Diastolic properties of the normal left ventricle during supine exercise.

Diastolic function in response to dynamic exercise was studied by biplane left ventriculography and by measuring left ventricular pressure with a high fidelity micromanometer tipped catheter at rest and during supine bicycle exercise in nine normal subjects. During exercise there was a fall in end systolic volume, in the time constant of left ventricular isovolumic pressure decay, and in the lowest diastolic pressure. Stroke volume, peak filling rate, mean passive filling rate, and the volume at the lowest diastolic pressure increased. There was an increase in the number of time constants that had elapsed before the lowest diastolic pressure was reached and the slope of the pressure-volume curves during passive filling (delta P/delta V) increased without changes in end diastolic pressure and volume. These results show that during exercise elastic recoil is enhanced and left ventricular relaxation is faster and more complete. Both phenomena reduce the lowest diastolic filling pressure. The observed increase in chamber stiffness from rest to exercise is probably related to increased resistance of the left ventricular wall caused by higher passive filling rates. The enhanced early diastolic pressure decay during exercise allows stroke volume to increase despite an increase in diastolic viscoelastic resistance and chamber stiffness.     

Contractile properties of the left ventricle with aneurysm

Twenty-five patients with an anterior wall acute myocardial infarction (AMI) were studied by 2-dimensional echocardiography (2-D echo) 3 to 5 days after the onset of chest pain, and serially over 3 to 24 months to determine if a particular pattern of contractility may predispose to left ventricular (LV) aneurysm formation. No subject had a prior AMI. In 8 subjects LV aneurysm eventually developed (group I), usually within 2 to 4 weeks of AMI; in 17 patients LV aneurysm did not develop (group II). Percent fractional shortening of the basal and midventricular segments was significantly better in group I subjects than in group II subjects (29 +/- 2% vs 20 +/- 2%, p less than 0.01, respectively, for the basal segment, and 23 +/- 1% vs 17 +/- 2%, p less than 0.02, respectively, for the midventricular segment). Infarct size as determined by peak creatine kinase isoenzyme levels was large in both groups, and there was no statistically significant difference between their mean values (2,099 +/- 620 IU vs 1,334 +/- 249 IU for groups I and II, respectively). Severe asynergy of the infarcted myocardium was present in all group I subjects and in 9 of 17 group II subjects on the initial 2-dimensional echocardiographic study. These results indicate that LV aneurysm formation depends on a critical imbalance of myocardial forces where strong LV segments cause bulging of weakened ones.     

Diastolic viscous properties of the intact canine left ventricle

The viscoelastic model of the ventricle predicts that the rate of change of volume (strain rate) is a determinant of the instantaneous pressure in the ventricle during diastole. Because relaxation is not complete before the onset of filling, one cannot distinguish the individual effects of relaxation and viscosity unless the passive and active components that determine the ventricular pressure are separated. To overcome this problem, we used the method of ventricular volume clamping to compare the pressures in the fully relaxed ventricle at a given volume at zero strain rate (static pressure) and high strain rate (dynamic pressure). Six open-chest, fentanyl-anesthetized dogs were instrumented with micromanometers and an electronically controlled mitral valve occluder in series with the electromagnetic flow probe. We reasoned as follows: If there were significant viscosity, then the dynamic pressure would be higher than the static pressure. The static pressure was measured when the ventricle was completely relaxed following a mitral valve occlusion after an arbitrary filling volume had been achieved. The dynamic pressure was determined by delaying the onset of filling until relaxation was complete and then measuring the pressure at the same volume that was achieved when the static pressure was measured. In 19 different hemodynamic situations, the dynamic and static pressures were identical (mean difference, 0.1 +/- 0.8 mm Hg), indicating that in the passive ventricle viscoelastic effects are insignificant and do not contribute to the left ventricular diastolic pressure under normal filling rates.     

Pseudoaneurysm of the left ventricle progressing from a subepicardial aneurysm.

