Case Report and Brief Review

Four Days of Percutaneous Cardiopulmonary Support and Sixteen Days of Percutaneous Left
Atrium-Artery Bypass: A Case Report of

Yoshiyuki Yamamoto, MD, Takashi Sueda, MD, Mitsunori Okamoto, MD
Yoshiyuki Yamamoto, MD, Takashi Sueda, MD, Mitsunori Okamoto, MD
Cardiogenic shock occurs in 7–10% of patients after acute myocardial infarction (AMI), and it has been one of the major causes of death following AMI.1,2 Intra-aortic balloon pumping (IABP) has been routinely used for AMI with cardiogenic shock, and may contribute to preventing mechanical complications or reocculusion.3 However, IABP does not appear to be sufficient to improve mortality rates, according to several clinical studies.4,5 In Japan, percutaneous cardiopulmonary support (PCPS) has been widely used since 1989 for resuscitation, severe heart failure and for temporal extracorporeal circulation.6 PCPS directly increases cardiac output compared with IABP. While PCPS has advantages in terms of its easy insertion of blood access tubes and rapid start-up of cardiac support, it is difficult to continue PCPS over several days due to the risk of leg ischemia and hemolysis. Ventricular assist systems have been recognized for their longer and stronger circulation support compared to PCPS, and percutaneous left atrium-artery bypass (LAAB) has also been employed to supply percutaneous circulation support.7,8 We present a case of severe AMI with cardiogenic shock. Acute renal failure caused by rhabdomyolysis and septic shock occurred during the patient’s course of treatment, but we were able to rescue him through the use of various circulatory assist devices (PCPS, IABP and LAAB). In particular, we were able to continue LAAB for 16 days with few complications. Case report. On November 30, 2002, a 46-year-old man developed sudden chest pain and was brought to our hospital by ambulance within 30 minutes of initial onset of pain. At the time of admission, his blood pressure was 90/60 mmHg, his pulse rate was 90/minute, and his limbs were cold and cyanotic. Hypertension and impaired glucose tolerance had been diagnosed in the past, but he was given no medical treatment. An electrocardiogram showed significant ST-elevation in V1–V6, I, and aVl. We performed emergent coronary angiography due to a suspicion of AMI. Coronary angiography showed a 99% stenosis in the proximal RCA, a 75% stenosis in the middle LCX and total occlusion in the proximal LAD (Figure 1). We determined that the LCA occlusion occurred due to an old myocardial infarction at the RCA basin. We began emergent percutaneous coronary intervention with the informed consent of the patient and his family. At first, we started IABP through the left femoral artery, and a 7 Fr sheath was inserted into the right femoral artery. A 3.5–15 mm Multi-Link Tristar™ stent (Guidant ACS, Indianapolis, Indiana) was implanted directly in the occluded LAD. As slow-flow occurred after the implantation of the stent, the patient’s systolic blood pressure dropped to 60 mmHg and his dyspnea worsened. The patient was intubated and artificial respiration was started. PCPS (Terumo, Japan) was then performed through the right femoral artery and vein, and a temporal pacemaker was inserted due to bradycardia. The patient’s hemodynamic status stabilized immediately after starting PCPS. We continued coronary intervention via the trans-right brachial approach under PCPS. Thrombus aspiration and thrombolysis (tisokinase 1,600,000 units) restored flow at the LAD from TIMI 1 to TIMI 3, residual stenosis became 0% (Figure 2), and the intervention was completed. We decided to delay intervention on the RCA lesion. Left ventriculography showed broad anterior wall akinesis. The patient’s ejection fraction was 20% and his CPK rose to 16,780 mg/dl. The clinical course of this patient is depicted in Figure 3 (unavailable). PCPS was continued for 4 days (3.0–1.5 l/min), and was removed surgically. IABP was continued for 4 days as well. FiO2 was maintained between 0.6–1.0, and inotropic agents (epinephrine 0.2–0.05 gamma, dopamine 10–3 gamma) were continued. The patient sustained a high fever (38–39º), though we changed antibiotics twice (ampicillin/sulbactam 1.5 g b.i.d. to vancomycin 0.5 g t.i.d. to meropenem 0.5 g t.i.d., clindamycin 0.6 g b.i.d.) and replaced catheters. His blood culture remained negative throughout the course of treatment. Red urine and CPK elevation occurred on the 11th day, followed by oliguria and renal dysfunction. As there was no lower leg ischemia, we thought that the cause of rhabdomyolysis could be due to sepsis or medications. Propofol and other alterable drugs were stopped and dantrolene was started, but the patient’s CPK continued to rise. Continuous hemodiafiltration was commenced on the 12th day. On the 13th day, the patient’s systolic blood pressure fell to 70 mmHg and cyanosis developed. LAAB was then started; using an 8 Fr dilator and Brockenbrough needle, a 0.035 inch Flexstiff wire (Terumo, Japan) was inserted under fluoroscopy from the right femoral vein through the left atrium to the left superior pulmonary vein (Brockenbrough method). The interatrial septum was then dilated with a 16 