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Biomedical subjects

Frits W Prinzen

Publications and source records attributed to Frits W Prinzen.

At least 19 recordsLinked to original sources
PubMed2006

Calculation of effective VV interval facilitates optimization of AV delay and VV interval in cardiac resynchronization therapy.

BACKGROUND: In hearts with left bundle branch block (LBBB), both atrioventricular (AV) delay and interventricular (VV) interval determine left ventricular (LV) pump function in cardiac resynchronization therapy (CRT). The optimal combination of AV delay and VV interval currently is determined by extensive hemodynamic testing. OBJECTIVES: The purpose of this study was to investigate whether the effective VV interval (VV(eff)) can be used to optimize AV delay and VV interval. METHODS: In eight canine hearts with chronic LBBB, LV pacing was performed at various AV delays as well as biventricular pacing at multiple AV delays and VV intervals. LV pump function was assessed from LVdP/dt(max) and stroke volume (conductance catheter). Interventricular asynchrony was calculated from the timing difference between upslope of LV and RV pressure curves. VV(eff) was defined as the time delay between activation of the RV apex and LV lateral wall, irrespective of the source of RV activation (RV pacing or intrinsic conduction). VV(eff) was determined from pacemaker settings and surface ECGs recorded during biventricular pacing at various AV delays (positive values denote LV preexcitation). RESULTS: For all animals, the relationship between VV(eff) and LVdP/dt(max) as well as LV stroke work was parabolic. Maximal improvement in LVdP/dt(max) was similar during LV pacing, simultaneous biventricular pacing, and sequential biventricular pacing and was obtained at similar values of VV(eff). VV(eff) was strongly correlated with interventricular asynchrony (R = 0.97 +/- 0.03). Optimum LVdP/dt(max) occurred at VV(eff) ranging from -24 to 12 ms (mean -6 +/- 13 ms). For each experiment, the optimal VV(eff) was virtually equal to the value halfway between its minimum (during LV pacing at short AV delay) and maximum (during LBBB) value (R = 0.91). CONCLUSION: Use of VV(eff) facilitates determination of the best combination of AV delay and VV interval during biventricular pacing. For each individual heart, VV(eff), resulting in optimum LV pump function, can be estimated using surface ECGs recorded during biventricular pacing.

Animals↗
PubMed2006

Pacing-induced dys-synchrony preconditions rabbit myocardium against ischemia/reperfusion injury.

BACKGROUND: Because increased mechanical load induces preconditioning (PC) and dys-synchrony increases loading in late-activated regions, we investigated whether dys-synchrony induced by ventricular pacing (VP) at normal heart rate leads to cardioprotection. METHODS AND RESULTS: Isolated working rabbit hearts were subjected to 35 minutes of global ischemia and 2 hours of reperfusion. Seven hearts underwent VP PC (3 periods of 5 minutes VP at the posterior left ventricular [LV] wall), 7 hearts underwent ischemic preconditioning (IPC) (3 periods of 5 minutes of global ischemia), and 9 hearts served as control (C). LV pressure and sonomicrometry were used to assess global hemodynamics and segment work (SW) and end-diastolic segment length (EDSL) in anterior and posterior LV myocardium. Myocardial release of lactate and expression of proBNP mRNA were determined to gain insight in molecular processes involved in VP PC (*P<0.05). Infarct size (triphenyl tetrazolium chloride staining) was 18.3+/-13.0% in group C, and was uniformly reduced in the VP PC and IPC groups (1.8+/-0.8%*, and 3.5+/-3.1%*, respectively; and not significant between VP PC and IPC). LV posterior wall pacing (VP PC group) increased EDSL (by 6.3+/-5.8%*) and SW (to 335+/-207%*) in the LV anterior wall, whereas posterior wall SW decreased to negative values (-23+/-63%*). LV pacing did not significantly change lactate release and coronary flow but significantly increased proBNP mRNA expression in both anterior and posterior myocardium as compared with controls. CONCLUSIONS: Intermittent dys-synchrony is equally cardioprotective as "classical" IPC. Stretch-mediated signaling is a more likely trigger for VP PC than ischemia. VP PC is potentially applicable in cardiac surgery.

