We have demonstrated the decreased FFR in the patients with SCF. Decreased FFR levels have been attributed to increased resistance in the epicardial coronary arteries due to diffuse atherosclerotic disease which has been demonstrated by IVUS.

SUMMARYIntravascular ultrasound imaging can detect intimal thickening and is suitable for detection of early atherosclerosis, which cannot be detected by conventional angiography. The aim of the present study was to investigate the epicardial coronary morphology and intracoronary pressure in relation to slow coronary flow (SCF). The study population consisted of 19 patients with SCF [11 (57.9%) females; 55.95 ± 9.42 years]. Proximal, middle, distal and mean total vessel area, lumen area, intima + media area (IMA), percent IMA, and maximal intima + media (I + M) thickness were calculated and compared to healthy subjects. Proximal, middle, distal and mean I + M thickness, IMA, and % IMA of patients with SCF were found to be significantly higher than those of control subjects. Longitudinally extended massive calcification throughout the epicardial arteries was found in 13 (68.4%) patients with SCF and regional calcification was found in 6 (31.6%) patients with SCF. Proximal and distal pressure gradients of patients with SCF were determined to be 15.84 ± 12.11 mmHg in the intracoronary pressure measurements. Fractional flow reserve values were significantly lower than the normal population (0.83 ± 0.13, P < 0.0001). This study indicates that patients with SCF have diffuse intimal thickening, widespread calcification along the vessel wall and atheroma which does not cause luminal irregularities in coronary angiography, and a pressure gradient between proximal and distal segments of epicardial coronary arteries with SCF. Based on these results, we believe that SCF may be a form of diffuse atherosclerosis involving both the microvascular system and epicardial coronary arteries. (Jpn Heart J 2003; 44: 907-919)

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Malignant and nonmalignant serosal fluids have been found to be associated with high serum levels of CA 125, suggesting that the presence of fluid in the serosal cavities may stimulate its release. In this study, we investigated the relationship between serum CA 125 levels and the presence of pleural fluid in patients with chronic heart failure (CHF). We performed a clinical study in 36 patients with CHF with and without pleural fluid. Patients with CHF were divided into two groups based on the presence of fluid in the pleural cavity. Group 1 included 18 CHF patients (6 females, 12 males) with pleural fluid. Group 2 consisted of 18 CHF patients (7 females, 11 males) without pleural fluid. The control group consisted of 30 healthy volunteers (12 females, 18 males). The serum CA 125 level was determined in all groups. Serum CA 125 levels were found to be 100.0 ± 129.4 U/ml in CHF patients with pleural fluids, whereas they were 36.5 ± 35.2 U/ml in CHF patients without pleural fluid and 8.9 ± 6.1 U/ml in the control group. Significantly high serum CA 125 levels were found in CHF patients with pleural fluids (p < 0.05) when compared with both CHF patients without pleural fluid and the control group. There was also a statistically significant difference in CA 125 levels between patients without pleural fluid and the control group (p < 0.05). We concluded that serum CA 125 levels should be interpreted with caution in patients with CHF in the presence of pleural fluid. Invasive procedures to define the etiology of elevated serum CA 125 levels may be unnecessary in this patient group.

Longitudinal myocardial systolic function assessed by STE, which is a sensitive marker of subclinical ventricular dysfunction is impaired in BD. Increased NT-proBNP levels may be a sign of subclinical ventricular dysfunction in these patients.

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