Significance of morphological abnormalities detected by MRI in patients undergoing successful ablation of right ventricular outflow tract tachycardia

BACKGROUND: MRI can demonstrate subtle morphological changes of the right ventricle in patients with idiopathic right ventricular outflow tract tachycardia (RVOT). The present study examines the incidence and significance of right ventricular (RV) abnormalities detected by MRI with respect to the site of successful radiofrequency catheter ablation of the clinical tachycardia. METHODS AND RESULTS: The study population comprised 20 patients (mean age, 40+/-12 years) undergoing elimination of recurrent RVOT by radiofrequency catheter ablation. MRI studies were performed before ablation to assess RV volumes and function, as well as structural abnormalities of the RV myocardium. Ten healthy age- and sex-matched subjects served as control subjects. The successful ablation sites, as documented by radiographs of the catheter position, were compared with MRI findings. Patients with RVOT showed no difference in respect to RV volumes and ejection fractions compared with control subjects. Whereas RV abnormalities were limited to prominent fatty deposits of the right atrioventricular groove extending into the inlet portion of the RV wall in 2 of 10 control subjects, MRI studies demonstrated morphological changes of the RV free wall in 13 (65%) of 20 patients with RVOT, including presence of fatty tissue (n=5), wall thinning (n=9), and dyskinetic wall segments (n=4). Eight of these patients had additional fat deposits, thinning, or a saccular aneurysm in the RV outflow tract, corresponding with the ablation site in 6 patients. CONCLUSIONS: In RVOT, structural abnormalities of the right ventricle can be detected in a substantial number of patients despite normal RV volumes and global function. MRI abnormalities within the RV outflow tract are significantly associated with the origin of tachycardia.     

The dose-dependent effects of halothane on right ventricular contraction pattern and regional inotropy in swine

The right ventricle (RV) is comprised of two embryologically distinct units, the inflow and outflow tracts, which normally contract sequentially and differ in the magnitude of increased inotropy during sympathetic nervous stimulation. The present study examined the dose-response effects of halothane on the RV contraction pattern and regional contractility in seven open-chest pigs instrumented for measurement of inflow and outflow tract pressures and segment lengths. The RV contraction pattern was evaluated by comparing the phase of inflow and outflow tract shortening, and regional contractility was determined by calculation of preload recruitable stroke work (PRSW) slope. Using this methodology, an inflow-outflow tract contraction phase difference of -27 degrees (inflow tract shortened earlier) was evident at baseline, but was abolished by 1.0 and 1.5 minimum alveolar anesthetic concentration (MAC) halothane; PRSW slope of both the inflow and outflow tracts, however, demonstrated similar dose-related change. To determine whether alterations in cardiac sympathovagal balance played a role in the RV response to halothane, an additional four animals were studied after pretreatment with hexamethonium, propranolol, and atropine. In these animals, there was no difference in the regional contraction phase either at baseline or during halothane administration, and dose-related depression of PRSW by halothane was again similar in both regions. However, when halothane effects on regional PRSW in animals with autonomic blockade were compared to those of neurally intact animals, a 20% greater depression of outflow tract PRSW by 0.5 MAC halothane was evident. This study demonstrates that halothane abolishes the normal sequential pattern of RV contraction without exerting markedly variant negative inotropic effects within different regions of the RV, and provides evidence to suggest that alterations in cardiac sympathovagal balance may contribute to the effect of halothane on RV contraction dynamics.     

Self-monitoring of blood pressure at home: how many measurements are needed?

Inappropriate sinus tachycardia and atrial arrhythmias have been reported after radiofrequency ablation. Previous studies have suggested that cardiac denervation is a possible explanation for these rhythm disturbances. The aim of this study was to investigate possible alterations in autonomic innervation of the heart after ablation using the techniques of heart rate variability (HRV) analysis and metaiodobenzylguanidine (I-123 MIBG) scintigraphy. The subjects of this study were 30 consecutive patients aged 25 to 40 years, without structural heart disease, who underwent radiofrequency ablation of atrioventricular nodal slow pathways, and posteroseptal and left lateral accessory pathways because of symptomatic recurrent reentrant tachycardias. Time and frequency domain analysis of HRV after ablation revealed a significant reduction in the indexes of the mean of all 5-minute standard deviation of RR intervals (p = 0.042), low frequency (p = 0.0005), and total frequency (p = 0.008) compared with preablation values in the group of patients who underwent atrioventricular nodal slow pathway ablation. Patients who underwent ablation of a posteroseptal accessory pathway also had significant attenuation of the indexes of standard deviation about the mean RR interval (p = 0.03), standard deviation of 5-minute mean RR intervals (p = 0.006), and low-frequency (p <0.0001), and high-frequency (p <0.0001) components. Significant I-123 MIBG map defects, indicating efferent cardiac sympathetic denervation, were also found in the same groups of patients: atrioventricular nodal group (p = 0.0024), posteroseptal accessory pathway group (p = 0.0007). None of the above changes in HRV and 123-I MIBG scintigraphy were seen in patients who underwent ablation of left lateral accessory pathways. We conclude that radiofrequency ablation in the anterior, mid-, and posterior regions of the low intraatrial septum may disrupt sympathetic fibers located in these regions, causing cardiac sympathetic denervation. The density of these fibers appear to be less along the left atrioventricular groove.     

