Changes in C-reactive protein levels following coronary stent implantation depend on the extent of periprocedural arterial injury
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Paawweełł KKrraalliisszz11,, HHaalliinnaa KKeemmoonnaa22,, SSłłaawwoommiirr DDoobbrrzzyycckkii11,, H
Haannnnaa BBaacchhóórrzzeewwsskkaa--GGaajjeewwsskkaa11,, KKoonnrraadd NNoowwaakk11,, ZZddzziissłłaaww SSaawwiicckkii33
1Zakład Kardiologii Inwazyjnej, Akademia Medyczna, Białystok, Poland
2Zakład Laboratoryjnej Diagnostyki Klinicznej, Akademia Medyczna, Białystok, Poland
3Klinika Medycyny Ratunkowej, Akademia Medyczna, Białystok, Poland
Address for correspondence:
lek. med. Paweł Kralisz, Zakład Kardiologii Inwazyjnej, SPSK Akademii Medycznej, ul. Skłodowskiej 24a, 15-276 Białystok, Poland, tel.: +48 85 746 84 96, fax: +48 85 746 88 28, e-mail: paqral@yahoo.com
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Reecceeiivveedd:: 31 October 2005. AAcccceepptteedd:: 21 December 2005 Abstract
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Baacckkggrroouunndd:: Coronary stenting is associated with acute inflammation within the arterial wall followed by neointimal growth. Acute inflammatory response is expressed by a marked systemic elevation of the inflammatory biomarker C-reactive protein (CRP). It has been shown that the degree and extent of CRP increase may be related to clinical presentation or periprocedural treatment.
A
Aiimm:: To investigate whether an increase in CRP level is associated with the extent of arterial injury during stent deployment.
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Meetthhooddss:: CRP levels were measured with a high-sensitivity CRP (hsCRP) assay. Seventy-three patients (51 males) with normal baseline plasma CRP (<3 mg/L) underwent percutaneous coronary intervention (PCI) with stent implantation for stable coronary disease. Blood samples for hsCRP were drawn before the intervention, and 6, 12 and 24 hours after the procedure.
Both quantitative (single vs multivessel coronary intervention) and qualitative analyses (including lesion classification according to the ACC/AHA grading system) were performed in all patients. The examined angiographic parameters and procedural data obtained included reference diameter, lesion location, lesion length, total stented segment length, diameter of stent after deployment, maximal deployment pressure, total inflation number and duration.
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Reessuullttss:: The mean hsCRP level increased in all patients between baseline and 24 hours (1.36±0.93 mg/L and 4.34±3.3 mg/L, p <0.0001). Single vessel procedure was performed in 51 patients and multivessel coronary intervention in 22 patients. Mean hsCRP was similar at baseline and after 6 hours in both groups and the increase after 12 and 24 hours was higher among patients with multivessel coronary intervention compared to patients with single vessel procedure (2.69±2.48 vs 4.15±3.17;
p=0.039 and 3.76±3.13 vs 5.69±3.38; p=0.021, respectively). There was no correlation between hsCRP and the degree of lesion complexity. Multiple regression analysis showed that the total stented segment length (p=0.01) contributed to the hsCRP increase after 24 hours.
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Coonncclluussiioonnss:: The inflammatory response expressed by hsCRP levels is higher in patients with multivessel coronary intervention with longer total segment stented.
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Keeyy wwoorrddss:: C-reactive protein, stable coronary disease, stent implantation, arterial injury
Kardiol Pol 2006; 64: 364-371
Introduction
The contribution of inflammation to the pathogenesis of coronary artery disease (CAD) has been proven in experimental and clinical trials [1]. An
evaluation of inflammation severity may play a crucial role in predicting the risk of unfavourable cardiovascular events and hence contribute to the adjustment of treatment and improve prognosis.
C-reactive protein (CRP) is one of the acute phase proteins that is produced in the liver in response to various cytokines, induced particularly by interleukine-6 [2]. CRP is a sensitive and non-specific marker of the inflammatory process, tissue injury and infection. CRP is commonly used for the evaluation of the clinical course of diverse inflammatory states owing to its long half life, stability and availability of specific and repeatable assay modalities.
It has been shown that CRP levels are independent predictors of myocardial infarction (MI), stroke and cardiovascular death in patients with CAD disease [3–6].
