Fragment reconstruction of coronary arteries using transesophageal echocardiography for coronary diagnostics.

AIMS: Ultrasound differs procedurally from the established methods for non-invasive coronary visualization and is therefore an interesting alternative for non-invasive diagnostics. In this study, fragment reconstruction of coronary arteries by transesophageal echocardiography (FRC-TEE) was investigated for the first time in a patient population being evaluated for coronary angiography. METHODS AND RESULTS: Ultrasonic and angiographic findings were compared visually and using quantitative measurements in 50 patients. One hundred and seventy-one vessels were examined by FRC-TEE. The total lengths visualized were 9.6 +/- 1.7 cm for the right coronary artery, 7.0 +/- 1.1 cm for left circumflex, 3.9 +/- 1.2 cm for left anterior descending (LAD), and 1.5 +/- 0.8 cm for the left main coronary artery. There was high concordance between results of both procedures. Sixty-three stenoses were detected using FRC-TEE. The mean difference in degree of stenosis between techniques was 0.2 +/- 5.1%. Stents could be visualized in 19 segments. FRC-TEE detected distal stenoses of the coronary arteries to only a limited extent: 14 stenoses and 2 stents, predominantly in the LAD artery (n = 13), were not identified. CONCLUSIONS: FRC-TEE is a potential method for diagnosing coronary artery disease. FRC-TEE and angiography yield comparable findings during the evaluation of coronary lesions. Further investigations are needed to verify the encouraging findings and define FRC-TEE's applications.

Vascular effects of class-III antiarrhythmic drugs: chromanol 293B, but not dofetilide blocks the smooth muscle delayed rectifier K+ channel.

Chromanol 293B and dofetilide are inhibitors of IKs and IKr, i.e., of the slow and the rapid component of the delayed rectifier potassium current. The specificity of these drugs was tested by investigating their effects on the delayed rectifier potassium current in vascular smooth muscle, regulating the tone of blood vessels. Using depolarizing step protocols with asymmetrical potassium concentrations (135/4.5 mM K+ in pipette/bath), voltage-dependent K+ currents (IKv) of enzymatically dispersed guinea pig portal vein cells were studied in the whole-cell patch-clamp technique. Peak currents were obtained within 20 ms (at +50 mV) after activation. During a 10 s test pulse to +60 mV, these currents exhibited a relatively fast inactivation with time constants of 384 ms (Tfast) and 4505 ms (Tslow). Dofetilide was totally ineffective in modulating currents; in contrast, after application of chromanol 293B, a steady-state block of IKv developed within 135 s. The block was concentration-dependent with an IC50 of 7.4 microM. Chromanol did not produce any shift in the normalized steady-state activation and inactivation curves and the recovery from inactivation was not significantly changed. Chromanol 293B similarly inhibited delayed rectifier K+ channels whether in their closed or open state, and produced an "apparent" acceleration of inactivation, i.e., the drug accelerated the faster time constant of inactivation during a 10 s test pulse from 384 ms (control) to 149 ms (100 microM chromanol). In recent studies, chromanol was described as a specific blocker of slowly activating delayed rectifier potassium channels (IKs) in cardiomyocytes. The results of this study, however, extend the inhibitory spectrum of the drug and demonstrate block of closed and open state delayed rectifier K+ currents in portal vein vascular smooth muscle. Such a block could possibly contribute to the generation of portal hypertension.