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Biomedical subjects

F W Prinzen

Publications and source records attributed to F W Prinzen.

At least 37 records · Page 2Linked to original sources

Cardiac output distribution in the chick embryo from stage 36 to 45.

OBJECTIVE: The distribution of cardiac output to different organs is well described in the mammalian fetus. Chick embryos are not often used in perinatal cardiovascular research and therefore it is not known whether they can serve as an animal model for this purpose. In this study we documented cardiac output distribution in chick embryos at increasing incubation time. METHODS: Fertilized eggs from day 10 to 19 with an incubation time of 21 days were studied in 3 increasing incubation time groups (10-13, 14-16 and 17-19 days). For the experiment, the egg was placed in a holder in an incubator. The egg was opened at the air cell and a small vein of the chorioallantoic membrane was catheterized. Twenty thousand fluorescent 15 microns microspheres in 0.2 ml were injected. After 5 min, the embryo was sacrificed and the different organs were dissected and digested for microsphere isolation and subsequent fluorescence analysis. RESULTS: The chorioallantoic membrane, which is the placenta equivalent of the chick embryo, received a relatively large fraction of the combined cardiac output: 52.08% (interquartile range [IQR] 12.67%) on days 10-13 and 40.95% (IQR 27.24%) on days 17-19. Relatively small fractions were distributed: to the heart 2.03% (IQR 1.58) on days 10-13 and 3.18% (IQR 1.95) on days 17-19, and to the brain 3.20% (IQR 1.80) on days 10-13 and 5.02% (IQR 3.39) on days 17-19. As incubation time advanced, the fraction of the combined cardiac output to the chorioallantoic membrane and yolk-sac decreased significantly in favor of the heart and brain. CONCLUSION: This distribution shows great similarity to the one found in the mammalian fetus. The chick embryo is an attractive model for perinatal cardiovascular research.

Allantois↗

Relation between torsion and cross-sectional area change in the human left ventricle.

During the ejection phase, motion of the left ventricular (LV) wall is such that all myocardial fibers shorten to the same extent. In a mathematical model of LV mechanisms it was found that this condition could be satisfied only if torsion around the long axis followed a unique function of the ratio of cavity volume to wall volume. When fiber shortening becomes non-uniform due to cardiac pathology, this pathology may be reflected in aberration of the torsional motion pattern. In the present study we investigated whether the predicted regular motion pattern could be found in nine healthy volunteers, using Magnetic Resonance Tagging. In two parallel short-axis cross-sections, displacement, rotation, and area ejection were derived from the motion of tags, attached non-invasively to the myocardium. Information from both sections was combined to determine area ejection, quantified as the change in the logarithm of the ratio of cavity area to wall area, and torsion, represented by the shear angle on the epicardium. Linear regression was applied to torsion as a function of area ejection. The slope thus found (-0.173 +/- 0.024 rad, mean +/- S.D.) was similar to the slope as predicted by the model of LV mechanics (-0.194 +/- 0.026 rad). In conclusion, the relation between area ejection and torsion could be assessed noninvasively in humans. In healthy volunteers, the relation was close to what was predicted by a mathematical model of LV mechanics, and also close to what was found earlier in experiments on animals.

Algorithms↗

Alleviation of the peripheral hemodynamic effects of dexmedetomidine by the calcium channel blocker isradipine.

BACKGROUND: Alpha 2-adrenergic agonists have peripheral vasoconstrictive effects and central sympatholytic and sedative effects. Whereas the latter are the basis of their use in anesthesia, the former could limit their clinical application. METHODS: To study whether a vasodilator could alleviate the systemic and coronary vasoconstrictor effects of dexmedetomidine without influencing the central sympatholytic effects, the calcium channel blocker isradipine was infused after a high dose of dexmedetomidine in anesthetized dogs. RESULTS: Dexmedetomidine 10 micrograms.kg-1 decreased plasma concentrations of norepinephrine and epinephrine by more than 90%, heart rate by 39%, cardiac output by 64%, dp/dtmax by 29% and increased mean arterial pressure by 55% and the left ventricular end-diastolic pressure (LVEDP) 4-fold as compared to baseline. In addition, coronary blood flow decreased by 52% and coronary venous oxygen saturation by 51%. Isradipine could completely antagonize all the coronary and systemic hemodynamic changes induced by dexmedetomidine, but only partially he increase in LVEDP. Isradipine caused no changes in plasma catecholamine levels. CONCLUSION: Isradipine could alleviate the peripheral hemodynamic actions of dexmedetomidine while having no effect on its central sympatholytic properties.

