Elevated B-type Natriuretic Peptide Levels in Patients Undergoing Coronary Stenting

ABSTRACT: Background. Release of B-type natriuretic peptide (BNP) may be triggered by tissue hypoxia even in the absence of left ventricular (LV) dysfunction, generating interest in studying changes in levels following percutaneous coronary intervention (PCI). Though the prognostic role of natriuretic peptides following elective PCI has been documented, most studies only assessed single pre-procedural levels. Previous studies assessing BNP rise following balloon angioplasty or coronary stenting have reported conflicting results; most of these studies excluded patients with recent acute coronary syndrome (ACS). Results. We studied the changes in BNP following coronary stenting in 100 patients across the entire spectrum of ACS and observed a significant rise in BNP following stenting. Baseline BNP levels > 100 pg/ml were observed in 31% of patients; following PCI, 45% of patients were noted to have BNP > 100 pg/ml. In patients with baseline BNP < 100 pg/ml, 20% had post-procedure BNP levels > 100 pg/ml. Post-PCI BNP levels were significantly higher in patients with recent ACS (versus those with stable angina), those with LV dysfunction, high baseline troponin I, visible angiographic thrombus and those with post-PCI TIMI 1–2 flow. Patients with post-PCI BNP levels > 100 pg/ml had a trend toward more frequent occurrence of TIMI no reflow following PCI (9.3 versus 1.7%; p = 0.07). Conclusion. Recent ACS, raised basal troponin, LV dysfunction, and presence of angiographic thrombus were all associated with high baseline and post-PCI BNP levels. Though recent ACS was the strongest predictor of elevated BNP levels, BNP levels rose following PCI even in patients with chronic stable angina.

J INVASIVE CARDIOL 2011;23:240–245

Key words: congestive heart failure; left ventricular dysfunction

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B-type natriuretic peptide (BNP) is a novel cardiac marker that is released into the circulation in response to ventricular dilatation and pressure overload.^1–3 It was originally introduced as a biomarker for congestive heart failure (CHF), where levels are known to be elevated in direct proportion to symptom severity as well as degree of left ventricular (LV) dysfunction.^4–6  Furthermore, BNP has been shown to have both diagnostic and prognostic value in a wide variety of other cardiac disorders, including acute coronary syndromes (ACS),^7,8 myocardial infarction,^9,10 and stable coronary heart disease.^11,12

Since it is known that tissue hypoxia by itself can also trigger BNP release, even in the absence of LV dysfunction,^13,14 there has been keen interest in changes in BNP levels following percutaneous coronary interventions (PCI), which also induces transient controlled myocardial ischemia. Studies in patients undergoing plain balloon angioplasty reported that although BNP levels did rise following PCI, there was variability with regard to the timing of the BNP peak.^15,16 Whether coronary stenting, which results in much more shortened ischemic times as compared to plain balloon angioplasty, is also associated with a rise in BNP is not well characterized, with studies reporting conflicting results.^17,18 Moreover, these studies excluded patients with ACS or recent myocardial infarction.

Given the increasing role of PCI in contemporary cardiology practice, we studied the changes in BNP following PCI in 100 patients across the entire spectrum of ACS.

Methods

The patient population comprised 100 consecutive patients undergoing coronary angioplasty for symptomatic coronary artery disease (CAD) at our institution from October 2010 to December 2010, who were included prospectively in the study. The study conformed to the institutional ethical guidelines and all patients were included after informed consent. Patients with symptomatic heart failure, significant valvular heart disease and hepatic or renal disease were excluded. All patients undergoing PCI were given 70 IU/kg unfractionated heparin before PCI, while the use of glycoprotein IIb/IIIa inhibitor and coronary stent type (bare-metal or drug-eluting stent) was in accordance with the operator’s discretion. Patients with > 70% stenosis of only 1 epicardial coronary artery vessel were classified as single-vessel disease and those with > 70% stenosis of > 1 epicardial coronary artery were classified as multivessel disease. Coronary artery lesions were classified qualitatively according to modified American College of Cardiology/American Heart Association (ACC/AHA) classification into type A, B, or C; types A and B1 lesions were categorized as simple, while types B2 and C were categorized as complex lesions.19 For each procedure, the duration, balloon inflation pressure, and number and type of stent were recorded. Any complications occurring during or within the first 24 hours of PCI were also recorded.