Segmental right ventricular function after acute myocardial infarction: two-dimensional echocardiographic study in 63 patients

Right ventricular (RV) segmental contraction was studied in 63 patients with acute myocardial infarction (MI), using 2-dimensional (2-D) echocardiography. Group A included 32 patients with ischemic RV dysfunction: 19 had a disproportionate increase in right atrial pressure at the time of the examination (Group AI) and in 13 patients, right atrial pressure was normal when the echocardiogram was obtained (Group AII). Group B included 31 patients without ischemic RV dysfunction. Alkinesia or dyskinesia of the RV wall was found in 30 patients: 19 from Group AI, 8 from Group AII, and 3 from Group B. Asynergy could be identified in all segments of the RV wall including the outflow tract, RV apex, and anterior wall, but was more frequently found in the posterior wall (29 patients), best seen in the transversal subcostal short-axis view. A significant difference was found either in the frequency of wall motion abnormalities or in the number of segments with asynergy among the 3 groups (p less than 0.001). However, asynergy of the RV wall may be present in some patients with normal right heart hemodynamic function, suggesting that asynergy may be more sensitive than hemodynamic function in the diagnosis of acute RV infarction. Paradoxical septal motion was found in 8 patients, all in Group AI, and all had a right atrial pressure equal to or greater than pulmonary capillary pressure.     

Demodex-associated folliculitis

We report a rare case of the rupture of the right ventricle which occurred in a minimally invasive direct coronary artery bypass grafting (MIDCABG) for a redo bypass surgery. A 52-year-old male patient underwent a left internal thoracic artery (LITA) to the left anterior descending artery (LAD) bypass. Rupture of the right ventricle occurred abruptly during dissection to find the LAD. Too much dissection of the interventricular groove under undue traction of the pericardium may cause a rupture of the heart.     

MRI semeiology of segmental contraction abnormalities in arrhythmogenic dysplasia of the right ventricle

The diagnosis of localized arrhythmogenic right ventricular dysplasia may be difficult to ascertain. Aside from electrophysiological arguments, visualization of an abnormal right ventricular contraction pattern is of crucial importance for diagnosis. Cine-MR is almost the only examination method which offers detailed informations on the right ventricular contraction pattern. Nine observations of segmental right ventricular contraction abnormalities assessed by cine-MR are described here: dyskinesia of the distal part of the anterior wall (2), of the inferior wall (2), of the right ventricular outflow tract (2); akinesia of the outflow tract (2) and of the inferior wall (1). Morphological abnormalities of the right ventricle are always associated with contraction abnormalities but seem to be less disease specific. Patients should be more readily referred for a cine-MR examination when the diagnosis of localized right ventricular dysplasia is suspected. Cine-MR sequences related to these observations may be reached via Internet at:http:@alsace.u-strasbg.fr/cardio/coeur.htm.     

Aortic outflow obstruction in visceral heterotaxy: a study based on twenty postmortem cases

Aortic outflow tract obstruction can complicate the clinical course and surgical management of patients with heterotaxy syndromes, but its anatomic basis has not been described in detail. In 20 postmortem cases with asplenia (n = 4) or polysplenia (n = 16), the anatomic causes of aortic outflow tract obstruction were absence of the subaortic conus in association with (1) narrowing of the subaortic outflow tract between the conal septum anteriorly and the common atrioventricular (AV) valve posteriorly in six (30%) patients; (2) aortic valvar atresia in four (25%), three with asplenia and one with polysplenia; (3) redundant AV valve leaflets in four (20%); (4) excessive AV valve fibrous tissue in four (20%); (5) marked hypoplasia of the mitral valve and left ventricle in two (10%); and (6) aneurysm of membranous septum in one (5%). One patient belonged to group (1) and (4). Aortic outflow tract obstruction was much more common with polysplenia (28%) than with asplenia (4%) (p < 0.001).     

