Laser ablation of normal and diseased human ventricle

The feasibility and safety of laser photoablation in patients with ventricular tachycardia (VT) and accessory pathways are currently being examined. We studied the qualitative and quantitative effects of argon laser radiation on normal and diseased human ventricle to determine the relationship between the size of tissue lesion and delivered energy. Twenty-nine human ventricle segments (normal ventricle = 10; diseased ventricle = 19) were excised from patients during mapping-guided subendocardial resection for VT (seven patients), mitral valve replacement (five patients), or immediately at autopsy (three patients). Lasing was performed with a 15 W argon laser coupled to a 300 micron optical fiber. Incremental laser discharges from 10 to 1000 J were delivered in air and saline with the optical fiber 5 mm from the endocardial surface. Gross and microscopic damage was quantified and correlated with laser discharges at low (10 to 100 J), intermediate (101 to 300 J), and high (greater than 300 J) energies. Histologic examination of laser-induced lesions in both normal and diseased human ventricle in either medium showed focal thermal injury with crater formation, vacuolization, and coagulation necrosis of endocardium and myocardium. In normal ventricle, mean lesion diameter and depth in air increased with increasing energies up to 300 J. Over 300 J, tissue perforation was frequently observed. In saline, the mean lesion depth was significantly reduced (p less than 0.02) at comparable energies. In diseased ventricle, mean lesion diameter and depth in air and saline also increased with increasing laser discharge energies up to 300 J. Higher energy laser discharges did not increase mean lesion dimensions or result in tissue perforation.(ABSTRACT TRUNCATED AT 250 WORDS)     

The effect of chemical ablation of the endocardium on ventricular fibrillation threshold

The purpose of this study was to examine the effects of ablation of the superficial endocardium and Purkinje network on left ventricular fibrillation threshold. Lugol's solution was applied through small ventriculotomies to the left and right ventricular endocardium of 10 dogs on cardiopulmonary bypass. Two control groups of five animals each underwent either endocardial application of saline or epicardial application of Lugol's solution. Ventricular fibrillation threshold was measured before and after each intervention by the single-stimulus technique. Application of Lugol's solution to the endocardium resulted in a 102 +/- 15% increase in ventricular fibrillation threshold from a control value of 26 +/- 2 to 53 +/- 6 mA (p less than .005). In two animals, ventricular fibrillation could not be initiated postoperatively. In the control groups, there were no significant changes in ventricular fibrillation threshold. Histologic examination revealed that Lugol's solution obliterated less than 0.5 mm of superficial endocardium while sparing the adjacent myocardium. Electrophysiologic and rheologic data confirmed the discrete nature of the chemical injury. Thus ablation of the superficial ventricular endocardium with Lugol's solution results in a profound increase in the ventricular fibrillation threshold with only minimal tissue destruction.     

Thermal effects of laser and electrical discharge on cardiovascular tissue: implications for coronary artery recanalization and endocardial ablation

To determine the thermal responses of cardiovascular tissues to laser and electrical ablation, and to characterize the effects of different superfusing media and temperatures on target tissue temperatures and resulting extent of tissue injury, 184 laser and 15 electrical discharges were delivered to segments of human and canine aorta and canine ventricular endocardium. Tissue temperatures were measured 2 mm from the point of contact of laser fiber tip and tissue. When superfusing media consisted of whole blood or plasma at room temperature, a standard 40 J laser discharge caused peak arterial temperatures to rise 29.2 +/- 1.6 degrees C and 30 +/- 1.4 degrees C, respectively; however, tissue cooling was significantly slower in blood than in plasma. When saline solution was superfused, tissue temperatures rose by 11.4 +/- 2.2 degrees C, and tissue cooling occurred significantly faster than with either plasma or blood. The dimensions of the resulting aortic lesions were larger when blood (1.69 +/- 0.26 mm) was superfused than when plasma (1.39 +/- 0.04 mm) or saline (0.77 +/- 0.13 mm) was superfused (p less than 0.0001). Similar findings were observed with ventricular endocardium using blood or saline as the superfusing medium. In arterial tissue, superfusion with cold blood or saline solution resulted in lower peak temperature elevations (22 +/- 3.8 degrees C and 13.5 +/- 1.3 degrees C, respectively) and faster tissue cooling after laser discharge. Corresponding aortic lesion sizes were significantly smaller (1.4 +/- 0.03 and 0.5 +/- 0.02 mm, respectively) than when blood or saline medium was superfused at room temperature (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Chronic myocardial infarction: assessment of morphology, function, and perfusion by gradient echo magnetic resonance imaging and 99mTc-methoxyisobutyl-isonitrile SPECT.

