No abstract

Decreased fibrinolytic activity has been reported in atherosclerotic cardiovascular diseases. To determine whether oxidized low-density lipoprotein (Ox-LDL), which accumulates in atherosclerotic arteries, modulates the endothelial fibrinolytic system, cultures of human umbilical vein endothelial cells were incubated with low-density lipoproteins or lipids, and levels of plasminogen activator inhibitor-1 (PAI-1) and tissue-type plasminogen activator (t-PA) antigens in the conditioned medium were measured by enzyme-linked immunosorbent assay. Ox-LDL (30 ,ug protein/mL) and its extracted lipid (50 ,g cholesterol/mL) stimulated PAI-1 release by 42±3% and 29±-3% of control cultures, respectively, whereas Ox-LDL and its lipid inhibited t-PA release by 42+4% and 53 ±3% of control cultures, respectively. Native LDL and its lipid were inactive on their release. Ox-LDL depleted of hydrophilic lipids, which was prepared by the incubation with defatted albumin (an acceptor for hydrophilic lipids), lost both the stimulatory action on PAI-1 and the inhibitory action on t-PA. The extracted lipid from the incubated albumin, which has been found to accept the hydrophilic lipids from Ox-LDL, gained the stimulatory action on PAI-1 and the inhibitory action on t-PA. Ox-LDL depleted of lysophosphatidylcholine (LPC), which was prepared by the incubation with phospholipase B, lost the stimulatory effect on PAIT1, whereas the inhibitory effect on t-PA remained present in the Ox-LDL depleted of LPC. The incubation with synthetic palmitoyl LPC (10 ,uM) stimulated PAI-1 release by 85±7% of control. 25-Hydroxycholesterol (50 ,uM) and 7-ketocholesterol (50 ,uM), both of which were generated in Ox-LDL and were found to be transferable from Ox-LDL to defatted albumin by the analysis using gas chromatography-mass spectrometry, inhibited t-PA release by 26+3% and 31±3% of control cultures, respectively.

The conduction properties of the crista terminalis (CT) and its influence on the right atrial activation sequence were analyzed in 14 patients with typical atrial flutter (AF). Atrial mapping was performed with 35 points of the right atrium during typical AF and during atrial pacing performed after linear ablation of inferior vena cava-tricuspid annulus (IVC-TA) isthmus. Atrial pacing was delivered from the septal isthmus at cycle lengths of 600 ms and the tachycardia cycle length (TCL). The right atrial activation sequence and the conduction interval (CI) from the septal to lateral portion of the IVC-TA isthmus were analyzed. During AF, the conduction block line (CBL) (detected by the appearance of double potentials along the CT and craniocaudal activation on the side anterior to CT) was observed along the CT in all patients. The TCL and CI during AF were 254 +/- 19 and 207 +/- 14 ms, respectively. During pacing at a cycle length of 600 ms, the CBL was observed along the CT in four patients, however, a short-circuiting activation across the CT was observed in the remaining ten patients. The CI during pacing at 600 ms was 134 +/- 38 ms, shorter than that during AF (P < .0001). During pacing at the TCL, the CBL was observed along the CT in all patients. The presence of the CBL along the CT prevented a short-circuiting activation across the CT and resulted in the same right atrial activation as observed during AF. With the formation of the CBL, the CI significantly increased to 206 +/- 17 ms and was not different from that during AF. These data suggest that the conduction block along the CT is functional. It was presumed that presence of conduction block at the CT has some relevance to the initiation of typical AF though it was not confirmed.

Background-The exact boundaries of the reentry circuit in atrioventricular nodal reentrant tachycardia (AVNRT) have not been convincingly defined. Methods and Results-To define the tachycardia circuit, single extrastimuli were delivered during AVNRT to 8 sites of the right intra-atrial septum: 3 arbitrarily divided sites of the AV junction extending from the His bundle (HB) site to the coronary sinus ostium (CSOS) (sites S, M, and I) and the superior (S-CSOS), inferior (I-CSOS), posterior (P-CSOS), and posteroinferior (PI-CSOS) portions of the CSOS and the CSOS in 18 patients. The mean tachycardia cycle length (TCL) was 368Ϯ52 ms. Retrograde earliest atrial activation was observed at the HB site in all patients. The longest coupling intervals of single extrastimuli that reset AVNRT at sites S, M, I, I-CSOS, CSOS, S-CSOS, P-CSOS, and PI-CSOS were 356Ϯ51, 356Ϯ51, 355Ϯ52, 357Ϯ51, 318Ϯ47, 305Ϯ53, 311Ϯ56, and 312Ϯ56 ms, respectively, and the following return cycles at these sites were 368Ϯ52, 368Ϯ53, 367Ϯ53, 367Ϯ53, 407Ϯ66, 431Ϯ73, 415Ϯ55, and 412Ϯ56 ms, respectively. The longest coupling intervals at sites S, M, I, and I-CSOS did not differ from each other and were longer than those at CSOS and S-, P-, and PI-CSOS (PϽ0.0001). The return cycles at sites S, M, I, and I-CSOS did not differ from the TCL, whereas those at CSOS and S-, P-, and PI-CSOS were longer than the TCL (PϽ0.0001). Conclusions-The perinodal atrium extending from the HB site to I-CSOS was involved in the tachycardia circuit. I-CSOS was thought to be the entrance of the slow pathway. (Circulation. 1999;100:621-627.)

A 39-year-old woman with Sanfilippo C syndrome was referred to our department for the treatment of bradycardia. An electrocardiogram revealed a second degree atrioventricular block, and pacemaker implantation was performed with the patient under general anesthesia. A transthoracic echocardiogram showed normal left ventricular systolic function, moderate mitral regurgitation due to mitral valve prolapse, and a high E/e' ratio, indicating left ventricular diastolic dysfunction. The present patient exhibited a rare case of Sanfilippo syndrome complicated with conduction disturbances, mitral regurgitation, and diastolic dysfunction.