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Title: Treatment options and long-term outcome of percutaneous coronary interventions in patients with angina recurrence after coronary artery bypass grafting

Abstract:

In spite of the rapid developments in invasive cardiology, coronary artery bypass grafting (CABG) remains the treatment of choice in diabetic patients with multivessel coronary artery disease, long-segment lesions and chronic total occlusion, and the left main coronary artery stenosis or its equivalent. High number of CABG procedures performed in the last decades has a great impact on the increasing number of patients (pts) with recurrent angina due to a saphenous vein graft (svg) disease or native vessel (nv) atherosclerosis progression. Atherosclerosis progression and bypass graft degeneration limit long-term outcome in pts after CABG. The surgical treatment has no effect on the mechanism of the atherosclerotic disease; bypass grafts (and in particular the venous ones) are known to degenerate with time. Thus surgical revascularization has created a new problem in cardiology – the problem of degenerative bypass graft disease. Inflammatory factors influence pathogenesis and natural course of native vessel and bypass graft atherosclerosis. Percutaneous procedures have become a natural, logical alternative to surgery in pts with recurrent angina after CABG. AIM: To assess the mechanism of angina recurrence in a series of consecutive pts after CABG and to evaluate the feasibility of re-revascularization by percutaneous coronary intervention (PCI ) or reCABG. To assess the relationship between non-specific (e.g., hs-CRP) and specific (e.g., chlamydia pneumoniae, ChP), inflammatory markers and immediate and mid-term outcome in patients undergoing PCI after CABG. To assess the immediate and long-term outcome of PCI in patients after CABG and identify prognostic factors of major adverse cardiac events (MACE) in a long term follow-up.Two hundred and thirty six consecutive pts (81.4% men, mean age 63.1±8.2, range 40-82 years) undergoing cardiac catheterizations for recurrent angina in the mean time of 93.2 ± 48.1 (1-267) months after CABG were evaluated. The culprit lesion was identified on the basis of angiography of native vessels and coronary bypass grafts. Then the pts were qualified to PCI, reCABG or conservative therapy. Patients underwent long term clinical follow up, including the CCS class, recurrent cardiovascular hospitalization or occurrence of MACE (such as death, heart infarct, repeated PCI). The underlying cause of symptom recurrence was identified as follows: svg insufficiency in 92 (39%) patients, atherosclerosis progression in native vessels in 44 (18.6%) patients. Both reasons for symptom recurrence were seen in 59 (25%) patients. In 41 (17.4%) pts patent, properly performing bypass grafts were found in the absence of nv atherosclerosis progression; thus the reason for symptom recurrence in those pts remains unidentified. In a great majority of pts (178, i.e. 91%) symptoms recurred over a year after CABG and the predominant reason was svg occlusion. A correlation was found between the time of symptom recurrence after CABG and age (p=0.026, r= -0.159) and white blood account (p=0.0004, r= -0.252). However, there was no correlation between the time of symptom recurrence and hs-CRP (p=0.038, r= - 0.181). The search for independent factors of the time of angina recurrence after CABG was performed. This revealed the following predictors: atherosclerosis progression in native vessels, lack of IMA use as a graft, hyperlidaemia, and elevated white blood count. Among the 195 pts with angiographically identified reason of symptom recurrence, 141 (72.3%) pts were referred to re-revascularization due to atherosclerosis progression in native vessels or/and coronary bypass grafts (svg insufficiency/degeneration). In the remaining 54 (27.7%) pts there was no anatomical option for re-revascularization (neither PCI nor reCABG).PCI was performed in 132 (67.7%) patients, and 9 (4.6%) pts were referred to re-CABG. Svg-PCI was performed in 39(25.5%) pts, nv-PCI in 80 (60.6%), and both nv- and svg-PCI in 13 (9.8%) pts. ; On average, there was 1.73 lesion treated per patient. PCI was considered successful in 127 (96.2%) patients. During 30 days follow-up MACE occurred in 3 (2.4%) patients, including 1 (0.8%) sudden death on 4-th day after PCI and 2 (1.6%) MIs, Following successful PCI, symptom reduction by at least one CCS class was seen in 101 (80.2%) pts, including all pts treated in the course of acute coronary syndrome (ACS). In the long-term follow up of 2.5 years (range 1-63 months), MACE occurred in 54 out of 127 pts subjected to PCI. There were 9 deaths, including 5 cardiac deaths. Due to symptom recurrence, another angiography was performed in 44 pts. This revealed restenosis in 26 pts, atherosclerosis progression in 10 pts, and both causes in 2 pts. In 27 pts rePCI was performed, 3 pts were referred for reCABG and 2 for cardiac transplantation. After successful PCI, MACE-free survival was noted in 81% pts at 1 year and 65% at 5 years. The likelihood of MACE-free survival was higher for those after nv-PCI as compared to svg-PCI (p=0.047). There was no difference in MACE-free survival for those with PCI in stable angina vs. ACS (89.2 vs. 93.6% at 6 months, 71.9 vs. 62.5% at 2 years). Among the 127 pts subjected to successful PCI, 64 (50.4%) had hs-CRP ≥ 3.5mg/dl and 47 (37%) fibrinogen >3.5 g/L. No relationship was revealed between non-specific inflammatory markers elevation (including hs-CRP) and the risk of MACE. Patients with elevated IgA or IgG against ChP had a higher risk of MACE (particularly death) (p=0.047 and p=0.045 respectively). To determine independent predictors of long-term MACE, 44 parameters were included in the Cox analysis. This showed the following independent factors: left main coronary artery PCI (OR 3.1), svg-PCI (OR 2.1) and anti-ChP IgA >12 EIU (OR 1.9).During a mean follow-up of 7.5 years after CABG, bypass graft degeneration was found in 64% pts and it was the main cause of angina recurrence. Native vessel atherosclerosis progression occurred in 44% pts; this was manifest clinically significantly earlier than bypass graft degeneration. Atherosclerosis progression in native vessels, lack of IMA use as a graft, hyperlidaemia, and elevated white blood count were identified as independent factors of earlier angina recurrence after CABG. The PCI procedure was feasible in ~3/4 of pts with angina recurrence after CABG. PCI was safe and successful in symptom resolution. Following PCI for nv atherosclerosis progression or bypass graft degeneration, MACE occurred in ~1/3 pts. During a mean follow-up of 2.5 years, one in four pts required another intervention. In this period, ~50% pts required hospitalization for various reasons (including e.g., angina, atrial fibrillation of heart failure). The probability of MACE was higher following bypass graft PCI vs. native vessel PCI. Postprocedural elevation of cardiac markers and elevated ChP IgA were related to a higher cardiac event rate. Left main coronary artery PCI, svg-PCI and anti-ChP IgA >12 EIU have been identified as independent predictors of long-term MACE.

Level of degree:

2 - studia doktoranckie

Degree discipline:

choroby układu krążenia

Degree grantor:

Wydział Lekarski

Promoter:

Tadeusz Przewłocki

Date issued:

2007

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application/pdf

Identifier:

oai:dl.cm-uj.krakow.pl:1144

Call number:

ZB-105757

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Location of original object:

Biblioteka Medyczna Uniwersytetu Jagiellońskiego - Collegium Medicum

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Jun 24, 2019

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Nov 21, 2012

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ZB-105757 Jun 24, 2019
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