To assess the ability of magnetic resonance imaging (MRI) to identify the anatomic and functional abnormalities associated with completely scarred myocardium, 20 patients with chronic transmural myocardial infarction confirmed by electrocardiography and cineventriculography were examined by gradient echo MRI. Myocardial perfusion at rest was assessed in corresponding transverse sections using 99mTc-methoxyisobutyl-isonitrile single-photon emission computed tomography (MIBI-SPECT). MRI scar was defined as diastolic wall thickness (DWT) 2.5 SD below corresponding normal values or systolic wall thickening (delta WT) less than or equal to 1 mm. For MIBI-SPECT images, scar was defined as a MIBI uptake less than 2.5 SD below normal values. By MIBI-SPECT, 152 segments contained normal tissue and 88 contained scarred myocardium. In 226 of 240 (94%) segments, MRI gradings by DWT and MIBI-SPECT gradings were identical. DWT by MRI was higher in normal than in scarred MIBI-SPECT segments (10 +/- 1 versus 4 +/- 2 mm, p less than 0.001). In 230 of 240 (96%) segments, MRI gradings by delta WT and MIBI-SPECT gradings were identical. Segments graded normal by MIBI-SPECT showed higher delta WT by MRI than scar segments (5 +/- 1 versus 0.3 +/- 1 mm, p less than 0.001). MIBI-SPECT perfusion defect size and regions with reduced DWT on MRI tomograms correlated well (r = 0.85). This study indicates that myocardial regions fulfilling electrocardiographic and ventriculographic criteria for transmural myocardial scar are clearly depicted by regional diastolic wall thinning and delta WT less than or equal to 1 mm on gradient echo MR images.(ABSTRACT TRUNCATED AT 250 WORDS)     

Use of electrogram characteristics during sinus rhythm to delineate the endocardial scar in a porcine model of healed myocardial infarction

INTRODUCTION: Substrate-based catheter ablation of postmyocardial infarction (post-MI) ventricular tachycardia necessitates electroanatomic definition of the scarred endocardium. We sought to determine whether electrogram criteria during sinus rhythm could identify the location and extent of the myocardial scar by electroanatomic mapping. METHODS AND RESULTS: A porcine model of healed MI was generated by injecting agarose microspheres into the mid left anterior descending coronary artery. At least 4 weeks post-MI, the animals (n = 24) underwent detailed left ventricular endocardial electroanatomic mapping using a 4-mm-tip catheter (BioSense-Webster, Inc.). Based upon mapping data in normal animals, infarcted tissue was defined as bipolar electrogram amplitude < 1.5 mV and electrogram duration > or = 50 msec. Radiofrequency ablation lesions (2-10 per animal) were placed to tag the endocardial borders of the electroanatomic mapping-defined scar. The area of the scar defined by abnormal voltage amplitude was 25.9 +/- 15.4 cm2 (range 6.9-60.5). This area correlated well with that defined as scar by the electrogram duration criteria (26.4 +/- 16 cm2). Of those points remote from the infarct with falsely low voltage amplitude resulting from presumed poor catheter-tissue contact, 94% were correctly identified as normal when using the electrogram duration criteria. Late potentials were observed predominantly along the borders of the infarcted myocardium. The radiofrequency lesions placed to tag the scar borders were located along the scar periphery during gross pathologic examination. CONCLUSION: During normal sinus rhythm, both bipolar electrogram voltage amplitude and electrogram duration criteria are able to help differentiate normal from scarred myocardial tissue. Using these criteria, a detailed reconstruction of the endocardial scar can be rendered by electroanatomic mapping of the heart.     

