Sound pressure correlates of the Austin Flint murmur. An intracardiac sound study.

Mitral valve motion and pressure correlates of the Austin Flint murmur (AFM) were investigated in nine patients with aortic regurgitation using high fidelity catheter tip micromanometers and the mitral valve echocardiogram (MVE). External phonocardiography demonstrated a mid-diastolic murmur (MDM) in eight subjects and a presystolic murmur (PSM) in five. Maximum intensity of both AFM components was found in the left ventricular (LV) inflow tract; the murmur was not recordable in the left atrium (LA). In two patients, an apparent AFM was recorded in the intracardiac phonocardiogram when absent externally. Only one subject had a significant late diastolic "reversed" or LV to LA gradient; in this patient, presystolic mitral regurgitation was shown angiographically but no PSM was present and MVE revealed absence of atriogenic mitral valve re-opening. In two subjects, a PSM disappeared from the external phono when a "reversed" gradient occurred during the diastolic pause following a ventricular premature systole; this LV to LA gradient was associated with diastolic mitral regurgitation recordable in the left atrial phono. In two patients, LV inflow phono showed the MDM to begin 80-120 msec after the aortic second sound and during the D to E phase of the MVE. The rate of early diastolic mitral valve closure in patients (152 +/- 24 mm/sec) was not significantly different from 13 normals (232 +/- 10 mm/sec). With regard to the genesis of the AFM, the present study concludes: 1) diastolic mitral regurgitation plays no role, and 2) antegrade mitral valve flow is required but simultaneous retrograde aortic flow may also be necessary.     

Early diastolic clicks after the Fontan procedure for double inlet left ventricle: anatomical and physiological correlates.

M mode echocardiograms and simultaneous phonocardiograms were recorded in four patients with early diastolic clicks on auscultation. All had double inlet left ventricle and had undergone the Fontan procedure with closure of the right atrioventricular valve orifice by an artificial patch. The phonocardiogram confirmed a high frequency sound occurring 60-90 ms after aortic valve closure and coinciding with the time of maximal excursion of the atrioventricular valve patch towards the ventricular mass. One patient had coexisting congenital complete heart block. The M mode echocardiogram showed "reversed" motion of the patch towards the right atrium during atrial contraction. Doppler flow studies showed that coincident with this motion there was forward flow in the pulmonary artery with augmentation when atrial contraction coincided with ventricular systole. The early diastolic click in these patients was explained by abrupt cessation of the motion of the atrioventricular valve patch towards the ventricular mass in early diastole. In one patient atrial contraction led to a reversal of this motion and was associated with forward flow in the pulmonary artery.     

Noninvasive stress testing. Methodology for elimination of the phonocardiogram.

Measurement by systolic time intervals (STI) of cardiac responses requires extremely careful recording during actual stress test performance. Previous work indicated no significant changes in the pulse transmission time (PTT) during exercise and other challenges. Since external STI depend on the carotid pulse offset by the PTT as an aortic curve equivalent, stable PTT implies that timing of the carotid upstroke (CARu) and the carotid incisura (CARIN) would respectively track the pre-ejection period (i.e., the externally calculated onset of the aortic upstroke) and the aortic incisura which is externally timed by the aortic component of SII (IIA). In ten subjects, STIs were recorded at supine rest, sitting, standing, during prompt and sustained squatting and during isometric and dynamic exercise. The results demonstrated the tracking of both points: regression slopes and correlation coefficients were close to 1.00 for each series and for each subset. Coefficients of correlation (r) and of determination (r2) were uniformly high for all challenges except isometric handgrip (IHG). Since left ventricular ejection time is obtained directly from the pulse curve, with the exception of IHG, STI responses during stress testing can be measured without a phonocardiogram.     

Time relation between apex cardiogram and left ventricular events using simultaneous high-fidelity tracings in man.

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.     

Time relation between apex cardiogram and left ventricular events using simultaneous high-fidelity tracings in man.

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.     