Early development of chronic active hepatitis in recurrent hepatitis C virus infection after liver transplantation: association with treatment of rejection

As the importance of the right ventricle in many diseases and conditions has been realized, the need for quantitative assessment of the motion and contraction of the right ventricular free wall (RVFW) has become apparent. This study applied the myocardial tagging magnetic resonance imaging (MRI) technique to the normal RVFW to elucidate normal heterogeneity in RV motion and contractile patterns. The RVFW was divided into three segments (inferior, mid and superior) in each of three slices (apical, mid and basal) to allow for a detailed analysis of the motion and contraction. Percent segmental shortening (PSS) was used to measure the amount of contraction, and a vector analysis was used to quantitate the trajectory of the RVFW through systole. PSS increased monotonically through time to an average across all segments of 12% in the basal slice, 14% in the mid-ventricular slice, and 16% in the apical slice of the heart. The trajectory of the RVFW was characterized by a wave of motion toward the septum and outflow tract. The data provided in this study provide a better understanding of normal RV kinematics and can serve as a comparison for disease states.     

Reflex control of cardiac sympathetic nerve activity in anesthetized rats

Reflex control of sympathetic outflow to the heart was evaluated by recording the efferent discharges of the interior cardiac sympathetic nerves in anesthetized rats. The reflex responses of inferior cardiac sympathetic nerve activity (ICNA) to arterial baroreceptor loading by phenylephrine and to arterial/atrial baroreceptor unloading by hemorrhagic hypotension were compared with those of renal sympathetic nerve activity (RNA) and adrenal sympathetic nerve activity (ANA). The reflex decrease in ICNA to the phenylephrine-induced graded increase in arterial blood pressure was smaller than that of RNA or ANA. Thus ICNA is less sensitive to arterial baroreceptor stimulation. Hemorrhage produced a volume-dependent decrease in ICNA. The response was significantly smaller than that in RNA and was directionally opposite to that in ANA. Cervical vagotomy but not sinoaortic denervation abolished the hemorrhage-induced ICNA response, suggesting an important role of vagal pathways. These findings demonstrate that the reflex responses of sympathetic outflow to the heart were quantitively and qualitatively different from those to the kidney and the adrenal gland, indicating the regional control of sympathetic nerve activity in the regulation of cardiovascular functions.     

Nonthoracotomy implantation of cardioverter defibrillators: preliminary experience with a defibrillation lead placed at the right ventricular outflow tract

Although morbidity and mortality associated with defibrillator implantation using a nonthoracotomy approach have decreased as compared with a thoracotomy approach, defibrillation thresholds have been higher and fewer patients satisfied implant criteria. It may be possible to improve on the success of nonthoracotomy defibrillator implantation by the placement of a right ventricular (RV) outflow defibrillation lead. Implantable cardioverter defibrillator implantation data of 30 consecutive patients with clinical VT or VF were reviewed. Three defibrillation leads were routinely used. When either pacing threshold at the RV apex was inadequate (n = 2) or 18-J shocks were not successful in terminating VF in 3 of 4 trials (n = 8), the RV apex lead was positioned to the RV outflow tract attaching to the septum. Defibrillation testing was first performed with the RV apex lead in combination with CS, SVC, and/or subcutaneous leads. Twenty patients satisfied implant criteria with a defibrillation threshold of 13.5 +/- 3.6 J. In 7 of the 10 patients, whose RV lead was repositioned to the RV outflow tract, this lead in combination with SVC, CS, or subcutaneous leads produced successful defibrillation at < or = 18 J or in 3 of 4 trials. This approach improved the overall success of nonthoracotomy implantation of defibrillators from 69% to 90%. After a follow-up of 27 +/- 6 months, there was no dislodgment of the RV outflow tract defibrillation leads. CONCLUSIONS: This article reports the preliminary observation that placement of defibrillation leads to the RV outflow tract in humans was possible and without dislodgment. RV outflow tract offers an alternative for placement of defibrillation leads, which may improve on the success of nonthoracotomy defibrillator implantation.     