Biochemistry. Blood samples were taken for analysis of routine biochemistry, including blood sugar, renal function and lipid profile (total cholesterol, low-density lipoprotein, high-density lipoprotein, triglyceride). Serum BNP and troponin I levels were estimated prior to PCI and at 24 hours after PCI. Samples were collected in EDTA tubes and analyzed with the use of a fluorescence immunoassay kit (Triage^®; Biosite Inc., San Diego, California) for quantitative estimation. The lower detectable ranges for serum BNP and troponin I were 5 pg/ml and 0.40 ng/ml, respectively.

Statistical analysis. SPSS version 15 was used for statistical analysis, with continuous data represented as means ± standard deviations and categorical data represented as percentages.  Difference of means between independent groups was analyzed with student’s t-test; categorical variables were analyzed with the Chi-square test. Univariate and multivariate logistic regression was used for analyzing predictors of high baseline/post-PCI BNP levels. Correlation of BNP level with variables was analyzed with Pearson and Spearman correlation tests.

Results

The demographic and clinical patient profiles are depicted in Table 1. The mean age was 56.14 ± 9.93 years (range: 25–82 years) and 87% were males. Diabetes was present in 44%, hypertension in 58%, 33% were smokers, and 60% of patients were categorized as obese (BMI > 25 kg/m2). Presentation with chronic stable angina was noted in 45%, while a history of recent ACS was present in 55%. The angiographic profile of the study population is shown in Table 2. The most common target vessel was the left anterior descending artery in 61%, followed by the right coronary artery in 31% and left circumflex artery in 25%. Baseline 0–1 TIMI flow was present in 30.2% of patients. Complex coronary lesions (types B2/C according to ACC/AHA classification) were present in 25%, while a visible angiographic thrombus was noted in 16% of cases. The mean left ventricular ejection fraction (LVEF) was 49.76% and mean left ventricular end diastolic pressure (LVEDP) was 14.4 ± 4.61 mmHg. No patient developed contrast-induced nephropathy.

Coronary angioplasty was performed through the radial route in 44% of cases; multivessel angioplasty was performed in 21%, while drug-eluting stents were deployed in 85% of cases. Glycoprotein IIb/IIIa inhibitors were used in 61% of cases undergoing PCI (abciximab in 24%, tirofiban in 67%, and eptifibatide in 9% of cases). Nearly all patients (97%) underwent balloon angioplasty followed by stent implantation, while only 3% underwent direct stenting. Post-procedural TIMI 3 flow was present in 94.8%, while only 5.2% had TIMI 1–2 flow.

Following PCI, mean BNP levels demonstrated a significant rise (mean BNP: 145.26 pg/ml pre-PCI and 194.65 pg/ml post-PCI; p < 0.01), while mean troponin I levels showed a trend toward reduction, though this was statistically not significant (mean troponin I: 2.07 ng/ml pre-PCI to 1.45 ng/ml post-PCI; p = not significant). Baseline BNP levels > 100 pg/ml were observed in 31% of patients; post-PCI, 45% of patients were noted to have BNP > 100 pg/ml. In patients with baseline BNP < 100 pg/ml, 20% had post-procedure BNP levels > 100 pg/ml (mean BNP: 38.45 pg/ml pre-PCI versus 224.36 pg/ml post-PCI; p < 0.001). Interestingly, in this group of patients, though troponin I levels also demonstrated a rise, this was of borderline statistical insignificance (mean levels troponin I: 0.99 ng/ml pre-PCI to 1.80 ng/ml post-PCI; p = 0.06).

