Biomedical subjects

T Delhaas

Publications and source records attributed to T Delhaas.

28 records · Page 2Linked to original sources

PubMed1996

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↗

PubMed1995

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↗

PubMed1994

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↗

PubMed1993

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↗

PubMed1993

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↗

PubMed1993

Subepicardial fiber strain and stress as related to left ventricular pressure and volume.

In a mathematical model of the mechanics of the left ventricle (LV) by Arts et al. (1), assuming uniformity of fiber stress (sigma f) and fiber strain (delta epsilon f) in the wall during the ejection phase, fiber stress and fiber strain were related to LV cavity pressure (Plv), LV cavity volume (Vlv) and wall volume (Vw) by the following pair of equations: sigma f = Plv (1 + 3 Vlv/Vw) and delta epsilon f = 1/3 delta ln (1 + 3 Vlv/Vw). The ratio of Vlv to Vw appeared to be the most important geometric parameter, whereas the actual LV shape was of minor importance. The relationships on fiber strain and stress were evaluated experimentally in six anesthetized open-chest dogs during normal and elevated (volume loading) end-diastolic LV pressure. Subepicardial fiber strain was measured simultaneously in 16 adjacent regions of the LV anterior wall, using optical markers that were attached to the epicardial surface and recorded on video. Changes in Vlv were measured by use of four inductive coils sutured to the LV in a tetrahedric configuration. Vw was measured postmortem. During control as well as hypervolemia the following results were found. At the anterior free wall of the LV, the slope of the estimated linear relationship between measured and calculated fiber strain was 1.017 +/- 0.168 (means +/- SD), which is not significantly different from unity. Calculated fiber stress corresponded qualitatively and quantitatively with experimental results reported on isolated cardiac muscle. Calculated subepicardial contractile work per unit of tissue volume was not significantly different from global pump work as normalized to Vw. These findings support the assumption of homogeneity of muscle fiber strain and stress in the left ventricular wall during the ejection phase. Furthermore, average values of fiber stress and strain can be estimated on the basis of measured left ventricular pressure and volume.

Animals↗

PubMed1992

The time sequence of electrical and mechanical activation during spontaneous beating and ectopic stimulation.

The relation between the sequence of electrical (E) and mechanical (M) activation was studied at the LV anterior wall of open-chest dogs (n = 11). M activation was defined as the onset of epicardial fibre shortening, as measured with a recently developed video technique. E activation was determined with a brush of extracellular electrodes. The delay between activation of basal and apical regions was consistently larger for M activation than for E activation: during spontaneous beating: 20.5 +/- 7.30 ms vs 8.8 +/- 3.31 ms, during right ventricular outflow tract pacing: 50.3 +/- 7.69 ms vs 39.0 +/- 5.31 ms and during left ventricular apex pacing 40.1 +/- 10.03 ms vs 25.4 +/- 9.30 ms, respectively (P less than 0.05 in all cases). The E-M time interval was consistently shorter in early than in late activated regions: 32 +/- 10 vs 41 +/- 8 ms during RV outflow tract pacing (P = 0.09) and 24 +/- 30 vs 40 +/- 24 ms during LV apex pacing (P less than 0.05). Electrical asynchronies larger than 40 ms resulted in decreases of systolic blood pressure and stroke volume. This study shows that the asynchrony of cardiac motion exceeds that of electrical activation because the time interval between electrical activation and onset of fibre shortening is larger the later a particular region is activated. Possible explanations for this phenomenon are discussed.

Animals↗

PubMed1992

Respiration and measurement of cardiac output by thermodilution and central or peripheral dye dilution.

Cardiac output as measured by indicator dilution methods during artificial ventilation shows differences up to +/- 35%. We studied the influence of spontaneous breathing on measurement of cardiac output by thermodilution (TD) and central (CDD) and peripheral dye dilution (PDD) in seven anesthetized dogs. Injection of indicator was timed at one of five chosen moments in a respiratory cycle. The indicator for TD was also used as solvent for indocyanine green. Results were normalized by the value obtained with injection at inspiratory onset. Results of the central dilution methods showed a slight but not significant difference between values measured with injection at 25 and 75% of the respiratory cycle: 105.7 and 98.0%, respectively, (TD) and 102.3 and 97.2% (CDD). Mean cardiac output determined by TD, CDD, or PDD was not significantly different. We conclude that 1) a reasonable estimate of cardiac output may be obtained by means of a single indicator-dilution curve and 2) the choice of the dilution method may be determined by practical considerations.

Animals↗

PubMedDate not supplied

Proximal left coronary artery occlusion in a 15-year-old boy with noonan syndrome and hypertrophic cardiomyopathy.

Whereas intra- and extramural coronary artery narrowing have been found in patients with hypertrophic cardiomyopathy, occlusion of extramural coronary arteries has not been reported. Also, only three cases with Noonan syndrome and congenital coronary artery anomalies have been described. We report a patient with Noonan syndrome, hypertrophic cardiomyopathy, and complete occlusion of the proximal left coronary artery.

Abnormalities, Multiple↗

PubMedDate not supplied

Asystole during outbursts of laughing in a child with Angelman syndrome.

A girl with Angelman syndrome had recurrent episodes of ventricular asystole and syncope caused by severe vagal hypertonia during outbursts of laughing. After intravenous administration of atropine, laughing no longer induced asystole or syncope. The vast majority of patients with Angelman syndrome have seizures. Since hypoxia associated with asystole can provoke convulsions, we suggest electrocardiographic evaluation of Angelman patients with symptomatic bradycardia, loss of consciousness, or convulsions related to laughing.

Adolescent↗