The adverse effect of catheter ablation on the AV junction in experimental dogs

The purpose of this study was to assess the adverse effects of catheter electrical ablation. Eighteen anesthetized mongrel dogs received 10-400 J of DC countershocks one to five times in each of them near the region of AVJ. Complete AV block was established, no pacemaker was implanted. Electrical unstability was seen nearly in all. Among the date of observation (1-547 days), 16 dogs died spontaneously and the other two were killed. Gross and microscopic examination revealed that cardiac damage produced by DC shock was diffusely spread over the endocardium/valve, myocardium and epicardial layers. The prominent lesions of the acute stage were myocytolysis and/or necrosis of myocardium/endocardium. In chronic stage, diffuse fibrosis and other types of tissue degeneration were revealed, some dogs had both acute and chronic lesions at the same time. Two dogs with perforated aortic valve revealed an elevation of PAEDP, one of them developed marked right heart failure and ascites. We proposed that the acute submicroscopic injury induced by DC shock may progress to a diffuse and irreversible pathologic changes. Therefore, the chronic adverse effects of catheter ablation should be evaluated carefully.     

Intramural activation of the human ventricle: findings in normal and abnormal myocardial segments in patients with coronary artery disease

To define the intramural electrical activation of normal and abnormal myocardial segments in patients with coronary artery disease, mapping was performed using a plunge electrode with 10 electrodes 1 mm apart. Five transmural bipolar electrograms (40 to 500 Hz) were recorded from 79 sites in 13 patients at the time of open-heart surgery. The results were correlated with ventriculography. In 64 sites with normal contraction, activation spread from endocardium to epicardium in 20.5 +/- 2 msec, and no electrograms were abnormal. Activation time did not differ between the different anatomic segments. In the eight hypokinetic sites, activation spread from endocardium to epicardium in 22.2 +/- 2 msec, and no electrograms were abnormal. In the seven sites with akinesis or dyskinesis, abnormal electrograms were noted and were concentrated towards the endocardium. In four patients, the 40% to 80% of electrograms closest to the endocardium were abnormal, while in three patients all transmural electrograms were abnormal. The variable depth of electrically abnormal tissue should be considered in operations and ablative procedures for ventricular arrhythmias.     

Comparison of epicardial cryoablation and irrigated radiofrequency ablation in a Swine infarct model

Epicardial Cryoablation in Swine. Introduction: Cryoablation is an alternative to radiofrequency (RF) energy used in some ablation procedures. Its role and effectiveness compared to irrigated RF in epicardial tissue and epicardial substrates is not yet fully established. Methods and Results: Using a swine chronic infarct model, we compared RF lesions produced by an open‐irrigated 3.5 mm tip catheter with those produced by an 8 mm tip cryocatheter in epicardial infarct border zone, epicardial normal tissue, and normal endocardium. In the infarct border zone, cryolesions were larger than RF lesions in maximum diameter (9.3 ± 2.9 mm vs 6.2 ± 2 mm, P < 0.001) and volume (171.7 ± 173.1 mm³ vs 77 ± 53.5 mm³, P = 0.021). In normal epicardial tissue, cryolesions were larger in maximum diameter (11.2 ± 4.3 mm vs 7.7 ± 3.1 mm, P = 0.012), depth (5.8 ± 1.6 mm vs 4.7 ± 1.4 mm, P = 0.034), and volume (274.7 ± 242.2 mm³ vs 112 ± 102.9 mm³, P = 0.002). In normal endocardium, no significant differences were found. Conclusions: Epicardial cryoablation with an 8 mm tip cryocatheter led to larger lesion volume in infarcted myocardium compared to a 3.5 mm irrigated RF catheter. This is likely related to a combination of cryoadherence, more efficient energy delivery with horizontal orientation, and lack of warming by circulating blood. Cryoablation merits further investigation as a modality for treating ventricular tachycardia of epicardial origin in humans. (J Cardiovasc Electrophysiol, Vol. 23, pp. 1016‐1023, September 2012)     

Effect of myocyte necrosis on strength, strain, and stiffness of isolated myocardial strips