Fr dilator, followed by the insertion of a custom-made 18 Fr inflow cannula (Medikit®, Delhi, India), curved at the tip, into the left atrium (Figure 4). We inserted a 14 Fr outflow cannula from the right femoral artery to the right common iliac artery, connected it to an ordinary PCPS system, and started circulatory support at 3 l/min. The patient recovered from shock and lung edema after starting LAAB (Figure 5). At the same time, we performed coronary intervention on the RCA (ballooning and stenting; Multi-Link 3.0–15 mm, Guidant ACS) under LAAB, and achieved satisfactory dilatation. The patient’s CPK elevation worsened and high fever continued after stopping propofol. His maximum CPK was 112,500 mg/dl on the 14th day. On the same day, we removed the IABP that had been in place for 2 weeks. The patient’s fever disappeared and his CPK elevation resolved. Staphylococcus epidermidis was detected in a culture of the IABP tip later. On the 17th day, the oxygenator was removed and LAAB was continued using only a centrifugal pump (Figure 6). The patient was extubated under LAAB on the 22nd day. LAAB was removed surgically on the 28th day, and LAAB (2.5–2.0 l/min) was continued with an oxygenator for 5 days, then without an oxygenator for 11 days, for a total of 16 days. The patient’s systolic blood pressure was maintained at 100–120 mmHg during LAAB. Because his renal failure became irreversible and oliguria persisted, we continued continuous hemodiafiltration and then changed to hemodialysis 3 times per week on the 40th day. The patient left the intensive care unit on the 41st day. Hemodialysis was changed to peritoneal dialysis after 3 months. Four months later, the patient underwent coronary angiography which confirmed no restenosis of the LAD or RCA. The patient required rehabilitation due to the loss of systematic muscle strength, and he was discharged on crutches 7 months later. The patient’s cardio-thorax ratio was less than 50% on chest X-ray, and his ejection fraction was 34% on echocardiography at 4 months post-discharge. The patient is well at over 1 year post-discharge, has required no hospitalization, and has resumed his work. No difficulty was encountered when inserting the inflow cannula via the Brockenbrough method. A total of 20 minutes were required from the time of puncture until circulatory support started. An inflow cannula and an outflow cannula were inserted in the right femoral vein and artery, with no bleeding at the puncture site or ischemia in the right lower limb during LAAB. Hemolytic anemia progressed, and an erythrocyte transfusion was performed 7 times, for a total of 14 units during LAAB. The patient’s platelet level decreased from 300,000/ml to 80,000/ml. His infection was under control after the IABP was removed. A small left atrium-right atrium shunt remained for 10 months after the LAAB was removed and disappeared naturally, but its influence during the clinical course of treatment seemed to be insignificant. Discussion Cardiogenic shock is the most common cause of death in AMI.1,2 It has been shown that mortality rates of acute myocardial infarction are reduced by emergency revascularization,9,10 but mortality rates of cardiogenic shock remain at an unacceptably high level in the reperfusion era.1 Although early reperfusion was achieved in this case, the patient’s hemodynamics crashed during coronary intervention and PCPS was started. PCPS was continued for 4 days and allowed the patient to survive cardiogenic shock. In Japan, PCPS has been widely used not only for cardiogenic shock, but also for resuscitation, pulmonary embolism, and other conditions.6 PCPS makes it possible to increase cardiac output directly and to maintain circulation, but it is thought that the continuous use of PCPS is limited to several days due to the risk of lower limb ischemia and hemolysis. Revascularization of the infarct-related artery may be important in light of the fact that PCPS should be stopped as early as possible. Because shock with sepsis and rhabdomyolysis occurred, LAAB was commenced on the 13th day. LAAB was continued for 5 days with an oxygenator and 11 days without am oxygenator, for a total of 16 days. In 1962, Dennis et al. reported the use of the first the percutaneous left atrial-to-femoral bypass system via the jugular approach.11 Thiele et al. reported 18 cases of LAAB use (left ventricular assist device) that showed the potential to decrease mortality in cardiogenic shock patients.8 LAAB offers the following advantages: (1) enables the use of PCPS for a longer than usual duration since an oxygenator is unnecessary and the activation of neutrophils and hemolysis may fall off; and (2) offers the potential for a more aggressive decrease in left ventricular overload by direct evacuation from the left atrium. Further clinical experiments and trials are needed to clarify the benefits of LAAB over PCPS. LAAB especially requires sufficient time for the insertion procedure and is not suitable for cardiac arrest or “seconds count” cases, because it takes certain time to insert an inflow cannula to left atrium via the Brockenbrough method. We used a custom-made inflow cannula (Medikit), but a