Myocardial Bundles Research Articles

The hyaluronic acid in intramyocardial sliding

Introduction and objectivesThe sliding between internal and external segments of the myocardium assumes opposite directions in their movements, during the systolic and suction phases of the heart, generating friction. Our objective was to considerer the possibility of the existence of a lubricant that prevents friction wear in myocardial torsion and detorsion movements. MethodsTwenty-four hearts were used: (a) Fifteen two-year-old bovine hearts weighing 800–1000g. (b) 9 human hearts (two 16- and 23-week gestation embryos, one from a 10-year-old child weighing 250g and 6 from adults, with an average weight of 300g). In the hearts 5 transverse, 2cm thick sections were made from base to apex to analyze the hyaluronic acid. All samples were subjected to histochemical analysis with Alcian blue staining, a reliable marker to identify the presence of hyaluronic acid, as an antifriction mechanism and even to provide a semi-quantitative assessment. ResultsIn all the hearts analyzed, hyaluronic acid was found in the cleavage planes between the myocardial bundles. Histological and histochemical studies of the myocardium and its ducts (Thebesian and Langer) have shown that hyaluronic acid could be considered the antifriction effect, which flows throughout the myocardial thickness. ConclusionsThis process involves opposite directions of the muscle segments and of these against the septal area. Sliding between these segments assumes opposite courses during the phases of the cardiac cycle (systole and suction) generating friction. In order to carry out this work, there is an antifriction lubricating mechanism represented by the venous Thebesian and Langer ducts together with the presence of hyaluronic acid. It is understandable that the fascicles of the myocardium, one on top on the other but in discordant directions, implies that the friction between them without a lubricating mechanism would be a decrease in the capacity of movement due to friction.

PO-683-01 THE MECHANISTIC ROLE OF INTRAMYOCARDIAL FAT IN VENTRICULAR TACHYCARDIA RE-ENTRY CIRCUITRY IN PATIENTS WITH ISCHEMIC CARDIOMYOPATHY

Post myocardial infarction (MI) ventricular tachycardia (VT) is due to circuit reentry through surviving myocardial bundles within scar, however, we have previously observed that critical VT circuits are more likely to be adjacent to lipomatous metaplasia (LM).

Cardiovascular and Cytogenetics Complications of Obesity Induced by Monosodium Glutamate in New Born Male Albino Rats

The present study was aimed to estimate cardiovascular and cytogenetic changes on rats induced obesity by monosodium glutamate (MSG). The study was performed on 90 newborn male rats which divided into 2 groups, the 1st group were treated with MSG at dose 4 mg/g IP once daily for 4 consecutive days, while as 2nd group served as control (Placebo). After 4 weeks from the first injection, five male rats were taken randomly from each group and the Body Weight (BW), Body Mass Index (BMI), leptin (LEP), Triglycerides (TG), Troponin-I (cTnI), cytogenetic study, myocardial fibrosis ratio and obese gene expression have been measured. All results revealed a significant increase in mean value (P<0.05) in treated group when compared with control group. While a results of myocardial fibrosis ratio photomicrograph showed myocardial interstitial fibrosis, collagen bundles and necrosis of myocytes forming a spaces in cardiac parenchyma. This study concluded the MSG have ability to induce obesity and its complications in rats by causing increasing of obese gene expression in adipose tissue, leptin resistance, in addition to increasing of BW, BMI and serum triglycerides levels, as well as increasing of serum Troponin-l, cardiac damage and inducing of different cytogenetic damage.

