Non-invasive assessment of left ventricular function after correction of severe aortic regurgitation. (1/46)

Twenty patients were studied with simultaneous left ventricular cavity echocardiograms and apex cardiograms during the first two weeks after correction of severe aortic regurgitation. Endocardial echoes and apex cardiograms were digitized, so that left ventricular dimensions, their rates of change, and echo dimension-apex cardiogram relations could be studied. After aortic valve replacement, there was an early reduction in end-diastolic dimension, within 2 days, from 7-0 +/- 0-8 cm to 5-7 +/- 1-0 cm (P less than 0-001), while peak normalized shortening rate (peak Vcf) dropped from 1-9 +/- 0-6 to 1-4 +/- 0-6 S-1 (P less than 0-01), and remained unchanged for the remainder of the study. Immediately after operation, striking abnormalities of isovolumic contraction and, to a lesser extent, of early relaxation, could be seen, which regressed over 4 to 7 days, except in 2 patients who developed a low output state. These changes in left ventricular dimension, Vcf, and isovolumic contraction could not have been described by an single "measure" of left ventricular function.  (+info)

Value of systolic time intervals in assessing severity of congenital aortic stenosis in children. (2/46)

Simultaneous recordings have been made of electrocardiogram, phonocardiogram, carotid pulse tracing, left ventricular pressure, and aortic pressure in 27 children with aortic valve stenosis and 3 children with membranous subaortic stenosis. Peak systolic pressure difference ranged from 10 to 110 mmHg (1.3 to 14.6 kPa). None of the patients had congestive heart failure and cardiac output was in the normal range in all. Total electromechanical systole, left ventricular ejection time, and pre-ejection time were corrected for heart rate, age, and sex. Mild stenosis (peak systolic pressure difference less than or equal to 50 mmHg (6.7 kPa)) was present in 18, severe stenosis (peak systolic pressure difference greater than 50 mmHg) in 12 patients. The externally measured pre-ejection time and ejection time proved to be nearly equal to the corresponding intervals measured internally; from these data it is concluded that pre-ejection time and ejection time in children with aortic stenosis can be measured reliably by non-invasive methods. Mean values for corrected total electromechanical systole and ejection time were prolonged, but the corrected pre-ejection time did not differ from the normal value. When corrected time intervals were plotted against severity of the aortic stenosis as expressed by the peak systolic pressure difference or the aortic valve orifice index, a wide scatter was found. It is concluded that a normal ejection time is strong evidence against a peak systolic pressure difference of more than 50 mmHg (6.7 kPa) or an aortic valve orifice index less than 0.70 cm2 per m2 BSA. A prolonged ejection time, however, may occur in mild as well as in severe stenosis. Total electromechanical systole and pre-ejection time have no value in predicting the severity of aortic stenosis in children.  (+info)

Effects of sustained isometric handgrip on praecordial accelerocardiogram in normal subjects and in patients with heart disease. (3/46)

The effects of isometric exercise on the maximum amplitude of the praecordial accelerocardiogram (as represented by the DE deflection) have been compared in 6 normal subjects (group 1), 12 patients with aortic stenosis (group 2), and 16 patients with myocardial disease (group 3). Whereas the tachycardia and pressor effects of isometric exercise were identical in all three groups, the normal subjects showed a significant decrease in DE during handgrip of 10 +/- 4 per cent (P less than 0.05) as compared with the insignificant increases of 8.5 +/- 6 per cent (P greater than 0.5), and 4 +/- 3.5 per cent (P greater 0.3) observed in the patients in groups 2 and 3. This response in the normal subjects differed significantly from the responses observed in the patients in groups 2 (P less than 0.02) and 3 (P less than 0.01). Of the patients in each of groups 2 and 3, 50 per cent responded abnormally to handgrip in that they showed a significant increase in DE. In the patients with aortic stenosis this subgroup of patients differed from the remainder in that they had a higher resting cardiac index (P less than 0.05). In the patients with myocardial disease this subgroup was characterized by a significantly lower resting left ventricular end-diastolic pressure (P less than 0.02). It seems, therefore, that those patients who increase DE in response to handgrip tend to have better left ventricular function at rest than those who do not. We suggest that this may be because of increased beta adrenergic activity at rest and during isometric exercise in the subgroup who respond to handgrip with an increase in DE.  (+info)