Cardiac rupture accounts for 8% to 10% of patient deaths after acute myocardial infarction, suggesting that myocyte necrosis weakens the ventricular wall in the initial days after occlusion. To test this theory, permanent occlusion of the left anterior descending coronary artery was performed in dogs. Twenty-four hours after occlusion, the tensile strength, strain at rupture, and stiffness of necrotic epicardium, midmyocardium, endocardium, subepicardium, and the visceral pericardium (VP) were quantified and compared with those of noninfarcted cardiac tissue. The relationship between tensile strength, stiffness, and collagen content was also examined. These material properties did not differ between necrotic and normal myocardium in any of the layers, indicating that myocyte necrosis, per se, does not weaken the myocardium. In both necrotic and normal tissue, marked transmural heterogeneity was observed; tensile strength of the endo- and epicardium (21.3 +/- 3.3 and 21.3 +/- 3.2 gm/mm2) was significantly greater (p less than 0.01) than that of the midmyocardium (4.0 +/- 0.3 gm/mm2) and subepicardium (5.0 +/- 0.5 gm/mm2), whereas the VP was substantially stronger (greater than 100 gm/mm2) than any myocardial layer. Similar results were obtained for stiffness. In contrast, strain at rupture did not vary significantly among myocardial layers and ranged from 0.40 +/- 0.03 (VP) to 0.53 +/- 0.03 (endocardium). Both tensile strength and stiffness of the myocardial layers were found to correlate directly with their collagen content: the higher the hydroxyproline concentration, the greater the tensile strength (r = 0.83). These results support the concept that the collagen fibroskeleton is an important determinant of the material properties of the myocardium. As myocyte necrosis, per se, did not affect tensile strength, we tentatively conclude that cardiac rupture may be a consequence of a defect or weakness in the collagenous framework of the heart.     

Comparison of radiofrequency ablation in normal versus scarred myocardium

INTRODUCTION: Reentrant circuits causing ventricular tachycardia are closely associated with previously scarred myocardium. The presence of scar has been blamed for the poor success rate of radiofrequency ablation (RFA) in that context. This article investigates the in vivo effects of radiofrequency ablation in myocardium scarred from acute myocardial infarction. METHODS AND RESULTS: Anterior myocardial infarction was induced in five dogs by ligating the left anterior descending artery. The mean left ventricular ejection fraction after infarction was 38%. At a mean of 15 weeks following myocardial infarction, 50 RFA lesions were created in random order, 25 in scarred and 25 in normal myocardium using a needle electrode (21 gauge, 5 mm in length) introduced from the epicardium of the left ventricle at thoracotomy. During unipolar temperature-controlled RFA (90 degrees C for 60 seconds), intramural temperatures were measured by thermistors at distances of 1, 2, 3, 4, and 5 mm from the ablating electrode. The margins of the lesions were clearly discernible in scar at histological examination in 64% of ablations where the scarring was patchy. There were no significant differences between lesion sizes, intramural temperatures at different distances, total energy required for ablation, or mean impedance during ablation of normal versus scarred myocardium. CONCLUSIONS: Scar does not affect lesion size or intramural temperature profile during RFA if electrode size, tissue contact, and tip temperature are controlled. More radiofrequency energy is not required to maintain tip temperature at 90 degrees C in scar compared to normal myocardium.     

Magnetic resonance tomography image of transmural myocardial infarct in comparison with 99mTc-methoxyisobutylisonitrile SPECT]

To assess the ability of magnetic resonance imaging (MRI) to identify morphologic and functional abnormalities associated with transmural anterior and inferior myocardial infarction, 18 patients with anterior myocardial infarcts and 11 patients with inferior myocardial infarcts confirmed by ECG and cine-ventriculography underwent gradient-echo MRI of transverse and short-axis imaging planes. Myocardial perfusion of corresponding imaging planes was measured by 99mTc-methoxyisobutyl-isonitrile single-photon emission computed tomography (MIBI-SPECT). Transmural scar by MRI was defined as diastolic wall thickness 2.5 SD below corresponding normal values of a healthy control group (n = 21). MIBI-SPECT scar was defined as a MIBI uptake less than 2.5 SD below mean values of a healthy control group (n = 11). By MIBI-SPECT, 231 segments contained normal tissue and 161 contained scarred myocardium. In 352/392 (90%) segments gradings based on diastolic wall thickness and MIBI-SPECT gradings were identical. Diastolic wall thickness was significantly higher in normal than in scarred MIBI-SPECT segments (10.3 +/- 1.5 vs 5.2 +/- 2 mm, p less than 0.0001). Additionally, normal segments by MIBI-SPECT showed significantly higher systolic wall thickening than scar segments (5.5 +/- 1.5 vs 0.6 +/- 1.6 mm, p less than 0.0001). The correlation between MRI and MIBI-SPECT assessed infarct size was r = 0.91 for anterior and r = 0.77 for inferior myocardial infarcts. The agreement between MIBI-SPECT perfusion defect size and regions with reduced diastolic wall thickness on MRI tomograms was significantly better for anterior myocardial infarcts than for inferior myocardial infarcts.(ABSTRACT TRUNCATED AT 250 WORDS)     