Analysis of baseline BNP levels in different subgroups. Baseline BNP levels were significantly higher in patients with recent ACS (235.88 pg/ml versus 33.58 pg/ml; p < 0.001), angiographic thrombus (485.16 pg/ml versus 114.36 pg/ml; p < 0.001), LV dysfunction (198.86 pg/ml versus 76.35 pg/ml; p = 0.03), and those with raised baseline troponin I levels (426.59 pg/ml versus 136.15 pg/ml; p < 0.001). Patients with recent ACS and LV dysfunction had the highest baseline BNP levels (281.14 pg/ml), followed by those with recent ACS and normal LV systolic function (140.29 pg/ml), chronic stable angina patients with LV dysfunction (34.31 pg/ml) and chronic stable angina with normal LV function (33.05 pg/ml). Though statistically not significant, patients with pre-PCI TIMI 0–1 flow demonstrated a trend toward higher baseline BNP levels as compared to those with TIMI 2–3 flow (181.21 pg/ml versus 129.7 pg/ml, respectively); similar trends toward higher baseline BNP levels were noted in patients with complex versus simple coronary lesions (178.72 pg/ml versus 134.11 pg/ml, respectively). Patients with post-PCI TIMI 1–2 flow had a trend toward higher baseline BNP values as compared to those with post-PCI TIMI 3 flow (188.3 pg/ml versus 143.45 pg/ml, respectively, though this was again statistically not significant). Obese patients (body mass index > 25 kg/m2) had significantly lower baseline BNP (89.03 ± 128.47 pg/ml) as compared to those with body mass index < 25 kg/m2 (238.99 ± 413.02 pg/ml; p < 0.001).

Predictors of raised baseline BNP (Table 3). Univariate predictors of high baseline BNP (> 100 pg/ml) included history of recent ACS (p < 0.001), LV dysfunction (p = 0.008), presence of thrombus (p = 0.006) and baseline troponin I > 0.40 ng/ml (p < 0.001); however, on multivariate analysis, only recent ACS was a statistically significant predictor of high baseline BNP (p = 0.004). Age was positively correlated with BNP (Pearson correlation coefficient = 0.32; p = 0.001) and BMI was negatively correlated with BNP (Pearson correlation coefficient = -0.248; p = 0.013).

Comparison between patients with baseline BNP > or ≤ 100 pg/ml (Table 4). This comparison revealed that those with higher BNP were older (mean age: 59.3 years versus 54.7 years; p = 0.03), had lower ejection fraction (44.27% versus 52.26%; p < 0.001), more frequently had history of recent ACS (90% versus 39%; p < 0.001), had significantly higher mean baseline troponin I levels (5.90 ng/ml versus 0.32 ng/ml; p < 0.001), higher incidence of angiographic thrombus (23% versus 1.5%; p < 0.001) and had more frequent use of intra-procedure glycoprotein IIb/IIIa inhibitors (77% versus 54%; p = 0.04). Presence of baseline TIMI 0–1 flow was more frequent in those with BNP > 100 pg/ml (37% versus 24%); however, this was of borderline statistical significance (p = 0.055). Patients with baseline BNP > 100 pg/ml continued to have high troponin I levels even after PCI (mean troponin I: 4.12 ng/ml versus 0.24 ng/ml in those with baseline BNP > or < 100 pg/ml). There was no difference between these 2 groups in terms of number of stents used, stent length or diameter, or balloon inflation pressures.

Analysis of post-PCI BNP levels in different subgroups (Table 5). Post-PCI BNP levels were significantly higher in patients with recent ACS as compared to those with stable angina (296.50 pg/ml versus 69.11 pg/ml; p < 0.001), LV dysfunction (275.26 pg/ml versus 91.01 pg/ml; p < 0.001), angiographic thrombus (490.38 pg/ml versus 167.76 pg/ml; p < 0.001), and those with high baseline troponin I (486.16 pg/ml versus 122.71 pg/ml; p < 0.001). Also, patients with post-PCI TIMI 3 flow had significantly lower BNP at 24 hours as compared to those with post-PCI TIMI 1–2 flow (176.36 pg/ml versus 527.40 pg/ml; p < 0.01). Patients with high BNP levels (> 100 pg/ml) at 24 hours post-PCI more frequently had history of ACS (83% versus 32%; p < 0.001) and higher baseline troponin I (4.36 ng/ml versus 0.28 ng/ml; p < 0.001) as compared to those with post-PCI BNP levels < 100 pg/ml. There was a trend toward more frequent occurrence of TIMI no reflow following PCI in this group as compared to those with BNP < 100 pg/ml following PCI (9.3% versus 1.7%; p = 0.07).