Evidence that the myocardium is a continuous helical muscle with one insertion

Introduction and objectivesAnatomically, the heart cannot be suspended in the thorax without structural continuity of the heart muscle to pump blood at a speed of 200cm/s with an efficacy that allows ejecting 70% of the left ventricular volume with only 12% shortening of its contractile unit, the sarcomere. The aim of this study was to investigate a) whether the myocardium is a single, continuous, helical muscle; b) the origin and end of the myocardial muscle; and c) the sliding movement between the myocardial segments during ventricular torsion–detorsion. This forces us to think of an antifriction mechanism. MethodsA total of 18 hearts (10 bovine and 8 human) were used for anatomical and histological studies. Histological an histochemical analysis of the samples were performed, using the Alcian Blue technique to confirm hyaluronic acid and its antifriction mechanism. ResultsThe myocardium could be defined as a single, continuous, and helical muscle that is inserted at its origin and end, according to the specimens analyzed, to an osseus-chondroid-tendinous nucleus called cardiac fulcrum, thus limiting the 2 ventricular chambers. Hyaluronic acid was found in the excision planes between the myocardial bundles. ConclusionsThe myocardium in its longitudinal continuity adopts a spiraling spatial configuration, inserted at its end to a nucleus called cardiac fulcrum. The Thebesian veins and hyaluronic acid could have an essential role in the antifriction mechanism, due to the resistance between the sliding myocardial muscle surfaces in their torsion (systole) and detorsion (suction) motions.

238-LB: Dietary Protein Restriction Induces Myocardial Dysfunction Despite Reducing Body Weight in Aged C57BL/6J Mice

Introduction: Type 2 diabetes (T2D) and obesity reduce healthspan in part by increasing risk of cardiovascular events including arrhythmias, heart attacks, cardiomyopathies, and coronary heart disease. Low protein diets and specific amino acid deficiencies, such as dietary methionine, have been observed to reduce body weight, improve glycemic control, and ultimately extend lifespan. However, little is known of how systemic protein deficiency may alter myocardial integrity and bioenergetic function. Methods: Twelve-month-old male C57BL/6J mice were randomized to a normal protein (NP; 20% casein), low protein (LP; 5% casein), high fat (HF; 60% fat), or high fat + low protein (HF + LP; 60% fat, 5% casein) diet for 16 weeks. Body weight was measured weekly. Oxidative phosphorylation (OXPHOS) and electron transport system (ETS) capacity was determined in permeabilized myocardial fiber bundles by high-resolution respirometry. Citrate synthase activity was determined by kinetic enzymatic assay. Cardiomyocyte diameter was determined by haemotoxylin and eosin (H&E) staining. Untargeted transcriptomic profiling was conducted by RNA sequencing. Changes in protein expression were determined by immunoblotting. Results: LP reduced body weight relative to NP and HF, whereas HF+LP reduced body weight relative to HF, but was greater than LP alone. LP and LP+HF increased heart weight relative to body weight and cardiomyocyte diameter relative to both NP and HF. Succinate linked OXPHOS and ETS (complex II coupled and uncoupled) was reduced in both LP and LP+HF compared to NP and HF alone. Conclusion: Protein restriction reduces cardiac OXPHOS capacity and induces cardiomyocyte hypertrophy in aging mice. These results question the applicability of chronic protein restriction for management of obesity-related diseases. Further investigation is required to determine if the alterations in cardiac bioenergetic function and structure are advantageous or maladaptive responses. Disclosure C.L. Axelrod: None. W.S. Dantas: None. G. Davuluri: None. W.T. King: None. C.M. Hill: None. C. Morrison: None. J.P. Kirwan: None. Funding National Institute of Diabetes and Digestive and Kidney Diseases (DK105032); National Institute of General Medical Sciences (GM104940)

A novel multielectrode catheter for high-density ventricular mapping: electrogram characterization and utility for scar mapping.

Multielectrode mapping catheters can be advantageous for identifying surviving myocardial bundles in scar. This study aimed to evaluate the utility of a new multielectrode catheter with increased number of small and closely spaced electrodes for mapping ventricles with healed infarction. In 12 swine (four healthy and eight with infarction), the left ventricle was mapped with investigational (OctarayTM) and standard (PentarayTM) multielectrode mapping catheters. The investigational catheter has more electrodes (48 vs. 20), each with a smaller surface area (0.9 vs. 2.0 mm2) and spacing is fixed at 2 mm (vs. 2-6-2 mm). Electrogram (EGM) characteristics, mapping efficiency and scar description were compared between the catheters and late gadolinium enhancement (LGE). Electrogram acquisition rate was faster with the investigational catheter (814 ± 126 vs. 148 ± 58 EGM/min, P = 0.02) resulting in higher density maps (38 ± 10.3 vs. 10.1 ± 10.4 EGM/cm2, P = 0.02). Bipolar voltage amplitude was similar between the catheters in normal and infarcted myocardium (P = 0.265 and P = 0.44) and the infarct surface area was similar between the catheters (P = 0.12) and corresponded to subendocardial LGE. The investigational catheter identified a higher proportion of near-field local abnormal ventricular activities within the low-voltage area (53 ± 16% vs. 34 ± 16%, P = 0.03) that were considered far-field EGMs by the standard catheter. The investigational catheter was also advantageous for mapping haemodymically non-tolerated ventricular tachycardias due to its higher acquisition rate (P < 0.001). A novel multielectrode mapping catheter with higher number of small, and closely spaced electrodes increases the mapping speed, EGM density and the ability to recognize low amplitude near-field EGMs in ventricles with healed infarction.

