 75 years in the SHould we emergently revascularize Occluded Coronaries in cardiogenic shocK (SHOCK) trial: Do elderly patients with acute myocardial infarction complicated by cardiogenic shock respond differently to emergent revascularization? Am Heart J 2005;149:1128–1134.

3. Dauerman HL, Ryan TJ, Piper WD, et al. Outcomes of percutaneous coronary intervention among elderly patients in cardiogenic shock: A multicenter, decadelong experience. J Invasive Cardiol 2003;15:380–384.

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9. Claeys MJ, Bosmans J, Ceuninck MD, et al. Effect of intracoronary adenosine infusion during coronary intervention on myocardial reperfusion injury in patients with acute myocardial infarction. Am J Cardiol 2004;94:9–13.

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12. Ely SW, Berne RM. Protective effects of adenosine in myocardial ischemia. Circulation 1992;85:893–904.

13. Hasdai D, Harrington RA, Hochman JS, et al. Platelet glycoprotein IIb/IIIa blockade and outcome of cardiogenic shock complicating acute coronary syndromes without persist ent ST-segment elevation. J Am Coll Cardiol 2000;36:685–692.

14. Chan AW, Chew DP, Bhatt DL, et al. Long-term mortality benefit with the combination of stents and abciximab for cardiogenic shock complicating acute myocardial infarction. Am J Cardiol 2002;89:132–136.