The 'rapid filling wave' of the apex cardiogram. Its relation to echocardiographic and cineangiographic measurements of ventricular filling. (4/46)

In order to study the relation between the 'rapid filling wave' of the apex cardiogram and left ventricular filling, simultaneous apex cardiograms, phonocardiograms, and echocardiograms were recorded in 57 patients. Continuous measurements of left ventricular dimension were derived from the echocardiograms by digitization using manual tracing and a computer. Possible errors in the use of a single dimension to assess left ventricular filling were investigated by frame-by-frame analysis of cineangiocardiograms in 37 patients, and the timing of changes in transverse diameter found to correlate closely with those in cavity area. Mitral valve opening, shown as the initial separation of the valve cusps by echocardiography, preceded the 'O' point of the apex cardiogram in all except 3 patients, the 'O' point appearing to correlate more closely with the time of peak rate of outward wall movement. A third heart sound was present in 29 patients, and in 25 of these it occurred later than the peak rate of wall movement (ment interval 51 ms). The end of rapid filling derived from the dimension trace occurred in relation to the third heart sound after a mean interval of 9 ms, with a range from 50 ms before to 80 ms after the third sound. Peak rates of wall movement were similar in patients with and without third heart sounds. The results show that outward left ventricular wall movement begins with a period of acceleration, with peak rates occurring synchronous with the 'O' point of the apex cardiogram and thus with the nadir of the ventricular pressure trace. Outward wall movement becomes less rapid thereafter, so that the rapid filling wave of the apex cardiogram does not reflect the time of rapid filling of the left ventricle. The 'O' point is not related to mitral valve movement nor does the third heart sound bear a consitent relation to any aspect of left ventricular wall movement.  (+info)

Time relation between apex cardiogram and left ventricular events using simultaneous high-fidelity tracings in man. (5/46)

In 10 patients without left heart valvular disease and having normal function of the left ventricle, the left ventricular apex cardiogram with its first derivative (dA/dt), left ventricular pressure with its first derivative (dP/dt), aortic pressure, electrocardiogram, and phonocardiogram were reocrded simultaneously during cardiac catheterization. The apex cardiographic tracings were obtained by means of a transducer with infinite time constant and very high resonant frequency and the LV and aortic pressures with catheter tip-manometers. The onset of the systolic rise of apex cardiographic and LV pressures were found to occur almost simultaneously with the upstroke of LV pressure, preceding that of the apex cardiogram by only 2 +/- 4 ms (mean +/- 1 SD). The summit of the systolic upstroke of the apex cardiogram (called E-point) occurred 37 +/- 9 ms after opening of the aortic valve and 41 +/- 9 ms after peak dP/dt. The peak of dA/dt preceded peak dP/dt by 10 +/- 4 ms. The protodiastolic nadir of the apex cardiogram (called-O-point) occurred slightly earlier (19 +/- 16 ms) than the nadir of the LV pressure curve, with considerable variation. In conclusion, this study using external and internal transducers with similar characteristics gives a new definition of the time relation between the externally recorded apex cardiogram and the haemodynamic events within the left heart in human subjects with normal left ventricular function.  (+info)

Transmission of audible praecordial gallop sounds to right supraclavicular fossa. (6/46)

