Letter: Significance of fourth heart sound and split first heart sound.
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BACKGROUND: The presence of third heart sounds in patients with valvular heart disease is often regarded as a sign of heart failure, but it may also depend on the type of valvular disease. METHODS: We assessed the prevalence of third heart sounds and the relation between third heart sounds and cardiac function in 1281 patients with six types of valvular heart disease. RESULTS: The prevalence of third heart sounds was higher in patients with mitral regurgitation (46 percent) or aortic regurgitation (28 percent) than in those with aortic stenosis (11 percent) or mitral stenosis (8 percent). The left ventricular ejection fraction was significantly lower (P less than 0.001) when a third heart sound was detected in patients with aortic stenosis (0.38, vs. 0.56 in those without third heart sounds) or mixed aortic valve disease (0.40 vs. 0.55). However, the ejection fraction was only slightly lower in patients with mitral regurgitation and third heart sounds (0.51 vs. 0.57, P = 0.03). The pulmonary-capillary wedge pressure was higher (P less than 0.001) when a third heart sound was detected in patients with aortic stenosis (18.6 mm Hg, vs. 12.1 mm Hg in those without third heart sounds). There was no association between the wedge pressure and third heart sounds in patients with mitral regurgitation. The prevalence of third heart sounds increased with the severity of mitral regurgitation. CONCLUSIONS: In patients with mitral regurgitation, third heart sounds are common but do not necessarily reflect left ventricular systolic dysfunction or increased filling pressure. In patients with aortic stenosis, third heart sounds are uncommon but usually indicate the presence of systolic dysfunction and elevated filling pressure.
The study investigates the genesis of the third heart sound (S3) in ischemic heart disease based on a mass-spring model. In such a system, the natural frequency of vibration, Fn, depends on the elastic constant, k, and the mass, m, according to the following relationship: Fn = 1/2 pi square root of k/m. To identify the cardiac structures representing k and m, the correlations between the energy of the S3 spectrum and the echocardiographic parameters were searched for. The results are consistent with a model in which k is represented by the thickness of the left ventricle and m by its blood content. The k/m ratio emerges as an important determining factor of the acoustic quality of S3, and yields information on the dysfunction of the left ventricle in ischemic heart disease.
Two main theories exist concerning the origin of the heart sounds. The first proposes that rapid pressure fluctuations cause the cardiac valve leaflets to vibrate and produce the sound. The second theory suggests that sudden pressure perturbations cause the entire cardiohemic mass to vibrate as a whole. In 35 patients (26 men and 9 women, aged 18 to 73) with various heart diseases microtransducer catheters (Millar) were used to simultaneously record aortic pressures and aortic internal phonocardiograms in order to determine if they had a common mode of origin and propagation. The propagation velocities of the first heart sound and the foot of the aortic pressure pulse were found to be similar, 5.24 +/- 0.61 m/s and 5.97 +/- 1.87 m/s respectively (+/- SE). It was possible to derive facsimiles of the aortic internal phonocardiogram by double differentiation of the corresponding aortic pressure pulse and conversely to derive the pressure pulse by double integration of the phonocardiogram. These data support the concept that the low-frequency pressure variations produced by the entire cardiohemic mass, which predominate in the aortic pressure pulse waveforms, are generated and propagated in the same manner as the high-frequency pressure variations, which are the first and second heart sounds.
The normal heart sounds, murmurs, opening and closing sounds of aortic and mitral valve prostheses were recorded on a tape and analyzed in terms of contour sonagrams in order to obtain the highest frequencies which were recordable on the chest wall. The peak frequencies showed a broad range, the maximum beeing reached at about 8000 c.p.s. in the case of the sounds of prosthetic valves. Furthermore, sound level examinations of the normal first and second heart sound, as well as of the opening and closing sounds of the aortic valve prostheses were performed. The highest sound level of all of these sounds was found to lie within the low frequency range of 40 to 100 c.p.s.
The normal heart sounds, murmurs, opening and closing sounds of aortic and mitral valve prostheses were recorded on a tape in order to obtain the highest frequencies which were recordable on the chest wall. Sections of these tapes were analyzed in terms of contour sonagrams. For this purpose six groups were formed and investigated: group I comprised persons without cardiovascular diseases, group II patients with mitral valve failure, group III patients with aortic valve failure, group IV patients with congenital heart disease, group V patients with Starr-Edwards aortic valve prostheses (model 1260) and group VI patients with various mitral valve prostheses. In each of these groups the highest recordable frequencies were measured. The peak frequencies varied widely in regard to frequency range in a comparison of the six groups. The maximum was reached at about 8000 c.p.s. in the case of the sounds of prosthetic valves. Furthermore, sound level examinations of the normal first and second heart sounds, as well as of the opening and closing sounds of the aortic valve prostheses were performed. The highest sound level of all of these sounds was found to lie within the low frequency range of 40 to 100 c.p.s. The results of both the measurements of the peak frequencies and of the maximal sound level were discussed on the basis of the presently accepted theories on the mechanism of heart sounds and murmurs.
