Dipyridamole-provoked chest pain implies severe coronary artery disease in children

The diagnostic significance of dipyridamole-provoked chest pain was studied in 17 children with severe coronary arterial stenotic lesions (CAL) complicated with Kawasaki disease. Although dipyridamole induced chest pain in seven patients (symptomatic group), 10 reported no pain (asymptomatic group). In the asymptomatic group, seven children had one vessel disease (1VD) of right coronary artery (RCA) and the other three had two vessel disease (2VD) involving the RCA and left anterior descending artery (LAD). Four multivessel disease patients, one three vessel disease (3VD) and three 2VD of LAD and RCA, and three 1VD of LAD, were symptomatic. In the thallium scans, all patients, except two of the asymptomatic group, showed perfusion abnormalities. In addition, the extent score of the symptomatic group was significantly worse than that of the asymptomatic group (P = 0.01). While only one in six of the asymptomatic group showed abnormal ST depression on treadmill exercise electrocardiography, all patients in the symptomatic group (P = 0.02) showed ischemic ST depression. These findings suggest that the occurrence of chest pain after medication with dipyridamole closely correlates with the severity of CAL in children.     

A case of ureteral reflux identified by ultrasound

Reflux nephropathy is known to be a major cause of renal failure in children. Vesico-ureteral reflux is usually diagnosed by voiding cysto-urethrography (VCG). However, it has been observed that conventional VCG is not always reliable for the diagnosis of ureteral reflux. In the case of a 5 year old girl with recurrent febrile urinary tract infection, VCG showed no ureteral reflux. Urodynamic study revealed a large bladder capacity and significant residual urine. Renal scintigram delineated a right renal scar. Simple ultrasound examination with videotape recording during voiding definitely demonstrated the presence of significant ureteral reflux when she voided, that is, there was marked dilatation of the right distal ureter and ballooning of the right renal pelvis on voiding, and quick refilling of the bladder concomitantly with the disappearance of the pelvic ballooning. Therefore, an ultrasound during voiding may be useful for diagnosing ureteral reflux in patients where a VCG does not reveal reflux.     

Vasopressin plus oxygen vs vasopressin alone in cirrhotic patients with portal-hypertensive gastropathy: Effects on gastric mucosal haemodynamics and oxygenation

The effects of vasopressin plus oxygen and vasopressin alone on gastric mucosal perfusion and oxygenation were studied using reflectance spectrophotometry and laser Doppler velocimetry in 23 cirrhotic patients with portal-hypertensive gastropathy. The measurements were performed under basal conditions and after double-blinded administration of placebo (n= 7), vasopressin (0.3 U/min; n= 8) or vasopressin (0.3 U/min) plus nasal oxygen (4 L/min; n= 8). No significant effects on gastric mucosal haemodynamics and oxygenation were observed after placebo. In contrast, vasopressin and vasopressin plus oxygen induced a similar reduction in haemoglobin content (-26 ± 2 and -21 ± 4%, respectively P < 0.01) and laser Doppler signal (-23 ± 2 and -22 ± 2%, respectively, P < 0.01). Although each treatment induced a significant reduction in oxygen saturation (-21 ± 2 and -7 ± 1%, respectively P < 0.01), the effect was less pronounced in patients receiving the combination than in those receiving vasopressin alone (P < 0.01). These data suggest that vasopressin and vasopressin plus oxygen reduce gastric mucosal hyperaemia and that the oxygen supplement partially protects against gastric mucosal hypoxia during vasopressin infusion in cirrhotic patients with portal-hypertensive gastropathy.     

Bile acid composition in primary hepatocellular carcinoma

Bile acid composition in human primary hepatocellular carcinoma (HCC) tissues from eight non-hyperbilirubinaemic patients was compared with that in the neighbouring liver tissues. Quantitation of bile acids was carried out using selected ion monitoring. Significant amounts (>14 pmol/mg liver) of bile acids were found to be present in HCC tissues of all patients. In four patients, the concentration of chenodeoxycholic acid was higher in HCC than the corresponding neighbouring liver tissues, whereas those of other bile acids were less. The ratio of cholic to chenodeoxycholic acid was lower in HCC than in adjacent liver tissues in seven out of eight patients. This may indicate predominant synthesis of chenodeoxycholic acid in HCC tissues. The large inter-individual variation in bile acid concentration and composition of HCC tissues may result from the grade of anaplasia of HCC cells. 3β-Hydroxy-5-cholenoic acid, thought to be excreted in increased amounts in the urine of HCC patients, was shown to be a minor constituent of HCC tissues and of the neighbouring liver tissues in most patients, indicating that the C26-hydroxylation pathway plays a minor role. Unusual bile acids, such as 23-nor-3α,7α,12α-trihydroxy-5β-cholanoic, 3β,7β-dihydroxy-5β-cholanoic, 7-oxo-3α,12α-dihydroxy-5β-cholanoic and 12-oxo-3α,7α-dihydroxy-5β-cholanoic acids, were found in trace amounts in HCC tissues but their significance is not clear at present.     

Intracellular Calcium Dynamics,Shortened Action Potential Duration,and Late‐Phase 3 Early Afterdepolarization in Langendorff‐Perfused Rabbit Ventricles

Calcium Dynamics, APD Shortening, and Late‐Phase 3 EAD. Introduction: To elucidate the mechanism of late‐phase 3 early after depolarization (EAD) in ventricular arrhythmogenesis, we hypothesized that intracellular calcium (Ca_i) overloading and action potential duration (APD) shortening may promote late‐phase 3 EAD and triggered activity, leading to development of ventricular fibrillation (VF). Methods and Results: In isolated rabbit hearts, we performed microelectrode recording and simultaneous dual optical mapping of transmembrane potential (V_m) and Ca_i transient on left ventricular endocardium. An I_KATP channel opener, pinacidil, was used to abbreviate APD. Rapid pacing was then performed. Upon abrupt cessation of rapid pacing with cycle lengths of 60–200 milliseconds, there were APD₉₀ prolongation and the corresponding Ca_i overloading in the first postpacing beats. The duration of Ca_i transient recovered to 50% (DCaT₅₀) and 90% (DCaT₉₀) in the first postpacing beats was significantly longer than baseline. Abnormal Ca_i elevation coupled with shortened APD produced late‐phase 3 EAD induced triggered activity and VF. In additional 6 preparations, the heart tissues were treated with BAPTA‐AM, a calcium chelator. BAPTA‐AM significantly reduced the maximal Ca_i amplitude (26.4 ± 3.5% of the control; P < 0.001) and the duration of Ca_i transients in the mapped region, preventing the development of EAD and triggered activity that initiated VF. Conclusions: I _KATP channel activation along with Ca_i overloading are associated with the development of late‐phase 3 EAD and VF. Because acute myocardial ischemia activates the I_KATP channel, late‐phase 3 EADs may be a mechanism for VF initiation during acute myocardial ischemia. (J Cardiovasc Electrophysiol, Vol. 23, pp. 1364‐1371, December 2012)     

Regression of plane warts following spontaneous inflammation

This paper describes the clinical and histopathological features in ten cases of spontaneously involuting plane warts. In all, rapid regression occurred after the sudden development of an inflammatory reaction. At an early stage a degenerative change appears in the upper epidermis and the typic features of the warts are masked. At the height of the reaction an intense mononuclear cell infiltrate in the dermis associated with epidermal spongiosis, exocytosis cell necrosis and focal parakeratosis is found. It is suggested that the development of cell mediated immunity may be responsible for spontaneous involution of warts.