CRP level monitoring has been validated in predicting the risk of unfavourable cardiovascular events in patients undergoing percutaneous coronary interventions (PCI).
Elevated baseline CRP concentration as well as its increase after PCI indicate a worse prognosis [7–8].
Percutaneous dilation of a stenosed coronary artery is associated with a mechanical wall injury. The trauma induces an inflammatory reaction which may depend on both the type of atherosclerotic plaque and the extent of artery injury during percutaneous intervention [9–11].
The aim of this study was to investigate whether an increase in CRP level is associated with the extent of arterial mechanical injury during stent deployment.
Methods Patients
The study included 73 consecutive patients with stable CAD scheduled for PCI with elective stent implantation. The severity of CAD symptoms ranged between CCS class 2 and 3. All patients had normal baseline CRP (≤3 mg/dL).
The exclusion criteria were as follows: acute coronary syndrome, fever, any active infective disease, autoimmune disease, neoplastic disease, severe heart failure, left ventricular ejection fraction below 30%, haemodynamically significant valvular disease, cardiac surgery within the past three months, cardiac revascularisation (CABG or PCI) within the past three months or long-term immunosuppression.
Percutaneous coronary intervention
The PCI procedures were performed using standard equipment (6F catheters) and femoral arterial access.
The procedure was successful if residual stenosis was
<20%, full restoration of flow TIMI 3 was achieved, and no procedural complications, i.e. MI, death or urgent CABG, occurred.
A quantitative coronary assessment (QCA) of all angiograms using digital computed technology was performed. The analysed parameters included proximal and distal reference diameters, lesion site, lesion length,
total length of deployed stent and diameter of deployed stent. Additionally, balloon inflation count and total duration as well as maximum stent deployment pressure were evaluated. Coronary artery lesion morphology before PCI was classified as A, B1, B2 or C according to the commonly accepted scheme of ACC/AHA [12].
Quantitative and qualitative evaluation (including classification of coronary artery lesion complexity) was carried out by an experienced invasive cardiologist who did not perform the procedure and was blinded to patient outcome.
Coronary angioplasty of one, two or three vessels was performed. The total length of the stented portion of the artery was measured as the sum of lengths of all stents deployed within the lesion. Moreover, if angioplasty of more than one artery was performed, the total stent length was considered as the sum of lengths of all the stents deployed in all treated coronary vessels.
The total stent area was calculated taking into account vessel diameter. To simplify measurements, the deployed stent was considered to be cylindrical (2 πrl, where r=stent radius, l=stent length).
It was assumed that the degree of procedure-related injury of a vessel depends on the total length of the arterial segment in which intervention was performed and the type of treated lesion. All patients were divided into two groups: those with intervention within one vessel, and those in whom stents were implanted in more than one coronary artery (double- or triple-vessel intervention).
Additionally, the qualitative analysis included simple vs.
complex lesions treated. Lesions classified as type A and/or B1 were assumed to be simple, whereas type B2 and/or C lesions were classified as complex.
All patients received aspirin (100 mg) and ticlopidine (2 x 250 mg) for at least three days before the procedure, and heparin (100 IU/kg of body weight) immediately before PCI in a catheterization laboratory to achieve ACT
>300 sec. Other therapeutic interventions were conduc- ted according to the current standards of CAD treatment.
CRP assaying
Venous blood for CRP determination was drawn from the antecubital vein prior to coronary angioplasty and at 6, 12 and 24 hours after stent deployment, using standard vacuum tubes. After clotting, samples were centrifuged and sera stored at –70°C until testing. Plasma CRP levels were measured using the nephelometric method (Dade Behring Diagnostics, Marburg, Germany).
Statistical analysis
Results are shown as means ± standard deviation.
Discrete variables were compared with χ2 test and
quantitative variables with Student’s t-test. Differences with p <0.05 were found significant.
Results
Successful coronary angioplasty with stent implantation was performed in all study patients.
Primary clinical and angiographic characteristics of the entire group are shown in Table I.
Single coronary artery stenting was performed in 51 (69.9%) patients, whereas two or three arteries were
stented in 22 (30.1%) cases. The procedures involved respective vessels with the comparable lengths of both stenosis and inserted stent. There was a difference in the total stent length and area, which were a sum of these results for relevant vessels (p=0.0005 and 0.002, respectively, Table II). After stent deployment a significant increase of mean CRP concentrations in the chosen timeframes was observed in both groups (Figure 1). At the same time, the elevation of the mean CRP level 12 and 24 hours after stenting was significantly higher in patients with multi-vessel coronary angioplasty (Table II). Multivariable regression analysis including basic clinical data and details of the procedure performed showed that the total length of stent was significantly related to the mean CRP level increase in a 24-hour follow-up (p=0.01).