Automic innervation of dog coronary arteries

The autonomic innervation of canine coronary arteries has been examined using the Falck and Owman technique for demonstrating catecholamines and a modification of the Koelle technique for the demonstration of cholinesterase. The experimental protocol included an examination of the neural innervation of the major coronary arteries: LCC, LAD, and RCA. A consistent, relatively dense adrenergic innervation was noted. A gradient in the degree of cholinergic innervation was: LAD less than RCA less than LCC. Light microscopic examination of the hearts of dogs subjected to either cervical vagotomy or total extrinsic cardiac denervation was performed. Additional surgical procedures included removal of the left stellate ganglion and a preferential stripping of the LCC. These studies demonstrated the intrinsic nature of parasympathetic coronary innervation. Following all surgical procedure no variations in density of cholinergic innervation were noted, indicating that these fibers are probably postganglionic parasympathetic fibers arising from intrinsic ganglia within the ventricles. These ganglia may be located at the base of the great vessels and send their fibers to the coronary vessels via the septal artery.     

Xenobiotics and xenoestrogens in fish: modulation of cytochrome P450 and carcinogenesis

The periaqueductal gray matter (PAG) serves as the midbrain link between forebrain emotional processing systems and motor pathways used in the defense reaction. Part of this response depends upon PAG efferent pathways that modulate cardiovascular-related sympathetic outflow systems, including those that regulate the heart. While it is known that the PAG projects to vagal preganglionic neurons, including possibly cardiovagal motoneurons, no information exists on the PAG circuits that may affect sympathetically mediated cardiac functions and, thus, the purpose of this study was to use neuroanatomical methods to identify these pathways. First, viral transneuronal retrograde tracing experiments were performed in which pseudorabies virus (PRV) was injected into the stellate ganglion of rats. After 4 days survival, five PAG regions contained transynaptically infected neurons; these included the dorsomedial, lateral and ventrolateral PAG columns as well as the Edinger-Westphal and precommissural nuclei. Second, the descending efferent PAG projections were studied with the anterograde axonal marker Phaseolus vulgaris leuco-agglutinin (PHA-L) with a particular focus on determining whether the PAG projects to the intermediolateral cell column (IML). Almost no axonal labeling was found throughout the thoracic IML suggesting that the PAG modulates sympathetic functions by indirect pathways involving synaptic relays through sympathetic premotor cell groups, especially those found in the medulla oblongata. This possibility was examined by a double tracing study. PHA-L was first injected into either the lateral or ventrolateral PAG and after 6 days, PRV was injected into the ipsilateral stellate ganglion. After an additional 4 days survival, a double immunohistochemical procedure for co-visualization of PRV and PHA-L was used to identify the sympathetic premotor regions that receive an input from the PAG. The PAG innervated specific groups of sympathetic premotor neurons in the hypothalamus, pons, and medulla as well as providing reciprocal intercolumnar connections within the PAG itself (Jansen et al., Brain Res. 784 (1998) 329-336). The major route terminates in the ventral medulla, especially within the medial region which contains sympathetic premotor neurons lying within the raphe magnus and gigantocellular reticular nucleus, pars alpha. Both serotonergic and non-serotonergic sympathetic premotor neurons in these two regions receive inputs from the PAG. Weak PAG projections to sympathetic premotor neurons were found in the rostral ventrolateral medulla (including to C1 adrenergic neurons), locus coeruleus, A5 cell group, paraventricular and lateral hypothalamic nuclei. In summary, both the lateral and ventrolateral PAG columns appear to be capable of modulating cardiac sympathetic functions via a series of indirect pathways involving sympathetic premotor neurons found in selected sites in the hypothalamus, midbrain, pons, and medulla oblongata, with the major outflow terminating in bulbospinal regions of the rostral ventromedial medulla.     

Subaortic obstruction and the Fontan operation

Systemic outflow tract obstruction in the heart with a functional single ventricle promotes myocardial hypertrophy, and this has been shown to be an unequivocal risk factor for poor outcome at Fontan procedure. Such systemic outflow tract obstruction may be congenital or acquired. Those factors contributing to acquired systemic outflow tract obstruction in those patients with a double-inlet left ventricle, a rudimentary right ventricle, and a discordant ventriculoarterial connection include the size of the ventricular septal defect, previous pulmonary artery banding, and other volume unloading surgical procedures. Staging with a bidirectional cavopulmonary connection and construction of a proximal pulmonary artery-aortic connection or ventricular septal defect enlargement has neutralized this factor.     

