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Ventricular Myocardium (ventricular + myocardium)
Kinds of Ventricular Myocardium Selected AbstractsACUTE CORONARY LIGATION IN THE DOG INDUCES TIME-DEPENDENT TRANSITIONAL CHANGES IN MITOCHONDRIAL CRISTA IN THE NON-ISCHAEMIC VENTRICULAR MYOCARDIUMCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 3 2007Craig Steven McLachlan SUMMARY 1The aim of the present study was to examine, in the dog myocardium, the incidence of zig-zag mitochondrial cristae over time in the non-ischaemic posterior wall, following an acute anterior wall infarct. 2Changes within the myocardial mitochondrial crista membrane in dogs were investigated following acute left anterior descending coronary artery ligation. Transmyocardial biopsy samples were taken serially from the posterior non-ischaemic wall in the same dog. Changes in heart mitochondrial cristae were examined by transmission electron microscopy prior to coronary ligation (control) and 40 min and 2, 4, 6 and 24 h postinfarction. 3In control hearts, 90% of mitochondrial cristae had a lamelliform appearance. Following infarction, there were twotransitional states with respect to mitochondrial cristae, the first characterized by undulating lamelliform cristae that are also found in 10% of control samples and a second transitional state that was zig-zag and reached a maximum between 6 and 24 h after infarction. 4In conclusion, an undulating lamelliform crista pattern is present in the non-ischaemic wall of the acute infarcted dog and we hypothesize that this may be an intermediate from, between ,normal' lamelliform and ,abnormal' zig-zag cristae. [source] Noncompaction of the Ventricular Myocardium: Report of Two Cases With Bicuspid Aortic Valve Demonstrating Poor Prognosis and With Prominent Right Ventricular InvolvementECHOCARDIOGRAPHY, Issue 4 2003Yuksel Cavusoglu Noncompaction of the ventricular myocardium is a rare, unclassified cardiomyopathy due to an arrest of myocardial morphogenesis. The characteristic echocardiographic findings consist of multiple, prominent myocardial trabeculations and deep intertrabecular spaces communicating with the left ventricular (LV) cavity. The disease typically involves the LV myocardium, but right ventricular (RV) involvement is not uncommon. The clinical manifestations include heart failure (HF) signs, ventricular arrhythmias and cardioembolic events. Noncompacted myocardium may occur as an isolated cardiac lesion, as well as it can be in association with congenital anomalies. We describe two illustrative cases of noncompaction of the ventricular myocardium, a 19-year-old male with bicuspid aortic valve and progressive worsening of HF, and a 61-year-old male with marked RV involvement in addition to LV apical involvement, both with the typical clinical and echocardiographic features of the disease. (ECHOCARDIOGRAPHY, Volume 20, May 2003) [source] Excitable Gap in Canine Fibrillating Ventricular Myocardium: Effect of Subacute and Chronic Myocardial InfarctionJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 6 2001TARESH TANEJA M.D. Excitable Gap in Infarcted Canine Myocardium.Introduction: The existence of an excitable gap during ventricular fibrillation (VF) has been suggested in several prior studies. However, the effects of myocardial infarction on the presence and duration of an excitable gap during VF have not been evaluated. Methods and Results: Electrophysiologic study was performed in normal dogs and in dogs with subacute and chronic infarction. Experimental infarction was produced by left anterior descending coronary ligation. The excitable gap was determined indirectly using either evaluation of intrinsic wavefronts during VF or from the shortest activation interval at individual sites using recordings from a 112- electrode plaque sutured to the epicardial surface of the left ventricle. The excitable gap also was correlated to local electrophysiologic and anatomic properties. The excitable gap using the wavefront propagation method and shortest activation method was significantly longer in subacute infarction dogs (48 ± 17 msec and 37 ± 18 msec, respectively) and chronic infarction dogs (41 ± 14 msec and 35 ± 14 msec, respectively) than normal dogs (32 ± 13 msec and 30 ± 11 msec, respectively; P < 0.05 normal vs subacute and chronic infarction dogs in both methods). The excitable gap occupied approximately 30% and 27% of the VF cycle length in all three groups using the wavefront propagation and shortest activation method, respectively. The excitable gap correlated better with local ventricular refractoriness determined using the wavefront propagation method than with the shortest activation method, but not at all with refractoriness determined using extrastimulus testing. Tissue necrosis was noted in subacute infarction dogs and fibrosis in chronic infarction dogs, but the gap was not highly correlated with anatomic changes. Conclusion: During VF, an excitable gap exists in both normal and infarcted canine ventricular myocardium. It is significantly longer in the presence of infarction. These finding have implications for understanding the pathophysiology of VF and targeting antiarrhythmic therapies. [source] Independent Autonomic Modulation of Sinus Node and Ventricular Myocardium in Healthy Young Men During SleepJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 10 2000PETER KOWALLIK M.D. Autonomic Modulation of Sinus Node and Ventricle. Introduction. The aim of this study was to investigate whether autonomic modulation of ventricular repolarization may spontaneousiy differ from that of the sinoatrial node. Methods and Results. Onset of P waves. QRS complexes, and the apex and end of T waves were detected heat to heat in high-resolution ECGs from nine healthy young men during the night. There were time-dependent fluctuations in the QT/RR slopes of consecutive 5-minute segments that could not he explained by the mean RR cycle length of the respective segment. Because the variahility found in QT intervals could not be explained hy either possible effects of rate dependence or hysteresis, autonomic effects were obvious. Power