Distal left main trifurcation disease in a patient with porcelain aorta




Abstract


Coronary trifurcation lesions are a complex subset of lesions and are substantially more complex than bifurcations when treated with percutaneous coronary intervention (PCI) because of higher rates of acute periprocedural complications (dissection, myocardial infarction, acute vessel closure) and less effective long-term outcomes (stent thrombosis, restenosis) as compared to non-bifurcation lesions.


We present the case of a 73-year-old man who was admitted to our hospital with symptomatic severe aortic stenosis who was found to have a distal left main trifurcation disease as well as porcelain aorta on work-up. Given the high risk of stroke during surgical aortic valve replacement and coronary artery bypass grafting, the patient was accepted by the heart team to proceed with percutaneous coronary intervention (PCI) and trans-catheter aortic valve replacement (TAVR). We describe a successful double mini-crush stenting technique approach for this case.


Highlights





  • Left main trifurcation stenting carries an overall high rate of adverse events and it should be reserved for patients who are at high risk or who refuse bypass surgery.



  • The double mini-crush technique can be safely performed using three DES stents with high procedural success in left main trifurcation disease.



  • Porcelain aorta is an extensive circumferential calcification of the ascending aorta in which TAVR is a safe and efficient option for patients with severe symptomatic aortic stenosis.




Case description


A 73-year-old male was admitted to the cardiology department with a diagnosis of severe symptomatic aortic stenosis.


The patient’s medical history included systemic hypertension diagnosed 15 years earlier treated with metoprolol 100 mg bid, chronic obstructive pulmonary disease (COPD) due intense cigarette smoking GOLD II, treated with intermittent bronchodilators and supplemental oxygen, as well as prostatic hyperplasia treated with tamsulosin and finasteride.


The patient had been in good health until 2 years prior to his current admission, when he was diagnosed with a systolic ejection heart murmur at a routine checkup. At that time he underwent an echocardiogram showing severe aortic stenosis. Since the patient was apparently asymptomatic, he rejected treatment. The patient did not undergo exercise stress testing at that time. He continued like this until 2 months prior to the current admission, when the patient presented a decline in NYHA functional class (III-IV), as well as repetitive episodes of typical angina with minimal exertion. The symptoms were so severe that he was admitted 3 times at the emergency department of his local hospital. The patient denied any episode of syncope. Given the previous diagnosis, the patient was referred to our hospital.


On arrival, he was hemodynamically stable. His weight was 82 kg and his height was 1.72 m. On examination the heart rate was 74 bpm, the blood pressure 115/60 mmHg, the respiratory rate of 20 bpm and the oxygen saturation of 90% while breathing ambient air. The carotid upstrokes were diminished in amplitude and delayed in time, the second heart sound was single and there was a murmur heard best in aortic area which peaked in late systole with Gallavardin’s phenomenon with an otherwise normal physical examination.


His laboratory data were within the normal range.


The echocardiogram revealed a LVEF of 48%, mid and basal inferior and inferolateral wall-motion abnormalities, moderate diastolic dysfunction, moderate mitral regurgitation as well as severe aortic stenosis (D1) with a mean gradient of 82 mmHg and an aortic valve area of 0.4. PASP was 30 mmHg.


Eventually, the patient underwent coronary angiography showing distal left main trifurcation disease involving all three branches Modified Medina 1–1–1-1 ( Fig. 1 ) as well as a severely diseased right coronary artery with a Syntax Score of 47. A relevant finding during cardiac catheterization was the presence a severely calcified ascending aorta. Given these findings, the patient underwent a CT-Angiogram, which confirmed the presence of circumferential calcification of the ascending aorta ( Fig. 2 ), compatible with porcelain aorta. The patient’s STS score was 5.5% risk of mortality.




Fig. 1


Spider view showing distal left main trifurcation disease modified Medina 1-1-1-1.



Fig. 2


Angio-CT reconstruction showing diffuse calcification of the ascending aorta and aortic arch.


The case was evaluated by the heart team, and owing the intermediate surgical risk, a severely calcified ascending aortic wall with very high risk of stroke during surgical aortic valve replacement (SAVR) and the presence of CPOD, the patient was accepted for PCI and TAVR.


After assessing the coronary anatomy, the patient underwent IVUS-guided PCI of distal left main trifurcation disease with a successful double mini-crush technique using three drug eluting stents (DES) with a 7F Voda guide catheter (Boston Scientific) through a femoral approach. Final kissing balloon was performed. The angiographic result was successful, without signs of stent thrombosis while on coronary care unit after the procedure ( Fig. 3 ).




Fig. 3


PA 0 Caudal 30 view of left main after successful double mini crush technique.


Three days later, the patient underwent successful TAVR with a balloon expandable valve. On clinical follow-up the patient is in NYHA class II and echocardiogram at 6 months showed adequate function of the prosthetic aortic valve.





Discussion and review of the published data


In approximately two thirds of patients, the left main coronary artery bifurcates into the LAD and LCx arteries; in one third of patients the left main coronary artery trifurcates into the LAD, LCx and ramus intermedius .


Among the various anatomic types of obstructive coronary artery disease (CAD), significant left main coronary artery disease is the highest risk lesion and is associated with poorer clinical outcomes compared with non-left main CAD .


Left main trifurcation is defined as a distal left main coronary artery dividing into three branches, each having a diameter of >2.25 mm and both side branches (SBs) originating <3 mm from the main branch (MB) ostium ; whereas distal left main trifurcation disease is defined as a >50% diameter stenosis within 5 mm from the carina involving the left anterior descending as the MB associated or not with significant disease in either one or both the SBs .


Coronary trifurcation lesions are a complex subset of lesions and are substantially more complex than bifurcations when treated with PCI because of higher rates of acute periprocedural complications (dissection, myocardial infarction, acute vessel closure) and less effective long-term outcomes (stent thrombosis, restenosis) as compared to non-bifurcation lesions .


The rationale to proceed with PCI previous to TAVR is that stenting after TAVR can sometimes be challenging, particularly with regard to adequate guide position, given the position of the aortic prosthesis, predominantly with certain valve designs, which may limit subsequent access to the coronary ostia .


The reason to choose a mini-crush stenting technique in this case relies on the fact that the limited length of the five layers of struts and the optimized expansion of the crushed side branch stents may reduce the acute and subacute stent thrombosis rate as observed in the series by Galassi et al. .


Different techniques used in these types of lesions requiring 3 stents as intention to treat are double crush technique, double mini-crush technique and double V-Stent technique .


In this case we performed IVUS-guided PCI of distal left main disease, demonstrating adequate expansion and apposition of the stents ( Fig. 4 ). This approach has shown a lower risk of mortality at 3 year-follow up in patients who undergo unprotected left main PCI with drug eluting stents as compared with conventional angiography guidance .


Nov 13, 2017 | Posted by in CARDIOLOGY | Comments Off on Distal left main trifurcation disease in a patient with porcelain aorta

Full access? Get Clinical Tree

Get Clinical Tree app for offline access