Early diastolic clicks after the Fontan procedure for double inlet left ventricle: anatomical and physiological correlates

M mode echocardiograms and simultaneous phonocardiograms were recorded in four patients with early diastolic clicks on auscultation. All had double inlet left ventricle and had undergone the Fontan procedure with closure of the right atrioventricular valve orifice by an artificial patch. The phonocardiogram confirmed a high frequency sound occurring 60-90 ms after aortic valve closure and coinciding with the time of maximal excursion of the atrioventricular valve patch towards the ventricular mass. One patient had coexisting congenital complete heart block. The M mode echocardiogram showed "reversed" motion of the patch towards the right atrium during atrial contraction. Doppler flow studies showed that coincident with this motion there was forward flow in the pulmonary artery with augmentation when atrial contraction coincided with ventricular systole. The early diastolic click in these patients was explained by abrupt cessation of the motion of the atrioventricular valve patch towards the ventricular mass in early diastole. In one patient atrial contraction led to a reversal of this motion and was associated with forward flow in the pulmonary artery.     

Considerations on the mechanism of the systolic click of mitral valve prolapse

The Authors briefly discuss the mechanism of production of the systolic click of mitral valve prolapse. A "valvular" mechanism seems inadequate to explain the genesis of vibrations that can be recorded, not only in the external phonocardiogram, but also in the intraventricular pressure tracing, in the apex cardiogram, and even in the left atrial pulse (esophagus). It seems more logical to postulate that the force of deceleration created by the sudden eversion of a mitral leaflet set the whole cardiohemic system (blood, myocardial walls, and the mitral apparatus) into vibration, thus producing the click. In mitral valve prolapse, the contribution to sound production of mitral leaflets and chordae is likely to be minor, as it had been demonstrated for the first heart sound.     

Noninvasive index of cardiac contractility during stress testing: a collaborative study

The present study was conducted in parallel in three different institutions with a similar purpose but using different technical setups. Based on the experimental demonstration that the external phonocardiogram is similar to the rate of acceleration (d3P/d3t) of the left ventricular pressure, and that catecholamines in a similar way increase the early positive wave of the left ventricular pressure and the first heart sound (S1) of the external phonocardiogram; knowing that exercise causes secretion of catecholamines and sympathetic reflexes, we have studied the S1 changes as a result of exertion in 34 normal young subjects. Blood pressure, heart rate, electrocardiograph, and phonocardiograph recordings of each subject were taken. In 10 subjects, cardiac output was also recorded by impedance cardiography. The result of the study was that the first heart sound increased routinely 4-5 times the normal amplitude; in a few subjects the increase was up to 15 times greater. While the extent of increase of S1 was proportional to the severity and duration of the effort and was usually proportional to the increase of other parameters, exceptions were noted as having marked increase of S1 with moderate increase of either blood pressure or heart rate. This was explained by the different receptors activated by the catecholamines and by the complexity of hormonal and neural influences acting on various organs in a stress test. The amplitude of S1 was found to be a reasonably reliable index for following changes of cardiac contractility during exercise, and the suggestion was made that this parameter should be studied in parallel with the others in routine stress tests.     

Genesis and clinical significance of the "low-pitched" aortic ejection sound

The genesis and clinical significance of the aortic ejection sound with a low-frequency predominance and delayed appearance were studied. This is recorded on the phonocardiogram in some patients with left ventricular dysfunction. Subjects studied consisted of 10 patients with a low-pitched ejection sound and seven patients with an ordinary high-pitched aortic ejection sound. No patients had echocardiographic findings suggestive of organic lesions of the aortic valve. Time relationships among the ejection sounds, aortic valve echograms and carotid artery pulses, and then movements of the aortic valve cusps and non-invasively estimated left ventricular systolic function were compared between the two groups. Results were as follows: 1. The low-pitched ejection sound: 1) The beginning of the sound was nearly coincident with the onset of the upstroke of the carotid artery pulse and the initial full opening of the aortic valve cusps. 2) The beginning of the ejection systolic murmur followed immediately after the ejection sound. 3) The amplitude of the sound was closely related to the height of the carotid artery pulse in a case of atrial fibrillation. 2. The low-pitched ejection sound vs the high-pitched ejection sound: 1) The onset of the low-pitched ejection sound was significantly delayed. 2) The amplitude and the velocity of the initial opening of the aortic valve cusps were significantly decreased. 3) The preejection period (PEP) was significantly prolonged; the ejection time (ET) was significantly shortened; and the PEP/ET ratio was significantly increased.(ABSTRACT TRUNCATED AT 250 WORDS)     

Complete right bundle-branch block: echophonocardiographic study of first heart sound and right ventricular contraction times.

