Plasma factor XI and XII activity in patients with slow coronary flow.

The exact pathophysiology of slow coronary flow (SCF) phenomenon, characterized by delayed opacification of coronary arteries during coronary angiography, is still unknown, although endothelial dysfunction, inflammation, vasomotor disorders and atherosclerosis are shown. The present study was conducted to investigate whether there is a coagulation pathway abnormality in patients with SCF measuring plasma factor XI and XII activity. The study included 55 patients with angiographically proven SCF (group I) and 40 individuals with normal coronary flow (NCF, group II). Baseline demographic properties were similar in both groups. Echocardiographic parameters were also similar in patients with SCF and NCF. Factor XI activity was significantly higher in group I when compared with group II. Factor XII activity was also significantly higher in group I when compared with group II (108.9 ±â€Š19 vs. 98.8 ±â€Š20, P = 0.018 and 131.2 ±â€Š17 vs. 119.1 ±â€Š16, P = 0.001, respectively). We conclude that SCF phenomenon appears to be associated with enhanced procoagulant state, which may support the role of inflammation and atherosclerosis in the pathogenesis of this phenomenon.

The effect of cilostazol on right heart function and pulmonary pressure.

INTRODUCTION: Cilostazol is a PDE3 inhibitor and used to treat peripheral arterial disease. There are few reports on the influence of cilostazol on heart. AIMS: The aim of this study was to assess this effect on right ventricular function and pulmonary artery pressure. METHODS: Forty patients with normal left and right ventricular ejection fraction and mild or moderate pulmonary artery hypertension were enrolled in the study. Right ventricular function was assessed by tricuspid annular plane systolic excursion (TAPSE), fractional area change (FAC), tissue Doppler imaging (TDI), and two-dimensional speckle-tracking echocardiography (2D-STE) before and after oral administration of cilostazol. Also pulmonary artery pressure assessed before and after administration of cilostazol. RESULTS: After cilostazol administration, there were significant increases in the TAPSE (1.9 ± 0.3 cm vs. 2.2 ± 0.3 cm, P < 0.001). Peak longitudinal strain (-18.7 ± 4.5% vs. -21.3  ± 3.7%, P = 0.001), isovolumetric acceleration (IVA) (176.6 ± 62.7 cm/sec(2) vs. 200.6 ± 61.9 cm/sec(2) , P = 0.025), right ventricular FAC increased significantly (37.6 ± 8.0% vs. 41.5 ± 8.9%, P < 0.001). Pulmonary artery pressure decreased significantly (39.9 ± 7.9 vs. 36.6 ± 5.5 mmHg, P = 0.001) after cilostazol administration. CONCLUSION: Our study demonstrated that cilostazol improved right ventricular systolic function and reduced pulmonary artery pressure.

Acute sleep deprivation is associated with increased atrial electromechanical delay in healthy young adults.

BACKGROUND: Sleep deprivation (SD) is known to be associated with an increased incidence of adverse cardiovascular outcome. Atrial electromechanical delay (AEMD) calculated from tissue Doppler imaging has been shown to detect atrial impairment in paroxysmal atrial fibrillation. The aim of the study was to investigate whether AEMD would increase in otherwise healthy young adults with acute SD. METHODS: Twenty-seven healthy volunteers were included into the study (mean age: 26 ± 3 years). The participants underwent an echocardiographic examination after a night with SD. AEMD defined as the interval from the onset of P wave to the onset of late diastolic Am wave (PA) was calculated from the lateral and septal mitral annulus, and lateral tricuspid annulus (PA lateral, PA septum, and PA tricuspid, respectively). RESULTS: Subjects had similar values of PA tricuspid duration in milliseconds after the night of sleep debt when compared after regular sleep, whereas they had significantly higher values of PA lateral and PA septal durations (69.05 ± 10.64 ms vs 51.31 ± 11.32 ms, P < 0.001 and 51.75 ± 7.15 ms vs 41.37 ± 8.52 ms, P < 0.001; respectively). Moreover, participants had higher inter-AEMD and intra-AEMD values after the night of sleep debt when compared after regular sleep [30.19 ± 9.84 ms vs 14.72 ± 6.81 ms, P < 0.001 and 12.82 ± 7.09 ms vs 4.41 ± 3.60 ms, P < 0.001; respectively]. Pearson's correlation analyses suggest that inter-AEMD and intra-AEMD were inversely correlated with sleep time (r =-0.628, r =-0.499, r =-0.696, and r =-0.572, respectively [all P < 0.001]). CONCLUSION: In conclusion, in this cross-sectional study, we clearly found that even one night of SD is associated with higher values of inter-AEMD and intra-AEMD in healthy young adults.

Increased urinary albumin excretion rates can be a marker of coexisting coronary artery disease in patients with peripheral arterial disease.

Coexisting coronary artery disease (CAD) is an important cause of morbidity and mortality in patients with peripheral arterial disease (PAD). Clinical evaluation and noninvasive tests have some important limitations for the detection of CAD in patients with PAD. The purpose of this study was to investigate whether urinary albumin excretion (UAE) was a sign of atherosclerotic involvement of coronary arteries in patients with PAD. Our study consisted of 65 consecutive patients (56 men, 9 women, mean age; 59.7+/-7.9 years) with PAD who underwent coronary angiography. Urinary albumin excretion was measured in 24-hour urine samples by immunoprecipitation technique. PAD was defined as the presence of > or =50% stenotic lesions in at least 1 of the iliac, femoral, popliteal, tibialis anterior, tibialis posterior, or peroneal arteries. CAD was defined as > or =25% diameter stenosis in at least 1 coronary artery. Patients without any coronary lesions were accepted as having normal coronaries. Age, sex, distributions of coronary risk factors, and UAE rates were compared between patients with and without CAD. Mean UAE was 17.9+/-15.6 mg/day in the total population. Thirty-seven percent of patients had CAD, and 63% had no coronary lesion. UAE rates were 22.33+/-18.74 and 15.32+/-13.01 mg/day in patients with CAD and those with normal coronary arteries, respectively (p = 0.021). Microalbuminuria was detected in 25% in patients with CAD and 12% in those without coronary artery lesions (p = 0.184). The difference was not statistically significant. The distributions of other risk factors and sex were not different between the 2 groups. These data suggest that in patients with PAD, urinary albumin excretion rates may be used to determine those with a high probability of CAD. Further studies are required to decide whether this noninvasive testing is appropriate in detecting high-risk patients.