A 56-year-old man presented with an inferior myocardial infarction and a huge pseudoaneurysm below the inferior surface of the left ventricle, which had progressed from a small subepicardial aneurysm over a 6-month period. Transthoracic echocardiography, Doppler color flow images, radionuclide angiocardiography, magnetic resonance imaging and contrast ventriculography all revealed an abrupt disruption of the myocardium at the neck of the pseudoaneurysm, where the diameter of the orifice was smaller than the aneurysm itself, and abnormal blood flows from the left ventricle to the cavity through the orifice with an expansion of the cavity in systole and from the cavity to the left ventricle with the deflation of the cavity in diastole. Coronary angiography revealed 99% stenosis at the atrioventricular nodal branch of the right coronary artery. At surgery the pericardium was adherent to the aneurysmal wall and a 1.5-cm orifice between the aneurysm and the left ventricle was seen. Pathological examination revealed no myocardial elements in the aneurysmal wall. The orifice was closed and the postoperative course was uneventful. Over-intense physical activity as a construction worker was considered to be the cause of the large pseudoaneurysm developing from the subepicardial aneurysm. These findings indicate that a subepicardial aneurysm may progress to a larger pseudoaneurysm, which has a propensity to rupture, however, it can be surgically repaired.     

Diastolic properties of the normal left ventricle during supine exercise

Diastolic function in response to dynamic exercise was studied by biplane left ventriculography and by measuring left ventricular pressure with a high fidelity micromanometer tipped catheter at rest and during supine bicycle exercise in nine normal subjects. During exercise there was a fall in end systolic volume, in the time constant of left ventricular isovolumic pressure decay, and in the lowest diastolic pressure. Stroke volume, peak filling rate, mean passive filling rate, and the volume at the lowest diastolic pressure increased. There was an increase in the number of time constants that had elapsed before the lowest diastolic pressure was reached and the slope of the pressure-volume curves during passive filling (delta P/delta V) increased without changes in end diastolic pressure and volume. These results show that during exercise elastic recoil is enhanced and left ventricular relaxation is faster and more complete. Both phenomena reduce the lowest diastolic filling pressure. The observed increase in chamber stiffness from rest to exercise is probably related to increased resistance of the left ventricular wall caused by higher passive filling rates. The enhanced early diastolic pressure decay during exercise allows stroke volume to increase despite an increase in diastolic viscoelastic resistance and chamber stiffness.     

Canine left ventricle electromechanical behavior under different pacing modes

Background

Cardiac resynchronization therapy may improve survival and quality of life in patients suffering from heart failure with left ventricular (LV) contraction dyssynchrony. While several studies have investigated electrical or mechanical determinants of synchronous contraction, few have focused on activation contraction coupling at a macroscopic level.

Objective

The objective of the study was to characterize LV electromechanical behavior and response to pacing in a heart failure model.

Methods

We analyzed data from 3D electroanatomic non-contact mapping and blood pool SPECT for 12 dogs with right ventricular (RV) tachycardia pacing-induced dilated cardiomyopathy. Surfaces generated by the two modalities were registered. Electrical signals were analyzed, and endocardial wall displacement curves were portrayed.

Results

Rapid pacing decreased the mean LV ejection fraction (LVEF) to 20.9?% and prolonged the QRS duration to 79?±?10?ms (normal range: 40?C50?ms). QRS duration remained unchanged with biventricular pacing (88.5?ms), while single site pacing further prolonged the QRS duration (113.3?ms for RV pacing and 111.6?ms for LV pacing). No trend was observed in LV systolic function. Activation duration time was significantly increased with all pacing modes compared to baseline. Finally, electromechanical delay, as defined by the delay between electrical activation and mechanical response, was increased by single site pacing (172.9?ms for RV pacing and 174.6?ms for LV pacing) but not by biventricular pacing (162.4?ms).

Conclusions

Combined temporal and spatial coregistration electroanatomic maps and baseline gated blood pool SPECT imaging allowed us to quantify activation duration time, electromechanical delay, and LVEF for different pacing modes. Even if pacing modes did not significantly modify LVEF or activation duration, they produced alterations in electromechanical delay, with biventricular pacing significantly decreasing the electromechanical delay as measured by surface tracings and endocardial non-contact mapping.     

