Stenting of an Unprotected Left Main Coronary Artery Stenosis in a Patient with Cardiogenic Shock and Ventricular Fibrillation C

Percutaneous coronary intervention (PCI) is a well recognized and accepted treatment modality in cases of cardiogenic shock where emergent angioplasty is the therapy of choice. Emergent PCI is, however, not without complications. Occlusion rates of 8–15% have been reported in studies of infarct angioplasty.1 In addition, 6-month restenosis rates of up to 45% have been reported.2 Despite improvements in coronary care, cardiogenic shock remains a lethal complication of acute myocardial infarction (AMI).1 Recently, it was suggested that angioplasty may reduce the mortality associated with cardiogenic shock complicating myocardial infarction.3 In a cohort of 27 patients with cardiogenic shock complicating AMI, O’Neill et al. reported an in-hospital mortality rate of 67%.4 The rate was dramatically reduced to 25% in patients treated with successful emergency angioplasty of the infarct-related artery. Lee et al. reported disappointing survival results in patients with multivessel disease who had an overall mortality rate of 62%.1 In a very small series of patients, stent implantation in patients with cardiogenic shock appears to give improved results.5 We describe a case of stenting an unprotected left main lesion complicated by cardiogenic shock. Case Report. An 81-year-old male with chest pain was brought to the emergency room by paramedics. The patient was awake, but blood pressure was 46/20 mmHg. Heart rate was 139/minute and irregular. He was cold, clammy and diaphoretic. Electrocardiogram showed atrial fibrillation with a rapid ventricular response, marked ST-T abnormalities and possible subendocardial injury (Figure 1). He was taken to the cardiac cath lab. Cordarone 100 mg intravenous bolus was given. A 9.5 French (Fr) intra-aortic balloon pump catheter was inserted through the left femoral artery. Blood pressure was 88/49 mmHg with augmentation. An 8 Fr sheath was placed in the right femoral artery. Heparin and intravenous abciximab were given per standard protocol. An 8 Fr, XB 3.5 guiding catheter was immediately positioned in the left main coronary artery. The initial coronary angiogram showed 95% stenosis of the distal left main and 70% stenosis of the origin of the left anterior descending (LAD) coronary artery with TIMI 1 flow. The mid LAD had 80% and 50% diffuse lesions and the circumflex had a 95% lesion proximally with TIMI 1 flow beyond in a very small vessel (Figure 2). A track wire was placed across the left main and proximal LAD. Then, a 3.0 x 20 mm Ranger balloon (Boston Scientific/Scimed, Inc., Maple Grove, Minnesota) was positioned at the left main and inflated to 6 bars for 15 seconds. The 70% stenosis of the left main remained. Flow was improved to TIMI 2. A 3.0 x 25 mm NIR stent (Boston Scientific/Scimed, Inc.) was placed across the left main and proximal LAD 95% and 70% lesions and inflated to 14 bars for 20 seconds. The patient developed ventricular tachycardia and fibrillation. Two hundred and fifty joules were delivered to his chest and he converted to sinus tachycardia at 112 beats/minute with left bundle branch block. Repeat coronary angiogram showed TIMI 3 flow in the LAD, yet significant residual stenosis was present in the mid LAD. Therefore, a 2.75 x 30 mm balloon was placed at the mid LAD lesion and inflated to 8 bars. Blood pressure was improved to 117/62, heart rate was 112 beats/minute and respiration rate was 44/minute. Repeat coronary angiogram showed TIMI 2 flow. However, there was a residual stenosis of 70% at the mid LAD (Figure 3). A 2.5 x 20 Ranger balloon was placed at the mid LAD and inflated to 6 bars and 15 bars. Subsequent coronary angiography showed TIMI 3 flow with residual 35–40% stenosis of the mid LAD. A 6 Fr, FR4 diagnostic catheter was utilized for the right coronary angiogram, which showed the dominant RCA with a 20% proximal irregularity and 30% distal irregularity. There were no collaterals seen to the left system. At the termination of the procedure, arterial pressure was 87/37 mmHg with aortic balloon pump. The patient was drowsy but awake, responding to verbal stimuli. Abciximab infusion was continued for 12 hours; activated clotting time was 309 seconds. The hospital course was complicated by congestive heart failure. However, he was able to go home seven days after admission with Lasix, Vasotec, Plavix, Zocor and aspirin. After discharge, he was able to walk one block without angina. Three months later, the patient had a stress thallium test for recurrent angina. He exercised for 3 minutes with a maximum heart rate of 125/minute. The test was terminated because of shortness of breath and fatigue. This showed a moderate fixed defect involving the antero-apical myocardium. There was a reversible perfusion defect in the septum, compatible with peri-infarction ischemia in the LAD territory. He was brought back to the hospital for coronary angiography, which showed no significant in-stent restenosis of the left main. There was a recurrent 70% lesion at the distal extent of the previous NIR stent in the proximal LAD and a recurrent 95% lesion in the mid LAD before the first diagonal branch. Slow distal LAD TIMI 1 flow was observed. A Rotowire was placed in the LAD across the 70% and 95% type B lesions. Rotational atherectomy with a 1.25 burr was performed and two 2.5 NIR stents (2.5 x 25 mm and 2.5 x 32 mm) were placed in overlapping positions. Final follow-up coronary angiogram showed the 70% and 95% lesions reduced to 10% residual. Initial slow TIMI 1 flow in the LAD was improved to TIMI 3. The patient had a 6-month follow-up stress thallium test. He exercised for four minutes with a maximum heart rate of 124/minute. The patient reported no chest pain. This showed a small fixed defect involving the apex. There was no perfusion defect. The patient has been seen in the office every four months without angina. He continues on his discharge medication. The patient has now done well for three years. Discussion. Despite the dramatic advances in the treatment of AMI, cardiogenic shock remains a devastating complication. In 1980, DeWood et al. were the first to show a survival advantage in patients with cardiogenic shock treated with emergency bypass surgery.6 The establishment of intra-aortic balloon pump counterpulsation has proven utility and is mandatory before catheterization in patients with AMI and cardiogenic shock, and is clinically useful in the broad range of high-risk patients represented in the PAMI-II registry, including patients with resistant heart failure, mechanical complication of AMI, refractory infarct-related vessel reocclusion and a bridge to the operation.2 Andersen et al. evaluated intra-aortic balloon pump use in patients presenting with cardiogenic shock. In patients treated with an early intra-aortic balloon pump, there was a trend toward lower 30-day and 1-year mortality. If counterpulsation is to be utilized, it should be utilized sooner rather than later.7 The Abciximab Before Direct Angioplasty and Stenting in Myocardial Infarction regarding Acute and Long Term Follow-Up (ADMIRAL) trial was a multicenter, randomized, double-blind, placebo-controlled study designed to examine the effects of abciximab on primary stenting in 300 patients with AMI. There was a significant 59% reduction at 30 days in the composite endpoint of death, recurrent myocardial infarction or urgent target vessel revascularization in the stent-abciximab group compared with the stent-placebo group (6.0% versus 14.6%, respectively; p = 0.01). This early benefit was maintained at 6 months, with a similar reduction in the composite endpoint of death, recurrent myocardial infarction or urgent target vessel revascularization (7.4% versus 15.9%, respectively; p = 0.02).8 Angioplasty of unprotected left main coronary artery disease has been controversial. Kusuga et al. reported initial and long-term results of angioplasty on unprotected left main coronary artery in patients with AMI.9 In-hospital mortality was 35.7% (36% in the elective group) (p Acknowledgment. Thank you to Nancy Atkisson for her assistance in preparing this manuscript.

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