speetral analysis was performed for consecutive 5-minute segments of PP and QT techograms. In a given subject. trends in the time course of low-frequency (LF) and high-frequency (HF) power in PP and QT often were similar, but they were quite different at other times. The mean LF/HF ratio for QTend (0.75 ± 0.1) was different from that of PP (1.8 ± 0.2; P = 0.002), indicating differences in sympathovagal balance at the different anatomic sites. Furthermore, at a given mean heart rate, averaged QT intervals were different on a time scale of several minutes to hours. The QT/RR slope of 5-minute segments correlated significantly with the HF power of QT variability but not with that of PP variability, indicating effects of the autonomic nervous system on ventricular action potential restitution. Conclusion. These differences demonstrate that changes in sinus node automaticity are not necessarily indicative of the autonomic control of ventricular myocardium. (J Cardiavasc Electrophysiol, Vol. II, pp. 1063-1070. October 2000) [source] The Three-Dimensional Arrangement of the Myocytes Aggregated Together Within the Mammalian Ventricular MyocardiumTHE ANATOMICAL RECORD : ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY BIOLOGY, Issue 1 2009Morten Smerup A 3-D helical arrangement of aggregates of myocytes in a pig's heart revealed by diffusion tensor MRI. See Smerup et al., on page 1, of this issue. [source] Myocardial growth before and after birth: clinical implications,ACTA PAEDIATRICA, Issue 2 2000AM Rudolph Perinatal changes in myocardial growth have recently evoked considerable interest with regard to cardiac chamber development with congenital cardiac lesions and to myocardial development in preterm infants. It is suggested that cardiac chamber development is influenced by blood flow. Experimental pulmonary stenosis in fetal lambs may induce either greatly reduced or markedly increased right ventricular volume. Ventricular enlargement appears to be associated with a large ventricular volume load resulting from tricuspid valve regurgitation. A small competent tricuspid valve is associated with reduced flow through the ventricle due to outflow obstruction and a small right ventricle. Postnatal growth of the ventricles in congenital heart disease is discussed. Increase in myocardial mass prenatally is achieved by hyperplasia, both during normal development and when myocardial mass is increased by right ventricular outflow obstruction. Postnatally, increases in myocardial mass with normal growth, as well as with ventricular outflow obstruction, are largely due to hypertrophy of myocytes. Myocardial capillary numbers do not increase in proportion with myocyte numbers in ventricular myocardium in association with outflow obstruction. The postnatal effects of these changes in congenital heart lesions are considered. Studies in fetal lambs suggest that the late gestational increase in blood cortisol concentrations is responsible for the change in the pattern of myocardial growth after birth. The concern is raised that prenatal exposure of the premature infant to glucocorticoids, administered to the mother to attempt to prevent hyaline membrane disease in the infant, may inhibit myocyte proliferation and result in a heart with fewer than normal myocytes. This would necessitate that each myocyte would have to hypertrophy abnormally to achieve a normal cardiac mass postnatally. [source] Evaluation of Right Ventricular Fibrosis in Adult Congenital Heart Disease Using Gadolinium-enhanced Magnetic Resonance Imaging: Initial Experience in Patients with Right Ventricular Loading ConditionsCONGENITAL HEART DISEASE, Issue 5 2006Lopa P. Hartke MD ABSTRACT Objective., Gadolinium-enhanced cardiac magnetic resonance imaging has been used to show myocardial fibrosis, a finding that appears as late gadolinium enhancement. Its role in the evaluation of right ventricular fibrosis in congenital heart disease is unclear. The purpose of this study was to demonstrate late gadolinium enhancement of the right ventricle in adult and adolescent congenital heart disease and to investigate the relationship between this enhancement and clinical and pathophysiological data. Design., In total, 24 patients, 16 patients with congenital heart disease and right ventricular loading conditions and 8 controls, underwent gadolinium-enhanced viability imaging. Diagnoses varied and included repaired, palliated, and unrepaired lesions. The presence and extent of right ventricular late gadolinium enhancement was compared with patient clinical and hemodynamic data. Exact Wilcoxon tests, Fisher's exact tests, and Spearman's rank correlation were used to compare variables. Results., Nine of 16 patients (56%) were found to have right ventricular late gadolinium enhancement, ranging from 5% to 80% of right ventricular myocardium affected (mean 36.1%, SD 29.7). The combination of right ventricular systolic pressure ,98 mm Hg and systemic oxygen saturation ,93% strongly suggested the presence of right ventricular late gadolinium enhancement (positive predictive value 100%), but no single variable or combination of variables could reliably predict its absence (negative predictive values ,75%). Extent of right ventricular late gadolinium enhancement did not correlate with degree of either hypoxia or right ventricular hypertension. Conclusions., Gadolinium-enhanced cardiac magnetic resonance demonstrates right ventricular late gadolinium enhancement in some patients with congenital heart disease and right ventricular loading conditions. Clinical variables were associated with the presence of fibrosis but did not reliably predict severity. Myocardial preservation is likely a multifactorial process that may affect the right and left ventricles differently. [source] Effects of right and left vagal stimulation on left ventricular acetylcholine levels in the catACTA PHYSIOLOGICA, Issue 1 2001T. Akiyama To test the effectiveness of, and the interactions between, right and left vagal stimulation on left ventricular acetylcholine (ACh) levels, we applied the dialysis technique to the heart of anaesthetized cats. Dialysis probes were