Animals↗
PubMed2006

The effects of esmolol and dexmedetomidine on myocardial oxygen consumption during sympathetic stimulation in dogs.

OBJECTIVE: The purpose of this study was to compare the potential of the beta(1)-adrenergic receptor blocker esmolol and the alpha(2)-adrenergic receptor agonist dexmedetomidine to suppress the cardiovascular and neuroendocrine response to a sympathetic stimulus. DESIGN: Experimental study. SETTING: Laboratory of university. PARTICIPANTS: Eleven anesthetized dogs. INTERVENTIONS: Catheters for arterial and coronary venous blood sampling and calculation of myocardial oxygen consumption were inserted. Pressure sensors were placed in the aorta, left ventricle, and a carotid artery. Flow probes were placed around the aortic root and around the left anterior descending coronary artery. Esmolol was infused (loading dose of 1 mg/kg, infusion of 0.3 mg/kg/h), and the adequacy of beta-blockade was checked. Thirty minutes after stopping esmolol, dexmedetomidine infusion was started (loading dose of 1 microg/kg, infusion of 1.5 microg/kg/min). Occlusion of both carotid arteries was used as a sympathetic stimulus before and during infusion of esmolol and before and during infusion of dexmedetomidine. MEASUREMENTS AND MAIN RESULTS: The variables were measured just before and during sympathetic stimulation, and changes were calculated. Both drugs suppressed the increase in dPdT(max). Dexmedetomidine suppressed the increase in plasma norepinephrine and the increase in systemic vascular resistance (dexmedetomidine 4% +/- 4% and esmolol 25% +/- 19% increase, p = 0.02). Esmolol attenuated the heart rate response (esmolol 2% +/- 2% and dexmedetomidine 20% +/- 18% increase, p = 0.02). However, dexmedetomidine decreased baseline heart rate more than esmolol; therefore, the absolute maximal heart rate during sympathetic stimulation was lower in the presence of dexmedetomidine (dexmedetomidine 119 +/- 14 and esmolol 141 +/- 15 beats/min, p = 0.01). Neither drug suppressed the increase in myocardial oxygen consumption. CONCLUSIONS: Both esmolol and dexmedetomidine have the potential to suppress some of the cardiovascular and neuroendocrine changes to a sympathetic stimulus but neither drug abolished the increase in myocardial oxygen consumption.

Adrenergic alpha-Agonists↗
PubMed2006

Ventricular remodeling during long-term right ventricular pacing following His bundle ablation.

To investigate ventricular remodeling during long-term right ventricular (RV) pacing after His bundle ablation (HBA) in patients with atrial arrhythmias, a retrospective analysis was performed on echocardiographic data from 45 patients (mean age 57 +/- 11 years) with atrial arrhythmias who underwent HBA and pacemaker implantation (HBA-PI) to control ventricular rate. Echocardiography was performed 1 year before HBA-PI, and up to 7 +/- 2 years of follow-up was conducted. An inverse linear relation was found between the relative increase of left ventricular (LV) end-diastolic diameter (EDD) during long-term RV pacing and LVEDD before HBA-PI (r = -0.61, p<0.001). Patients were divided into 2 groups: those with LVEDDs smaller than the mean LVEDD of 50 mm (group I, 46 +/- 2 mm, n = 28) and those with LVEDDs >50 mm (group II, 56 +/- 4 mm, n = 17). Before HBA-PI, patients in group I had significantly smaller LV weights (167 +/- 44 vs 238 +/- 56 g) and LV end-systolic diameters (30 +/- 2 vs 42 +/- 7 mm) and higher LV ejection fractions (64 +/- 5% vs 49+/- 12%) than those in group II. In group I, long-term RV pacing increased LVEDD, LV end-systolic diameter, LV weight, and left atrial diameter; increased mitral regurgitation; and decreased the LV ejection fraction and LV fractional shortening. No significant changes were observed during long-term RV pacing in group II. In conclusion, long-term RV pacing after HBA adversely affects LV structure and function in patients with initially normal LV dimensions and function.

