Occlusion of azygos vein via direct percutaneous puncture of innominate vein following cavopulmonary anastomosis. (17/450)

A 2-year-10-month-old boy was diagnosed with a complex congenital heart disease: right atrial isomerism, left superior vena cava (LSVC), complete atrioventricular septal defect, secundum type atrial septal defect, transposition of the great arteries with pulmonary atresia, patent ductus arteriosus, absence of a right superior vena cava (RSVC), and dextrocardia. He had received a left Blalock-Taussig (BT) shunt at the age of 3 months and a left bidirectional Glenn shunt one year after BT shunt. Progressive cyanosis was noted after the second operation and cardiac catheterization showed a functional Glenn shunt with an engorged azygos vein, which was inadvertently skipped for ligation. Because of the absence of RSVC, transcatheter occlusion of the azygos vein was performed successfully via direct puncture of the innominate vein.  (+info)

Initiation of atrial fibrillation by ectopic beats originating from the superior vena cava: electrophysiological characteristics and results of radiofrequency ablation. (18/450)

BACKGROUND: The superior vena cava (SVC) has cardiac musculature extending from the right atrium. However, no previous study in humans has given details regarding the ectopic foci that initiate paroxysmal atrial fibrillation (PAF), which may originate from the SVC. METHODS AND RESULTS: A total of 130 patients with frequent attacks of PAF initiated by ectopic beats were included. Eight patients (6%) had spontaneous AF initiated by a burst of rapid ectopic beats from the SVC (located 19+/-7 mm above the junction of the SVC and right atrium), which was confirmed by multiplane angiographic and intracardiac echocardiographic visualization and was marked by a sharp SVC potential preceding atrial activity. During initial repetitive discharges, the group with SVC ectopy had a higher incidence of intravenous conduction block than the group with pulmonary vein ectopy (75% versus 37%; P=0.03). The activation time of the earliest intracardiac ectopic activities relative to ectopic P wave onset was significantly shorter in the SVC ectopy than the pulmonary vein ectopy group (37+/-15 versus 84+/-32 ms; P<0. 001). After 5+/-3 applications of radiofrequency energy, AF was eliminated. SVC angiography after ablation revealed a local indentation of the venous wall in one patient. Two patients manifested coexisting sinus rhythm and a "focal" fibrillating activity confined inside the SVC after radiofrequency ablation. During a follow-up period of 9+/-3 months, all 8 patients were free of antiarrhythmic drugs, without tachycardia recurrence or symptoms of SVC obstruction. CONCLUSIONS: Ectopic beats initiating PAF can originate from the SVC. A radiofrequency current delivered to eliminate these ectopies is a highly effective and safe way to prevent PAF.  (+info)

Evaluation of right atrial appendage blood flow by transesophageal echocardiography in subjects with a normal heart. (19/450)

Right atrial appendage (RAA) blood flow pattern was analyzed in 42 normal subjects-without cardiovascular disease (aged 30 to 48 years, mean 40 +/- 6) who underwent transesophageal echocardiography. RAA flow pattern was demonstrated to be bi-, tri- or quadriphasic and heart rate dependent (p < 0.01) in this study. In 15 subjects (36%), a biphasic pattern was observed. A triphasic pattern was observed in 12 subjects (28%). Fifteen subjects (36%) had a quadriphasic pattern. In these subjects, we observed a pattern consisting of two diastolic forward flow waves, each followed by a backward flow wave. Mean heart rates among subjects with bi-, tri- and quadriphasic patterns were 110 +/- 6, 91 +/- 4 and 72 +/- 13 beats/min, respectively. In the triphasic pattern, the onset of superior vena cava diastolic forward flow began 18 +/- 4 ms after the onset of tricuspid E wave, whereas the first diastolic forward flow wave in the RAA began 40 +/- 7 ms after onset of the tricuspid E wave. A similar relation was also noted in the quadriphasic pattern. This sequence was constant and independent of heart rate (p < 0.05), suggesting a temporal relation between right ventricular relaxation and the first diastolic forward flow wave in the RAA. In normal subjects, the RAA flow pattern is heart rate dependent and three distinct flow patterns can be differentiated. Right ventricular relaxation appears to induce both the superior vena cava diastolic forward flow wave and the first diastolic forward flow wave of the RAA. These results can be used for comparison with patterns found in disease states.  (+info)