implanted in the left ventricular myocardium and perfused with Krebs,Henseleit buffer containing eserine. Dialysate ACh content was measured as an index of ACh release from post-ganglionic vagal nerve terminals in the left ventricular myocardium. We electrically stimulated the right and left cervical vagal nerves separately or together and investigated the dialysate ACh response. In two different regions of the left ventricle, substantial dialysate ACh responses were observed by the stimulation (20 Hz) of both right and left cervical vagal nerves. At stimulation frequencies of both 10 and 20 Hz, the dialysate ACh response to the bilateral vagal stimulation was almost algebraically the calculated sum of the individual dialysate ACh responses to unilateral vagal stimulation. In conclusion, ACh levels in the left ventricle are affected by both right and left vagal nerves and show little evidence of interactions between right and left vagal nerves at the level of the cardiac ganglia. [source] Noncompaction of the Ventricular Myocardium: Report of Two Cases With Bicuspid Aortic Valve Demonstrating Poor Prognosis and With Prominent Right Ventricular InvolvementECHOCARDIOGRAPHY, Issue 4 2003Yuksel Cavusoglu Noncompaction of the ventricular myocardium is a rare, unclassified cardiomyopathy due to an arrest of myocardial morphogenesis. The characteristic echocardiographic findings consist of multiple, prominent myocardial trabeculations and deep intertrabecular spaces communicating with the left ventricular (LV) cavity. The disease typically involves the LV myocardium, but right ventricular (RV) involvement is not uncommon. The clinical manifestations include heart failure (HF) signs, ventricular arrhythmias and cardioembolic events. Noncompacted myocardium may occur as an isolated cardiac lesion, as well as it can be in association with congenital anomalies. We describe two illustrative cases of noncompaction of the ventricular myocardium, a 19-year-old male with bicuspid aortic valve and progressive worsening of HF, and a 61-year-old male with marked RV involvement in addition to LV apical involvement, both with the typical clinical and echocardiographic features of the disease. (ECHOCARDIOGRAPHY, Volume 20, May 2003) [source] Fatty acid metabolism assessed by 125I-iodophenyl 9-methylpentadecanoic acid (9MPA) and expression of fatty acid utilization enzymes in volume-overloaded heartsEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 3 2004T. Miyamoto Abstract Background, The peroxisome proliferator-activated receptor (PPAR) , is a member of the nuclear receptor superfamily and regulates gene expression of fatty acid utilization enzymes. In cardiac hypertrophy and heart failure by pressure-overload, myocardial energy utilization reverts to the fetal pattern, and metabolic substrate switches from fatty acid to glucose. However, myocardial metabolism in volume-overloaded hearts has not been rigorously studied. The aim of the present study was to examine fatty acid metabolism and protein expressions of PPAR, and fatty acid oxidation enzymes in volume-overloaded rabbit hearts. Methods, Volume-overload was induced by carotid-jugular shunt formation. Sham-operated rabbits were used as control. Chronic volume-overload increased left ventricular weight and ventricular cavity size, and relative wall thickness was decreased, indicating eccentric cardiac hypertrophy. 125I-iodophenyl 9-methylpentadecanoic acid (9MPA) was intravenously administered, and animals were sacrificed at 5 min after injection. The 9MPA was rapidly metabolized to iodophenyl-3-methylnonanoic acid (3MNA) by ,-oxidation. Lipid extraction from the myocardium was performed by the Folch method, and radioactivity distribution of metabolites was assayed by thin-layer chromatography. The protein was extracted from the left ventricular myocardium, and levels of PPAR, and fatty acid oxidation enzymes were examined by Western blotting. Results, Myocardial distribution of 9MPA tended to be more heterogeneous in shunt than in sham rabbits (P = 0·06). In volume-overloaded hearts by shunt, the conversion from 9MPA to 3MNA by ,-oxidation was faster than the sham-control hearts (P < 0·05). However, protein levels of PPAR, and fatty acid utilization enzymes were unchanged in shunt rabbits compared with sham rabbits. Conclusions, These data suggest that myocardial fatty acid metabolism is enhanced in eccentric cardiac hypertrophy by volume-overload without changes in protein expressions of PPAR, and fatty acid utilization enzymes. Our data may provide a novel insight into the subcellular mechanisms for the pathological process of cardiac remodelling in response to mechanical stimuli. [source] Correlation of ,-skeletal actin expression, ventricular fibrosis and heart function with the degree of pressure overload cardiac hypertrophy in ratsEXPERIMENTAL PHYSIOLOGY, Issue 3 2006Donatella Stilli We have analysed alterations of ,-skeletal actin expression and volume fraction of fibrosis in the ventricular myocardium and their functional counterpart in terms of arrhythmogenesis and haemodynamic variables, in rats with different degrees of compensated cardiac hypertrophy induced by infra-renal abdominal aortic coarctation. The following coarctation calibres were used: 1.3 (AC1.3 group), 0.7 (AC0.7) and 0.4 mm (AC0.4); age-matched rats were used as controls (C group). One month after surgery, spontaneous and sympathetic-induced ventricular arrhythmias were telemetrically recorded from conscious freely moving animals, and invasive haemodynamic measurements were performed in anaesthetized animals. After killing, subgroups of AC and C rats were used to evaluate in the left ventricle the expression and spatial distribution of ,-skeletal actin and the amount of perivascular and interstitial fibrosis. As compared with C, all AC groups exhibited higher values of systolic pressure, ventricular weight and ventricular wall thickness. AC0.7 and AC0.4 rats also showed a larger amount of fibrosis and upregulation of ,-skeletal actin expression associated with a higher vulnerability to ventricular arrhythmias (AC0.7 and AC0.4) and enhanced myocardial