Coronary angiography revealed simple coronary stenoses in 49 (67.1%) and complex lesions in 24 (32.9%) patients. Type A stenosis predominated in patients with simple coronary lesions and the majority of these subjects had angioplasty of one vessel (37 patients, 75.5%). Type B2 stenosis was most frequent in the group with complex lesions, of which 8 patients with angioplasty of >1 artery apart from at least one complex stenosis also had simple lesions (type A or B1).
Coronary angioplasty of complex lesions required more frequent balloon inflations, higher maximum pressures and longer inflation time; however, the differences failed to reach statistical significance.
Both the total length of stenosis and the total length of stent were higher in the group with complex lesions, due to the type of lesion itself and the greater number of multi-vessel procedures performed in this group
Age 59.2±10.84
Gender (M/F) 51/22
BMI 28.7 (min 21.1. max 44.9)
Hypercholesterolaemia 52 (71.2%)
Diabetes mellitus 13 (17.8%)
Arterial hypertension 50 (68.5%) Past myocardial infarction 32 (43.8%)
Class 2/3 CCS 30 (41.1%)/43 (58.9%)
Coronary artery disease:
1 vessel 32 (43.8%)
2 vessels 30 (41.1%)
3 vessels 11 (15.1%)
PTCA with stent implantation:
1 vessel 51 (69.9%)
2 vessels 19 (26%)
3 vessels 3 (4.1%)
T
Taabbllee II.. Primary clinical characteristics of study patients
9 8 7 6 5 4 3 2 1 0
P PCCII ++ sstteenntt
11 aarrtteerryy
P PCCII ++ sstteenntt
>
>11 aarrtteerryy 0 6 12 24
hours p=0.000002
p=0.003
p=0.007
p=0.00007
p=0.00001 p=0.002
0 6 12 24 hours
FFiigguurree 11.. Mean CRP concentrations at the examined time-points in patients treated with single- or multi-vessel angioplasty
P PCCII ++ sstteenntt ssiimmppllee lleessiioonnss
P PCCII ++ sstteenntt ccoommpplleexx lleessiioonnss p=0.000001
p=0.007
p=0.03
p=0.002
p=0.00003 p=0.0007
FFiigguurree 22.. Mean CRP concentrations at the examined time-points in patients treated with angioplasty of coronary arteries with single or complex lesions
9 8 7 6 5 4 3 2 1
0 0 6 12 24 hours
0 6 12 24 hours
(p=0.001 and p=0.001, respectively, compared with the simple lesions group). A significant increase in mean concentrations of CRP at the examined time-points was observed in both groups (Figure 2). Greater stented lesion complexity was not associated with an additional increase of CRP levels (Table III).
Discussion
Concentration of CRP is one of the most important prognostic factors of theoccurrence of major adverse cardiac events (MACE) in patients with CAD. Although the CRP itself has the potential to contribute to the development of atherosclerosis, the correlation between elevated CRP level and the risk of MACE is stronger than that between CRP and the severity of CAD. C-reactive protein plays an important role as a proinflammatory and, simultaneously, proco- agulatory factor.
C-reactive protein level may reflect the intensity of inflammation in the coronary artery and discriminate patients with more severe or with a higher risk of atherosclerosis [13]. On the other hand, the inflammatory process within the arterial wall contributes to the development of unstable atherosclerotic plaque, which may result in its rupture, thrombosis and acute coronary syndrome [3, 14–15]. C-reactive protein plays a key role in the sequence of events that lead to thrombotic complications, effecting monocyte recruitment and activation, increased expression of adhesive molecules (ICAM-1, VCAM-1) and tissue factor (TF), increased MCP-1 production and induction of plasminogen activator inhibitor expression (PAI–1) [16–19]. Thrombotic complications play the key role in pathogenesis of recurrence of ischaemia, reinfarction, the need of repeated revascularisation and death.