Arrhythmias, Cardiac↗
PubMed2006

A new paradigm for physiologic ventricular pacing.

Clinical trials in patients with pacemakers for sinus node dysfunction or atrioventricular block (AVB) and implantable cardioverter-defibrillators provide increasing evidence showing that desynchronization of ventricular electrical activation and contraction, induced by conventional right ventricular apex (RVA) pacing, is a serious threat for long-term cardiac morbidity and mortality. The risk of heart failure is increased even in hearts with initially normal pump function and in case of part-time ventricular pacing. These epidemiologic data fit with knowledge from decades of pathophysiological research, indicating that right ventricular (RV) pacing creates abnormal contraction, reduced pump function, hypertrophy, and ultrastructural abnormalities. This paper presents a new paradigm that aims to tailor ventricular pacing to the individual patient to achieve a way of pacing that is as physiologic as possible. In patients without AVB and no intraventricular conduction abnormalities, ventricular pacing should be avoided as much as possible, using atrial-based pacing. In patients with AVB, alternate single-site RV or left ventricular pacing or biventricular pacing may be superior to RVA pacing. Efforts to optimize the pacing mode or site should be greater in patients with a longer expected duration of pacing, poorer cardiac function, and larger mechanical asynchrony. Awareness of the problem of desynchronization should also lead to more regular monitoring of cardiac pump function and mechanical asynchrony in any patient with ventricular pacing.

Animals↗
PubMed2006

Electrocardiographic changes predicting sudden death in propofol-related infusion syndrome.

BACKGROUND: The occurrence of metabolic acidosis, rhabdomyolysis, hyperkalemia, and sudden cardiac death after long-term, high-dose propofol infusion has been referred to as propofol infusion syndrome (PRIS). OBJECTIVES: The purpose of this study was to explore the ECG abnormalities observed in a patient with PRIS in order to identify possible pathophysiologic mechanisms of the syndrome. METHODS: ECG changes in the index case were characterized by down-sloping ST-segment elevation in precordial leads V1 to V3 (Brugada-like ECG pattern). We subsequently assessed the relationship between this ECG pattern and the propofol infusion rate, the development of arrhythmias, and the occurrence of sudden death in a previously described cohort of 67 head-injured patients, seven of whom had been identified as having PRIS. RESULTS: Six of the PRIS patients developed the ECG pattern of ST-segment elevation in leads V1 to V3 and died within hours of irrecoverable electrical storm. This ECG pattern was the first aberration recorded hours before the death of these patients. ECGs that were available for 30 of 60 unaffected patients exhibited a normal pattern. None of the 60 patients developed ventricular arrhythmias. CONCLUSION: Our findings indicate that development of an acquired Brugada-like ECG pattern in severely head-injured patients is a sign of cardiac electrical instability that predicts imminent cardiac death. Future studies will determine whether such an ECG pattern also predicts imminent cardiac arrhythmia in other patient populations.

Acidosis↗
PubMed2006

Systemic and regional hemodynamics in pigs with acute liver failure and the effect of albumin dialysis.

OBJECTIVE: Acute liver failure (ALF) is haemodynamically characterized by a hyperdynamic circulation. The aims of this study were to investigate the systemic and regional haemodynamics in ALF, to measure changes in nitric oxide metabolites (NOx) and to evaluate whether these haemodynamic disturbances could be attenuated with albumin dialysis. MATERIAL AND METHODS: Norwegian Landrace pigs (23-30 kg) were randomly allocated to groups as controls (sham-operation, n = 8), ALF (hepatic devascularization, n = 8) and ALF + albumin dialysis (n = 8). Albumin dialysis was started 2 h after ALF induction and continued for 4 h. Systemic and regional haemodynamics were monitored. Creatinine clearance, nitrite/nitrate and catecholamines were measured. A repeated measures ANOVA was used to analyse the data. RESULTS: In the ALF group, the cardiac index increased (PGT < 0.0001), while mean arterial pressure (PG = 0.02) and systemic vascular resistance decreased (PGT < 0.0001). Renal resistance (PG = 0.04) and hind-leg resistance (PGT = 0.003) decreased in ALF. There was no difference in jejunal blood flow between the groups. ALF pigs developed renal dysfunction with increased serum creatinine (PGT = 0.002) and decreased creatinine clearance (P = 0.02). Catecholamines were significantly higher in ALF, but NOx levels were not different. Albumin dialysis did not attenuate these haemodynamic or renal disturbances. CONCLUSIONS: The haemodynamic disturbances during the early phase of ALF are characterized by progressive systemic vasodilatation with no associated changes in metabolites of NO. Renal vascular resistance decreased and renal dysfunction developed independently of changes in renal blood flow. After 4 h of albumin dialysis there was no attenuation of the haemodynamic or renal disturbances.