Histological study on the heart ventricle of Egyptian bovines (Bos aegyptiacus).

Background:The heart ventricles have thicker walls than atrium as they pump blood through blood vessels into all body organs.Aim:This study aimed to describe the histological changes of the heart ventricles in Egyptian bovine (Bos aegyptiacus) with special reference to Purkinje fibers.Methods:A total of 10 male Egyptian bovines of 1–10 years old were divided into three groups according to age; immature, mature, and adult animals.Results:The histological sections from all examined animals’ groups revealed three different layers of the wall of both right and left ventricles; endocardium, myocardium, and epicardium. The endocardium was lined with endothelium and filled with fibrous connective tissue. The endocardium of adult bovine was the thickest. Purkinje fibers appeared of pale cytoplasm with few myofibrils. They were present in the deep layer of the endocardium and in the myocardium. The size of Purkinje fibers and the amount of their myofibrils appeared to be increased with advanced age. Bundles of cardiac muscles were the main constituent of the myocardium. The myocardial bundles were separated by fine connective tissue in immature animals that showed an increased amount in the adult animals. The hypereosinophilic cardiac muscle cells were observed in the ventricles of both mature and adult animals suggesting hypercontraction during rigor mortis. An external layer of the ventricles was the epicardium which consisted of connective tissue and covered with mesothelium.Conclusion:Overall, this study revealed histological changes in the wall of the ventricle and Purkinje fibers of Egyptian bovines (B. aegyptiacus) in relation to age. Additionally, the hypereosinophilia of the cardiac muscle cells was recorded in the ventricles of mature and adult bovines.

A swine model of infarct-related reentrant ventricular tachycardia: Electroanatomic, magnetic resonance, and histopathological characterization

Human ventricular tachycardia (VT) after myocardial infarction usually occurs because of subendocardial reentrant circuits originating in scar tissue that borders surviving myocardial bundles. Several preclinical large animal models have been used to further study postinfarct reentrant VT, but with varied experimental methodologies and limited evaluation of the underlying substrate or induced arrhythmia mechanism. We aimed to develop and characterize a swine model of scar-related reentrant VT. Thirty-five Yorkshire swine underwent 180-minute occlusion of the left anterior descending coronary artery. Thirty-one animals (89%) survived the 6-8-week survival period. These animals underwent cardiac magnetic resonance imaging followed by electrophysiology study, detailed electroanatomic mapping, and histopathological analysis. Left ventricular (LV) ejection fraction measured using CMR imaging was 36% ± 6.6% with anteroseptal wall motion abnormality and late gadolinium enhancement across 12.5% ± 4.1% of the LV surface area. Low voltage measured using endocardial electroanatomic mapping encompassed 11.1% ± 3.5% of the LV surface area (bipolar voltage ≤1.5 mV) with anterior, anteroseptal, and anterolateral involvement. Reentrant circuits mapped were largely determined by functional rather than fix anatomical barriers, consistent with "pseudo-block" due to anisotropic conduction. Sustained monomorphic VT was induced in 28 of 31 swine (90%) (67 VTs; 2.4 ± 1.1; range 1-4) and characterized as reentry. VT circuits were subendocardial, with an arrhythmogenic substrate characterized by transmural anterior scar with varying degrees of fibrosis and myocardial fiber disarray on the septal and lateral borders. This is a well-characterized swine model of scar-related subendocardial reentrant VT. This model can serve as the basis for further investigation in the physiology and therapeutics of humanlike postinfarction reentrant VT.

Myocardial bridge and coronary arteries: morphological study and clinical significance.