P
PCCII ++ sstteenntt PPCCII ++ sstteenntt pp 11 aarrtteerryy >>11 aarrtteerryy
N
N==5511 NN==2222
CRP 0 (mg/L) 1.30±0.91 1.52±0.99 0.375
CRP 6 h (mg/L) 1.96±2.09 2.64±2.59 0.237
CRP 12 h (mg/L) 2.69±2.48 4.15±3.17 0.039
CRP 24 h (mg/L) 3.76±3.13 5.69±3.38 0.021
Stented vessel: (LAD/Cx/RCA) (LAD-Cx/LAD-RCA/Cx-RCA/LAD-Cx-RCA) –
(24/16/11) (9/9/1/3)
Stenosis length [mm]
LAD 13.39±4.89 12.30±3.17 0.395
Cx 12.21±4.83 11.52±4.18 0.696
RCA 14.39±6.06 13.83±7.56 0.840
Reference diameter [mm]
LAD 3.25±0.51 3.17±0.43 0.581
Cx 2.87±0.28 2.95±0.54 0.621
RCA 3.57±0.39 3.38±0.29 0.186
Post PCI stent diameter [mm]
LAD 3.39±0.50 3.21±0.39 0.188
Cx 2.98±0.23 3.14±0.51 0.409
RCA 3.69±0.32 3.52±0.33 0.259
Stent length [mm]
LAD 18.75±7.22 15.47±3.76 0.081
Cx 17.33±9.19 16.00±5.34 0.712
RCA 21.30±6.67 20.40±8.69 0.798
Total stent length [mm] 19.04±7.48 29.18±14.95 0.0005
Total stent area [mm2] 204.32±88.22 300.51±160.48 0.002
T
Taabbllee IIII.. CRP levels at the examined time-points with respect to coronary arteries treated with deployment of stent and selected angiographic details
Abbreviations: LAD – left anterior descending, CX – circumflex, RCA – right coronary artery
PCI is an effective method for treating coronary artery disease. Mechanical dilation of the artery lumen is, however, associated with its injury and a local inflammatory reaction [20–21]. Animal models of artery injury have demonstrated the considerable role of CRP in the development of this effect [19].
Stent deployment causes greater injury to the arterial wall and a more intense inflammatory response than balloon angioplasty [10]. An inflammatory response to the insertion of stent is reflected by a marked increase in plasma CRP level.
Gottsauner-Wolf et al. [7] observed a CRP increase pattern within 120 hours following stent deployment. In all patients, the greatest increase in CRP was observed 48 hours after stent implantation. In patients who had restenosis at 6-month follow-up, the mean plasma CRP after stent implanation was higher and peaked at 36 hours. Moreover, significantly higher CRP
levels after stent deployment were found in patients with complex lesions (type C according to ACC/AHA).
These findings may indicate an individually diverse inflammatory response to stent insertion. It may also be assumed that angioplasty of complex lesions may be associated with more intense local injury to the arterial wall and a more expressed inflammatory response.
Almagor et al. [22] analysed alterations of CRP levels following stent deployment in patients with various types of CAD. Increased CRP level was shown to be higher in patients with acute coronary syndromes without ST segment elevation than in patients with stable CAD [22]. This may confirm previous observations that complex stenoses correspond more frequently to unstable atherosclerotic plaques which are more vulnerable, mainly due to more intense local inflammation [23]. Interventional treatment of such lesions may cause a more severe inflammatory reaction.