Predictors of raised post-PCI BNP (Table 6). Univariate predictors of high BNP at 24 hours (> 100 pg/ml) were recent ACS (p < 0.001), LV systolic dysfunction (p < 0.001), peri-procedure TIMI flow < 3 (p = 0.03), and basal troponin I > 0.40 ng/ml (p = 0.001). On multivariate analysis, recent ACS (p = 0.003) and raised baseline troponin I > 0.40 ng/ml (p = 0.02) were the only predictors of raised BNP at 24 hours.

There was no significant difference in baseline (173.13 pg/ml versus 139.33 pg/ml; p = not significant) or 24-hour post-PCI BNP (220.77 pg/ml versus 185.38 pg/ml; p = not significant) levels in those undergoing single-vessel or multi-vessel PCI, respectively.  Though patients with ACS had significantly higher baseline BNP as compared to those with chronic stable angina (235.88 pg/ml versus 33.58 pg/ml; p < 0.001), both groups demonstrated a significant rise in post-PCI BNP (296.5 pg/ml in those with ACS and 69.11 pg/ml in those with chronic stable angina; p < 0.01).

Discussion

The natriuretic hormone BNP is a novel cardiac biomarker that is secreted by the ventricles in response to volume and pressure overload and was initially introduced as a prognostic marker for patients with congestive heart failure.^20,21 Presently, there are sufficient data to establish the diagnostic and prognostic utility of BNP across the spectrum of ACS as well as in those with stable CAD.^8,22–24 Ischemia-induced transient ventricular dysfunction can by itself lead to BNP release even in the absence of evident myocardial necrosis, accounting for elevated BNP levels in patients with ACS and stable CAD.

There is also evidence that tissue hypoxia can trigger BNP release, even in the absence of LV dysfunction, either reflecting cleavage of stored propeptides or increase in BNP gene expression, with consequent BNP release from the ventricles.^13,14,25 Hence, interest has focused on changes in BNP levels following PCI, which also induces transient controlled myocardial ischemia followed by mechanical establishment of reperfusion. Release of BNP in patients undergoing plain balloon angioplasty was confirmed in initial studies; however, there was inconsistency with regard to the timing of the BNP peak following PCI, with some studies showing transient increase in BNP levels 24 hours following balloon angioplasty,¹⁵ and others reporting that peak BNP levels occurred immediately after balloon angioplasty, and returned to baseline 4 hours later.¹⁶

Though the prognostic role of natriuretic peptides following elective PCI and stenting has been documented, only single pre-procedural levels were evaluated in these studies.^26,27 Whether coronary stenting, which results in shorter procedural ischemic times as compared to plain balloon angioplasty, is also associated with rise in BNP following PCI, has not been well characterized, with studies reporting conflicting results.

We observed a significant rise in overall mean BNP levels at 24 hours post-PCI, despite a trend toward reduction in troponin I levels. Following PCI, 45% of patients had BNP > 100 pg/ml; nearly 20% of patients had post-PCI BNP levels > 100 pg/ml despite pre-PCI BNP levels < 100 pg/ml (mean BNP: 38.45 pg/ml pre-PCI versus 224.36 pg/ml post-PCI; p < 0.001). Patients with high post-PCI BNP more frequently had ACS, higher pre-procedure troponin I levels, more LV dysfunction and angiographic presence of thrombus; the incidence of no reflow following PCI was also more common in these patients. Though Tateishi et al15 also reported a rise in BNP at 24 hours following plain balloon angioplasty, our results contrast with previous studies of temporal changes in BNP levels following coronary stenting.^17,18 Cantor et al, in a study of 55 patients undergoing elective PCI, showed that though BNP levels did not change significantly at 6 hours post-PCI, there was an insignificant trend toward higher values at 18–24 hours post-PCI.17 Yildirir et al demonstrated that in patients undergoing coronary stenting, PCI did not cause any significant alteration in plasma BNP levels measured either at 1 or 24 hours; those with complex coronary lesions were more likely to have higher baseline BNP, a difference that persisted after stenting.¹⁸ These differences may be partly explained by the fact that patients with ACS were excluded in both of these studies, while our patient population was a relatively heterogeneous group, with nearly 55% of patients having a recent ACS. However, despite this, we observed that even patients with chronic stable angina demonstrated a significant rise in BNP following PCI (from 33.58 pg/ml to 69.11 pg/ml; p < 0.001).