Mitral Ebstein's Anomaly Modified with a Scarred Rhabdomyoma in Tuberous Sclerosis: An Extremely Rare Cause of Mitral Insufficiency

We present an extremely rare case of mitral Ebstein''s anomaly that resulted in severe mitral regurgitation (MR). A 41-year-old woman with a history of tuberous sclerosis underwent surgery. Preoperatively, it was assumed that MR had occurred due to leaflet tethering related to left ventricular posterior wall motion asynergy due to a scarred rhabdomyoma. However, surgical inspection revealed a dysplastic posterior leaflet adhering to the ventricular wall, which was completely covered by the endocardium. Both congenital mitral Ebstein''s anomaly and acquired wall motion abnormality due to a scarred rhabdomyoma may have contributed to the development of severe MR in this case.     

Regional reduction in ventricular norepinephrine after healing of experimental myocardial infarction in cats

Regional ventricular norepinephrine and myosin heavy chain concentrations were measured in two models of healed left ventricular myocardial infarction in cats. One model was characterized by a well-defined dense transmural scar (discrete myocardial infarction), while the other demonstrated a pattern of nontransmural diffuse patchy fibrosis in the infarct area (diffuse myocardial infarction). Norepinephrine and myosin heavy chain concentrations were measured in the scarred area, the non-infarcted zone surrounding the scar(s), and in sites remote from the scar. Corresponding tissue sites from unoperated animals and sham operated animals served as controls. Myosin heavy chain concentration was used as an index of surviving muscle mass to express norepinephrine concentration. Norepinephrine concentration, as a function of crude tissue mass, was significantly reduced in both the scarred tissues and the non-scarred tissues surrounding the scar in the discrete infarction model but was significantly reduced only in non-scarred tissues adjacent to the dense scar when expressed as a function of myosin heavy chain. The heavily scarred area of the discrete preparation approached normal values when corrected for myosin heavy chain content. The diffuse infarct preparation demonstrated normal norepinephrine concentration at all three sites studied, whether expressed as a function of tissue mass or myosin heavy chain. These data indicate a long-term regional reduction in norepinephrine concentration specific to non-infarcted tissues adjacent to a dense transmural myocardial infarction scar. This regional reduction in norepinephrine concentration corresponds to reported regions of increased sensitivity to sympathetic nerve stimulation in the discrete myocardial infarction model.     

Reconstruction of the left ventricle by circular endoventriculoplasty with septal exclusion

Since 1984 the authors have developed a technical modification of left ventricular surgery after myocardial infarction. The principle is to reorganise the contractile muscle in a circumferential manner by excluding the fibrous akinetic parts of the interventricular septum. The operation consists of implanting sutures distally then resecting the exteriorized fibrous zones and finally mobilising the scarred endocardium in the zones inaccessible to resection (septum and the base of the anterior and posterior papillary muscles) up to the limits of the viable myocardium. A patch of septal endocardium or dacron lined with pericardium is sutured in the contractile muscular zone. One hundred and fifty patients have been operated for cardiac failure (37%), angina (40%) or arrhythmias (10%). One third of patients required intra-aortic balloon pumping in the preoperative period. Myocardial revascularisation was associated in 75% of cases. Surgery was performed as an emergency in 33 cases (25% mortality); in the remaining 117 cases the mortality was 5%. Postoperative control assessment (115 immediate postoperative and 60 one year controls) showed the left ventricular geometry to be almost normal and the global ejection fraction to have increased by an average of 17%. This technique of left ventricular remodelling with septal exclusion enables the surgeon to perform a more physiological repair in patients without cardiac failure and to extend the surgical indications in patients with cardiac failure.     