P
PCCII ++ sstteenntt PPCCII ++ sstteenntt pp S
Siimmppllee sstteennoossiiss CCoommpplleexx sstteennoossiiss a
acccc.. ttoo AAHHAA ((AA//BB11)) aacccc.. ttoo AAHHAA ((BB22//CC)) N
N==4499 NN==2244
CRP 0 [mg/L] 1.42±0.95 1.25±0.89 0.448
CRP 6 h [mg/L] 2.21±2.18 2.06±2.46 0.794
CRP 12 h [mg/L] 3.02±2.46 3.35±3.36 0.638
CRP 24 h [mg/L] 4.39±3.07 4.25±3.81 0.870
Stenosis length [mm] 14.17±6.29 23.88±11.19 0.001
Reference diameter [mm]
LAD 3.26±0.53 3.16±0.39 0.485
Cx 2.86±0.27 2.97±0.56 0.529
RCA 3.44±0.36 3.51±0.34 0.671
AHA lesion type
LAD (A/B1/B2/C) 27 (15/12/0/0) 17 (0/1/15/1)
Cx (A/B1/B2/C) 16 (7/9/0/0) 12 (3/3/5/1) –
RCA (A/B1/B2/C) 19 (9/10/0/0) 8 (2/3/2/1)
PTCA + stent:
1 vessel 37 (75.5%) 14 (58.3%)
2 vessels 12 (24.5%) 7 (29.2%) –
3 vessels – 3 (12.5%)
Inflations
Frequency 2.14 (1–5) 2.23 (1–6) 0.126
Max pressure [atm.] 13.01 (7–18) 13.89 (14–22) 0.068
Total time [s] 89.60 (7–254) 92.38 (21–300) 0.31
Total stent length [mm] 18.71±7.96 26.75±15.82 0.001
Total stent area [mm2] 177.47±109.26 279.2±169.69 0.012
T
Taabbllee IIIIII.. CRP levels in the examined time-points with respect to the type of coronary artery stenosis treated with deployment of stent (acc. to ACC/AHA) and selected angiographic details
Abbreviations: as in Table II
Our study intended to establish the relationship between plasma CRP levels and the extent of periprocedural artery injury. It was assumed that the degree of iatrogenic injury of a vessel depends on the total length of the arterial segment in which intervention was performed and the complexity of the treated lesion.
The results of our study confirm that stent deployment is associated with an inflammatory response expressed with a marked increase in plasma C-reactive protein concentration. This effect was clearly observed regardless of the established criteria of the analysis (single or multivessel intervention, angioplasty of simple or complex lesions). At the same time, intervention within >1 vessel and, thus, involving an injury to the larger artery area was associated with a greater increase in CRP level already at 12 hours and was more evident after 24 hours (3.74- vs 2.89-time/fold increase for single vessel intervention).
A similar relationship was not observed in subjects with complex lesions in whom the increased CRP level was similar to patients with simple stenoses. Although the total length of deployed stent in patients with complex lesions was greater than for the simple lesion group, it was less obvious than in single- and multi-vessel interventions. Multivariable regression analysis showed that the total length of inserted stent significantly contributed to the increase in CRP concentration.
Available studies on CRP levels after coronary intervention involved maximum follow-up of 48–120 hours. In the present study, the shorter follow-up was mainly due to the fact that following effective coronary angioplasty the patients were discharged after one or two days. It may be assumed that peak and persistent increased levels of CRP subsequent to the deployment of stent would have different patterns in the analysed groups. However, it seems that this effect would depend on individual differences in inflammatory response rather than on the acute reaction associated with the extent of arterial injury.
The limitations of this study include the relatively small study group of patients and the lack of long-term clinical follow-up required to determine the influence of the observed CRP level increase on the rate of MACE. It remains unclear whether a larger increase in CRP level may be indicative of a worse prognosis in patients with more extensive coronary intervention.
The presented outcomes may affect the process of clinical decision-making. Additionally, they justify the requirement to place emphasis on minimising periprocedural artery injury, e.g. by planning procedures to avoid more extended interventions. The results also indicate the need to make more intense use of anti-inflammatory features of cardiac drugs (such as statins), particularly in multi-vessel interventions.
Conclusions
1. Percutaneous coronary intervention with stent deployment in patients with stable coronary artery disease is associated with an inflammatory reaction reflected by a significant increase in plasma CRP levels.
2. In the study group the increase in CRP concentration at 12 and 24 hours following the insertion of stent was higher in multi-vessel interventions than in single vessel procedures. This effect was significantly enhanced by the greater total stent length in multi-vessel interventions.
3. In the study group stent deployment within complex coronary lesions (classified according to ACC/AHA) was not associated with a greater increase in CRP levels compared to simple lesions.