contractility (AC0.4). Our results illustrate the progressive changes in the extracellular matrix features accompanying early ventricular remodelling in response to different degrees of pressure overload that may be involved in the development of cardiac electrical instability. We also demonstrate for the first time a linear correlation between an increase in ,-skeletal actin expression and the degree of compensated cardiac hypertrophy, possibly acting as an early compensatory mechanism to maintain normal mechanical performance. [source] Tissue-specific expression of Cre recombinase from the Tgfb3 locusGENESIS: THE JOURNAL OF GENETICS AND DEVELOPMENT, Issue 2 2008Liang-Tung Yang Abstract Tgfb3, a member of the TGF-, superfamily, is tightly regulated, both spatially and temporally, during embryogenesis. Previous mouse knockout studies have demonstrated that Tgfb3 is absolutely required for normal palatal fusion and pulmonary development. We have generated a novel tool to ablate genes in Tgfb3 -expressing cells by targeting the promoterless Cre-pgk-Neo cassette into exon 1 of the mouse Tgfb3 gene, which generates a functionally null Tgfb3 allele. Using the Rosa26 reporter assay, we demonstrate that Cre -induced recombination was already induced at embryonal day 10 (E10) in the ventricular myocardium, limb buds, and otic vesicles. At E14, robust recombination was detected in the prefusion palatal epithelium. Deletion of the TGF-, type I receptor Alk5 (Tgfbr1) specifically in Tgfb3 expressing cells using the Tgfb3-Cre driver line lead to a cleft palate phenotype similar to that seen in conventional Tgfb3 null mutants. In addition, Alk5/ Tgfb3-Cre mice displayed hydrocephalus, and severe intracranial bleeding due to germinal matrix hemorrhage. genesis 46:112,118, 2008. © 2008 Wiley-Liss, Inc. [source] Synchronous Ventricular Pacing without Crossing the Tricuspid Valve or Entering the Coronary Sinus,Preliminary ResultsJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 12 2009BENHUR D. HENZ M.D. Background: Right ventricular apical (RVA) pacing promotes tricuspid regurgitation (TR), electromechanical dyssynchrony, and ventricular dysfunction. We tested a novel intramyocardial bipolar lead to assess whether stimulation of the atrioventricular septum (AVS) produces synchronous ventricular activation without crossing the tricuspid valve (TV). Methods: A lead with an active external helix and central pin was placed on the AVS and the RVA in three dogs. High-density electroanatomic (EA) mapping was performed of both ventricles endocardially and epicardially. Intracardiac echocardiography was used to access ventricular synchrony. Results: The lead was successfully deployed into the AVS in all cases with consistent capture of the ventricular myocardium without atrial capture or sensing. The QRS duration was less with AVS compared with RVA pacing (89 ± 4 ms vs. 100 ± 11 ms [P < 0.0001, GEE P = 0.03]). There was decreased delay between color Doppler M-mode visualized peak contraction of the septum and the mid left ventricular free wall with AVS compared with RVA pacing (89 ± 91 ms vs. 250 ± 11 ms [P < 0.0001, GEE P = 0.006]). Activation time between the mid septum and mid free wall was shorter with AVS versus RVA pacing (20.4 ± 7.7 vs. 30.8 ± 11.6 [P = 0.01, GEE P = 0.07]). The interval between QRS onset to earliest free wall activation was shorter with AVS vs. RVA pacing (19.2 ± 6.4 ms vs. 31.1 ± 11.7 ms [P = 0.005, GEE P = 0.02]). Conclusion: The AVS was successfully paced in three dogs resulting in synchronous ventricular activation without crossing the TV. [source] Effects of Wall Stress on the Dynamics of Ventricular Fibrillation: A Simulation Study Using a Dynamic Mechanoelectric Model of Ventricular TissueJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 7 2008SATOKO HIRABAYASHI master of environment Introduction: To investigate the mechanisms underlying the increased prevalence of ventricular fibrillation (VF) in the mechanically compromised heart, we developed a fully coupled electromechanical model of the human ventricular myocardium. Methods and Results: The model formulated the biophysics of specific ionic currents, excitation,contraction coupling, anisotropic nonlinear deformation of the myocardium, and mechanoelectric feedback (MEF) through stretch-activated channels. Our model suggests that sustained stretches shorten the action potential duration (APD) and flatten the electrical restitution curve, whereas stretches applied at the wavefront prolong the APD. Using this model, we examined the effects of mechanical stresses on the dynamics of spiral reentry. The strain distribution during spiral reentry was complex, and a high strain-gradient region was located in the core of the spiral wave. The wavefront around the core was highly stretched, even at lower pressures, resulting in prolongation of the APD and extension of the refractory area in the wavetail. As the left ventricular pressure increased, the stretched area became wider and the refractory area was further extended. The extended refractory area in the wavetail facilitated the wave breakup and meandering of tips through interactions between the wavefront and wavetail. Conclusions: This simulation study indicates that mechanical loading promotes meandering and wave breaks of spiral reentry through MEF. Mechanical loading under pathological conditions may contribute to the maintenance of VF through these mechanisms. [source] Optical Mapping of Transmural Activation Induced by Electrical Shocks in Isolated Left Ventricular Wall Wedge PreparationsJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 11 2003OLEG F. SHARIFOV Ph.D. Introduction: It is believed that electrical shocks interrupt fibrillation by directly stimulating the bulk of ventricular myocardium in excitable states, but how shocks activate intramural tissue layers is not known. In this study, Vm responses and transmural activation patterns induced by shocks during diastole were measured in isolated coronary perfused preparations of porcine left ventricle. Methods and Results: Rectangular shocks (duration = 10 ms; field strength, E = 1,44 V/cm) were