Dual interaction of agmatine with the rat alpha(2D)-adrenoceptor: competitive antagonism and allosteric activation. (20/450)

In segments of rat vena cava preincubated with [(3)H]-noradrenaline and superfused with physiological salt solution, the influence of agmatine on the electrically evoked [(3)H]-noradrenaline release, the EP(3) prostaglandin receptor-mediated and the alpha(2D)-adrenoceptor-mediated inhibition of evoked [(3)H]-noradrenaline release was investigated. Agmatine (0.1-10 microM) by itself was without effect on evoked [(3)H]-noradrenaline release. In the presence of 10 microM agmatine, the prostaglandin E(2)(PGE(2))-induced EP(3)-receptor-mediated inhibition of [(3)H]-noradrenaline release was not modified, whereas the alpha(2D)-adrenoceptor-mediated inhibition of [(3)H]-noradrenaline release induced by noradrenaline, moxonidine or clonidine was more pronounced than in the absence of agmatine. However, 1 mM agmatine antagonized the moxonidine-induced inhibition of [(3)H]-noradrenaline release. Agmatine concentration-dependently inhibited the binding of [(3)H]-clonidine and [(3)H]-rauwolscine to rat brain cortex membranes (K(i) values 6 microM and 12 microM, respectively). In addition, 30 and 100 microM agmatine increased the rate of association and decreased the rate of dissociation of [(3)H]-clonidine resulting in an increased affinity of the radioligand for the alpha(2D)-adrenoceptors. [(14)C]-agmatine labelled specific binding sites on rat brain cortex membranes. In competition experiments. [(14)C]-agmatine was inhibited from binding to its specific recognition sites by unlabelled agmatine, but not by rauwolscine and moxonidine. In conclusion, the present data indicate that agmatine both acts as an antagonist at the ligand recognition site of the alpha(2D)-adrenoceptor and enhances the effects of alpha(2)-adrenoceptor agonists probably by binding to an allosteric binding site of the alpha(2D)-adrenoceptor which seems to be labelled by [(14)C]-agmatine.  (+info)

Effect of phenylephrine on focal atrial fibrillation originating in the pulmonary veins and superior vena cava. (21/450)

OBJECTIVES: This study was aimed at evaluating the effects of phenylephrine infusion on the occurrence of focal atrial fibrillation (AF). BACKGROUND: Paroxysmal AF can be initiated by ectopic atrial beats originating in the pulmonary vein (PV) or superior vena cava (SVC). The effect of change in autonomic tone on this focal AF is unknown. METHODS: This study included 12 patients with frequent bursts of AF documented by 24-h Holter monitoring. The number and coupling interval of spontaneous ectopic activity and bursts of AF were evaluated for 1 min before and after phenylephrine (2 to 3 microg/kg) injection. RESULTS: After detailed mapping, four patients had a focus located in the left superior PV, six in the right superior PV and two in the SVC. In 10 patients with AF foci originating in the PVs, the frequency of ectopic activity (19.5 +/- 27.4 vs. 11.4 +/- 22.9 beats/min, p = 0.059) was reduced as well as AF bursts (14 +/- 3 vs. 1.8 +/- 2.7 bursts/min, p = 0.005) before versus after phenylephrine injection; the minimal coupling interval of ectopic activity and AF bursts became longer compared with baseline. The maximal percent increase in sinus cycle length after phenylephrine injection was significantly greater in patients with complete suppression of AF compared with those with partial suppression (43 +/- 19 vs. 14 +/- 5%, p = 0.01). However, no significant effect of phenylephrine on AF originating in the SVC was found. CONCLUSIONS: Change in autonomic tone induced by phenylephrine injection was effective in suppressing focal AF originating in the PVs but not in the SVC.  (+info)

