Nevşehir State Hospital Cardiology Clinic
A 75-year-old man admitted to anestesiology intensive care due to respiratory distress due to pneumonia. In the following days, troponin level has been increased 3to4 times. Cardiology consultant recieved the patient and critical left main and left circumflex stenoses were shown on coronary angiography (Video 1). Bypass surgery is indicated. The RCA was patent (Video 2). On ECHO, LVEF was %60 with minimal MI. Other findings were unremarkable. Renal function was normal. High surgical risk from surgeons and patient’s tendency to PCI let us to plan a high risk LM PCI, which has been declared him as a second option.
Although we first planned a simple LMtoLAD crossover stenting, our proctor advised wiring of LCX, ostium of which is festival with slow flow (Video 3), DK CRUSH was attempted. After wiring LCX, a 2.0×20 balloon did not cross the lesion despite inflation of a 4.0×12 mm anchor balloon in the LAD (Video 4). Then, we predilated the LM lesion with anchor balloon (Video 5). Before second attempt of LCX balloon crossing, we took a picture and decided to perform LM-to-LAD crossover stenting (Video 6). If you see Video, you would realize bulging of LCX in to the LAD, U-shape prolapsus. This is corrected before implantation of a 4.0×18 BMS stent at 18-22 atm to prevent wire entrapment (Video 7). After stenting, LCX flow got slower, and ostium became much more critical (Video 8). Present hipotension became worse with symptoms. First we performed a rapid 3 postdilatation with a 4.5×9 balloon at 14-20 atm and achieved optimization (Video 9). After that, LCX flow was worse (Video 10). Despite fluid replacement, BP was decreased more and more (60/40 mmHg) and dopamine was started at vasopressive dosage. We quickly rewired LCX with LAD wire and delivered a 1.2×9 mm balloon and then pulled back the jailed wire. Inflation of the ostium at 18 atm was done at 3 locations (Video 11). Despite increase in LCX flow and optimal treatment, BP was the same as low as 60/40 mm Hg. We performed bed-side hand ECHO. We detected severe acute mitral insufficiency which was probably due to papillary muscle malfunction associated with ischemia of LCX. We ordered intraaortic balloon pump. LM lesion was ulcerated (not shown here) and became a type 1 perforation at the site of ulceration (Video 12). When patient was unconcious with gasping, we performed a short term CPR. Bradycardia was developed but not VT or VF. In total, 1000 ml saline, 2 mg atropin and 2 mg adrenaline were given. After IABP implantation, BP was 90/40 mm Hg with spontaneous movements and partial conciousness. MI was markedly decreased 2 hours katar and BP became 130/80. Conciousness was complete 6 hours later without any neurological deficit. IABP was programmed 2:1 and pulled back next morning.