Albumins↗
PubMed2006

Effect of albumin dialysis on intracranial pressure increase in pigs with acute liver failure: a randomized study.

BACKGROUND: Increased intracranial pressure (ICP) worsens the outcome of acute liver failure (ALF). This study investigates the underlying pathophysiological mechanisms and evaluates the therapeutic effect of albumin dialysis in ALF with use of the Molecular Adsorbents Recirculating System without hemofiltration/dialysis (modified, M-MARS). METHODS: Pigs were randomized into three groups: sham, ALF, and ALF + M-MARS. ALF was induced by hepatic devascularization (time = 0). M-MARS began at time = 2 and ended with the experiment at time = 6. ICP, arterial ammonia, brain water, cerebral blood flow (CBF), and plasma inflammatory markers were measured. RESULTS: ICP and arterial ammonia increased significantly over 6 hrs in the ALF group, in comparison with the sham group. M-MARS attenuated (did not normalize) the increased ICP in the ALF group, whereas arterial ammonia was unaltered by M-MARS. Brain water in the frontal cortex (grey matter) and in the subcortical white matter at 6 hrs was significantly higher in the ALF group than in the sham group. M-MARS prevented a rise in water content, but only in white matter. CBF and inflammatory mediators remained unchanged in all groups. CONCLUSION: The initial development of cerebral edema and increased ICP occurs independently of CBF changes in this noninflammatory model of ALF. Factor(s) other than or in addition to hyperammonemia are important, however, and may be more amenable to alteration by albumin dialysis.

Albumins↗
PubMed2005

Tailoring cardiac resynchronization therapy using interventricular asynchrony. Validation of a simple model.

This study explores the use of interventricular asynchrony (interVA) for optimizing cardiac resynchronization therapy (CRT), an idea emerging from a simple pathway model of conduction in the ventricles. Measurements were performed in six dogs with chronic left bundle branch block (LBBB) and in 29 patients of the Pacing Therapies for Congestive Heart Failure (PATH-CHF)-I study. In the dogs, intraventricular asynchrony (intraVA) was determined using left ventricular (LV) endocardial activation maps. In dogs and patients, the maximum rate of rise of LV pressure (LV dP/dt(max)) and the pulse pressure (PP) and interVA [time delay between upslope of LV and right ventricular (RV) pressure curves] were measured during LV, RV, and biventricular (BiV) pacing with various atrioventricular (AV) delays. Measurements in the canine hearts supported the pathway model in that optimal resynchronization occurred at approximately 50% reduction of intraVA and at an interVA value halfway that during LBBB and LV pacing. In patients with significant hemodynamic response during pacing (n = 22), intrinsic interVA and interVA at peak improvement (interVA(p)) varied widely between patients (from -83 to -15 ms and from -42 to +31 ms, respectively). However, the model predicted individual interVA(p) accurately (SD of +/-6 ms and +/-12 ms for LV dP/dt(max) and PP, respectively). At equal interVA, LV and BiV pacing produced equal hemodynamic response, but in 11 of 22 responders, BiV pacing reduced interVA insufficiently to reach the maximum hemodynamic response. LV pacing at short AV delay proved to result in better hemodynamics than predicted by the model, indicating that additional factors determine hemodynamics during LV preexcitation. Guided by a simple pathway model, interVA measurements accurately predict optimal hemodynamic performance in individual CRT patients.