An index to quantify the contamination of lung sounds by heart sounds is described. Using the index, the efficacy of high pass filtering and adaptive filtering methods for the reduction of heart sounds is evaluated.
A 32-week fetus was demonstrated phonocardiographically and echocardiographically to have a regular atrial rate of 150 per minute and a regular ventricular rate of 39 per minute, indicating complete heart block. The diagnosis was suspected when two groups of heart sounds at two distinct rates were heard on auscultation, and was confirmed by the postnatal ECG. The maternal history was significant for the presence of systemic lupus erythematosus. The basis for the echocardiographic diatnosis of complete heart block, the presence of atrial heart sounds in complete heart block, and the relationship of maternal SLE to congenital heart block are discussed.
The third heart sound (S3) is observed for various hemodynamic conditions in both the normal and diseased heart. A theory is proposed in which myocardial viscoelasticity is primarily responsible for S3. A mathematical model is developed based on the mechanical aspects of diastolic function: nonlinear elasticity, viscoelasticity, and pressure generation. The model is provided as an electrical analogy of the left ventricle and circulatory system. S3 is predicted for the normal heart and the heart with dilated cardiomyopathy. An elevation of S3 intensity is indicated for cardiomyopathy, as is often observed in the clinic. S3 is produced experimentally by volume loading of the open-chest canine preparation and mathematically by imposing the conditions of volume loading on the model. Consistency of theory and experiment imply that it is valid to attribute S3 to myocardial viscoelasticity. The animal whose heart possessed the largest constant of viscoelasticity produced the greatest level of S3, in both cases. Nonlinear ventricular compliance is not found to be an essential requirement for sound generation, although increased compliance led to an increase in sound. S3 is predicted to change in response to venous return, ventricular stiffness, contractility, heart rate, and duration of contraction, as observed by others. In general, the coupling of these quantities to S3 is explained in terms of an excitation of viscous properties of the ventricle.
The occurrence and timing of heart sounds were examined from phonocardiograms taken from the mitral, aortic and tricupsid recording areas in each of 18 horses. 10 sound events could be identified with each cardiac cycle. Atrial contraction produced up to 3 sound events. The first heart sound consisted of 4 components whereas the second sound was single. Two sound events were associated with the 3rd heart sound in early diastole. The occurrence of third and fourth heart sound components varied between horses and between recording areas. The mitral recording area was considered most satisfactory for routine phonocardiographic studies in horses.
An early diastolic sound in a patient with apical left ventricular disease is reported. Pulsed Doppler echocardiography showed blood flow within the left ventricular cavity during the isovolumic relaxation period whose peak flow velocity was synchronous with the onset of this diastolic sound. Because it occurred before filling started it could not have been either a third or fourth heart sound. It must thus represent a distinct and apparently unrecognised class of diastolic sound.
Although the third heart sound (S3) is well recognized as an important sign in the evaluation of patients with congestive heart failure, the interobserver variability with its observation needs to be known before general applicability can be determined. Therefore, we determined the agreement among four trained observers on the presence of S3 in 81 hospitalized patients. Agreement between pairs of observers varied between 48 and 73 percent. The kappa statistic, which adjusts for agreement by chance alone, showed that agreement between various observer pairs was moderate (kappa = 0.40-0.50) at best and slight (kappa = 0.10-0.30) at worst. The rate of agreement did not appear to be affected by the time interval between measurements, by the sex of the patient or by a training effect over the time of the study. In conclusion, although S3 may be important as a clinical sign, clinicians cannot agree reliably about whether or not it is present.
A phonocardiological analysis of the first heart sound was made and systolic time intervals were measured in 40 patients (ischaemic heart disease, hypertensive heart disease, cardiomyopathies) with incipient cardiac failure (functional groups I--II according to the NYHA) with auscultatory changes of the first heart sound and in controls of randomly selected healthy persons or patients in whom cardiopulmonary disease was excluded. The patients in all diagnostic groups differed significantly (P less than 0.05--0.001) in practically all the phonocardiographic indicators from the controls. The most constant abnormal finding was a pathological split of the first heart sound which may be divided into three phonocardiographic forms. Simultaneously, systolic time intervals alterations (P less than 0.02--0.001) were also found in these patients and indicated a lowered performance of the left ventricle. The results suggest that 1) a certain relation exists between systolic time intervals and the phonocardiographic pattern of the first heart sound in patients with cardiovascular diseases and those without it; 2) the modified (pathologically splitted and prolonged) first heart sound could be a sign of incipient cardiac failure.
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When a loud second heart sound is heard in a child, the possibility of pulmonary hypertension must be borne in mind. The second heart sound is also loud in patients with congenitally corrected transposition (CGT) because of the anterior position of the aortic valve. Therefore, it is difficult to distinguish the relatively rare isolated CGT from cardiac disease with high pressure in the pulmonary artery. We discuss this diagnostic problem on the basis of a two year old boy with a loud second heart sound.