Heart-sound screening in children. Use of a portable analog-digital computer (field study--Los Angeles 1966).
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OBJECTIVE: To review evidence as to the precision and accuracy of clinical examination for aortic regurgitation (AR). METHODS: We conducted a structured MEDLINE search of English-language articles (January 1966-July 1997), manually reviewed all reference lists of potentially relevant articles, and contacted authors of relevant studies for additional information. Each study (n = 16) was independently reviewed by both authors and graded for methodological quality. RESULTS: Most studies assessed cardiologists as examiners. Cardiologists' precision for detecting diastolic murmurs was moderate using audiotapes (kappa = 0.51) and was good in the clinical setting (simple agreement, 94%). The most useful finding for ruling in AR is the presence of an early diastolic murmur (positive likelihood ratio [LR], 8.8-32.0 [95% confidence interval [CI], 2.8-32 to 16-63] for detecting mild or greater AR and 4.0-8.3 [95% CI, 2.5-6.9 to 6.2-11] for detecting moderate or greater AR) (2 grade A studies). The most useful finding for ruling out AR is the absence of early diastolic murmur (negative LR, 0.2-0.3 [95% CI, 0.1-0.3 to 0.2-0.4) for mild or greater AR and 0.1 [95% CI, 0.0-0.3] for moderate or greater AR) (2 grade A studies). Except for a test evaluating the response to transient arterial occlusion (positive LR, 8.4 [95% CI, 1.3-81.0]; negative LR, 0.3 [95% CI, 0.1-0.8]), most signs display poor sensitivity and specificity for AR. CONCLUSION: Clinical examination by cardiologists is accurate for detecting AR, but not enough is known about the examinations of less-expert clinicians.
Right ventriculography was used to assess the tricuspid valve in 61 patients with systolic murmur-click syndrome. Systolic murmurs were present in 47 cases, and 32 had clicks. Mitral valve prolapse was present in 52 patients. Late systolic prolapse of the tricuspid valve was demonstrated in 32 patients (52.4%). In 9 cases, prolapse involved the tricuspid valve alone. In the systolic murmur-click syndrome, prolapse may involve either or both of the atrioventricular valves.
The present report describes a patient with a whooping murmur secondary to tricuspid insufficiency. The main features of this tricuspid whoop were as follows: variable in time, moving from mid to late systole; unpredictably associated with normal respiratory phases; after deep inspiratory apnea was almost constantly present.
We evaluated the relationship of S1 recorded by phonocardiography at the mitral area with motion of the mitral, tricuspid, and aortic valves, recorded by simultaneous echocardiography in 20 cardiac patients with a normal PR interval. The first major component of S1 coincided with mitral valve closure in 20 of 20 patients (100%) and also with tricuspid valve closure in 14 of 20 patients (70%). The second major component of S1 coincided with aortic valve opening in 20 of 20 patients and also with tricuspid valve closure in six of 20 patients (30%). We conclude that the first major component of S1 coincides with mitral valve closure in all patients but may also coincide with tricuspid valve closure in many patients, and the second major component of S1 coincides with aortic valve opening in all patients but may also coincide with tricuspid valve closure in some patients.
A patient with a loud intermittent midsystolic click presented a problem in differential diagnosis between mitral valve prolapse (intracardiac origin of the click) and left pneumothorax (extracardiac origin). External phonocardiography performed at the time of cardiac catheterization revealed that this loud midsystolic click disappeared whenever a catheter was positioned across the mitral valve. It reappeared whenever the catheter was removed from the transmitral position. Selective left ventriculography confirmed the diagnosis of mitral valve prolapse.
Sudden momentary fluctuations of left ventricular, aortic, right ventricular, and pulmonary arterial pressure were noted during isovolumic relaxation of the respective ventricles. The presence of such transients raised questions related to their meaning and significance. The purpose of this report is to emphasize the nonartifactural nature of these pressure transients and to describe their origin and significance in the cardiac cycle. Pressure transients were observed in 31 of 32 patients with normal aortic valves, and in 17 patients with normal pulmonary valves in whom right-sided measurements were made. Such transients, however, were absent on the left ventricular and aortic pressure recordings of three patients with calcific aortic stenosis. These sudden changes in pressure are indicative of momentary compressions and rarefactions of the blood that occur within the ventricles and their respective arterial chambers. Whenever present, pressure transients were noted to occur coincident with the major aortic or pulmonary components of the second sound. Since intraaterial sound pressure is derived from the pressure signal by litering the low frequencies and amplifying the high frequencies, one can deduce that intraarterial sound pressure is in fact a representation of these pressure changes. The recognition of these pressure transients on an otherwise smooth ventricular, aortic, or pulmonary arterial pressure places in proper perspective their role in the production of the second heart sound.
