Case Report. A 72-year-old male with a history of hypertension and rheumatoid arthritis presented to the emergency room with complaints of epigastric discomfort and lightheadedness for the preceding 4 weeks. On the day of admission, he experienced severe diaphoresis, blurry vision and exercise intolerance. His admission vital signs and physical examination were unremarkable, and 12-lead electrocardiogram demonstrated anteroseptal Q-waves and biphasic T-waves in leads II, III and AVF. The initial troponin I was 29.2 and the creatine was 2.2. He was admitted to the cardiac intensive care unit and started on aspirin, eptifibatide, unfractionated heparin, beta-blocker, angiotensin converting enzyme inhibitor and HMG-co-A reductase inhibitor. The following day, coronary angiography demonstrated a chronically occluded mid-left anterior descending artery and an ulcerated, thrombotic proximal right coronary artery (RCA) lesion (Figure 1). A Spider™ distal embolic protection device (ev3, Inc., Plymouth, Minnesota) was deployed in the distal RCA. Balloon angioplasty of the proximal lesion resulted in massive distal embolization and no-reflow phenomenon in the RV marginal artery, posterior descending artery and posterolateral artery (Figure 2). Moments after balloon inflation, the patient suffered ventricular fibrillation requiring cardiopulmonary resuscitation, defibrillation, intubation and mechanical ventilation.
A Pronto™ aspiration catheter (Vascular Solutions, Inc., Minneapolis, Minnesota) failed to retrieve any significant thrombus. An IABP was inserted, 2 drug-eluting stents (DES) were deployed in the proximal RCA, intravenous dopamine was initiated, and intracoronary nitroglycerin, adenosine and verapamil were administered without significant improvement in distal flow. The Spider™ distal embolic protection device was removed and contained no embolic material. The patient was transported back to the intensive care unit hypotensive and in critical condition.
Immediately following the initial procedure, the patient developed anuria and his mean arterial blood pressure remained below 45 mmHg, despite the administration of 10 L of normal saline and the addition of intravenous norepinephrine and dobutamine infusions. The arterial pH was 7.17 with a severe metabolic acidosis (lactate = 7.8). A Swan-Ganz catheter demonstrated a central venous pressure of 15 mmHg, RV pressure of 36/15 mmHg, pulmonary artery pressure of 36/33 mmHg and pulmonary artery wedge pressure of 22 mmHg. Echocardiography demonstrated a dilated RV with severely depressed function, a large inferoposteroseptal infarct, severely depressed LV function and an LV ejection fraction of 20%. The patient was brought back to the cardiac catheterization laboratory for pRVAD insertion.
Both femoral veins were cannulated. A 6 Fr multipurpose catheter was advanced over a 0.035 inch floppy J-tipped wire from the right femoral vein to the right pulmonary artery. The floppy guidewire was exchanged for a 0.035 inch Amplatz Super Stiff™ wire (Boston Scientific Corp., Natick, Massachusetts) and the multipurpose catheter was removed. A 21 Fr nonreinforced ventricular assist device outflow cannula was advanced over the wire to the main pulmonary artery. A second Amplatz Super Stiff™ wire was then advanced from the left femoral vein to the superior vena cava, a 21 Fr reinforced ventricular assist device inflow cannula was advanced over the wire to the right atrium, and both guidewires were removed (Figure 3). Anticoagulation was initiated with unfractionated heparin with a target activated clotting time of > 250 seconds. The system was primed and the cannulas were connected to the TandemHeart® centrifugal pump in an air-free fashion. RV assist was started at 2 L/minute and quickly titrated to 3.5 L/minute. Systemic mean arterial pressure immediately improved from 45 mmHg to 65 mmHg.
On post-procedure day 1, the patient experienced upper gastrointestinal bleeding and formed large (> 15 cm) bilateral groin hematomas requiring transfusion of 8 units of packed red blood cells. The pRVAD shuttered occasionally, indicating poor inflow. The patient was brought back to the catheterization laboratory for adjustment of the inflow and outflow cannulas. The pRVAD shuttering continued and pump flows were reduced to < 2 L/minute. Urine output returned to normal and the dopamine and norepinephrine were weaned off within 48 hours. The pRVAD and IABP were removed shortly thereafter. The patient was maintained on dobutamine and furosemide drips for 1 week and was discharged on post-procedure day 14. He made a full recovery and lives at home independently with NYHA class II symptoms. A transthoracic echocardiogram performed 2 months after the initial MI demonstrated normal RV function and a LV ejection fraction of 20%.
