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The causes of coronary artery spasm in patients with variant angina remain unknown. The segmental location of spasm indicates local hyperreactivity, but a diffuse increased coronary vasoconstriction, suggesting a substrate which could facilitate spasmogenic modifications, has been reported in many patients.1 The membrane sodium–hydrogen (Na+–H+) exchanger (NHE) is a major regulator of intracellular pH (pHi).2 An increased activity of the NHE isoform 1 (NHE-1) in smooth muscle cells has been suggested to favour vasoconstriction by causing intracellular alkalinisation and calcium overload.3 Furthermore, potential triggers of spasm (catecholamines, endothelin-1) have been shown to increase NHE-1 activity.4 In this study we investigated NHE-1 activity in platelets of patients with variant angina.
The study group included 17 patients (13 men, 58 (9) years) with variant angina (angina attacks at rest, associated with transient ST segment elevation). Patients with hypertension and diabetes were excluded. The control group included 17 healthy subjects (13 men, 55 (6) years) without any history of chest pain, and with normal physical examination, ECG, and laboratory tests.
Because of ethical reasons, calcium antagonist drugs could not be withdrawn in patients, who, however, were invited not to take these drugs on the day of the study. Other drugs were withdrawn for more than one week before the study.
A blood sample of 50 ml was drawn from an antecubital vein. To …
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