J Minten

Diastolic properties of the left ventricle in normal adults and in patients with third heart sounds.

To explore the pathogenesis of the third heart sound (S3), left ventricular hemodynamics in early diastole were studied during catheterization in normal adults without S3S (group I, n = 12) and in cardiac patients with S3S as the result of severe mitral regurgitation (group II, n = 11), dilated cardiomyopathy (group III, n = 24) or restricted left ventricular filling (group IV, n = 4). The height and steepness of the rise in left ventricular pressure after minimum diastolic pressure (the so-called rapid filling wave), maximum dV/dt, and the time constant of fall in isovolumetric pressure were measured. The completeness of relaxation was evaluated from the number of time constants elapsed at the time of minimum diastolic pressure. Pressure-volume data were fitted to simple elastic and viscoelastic models incorporating inflow rate into the equation. In all patients with S3S a significantly higher and steeper rapid filling wave was found than in normal adults. Maximum dV/dt was significantly greater in group II (1084.9 +/- 416 ml/sec; mean +/- SD) than in the other groups (463.9 +/- 177.1 ml/sec in group I, 448.8 +/- 134.0 ml/sec in group III, and 709.9 +/- 226.8 ml/sec in group IV). No significant differences in left ventricular chamber elastic properties in the different groups were found. However, intrapatient comparisons of the results of the use of elastic and viscoelastic equations revealed a significantly better curve fit (r = .930 vs .968, p less than .005) and a much higher viscous constant for group III. Similar results were found in group IV.(ABSTRACT TRUNCATED AT 250 WORDS)

The genesis of the third and fourth heart sounds. A pressure-flow study in dogs.

To examine the mechanism of mitral flow deceleration in diastole and its potential influence on the genesis of third (S3) and fourth (S4) heart sounds, we simultaneously recorded left atrial and left ventricular pressures (micromanometers), mitral flow velocity (electromagnetic catheter-tip flow velocity meter), and internal and external phonocardiograms in 25 open-chest dogs. Diastolic time intervals, transmitral pressure gradients (planimetry), maximum mitral flow velocity, and acceleration and deceleration of flow were measured under different loading conditions. It was found that deceleration of mitral flow in early and late diastole is always caused by a negative transmitral pressure gradient. After volume loading, diastolic pressures, positive (forward) and negative (backward) transmitral pressure gradients, and acceleration and deceleration of flow increased, and an S3 or S4 appeared (20:25 dogs). These sounds occurred during the phase of flow deceleration and could be recorded from the chest wall, inside the left ventricle, and directly from the epicardial surface of the freely exposed left ventricular wall. After balloon occlusion of the inferior vena cava (17:25 dogs), the opposite changes were observed and gallop sounds disappeared. The results indicate that the left ventricular pressure rise in response to filling reverses the transmitral pressure gradient and decelerates flow. Deceleration of inflow by the left ventricular wall in early and late diastole may represent a key mechanism in the genesis of S3 and S4.

Relation between coronary artery stenosis and myocardial purine metabolism, histology and regional function in humans

In 54 patients undergoing elective or emergency aortocoronary bypass grafting, angiographic and electrocardiographic changes were studied. Five patients with unstable angina and five patients with evolving myocardial infarction were included. High energy phosphate metabolism and the histologic appearance of the myocardium were analyzed in transmural biopsy specimens acquired at the time of surgery. In patients without anterior infarction on the electrocardiogram, severe stenosis of the left anterior descending coronary artery resulted in a reduction of anterior wall motion that was associated with a partial depletion of the adenylate pool. Mitochondrial function, however, remained intact: the adenosine diphosphate/adenosine triphosphate ratio, the energy charge and the creatine phosphate/adenosine triphosphate ratio were in the normal range. Histologic assessment demonstrated viable myocardium with a high incidence of atrophic cells. In evolving myocardial infarction, 170 minutes of acute coronary artery obstruction resulted in anterior wall akinesia associated with a decrease of the sum of the adenylates to 52% and of creatine phosphate to 16% of their normal value (p less than 0.05). The nucleosides accumulated; their major fraction (91%) was inosine. The adenosine diphosphate/adenosine triphosphate ratio increased from 0.14 +/- 0.04 to 0.49 +/- 0.20 (p less than 0.01) and the energy charge decreased from 0.924 +/- 0.021 to 0.660 +/- 0.169 (p less than 0.01). Ultrastructure examination revealed irreversible cell damage in at least the subendocardial layer. These results suggest that the energetic base of reduced contractility due to severe coronary artery stenosis is different from that in acute coronary obstruction.(ABSTRACT TRUNCATED AT 250 WORDS)