Animals↗
PubMed2005

Acute hemodynamic benefit of left ventricular apex pacing in children.

BACKGROUND: Despite the fact that pacing at the right ventricular apex acutely and chronically decreases left ventricular contractile function, this pacing site is still conventionally used in adults and children. Because animal studies showed beneficial effects of left ventricular pacing, we compared the hemodynamic performance of left ventricular apex, left ventricular free wall, and right ventricular apex pacing in children. METHODS: Studies were performed in 10 children (median age, 2.5 years; range, 2 months to 17 years) undergoing surgery for congenital heart disease with normal systemic left ventricular anatomy and intraventricular conduction. High-fidelity left ventricular and arterial pressure measurements were performed during epicardial right ventricular apex and left ventricular apex and free wall pacing. RESULTS: Left ventricular apex pacing increased the maximum rate of rise of left ventricular pressure and pulse pressure significantly relative to right ventricular apex pacing (by 7.7% +/- 7.2% and 7.7% +/- 7.0%, respectively) without changes in end-diastolic left ventricular pressure. Left ventricular free wall pacing did not significantly improve hemodynamics as compared with right ventricular apex pacing. The QRS duration was not different among pacing at the three sites. CONCLUSIONS: In this short-term study left ventricular apex pacing is hemodynamically superior to right ventricular apex and left ventricular free wall pacing in children. Therefore, the left ventricular apex appears a favorable pacing site after pediatric cardiac surgery.

Adolescent↗
PubMed2004

Left bundle branch block induces ventricular remodelling and functional septal hypoperfusion.

AIMS: Left ventricular (LV) dilatation, hypertrophy, and septal perfusion defects are frequently observed in patients with left bundle branch block (LBBB). We investigated whether isolated LBBB causes these abnormalities. METHODS AND RESULTS: In eight dogs, LBBB was induced by radio frequency ablation. Two-dimensional echocardiography showed that 16 weeks of LBBB decreased LV ejection fraction (by 23+/-14%) and increased LV cavity volume (by 25+/-19%) and wall mass (by 17+/-16%). The LV septal-to-lateral wall mass ratio decreased by 6+/-9%, indicating asymmetric hypertrophy. After onset of LBBB, myocardial blood flow (MBF, fluorescent microspheres) and systolic circumferential shortening [CS(sys), magnetic resonance (MR) tagging] decreased in the septum to 83+/-16% and -11+/-20% of baseline, respectively, and increased in LV lateral wall to 118+/-12% and 180+/-90% of baseline, respectively. MBF and CS(sys) values did not change over 16 weeks of LBBB. Changes in external mechanical work paralleled those in CS(sys). Glycogen content was not significantly different between septum and LV lateral wall of LBBB hearts (16 weeks) and control samples, indicating absence of hibernation. CONCLUSIONS: The asynchronous ventricular activation during LBBB leads to redistribution of circumferential shortening and myocardial blood flow and, in the long run, LV remodelling. Septal hypoperfusion during LBBB appears to be primarily determined by reduced septal workload.

Animals↗
PubMed2004

Adaptation to mechanical load determines shape and properties of heart and circulation: the CircAdapt model.

With circulatory pathology, patient-specific simulation of hemodynamics is required to minimize invasiveness for diagnosis, treatment planning, and followup. We investigated the advantages of a smart combination of often already known hemodynamic principles. The CircAdapt model was designed to simulate beat-to-beat dynamics of the four-chamber heart with systemic and pulmonary circulation while incorporating a realistic relation between pressure-volume load and tissue mechanics and adaptation of tissues to mechanical load. Adaptation was modeled by rules, where a locally sensed signal results in a local action of the tissue. The applied rules were as follows: For blood vessel walls, 1) flow shear stress dilates the wall and 2) tensile stress thickens the wall; for myocardial tissue, 3) strain dilates the wall material, 4) larger maximum sarcomere length increases contractility, and 5) contractility increases wall mass. The circulation was composed of active and passive compliances and inertias. A realistic circulation developed by self-structuring through adaptation provided mean levels of systemic pressure and flow. Ability to simulate a wide variety of patient-specific circumstances was demonstrated by application of the same adaptation rules to the conditions of fetal circulation followed by a switch to the newborn circulation around birth. It was concluded that a few adaptation rules, directed to normalize mechanical load of the tissue, were sufficient to develop and maintain a realistic circulation automatically. Adaptation rules appear to be the key to reduce dramatically the number of input parameters for simulating circulation dynamics. The model may be used to simulate circulation pathology and to predict effects of treatment.