applied across preparations (thickness = 14.9 ± 2.5 mm, n = 9) via large mesh electrodes during diastole or action potential (AP) plateau. Vm responses at the transmural surface were measured using optical mapping technique (resolution = 1.2 mm). Depending on shock strength, three types of Vm responses were observed. (1) Weak shocks (E , 1,4 V/cm) applied in diastole induced APs with simple monophasic upstrokes. The latency and time of transmural activation (TTA) rapidly decreased with increasing shock strength. Earliest activation occurred predominantly at the cathodal side of preparations in the areas that exhibited maximal ,Vm during AP plateau. (2) Intermediate shocks (E , 4,23 V/cm) induced monophasic and biphasic upstrokes that were paralleled with predominantly negative plateau ,Vm. Activation was initiated at multiple transmural sites and rapidly spread across the myocardial wall (TTA = 0.6 ± 0.2 ms). (3) Very strong shocks (E , 23,44 V/cm) could cause triphasic upstrokes, likely reflecting occurrence of membrane electroporation, and delayed activation (TTA = 6.7 ± 3.8 ms) at sites of largest negative plateau ,Vm. Conclusion: Shocks applied during diastole cause direct and rapid (within 1 ms) activation of ventricular bulk over a wide range of shock strengths, supporting the excitatory hypothesis of defibrillation. Very strong shocks can cause multiphasic Vm responses and delayed activation. (J Cardiovasc Electrophysiol, Vol. 14, pp. 1215-1222, November 2003) [source] Excitable Gap in Canine Fibrillating Ventricular Myocardium: Effect of Subacute and Chronic Myocardial InfarctionJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 6 2001TARESH TANEJA M.D. Excitable Gap in Infarcted Canine Myocardium.Introduction: The existence of an excitable gap during ventricular fibrillation (VF) has been suggested in several prior studies. However, the effects of myocardial infarction on the presence and duration of an excitable gap during VF have not been evaluated. Methods and Results: Electrophysiologic study was performed in normal dogs and in dogs with subacute and chronic infarction. Experimental infarction was produced by left anterior descending coronary ligation. The excitable gap was determined indirectly using either evaluation of intrinsic wavefronts during VF or from the shortest activation interval at individual sites using recordings from a 112- electrode plaque sutured to the epicardial surface of the left ventricle. The excitable gap also was correlated to local electrophysiologic and anatomic properties. The excitable gap using the wavefront propagation method and shortest activation method was significantly longer in subacute infarction dogs (48 ± 17 msec and 37 ± 18 msec, respectively) and chronic infarction dogs (41 ± 14 msec and 35 ± 14 msec, respectively) than normal dogs (32 ± 13 msec and 30 ± 11 msec, respectively; P < 0.05 normal vs subacute and chronic infarction dogs in both methods). The excitable gap occupied approximately 30% and 27% of the VF cycle length in all three groups using the wavefront propagation and shortest activation method, respectively. The excitable gap correlated better with local ventricular refractoriness determined using the wavefront propagation method than with the shortest activation method, but not at all with refractoriness determined using extrastimulus testing. Tissue necrosis was noted in subacute infarction dogs and fibrosis in chronic infarction dogs, but the gap was not highly correlated with anatomic changes. Conclusion: During VF, an excitable gap exists in both normal and infarcted canine ventricular myocardium. It is significantly longer in the presence of infarction. These finding have implications for understanding the pathophysiology of VF and targeting antiarrhythmic therapies. [source] Pacing During Ventricular Fibrillation: Factors Influencing the Ability to CaptureJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 1 2001JONATHAN C. NEWTON M.S. Pacing During Ventricular Fibrillation.Introduction: Recent studies showed that pacing atrial and ventricular fibrillation (VF) is possible. The studies presented here determined which parameters influence the efficacy of a pacing train to capture fibrillating ventricular myocardium. Electrode type, current strength, order of pacing trains, polarity, and VF morphology preceding the pacing trains were investigated. Methods and Results: A 504-electrode recording plaque sutured to the right ventricle of pig hearts was used to record the activations of VF and those resulting from the pacing stimulation. Capture of VF by pacing was determined by observing an animated display of the first temporal derivative of the electrograms. A series of electrodes in a line captured the heart more frequently during VF than did a point electrode. Increasing the current strength to 10× diastolic pacing threshold increased the incidence of capture, but increasing this strength further did not. The second or third train of 40 stimuli had greater capture rates than did the first train during the same VF episode. Anodal and cathodal unipolar, and bipolar stimulation were equally efficacious in capturing VF. VF activation during the 1-second interval preceding pacing was more organized for pacing trains that captured than those that did not. The highest incidence of capture, 46% to 61% of pacing trains, occurred with a line of electrodes at 10× diastolic pacing threshold delivered by the second or third train. Conclusion: The probability of a pacing train capturing fibrillating myocardium can be influenced by the pacing protocol parameters. [source] Membrane-bound and cytosolic forms of heterotrimeric G proteins in young and adult rat myocardium: Influence of neonatal hypo- and hyperthyroidismJOURNAL OF CELLULAR BIOCHEMISTRY, Issue 2 2001Jiri Novotny Abstract Membrane and cytosolic fractions prepared from ventricular myocardium of young (21-day-old) hypo- or hyperthyroid rats and adult (84-day-old) previously hypo- or hyperthyroid rats were analyzed by immunoblotting with specific anti-G-protein antibodies for the relative content of Gs,, Gi,/Go,, Gq,/G11,, and G,. All tested