Adrenergic alpha-Agonists↗

Hemodynamic and coronary vascular effects of dexmedetomidine in the anesthetized goat.

BACKGROUND: In phase III trials, the hemodynamic stabilising effect of the alpha 2-adrenergic agonist dexmedetomidine (DEX) is being investigated in patients with coronary artery disease, Coronary vascular effects of alpha 2-agonists have been studied in dogs and pigs, but both species have a different hemodynamic response to DEX than man. The aim of this study was to investigate the hemodynamic and coronary vascular effects in goats. METHODS: In 6 open-chest goats anesthetized with halothane, central and coronary hemodynamics and oxygen supply and demand were measured before and following IV bolus infusion of DEX in doses ranging from 0.1 to 10 micrograms/kg. RESULTS: With DEX doses of 1 microgram/kg or higher, mean arterial pressure (MAP), systemic vascular resistance, coronary vascular resistance and arterio-mixed venous oxygen content increased within 2 min, but returned to baseline within 15 min. In contrast, there was a progressive and cumulative decrease in cardiac output (CO), heart rate, and dP/dtmax, Regional coronary venous oxygen extraction (C(a-cv)O2) transiently increased after 3 micrograms/kg DEX and decreased 15 min after 10 micrograms/kg DEX. LVEDP transiently increased after 3 and 10 micrograms/kg DEX. The changes after DEX 10 micrograms/kg differed from those after lower doses: MAP (35%), CO (50%), stroke volume (33%), C(a-cv)O2 (15%) and myocardial oxygen extraction (33%) were all decreased. Myocardial oxygen supply and demand decreased in parallel. CONCLUSIONS: 1) The cardiovascular response to IV DEX in goats is similar to man. 2) In goats after DEX, systemic and coronary vasoconstriction are short-lived, and 3) the balance between myocardial oxygen supply and demand is maintained.

Adrenergic alpha-Agonists↗

Coronary vascular effects of dexmedetomidine during reactive hyperemia in the anesthetized dog.

OBJECTIVE: The central sympatholytic effects of alpha2-adrenergic agonists are believed to be beneficial during myocardial ischemia, but the peripheral vasoconstrictive effects are controversial. The aim of this study was to investigate the coronary vascular effects of dexmedetomidine (DM) during reactive hyperemia. DESIGN: The study had a prospective, randomized, open-comparative design. SETTING: University animal laboratory. PARTICIPANTS: Nine mongrel dogs. INTERVENTIONS: Coronary artery occlusions lasting 2 minutes were induced five times at 40-minute intervals. DM, 0.1, 1, and 10 micrograms/kg was administered 15 minutes before the second, third, and fourth coronary occlusion, respectively. The alpha2-antagonist atipamezole was administered before the fifth coronary occlusion. MEASUREMENTS AND MAIN RESULTS: DM, 1 microgram/kg, significantly decreased heart rate (from 128 +/- 13 to 96 +/- 21 beats/min); 10 micrograms/kg of DM also significantly decreased cardiac output (from 3.4 +/- 1.1 to 1.4 +/- 0.4 L/min). DM decreased myocardial blood flow in all layers of normally perfused myocardium. In hyperemic myocardium, DM significantly decreased epicardial blood flow (from 3.30 +/- 1.43 to 1.44 +/- 0.49 mL/min/g after DM 10 micrograms/kg), whereas endocardial blood flow did not change, hereby significantly increasing the endo/epi blood flow ratio (from 0.99 +/- 0.54 to 2.28 +/- 0.78). CONCLUSIONS: In the postischemic hyperemic subendocardial layer, coronary blood flow was preserved after DM. DM reduced primary determinants of myocardial oxygen demand. These effects of DM may be beneficial in conditions of temporary coronary artery occlusion and subsequent reperfusion.

Adrenergic alpha-Agonists↗

Beneficial effects of dexmedetomidine on ischaemic myocardium of anaesthetized dogs.