Lifestyle and 15-year survival free of heart attack, stroke, and diabetes in middle-aged British men

BACKGROUND: Arrhythmogenic right ventricular dysplasia (ARVD) is characterized by local or diffuse wall motion abnormalities in the right ventricle (RV), associated with recurrent ventricular tachycardia (VT) of RV origin. Brain natriuretic peptide (BNP) was first isolated from a porcine brain extract. In humans, BNP is expressed predominantly in the ventricles of failing hearts, and its expression has been observed primarily in myocytes in the interstitial fibrous area in dilated cardiomyopathy. We hypothesized that BNP is increasingly secreted from the residual myocytes within the atrophic tissue in patients with ARVD. METHODS AND RESULTS: Plasma BNP levels were measured in 17 patients with ARVD, 12 patients with idiopathic RV outflow tract tachycardia (RVOT), and 120 control subjects. We performed cardiac catheterization, RV endomyocardial biopsy, electron- beam CT, and biventricular endomyocardial mapping in the ARVD patients. There was a significant increase in plasma BNP levels in the ARVD patients compared with the RVOT patients and control subjects (61.4+/-59.6 pg/mL versus 8.3+/-5. 5 pg/mL and 9.3+/-5.8 pg/mL; P<0.0001, respectively). The plasma BNP levels had no correlation with any of the hemodynamic data, but they had a significant correlation with the RV ejection fraction (r=-0. 588, P=0.025) and with the fractionated-area scores (r=0.705, P=0. 005). Light microscopic immunohistochemistry showed strong BNP immunoreactivity in residual myocytes with fibrofatty replacement. CONCLUSIONS: These results suggest that plasma BNP levels were not increased in RVOT patients but were increased in ARVD patients, and that the increased BNP levels indicate the severity of both the RV dysfunction and the arrhythmogenic substrate.     

Double outlet right ventricle with L-position of the aorta, D-loop, subaortic VSD, and pulmonary stenosis

We describe a case of double outlet right ventricle with subaortic ventricular septal defect and pulmonary stenosis treated successfully with cardiopulmonary bypass. We consider the clinical history and angiocardiographic and surgical findings of this rare anomaly. We stress the difficulties of reconstruction of the outflow tract of the right ventricle, because of the anomalous pathway of the right coronary artery, the posterior situation of the pulmonary artery, and the abnormal anatomy present in the outflow tract of the right ventricle.     

Cardiac pressoreceptors and peripheral resistance

The results obtained show that the pressoreceptors, probably ubicated in the left ventricle of the rat, respond to the distention with vasodilatation. The afferent tract of this reflex is in the vagus nerve and the efferent one is in the sympathetic nervous system. The probable function of this reflex is discussed.     

The effects of eprosartan, an angiotensin II AT1 receptor antagonist, on uric acid excretion in patients with mild to moderate essential hypertension

To test our hypothesis that arginine (Arg) and lysine (Lys) enhance immune activities via neuronal control of the thymus and the spleen, a jugular vein was cannulated for amino acid administration in male Wistar rats (approximately 300 g). In one group (n = 5), an efferent nerve filament of the vagal thymus was isolated. In another group (n = 5), splenic nerve efferents were isolated. Efferent firing rates were recorded before and for 60-90 minutes after 10 mM Arg-Lys in 0.5 ml saline intravenously (i.v.). Differences in firing rates were evaluated using analysis of variance (ANOVA) and t-test. I.v. Arg-Lys increased vagal efferent firing rate to the thymus; enhancing thymic lymphocyte release. I.v. Arg-Lys decreased firing rate in splenic efferents; enhancing natural killer (NK) cell activity. Therefore, Arg-Lys are detected by hepatoportal sensors, stimulating hepatic vagal afferents to the hypothalamus, with the efferent neuronal impulses from the hypothalamus modulating immune function in thymus and spleen, thereby demonstrating the mechanism of Arg and Lys immune enhancing activity.     

Olivocochlear innervation of inner and outer hair cells during postnatal maturation: evidence for a waiting period

Reconstructions of the efferent innervation of the hamster (Mesocricetus auratus) cochlea were done during postnatal development. Efferent neurons were labeled via injections of biocytin and horseradish peroxidase into the crossed olivocochlear (OC) bundles using an in vitro brainstem technique. Such injections retrogradely labeled cell bodies in ventral periolivary regions of the superior olive consistent with their being medial OC neurons. Anterogradely labeled axons were traced to the cochlea, where they terminated on or below inner hair cells (IHCs) prior to postnatal day 5 (P5). After P5, labeled axons terminated on IHCs and outer hair cells (OHCs) and after P10, the majority of labeled axons terminated on the OHCs. In the electron microscope, small labeled terminals containing densely packed synaptic vesicles were found both adjacent to IHCs (axosomatic) as well as apposed to afferent and efferent fibers below IHCs prior to P5. By P10, large labeled terminals were axosomatic to OHCs and no longer found on IHCs. Consistent with previous reports, these data suggest that medial OC axons form part of an early primary innervation on and below IHCs before terminating on OHCs. This raises the possibility that OC neurons demonstrate a period of waiting below an intermediate target similar to that described in the development of thalamocortical projections.     