Adaptation, Physiological↗
PubMed2004

Increase in left ventricular torsion-to-shortening ratio in children with valvular aortic stenosis.

Perfusion of left ventricular (LV) subendocardium in valvular aortic stenosis (AS) patients is impaired. It was expected that this may lead to a reduction of subendocardial fiber contraction and, consequently, to an increase of LV torsion per amount of ejection. Using MR tagging (MRT), it was investigated whether the torsion-to-shortening ratio (TSR) is elevated in valvular AS patients. Six asymptomatic children with valvular AS were investigated using echo Doppler, ECG, exercise test, and MRT. LV torsion and natural strain of the inner diameter were determined from measured tag displacements in two short-axis slices of the LV. In all AS patients TSR was approximately 40% increased (0.62 +/- 0.04 rad; mean +/- SD) as compared to pediatric (0.44 +/- 0.08 rad; n=5) and adult controls (0.46 +/- 0.08 rad; n=9), indicating subendocardial contractile dysfunction. With other techniques hitherto used this type of dysfunction could not be detected.

Adolescent↗
PubMed2004

The left ventricular apex is the optimal site for pediatric pacing: correlation with animal experience.

Pacing at the commonly used right ventricular (RV) apex results in impaired ventricular performance. Previous animal studies indicated that the left ventricular (LV) apex is a superior pacing site. The purpose of this study was to investigate in dogs whether this good performance is associated with a more synchronous electrical activation pattern of the LV and whether the LV apex is also a good pacing site in children. In 11 healthy dogs and 8 children undergoing cardiac surgery, dual chamber pacing was performed at the RV apex, LV apex and LV lateral free wall (LVFW). In dogs, a basket electrode was inserted into the LV to assess pattern and timing of LV endocardial activation. In the children, hemodynamic measurements were performed immediately after recovery from cardiopulmonary bypass. In dogs, LV apex pacing resulted in synchronous activation around the LV circumference whereas RV apex and LVFW pacing resulted in asynchrony of activation between the septum and LVFW. In both canine and children's hearts most hemodynamic variables remained at sinus rhythm level during LV apex pacing, but LVdPdtmax, stroke work (dogs), and pulse pressure (children) were reduced as compared with sinus rhythm during RV apex and LVFW pacing. LV apex pacing results in synchronous activation of the LV and is, in adult dogs and in children, associated with superior hemodynamic performance.

Adolescent↗
PubMed2003

Intra-ventricular resynchronization for optimal left ventricular function during pacing in experimental left bundle branch block.

OBJECTIVES: We sought to investigate to what extent intra-ventricular asynchrony (intraVA) and inter-ventricular asynchrony (interVA) determine left ventricular (LV) function in canine hearts with left bundle branch block (LBBB) during ventricular pacing. BACKGROUND: Pacing therapy improves LV pump function in patients with heart failure and abnormal ventricular conduction supposedly due to resynchronization. However, the relationship between LV pump function and measures of asynchrony is not well established. METHODS: In 15 experiments, LV (various sites) and biventricular (BiV) pacing was performed at atrioventricular (AV) delays of 20 to 140 ms. Measured were the maximum rate of increase (dP/dt(max)) of LV pressure and LV stroke work (SW) (conductance catheter), interVA (time delay between the upslope of LV and RV pressures), and intraVA (from endocardial electrical activation maps). RESULTS: Induction of LBBB increased interVA (-6.4 +/- 8.6 to -28.4 +/- 8.5 ms [RV earlier]) and intraVA (4.9 +/- 2.4 to 18.0 +/- 3.3 ms), whereas LV dP/dt(max) and SW decreased (-13 +/- 18% and -39 +/- 24%, respectively). During LBBB, LV and BiV pacing increased LV dP/dt(max) and SW (mean increases 14% to 21% and 11% to 15%, respectively) without changing diastolic function or preload. Optimal improvement in LV function was obtained consistently when intraVA returned to pre-LBBB values, while interVA remained elevated. Normalization of intraVA required AV delays shorter than the baseline PQ time during LV apex and BiV pacing, thus excluding endogenous LV activation, but AV delays virtually equal to the baseline PQ time (difference 4 +/- 9 ms, p = NS) during pacing at (mid)lateral LV sites to obtain fusion between pacing-induced and endogenous activation. CONCLUSIONS: In LBBB hearts, optimal restoration of LV systolic function by pacing requires intra-ventricular resynchronization. The optimal AV delay to achieve this depends on both the site of pacing and baseline PQ time.

