Myocardial ischemia-reperfusion damage after pacing-induced tachycardia in patients with cardiac syndrome X

Abstract

The presence of myocardial ischemia in syndrome X (chest pain, "ischemia-like" electrocardiogram changes, and normal coronary angiograms) is uncertain possibly because, when focally distributed, it may not cause contractile dysfunction or lactate production. We measured lipid hydroperoxides (ROOHs) and conjugated dienes (CDs), two sensitive, independent markers of ischemia-reperfusion oxidative stress, in paired aortic and great cardiac vein blood samples before and after pacing-induced tachycardia in nine patients with syndrome X. Diagnostic ischemic S-T segment changes during pacing were followed by a consistent increase in ROOH and CD levels in the great cardiac vein (from 4.83 +/- 1.18 micromol/l at baseline to 7.88 +/- 1.12 micromol/l and from 0.038 +/- 0.002 to 0.051 +/- 0.003 arbitrary units, respectively, P < 0.01). In controls, ROOH and CD levels did not change after pacing. The large postpacing cardiac release of lipid peroxidation products, consistently observed in all patients and similar to that previously observed after ischemia caused by percutaneous transluminal coronary angioplasty, is consistent with an ischemic origin of syndrome X.

Role of Coronary Vasoconstriction in Ischemic Heart Disease and Search for Novel Therapeutic Targets

“…30 This possibility is strongly supported by the release of ischemic reperfusion products into the coronary sinus at the end of pacing-induced ischemia. 31 Coronary microvascular constriction or inadequate dilation might also be related to medial smooth muscle hypertrophy of pre-arterial vessels in hypertrophied myocardium. • Strong stimuli capable of causing critical constriction also in normal vessels.…”

Acute Intravenous l -Arginine Infusion Decreases Endothelin-1 Levels and Improves Endothelial Function in Patients With Angina Pectoris and Normal Coronary Arteriograms

“…In agreement with this hypothesis, a recent study demonstrated that patients with CSX showed enhanced concentrations of lipid hydroxyperoxides and conjugated dienes, 2 sensitive and independent markers of oxidative stress. 28 However, this hypothesis is highly speculative and deserves further research to better understand this important issue.…”

Relation Between Platelet Response to Exercise and Coronary Angiographic Findings in Patients With Effort Angina

“…In these patients, a coronary microvascular dysfunction has been reported, 29,30 with several abnormalities potentially capable of promoting platelet activation, including endothelial dysfunction (with possible impaired NO production [31][32][33] and increased endothelin release 34,35 ), abnormal autonomic function, 36 increased sodiumhydrogen exchanger activity, 37,38 and oxidative stress. 39 On the other hand, during stress conditions, an enhanced myocardial release of adenosine, the main metabolic regulator of coronary blood flow, has been hypothesized to occur in patients with syndrome X and to have a major role in determining the main pathophysiological features of the syndrome. 40 Because adenosine is also a powerful antiplatelet agent, [41][42][43] we recently investigated whether adenosine might be involved in the reduction of platelet reactivity that occurs with exercise in these patients.…”