A novel procedure for mediastinal vagotomy inhibits neurogenic inflammation in rat bronchial tree

Tachykinin-containing sensory axons originating from the cervical vagal nerves and the first several pairs of thoracic spinal nerves are involved in neurogenic inflammation evoked by capsaicin in the bronchial tree. Unilateral degeneration of the cervical vagal trunk by surgical lesion inhibits neurogenic inflammation in the ipsilateral bronchial airways. The vagal trunk has two main branches, the thoracic vagus nerve and recurrent laryngeal nerve in the thorax. The main purpose of this study was to determine whether the thoracic vagus nerve or recurrent laryngeal nerve was significantly involved in the neural control of bronchial inflammation in the rat. A novel and safe surgical procedure was used for selectively cutting the right thoracic vagal trunk, thoracic vagus nerve, or recurrent laryngeal nerve by introducing the surgical instrument through an aperture between the first and second ribs in the ventral wall of the rostral mediastinum. This surgical operation could be completed without causing a pneumothorax. After 2 postoperative weeks, the effects of denervation on capsaicin-induced plasma extravasation in the respiratory tract were tested. Either right thoracic vagal trunk transection or thoracic vagus section significantly decreased plasma extravasation in the right bronchial tree. Thoracic vagus section was obviously more effective. Evans blue extravasation in the right lobar bronchi was reduced by 44-78% after thoracic vagal trunk transection, while that in the right mainstem and lobar bronchi was reduced by 58-81% after thoracic vagus section. Area densities of India ink-labeled leaky blood vessels in the right lobar bronchi were reduced by 40-65% after thoracic vagal trunk transection, and those in the right mainstem and lobar bronchi were reduced by 83-88% after thoracic vagus neurectomy. Recurrent laryngeal neurectomy did not change the plasma extravasation induced by capsaicin in the trachea and bronchi. These results suggest that capsaicin-sensitive fibers running in the vagal trunk, which largely mediated neurogenic inflammation in the bronchial tree, were projected into the thoracic vagus nerve which, in turn, sent these nerve fibers to the ipsilateral bronchial tree. For the trachea, the remaining sensory fibers surviving denervation might provide sufficient tachykinins to trigger neurogenic inflammation.     

Significance of cardiac innervation on spontaneous ventricular arrhythmias elicited by left stellate ganglion stimulation in dogs 4 days after myocardial infarction: comparison of two experimental models

The effects of cardiac sympathetic overactivity on spontaneous arrhythmias and transmural left ventricular effective refractory period (LVERP) were assessed by left stellate stimulation (LSS) in 16 anesthetized dogs. The experiments were performed 4 days after proximal occlusion of the left anterior descending (LAD) coronary artery produced by either ligation (9 dogs) or embolization with histoacryl (7 dogs). The innervation of left ventricular myocardium was studied by light and electron microscopies. Synaptophysin (SYN)- and neuropeptide Y (NPY)-immunoreactive nerve fibers and terminals were thereby detected. In dogs subjected to ligation, LSS elicited negligible arrhythmias in spite of a decrease in LVERP by 6.9 +/- 2.2% (mean +/- SD, p < 0.001). However, dogs with intravascular occlusion were more susceptible to LSS, as indicated by development of sustained ventricular rhythms. In these animals, the LVERP decreased with LSS by 14.6 +/- 3.4% (p < 0.001). The innervation of the anterior left ventricular wall distal to the place of occlusion revealed a higher reduction of SYN- and NPY-immunoreactive nerves in infarcted myocardium and a more heterogeneous distribution of nerves in undamaged regions after ligation, compared to intravascular occlusion. Ultrastructurally, nerve terminals containing small agranular and large dense-core vesicles were found innervating ischemically damaged myocardiocytes. Our findings indicate a higher preservation of nerves in infarcted and noninfarcted myocardium of animals subjected to embolic occlusion of the LAD. Because LSS apparently elicited more arrhythmias in these animals, we suggested a proarrhythmic effect of intact myocardial innervation after infarction.