High speed enchocardiograms of the mitral, tricuspid, and pulmonary valves were recorded with a simultaneous electrocardiogram and phonocardiogram in 20 patients with complete right bundle-branch block and in 67 normal subjects. Late opening of the pulmonary valve indicating late right ventricular ejection was found in all patients. In 8 patients with wide splitting of the first heart sound the late ejection was related mainly to delay in tricuspid valve closure, suggesting a late onset of the right ventricular pressure pulse. In 10 patients with a single first heart sound the delayed ejection was associated with a long interval between tricuspid valve closure and pulmonary valve opening, suggesting a slow rising right ventricular pressure pulse; 3 of these patients also had late tricuspid valve closure but the tricuspid component of the first sound was absent. Late onset of pressure rise is thought to result from block in the main right bundle-branch, and a slow rising pulse from block in the distal Purkinje network. These findings explain the conflicting results in previous studies of the first heart sound and right ventricular pressure pulse in patients with right bundle-branch block, and may have prognostic significance.     

The double femoral sound

A double femoral sound is described in patients with congestive heart failure of varied etiology. The factor common to all patients was a powerful atrial contraction secondary to increased right ventricular diastolic pressure or increased resistance to right ventricular filling. The first sound is produced by atrial systole transmitted by the venae cavae to the femoral veins; the second sound by left ventricular systole transmitted by the aorta to the femoral arteries.     

Complete right bundle-branch block: echophonocardiographic study of first heart sound and right ventricular contraction times.

High speed enchocardiograms of the mitral, tricuspid, and pulmonary valves were recorded with a simultaneous electrocardiogram and phonocardiogram in 20 patients with complete right bundle-branch block and in 67 normal subjects. Late opening of the pulmonary valve indicating late right ventricular ejection was found in all patients. In 8 patients with wide splitting of the first heart sound the late ejection was related mainly to delay in tricuspid valve closure, suggesting a late onset of the right ventricular pressure pulse. In 10 patients with a single first heart sound the delayed ejection was associated with a long interval between tricuspid valve closure and pulmonary valve opening, suggesting a slow rising right ventricular pressure pulse; 3 of these patients also had late tricuspid valve closure but the tricuspid component of the first sound was absent. Late onset of pressure rise is thought to result from block in the main right bundle-branch, and a slow rising pulse from block in the distal Purkinje network. These findings explain the conflicting results in previous studies of the first heart sound and right ventricular pressure pulse in patients with right bundle-branch block, and may have prognostic significance.     

Systolic time intervals in induced atrial fibrillation in the dog.

The effect of induced atrial fibrillation on ventricular performance in the dog as measured by changes in the systolic time intervals (STI), was investigated. Atrial fibrillation was induced by enhancement of vagal tone with morphine sulfate, followed by direct mechanical stimulation of the atrium. Dogs received 15 mg. per kilogram of morphine sulfate subcutaneously, followed by 3 mg. per kilogram of pentobarbital sodium. ECG, atrial electrogram, phonocardiogram, and direct arterial blood pressure were recorded during periods of sinus rhythm and during periods of induced atrial fibrillation. Data were analyzed by selecting 20 representative cardiac cycles from each condition in each of 15 dogs. Cycles were selected so that the broadest spectrum of rates was examined for each animal. Three hundred cycles were examined from each condition, or a total of 600 cycles. Heart rate (HR), left ventricular end-diastolic pressure, and aortic end-diastolic pressure were unchanged during atrial fibrillation. The left ventricular pre-ejection period (LVPEP), externally derived isovolumic contraction time (EICT), and total mechanical systole (S1-S2 interval) were all found to increase significantly in duration after the induction of atrial fibrillation. The left ventricular ejection time (LVET) and the electromechanical delay (Q-S1 interval) were significantly decreased in duration following the induction of atrial fibrillation.     

