The Importance of von Willebrand Factor Level and Heart Rate Changes in Acute Coronary Syndromes: A Comparison with Chronic Ischemic Conditions

Abstract

The pathogenesis of acute coronary syndrome (ACS) and transient myocardial ischemia (TMI) is not completely understood. Therefore, the authors studied the biological indicators of thrombogenesis and sympathetic activity. The study was conducted on 50 patients with acute coronary syndrome and 30 patients with stable angina pectoris. Treatment was standardized with low-molecular-weight heparin and 300 mg aspirin/day but with no IIb/IIIa inhibitors, an oral beta-blocker, diltiazem 60 mg tid, glyceryl trinitrate i.v. in patients with ACS but with mononitrates orally and low-molecular-weight heparin in patients with stable angina. Twenty-four-hour continuous ECG monitoring and ST segment analysis were performed on day 2 of admission and heart rate analysis was performed 10, 5, and 1 minute before and during the myocardial ischemia periods. Blood sampling for von Willebrand factor (vWf) determination was performed through a peripheral vein at 8 AM, noon, 6 PM and 10 PM and half an hour after the description of angina. The patients with ACS were grouped as transient myocardial ischemia positive (n = 20) and negative (n = 30). The patients with stable angina were designated as the control group (n = 30). The detected vWf levels at 4 different daytime periods in patients with ACS were significantly higher than those in patients with stable angina. At the 6 PM to 10 PM period, the vWf level increase was significantly higher in patients with TMI than in the patients without TMI. At the 8 AM to noon period, the detected vWf levels decreased significantly in both TMI groups. During the nocturnal ischemia periods, the increase in vWf levels immediately after angina was significantly more apparent than the detected changes during daytime ischemia. Analysis showed that heart rates before the ischemia during stable angina episodes were significantly higher than those in TMI (-) (silent) angina. The heart rate difference between 10 minutes before and during the ischemia in the angina group was significantly different from that during TMI (-) (silent) ischemia. The heart rates at the times related to ischemia in the nocturnal period were significantly lower than those in the daytime period. The heart rate differences between the ischemia-related times and during the ischemia were significantly higher in daytime ischemic attacks than in nocturnal ischemic attacks. The study confirms that the vWf level, which is an indicator of thrombogenesis, was significantly increased in patients with ACS. Nocturnal ischemia is associated with thrombogenesis. Daytime ischemia is associated with increased sympathetic activity, and symptomatic ischemia is usually associated with increased sympathetic activity.

Relationship between Hemostatic Factors and the Platelet Index in Patients with Ischemic Heart Disease

“…Plasma VWF:Ag levels have been reported to be significantly increased in patients with ACS [11] . Although increased VWF is considered to be one of the acute phase reactants in patients with AMI, it is generally considered that the plasma VWF level is an independent risk factor in patients with myocardial infarction [12] .…”

“…Furthermore, it has recently been proposed that an elevated platelet volume is an independent risk factor for acute myocardial infarction (AMI) or acute coronary syndrome (ACS), but not for chronic coronary artery disease [3] . Hemostatic factors such as von Willebrand factor (VWF), D-dimer and thrombin-antithrombin III complex (TAT) [4][5][6][7] have been reported to be profoundly related to thrombin formation and, therefore, to platelet activation in coronary artery disease. It is important to study platelet heterogeneity in the circulation in patients with IHD.…”

Resistance to aspirin is increased by ST-elevation myocardial infarction and correlates with adenosine diphosphate levels

“…This is probably due to a general activation of the platelets, because platelet aggregation was also increased in patients not treated with aspirin. The increased aspirin resistance could be explained by increased activity of important positive feedback systems such as ADP and thromboxane [19], but also by an increase in vW factor that are released from endothelial cells under high shear stress [20]. …”

“…Several studies have shown sufficient inhibition of platelet aggregation with the 75 mg dose [1,20]. Recently though, a randomized study of 60 patients with stable coronary artery disease showed that the effect of aspirin was dose-dependent and the conclusion was that doses of less than 100 mg of aspirin was less effective inhibiting platelet aggregation than doses greater than 100 mg [22].…”

Cardiac Biomarkers for the Prediction and Diagnosis of Atherosclerotic Disease and its Complications

“…In a study that looked at the relationship between vWF levels and time of day in subjects with ACS, Heper et al found vWF levels to be higher in subjects with ACS as compared to those with stable angina [125]. Spaziani and colleagues found that in patients with unstable angina, both IL-6 and vWF levels decreased 1 month following stent placement [126].…”