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Zmiany stężenia białka C reaktywnego po angioplastyce wieńcowej z implantacją stentu w zależności od rozległości
uszkodzenia naczynia w czasie zabiegu
P
Paawweełł KKrraalliisszz11,, HHaalliinnaa KKeemmoonnaa22,, SSłłaawwoommiirr DDoobbrrzzyycckkii11,, H
Haannnnaa BBaacchhóórrzzeewwsskkaa--GGaajjeewwsskkaa11,, KKoonnrraadd NNoowwaakk11,, ZZddzziissłłaaww SSaawwiicckkii33
1Zakład Kardiologii Inwazyjnej, Akademia Medyczna, Białystok
2Zakład Laboratoryjnej Diagnostyki Klinicznej, Akademia Medyczna, Białystok
3Klinika Medycyny Ratunkowej, Akademia Medyczna, Białystok
Adres do korespondencji:
lek. med. Paweł Kralisz, Zakład Kardiologii Inwazyjnej, SPSK Akademii Medycznej, ul. Skłodowskiej 24a, 15-276 Białystok, tel.: +48 85 746 84 96, faks: +48 85 746 88 28, e-mail: paqral@yahoo.com
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Prraaccaa wwppłłyynnęęłłaa:: 31.11.2005. ZZaaaakkcceeppttoowwaannaa ddoo ddrruukkuu:: 21.12.2005 Streszczenie
W
Wssttęępp:: Przezskórne rozszerzenie tętnicy wieńcowej i implantacja stentu indukują ostry proces zapalny w obrębie ściany na- czynia. Odpowiedź zapalna jest odzwierciedlona istotnym systemowym wzrostem stężenia białka C-reaktywnego (CRP). Wyka- zano, że stopień wzrostu stężenia CRP może zależeć od klinicznego zaawansowania choroby wieńcowej oraz od leczenia zasto- sowanego w okresie okołozabiegowym.
C
Ceell:: Ocena zależności wzrostu stężenia białka CRP od rozległości mechanicznego uszkodzenia naczynia w czasie implanta- cji stentu.
M
Meettooddyy:: 73 kolejnych pacjentów (51 mężczyzn) ze stabilną chorobą wieńcową i z prawidłowym stężeniem białka C-reaktywne- go (≤3 mg/dL) poddano zabiegom przezskórnej angioplastyki wieńcowej z elektywną implantacją stentu. Stężenia CRP oznaczono metodą wysokiej czułości (high–sensitivity CRP, hsCRP) przed zabiegiem angioplastyki wieńcowej, po 6, 12 i 24 godz. od implantacji stentu. Angiogramy wszystkich pacjentów poddano analizie ilościowej (interwencja jedno- vs wielonaczyniowa) oraz jakościowej (obejmującej ocenę zwężenia wg klasyfikacji ACC/AHA). Uzyskano następujące dane angiograficzne i szczegóły dotyczące zabiegu:
wymiar referencyjny, lokalizacja i długość zwężenia, całkowita długość stentowanego segmentu, średnica stentu po implantacji, maksymalne ciśnienie, częstość i łączny czas inflacji balonu w naczyniu.
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Wyynniikkii:: W badanej grupie pacjentów obserwowano istotny wzrost średniego stężenia hsCRP po 24 godz. w stosunku do po- miaru wyjściowego (1,36±0,93 mg/L i 4,34±3,3 mg/L, p <0,0001). Przezskórną interwencję wieńcową, jednonaczyniową z implanta- cja stentu, przeprowadzono wśród 51 pacjentów i interwencję wielonaczyniową wśród 22 pacjentów. Średnie stężenie hsCRP było takie samo przed interwencją i po 6 godz. w obu grupach. Wzrost stężenia hsCRP po 12 i 24 godz. był istotnie wyższy wśród pa- cjentów z wielonaczyniową interwencja wieńcową z implantacja stentu w stosunku do grupy pacjentów z interwencja jednonaczy- niową (odpowiednio 2,69±2,48 vs 4,15±3,17; p=0,039 i 3,76±3,13 vs 5,69±3,38; p=0,021). Nie wykazano zależności pomiędzy stop- niem wzrostu stężenia hsCRP a stopniem złożoności zwężenia poddanego zabiegowi. Analiza wieloczynnikowej regresji wskazała, że łączna długość stentu istotnie przyczyniła się do przyrostu średniego stężenia białka CRP w 24. godzinie obserwacji (p=0,01).
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Wnniioosskkii:: W badanej grupie pacjentów, odpowiedź zapalna, wyrażona przez osoczowe stężenie hsCRP, była większa wśród pacjentów z wielonaczyniowa interwencją wieńcową z implantacja stentu i do tego efektu istotnie przyczyniła się większa cał- kowita długość implantowanego stentu.
S
Słłoowwaa kklluucczzoowwee:: białko C-reaktywne, stabilna choroba wieńcowa, implantacja stentu, choroba naczyń
Kardiol Pol 2006; 64: 364-371