We have studied the effect of dexmedetomidine during coronary artery stenosis (CAS) in dogs. Three periods of 15 min of CAS were induced at 40-min intervals in two groups of dogs (dexmedetomidine compared with placebo). Dexmedetomidine was administered before the second and third periods of CAS in doses of 1 and 3 micrograms kg-1, respectively. Dexmedetomidine decreased plasma concentrations of noradrenaline by mean 71 (SEM 9)%, heart rate by 8 (4)%, cardiac output by 30 (6)% and increased mean arterial pressure by 23 (10)%. Dexmedetomidine reduced blood flow in non-ischaemic myocardium and in the ischaemic epicardial layer by 16 (8)%, but blood flow was preserved in the ischaemic mid-myocardial and subendocardial layers. Consequently, dexmedetomidine increased the ischaemic-non-ischaemic blood flow ratio. Dexmedetomidine did not change myocardial oxygen consumption but decreased myocardial oxygen demand from 4.91 (0.33) to 3.76 (0.25) mumol min-1 g-1, thereby reducing the oxygen deficiency of the ischaemic myocardium from 1.47 (0.37) to 0.29 (0.32) mumol min-1 g-1.

Adrenergic alpha-Agonists↗

The effect of dexmedetomidine on the balance of myocardial energy requirement and oxygen supply and demand.

The effect of the alpha(2)-adrenergic agonist dexmedetomidine on the balance between myocardial energy requirement and oxygen supply and demand was investigated in 16 open-chest dogs anesthetized with either chloralose/urethane (CU) or fentanyl/halothane (FH). Myocardial energy requirement (estimated from the pressure work index), blood flow and its transmural distribution (radioactive microspheres), as well as myocardial oxygen and lactate extraction, were measured before and after administration of dexmedetomidine in doses ranging from 0.1 to 10 micrograms/kg intravenously. Under CU anesthesia, dexmedetomidine decreased heart rate, arterial blood pressure, and cardiac output. During FH anesthesia, dexmedetomidine reduced heart rate and cardiac output whereas arterial blood pressure increased. Dexmedetomidine decreased myocardial energy requirement only during CU anesthesia; myocardial oxygen supply and demand decreased in parallel. At the (large) dose of 10 micrograms/kg, myocardial oxygen extraction increased during both types of anesthesia. Dexmedetomidine >/= 1 microgram/kg increased endocardial/epicardial blood flow ratio during FH anesthesia. These data indicate that dexmedetomidine >/= 1 microgram/kg reduces myocardial energy requirements, especially when baseline heart rate and blood pressure are increased. Dexmedetomidine preserves endocardial perfusion and reduces oxygen demand in parallel with oxygen supply and energy requirements.

Adrenergic alpha-Agonists↗

The effects of alpha 2-adrenergic stimulation with mivazerol on myocardial blood flow and function during coronary artery stenosis in anesthetized dogs.

The central sympatholytic effect of alpha 2 agonists may be beneficial during myocardial ischemia, but could be opposed by their peripheral vasoconstrictive effect. We studied the effects of mivazerol during periods of moderate coronary artery stenosis in anesthetized dogs. Mivazerol decreased heart rate (from 125 +/- 6 to 106 +/- 6 bpm) and cardiac output (from 4.4 +/- 0.6 to 1.8 +/- 0.2L/min) under normal conditions, while mean arterial pressure did not change. Mivazerol reduced blood flow in nonischemic myocardium and in the ischemic epicardial layer, but blood flow was preserved in the ischemic midmyocardial and subendocardial layer. Mivazerol had no effect on myocardial oxygen extraction during the stenoses, and regional myocardial oxygen consumption was unchanged. However, mivazerol decreased myocardial oxygen demand from 4.51 +/- 0.51 to 3.17 +/- 0.24 mumol.min-1.g-1, thereby reducing oxygen deficiency of ischemic myocardium to values significantly lower than in the placebo group (from 1.07 +/- 0.32 to 0.47 +/- 0.41 mumol.min-1.g-1). Mivazerol had no effect on myocardial lactate production during the stenoses. We conclude that mivazerol reduced myocardial oxygen demand while blood flow was preserved in the inner layers of ischemic myocardium.

Adrenergic alpha-Agonists↗

The effect of dexmedetomidine on nutrient organ blood flow.

The alpha 2-adrenergic agonist dexmedetomidine decreases not only heart rate, myocardial contractility, and oxygen demand, but also cardiac output (Q). To investigate whether this reduction in Q could critically impair perfusion of individual organs, we studied the effect of dexmedetomidine on nutrient blood flow to the heart, brain, kidney, spleen, skin, intestine, liver, and arteriovenous anastomoses using the radioactive microsphere technique. Studies were conducted in 14 dogs with an open chest and anesthetized with either chloralose/urethane (CU) or fentanyl/halothane (FH), to create different baseline conditions. Hemodynamic variables, organ blood flow, arterial and mixed venous oxygen, and lactate content were measured before and after administration of 0.1, 1, and 10 micrograms/kg dexmedetomidine intravenously (IV). After 10 micrograms/kg dexmedetomidine Q decreased in both groups by 50%. The decrease in blood flow varied greatly between the organs. While flow through arteriovenous anastomoses and skin decreased by 70% to 90%, renal blood flow decreased by 30%, cerebral blood flow only when baseline blood flow was high (FH dogs), and left ventricular blood flow only in the CU group, where the largest decrease in hemodynamic variables occurred. Oxygen consumption decreased only in CU dogs, but so did arterial lactate levels. These data indicate that dexmedetomidine causes considerable redistribution of Q, predominantly reducing blood flow to less vital organs and shunt flow.