Myocardial bridge (MB) is the myocardial bundles covering a segment of a coronary artery or one of its branches. This work aimed to study the morphological properties of MB and their effects on the structure of the dominant coronary artery. Sixty adult human hearts (40 male and 20 female) were obtained from the Anatomy Department, Faculty of Medicine, King Abdulaziz University. Dissection o fthe coronary arteries and their main branches was done. Number, site, length and thickness of MB were determined in correlation with coronary dominancy. External diameter of proximal and distal segments of bridged branches and histology of the different segments of the anterior interventricular artery were examined as well. Thirty-six MB were observed in 27 (45%) hearts (18 male and 9 female). MB were mostly observed on the middle segment of the anterior interventricular artery (52.8%) and to a lesser extent on its diagonal branch (13.8%), posterior interventricular artery (13.8%), median and left marginal branches (5.6%), and right coronary artery stem (2.8%). In 30% out of 56.7% of right, in 8.3% out of 26.7% of balanced and in 6.7% out of 16.7% of left dominant hearts revealed MB. The mean length of MB was 24.9 ± 1.98 mm and that of their thickness was 2.28 ± 0.13 mm. Morphological differences in external diameter and histological structure of the different parts of bridged branch were observed. Knowledge of morphological aspects and effects of MB provide better therapeutic and surgical interventions for clinicians dealing with patients having MB.

The relationship between the first layer of the myocardial bridge and the longitudinal axis of the under-bridge arterial segment

Complete myocardial bridges (CMB) are myocardial bundles which cover a portion of the underepicardial coronary artery on one or more of its parts. Most frequently CMB cover the anterior interventricular branch, followed by the diagonal branches of both ventricles, first marginal branch and posterior interventricular branch. It is important to consider the association of several bridges on the same vessel or on different vessels. Microscopic picture of the under-bridge segments indicates that the term of myocardial bridge is arbitrary. Thus, while in thin myocardial bridges the direction of the myocardial fibers is similar to the basic layer, in thick bridges, especially those located on the anterior interventricular branch, myocardial fibers surround the vessel from all the parts and present a spiral orientation. Depending on the topography of the myocardial bridges, intramural vascular segment can be intersected by muscle bundles perpendicular, under an acute angle according to the longitudinal axis of the vessel or they can be oriented parallel to the vessel. According to the angle of intersection of the vessel by the muscle bundles, we could explain the different compression and strength levels of intramural vascular segment in different arterial segments. Histological study shows some morphological features, which would explain myocardial ischemia in some cases of intramural trajectory of large coronary arteries, such as deformation of the vessel, persistent vessel narrowing and narrow perivascular space. Scripta Scientifica Medica 2013; 45(4): 59-65.

Histopathological Verification for Successful Ablation of Mitral Isthmus Ventricular Tachycardia Complicated with Cardiac Sarcoidosis

A 68-year-old man died a few days after catheter ablation of drug-resistant, monomorphic ventricular tachycardia (VT) complicated with cardiac sarcoidosis. The diagnosis of mitral isthmus VT was made from electrophysiological observations, including electro-anatomical activation and voltage map, pace-mapping, entrainment mapping and ablation outcome. On autopsy of the heart, sarcoidic lesion with scattered fibrous tissue in the mitral isthmus was non-transmural, and the surviving myocardium serving as the reentry circuit in the endomyocardium was isolated from the adjacent viable epimyocardium, enabling the sustenance of macroreentry across the mitral isthmus. Non-transmural lesions produced by RF delivery created a barrier sufficient to interrupt the myocardial bundles located in the mitral isthmus, eliminating the mitral isthmus VT.

The infarct characteristics on magnetic resonance imaging and ventricular tachycardia: do we see what we need to see?

