Enhanced red cell sodium-hydrogen exchange in microvascular angina

Koren, Wladimir; Koldanov, R.; Peleg, Edna; Rabinowitz, Betty; Rosenthal, Ted L.

doi:10.1093/oxfordjournals.eurheartj.a015441

Cited by 32 publications

(18 citation statements)

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“…6 The cause of the increased baseline platelet reactivity in anginal NCA patients remains to be ascertained. 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.…”

Section: Pathophysiological Considerationsmentioning

confidence: 99%

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

et al. 2003

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Background-Platelet reactivity is increased by exercise in patients with obstructive coronary artery disease (CAD) but not in patients with syndrome X. In this study, we prospectively investigated whether the platelet response to exercise might help distinguish, among patients with angina, those with obstructive CAD from those with normal coronary arteries (NCAs). Methods and Results-Venous blood samples were collected before and 5 minutes after exercise from 194 consecutive patients with stable angina. Platelet reactivity was measured by the platelet function analyzer (PFA)-100 system as the time for flowing whole blood to occlude a collagen-adenosine diphosphate ring (closure time). Coronary angiography showed CAD in 163 patients (84%) and NCA in 31 patients (16%

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Section: Pathophysiological Considerationsmentioning

confidence: 99%

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

et al. 2003

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“…In order to explain Gamze Babur Güler et al, Factor XIII Val34Leu polymorphism in patients with cardiac syndrome X the pathophysiological abnormality, various theories such as abnormal coronary flow reserve [8], insulin resistance [9], enhanced red cell sodium--hydrogen exchange [10], and abnormal cardiac sensitivity [11] were suggested. The most proven and accepted ideas are endothelial dysfunction and inflammation, and increased sensitivity to pain [3,12].…”

Section: Discussionmentioning

confidence: 99%

Factor XIII Val34Leu polymorphism in patients with Cardiac Syndrome X

et al. 2013

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“…Other potential causes of CMVD, reported in several studies, include increased insulin resistance, which may facilitate endothelial activation and dysfunction 24 , estrogen deficiency in women 25 , enhanced activity of the membrane sodium-hydrogen exchanger 26 and more recently, subclinical inflammation 27,28 .…”

Section: Causes Of Cmvdmentioning

confidence: 99%

Cornary microvascular dysfunction: an under- appreciatwed segment of coronary artery disease

et al. 2015

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Background:Coronary artery disease (CAD) is predicted to be the most common cause of death and disability globally by 2020 1 . Early detection and management of coronary artery disease can improve CAD related morbidity and mortality. Coronary angiogram remains the final diagnostic procedure for CAD. The current treatment strategy for CAD is confined mainly on disease of the epicardial coronary arteries. But, normal epicardial coronary arteries are found in 20% of cases undergoing coronary angiography for chest pain evaluation 2 . Detection of normal coronary arteries in patients having angina pectoris does not exclude further coronary events; rather these patients bear more risk of future cardiac ischemic syndromes. Several studies tried to discover the dilemma of non-obstructive CAD.They concluded with proposition of coronary microvascular dysfunction. Normal epicardial coronary arteries at angiography in patients with angina: Proposition of coronary microvascular dysfunction. Dysfunction of the coronary microcirculation was explained earlier by 3,4 . Cannon and Epstein termed the condition as microvascular angina (MVA) 5 . Lanza and Crea described as Coronary microvascular dysfunction (CMVD) and demonstrated the pathophysiology with the following figure 6 : Prognosis of Coronary microvascular dysfunction (CMVD):Microvascular circulatory disease was previously considered not to confer elevated risk of future adverse cardiovascular events or early mortality 7,8

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Enhanced red cell sodium-hydrogen exchange in microvascular angina

Abstract: Microvascular angina is associated with enhanced Na+/H+ exchange in erythrocytes, probably due to more extensive phosphorylation of the membrane antiporter sites.

Cited by 32 publications

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

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

Factor XIII Val34Leu polymorphism in patients with Cardiac Syndrome X

Cornary microvascular dysfunction: an under- appreciatwed segment of coronary artery disease

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