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Mast Cell Tryptase Measurements During Cardiac Catheterization and the Effect of Heparin Administration Farhad Ardeshirpour Joseph P. Pye, BS Gregory J. Dehmer, MD Efthymios N. Deliargyris, MD Cardiac Catheterization Laboratory University of North Carolina School of Medicine
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Mast Cell Tryptase Measurements During Cardiac Catheterization and the Effect of Heparin Administration
Joseph P. Pye, BS
Gregory J. Dehmer, MD
Efthymios N. Deliargyris, MD
Cardiac Catheterization Laboratory
University of North Carolina School of Medicine
Chapel Hill, North Carolina, USA
It is now well recognized that inflammation plays a central role in the development and progression of atherosclerotic vascular disease (ASVD). Mast cells are part of this response and are activated at sites of plaque rupture, the central event in the genesis of myocardial infarction. (Figure 1).
When activated, mast cells release mediators that regulate plaque inflammation and the progression to myocardial infarction. We recently demonstrated that tryptase, a mediator specific to mast cells, is indeed elevated in patients with ASVD (Figure 2). Measurement of tryptase levels may therefore emerge as a novel means for the detection of ASVD.
Tryptase, which is normally bound to heparin within mast cells, is released in an unbound state upon activation. Heparin is routinely used both for the treatment of patients with myocardial infarction and also as a prophylactic measure during cardiac catheterization. We hypothesized that heparin’s strong affinity for tryptase might effect tryptase measurements during cardiac catheterization. To test this hypothesis we measured tryptase levels in patients undergoing cardiac catheterization in the presence or absence of heparin.
1. Patient Selection: Study subjects were recruited from patients referred for cardiac catheterization for recognized clinical indications. All patients provided informed consent.
2. Sample Collection and Analysis: Blood samples from the left main coronary artery and coronary sinus were collected in 47 patients before and after cardiac catheterization. Heparin was administered to 24/47 patients (51%), based on the operator’s discretion. Four serial samples were obtained in patients who did not receive heparin (control group), while two samples were obtained both before and after heparin administration in the test group. Samples were processed and serum was stored at -80C for later analysis. Tryptase was measured by immunoassay (UniCap, Pharmacia, Kalamazoo, MI), and values were expressed in g/l.
3. Statistical Analysis: All values are expressed as the mean standard deviation. Paired and unpaired student t-tests were used to compare differences between groups. P‑values less than 0.05 were considered significant.
Table 1. Baseline Characteristics
Baseline characteristics for the two study groups are shown in Table 1. Patients in the heparin group were younger and had a lower LVEF, however these differences were not significant.
*left ventricular ejection fraction; †erythrocyte sedimentation rate
Tryptase levels before and after cardiac catheterization in the 23 patients that did not receive heparin (control group) are shown in Figure 3. Mean tryptase levels did not demonstrate a significant difference before and after cardiac catheterization in either the left main or coronary sinus sampling sites (8.3 ± 4.0 vs. 7.9 ± 4.1µg/ml, and 8.3 ± 4.1 vs. 7.9 ± 3.8 µg/ml respectively, p=ns).
Samples obtained before and after cardiac catheterization in the heparin-treated group are shown in Figure 4. There was a significant (57%) reduction in the tryptase levels obtained from the left main (7.6 ± 4.5 vs. 3.3 ± 3.5µg/ml, p<0.01). Similarly, there was a significant (51%) reduction in tryptase levels obtained from the coronary sinus (7.6 ± 4.4 vs. 3.7 ± 4.3 µg/ml, p<0.02).
Heparin administration during cardiac catheterization resulted in a significant decrease in measured serum tryptase levels. Tryptase levels obtained following heparin administration were >50% reduced compared to baseline levels.
In the absence of heparin there was no difference in tryptase levels obtained before or after cardiac catheterization, suggesting that it was the presence of heparin and not the procedure itself that led to the reduction in tryptase levels.
As inflammation emerges as a central mechanism in the development of ASVD, there is an increasing need for identification and measurement of sensitive inflammatory markers.
Tryptase is a promising novel marker for the presence of ASVD, however, as our study demonstrates, levels obtained in the presence of heparin may underestimate the actual underlying risk for significant ASVD.