This editorial refers to ‘The heart rate of ventricular tachycardia following an old myocardial infarction is inversely related to the size of scarring’ by L. Woie et al., on page 864. The underlying mechanism of most ventricular tachycardias (VTs) after myocardial infarction (MI) is reentry involving areas of ventricular scar. Dense fibrous scars alone cannot cause arrhythmias; however, when surrounded by bundles of surviving myocytes in the peri-infarction zone, an arrhythmogenic substrate may arise. Areas of dense fibrosis intersperse with surviving myocardial bundles and form regions of conduction block that define reentry circuit borders. The presence of fibrosis between these surviving bundles prolongs the pathway for impulse propagation, creating slow conduction through the scar.1 The complex structure of these scars is likely to determine reentrant circuit characteristics and thereby VT characteristics.2 Late gadolinium-enhancement cardiac magnetic resonance (LGE-CMR) has increasingly been used to visualize the three-dimensional (3D) geometry of myocardial fibrosis and has become the gold standard for detection of non-transmural scars because of its superior spatial resolution.3 Woie et al .4 have addressed an interesting question of whether myocardial scar characteristics as visualized and defined by LGE-CMR correlate with VT characteristics, specifically with the VT cycle length (VTCL). They hypothesized that the rate of spontaneous VTs is related to the size of the post-infarction scar or its border zone. They studied 24 patients with remote MI and indication for implantation of an internal cardioverter-defibrillator for primary or secondary prevention who underwent LGE-CMR for quantification of left ventricular (LV) volumes, function, size of core infarct, and size of the infarct border zone prior to device implantation. Patients were followed every 3 months during the first year after implantation. Twenty out of 24 patients had VTs with a median VTCL of 325 ms (range 239–438 ms). None of …

Transmurality mapping of left ventricular scar: impact of spatial resoluton

Left ventricular (LV) scar is associated with ventricular tachycardia (VT), related to regions of slow conduction. Endocardial LV voltage maps reveal regions of low voltage near the site of VT origin, corresponding to myocardial fiber bundles trapped in areas of extensive fibrosis. Scar transmurality (i.e. the percent of myocardial wall thickness which is scarred, measured in 6-12 sectors around the LV myocardium) is an indicator of myocardial viability after reperfusion (1). Intermediate infarct transmurality has been correlated with non-ischemic VT (2). Furthermore, lower voltages are found in regions of more transmural scarring (3). We have expanded the transmurality concept to generate LGE transmurality maps of the LV.

Comparison of assessment methods used to diagnose Hematodinium sp. infections in Cancer pagurus

Abstract Ní Chualáin, C., and Robinson, M. 2011. Comparison of assessment methods used to diagnose Hematodinium sp. infections in Cancer pagurus. – ICES Journal of Marine Science, 68: . Endoparasitic dinoflagellates of the genus Hematodinium have recently gained attention as significant pathogens of the brown crab Cancer pagurus in Ireland. Patent infections, which are characterized by a hyperpigmented carapace and moribund condition, are limited to the discrete periods when macroscopic identification is possible. Three methods are assessed for diagnosing Hematodinium sp. infections in brown crab at the times when macroscopic identification is not always possible. Haemolymph smears, histological sections of gill, heart, midgut, hepatopancreas, muscle, and gonad, and a polymerase chain reaction (PCR) assay provided virtually equivalent accuracy in gauging infection prevalence, regardless of season. Sequences of PCR amplicons from the 18S ribosomal RNA gene confirmed the identity of the parasite as belonging to the genus Hematodinium. Infection intensity values (&lt;1–87%) obtained from haemolymph smears underscored infection levels within tissues, 90% of which contained advanced levels of infection. Alterations to tissues of infected crabs included haemocytopoenia, oedema, which caused dilation of the haemal sinuses resulting in pressure necrosis to the connective tissues around the oocytes, myocardial bundles, and hepatopancreatic tubules. The claw muscle of infected animals contained the fewest parasites.

The Pathophysiologic Basis of Fractionated and Complex Electrograms and the Impact of Recording Techniques on Their Detection and Interpretation