G protein subunits were present not only in myocardial membranes but were at least partially distributed in the cytosol, except for Go,2, and G11,. Cytosolic forms of the individual G proteins represented about 5,60% of total cellular amounts of these proteins. The long (Gs,-L) isoform of Gs, prevailed over the short (Gs,-S) isoform in both crude myocardial membranes and cytosol. The Gs,-L/Gs,-S ratio in membranes as well as in cytosol increased during maturation due to a substantial increase in Gs,-L. Interestingly, whereas the amount of membrane-bound Gi,/Go, and Gq,/G11, proteins tend to lower during postnatal development, cytosolic forms of these G proteins mostly rise. Neonatal hypothyroidism reduced the amount of myocardial Gs, and increased that of Gi,/Go, proteins. By contrast, neonatal hyperthyroidism increased expression of Gs, and decreased that of Gi, and G11, in young myocardium. Changes in G protein content induced by neonatal hypo- and hyperthyroidism in young rat myocardium were restored in adulthood. Alterations in the membrane-cytosol balance of G protein subunits associated with maturation or induced by altered thyroid status indicate physiological importance of cytosolic forms of these proteins in the rat myocardium. J. Cell. Biochem. 82: 215,224, 2001. © 2001 Wiley-Liss, Inc. [source] Heart rate variability , a therapeutic target?JOURNAL OF CLINICAL PHARMACY & THERAPEUTICS, Issue 2 2002H. C. Routledge Reduced heart rate variability (HRV) is a powerful and independent predictor of an adverse prognosis in patients with heart disease and in the general population. The HRV is largely determined by vagally mediated beat to beat variability, conventionally known as respiratory sinus arrhythmia. Thus, HRV is primarily an indicator of cardiac vagal control. It is still unclear whether the relationship between measures of cardiac vagal control and mortality is causative or mere association. Possible mechanisms by which cardiac vagal activity might beneficially influence prognosis include a decrease in myocardial oxygen demand, a reduction in sympathetic activity and a decreased susceptibility of the ventricular myocardium to lethal arrhythmia. In animals, augmentation of cardiac vagal control by nerve stimulation or by drugs is associated with a reduction in sudden death in susceptible models. In humans a number of drugs which have been shown to reduce mortality and sudden death in large randomised trials can also be demonstrated to increase HRV. As a result of this evidence, it has been suggested that the effect of drugs or other therapeutic manoeuvres on HRV might be used to predict clinical efficacy. The use of HRV as a therapeutic target is discussed in this review. [source] Determination of cardiac involvement in sarcoidosis by magnetic resonance imaging and Doppler echocardiographyJOURNAL OF INTERNAL MEDICINE, Issue 5 2002C. M. Sköld Abstract. Sköld CM, Larsen FF, Rasmussen E, Pehrsson SK, Eklund AG (Karolinska Hospital and Institutet, Stockholm, Sweden). Determination of cardiac involvement in sarcoidosis by magnetic resonance imaging and Doppler echocardiography. J Intern Med 2002; 252: 465,471. Objectives. To elucidate whether cardiac magnetic resonance imaging (MRI) could be useful in disclosing structural changes in the myocardium in sarcoidosis patients and to relate echo-Doppler derived indices of left ventricular function to electrocardiogram (ECG) findings. Design. The MRI was performed in 18 consecutive patients with sarcoidosis. Left ventricular ejection fraction (LVEF), i.e. systolic function, was estimated echocardiographically by Simpson's two-dimensional method (n = 16). Diastolic function was estimated by age-corrected Doppler-derived indices: isovolumetric relaxation time (IVRT), deceleration time (DT) and early filling/atrial contraction ratio (E/A ratio). Results. Eleven patients had conduction defects or dysrhythmias (ECG+) whilst seven patients had a normal ECG (ECG,). In two patients, high signalling, contrast-enhanced, isolated regions, suggestive of deposits, were seen in the left ventricular myocardium on MRI. Both these patients had abnormal ECGs and signs of systolic and/or diastolic dysfunction on echocardiography. LVEF was subnormal in seven of 10 of the ECG+ patients and in two of six of the ECG,. Signs of diastolic dysfunction were found in 59% and 56% of the measurements in the ECG+ and ECG, patients, respectively. Conclusion. We conclude (i) that myocardial deposits on MRI in sarcoidosis patients have a high specificity for cardiac involvement but a rather low sensitivity; (ii) that a substantial proportion of sarcoidosis patients with abnormal ECGs have echocardiographic signs of systolic and/or diastolic dysfunction. [source] Stereology of the myocardium in Leontopithecus (Lesson, 1840) callitrichidae , primatesJOURNAL OF MEDICAL PRIMATOLOGY, Issue 3 2003A. Pissinatti Abstract: Rare morphological features of the Leontopithecus cardiovascular system have been reported in the literature. The samples analyzed in this study came from 33 specimens of Leontopithecus from the collection of the Center of Primatology of Rio de Janeiro-FEEMA (CPRJ-FEEMA). Morphometry and stereological data were obtained from all animals. Adult body weights of L. rosalia were the lowest, the greatest being those of L. chrysopygus caissara; body weights of L. chrysomelas and L. c. chrysopygus were similar and in between those of the two former species. Cardiomyocytes (left ventricular myocardium) were bigger in adults than in infants. The myocardium of L. rosalia showed focal fibrosis, fatty vacuoles, and hyalinization. In L. chrysomelas the myocardium showed areas of fibrosis and presence of mononuclear cells. Fibrosis and areas of congestion were observed in L. c. chrysopygus; areas of disorganization and vascular congestion were found in L. c. caissara. In L. rosalia infants, a greater density of vessels per myocardial area and a greater length density of vessels were observed as compared with those of L. chrysomelas. In adults, L. chrysomelas showed greater density of connective tissue in the myocardium than L. c. chrysopygus and L. c. caissara