The mechanism of post-PCI BNP rise is possibly related to peri-procedural ischemia, although other factors, like rise in LVEDP, contrast load and fluid administration, may also contribute. However, in our study, there was no difference in LVEDP between patients with pre-PCI BNP ≤ or > 100 pg/ml. Contrast- and fluid-related factors were also probably not significantly responsible for rise in BNP, as we observed that there was no difference in post-PCI BNP levels in patients undergoing single- or multivessel angioplasty. Though BNP may have multiple postulated beneficial effects on the coronary vasculature, including vasodilatation (of coronary microvessels as well as epicardial coronary arteries), and anti-proliferative and anti-migratory effects on vascular smooth muscle cells,^28–30 higher levels following PCI are correlated with development of higher adverse events at follow-up.

We measured baseline and 24-hour BNP levels (not at 1 or 6 hours after PCI as done previously), since only higher 24-hour post-PCI BNP levels (and not at baseline or 1-hour post-PCI) are reported to correlate with development of events at follow-up.³¹ Categorization of patients according to clinical presentation and LVEF revealed that irrespective of LV function, those with recent ACS had the highest baseline BNP levels. Among the 4 thus categorized groups, patients with recent ACS and LV dysfunction had mean baseline BNP levels of 281.14 pg/ml, followed by those with recent ACS and normal LV systolic function (140.29 pg/ml), chronic stable angina patients with LV dysfunction (34.31 pg/ml) and chronic stable angina with normal LV function (33.05 pg/ml).

Although patients with complex coronary lesions on angiography and pre-PCI TIMI 0–1 flow had higher baseline BNP levels (178.72 pg/ml in complex versus 134.11 pg/ml in simple coronary lesions; 181.21 pg/ml in TIMI 0–1 flow versus 129.7 pg/ml in TIMI 2–3 flow), this did not reach statistical significance. The positive correlation of complex coronary lesions with higher baseline BNP levels has also been demonstrated in previous studies and has been attributed to chronic or repetitive ischemia in these patients.¹⁸ Following PCI, those with TIMI 3 flow demonstrated a trend toward lower BNP levels as compared to those with post-PCI TIMI 0–2 flow; also, the incidence of no reflow after PCI was more common in those with higher BNP levels. Grabowski et al also observed that although BNP levels ≤ or > 100 pg/ml did not discriminate between pre-PCI TIMI flow grade 3, post-PCI, patients with TIMI flow < 3 had higher BNP levels.³² Persistent elevations in BNP (> 80 pg/ml) at 24 hours and 7 days following successful PCI have also been shown to be correlated with development of LV dysfunction, despite a normal baseline ejection fraction.³³

Conclusion

In patients with CAD undergoing coronary stenting, levels of BNP frequently rise after coronary stenting. Recent ACS, raised basal troponin, LV systolic dysfunction, and presence of angiographic thrombus are all associated with high baseline and post-PCI BNP levels. Although recent ACS is the strongest predictor of elevated BNP levels, BNP levels rise after PCI even in patients with chronic stable angina.

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From the Department of Cardiology, Sanjay Gandhi PGIMS, Lucknow, India.
The authors report no conflicts of interest regarding the content herein.
Manuscript submitted February 18, 2011, provisional acceptance given March 28, 2011, final version accepted April 21, 2011.
Address for correspondence: Aditya Kapoor, MD, DM, FACC, Sanjay Gandhi PGIMS, Cardiology, Rae Bareli Rd., Lucknow, Uttar Pradesh 226014, India. Email: akapoor65@gmail.com