Extracellular electrograms, recorded directly from the heart, are the hallmarks of invasive cardiac electrophysiology and provide information about the electric status of the underlying myocardium. These electrograms are generated by depolarization of cardiomyocytes that generates transmembrane currents in extracellular space and potential differences due to electric resistance of the extracellular medium. In healthy myocardium, the basic configuration of the extracellular electrogram is simple. Under pathological conditions, however, electrograms may consist of multiple components and long duration, which have been attributed to abnormal conduction and arrhythmogenicity. Although complex and fractionated electrograms are presently considered to be a real phenomenon, this was not the case some 20 years ago. Debates about the “fact or artifact” of complex and fractionated electrograms were common.1 At that time, electrograms consisting of multiple “high frequency” components with low amplitudes and long duration, termed “fractionated,” were recorded in patients with healed myocardial infarction during endocardial mapping. Several investigators presumed that fractionated electrograms were artifacts, resulting from movements between electrode and myocardium, filter characteristics of amplifiers, or represented far field effects. A classic example to support the “artifact theory” was the recording of continuous activity from the jello brain.2 In those days, much attention had been paid to fractionated electrograms in healed myocardial infarction to guide catheter ablation or antiarrhythmic surgery.3–5 Although artifacts indeed may cause complex electrograms, most of the complex and fractionated electrograms are a “fact” and caused by the peculiar behavior of activation fronts, due to structural and electric complexity of the underlying myocardium. This article delineates the origin of the unipolar extracellular electrogram, reviews the circumstances that cause fractionated and complex electrograms, and discusses the impact of the recording technique on detection and interpretation of multifaceted electrograms. Extracellular electrograms arise because of transmembrane currents that occur due to differences in the …

New ECG Criteria in Arrhythmogenic Right Ventricular Dysplasia/Cardiomyopathy

Desmosomal changes, electric uncoupling, and surviving myocardial bundles in fibrofatty tissue characterize arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C). Resultant activation delay is pivotal for reentry and thereby ventricular tachycardia (VT). Current task force criteria (TFC) for diagnosis have limited sensitivity. The aim of this study was to assess the diagnostic value of additional criteria on activation delay and VT to improve identification of affected individuals. ECG criteria were studied, while off drugs, in 50 index patients with proven ARVD/C according to TFC (TFC > or = 4 points) and 33 patients with probable ARVD/C (TFC 3 points, or TFC3), being 21 index patients and 12 family members of proven ARVD/C patients. Newly proposed additional criteria are (1) prolonged terminal activation duration in V(1)-V(3), an indicator of activation delay, (2) VT with left bundle-branch block morphology and superior axis, and (3) multiple VT morphologies. All index patients were screened for mutations in ARVD/C-related genes encoding desmosomal proteins. Altogether, 23 of 33 (70%) TFC3 patients fulfilled ARVD/C diagnosis when newly proposed criteria were applied additionally to current TFC. VT with left bundle-branch block morphology and superior axis or multiple VT morphologies were recorded in 12 and 9 of 33 TFC3 patients, respectively, all being index patients. When applying prolonged terminal activation duration additionally to TFC on depolarization/conduction abnormalities, 14 (42%) TFC3 patients fulfilled ARVD/C diagnosis. Results were not significantly different between mutation carriers and noncarriers. Adding the newly proposed criteria to current TFC for ARVD/C will improve identification of affected individuals importantly, independent of outcome of DNA analyses.

Activation Delay and VT Parameters in Arrhythmogenic Right Ventricular Dysplasia/Cardiomyopathy: Toward Improvement of Diagnostic ECG Criteria

Desmosomal changes, electrical uncoupling, and surviving myocardial bundles embedded in fibrofatty tissue are hallmarks of activation delay in arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C). Currently, generally accepted task force criteria (TFC) are used for clinical diagnosis. We propose additional criteria based on activation delay and ventricular tachycardia (VT) to improve identification of affected individuals. Activation delay and VT-related 12-lead electrocardiographic (ECG) criteria were studied, while off drugs, in 42 patients with proven ARVD/C according to TFC, and 27 controls with idiopathic VT from the RV outflow tract. Two of three measured TFC could only be identified in a small minority of ARVD/C patients. Additional ECG criteria proposed in this study included (a) prolonged terminal activation duration, an indicator of activation delay; (b) VT with LBBB morphology and superior axis; and (c) multiple different VT morphologies. These criteria were met in 30 (71%), 28 (67%), and 37 (88%) ARVD/C patients, respectively, and in one control patient (P < 0.001). Electrophysiologic studies contributed importantly to yield different VT morphologies. Pathogenic plakophilin-2 mutations were identified in 25 (60%) of ARVD/C patients and in none of the controls. In ARVD/C patients, parameters measured were not significantly different between mutation carriers and noncarriers, except for negative T waves in V1-3, occurring more frequently in patients with mutation. The proposed additional criteria are specific for ARVD/C and more sensitive than the current TFC. Therefore, adding the newly proposed criteria to current TFC could improve ARVD/C diagnosis, independent of DNA analysis.