did. In L. rosalia, cardiomyocyte nuclei had a greater area density than those of the other forms of Leontopithecus. These characteristics may explain the faster development of L. rosalia infants as compared with that of L. chrysomelas and L. c. chrysopygus kept under the same handling conditions at the CPRJ-FEEMA. [source] Manganese ions as intracellular contrast agents: proton relaxation and calcium interactions in rat myocardiumNMR IN BIOMEDICINE, Issue 2 2003Wibeke Nordhųy Abstract Paramagnetic manganese (Mn) ions (Mn2+) are taken up into cardiomyocytes where they are retained for hours. Mn content and relaxation parameters, T1 and T2, were measured in right plus left ventricular myocardium excised from isolated perfused rat hearts. In the experiments 5,min wash-in of MnCl2 were followed by 15,min wash-out to remove extracellular (ec) Mn2+ MnCl2, 25 and 100,µM, elevated tissue Mn content to six and 12 times the level of control (0,µM MnCl2). Variations in perfusate calcium (Ca2+) during wash-in of MnCl2 and experiments including nifedipine showed that myocardial slow Ca2+ channels are the main pathway for Mn2+ uptake and that Mn2+ acts as a pure Ca2+ competitor and a preferred substrate for slow Ca2+ channel entry. Inversion recovery analysis at 20,MHz revealed two components for longitudinal relaxation: a short T1,,,1 and a longer T1,,,2. Approximate values for control and Mn-treated hearts were in the range 600,125,ms for T1,,,1 and 2200,750,ms for T1,,,2. The population fractions were about 59 and 41% for the short and the long component, respectively. The intracellular (ic) R1,,,1 and R2,,,1 correlated best with tissue Mn content. Applying two-site exchange analyses on the obtained T1 data yielded results in parallel to, but also differing from, results reported with an ec contrast agent. The calculated lifetime of ic water (,ic) of about 10,s is compatible with a slow water exchange in the present excised cardiac tissue. The longitudinal relaxivity of Mn ions in ic water [60 (s mM),1] was about one order of magnitude higher than that of MnCl2 in water in vitro [6.9 (s mM),1], indicating that ic Mn-protein binding is an important potentiating factor in relaxation enhancement. Copyright © 2003 John Wiley & Sons, Ltd. [source] Determinants of Lesion Sizes and Tissue Temperatures During Catheter CryoablationPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 5 2007MARK A. WOOD M.D. Background:Factors which influence lesion size from catheter-based cryoablation have not been well described. This study describes factors which influence lesion size during catheter cryoablation. Methods and Results:Cryoablation was delivered to porcine left ventricular myocardium in a saline bath using 4- or 8-mm electrode catheters. Ablation was delivered with the electrodes either vertical or horizontal to the tissue and both with and without superfusate flow over the electrode. The effect of electrode contact pressure was tested. Lesion dimensions were measured. All experiments were duplicated to measure tissue temperatures at 1-, 2-, 3-, and 5-mm deep to the ablation electrode. The 8-mm electrode produced lower tissue temperatures and larger lesion volumes when compared with the 4-mm electrode (all P < 0.05). Superfusate flow slowed the rate of tissue cooling, markedly warmed tissue temperatures, and reduced lesion volume when compared with no flow conditions. By linear regression modeling, lesion sizes and tissue temperatures were related to the presence of superfusate flow, electrode orientation, contact pressure and electrode size, or catheter refrigerant flow rate (r2 for models = 0.90,0.96, all P < 0.001). Electrode temperature predicted lesion size or tissue temperatures only when analyzed independent of electrode size or refrigerant flow rate. Conclusions:Lesion sizes and tissue temperatures during catheter cryoablation are related to convective warming, electrode orientation, electrode contact pressure, and any of the following: electrode size, catheter refrigerant flow rate or electrode temperature. However, electrode temperature may be a poor predictor of lesion size and tissue temperature for a given catheter size. [source] Isolated Giant Cell Myocarditis in the Atrium: An Incidental Finding?PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 10 2006IMRAN AHMAD M.D. Giant cell myocarditis (GCM) is an uncommon disorder that affects ventricular myocardium causing severe left ventricular dysfunction and ventricular arrhythmias. We report a case of GCM that only affected the atrium sparing the ventricle. [source] Epicardial Ablation of Ventricular Tachycardia Associated with Isolated Ventricular NoncompactionPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 7 2006HONG EUY LIM A 52-year-old man presented with sudden onset of palpitations and dizziness. Echocardiogram confirmed the diagnosis of isolated noncompaction of ventricular myocardium with moderated systolic dysfunction, and the electrocardiogram (ECG) revealed ventricular tachycardia (VT), of which the focus seemed to match an area of prominent left ventricular noncompaction on the 12-lead surface ECG. Through the activation mapping from the endo- and epicardium, simultaneously, a discrete potential preceding the QRS during VT was observed at the anterolateral epicardial wall. He subsequently underwent radiofrequency ablation, and VT was successfully eliminated. [source] Radiofrequency Catheter Ablation of an Incessant Ventricular Tachycardia Following Valve SurgeryPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 1 2002THORSTEN LEWALTER LEWALTER, T., et al.: Radiofrequency Catheter Ablation of an Incessant Ventricular Tachycardia Following Valve Surgery. Sustained monomorphic ventricular tachycardia (VT) after valve surgery represents a clinical entity with different tachycardia mechanisms. This case report describes an incessant VT after tricuspid and aortic valve replacement that did not respond to antiarrhythmic drug treatment. The tachycardia exhibited VA block and a right bundle branch block pattern with left-axis deviation, suggesting ventricular excitation via the left posterior fascicle. The