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Ventricular Free Wall (ventricular + free_wall)
Selected AbstractsSynchronous 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] Timing of Depolarization and Contraction in the Paced Canine Left Ventricle:JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 2003Experiment, Model Introduction: For efficient pump function, contraction of the heart should be as synchronous as possible. Ventricular pacing induces asynchrony of depolarization and contraction. The degree of asynchrony depends on the position of the pacing electrode. The aim of this study was to extend an existing numerical model of electromechanics in the left ventricle (LV) to the application of ventricular pacing. With the model, the relation between pacing site and patterns of depolarization and contraction was investigated. Methods and Results: The LV was approximated by a thick-walled ellipsoid with a realistic myofiber orientation. Propagation of the depolarization wave was described by the eikonal-diffusion equation, in which five parameters play a role: myocardial and subendocardial velocity of wave propagation along the myofiber cm and ce; myocardial and subendocardial anisotropy am and ae; and parameter k, describing the influence of wave curvature on wave velocity. Parameters cm, ae, and k were taken from literature. Parameters am and ce were estimated by fitting the model to experimental data, obtained by pacing the canine left ventricular free wall (LVFW). The best fit was found with cm= 0.75 m/s, ce= 1.3 m/s, am= 2.5, ae= 1.5, and k= 2.1 × 10,4 m2/s. With these parameter settings, for right ventricular apex (RVA) pacing, the depolarization times were realistically simulated as also shown by the wavefronts and the time needed to activate the LVFW. The moment of depolarization was used to initiate myofiber contraction in a model of LV mechanics. For both pacing situations, mid-wall circumferential strains and onset of myofiber shortening were obtained. Conclusion: With a relatively simple model setup, simulated depolarization timing patterns agreed with measurements for pacing at the LVFW and RVA in an LV. Myocardial cross-fiber wave velocity is estimated to be 0.40 times the velocity along the myofiber direction (0.75 m/s). Subendocardial wave velocity is about 1.7 times faster than in the rest of the myocardium, but about 3 times slower than as found in Purkinje fibers. Furthermore, model and experiment agreed in the following respects. (1) Ventricular pacing decreased both systolic pressure and ejection fraction relative to natural sinus rhythm. (2) In early depolarized regions, early shortening was observed in the isovolumic contraction phase; in late depolarized regions, myofibers were stretched in this phase. Maps showing timing of onset of shortening were similar to previously measured maps in which wave velocity of contraction appeared similar to that of depolarization. (J Cardiovasc Electrophysiol, Vol. 14, pp. S188-S195, October 2003, Suppl.) [source] Site-Specific Arrhythmogenesis in Patients with Brugada SyndromeJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 4 2003HIROSHI MORITA M.D. Introduction: It has been believed that electrophysiologic abnormality of the epicardial region of the right ventricular free wall may play an important role in arrhythmogenesis of phase 2 reentry in Brugada syndrome, but clinical evidence of the occurrence of ventricular arrhythmias at the right ventricular free wall has not been evaluated. In this study, we evaluated the site-specific inducibility of ventricular fibrillation (VF) and the origin of spontaneous premature ventricular contractions (PVCs) in patients with Brugada syndrome. Methods and Results. Forty-five patients with Brugada-type ECG were enrolled in this study. Spontaneous PVCs were recorded in 9 patients. Programmed electrical stimulation (PES) was performed at the right ventricular apex (RVA), the free wall and septal region of the right ventricular outflow tract (RVOT), and the left ventricle (LV). The inducibility of PVT/VF was evaluated at each ventricular site, and the origin of PVC was determined by pace mapping. Sustained VF was induced in 17 patients. VF was induced in all 17 patients by PES at RVOT. Although PES at the septal region of the RVOT induced VF in only 5 patients (29%), PES at the free-wall region of the RVOT induced PVT/VF in 13 patients (76%). PES at RVA induced VF in only 2 patients (12%), and PES at LV failed to induce any arrhythmic events. Ventricular pace mapping showed that 64% of PVCs occurred at the free-wall region of the RVOT, 18% at the septal region of the RVOT, 9% at RVA, and 9% at LV. Conclusion: VF in patients with Brugada syndrome frequently is induced at the free-wall region of the RVOT area. The origin of PVC appears to be related to the site of PVT/VF induction by PES.