“Mapping” the precordium I. Heart sounds of normal subjects

A systematic study of the amplitude of the heart sounds was made in 30 normal subjects (10 young men, 10 young women, and 10 children). It was based on the graphic recording of the amplitude of the main component of the first heart sound, the aortic component of the second heart sound, and the pulmonary component of the second heart sound. Special attention was paid to the exact constancy of amplification and condition of recording. Tracings were recorded over eight precordial areas.

The first heart sound was found generally largest over the left parasternal areas; exceptions were represented by cases having a largest first sound at the apex, at the fifth sternal or fourth right parasternal area, or even at the second right space. No basic difference existed in the maximal amplitude and spread of the first two components of the first sound.

The aortic component of the second heart sound was found largest generally in the third left parasternal area. Exceptions were represented by cases having a largest aortic component over the second or fourth left parasternal area.

The third and fourth sounds, when recorded in children, had maximal amplitude in the left parasternal areas.

These data confirm a recent systematization of the auscultatory areas of the precordium but are in contrast with older views on the classic areas of auscultation of the heart.     

Effect of turbulent blood flow on systolic pressure contour in the ventricles and great vessels: Significance related to anacrotic and bisferious pulses

The effect of turbulent blood flow on the contour of systolic pressure in the left and right ventricles and great vessels was investigated in 64 patients undergoing diagnostic cardiac catheterization. Intracardiac pressure and sound were recorded using a catheter-tip micromanometer. Measurements were made in normal subjects and patients with a variety of disorders including aortic stenosis, hypertrophic obstructive cardiomyopathy, coarctation of the aorta and atrial septal defect. Observations showed a consistent association of the intracardiac murmur, which is indicative of turbulence, with a transient reduction of the centrally recorded systolic pressure. The resultant abnormal systolic pressure contour can be explained on the basis of fluid dynamic considerations related to turbulence.     

Left to right atrial shunting in tricuspid atresia.

In tricuspid atresia, an obligatory right to left shunt occurs at the atrial level. We have observed several patients with left to right interatrial shunts. Data from cardiac catheterisation in 40 consecutive patients were reviewed to determine the frequency and mechanism of left to right shunting in tricuspid atresia. An increase of 6% or more in oxygen saturation between the superior vena cava and the right atrium in two or more sets of saturations, representing a left to right shunt, was present in 29 out of 50 (58%) catheterisations in which the data were adequate. In most, the shunt was also seen cineangiographically in the laevophase. In only two catheterisations was an anatomical cause (ostium primum atrial septal defect in one and anomalous pulmonary venous return in the other) found. In the remaining 27 catheterisations, no anatomical cause was found. Age, Qp:Qs, and mean atrial pressure difference were similar between the shunt and non-shunt groups. In the shunt group right atrial "a" waves were equal to or higher than left atrial "a" waves and left atrial "v" waves were equal to or higher than right atrial "v" waves. Simultaneous pressure recordings (in one patient with left to right atrial shunt) from the left atrium and right atrium with isosensitised miniature pressure transducers mounted 5 cm apart showed (1) a higher pressure in the right atrium than in the left atrium during atrial systole and (2) a higher pressure in the left atrium than in the right atrium during atrial disatole. It is concluded that (a) left to right shunt across the atrial septum occurs frequently in tricuspid atresia and (b) the left to right shunt is the result of instantaneous pressure differences between the atria.     

Polycardiographic study of atrial flutter.

The modifications that atrial flutter determines on the phonocardiogram, apexcardiogram, carotid pulse tracing, jugular venous pulse tracing, and indirect (esophageal) left atrial pulse tracing were studied. On the basis of the data here presented and that of the literature, a polygraphic profile of atrial flutter has been constructed as follows: notable variability of the intensity and of the richness of the vibratory components of the first and second heart sound; regularly alternating intervals between successive atrial sounds, each one of which consists of two groups of vibrations; deformations of all mechanographic tracings corresponding with "F" waves of the ECG. The interpretation of various polygraphic reports contributes to the understanding of the physiopathogenesis of atrial flutter.     