electrophysiological study was limited by the prosthetic tricuspid and aortic valve replacement, therefore a transseptal approach was necessary to obtain access to the ventricular myocardium. Radiofrequency catheter ablation was performed in the proximal left bundle or distal His region with termination of the incessant VT followed by complete AV block. After pacemaker implantation using a transvenous right atrial and an epicardial ventricular lead, no VT reoccurrence could be documented. [source] X-linked fetal cardiomyopathy caused by a novel mutation in the TAZ genePRENATAL DIAGNOSIS, Issue 5 2006April N. Brady Abstract Objectives Mutations in the tafazzin (TAZ) gene at chromosomal locus Xq28 are responsible for Barth syndrome (BTHS), X-linked endocardial fibroelastosis (EFE), X-linked fatal infantile dilated cardiomyopathy (CMD3A), and familial isolated noncompaction of left ventricular myocardium (INVM). This evaluation was performed to determine if a known familial TAZ gene mutation might present with abnormal fetal cardiac pathology findings as early as the second trimester of pregnancy. Methods Prenatal diagnosis revealed that a male fetus was positive for a known familial arg94his TAZ gene mutation. An elective termination with subsequent fetal pathology examination was performed at 18 weeks' gestation. Results Fetal examination revealed cardiomegaly, EFE, and subendocardial vacuolization of the myocytes. Conclusion Characteristic cardiac pathology findings of a TAZ gene mutation are seen in a fetus at 18 weeks' gestation. To our knowledge, this case provides the earliest fetal pathologic description of a TAZ cardiomyopathy. Copyright © 2006 John Wiley & Sons, Ltd. [source] Three-dimensional architecture of the left ventricular myocardiumTHE ANATOMICAL RECORD : ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY BIOLOGY, Issue 6 2006Paul P. Lunkenheimer Abstract Concepts for ventricular function tend to assume that the majority of the myocardial cells are aligned with their long axes parallel to the epicardial ventricular surface. We aimed to validate the existence of aggregates of myocardial cells orientated with their long axis intruding obliquely between the ventricular epicardial and endocardial surfaces and to quantitate their amount and angulation. To compensate for the changing angle of the long axis of the myocytes relative to the equatorial plane of the ventricles with varying depths within the ventricular walls, the so-called helical angle, we used pairs of cylindrical knives of different diameters to punch semicircular slices from the left ventricular wall of pigs, the slices extending from the epicardium to the endocardium. The slices were pinned flat, fixed in formaldehyde, embedded in paraffin, sectioned, stained with azan or hematoxilin and eosin, and analyzed by a new semiautomatic procedure. We made use of new techniques in informatics to determine the number and angulation of the aggregates of myocardial cells cut in their long axis. The alignment of the myocytes cut longitudinally varied markedly between the epicardium and the endocardium. Populations of myocytes, arranged in strands, diverge by varying angles from the epicardial surface. When paired knives of decreasing diameter were used to cut the slices, the inclination of the diagonal created by the arrays increases, while the lengths of the array of cells cut axially decreases. The visualization of the size, shape, and alignment of the myocytic arrays at any side of the ventricular wall is determined by the radius of the knives used, the range of helical angles subtended by the alignment of the myocytes throughout the thickness of the wall, and their angulation relative to the epicardial surface. Far from the majority of the ventricular myocytes being aligned at angles more or less tangential to the epicardial lining, we found that three-fifths of the myocardial cells had their long axes diverging at angles between 7.5 and 37.5° from an alignment parallel to the epicardium. This arrangement, with the individual myocytes supported by connective tissue, might control the cyclic rearrangement of the myocardial fibers. This could serve as an important control of both ventricular mural thickening and intracavitary shape. Anat Rec Part A 288A:565,578, 2006. © 2006 Wiley-Liss, Inc. [source] Isolated noncompaction of the ventricular myocardium: contemporary Diagnosis and ManagementCLINICAL CARDIOLOGY, Issue 4 2007Michael P. Chrissoheris M.D. Abstract Noncompaction of the ventricular myocardium is a rare form of cardiomyopathy that has been described since the early 1990s. However, noncompaction remains frequently overlooked, in part due to the limited awareness of its unique clinical and imaging characteristics. Contemporary diagnosis has been facilitated by the introduction of specific morphologic criteria by echocardiography and cardiac magnetic resonance. Management issues revolve around the management of heart failure, arrhythmias, and thromboembolic events in order to prevent the significant morbidity and even mortality that has been associated with this entity. Finally, the genetics of noncompaction have been diverse and an issue of clinical importance as it relates to screening of first-degree relatives of affected patients. Two recent cases are presented and many of the contemporary issues in diagnosis and management, based on an extensive review of the literature, are addressed. Copyright © 2007 Wiley Periodicals, Inc. [source] Mutations in sarcomeric protein genes not only lead to cardiomyopathy but also to congenital cardiovascular malformationsCLINICAL GENETICS, Issue 1 2008Marja W. Wessels Noncompaction of the ventricular myocardium is associated with de novo mutation in the beta-myosin heavy chain gene Budde et al. (2007) PLoS ONE 2: e1362 Homozygosity for a novel splice site mutation in the cardiac myosin-binding protein C gene causes severe neonatal hypertrophic cardiomyopathy Xin et al. (2007) Am J Med Genet 143: 2662,2667 Alpha-cardiac actin mutations produce atrial septal defects Matsson et al. (2008) Hum Mol Genet 17: 256,265 [source] | ||||||||||||||||||||||||||||