(J Cardiovasc Electrophysiol, Vol. 14, pp. 373-379, April 2003) [source] Noninvasive Assessment of Cardiac Resynchronization Therapy for Congestive Heart Failure Using Myocardial Strain and Left Ventricular Peak Power as Parameters of Myocardial Synchrony and FunctionJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 12 2002Ph.D., ZORAN B. POPOVI Resynchronization Therapy for Heart Failure.Introduction: Although invasive studies have shown that cardiac resynchronization therapy by biventricular pacing improves left ventricular (LV) function in selected heart failure patients, it is impractical to apply such techniques in the clinical setting. The aim of this study was to assess the acute effects of cardiac resynchronization therapy by noninvasive techniques. Methods and Results: Twenty-two patients enrolled in the InSync trial (age 64 ± 9 years, 18 men and 4 women; all with ejection fraction <35% and QRS >130 msec) were studied 1 to 12 months after pacemaker implantation during pacing, and while ventricular pacing was inhibited. Regional myocardial strains of the interventricular septum, LV free wall, and right ventricular free wall were derived from color Doppler tissue echocardiography. Peak power index was calculated as a product of simultaneously recorded noninvasive blood pressure and pulse-wave (PW) Doppler velocity of the LV outflow tract. The Z ratio (sum of LV ejection and filling times divided by RR interval) and tei index were calculated from PW Doppler data. During pacing, overall regional strain improved (P = 0.01), while the LV strain coefficient of variation decreased from 2.7 ± 2.4 to 1.3 ± 0.7 (P = 0.009). Additionally, peak power index improved from 84 ± 24 to 94 ± 27 cm· mmHg/sec (P = 0.004). The Z ratio increased from 0.71 ± 0.08 to 0.78 ± 0.07 (P = 0.0005), while the tei index decreased from 0.86 ± 0.33 to 0.59 ± 0.16 (P = 0.0002). Conclusion: Using novel noninvasive indices, we demonstrated that cardiac resynchronization therapy improves LV performance. [source] Quantitative Assessment of Regional Right Ventricular Myocardial Velocities in Awake Dogs by Doppler Tissue Imaging: Repeatability, Reproducibility, Effect of Body Weight and Breed, and Comparison with Left Ventricular Myocardial VelocitiesJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 6 2005Valérie Chetboul Right ventricular myocardial (RVM) motion is poorly documented. The objective of this study was to determine the variability of RVM velocities by tissue Doppler imaging (TDI) in healthy dogs (study 1), to analyze RVM motion in a large healthy canine population (study 2), and to compare the results with those obtained for the left ventricular free wall. Six healthy Beagle Dogs were monitored in study 1, and 64 healthy dogs of 14 different breeds were monitored in study 2. Velocities were recorded in 2 segments (basal and apical) of the right and left myocardial walls. In study 1, 36 TDI examinations were performed for 4 days, whereas a single TDI examination was performed on each dog in study 2. All velocity profiles included 1 positive systolic wave and 2 negative diastolic waves. The lowest intraday and interday coefficient of variation values of the right TDI variables were observed at the base (3.5,16.1%). The variability of the right apical velocities was much higher, with most coefficient of variation values >15%. RVM velocities were higher in the basal than in the apical segments (P < .001) and were higher than the left velocities of the corresponding segment (P < .01). Body weight and breed had an effect on only a few right and left TDI variables. TDI provides a repeatable and reproducible method for evaluating basal RV function in the dog. These data also demonstrate