低能量心脏除颤心肌损伤的实验研究

在 13只犬的低能量心脏除颤实验中 ,应用病理检查、除颤心电图记录以及除颤前后肌酸磷酸激酶及其同工酶 (CPK和CPK MB)测定三种方法探测心肌损伤。肉眼观察和显微镜检查见到 5只犬 (除颤 7～ 2 1次 ,能量 10～ 4 0J)电极处心脏轻度充血 ,2只犬 (除颤 9～ 2 0次 ,能量 2 0～ 5 0J)心肌苍白、心内膜附有血栓 ,6只犬 (除颤 7～ 2 9次 ,能量 10～ 60J)心内膜水肿、血栓形成、局部心肌断裂和退行性变、心肌间质出血等病理变化。记录到 4只犬 (除颤 8～2 4次 ,能量 2 0～ 5 0J)除颤放电后ST段压低或ST段抬高心电图波形。测得 2只犬 (除颤 10～ 19次 ,能量 5～ 4 0J)除颤后CPK和CPK MB有轻度升高 ( 1只CPK由 10 4升至 110IU ,另 1只CPK MB由 4 7.1升至 60 .9IU)。本实验提示 :低能量心脏除颤可导致心肌损伤 ;损伤可能由热和电等因素造成 ;损伤程度与除颤能量和除颤脉冲间隔时间等因素有关 ;损伤范围为局灶性且可能愈合。     

Sulphinpyrazone reduces endocardial injury and mural thrombosis

STUDY OBJECTIVE--The aim of the study was to investigate the effectiveness of sulphinpyrazone, a drug which stabilises endothelial cell membranes, in reducing endocardial injury and mural thrombosis produced by lactic acid in the left ventricle. DESIGN--The left ventricular endocardium of isolated beating rat hearts, perfused via the aorta with oxygenated Krebs-Henseleit buffer, was exposed for up to 4 h to additional lactic acid (pH 6.4), with and without sulphinpyrazone (100 ng x ml-1). After flushing with buffer, passage of 10 ml blood, and further flushing, the hearts were fixed by coronary perfusion and the endocardium examined by scanning electron microscopy. EXPERIMENTAL MATERIAL--Hearts from 48 male albino Wistar rats, weight 270-380 g, were used. MAIN RESULTS--Morphometric analysis of the surface of the papillary muscles showed that lactic acid caused membrane injury in endothelial cells, up to 30% of which exfoliated. However when sulphinpyrazone was present, endothelial cell damage was reduced and there was up to 75% reduction in the area of exposed basal lamina or connective tissue. This was associated with a corresponding reduction in the extent of platelet adhesion (79%) and thrombus formation (94%). CONCLUSIONS--The results show that sulphinpyrazone has the potential to reduce the risk of mural thrombosis following endocardial injury.     

Selective ablation of atheromas using a flashlamp-excited dye laser at 465 nm.

Ablation of human atheromas with laser pulses that had only a small effect on normal artery tissue was shown in vitro in air and under saline using 1-mu sec pulses at 465 nm from a flashlamp-excited dye laser. At this wavelength, there is preferential absorption in atheromas due to carotenoids. The threshold fluence for ablation was 6.8 +/- 2.0 J/cm2 for atheromas and 15.9 +/- 2.2 J/cm2 for normal aorta tissue. At a fluence of 18 J/cm2 per pulse, the ablated mass per unit of energy ranged from 161 to 370 micrograms/J for atheromas and from 50 to 74 micrograms/J for normal aorta tissue. Ablation products consisted of cholesterol crystals, shredded collagen fibers, and small bits of calcific material. Most debris was less than 100 micron in diameter, but a few pieces were as large as 300 micron. High-speed photography of ablation in air suggested explosive ejection of debris, caused by vapor formation, at speeds on the scale of 300 m/sec. Histological analysis showed minimal thermal damage to residual tissue. These data indicate that selective laser ablation of atheromas is possible in vitro.     

Passive current redistribution in the heart

INTRODUCTION: Electrical stimuli produce a spatial distribution of voltage across the heart. We hypothesized that the potential difference between tissue near a stimulating electrode and a remote site could cause sufficient current to flow through a highly conductive wire connecting the two sites to directly stimulate the remote tissue. METHODS AND RESULTS: In six open chest pigs, we inserted a catheter with right ventricular (RV) and superior vena cava (SVC) coil electrodes. A wire was placed with one end contacting the epicardium 10 +/- 2 mm away from the RV electrode and the other end on left ventricular (LV) epicardium 56 +/-14 mm from the RV end of the wire. Stimuli of 10 to 100 V were delivered to the RV and SVC electrodes. Potentials were recorded from two 252-electrode arrays placed over the RV and LV ends of the passive wire. The current induced in the wire was measured. A minimum stimulus of 15 +/- 6 V was needed between RV --> SVC electrodes to not only pace the RV but also to pace the LV through the passive wire as detected by the electrode array recordings. Current in the wire varied linearly with RV-SVC stimulus strength. CONCLUSION: Coupling RV and LV epicardium with a passive wire while stimulating the RV endocardium induced sufficient current in the wire to synchronously pace the LV.     