Laser method for recording displacement of the heart and chest wall

Several non-invasive methods are in use for recording mechanocardiograms. In this paper a new laser technique will be presented to measure heart motion, chest wall displacement and other displacement curves of cardiovascular structures. Principles of the laser displacement technique are described. The measurement range within which displacement is sensed, is 32 mm with a detector to object distance of 25 cm and a resolution of 8 micron (digital output) or 16 micron (analogue output). The specific surface of which motion is sensed is 1 mm2. The sensitivity of the system is 156 mV/mm at a frequency bandwidth of 0-2 kHz. Assessment of the laser displacement technique was carried out during 6 dog experiments on the closed chest, on the exposed heart, on blood vessels and also on the chest wall of 5 normal subjects. Displacement of the chest wall at the apical site ranges between 0.3-0.8 mm and of the exposed heart between 3-10 mm.

Energy state of the myocardium during long-term cold storage and subsequent reperfusion.

Long-term preservation of dog hearts was performed over 24 h using Bretschneider-HTK cardioplegia and cold storage. Preservation was assessed in terms of conservation of myocardial tissue levels of high-energy phosphates (HEP) and functional outcome after cardiac transplantation. Serial left ventricular biopsies were taken and analysed for ATP, ADP, AMP, adenosine, inosine, hypoxanthine, xanthine and creatine phosphate. Myocardial structure was studied by electron microscopical examination of a similar biopsy specimen. Cardiac performance was measured before and after cardiac transplantation. Several techniques of cardioplegic arrest were studied: single dose cardioplegia, multidose cardioplegia and continuous perfusion with the cardioplegic solution. In all groups, the hearts were stored at 0.5 degree C for 24 h. In the group of single dose Bretschneider-HTK cardioplegia, myocardial ATP content after 24 h of cold storage was only 25% of control. The total sum of nucleotides at that time interval was however 65% of the control value. Reperfusion of these hearts using a support dog (whole blood reperfusion) did not result in any recovery of ATP. Creatinine phosphate however showed an overshoot. Accumulated nucleosides were washed out. The hearts showed electrical activity but were severely arrhythmic. Contractility was poor. In the group of multidose Bretschneider-HTK cardioplegia, HEP preservation was better than after single dose cardioplegia. ATP content was about 50% of control. The total sum of nucleotides was 85% of control. Ultrastructural assessment of the myocytes revealed only slight ischaemic damage to the mitochondria. Reperfusion on cardiopulmonary bypass after cardiac transplantation did not show any restoration of ATP, but a steady catabolism of HEP. The nucleosides adenosine and inosine were not washed out upon reperfusion. After cardiac transplantation, none of these hearts could be weaned from cardiopulmonary bypass due to irreversible low cardiac output. Histological examination demonstrated irreversible myocardial tissue damage. In the group of continuous cold Bretschneider cardioplegia, HEP content was completely preserved throughout the 24 h of perfusion. Ultrastructure of the myocytes was normal. Reperfusion of the transplanted hearts showed a mild breakdown of ATP to 70% of control values accompanied by a slight accumulation of nucleosides. Haemodynamic recovery however was perfect and none of the hearts needed positive inotropic support. Myocytes after reperfusion had a normal subcellular appearance.(ABSTRACT TRUNCATED AT 400 WORDS)

Cardioprotective effects of carnitine in extensive aortocoronary bypass grafting: a double-blind, randomized, placebo-controlled clinical trial

The cardioprotective effects of carnitine were tested in patients undergoing multiple aortocoronary bypass grafting. Intermittent aortic cross-clamping at 28°C was used. Mean total cross-clamping time was 30 ± 11 min. Patients were randomized into three groups: a control group receiving placebo (group 1), a group preheated with 3 g carnitine intravenously before cardiopulmonary bypass (CPB) (group 2), and a group preheated with 6 g carnitine intravenously (group 3). The markers of myocardial ischemia included levels of adenosine triphosphate, its catabolites, and creatine phosphate in transmural left ventricular biopsy specimens taken at the beginning and end of CPB, as well as hemodynamic recovery during weaning from CPB and for the next 24 h. The intravenous infusion of carnitine (3 or 6 g) had no hemodynamic effect. At the end of CPB myocardial tissue levels of adenosine triphosphate and creatine phosphate did not differ significantly among the groups (P > 0.05). Recovery of cardiac function during weaning from CPB and for the following 24 h was similar in all three groups (P > 0.05). It is concluded that pretreatment with carnitine neither facilitates weaning from cardiopulmonary bypass in patients undergoing aortocoronary bypass surgery nor favorably affects hemodynamic function during the next 24 h.