The carina as a landmark in central venous catheter placement. (22/450)

Location of the tip of a central venous catheter (CVC) within the pericardium has been associated with potentially lethal cardiac tamponade. Because the pericardium cannot be seen on chest x-ray (CXR), an alternative radiographic marker is needed for correct placement of CVCs. The anatomy of the region was studied in 34 cadavers. The carina was a mean (SEM) distance of 0.4 (0.1) cm above the pericardial sac as it transverses the superior vena cava (SVC). In no case was the carina located below the pericardial sac. The carina is a reliable, simple anatomical landmark for the correct placement of CVCs. In almost all cases, the carina is radiologically visible even in poor quality, portable CXRs. CVC tips should be located in the SVC above the level of the carina in order to avoid cardiac tamponade.  (+info)

Inotropic, chronotropic, and dromotropic effects mediated via parasympathetic ganglia in the dog heart. (23/450)

Some parasympathetic ganglionic cells are located in the epicardial fat pad between the medial superior vena cava and the aortic root (SVC-Ao fat pad) of the dog. We investigated whether the ganglionic cells in the SVC-Ao fat pad control the right atrial contractile force, sinus cycle length (SCL), and atrioventricular (AV) conduction in the autonomically decentralized heart of the anesthetized dog. Stimulation of both sides of the cervical vagal complexes (CVS) decreased right atrial contractile force, increased SCL, and prolonged AV interval. Stimulation of the rate-related parasympathetic nerves to the sinoatrial (SA) node (SAPS) increased SCL and decreased atrial contractile force. Stimulation of the AV conduction-related parasympathetic nerves to the AV node prolonged AV interval. Trimethaphan, a ganglionic nicotinic receptor blocker, injected into the SVC-Ao fat pad attenuated the negative inotropic, chronotropic, and dromotropic responses to CVS by 33 approximately 37%. On the other hand, lidocaine, a sodium channel blocker, injected into the SVC-Ao fat pad almost totally inhibited the inotropic and chronotropic responses to CVS and partly inhibited the dromotropic one. Lidocaine or trimethaphan injected into the SAPS locus abolished the inotropic responses to SAPS, but it partly attenuated those to CVS, although these treatments abolished the chronotropic responses to SAPS or CVS. These results suggest that parasympathetic ganglionic cells in the SVC-Ao fat pad, differing from those in SA and AV fat pads, nonselectively control the atrial contractile force, SCL, and AV conduction partially in the dog heart.  (+info)

Lessons learned from a 6-year clinical experience with superior vena cava Greenfield filters. (24/450)

PURPOSE: Therapy to prevent pulmonary embolism (PE) resulting from upper extremity deep venous thrombosis (UEDVT) remains controversial despite an increasing incidence of DVT of upper extremity origin. The purpose of this study was to evaluate the results of 72 superior vena cava Greenfield filters (SVC-GFs) placed in patients at risk for PE arising from UEDVT. METHODS: During the past 78 months, we placed SVC-GFs in 72 patients with UEDVT in whom anticoagulation was either deemed contraindicated (n = 67) or proved ineffective in preventing recurrent PE (n = 4) or extension of the thrombus (n = 1). There were 25 male (35%) and 47 (65%) female patients whose ages ranged from 25 to 99 years (mean, 74 years). Follow-up ranged from 10 days to 78 months (mean, 7.8 months). Sequential chest radiographs revealed no filter migration or displacement in 26 patients. RESULTS: Thirty-four patients died in the hospital of causes unrelated to the SVC filter or recurrent thromboembolism (mean time to death, 20 days). Follow-up of the surviving 38 patients ranged from 1 month to 78 months (mean, 22 months); none of these patients were seen with any evidence of PE. One SVC-GF was incorrectly discharged into the innominate vein and left in place. This vein remains patent 2 months after insertion without evidence of filter migration. CONCLUSIONS: We think that insertion of SVC-GFs is a safe, efficacious, and feasible therapy and may prevent recurrent thromboembolism in patients with UEDVT who are resistant to anticoagulation or have contraindications to anticoagulation.  (+info)