Slow intramural heating with diffused laser light: A unique method for deep myocardial coagulation

BACKGROUND: Catheter ablation of postinfarction ventricular tachycardia (VT) may be limited by insufficient myocardial coagulation or excessive endocardial or epicardial damage. We propose that volumetric heating restricted to intramural sites may improve the outcome and safety of this procedure, especially if delivered at rates that enhance heat conduction and forestall adverse tissue changes. METHODS AND RESULTS: A novel optical fiber with a diffusing tip for direct intramural, volumetric laser heating was tested via thoracotomy and percutaneously in normal dogs. Low-power (2.0- to 4.5-W) diode laser light (805 nm) diffused within tissue induced large lesions but no visible surface damage, mural thrombi, or transmural perforation. Mean lesion depth approximated tip length (10 mm). Mean lesion widths in the thoracotomy and percutaneous groups were 5.8+/-0.5 to 9.1+/-0.84 mm and 5.2+/-0.85 to 7.9+/-1.1 mm, respectively, depending on the light dose. Mean volumes in the percutaneous group were 1006+/-245 to 2471+/-934 mm. ST-segment depression, appearing in unfiltered bipolar electrograms recorded from the guiding catheter, was specific for lesion induction. All dogs survived the protocol, which included a 1-hour observation period. In cross section, lesions were elliptical to spherical and characterized by extensive contraction-band necrosis abruptly bordering viable tissue. No platelets or fibrin adhered to the endocardium. CONCLUSIONS: Slow, volumetric, and direct intramyocardial heating induces large, deep lesions without hazardous tissue damage. Such heating might cure postinfarction VT more successfully and safely than present techniques. Further testing and development of this method seem warranted.     

Platelet and fibrinogen turnover at the exposed subendothelium measured over 1 year after a balloon catheter de-endothelializing injury to the rabbit aorta: thrombotic eruption at the late re-endothelialization stage

Balloon catheter de-endothelialization of the rabbit aorta in vivo causes a rapid release of thrombin and a consequent hemostatic response at the surface of the exposed subendothelium. Previously, we have compared the net fluxes of several hemostatic proteins from plasma into the exposed aorta subendothelium for up to 600 days after injury. We now report the turnover of platelets, compared to fibrinogen, at the de-endothelialized aorta for up to 390 days after injury. Anesthetized NZW rabbits received either a de-endothelializing or a sham injury (controls) to their aortas. At a predetermined time (either 10 min before or up to 390 days after injury), each rabbit was infused with known quantities of rabbit (51)Cr-platelets and rabbit (125)I-fibrinogen; the radiolabels were allowed to circulate for 10 min before the rabbit was rapidly exsanguinated. Radioactivity measurements and tissue analysis revealed that at 10 min after balloon injury, approximately 165,000 platelets/mm(2) were associated with the aorta surface, and platelet turnover was 840/min/mm(2). Turnover had decreased to <200/min/mm(2) at 10-21 days but, from 65 to 390 days, had increased to approximately 1500/min/mm(2). In comparison, approximately 17 pmol of fibrinogen/cm(2) saturated the ballooned surface by 10 min after injury. Fibrinogen turnover at the aorta surface at 10 min after injury amounted to 0.2 pmol/min/cm(2), increasing to 0.7 at 10 days but decreasing to 0.25 at 21 days. Between 65 and 390 days, fibrinogen turnover increased slowly to 1.3 pmol/min/cm(2). Fibrinogen turnover at the surface of the aorta paralleled that within the intima-media over 390 days. Platelet and fibrin(ogen) deposits within the aorta wall increased over the 21-390 days interval as shown by immunostaining. The results are consistent with the re-endothelializing aorta tending to support thrombosis and ulceration in the late healing stage.