the heterogeneity of the myocardial velocities between the left and the right ventricles and between the base and the apex. [source] Spontaneous Feline Hypertension: Clinical and Echocardiographic Abnormalities, and Survival RateJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 1 2003Valerie Chetboul Systemic hypertension was diagnosed in 58 of 188 untreated cats referred for evaluation of suspected hypertension-associated ocular, neurologic, cardiorespiratory, and urinary disease, or diseases frequently associated with hypertension (hyperthyroidism and chronic renal failure). Hypertensive cats were significantly older than normotensive subjects (13.0 ± 3.5 years versus 9.6 ± 5.0 years; P < .01), and had a greater prevalence of retinal lesions (48 versus 3%; P < .001), gallop rhythm (16 versus 0%; P < .001), and polyuria-polydipsia (53 versus 29%; P < .01). Blood pressure was significantly higher (P < .001) in cats with retinopathies (262 ± 34 mm Hg) than in other hypertensive animals (221 ± 34 mm Hg). Hypertensive cats had a thicker interventricular septum (5.8 ± 1.7 versus 3.7 ± 0.64 mm; P < .001) and left ventricular free wall (6.2 ± 1.6 versus 4.1 ± 0.51 mm; P < .001) and a reduced diastolic left ventricular internal diameter (13.5 ± 3.2 versus 15.8 ± 0.72 mm; P < .001) than control cats. Left ventricular geometry was abnormal in 33 of 39 hypertensive subjects. No significant difference was found in age or blood pressure at the initial visit between cats that died or survived over a 9-month period after initial diagnosis of hypertension. Mean survival times were not significantly different between hypertensive cats with normal and abnormal left ventricular patterns. Further prospective studies are needed to clearly identify the factors involved in survival time in hypertensive cats. [source] Cardiac Troponin I in Feline Hypertrophic CardiomyopathyJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 5 2002William E. Hemdon Measurement of plasma cardiac troponin I concentration ([cTnI]) is a sensitive and specific means for detecting myocardial damage in many mammalian species. Studies have shown that [cTnI] increases rapidly after cardiomyocyte injury. The molecular structure of cTnl is highly conserved across species, and current assays developed for its detection in humans have been validated in many species. In this study, [cTnI] was quantified using a 2-site sandwich assay in plasma of healthy control cats (n = 33) and cats with moderate to severe hypertrophic cardiomyopathy (HCM) (n = 20). [cTnI] was significantly higher in cats with HCM (median, 0.66 ng/mL; range, 0.05,10.93 ng/mL) as compared with normal cats (median, <0.03 ng/mL; range, <0.03-0.16 ng/mL) (P < .0001). An increase in [cTnI] was also highly sensitive (sensitivity = 85%) and specific (specificity = 97%) for differentiating cats with moderate to severe HCM from normal cats. [cTnI] was weakly correlated with diastolic thickness of the left ventricular free wall (r2= .354; P= .009) but not with the diastolic thickness of the interventricular septum (P= .8467) or the left atrium: aorta ratio (P= .0652). Furthermore, cats with congestive heart failure at the time of cTnl analysis had a significantly higher [cTnI] than did cats that had never had heart failure and those whose heart failure was controlled at the time of analysis (P= .0095 and P= .0201, respectively). These data indicate that cats with HCM have ongoing myocardial damage. Although the origin of this damage is unknown, it most likely explains the replacement fibrosis that is consistently identified in cats with moderate to severe HCM. [source] Regional Differences in Arrhythmogenic Aftereffects of High Intensity DC Stimulation in the VentriclesPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 5 2000ITSUO KODAMA Regional differences of the aftereffects of high intensity DC stimulation were investigated in isolated rabbit hearts stained with a voltage-sensitive dye (di-4-ANEPPS). Optical action potential signals were recorded from the epicardial surface of the right and left ventricular free wall (RVep, LVep) and from the right endocardial surface of the interventricular septum (IVS). Ten-millisecond monophasic DC stimulation (S2, 20,120 V) was applied to the signal recording spots during the