Adrenergic alpha-Agonists↗

Regional electrical activation and mechanical function in the partially ischemic left ventricle of dogs.

During normoxia, asynchronous electrical activation of the left ventricle significantly affects regional mechanical performance. Regional fiber strain and external work during the ejection phase are found to be lower in early-activated than in late-activated regions. Because electrical activation is known to be delayed during ischemia, the present study was designed to investigate the influence of this electrical asynchrony on regional fiber strain, if any, during moderate and severe myocardial ischemia. Regional electrical activation time (t(ea)) and fiber strain during the ejection phase (ef,e) were measured in the epicardial layers of the left ventricular anterior wall during normoxia and after 15 min of total occlusion (n = 5) or 30, 60, 120, and 180 min of partial occlusion of the left anterior interventricular coronary artery (LAICA; n = 11). Myocardial blood flow (MBF) was assessed with radioactive microspheres. Blood gases, pH, and lactate and Pi contents were determined in arterial, local venous, and coronary sinus blood. During normoxia, t(ea) and ef,e were similar in various epicardial regions of the left ventricular anterior wall. During total LAICA occlusion, in the ischemic area, subepicardial MBF decreased from 0.86 +/- 0.36 (SD) to 0.18 +/- 0.09 ml.g-1.min-1 and subepicardial ef,e decreased from -0.11 +/- 0.02 to -0.01 +/- 0.01, whereas the delay in t(ea) between the normoxic basal-lateral and ischemic apical-medial areas increased slightly but significantly from 1.9 +/- 8.0 to 7.5 +/- 8.0 ms. After a 180-min partial occlusion of the LAICA, in the ischemic area, subepicardial MBF decreased from 0.62 +/- 0.17 to 0.49 +/- 0.18 ml.g-1.min-1 and ef,e decreased from -0.08 +/- 0.01 to -0.03 +/- 0.01. No significant change in the difference in t(ea) between the normoxic and ischemic areas could be detected (5.1 +/- 4.8 and 5.2 +/- 5.8 ms in the control situation and after 180-min partial occlusion, respectively). These findings indicate that in the ischemic epicardium 1) mechanical function is more affected than electrical impulse conduction and 2) delayed activation, if any, is accompanied by decreased instead of increased fiber strain, as found in the normoxic left ventricle.

Animals↗

A model approach to the adaptation of cardiac structure by mechanical feedback in the environment of the cell.

The uniformity of the mechanical load of the cardiac fibers in the wall is maintained by continuous remodeling. In this proposed model the myocyte changes direction in optimizing systolic sarcomere shortening. Early systolic stretch and contractility increases the mass of contractile proteins. Cyclic strain of the myocardial tissue diminishes passive stiffness, resulting in the control of ventricular end-diastolic volume. Utilizing these rules of remodeling in our mathematical model yields that the natural helical pathways of the myocardial fibers in the wall are formed automatically.

Adaptation, Physiological↗

Asymmetric thickness of the left ventricular wall resulting from asynchronous electric activation: a study in dogs with ventricular pacing and in patients with left bundle branch block.

Various kinds of abnormal, asynchronous electric activation of the left ventricle (LV) decrease mechanical load in early versus late activated regions of the ventricular wall. Because myocardium usually adapts its mass to changes in workload, we investigated by echocardiography whether regional differences in wall thickness are present in two kinds of asynchronous electric activation of different origin and conduction pathway: epicardial ventricular pacing in dogs and left bundle branch block (LBBB) in patients. In six dogs, 3 months of epicardial LV pacing at physiologic heart rates decreased the thickness of the early activated anterior wall by 20.5 +/- 8.1% without significantly changing LV cavity area and septal thickness. In a retrospective study of 228 LBBB patients, the early activated septum was significantly thinner than the late activated posterior wall. The asymmetry most pronounced was as large as 10% in 28 patients with LBBB and paradoxic septal motion. No difference in regional wall thickness was present in 154 control patients. In conclusion, chronic asynchronous electric activation in the heart induces redistribution of cardiac mass. This redistribution occurs in hearts, which differ in impulse conduction pathway, disease, and species and is characterized by thinning of early versus late activated myocardium.