Factors affecting the relaxation and diastolic properties of the left ventricle

The myocardium is an integrated functional unit. The separation of the cardiac cycle into three phases on simultaneous ventricular and arterial pressure curves:contraction, relaxation, diastole, is an artificial distinction of interdependent functions which are superimposed in time in the real mechanical and biochemical phenomena. At the level of the sarcomeres and myofilaments, relaxation is the active process of liberation of the bridges formed between actin and myosin during contraction; diastole is the phase during which there is no cyclic renewal of these bridges, it is the passive phase. Myocardial relaxation in mammals is controlled by the rapid recapture of Ca2+ by the sarcoplasmic reticulum. It plays an important mechanical role during the closure of the aortic semilunar valves, the opening of the mitral valve, the rapid filling of the right ventricle and the diastolic perfusion of the coronary arteries. It is dependent on the load and is influenced by myocardial metabolism (hypoxia, acidosis, ischaemia), temperature and a number of pharmacological agents. Amongst the passive properties of the left ventricle, we need to distinguish between the distensibility of the left ventricle as a filling chamber (parietal rigidity) and the rigidity of each of the myocardial fibres which make up the ventricular wall (myocardial rigidity). The passive properties of the left ventricle can be modified by ventricular geometry, passive mechanical properties of the ventricular wall (thickening, myocardial changes, heart rate and filling rate, cellular oedema, hypoxia, ischaemia, coronary artery filling pressure), the interaction between the pericardium, the right ventricle and the left ventricle and intrathoracic pressure. The large number of factors which are capable of modifying left ventricular relaxation and diastole explains the problems associated with in vivo investigations, which depend on a large number of indices of limited value.     

Diastolic anisotropic properties of the left ventricle in the conscious dog

The role of myocardial anisotropy in determining change in left ventricular shape during diastolic filling has not yet been demonstrated. Therefore, 11 conscious dogs were instrumented with global ultrasonic dimension transducers to measure left ventricular major and minor axis diameters and equatorial wall thickness. Myocardial geometry was represented as a three-dimensional ellipsoidal shell. Left ventricular transmural pressure was measured with micromanometers, and ventricular volume was varied by inflation of vena caval occluders. Left ventricular wall strains and stresses calculated from the ellipsoidal shell model agreed closely with those measured directly by myocardial force and dimension transducers. Unequal normalized diastolic stress-strain relations were observed in the latitudinal, longitudinal, and wall thickness directions, reflecting anisotropic mechanical properties of the myocardium. Although a greater wall stress in the latitudinal versus longitudinal axis was predicted adequately from left ventricular geometry alone, the observed latitudinal strain exceeded longitudinal strain by an amount greater than was predicted by geometric considerations alone, suggesting that myocardial anisotropy contributes significantly to changes in ventricular shape during diastolic filling.     

Two-chambered right ventricle: simulating two-chambered left ventricle.

Two cases are described of a most unusual variant of two-chambered right ventricle. In both the ventricular septal defect was between the distal chamber of the right ventricle and the left ventricle. However the extensive dividing 'septum' between proximal and distal parts of the right ventricle converted the latter, haemodynamically, into part of the left ventricle. In the first case the distal chamber supported the aorta in the left anterior position, the pulmonary artery arising from the proximal part of the right ventricle. In the second the pulmonary artery arose from the distal chamber and the aorta from the proximal chamber. Though in both the ventriculoarterial connection was double outlet right ventricle, functionally there was arterial concordance in case 1 and discordance in case 2. A further disconcerting feature was the resemblance of the distal right ventricular chamber to the rudimentary chamber of a univentricular heart of left ventricular type.     

Long-term behavior of echocardiography findings of the left ventricle following myocardial infarct

110 patients at the age of 62.5 +/- 10.7 years were echocardiographically investigated by means of M-mode and section-picture on the 6th and 27th day as well as 3 and 12 months after the infarction. In all investigations patients with anterior wall infarctions showed lower systolic thickenings of the septum, disturbances of the kinetics of the anterior wall of higher degree and up to the 3rd month a compensatorily increased systolic thickening of the posterior wall. Up to the 1st year this was replaced by an increasing hypertrophy of the posterior wall. After a posterior wall infarction the systolic thickening of the posterior wall and the disturbance of the kinetics had less clear results so that compensation mechanisms in the anterior wall were not proved.     

Two-chambered right ventricle: simulating two-chambered left ventricle.

Two cases are described of a most unusual variant of two-chambered right ventricle. In both the ventricular septal defect was between the distal chamber of the right ventricle and the left ventricle. However the extensive dividing 'septum' between proximal and distal parts of the right ventricle converted the latter, haemodynamically, into part of the left ventricle. In the first case the distal chamber supported the aorta in the left anterior position, the pulmonary artery arising from the proximal part of the right ventricle. In the second the pulmonary artery arose from the distal chamber and the aorta from the proximal chamber. Though in both the ventriculoarterial connection was double outlet right ventricle, functionally there was arterial concordance in case 1 and discordance in case 2. A further disconcerting feature was the resemblance of the distal right ventricular chamber to the rudimentary chamber of a univentricular heart of left ventricular type.