early plateau phase of the action potential induced by basic stimuli (S1, 2.5 Hz). There was a linear relationship between S2 voltage and the S2 field intentisy (FI). S2 caused postshock additional depolarization. giving rise to a prolongation of the shocked action potential. With S2, 40 V (FI ,,20 V/cm), terminal repolarization of action potential was inhibited, and subsequent postshock S1 action potentials for 1,5 minutes were characterized by a decrease in the maximum diastolic potential and a decrease in the amplitude and a slowing of their upstroke phase. The higher the S2 voltage, the larger the aftereffects. The changes in postshock action potential configuration in RVep were significantly greater than those observed in LVep and IVS when compared at the same levels of S2 intensity. In RVep, 12 of 20 shocks of 120 V resulted in a prolonged refractoriness to S1 (> 1 s), and the arrest was often followed by oscillation of membrane potential. Ventricular tachycardia or fibrillation ensued from the oscillation in five cases. No such long arrest or serious arrhythmias were elicited in LVep and IVS. These results suggest that RVep is more susceptible than LVep and IVS for arrhythmogenic aftereffects of high intensity DC stimulation. [source] Anaesthetic implications of arrhythmogenic right ventricular dysplasia/cardiomyopathyANAESTHESIA, Issue 1 2009A. K. Alexoudis Summary Arrhythmogenic right ventricular dysplasia, also called right ventricular cardiomyopathy, is a genetically determined heart muscle disease, characterised by life-threatening ventricular arrhythmias in apparently healthy young people. The primary myocardial pathology is that the myocardium of the right ventricular free wall is replaced by fibrous or fibrofatty tissue, with scattered residual myocardial cells. Right ventricular function is abnormal and in severe cases is associated with global right ventricular dilation and overt biventricular heart failure. Although still relatively rare, arrhythmogenic right ventricular cardiomyopathy is a well recognised cause of sudden unexpected peri-operative death. In this review, we describe the basic characteristics of this disease, emphasising the diagnosis and we offer some suggestions for the anaesthetic management of these patients in the peri-operative period. [source] Role of Structural Complexities of Septal Tissue in Maintaining Ventricular Fibrillation in Isolated, Perfused Canine VentricleJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 1 2001TAKANORI IKEDA M.D. Tissue Structure and VF.Introduction: It is unclear how the patterns of wavelet propagation during ventricular fibrillation (VF) vary between structurally different tissues. We hypothesized that the structural complexities of septal tissue influence the maintenance of reentrant wavelets in the ventricle. Methods and Results: Endocardial activation patterns during VF were analyzed in the isolated, perfused canine right ventricular (RV) free wall (n = 9), interventricular septum (n = 5), and left ventricular (LV) free wall (n = 6) using a computerized mapping system (2-mm resolution) with 120-msec consecutive windows. Each tissue sample was cut progressively to reduce the tissue mass until the VF was terminated. More wavelets were seen in the septa than in the RV and LV free walls at baseline (P = 0.004), and VF in the septa displayed a shorter cycle length than in the RV and LV free walls (P = 0.017). As the tissue mass decreased, VF became successively more organized in all regions: the number of wavelets decreased and the cycle length of VF lengthened. Single and "figure-of-eight" stationary, reentrant wavelets often were mapped after tissue mass reduction in the RV free walls and rarely in the LV free walls, but they were not observed in the septa. Less critical mass was required to maintain VF in the septa than in the RV and LV free walls (P = 0.0006). Gross anatomic and histologic examinations indicated that the tissue structure of the septa is more complex than that of the RV and LV free walls. Conclusion: VF activation patterns with progressive reduction of tissue mass differ for the septum and the ventricular free walls. The structural complexities of the septal tissue influence the maintenance of fibrillation in the ventricle. [source] | ||||||||||