Adaptation, Physiological↗

Fluorescent microspheres to measure organ perfusion: validation of a simplified sample processing technique.

A disadvantage of nonradioactive microsphere techniques is that the processing of samples is time-consuming and complex. We developed and validated a simplified processing method for the fluorescent microsphere (FM) technique. In seven anesthetized dogs with coronary artery stenosis up to six different FM and five different radioactivity labeled microspheres (RM) were injected. Two FM and two RM labels were injected simultaneously to enable inter- and intramethod comparison. After gamma-counting samples of blood, myocardium (n = 168), and other organs (n = 59) were digested in test tubes with 2 N ethanolic KOH (60 degrees C, 48 h), microspheres were sedimented by centrifugation, dye was extracted in the same tube, and fluorescence was measured. With this processing method, recovery of FM was approximately 100%. Good correlations for inter- and intramethod comparisons were found [r = 0.985 +/- 0.01 (mean +/- SD)]. The lower intermethod correlation for blue microspheres (r = 0.958) indicates that the use of this label is less desirable. RM and FM endocardial-to-epicardial blood flow ratios correlated well (r = 0.974). With this one-vessel centrifugal sedimentation method and at least five fluorescently labeled microspheres, blood flow can be reliably measured in various organs, including ischemic myocardium.

Animals↗

Regional fibre stress-fibre strain area as an estimate of regional blood flow and oxygen demand in the canine heart.

1. In the present study the relation between regional left ventricular contractile work, regional myocardial blood flow and oxygen uptake was assessed during asynchronous electrical activation. 2. In analogy to the use of the pressure-volume area for the estimation of global oxygen demand, the fibre stress-fibre strain area, as assessed regionally, was used to estimate regional oxygen demand. The more often used relation between the pressure-sarcomere length area and regional oxygen demand was also assessed. 3. Experiments were performed in six anaesthetized dogs with open chests. Regional differences in mechanical work were generated by asynchronous electrical activation of the myocardial wall. The ventricles were paced from the right atrium, the left ventricular free wall, the left ventricular apex or the right ventricular outflow tract. Regional fibre strain was measured at the epicardial anterior left ventricular free wall with a two-dimensional video technique. 4. Regional fibre stress was estimated from left ventricular pressure, the ratio of left ventricular cavity volume to wall volume, and regional deformation. Total mechanical power (TMP) was calculated from the fibre stress-fibre strain area (SSA) and the duration of the cardiac cycle (tcycle) using the equation: TMP = SSA/tcycle. Regional myocardial blood flow was measured with radioactive microspheres. Regional oxygen uptake was estimated from regional myocardial blood flow values and arteriovenous differences in oxygen content. 5. During asynchronous electrical activation, total mechanical power, pressure-sarcomere length area, myocardial blood flow and oxygen uptake were significantly lower in early than in late activated regions (P < 0.05). 6. Within the experiments, the correlation between the pressure-sarcomere length area and regional oxygen uptake was not significantly lower than the one between total mechanical power (TMP) and regional oxygen uptake (VO2,reg). However, variability of this relation between the experiments was less for total mechanical power. Pooling all experimental data revealed: VO2,reg = k1 TMP+k2, with k1 = 4.94 +/- 0.31 mol J-1 k2 = 24.2 +/- 1.9 mmol m-3 s-1 (means +/- standard error of the estimate). 7. This relation is in quantitative agreement with previously reported relations between the pressure-volume area and global oxygen demand. The results indicate that asynchronous electrical activation causes a redistribution of mechanical work and oxygen demand and that regional total mechanical power is a better and more general estimate of regional oxygen demand than the regional pressure-sarcomere length area.

Animals↗

Adaptation of cardiac structure by mechanical feedback in the environment of the cell: a model study.

