Elevated level of plasma homocysteine in patients with slow coronary flow.

BACKGROUND: Elevated plasma levels of homocysteine are currently considered a major, independent risk factor for cardiovascular diseases. Recently, several investigators have suggested that even mild elevation in plasma homocysteine level can severely disturb vascular endothelial function and subsequently impair coronary blood flow. Accordingly, we investigated plasma homocysteine level in patients with slow coronary flow. METHOD: Study population included 53 patients with angiographically proven normal coronary arteries and slow coronary flow in all three coronary vessels (group I, 21 females, 32 males, mean age=48+/-9 years), and 50 subjects with angiographically proven normal coronary arteries without associated slow coronary flow (group II, 22 females, 28 males, mean age=50+/-8 years). Coronary flow rates of all patients and control subjects were documented by Thrombolysis In Myocardial Infarction frame count (TIMI frame count). All patients in group I had TIMI frame counts greater than two standard deviations above those of control subjects (group II) and, therefore, were accepted as exhibiting slow coronary flow. The mean TIMI frame count for each patient and control subject was calculated by adding the TIMI frame counts for each major epicardial coronary artery and then dividing the obtained value into 3. Plasma homocysteine level was measured in all patients and control subjects using commercially available homocysteine kits. RESULTS: There was no statistically significant difference between two groups in respect to age, gender, hypertension, diabetes mellitus, hyperlipidemia and cigarette smoking (p>0.05). Plasma homocysteine level of patients with slow coronary flow were found to be significantly higher than those of control subjects (15.5+/-5.7 vs. 8.7+/-4.2 microM/l, respectively, p<0.001). Moreover, we found a significant positive correlation between plasma homocysteine level and mean TIMI frame count (r=0.660, p<0.001). CONCLUSION: We have shown that patients with slow coronary flow have raised level of plasma homocysteine compared to control subjects with normal coronary flow. This data suggests that elevated level of plasma homocysteine may play a role in the pathogenesis of slow coronary flow.

P-wave duration and P-wave dispersion in patients with dilated cardiomyopathy.

BACKGROUND: P-wave dispersion (PWD) has been reported to be associated with inhomogeneous and discontinuous propagation of sinus impulses. In the present study, we aimed to investigate PWD in patients with dilated cardiomyopathy. METHOD: The study population consisted of 72 patients with dilated cardiomyopathy and 72 healthy control subjects. Left atrial diameter, left ventricular end-diastolic and end-systolic diameters and left ventricular ejection fraction of all patients and control subjects were measured by means of transthoracic echocardiography. Maximum P-wave duration (Pmaximum) and minimum P-wave duration (Pminimum) were measured from the 12-lead surface electrocardiogram. PWD was calculated as the difference between Pmaximum and Pminimum. RESULTS: Pmaximum and PWD of patients with dilated cardiomyopathy were significantly higher than those of control subjects (Pmaximum: 126+/-12 ms vs. 116+/-10 ms, PWD: 47+/-6 ms vs. 38+/-7 ms, respectively, P<0.001 for all). However, there was no statistically significant difference between patient group and control group regarding Pminimum (79+/-7 ms vs. 78+/-6 ms, respectively, P=0.27). Left atrial diameter was significantly higher in patients with dilated cardiomyopathy compared to control subjects (4.51+/-0.62 cm vs. 3.60+/-0.43 cm, respectively, P<0.001). Left ventricular ejection fraction was found to be significantly lower in patients with dilated cardiomyopathy compared to control subjects (33+/-5% vs. 63+/-7%, respectively, P<0.001). CONCLUSION: PWD was found to be significantly higher in patients with dilated cardiomyopathy than in healthy control subjects.

Activation of coagulation system in dilated cardiomyopathy: comparison of patients with and without left ventricular thrombus.

OBJECTIVES: We aimed to investigate plasma levels of molecular markers for platelet activity, thrombin activation and fibrinolytic status in patients with dilated cardiomyopathy (DCM) with and without left ventricular (LV) thrombus and to compare these markers between patients with DCM and control participants. MATERIALS AND METHODS: The study population comprised 60 patients with DCM who met the inclusion criteria. Patients were divided into two groups: 22 patients with LV thrombus and 38 patients without LV thrombus. The age-matched control group consisted of 23 healthy participants (18 men and five women with a mean age of 49). Patients with DCM and healthy participants were compared with respect to platelet activity, thrombin activation and fibrinolytic status. These comparisons were also performed in patients with DCM with and without LV thrombus. RESULTS: Platelet factor 4 (28.2+/-4.4 ng/ml compared with 20+/-3.1 ng/ml, P<0.01) and beta-thromboglobulin (40+/-2 ng/ml compared with 17+/-3 ng/ml) levels, reflecting platelet activity, were significantly higher in patients with DCM than in control participants. Fibrinopeptide A (6.94+/-0.69 ng/ml compared with 1.96+/-0.1 ng/ml, P<0.001) and thrombin-antithrombin III complex (5.26+/-2.60 ng/ml compared with 3.17+/-1.23 ng/ml, P<0.001) levels, as markers of fibrin generation, were also higher in patients with DCM than in normal participants. Plasma levels of D-dimer (118+/-16 ng/ml compared with 85+/-3 ng/ml, P<0.001) and plasmin-alpha2-plasmin inhibitor complex (0.8+/-1.1 microg/ml compared with 0.6+/-1.7 microg/ml, P<0.001) in patients with DCM significantly exceeded those in the normal participants. There were no statistically significant differences between patients with and without LV thrombus in DCM with respect to platelet activity, thrombin activation and fibrinolytic status. CONCLUSION: We have shown that platelet activation, thrombin activation and fibrinolytic activity are increased in patients with DCM compared to control participants. However, these markers reflecting coagulation activation in patients with LV thrombus are comparable to those in patients without LV thrombus.

Migraine headache induced recurrent atrial fibrillation: a case report.

A variety of symptoms that accompany migraine are mediated by the autonomic nervous system. The autonomic nervous system has long been known to play a potentially important role in the occurrence of atrial fibrillation. Clinically significant effects on cardiac rhythm are uncommon during migraine attacks. In the present case, we report a man who experienced recurrent episodes of atrial fibrillation, which were likely secondary to the vomiting component of migraine.