To evaluate the significance of audible gallop sounds in the right supraclavicular fossa we performed simultaneous external heart sound recordings at 50 and 100 Hz at the left ventricular apex, left sternal border, and right supraclavicular fossa in 50 patients with audible gallop sounds at the left ventricular apex. In each patient heart sounds were recorded with a simultaneous jugular phlebogram, apex cardiogram, and carotid pulse tracing. In 44 patients an apical fourth heart sound coincident with the 'a' wave of the apex cardiogram was recorded, and in 32 (73%) the fourth heart sound was audible and recordable in the right supraclavicular fossa. A left ventricular third heart sound, coincident with the rapid filling wave of the apex tracing, was present in 25 patients but was recorded in the right supraclavicular fossa in only 7 (28%). Intracardiac phonocardiography (high-fidelity catheter) was performed in six patients with left ventricular gallop sounds and in each instance arterial transmission of the third or fourth heart sound, or both, was present. Five additional patients had a prominent jugular venous 'a' wave, but only two had a soft parasternal fourth heart sound. Intracardiac phonocardiography in these five patients failed to reveal transmission of right ventricular gallop sounds to the superior vena cava. We conclude that since left ventricular gallop sounds commonly are transmitted to the right supraclavicular fossa auscultation in this area is often helphful in their detection. In addition, a prominent jugular venous 'a' wave sometimes produces recordable presystolic vibrations that are occasionally audible as well.  (+info)

Use of tissue velocity imaging in the diagnosis of fetal cardiac arrhythmias. (7/46)

BACKGROUND: Precise diagnosis of cardiac arrhythmias in the fetus is crucial for a managed therapeutic approach. However, many technical, positional, and gestational age-related limitations may render conventional methods, such as M-mode and Doppler flow methodologies, or newer techniques, such as fetal electrocardiography or magnetocardiography, difficult to apply, or these techniques may be unsuitable for the diagnosis of fetal arrhythmias. METHODS AND RESULTS: In this prospective study, we describe a novel method based on raw scan-line tissue velocity data acquisition and analysis. The raw data are available from high-frame-rate 2D tissue velocity images and allow simultaneous sampling of right and left atrial and ventricular wall velocities to yield precise temporal analysis of atrial and ventricular events. Using this timing data, a ladder diagram-like "fetal kinetocardiogram" was developed to diagram and diagnose arrhythmias and to provide true intervals. This technique was feasible and fast, yielding diagnostic results in all 31 fetuses from 18 to 38 weeks of gestation. Analysis of various supraventricular and ventricular arrhythmias was readily obtained, including arrhythmias that conventional methods fail to diagnose. CONCLUSIONS: The fetal kinetocardiogram opens a new window to aid in the diagnosis and understanding of fetal arrhythmias, and it provides a tool for studying the action of antiarrhythmic drugs and their effects on electrophysiological conduction in the fetal heart.  (+info)

Correlation between praecordial accelerocardiogram and left ventricular pressure. (8/46)

The praecordial accelerocardiogram possesses important practical advantages over more familiar techniques of recording praecordial pulsations. We have compared the amplitude of the P wave of the praecordial accelerocardiogram in 6 normal subjects (group 1) and 21 patients with heart disease (group 2) at rest and after 3 minutes of isometric handgrip at 30 per cent maximum voluntary contraction. At rest in group 2 there was a significant linear correlation between the amplitude of the P wave of the accelerocardiogram, relative to the maximum systolic amplitude (P/DE), and the left ventricular end-diastolic pressure (P less than 0-01). However, comparison of the data for P/DE showed that the mean value (+/-SEM) of 29+/-5 per cent in group 1 was not significantly different from the mean value of 37+/-4 per cent in group 2 (P g .reater than 0-30). During handgrip the mean amplitude of the P wave did not increase significantly in group 1 (P greater than 0-20) but increased significantly in group 2 (P less than 0-02). In group 2 there was a significant linear correlation between the percentage increase in the amplitude of the P wave of the accelerocardiogram during handgrip and the percentage increase in the left ventricular end-diastolic pressure (P less than 0-01).  (+info)

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