The first heart sound in normal and pathological conditions

Considerations of the physical basis of cardiac contraction and sound generation explain the mechanism of the first sound. Older theories examining this sound as the result of valve closure or stiffening are refuted. It has been demonstrated that the normal first sound originates in the left ventricle alone and that accelerations and decelerations, "timed" by mitral and aortic valves events, are its cause. Three components have been recognized in the first sound: a occurs when the left ventricular wall and septum have reached a certain tension; b when the aortic valve opens; c when the peak of the aortic pulse has been reached. The ventricular septum is an integral and essential part of the left ventricle. In left bundle branch block, abnormal activation of the septum transforms this into a passive structure resulting in a slower rise of left ventricular pressure and a longer isovolumic period. This causes a small and delayed first sound, whose components, however, are still separated by normal intervals. In right bundle branch block, the first sound has a normal amplitude and its components are separated by normal intervals. If there is a larger late component, it is a c component, similar to that of normal elderly subjects. A larger c component may also be found in atrial septal defect. The cannon sound of AV block is caused by more rapid deceleration due to higher atrial pressure at the onset of ventricular contraction resulting in intense vibrations. The first sound of arrhythmias varies in the different conditions and even in different subjects, due to the effect of several variable factors. Elevated left atrial pressure, stiffening of the mitral valve in mitral stenosis, causes a slow onset and a more rapid rise of LV pressure. This results in a delayed, but larger, first sound. The action of catecholamines on the myocardium dramatically increases the first sound. The latter can be considered as an index of contractility and may be of great interest during stress tests.     

A case of secundum atrial septal defect combined with aortic stenosis and coronary artery disease showing a single second heart sound

We describe an extremely rare case of secundum atrial septal defect with aortic stenosis and coronary artery disease showing a single second heart sound throughout the respiratory cycle by echocardiogram with simultaneous phonocardiogram. Aortic valve closure corresponded to the single second heart sound. We were unable to detect pulmonary valve closure (PVC) on echocardiogram. Because of the presence of pulmonary hypertension, the pulmonary component of the second heart sound (P2) was presumed to be increased in intensity, and the PVC-P2 interval was thought to be abbreviated. Carotid pulse tracing showed a prolongation of the left ventricular ejection time. We concluded that the single second heart sound was due to both prolongation of left ventricular systole and pulmonary hypertension.     

Aortic valve closure: echocardiographic, phonocardiographic, and hemodynamic assessment.

The temporal relationship between the closure of the aortic valve (AoV) and the onset of the aortic component of the second heart sound (A2) was defined by simultaneous recording of AoV echogram, phonocardiogram (PCG), and electrocardiogram in 25 subjects. Ten subjects had no heart disease (normal); 15 suffered from various cardiac conditions other than AoV disease (patients). The point of coaptation (C) of the AoV cusps to the onset of A2, the C-A2 interval, was measured to the nearest 5 msec. in 125 cycles. Fifty-eight cycles had a C-A2 of 10 msec., and 47 cycles had a C-A2 of 15 msec. The remainder were distributed at intervals below 10 or above 15 msec. The average C-A2 interval was 11.48 +/- 0.38 msec. (mean +/- 1 S.D.). A similar distribution pattern was observed when the total number of cycles was divided into "normal" and "patient" groups. In 3 subjects, simultaneous equisensitive (catheter-tip micromanometer) left ventricular and central aortic pressures, PCG, and AoV echograms were recorded. C-A2 ranged from 0 to 10 msec.; the interval between left ventricular and aortic pressure at the level of the incisura-hangout interval-ranged from 8 to 20 msec. Inhalation of amyl nitrite in one subject produced a significant fall in arterial pressure, accompanied by prolongation of the hangout interval from 10 to 20 msec. and of the C-A2 interval from 0 to 8 msec. Thus, the C-A2 interval is an integral part of the hangout time. Data suggest that A2 does not originate from the coaptation of the aortic valve cusps per se, but is related to events that occur at the time of or slightly after coaptation.