Platelet function disorder in patients with coronary slow flow

Abstract

SummaryBackground: Some patients evaluated for chest pain with angiographically normal coronary arteries show coronary slow flow phenomenon (CSFP) on angiography. Slow flow of dye in epicardial coronary arteries is also not an infrequent finding in patients during routine coronary angiography. The precise pathophysiology of CSFP is not known yet.Hypothesis: This study investigates the presence of platelet function disorders in patients with CSFP.Methods: The patient group included 24 patients with CSFP detected by coronary angiography via the TIMI "frame count" method, and a control group included 23 patients with normal coronary flow. Platelet aggregability induced by use of ristocetin, collagen, and adenosine diphosphate (ADP), was measured from all blood samples in both control and patient groups.Results: The ratio of platelet aggregability increased significantly in patients with CSFP compared with patients with normal coronary flow (ristocetin 57.6 ± 15 vs. 45.4 ± 17.1, collagen 62.9 ± 16.4 vs. 48.9 ± 25.3, ADP 59.4 ± 18 vs. 42.4 ± 15.2, p < 0.05).Conclusion: Platelet aggregability is increased in patients with CSFP.

Assessment of the relationship between a narrow fragmented QRS complex and coronary slow flow

“…However, we were unable OR -odds ratio; CI -confidence interval; GFR -glomerular filtration rate; BP -blood pressure a significant independent predictor for a narrow fQRS complex, after adjustment for other parameters that univariate analysis had identified as to show any difference between the CSF and control groups in terms of age, gender, or other risk factors for CAD, including hypertension, diabetes, dyslipidemia, family history, and smoking; the exception was BMI, which was found to be higher in patients with CSF, consistently with some other previous studies [19,20]. Several important mechanisms have been proposed for the development of CSF, including endothelial dysfunction, diffuse atherosclerosis, microvascular vasomotor dysfunction, smallvessel disease, imbalance of vasoactive substances, and raised platelet aggregability [3][4][5][6]. Inflammation has also been reported to play an important role in the development of CSF [7].…”

“…It is not a rare angiographic finding, having a reported incidence of 1-7% in patients undergoing coronary angiography for suspected CAD [2]. Although neither the exact etiologies nor the pathophysiological mechanisms are yet fully understood, several potential mechanisms have been proposed, including microvascular and endothelial dysfunction, small-vessel disease, diffuse atherosclerosis, increased platelet aggregability, and inflammation [3][4][5][6][7]. CSF has been linked to various clinical manifestations, such as hypertension, stable and unstable angina pectoris, acute myocardial infarction, life-threatening arrhythmias, and sudden cardiac death [8].…”

Increased circulating soluble CD40 levels in patients with slow coronary flow phenomenon: an observational study

“…Abnormal slow flow pattern in coronary arteries has been concluded to be a manifestation of diffuse atherosclerotic disease due to endothelial injury without creating an angiographically visible coronary lesion (16); therefore, SCF may be an early manifestation of diffuse atherosclerosis involving both microvascular system and epicardial coronary arteries (4). Additionally, inflammation (17,18), platelet function disorder (19,20), and imbalance of vasoactive substances (15,21) have also been implicated in the pathogenesis of the SCF phenomenon. Serum paraoxonase (PON), a high-density lipoprotein bound antioxidant enzyme, acts against atherosclerosis and endothelial dysfunction.…”

Pharmacological Management of Cardiac Syndrome Y: A Focused Review

“…An increased resistance to blood flow at the level of the microvascular coronary artery beds is thought to account for the myocardial ischemia occurring mostly at rest in these patients [11,12]. Inappropriate release and increased levels of the vasoconstrictor alkaloids neuropeptide Y [13], endothelin-1 [14], thromboxane A2 [15] and platelet aggregation [16] have been reported to play a role in the pathophysiology of this disorder. Moreover, endothelial cell dysfunction have been proposed based on studies reporting histological evidence of swelling and degeneration of endothelial cells, along with narrowing of the vascular lamina and fibromuscular hyperplasia [17][18][19].…”