Abstract 1830: New ECG Criteria for Diagnosis of Arrhythmogenic Right Ventricular Dysplasia/Cardiomyopathy

Introduction Desmosomal changes, electrical uncoupling and surviving myocardial bundles embedded in fibrofatty tissue are hallmarks of activation delay (AD) in arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C). AD is pivotal for reentrant mechanisms and thereby ventricular tachycardia (VT). At present, generally accepted Task Force Criteria (TFC) are used for clinical diagnosis of ARVD/C. We propose additional criteria (AC) on AD and VT to improve identification of affected individuals. Methods AD and VT-related electrocardiographic criteria were studied, while off drugs, in 42 patients with proven ARVD/C according to TFC, and 23 controls with idiopathic VT from the RV outflow tract. TFC assessed: epsilon waves, QRS width &gt;110ms in V1–3 in absence of RBBB and negative T-waves in V2 and beyond. The 3 new AC are: prolonged S-wave upstroke in V1–3 (≥55ms from nadir of S to end of depolarization) occurrence of LBBB like VT with axis −30° to −150°and number of different monomorphic VT morphologies (different when Δ axis ≥30°; spontaneous and induced by programmed electrical stimulation (PES)). All ARVD/C patients were screened for mutations in genes encoding desmosomal proteins. Results For comparison of ARVD/C patients (pts) and controls: see table . In ARVD/C pts mean S-wave upstroke duration was 63±20 ms (range 40–140), mean number of different spontaneous VTs 1.8±0.95 (range 0–5) and mean number of spontaneous+induced VTs 2.8±1.08 (range 1–5). All VTs showed LBBB morphology. Plakophilin-2 mutations were identified in 25 (60%) of ARVD/C pts. Parameters measured were not significantly different between mutation carriers and non-carriers. Conclusions The newly proposed criteria are sensitive and specific for ARVD/C and thereby useful for its diagnosis, independent of outcome of DNA analysis. Prolonged S-wave upstroke is the most sensitive ECG indicator of activation delay during sinus rhythm. PES contributes to yield of VT morphologies.

Diverse Myocardial Extension and Autonomic Innervation on Ligament of Marshall in Humans

The ligament of Marshall (LOM) or the oblique vein of Marshall (VOM) in the left atrium (LA) is one of the origins of nonpulmonary vein ectopies causing atrial fibrillation. The distributions of myocardial bundles (Marshall bundles; MBs) and autonomic nerves adjacent to the LOM have not been completely elucidated. Twenty-eight human hearts were examined postmortem. The inferolateral LA myocardium was dissected en block and cut perpendicularly to the atrioventricular ring. The specimens were sectioned at 1-mm intervals and stained with hematoxylin and eosin, and Azan-Mallory. In addition, S-100 and tyrosine hydroxylase (TH) were employed for the immunohistochemical analysis of the sympathetic and parasympathetic fibers. In 25 cases, MBs were observed. Although the MBs surrounded the VOM at the coronary sinus (CS) juncture, they gradually diminished in density toward the distal venous branch. The connections of the MBs and LA myocardium were frequently observed in the CS juncture and anterior wall of the left pulmonary vein (PV)-LA junctions. TH-stained sympathetic nerve fibers were densely distributed around the PV-LA junctions. On the other hand, non-TH-stained parasympathetic ganglions were mainly observed at the CS juncture. MB-LA connections were mainly observed at the CS juncture and PV-LA junctions. The association between sympathetic nerve fibers and MBs was distinct at the PV-LA junctions. At the CS juncture, the regression of the sympathetic nerve fibers and the increase of parasympathetic ganglions were observed. The diverse arrangement and autonomic innervation of MBs seem to characterize the LOM region in humans.

Achievement of complete isthmus block by catheter ablation performed only at the tricuspid-valve side of the isthmus in 2 patients with typical atrial flutter: role of the &ldquo;dead-end&rdquo; myocardial bundles in the membranous sector adjacent to the inferior caval vein

Achievement of complete isthmus block by catheter ablation performed only at the tricuspid-valve side of the isthmus in 2 patients with typical atrial flutter: role of the &ldquo;dead-end&rdquo; myocardial bundles in the membranous sector adjacent to the inferior caval vein