ready-made inflow cannula (Medikit) is now available in Japan. A small LA-RA shunt remained 6 months after LAAB in our patient, but its effect is considered minimal for the clinical course of treatment. Potential complications of LAAB are similar to those of PCPS: bleeding at the puncture site, arterial and venous injury, hemolysis, infection, thrombosis, bleeding tendency caused by heparin, and so forth. The partticular complications of LAAB use include cardiac tamponade and LA-RA shunt associated with the Brockenbrough method. Pulmonary embolism is contraindicated for LAAB. In our patient, significant CPK elevation appeared on the 12th day and his maximum CPK reached 112,500 mg/dl. The causes of rhabdomyolysis may include drugs, alcohol, ischemia, infection and many other factors.12 In this case, there was no manifest lower limb ischemia, and CPK elevation continued after stopping propofol. The patient’s CPK elevation finally decreased with and his fever fell after removal of the IABP. Considering that Staphylococcus epidermidis was detected in the culture of the IABP tip, sepsis may have played an important role in rhabdomyolysis in this case. Bacterial sepsis-induced rhabdomyolysis occurs in approximately 7% of all rhabdomyolysis cases, and Gram-positive bacteria seem to be predominant.1,3 High fever continued from the second day, and antibiotics were ineffective. Catheter-induced infection is always problematic for such patients. It was difficult to know whether the IABP should be removed while the patient was unstable, but the IABP turned out to be the cause of sepsis. Percutaneous LAAB supported circulation sufficiently after the IABP was removed and contributed to our patient’s long-term survival. Slow-flow occurred in the initial procedure and adversely affected the patient’s hemodynamics. A distal protection device was not available at that time. During the initial procedure, the coronary intervention could have been continued through the right femoral artery if a PCPS had been placed through the left side, as a substitute for the IABP, but we considered IABP useful in cases of AMI with cardiogenic shock. We performed a coronary intervention to the RCA on the 13th day, but could have considered earlier PCI to the RCA. We did not use a S-G catheter, and there were no invasive hemodynamic data. The patient survived at extraordinary cost. The application of the LAAB may be limited to special cases within the overall population of AMI patients. Conclusion In conclusion, we used PCPS for 4 days in the acute phase of AMI with cardiogenic shock, followed by LAAB for 16 days (with an oxygenator for 5 days, without an oxygenator for 11 days) during the patient’s sepsis- and rhabdomyolysis-induced shock. We believe that this case in which multiple circulatory assistance devices were used contributed to our patient’s long-term survival. Percutaneous LAAB assisted our patient’s circulation sufficiently with few complications.
References
1. Goldberg RJ, Samad NA, Yarzebski J, et al. Temporal trends in cardiogenic shock complicating acute myocardial infarction. N Eng J Med 1999;340:1162–1168. 2. Holmes DR Jr, Bates ER, Kleinman NS, et al. for the GUSTO-I Investigators. Contemporary reperfusion therapy for cardiogenic shock: The GUSTO-I trial experience. Global utilization of streptokinase and tissue plasminogen activator for occluded coronary arteries. J Am Coll Cardiol 1995;26:668–674. 3. Stone GW, Ohman EM, Miller MF, et al. Contemporary Utilization and outcome of intra Aortic Balloon Counterpulsation in acute myocardial infarction. J Am Coll Cardiol 2003;41:1940–1945. 4. Scheidt S, Wilner G, Mueller H, et al. Intra-aortic balloon counterpusation in cardiogenic shock: Report of a co-operative clinical trial. N Engl J Med 1973;288:979–984. 5. DeWood MA, Notske RN, Hensley GR, et al. Intraaortic balloon counterpulsation with and without reperfusion for myocardial infarction shock. Circulation 1980;61:1105–1112. 6. Sawa Y. In: Matsuda H (ed.) Percutaneous Cardiopulmonary Support (in Japanese). Tokyo: Shujunsha. 1998, pp. 19–24. 7. Kyo S, Miyamoto N, Motoyama T, et al. Transesophageal echo-guided percutaneous left heart bypass (LA-aorta) for cardiogenic shock patients. Jpn J Artif Organs 1994;23:931–935. 8. Thiele H, Lauer B, Hambrecht R, et al. Reversal of cardiogenic shock by percutaneous left atrial-to-femoral arterial bypass assistance. Circulation 2001;11:2917–2923. 9. Hochman JS, Sleeper LA, Webb JG, et al. Early revascularization in acute myocardial infarction complicated by cardiogenic shock. N Engl J Med 1999;341:625–634. 10. Hochman JS, Buller CE, Sleeper LA, et al. Cardiogenic shock complicating acute myocardial infarction — Etiologies, management and outcome: A report from the SHOCK trial registry. J Am Coll Cardiol 2000;36:1063–1070. 11. Dennis C, Carlens E, Senning A, et al. Clinical use of a cannula for left heart bypass without thoracotomy. Ann Surg 1962;156:623–637. 12. Holt SG, Moore KP. Pathogenesis and treatment of renal dysfunction in rhabdomyolysis. Intensive Care Med 2001;37:803–811. 13. Betrosian A, Thireos E, Kofinas G, et al. Bacterial sepsis-induced rhabdomyolysis. Intensive Care Med 1999;25:469–474.