Systolic honks have so far been synonymous with prolapse of the mitral valve leaflet. Evidence of tricuspid valve involvement in two cases is presented. These patients developed systolic honk during the deterioration of their congestive heart failure. Simultaneous recordings of echocardiograms and phonocardiograms showed fluttering of the tricuspid valve, coinciding with the systolic honk. This fluttering was not seen when honk was absent. The mechanism of production of this honk is discussed.
To enhance the bedside diagnosis of tricuspid regurgitation, the influence of manual pressure applied below the liver on lower left sternal border murmurs was determined in 23 patients. All 23 subjects had right ventriculograms and right atrial phonocardiograms. The sign was positive in 13 cases, including 3 who were without a Carvallo sign. The application of manual pressure below the liver is a simple and valid additional maneuver for identifying the murmur of tricuspid regurgitation.
A 37-year-old man was admitted to the hospital in order to evaluate the cause of systolic ejection heart murmur and to treat his easy fatigability. The chest roentgenogram showed a marked protrusion of the left second and third arches of the cardiac silhouette. At the diagnostic procedure, 200 ml of air was injected into the left thoracic space. The chest roentgenogram revealed no sign of pneumopericardium, but an abnormal extra heart sound was audible. Addition of another 200 ml of air was needed to reveal a pneumopericardium on the chest roentgenogram. A peculiar extra heart sound after artificial pneumothorax may be useful for the early recognition of congenital pericardial defect.
A systolic murmur discovered in antenatal care is the most common reason for cardiological assessment during pregnancy. We have assessed the value of clinical and echocardiographic assessment in 50 consecutive patients who were referred to our cardiac clinic following the discovery of a cardiac murmur at an antenatal clinic. Most of the murmurs occurred at 10-12 weeks gestation; 46 subjects had cardiac murmurs confirmed at the cardiac clinic, of whom 16 gave a history suggestive of a previous cardiovascular disorder. Of the 16 patients, 13 had been found to have a murmur earlier in life which was thought to be of no clinical significance. Complications during pregnancy were infrequent. The most frequent murmur discovered was a soft midsystolic murmur heard with greatest intensity at the left sternal edge. The results of electrocardiography and echocardiography were not helpful in assisting with the diagnosis or substantially altering antenatal management in these patients. We do not feel that echocardiography has an important role in the assessment of systolic murmurs in pregnancy in the absence of other clinical or ECG abnormalities.
Frequency analysis of first heart sound in elderly and expired cases was performed to reveal changes of the cardiovascular system accompanying aging. The vibration was analyzed for isometric contraction phase or 0.06 seconds following the main vibration of first sound by means of fast Fourier transform technique, and main frequency was compared. Mean main frequencies were 43.0 +/- 15.4 cps (mean +/- SD) in 21 cases from 54 years to 69 years, 41.4 +/- 12.6 cps in 34 cases from 70 years to 79 years, 40.0 +/- 14.4 cps in 19 cases from 80 years to 89 years, and 44.2 +/- 4.5 cps in 4 cases from 90 years to 94 years. It was 44.4 +/- 8.0 cps in 6 cases with left ventricular hypertrophy (LVH) on ECG, and 37.2 +/- 7.5 cps in 18 cases without LVH. It was 35.7 +/- 6.5 cps in 9 cases who expired and 32.6 +/- 5.8 cps in cases of those who died within a year. Though mean main frequencies were almost equal in these groups, it is higher than that of younger subjects, which suggests stiffness of the cardiovascular system of the aged. It was suggested that the stiffness of the cardiovascular system is greater than the increase in cardiac weight of elderly subjects with LVH. Mean main frequency was low in subjects who dies within a year, which may be due to cardiomegaly.
Between January and September 1985, 476 patients underwent two-dimensional and M-mode echocardiography. Left ventricular bands were noted in 104 of these individuals. Of these patients, 89 (85.6%) were referred for evaluation of a systolic murmur. In view of this high incidence of association between left ventricular bands and systolic murmurs, we decided to perform a prospective analysis on patients with the classical vibratory systolic murmur (Still's murmur) which is commonly found in children and young adults. The incidence of left ventricular bands would be compared with a group of individuals in whom no cardiac murmurs could be detected. It was hoped in this way to possibly determine whether there was a definite relationship between the vibratory systolic murmur and left ventricular bands. Echocardiographs were performed using an Advanced Technical Laboratories machine and gain settings were adjusted such that all artefacts and normal structures could easily be distinguished from the ventricular bands. The ventricular bands were divided into two types. Of significance, we felt, were those which crossed the left ventricular outflow tract and which could therefore have been responsible for the production of turbulence and thus a murmur reminiscent of the Still's murmur. This type of left ventricular band was noted in 76% of our patients with Still's murmurs as opposed to only 14% of the individuals without any murmur (p less than 0.001). This statistically significant difference led us to conclude that left ventricular bands might be the cause of the Still's murmur. Further investigation, particularly with Doppler studies would be required to confirm this interesting association.
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