Discussion. Simultaneous right and left heart failure in the setting of acute MI is clinically manifested as profound cardiogenic shock occurring very shortly after symptom onset.6 The injured RV cannot deliver adequate LV preload, resulting in decreased LV end-diastolic volume. Extension of injury to the inferoposterior LV walls also reduces LV contractility, further reducing an already compromised LV stroke volume. In our case, this resulted in hemodynamic collapse that was refractory to standard treatments such as vasopressor and IABP support. Providing RV assistance to improve LV preload while providing IABP support to reduce LV afterload and improve coronary perfusion dramatically improved cardiac output, eliminated shock physiology and resulted in an excellent patient outcome.
RV systolic function usually recovers within several days of acute infarction.7 In our case, only 2 days of RV assistance were needed before RV systolic function was sufficient to generate adequate LV preload. Previous reports demonstrate accelerated RV recovery during RV assistance.5 This may be related to decreased myocardial oxygen consumption from decreased wall stress. Future studies are needed to determine the optimal duration of device support.
The pRVAD shuttered on several occasions during assist therapy, forcing us to reduce pump flow. Shuttering is usually caused by underfilling of the inflow cannula and can be due to one of several causes: 1) The nonreinforced inflow cannula can collapse with high pump flow rates.4 We attempted to eliminate this possibility by using a reinforced inflow cannula in the right atrium; 2) Ongoing groin and gastrointestinal bleeding which can cause intravascular hypovolemia. We attempted to correct this with blood transfusion without improvement; 3) PRVAD flow may be reduced if the inflow cannula tip is pulled against the right atrial wall. We adjusted the cannula under fluoroscopy on several occasions without improvement; 4) Insertion of both the 21 Fr inflow and 21 Fr outflow cannula in the femoral veins through the inferior vena cava to the right heart may partially occlude the inferior vena cava, reducing right atrial blood return sufficiently to reduce pRVAD inflow. A previous report documents successful, safe insertion of a 8 mm (25 Fr) coaxial inflow/outflow cannula (A-Med Systems, Inc., West Sacramento, California) in the right internal jugular vein for temporary right heart bypass during off-pump coronary artery bypass surgery in 10 patients.8 A right internal jugular approach for insertion of the TandemHeart® device inflow cannula may improve right atrial blood return, inflow cannula pRVAD flow, and the ability to maximally support RV function.
We placed 2 overlapping drug-eluting stents (DES) in the proximal RCA after the patient developed massive distal embolization with balloon angioplasty. The use of DES in the percutaneous management of non-ST-segment elevation acute coronary syndromes is controversial and has evolved over time. Formerly, patients with non-ST-segment elevation acute coronary syndromes were routinely treated with DES across the United States.9 More recent concerns of late stent thrombosis have shifted practice patterns toward the use of bare-metal stents in this clinical setting. In conclusion, we report a case of successful long-term survival after using entirely percutaneous biventricular support with pRVAD and an IABP for the treatment of cardiogenic shock from acute simultaneous RV and LV MI. Concurrent augmentation of LV preload using a pRVAD and reduction in afterload and improved coronary perfusion using an IABP dramatically improved cardiac output, quickly resolved cardiogenic shock and resulted in an excellent patient outcome. Further studies of this approach are warranted.
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- Kinch J, Ryan T. Right ventricular infarction. N Engl J Med 1994;330:1211–1217.
- Pfisterer M. Right ventricular involvement in myocardial infarction and cardiogenic shock. Lancet 2003;362:392–394.
- Giesler G, Gomez J, Letsou G, et al. Initial report of percutaneous right ventricular assist for right ventricular shock secondary to right ventricular infarction. Catheter Cardiovasc Interv 2006;68:263–266.
- Atiemo A, Conte J, Heldman A. Resuscitation and recovery from acute right ventricular failure using a percutaneous right ventricular assist device. Catheter Cardiovasc Interv 2006;68:78–82.
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- Mendes L, Picard M, Sleeper L, et al. Cardiogenic shock: Predictors of outcome based on right and left ventricular size and function at presentation. Coron Artery Dis 2005;16:209–215.
- Wirtz S, Schmidt C, Aken H, et al. Temporary right heart support with percutaneous jugular access. Ann Thorac Surg 2006;81:701–705.
- Kandzari D, Roe M, Ohman E, et al. Frequency, predictors, and outcomes of drug-eluting stent utilization in patients with high-risk non-ST-segment elevation acute coronary syndromes. Am J Cardiol 2005;96:750–755.