Animals↗
PubMed2003

Absence of reverse electrical remodeling during regression of volume overload hypertrophy in canine ventricles.

OBJECTIVE: Ventricular hypertrophy predisposes for cardiac arrhythmias, presumably due to prolongation of repolarization (electrical remodeling). The temporal relation between the development of hypertrophy and electrical remodeling, as well as their reversibility upon restoration of normal load, however, are poorly understood. This was investigated in the present study using volume overload hypertrophy induced by atrio-ventricular (AV) block and normalization of load by pacing. METHODS: Dogs were subjected to either 16 weeks of AV-block (CAVB group, n=9) or 8 weeks of AV-block followed by 8 weeks of right ventricular (RV) pacing at physiological heart rate (CAVB+PACE group, n=9). RESULTS: Left ventricular (LV) mass (2D-echocardiography) increased after 8 weeks of AV-block to approximately 30% above baseline and returned to 10+/-14% after 8 weeks of pacing. QT-time (surface ECG) also increased after AV-block. However, 8 weeks of pacing did not decrease QT and QTc-time (c=corrected for heart rate), neither during physiological pacing nor during temporary pacing at 100 beats/min. Lack of reverse electrical remodeling was confirmed by the absence of changes in LV and RV action potential duration (monophasic action potentials) at week 8 and 16. CONCLUSIONS: In volume overload hypertrophy due to AV-block, structural and electrical remodeling develop in parallel but restoration of physiological heart rate causes dissociation between reverse structural remodeling and reverse electrical remodeling.

Action Potentials↗
PubMed2003

Left ventricular septal and apex pacing for optimal pump function in canine hearts.

OBJECTIVES: The goal of this study was to test the hypothesis that left ventricular (LV) pump function is optimal when pacing is performed at the LV near the sites where the impulses exit the Purkinje system. BACKGROUND: Pacing at the conventional site, the right ventricular (RV) apex, adversely affects hemodynamics. During normal sinus rhythm (SR), electrical activation of the working myocardium starts at the LV septal endocardium and spreads from apex to base. METHODS: Experiments were conducted in anesthetized open-chest dogs with normal ventricular conduction to investigate hemodynamic effects of pacing at various epicardial LV sites, the RV apex, and combinations of these sites (n = 11) and of RV and LV septal pacing (n = 8). The LV septal endocardium was reached via the RV by puncturing through the septum with a barbed electrode. Left ventricular systolic (LVdP/dtpos and stroke work) and diastolic (LVdP/dtneg and Tau) function were assessed using pressure-volume relations (conductance catheter technique). RESULTS: Left ventricular systolic and diastolic function were highly dependent on the site of pacing, but not on QRS duration. Left ventricular function was maintained at SR level during LV septal, LV apex, and multisite pacing, was moderately depressed during pacing at epicardial LV free wall sites, and was most severely depressed during RV apex pacing. On average, RV septal pacing did not improve LV function, compared with RV apex pacing, but in each experiment one (variable) RV pacing site was found, which only moderately reduced LV function. CONCLUSIONS: During ventricular pacing, LV pump function is maintained best (i.e., at SR level) when pacing at the LV septum or LV apex, potentially because pacing from these sites creates a physiological propagation of electrical conduction.

Analysis of Variance↗