Platelet hyperaggregability in patients with chest pain and angiographically normal coronary arteries

Rubenfire, Melvyn; Blevins, Roger D.; Barnhart, Marion I.; Housholder, S. D.; Selik, Nancy R.; Mammen, Eberhard F.

doi:10.1016/0002-9149(86)90854-4

Cited by 54 publications

(23 citation statements)

References 28 publications

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“…These data are in agreement with an earlier report that some AMI patients exhibited significantly reduced F 1+2 and TAT plasma levels when compared with control individuals and patients with angina pectoris [25]. It has been shown recently that patients with chest pain and normal coronary arteries exhibit heightened platelet aggregability [26], and increased platelet P-selectin expression [27]resultant in excessive TG. This fact limits our abilities to regard such patients as ‘controls’, and similarly to distinguish this group from patients with acute coronary syndromes.…”

Section: Discussionsupporting

confidence: 92%

Failure of Thrombin Generation Markers to Triage Patients Presenting with Chest Pain

et al. 1999

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Thrombin generation (TG) is an important pathogenic factor in acute coronary syndromes including acute myocardial infarction (AMI). Since the diagnostic utility of TG remains uncertain we sought to determine whether markers of TG may triage patients presenting to the Emergency Department with chest pain. Soluble plasma levels of prothrombin fragment 1+2 (F₁₊₂), and thrombin/antithrombin III complexes (TAT) were determined by ELISA in 80 patients presenting with chest pain to the Emergency Department and compared with 20 controls. There were no differences in TG markers between patients with non-cardiac chest pain and healthy controls. Patients with unstable angina (UA), and congestive heart failure (CHF) did not differ from controls with respect to F₁₊₂, and TAT was elevated in UA patients (6.05 ± 1.15 ng/ml, p = 0.033) when compared with controls (3.34 ± 0.20 ng/ml). Contrary to expectations, TAT levels at presentation with AMI were well below the concentrations observed in patiens with UA and CHF. Moreover, plasma F₁₊₂ levels were significantly lower than in healthy controls (0.84 ± 0.10 ng/ml versus 1.22 ± 0.11, p = 0.026). At the time of presentation to the Emergency Department, F₁₊₂ and TAT failed to suitably triage patients with chest pain. The surprisingly low levels of TG markers in AMI patients before applying intensive therapy and reperfusion strategies deserves further investigation.

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Section: Discussionsupporting

confidence: 92%

Failure of Thrombin Generation Markers to Triage Patients Presenting with Chest Pain

et al. 1999

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“…A single report indicates that non-specific pain itself does not affect the concentrations of cytokines and soluble adhesion molecules [39]. It has been reported that patients with chest pain and normal coronary arteries exhibited increased platelet aggregation induced by adenosine diphosphate and epinephrine, and therefore indicating platelet activation [40]. Moreover, patients with the noncardiac chest pain exhibited similar β-thromboglobulin release [41], mean platelet volume, and aggregate ratios with patients with coronary artery disease [42].…”

Section: Discussionmentioning

confidence: 99%

Soluble PECAM-1, but Not P-Selectin, Nor Osteonectin Identify Acute Myocardial Infarction in Patients Presenting with Chest Pain

et al. 1999

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We sought to determine plasma levels of platelet/endothelial cell adhesion molecule-1 (PECAM-1), P-selectin, and platelet-derived osteonectin, and prospectively compare these data with the discharge diagnosis in patients presenting with chest pain in a community hospital Emergency Department. Soluble antigens were measured by ELISA in 44 subjects including patients with acute myocardial infarction (AMI) (n = 13), chest pain of noncardiac origin (n = 17), and compared to those of age- and sex-matched healthy controls (n = 14). Elevated soluble PECAM-1 (64.5 ± 18.3 ng/ml, p = 0.019), but not P-selectin (149.5 ± 49.8 ng/ml, p = NS), nor osteonectin (549.5 ± 159.1 ng/ml, p = NS), occurred in the AMI group as compared to patients with noncardiac chest pain (46.2 ± 7.5 ng/ml, 118.2 ± 40.1 ng/ml, and 619.4 ± 74.4 ng/ml, respectively). Increased plasma PECAM-1 may serve as a useful marker in the early detection of patients with AMI. Larger studies will be necessary to confirm the utility of soluble PECAM-1 in identifying AMI among patients presenting with chest pain.

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“…SPS was first described by Mammen and associates in 1983 at the Ninth International Joint Conference on Stroke and Cerebral Circulation (31). Subsequently, Mammen and associates described 41 patients with coronary artery disease and SPS; this was followed by a report in 1986 delineating this syndrome in a number of individuals with cerebrovascular disease; the inheritance was noted to be autosomal dominant (32). Finally in 1995 over 200 families, with a variety of arterial and venous thrombotic events due to SPS were described (33).…”

Section: Sticky Platelet Syndromementioning

confidence: 99%

Hereditary and Acquired Thrombophilic Disorders

Bick

2006

Clin Appl Thromb Hemost

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Platelet hyperaggregability in patients with chest pain and angiographically normal coronary arteries

Cited by 54 publications

References 28 publications

Failure of Thrombin Generation Markers to Triage Patients Presenting with Chest Pain

Failure of Thrombin Generation Markers to Triage Patients Presenting with Chest Pain

Soluble PECAM-1, but Not P-Selectin, Nor Osteonectin Identify Acute Myocardial Infarction in Patients Presenting with Chest Pain

Hereditary and Acquired Thrombophilic Disorders

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