Optimal storage temperature and benefit of hypothermic cardioplegic arrest for long-term preservation of donor hearts: a study in the dog

Currently, for practical clinical purposes, the preservation of donor hearts is limited to about 4 h. Transplantation must be finished within this period to assure complete functional recovery upon reperfusion. From the clinical setting it is well known that hypothermia results in a better myocardial preservation during ischemia. During ischemia, rapid catabolism of high-energy phosphates (e.g., ATP and creatine phosphate) occurs. The purpose of this study was to investigate the influence of temperature during a 24-h preservation period on the rate of catabolism of ATP and on the rate of accumulation of breakdown products (ADP, AMP, adenosine, inosine, hypoxanthine, and xanthine). For this purpose, hearts were excised and stored for 24 h at 0.5°, 12°, or 18 °C. In addition, the effect of initial cardioplegic arrest was compared with simple normothermic excision of the heart followed by 24 h in cold storage. It was found that the higher the storage temperature, the higher the rate of catabolism of high-energy phosphates and, hence, after 24 h, the lower the final ATP level and the higher the level of breakdown products, mainly nucleosides. It was also found that the initial cardioplegic arrest strongly benefits the preservation of high-energy phosphates as a result of the ATP-sparing effect.

Correlation between mechanical properties and wall composition of the canine superior vena cava.

The mechanical properties (modulus of elasticity and stress-relaxation) of different venous segments of the canine superior vena cava were determined as well as the composition of the vessel wall by means of physical, biochemical and histological methods. It was found that the wall of the vena cava was structurally and mechanically a function of the metric position with respect to the right heart: the modulus of elasticity increased, the stress-relaxation decreased, the concentration of hydroxyproline, collagen and elastin increased and the amount of muscle fibres decreased with increasing distal distance from the right heart. A significant linear correlation coefficient was observed between the modulus of elasticity and the structural wall components. The data presented show the axial heterogeneity and the dependency of the mechanical properties upon the venous vessel wall composition.

Geometrical variations of the canine superior vena cava: Relationship between diameter, segment length and transmural venous pressure

The dimensional variations of the superior vena cava throughout the cardiac cycle were investigated by means of angiographic and ultrasonic techniques. Results obtained by both methods were largely in agreement. In frontal direction the diameter curve resembled the transmural pressure variations, the sagittal diameter curve was not related to the venous pressure variations during certain phases of the cardiac cycle and compressional and/or stretching forces exerted by respectively the distending aorta and/or pulmonary artery and the contracting heart may have been responsible. Also segment length variations occurred: during atrial contraction, ventricular systole and early diastole the vein elongated, indicating the varying longitudinal traction forces, possibly exerted by the rotational movement of the contracting heart. Assuming elliptical symmetry the vena caval cross-section could be reconstructed, and the cross-sectional area, perimeter and segmental volume could be calculated throughout the cardiac cycle. Despite the high venous distensibility, no extreme collapse of the vein was observed during the cardiac cycle at low transmural pressures.

Influence of transmural pressure on retrograde pressure pulse transmission velocity in the canine superior vena cava

The influence of intrathoracic and intraluminal pressure on venous pressure pulse propagation velocity in the superior vena cava was investigated in acute canine experiments. The propagation velocity of distinct points of the venous pressure curve was measured under different conditions of preload, during expiratory and inspiratory apnea and during positive-negative pressure respiration. Under control conditions transmission velocities varied from 1.07 m/s to 3.29 m/s. After volume expansion propagation velocities rose significantly and varied from 1.09 m/s to 6.48 m/s. During expiratory apnea and at peak negative expiratory pressure, the propagation speed of distinct pressure points was higher than during inspiratory apnea and at peak positive inspiratory pressure. Significant linear correlation coefficients were found between the transmission velocities of different distinct pressure points and the transmural pressure, but not between the propagation speed and the intraluminal pressure.