In the cardiac left ventricle during systole mechanical load of the myocardial fibers is distributed uniformly. A mechanism is proposed by which control of mechanical load is distributed over many individual control units acting in the environment of the cell. The mechanics of the equatorial region of the left ventricle was modeled by a thick-walled cylinder composed of 6-1500 shells of myocardial fiber material. In each shell a separate control unit was simulated. The direction of the cells was varied so that systolic fiber shortening approached a given optimum of 15%. End-diastolic sarcomere length was maintained at 2.1 microns. Regional early-systolic stretch and global contractility stimulated growth of cellular mass. If systolic shortening was more than normal the passive extracellular matrix stretched. The design of the load-controlling mechanism was derived from biological experiments showing that cellular processes are sensitive to mechanical deformation. After simulating a few hundred adaptation cycles, the macroscopic anatomical arrangement of helical pathways of the myocardial fibers formed automatically. If pump load of the ventricle was changed, wall thickness and cavity volume adapted physiologically. We propose that the cardiac anatomy may be defined and maintained by a multitude of control units for mechanical load, each acting in the cellular environment. Interestingly, feedback through fiber stress is not a compelling condition for such control.

Adaptation, Physiological↗

Developments in non-radioactive microsphere techniques for blood flow measurement.

Considerable progress is being made in the development of non-radioactive microsphere methods. Validation studies of the three commercially available non-radioactive microspheres are promising. In most experimental conditions the use of non-radioactive microspheres saves money. Avoiding the use of radioactivity facilitates the use of microspheres in chronic animal experiments and when blood flow and chemical measurements are performed in the same sample. Moreover, using histological techniques, distributions of coloured or fluorescent microspheres in subunits of organs could be quantified, opening new scientific possibilities. Currently, the fluorescent microsphere technique seems to be the most promising non-radioactive microsphere method. Due to the high sensitivity and good spectral separation, the number of microspheres injected can be as small as that used, for radioactive microspheres, at least six labels can be used, and the relatively large volume in which fluorescence is measured (approximately 1-3 ml) enables the use of time saving microsphere isolation techniques. Development of these methods and further automation of the quantification process (using either automised spectrometry or FACS analysis) will considerably increase interest in the non-radioactive microsphere techniques. To accelerate these developments, investigators are encouraged to share their experiences.

Animals↗

Asymmetrical changes in ventricular wall mass by asynchronous electrical activation of the heart.

Ventricular pacing causes asynchronous electrical activation of the ventricular wall, because impulse conduction occurs via muscle fibers rather than via the Purkinje system. Chronic (up to 3 months) ventricular pacing caused about 30% decrease of wall mass in early activated regions but did not change wall mass in late activated regions. These are the first data indicating that chronic asynchronous activation induces asymmetrical structural adaptations. This asymmetry is likely to be evoked by regional differences in contractile work, as demonstrated in previous experiments from our laboratory. The nature of the structural adaptation as well as its clinical implications deserve more detailed investigation.

Adaptation, Physiological↗

Relation between regional electrical activation time and subepicardial fiber strain in the canine left ventricle.

To determine the relation between regional electrical activation time and fiber strain, epicardial electrical activation and deformation were measured in six open-chest dogs at the left ventricular anterior free wall after 15 min of right atrial, left ventricular free wall, left ventricular apex, or right ventricular outflow tract pacing, when end-diastolic pressure was normal or elevated (volume-loading). Regional electrical activation was measured using a 192-electrode brush. Regional subepicardial fiber strain (ef) was measured simultaneously in 16 regions, using optical markers which were attached to the epicardial surface and recorded on video. When relating regional ef during the ejection phase to regional activation time, the best correlation was found when a hemodynamic time reference rather than an electrophysiological one is used. Using the moment of the maximum rate of change of left ventricular pressure as the time reference for electrical activation, regional electrical activation time (t(ea)) and the degree of ef during the ejection phase could be fitted by a linear regression equation ef = a t(ea) + b, in which a = -3.46 +/- 0.73 s-1 an b = -0.28 +/- 0.05. For electrical activation times ranging from -40 to -80 ms, fiber strain was estimated with an accuracy of +/- 0.026 (+/- SE) with this relation. During right atrial pacing, t(ea) and ef were on the average -48 ms and -0.10 respectively. On further investigation, the relation between ef and t(ea) appeared to be influenced by end-diastolic pressure. For normal (1.1 kPa) and elevated end-diastolic pressure (1.8 kPa), the slope of the linear regression line was -3.96 and -2.86 s-1, respectively. Three conclusions may be drawn. Firstly, the time interval between the moment of regional electrical activation and the moment of the maximum rate of change of left ventricular pressure is an index of regional fiber strain. Secondly, it can be concluded from the above equations that electrical asynchrony of more than 30 ms causes non-uniformities in the degree of ef of the order of mean ef during pacing from the right atrium. Finally, differences in fiber strain during asynchronous electrical activation are less pronounced at larger filling pressures.

Animals↗