Electrocardiographic (ECG) artefacts may closely simulate both supraventricular and ventricular tachycardias. We describe a case initially diagnosed as rapid atrial fibrillation, based on 12-lead surface ECG (especially the limb leads) and monitor tracing. The arrhythmia was resistant to beta blockers. Because of the at times apparently regular rhythm, an esophageal ECG recording was performed, and adenosine was administered. When the presumed atrial fibrillation terminated after sodium pentothal was administered while preparing for electrical cardioversion, the oesophageal ECG recordings and the ECGs during adenosine administration were reviewed. An ECG artefact diagnosis was suspected, and then confirmed, during relapse of the "arrhythmia," with simple palpation of the radial pulse and cardiac auscultation.
Adenosine/diagnostic use ; Adult ; *Artifacts ; Atrial Fibrillation/*diagnosis/physiopathology/therapy ; *Diagnostic Errors ; *Electrocardiography ; Female ; Humans ; Predictive Value of Tests ; Tachycardia, Supraventricular/*diagnosis/physiopathology/therapy ; Time Factors ; *Unnecessary Procedures

Herein we report about the adenosine stress perfusion MR imaging findings of a 50-year-old man who exhibited two different perfusion defects resulting from two different mechanisms after a coronary artery bypass surgery. An invasive coronary angiography confirmed that one perfusion defect at the mid-anterior wall resulted from an ischemia due to graft stenosis. However, no stenosis was detected on the graft responsible for the mid-inferior wall showing the other perfusion defect. It was assumed that the perfusion defect at the mid-inferior wall resulted from delayed perfusion owing to the long pathway of the bypass graft. The semiquantitative analysis of corrected signal-time curves supported our speculation, demonstrating that the rest-to-stress ratio index of the maximal slope of the myocardial territory in question was similar to those of normal myocardium, whereas that of myocardium with the stenotic graft showed a typical ischemic pattern. A delayed perfusion during long graft pathway in a post-bypass graft patient can mimick a true perfusion defect on myocardial stress MR imaging. Radiologists should be aware of this knowledge to avoid misinterpretation of graft and myocardial status in post bypass surgery patients.
Adenosine/diagnostic use ; Contrast Media/diagnostic use/*pharmacokinetics ; Coronary Angiography/*methods ; Coronary Artery Bypass/*methods ; Coronary Stenosis/*diagnosis ; Humans ; Magnetic Resonance Imaging/*methods ; Male ; Middle Aged ; Myocardial Perfusion Imaging/methods

OBJECTIVE: We wanted to prospectively assess the adverse events and hemodynamic effects associated with an intravenous adenosine infusion in patients with suspected or known coronary artery disease and who were undergoing cardiac MRI. MATERIALS AND METHODS: One hundred and sixty-eight patients (64 +/- 9 years) received adenosine (140 microg/kg/min) during cardiac MRI. Before and during the administration, the heart rate, systemic blood pressure, and oxygen saturation were monitored using a MRI-compatible system. We documented any signs and symptoms of potential adverse events. RESULTS: In total, 47 out of 168 patients (28%) experienced adverse effects, which were mostly mild or moderate. In 13 patients (8%), the adenosine infusion was discontinued due to intolerable dyspnea or chest pain. No high grade atrioventricular block, bronchospasm or other life-threatening adverse events occurred. The hemodynamic measurements showed a significant increase in the heart rate during adenosine infusion (69.3 +/- 11.7 versus 82.4 +/- 13.0 beats/min, respectively; p < 0.001). A significant but clinically irrelevant increase in oxygen saturation occurred during adenosine infusion (96 +/- 1.9% versus 97 +/- 1.3%, respectively; p < 0.001). The blood pressure did not significantly change during adenosine infusion (systolic: 142.8 +/- 24.0 versus 140.9 +/- 25.7 mmHg; diastolic: 80.2 +/- 12.5 mmHg versus 78.9 +/- 15.6, respectively). CONCLUSION: This study confirms the safety of adenosine infusion during cardiac MRI. A considerable proportion of all patients will experience minor adverse effects and some patients will not tolerate adenosine infusion. However, all adverse events can be successfully managed by a radiologist. The increased heart rate during adenosine infusion highlights the need to individually adjust the settings according to the patient, e.g., the number of slices of myocardial perfusion imaging.
Adenosine/administration & dosage/*adverse effects ; Adult ; Aged ; Aged, 80 and over ; Blood Pressure/drug effects ; Contrast Media/diagnostic use ; Coronary Disease/*diagnosis ; Female ; Gadolinium DTPA/diagnostic use ; Heart Rate/drug effects ; Hemodynamics ; Humans ; Infusions, Intravenous ; *Magnetic Resonance Imaging ; Male ; Middle Aged ; Oxygen/blood ; Prospective Studies ; Vasodilator Agents/administration & dosage/*adverse effects

Protein tyrosine phosphorylation and dephosphorylation are important in the regulation of cell proliferation and signaling cascade. In order to examine whether phosphatase activity of CPTP1 and HPTP1B, typical nontransmembrane protein tyrosine phosphatase, could be controlled by phosphorylation, affinity-purified PTPs were phosphorylated by CKII and p56lck in vitro. Phosphoamino acid analysis revealed that CPTP1 was phosphorylated on both serine and threonine residues by CKII, and tyrosine residue by p56lck. Phosphatase activity of CPTP1 was gradually increased by three-fold concomitant with phosporylation by CKII. Phosphorylation of HPTP1B by CKII resulted in quick two-fold enhancement of its phosphatase activity within 5 min of incubation and remained in that state. In the presence of CKII inhibitor, heparin or poly(Glu.Tyr), both phosphorylation and enhancement of phosphatase activity of CPTP1 and HPTP1B were mostly blocked. p56lck catalyzed tyrosine phosphorylation of CPTP1 and HPTP1B was only observed by inhibiting the intrinsic tyrosine phosphatase activity. Taken together, these results indicate that CPTP1 or HPTP1B possesses a capability to regulate its phosphatase activity through phosphorylation processes and may participate in the cellular signal cascades.
Adenosine Triphosphate/metabolism ; Animal ; Chickens ; Dose-Response Relationship, Drug ; Heparin/pharmacology ; Human ; Hydrogen Peroxide/pharmacology ; Lymphocyte Specific Protein Tyrosine Kinase p56(lck)/metabolism* ; Peptides/pharmacology ; Phosphorus Radioisotopes/diagnostic use ; Phosphorylation/drug effects ; Protein-Serine-Threonine Kinases/metabolism* ; Protein-Tyrosine-Phosphatase/metabolism* ; Tyrosine/metabolism ; Vanadates/pharmacology