The Austin Flint Murmur

Phonocardiographic and Patho-anatomical Study

Hideo UEDA, M. D., Tsuguya SAKAMOTO, M. D., Nobuyoshi KAWAI, M. D., Hiroshi WATANABE, M. D., Zen'ichiro UozuMI, M. D., Ryozo OKADA, M. D., Tohru KOBAYASHI, M. D., Tetsuro YAMADA, M. D., Kiyoshi INOUE, M. D., and Goro KAITO, M. D.

Clinical, phonocardiographic and patho-anatomical studies were made on 15 cases with the Austin Flint murmur. The phonocardio- graphic characteristics were pointed out, and the mode of production of this murmur was explained based on the patho-anatomy of the . Several typical cases were illustrated.

INCE the last century, the Austin Flint murmur, a well-known apical diastolic rumble in ,1) has been extensively debated by many authors. 2)-49) However, despite the ample arguments on the incidence, acoustic and graphic characteristics, clinical background and cardiac patho- logy, a comprehensive study with the phonocardiographic as well as patho- logic confirmation has not been attempted up to the present time. The purpose of the present study is, therefore, to investigate these figures based on the clinico-pathological observations. Particular attention was paid to search for the auscultatory and phonocardiographic characteristics of the Austin Flint murmur, and to observe whether any patho-anatomical factors seem to be responsible for the production of this murmur.

MATERIAL AND METHOD

Out of the autopsy cases from the Second Department of Internal Medicine,

Tokyo University Hospital, 14 cases of •gisolated•h aortic insufficiency had com-

plete clinical examination including phonocardiography. The cases with con- comitant •gorganic•h mitral insufficiency were not included in this series. All

cases but one were male, and the age ranged from 19 to 59 with an average of 44.

In all cases except one, the cause of death was congestive failure due to val-

vular disease. An exceptional case died of acute myocardial infarction in the early

stage of syphilitic aortic insufficiency and was excluded from this study because of

the absence of the manifest clinical pictures of aortic insufficiency. In addition to

these 13 cases, 2 autopsy cases of dissecting with the Austin Flint

From the Second Department of Internal Medicine, Faculty of Medicine, University of Tokyo Tokyo. 294 Vol. 6 No. 4 AUSTIN FLINT MURMUR 295 murmur were included in this study. Both were male and aged 25 and 38, re- spectively. All 15 patients had significant aortic insufficiency and had a wide pressure with undetermined diastolic pressure level (0mm.Hg). In all cases, was repeatedly performed and phonocardiographic investigation was made at least 2 times or more. The phonocardiograms were taken by the use of a multi-filter system phonocardiograph 50) and a dynamic microphone. During past 3 years, the phonocardiograms with same filter system were simultaneously recorded from 2 or more auscultatory areas using a photographic paper of 150mm. in width. In most cases in this study, both Low (L) and High (H) Frequency PCG were sim- ultaneously recorded from 2 areas, namely the maximal point of intensity of blow- ing and rumbling murmurs. This technique makes it easy and accurate to compare the exact time relationship and various graphic features of 2 kinds of murmur. Combined auscultatory and phonocardiographic investigation was attempted to determine the location, intensity, transmission, and all other characteristics of the Austin Flint murmur and the other auscultatory and phonocardiographic findings. The method was partly described in the previous paper. 51) For the analysis of diastolic rumble, 100 cases of proved pure mitral stenosis with sinus rhythm were utilized as a control. Patho-anatomical study was performed on the fresh specimen as well as after fixation in 20 % of Formalin. Microscopic examination was car- ried on the Hematoxylin-Eosin, Mallory's azan and Weigert van Gieson's stainings.

RESULT A. Auscultatory and Phonocardiographic Study of the Austin Flint Murmur 1) Incidence: All 15 cases had this murmur , irrespective of the ex- istence of congestive heart failure. Once it was noticed, it usually continued during life. No case was encountered in whom this murmur completely dis- appeared after appropriate therapy. 2) Cardiac rhythm: Almost all cases had sinus rhythm. Prolongation of P-R interval was in only one case. Atrial fibrillation was observed trans- iently in one case and in later stage in 2 including a case of dissecting aneurysm. 3) Maximal point of intensity: In all cases, this murmur was best heard and recorded around the cardiac apex. 4) Intensity: Eight cases had the Levine's grade 43)of more than III . Relatively faint murmur was observed in 4, whereas it was extremely loud (grade V) in one. 5) Transmission: Generally, loud Austin Flint murmur transmitted widely. Nine cases had clearly recordable murmur over 2 intercostal spaces. One case showed an extreme transmission over the entire precordium . In this case, the phonocardiogram at the maximum point of the blowing murmur showed the low-pitched rumbling murmur on the Low PCG, whereas High PCG showed the blowing murmur. Jap. Heart J. J 296 UEDA, ET AL. uly, 1965

6) Quality: The Austin Flint murmur had predominantly low-pitched components. Two cases frequently revealed musical quality of this murmur as well as of the first heart sound.

7) Timing: All cases had the mid-diastolic component. Presystolic

(atrio-systolic) component without unequivocal crescendo was observed in 12 cases. Two cases had no presystolic component even with the sinus rhythm.

8) Diastolic sounds: The third heart sound was recorded in all cases, but the auscultation was not able to separate clearly the third sound and mid-diastolic rumble in most cases. The atrial sound was recorded in 5 cases, but it was not clearly separable from the atrio-systolic murmur in 3 cases. A distinct mitral opening •gsnap•h was not observed, but an opening sound 52) was sometimes recorded.

9) Graphic configuration of the Austin Flint murmur: This murmur was exclusively recorded on the Low to Medium PCG and never inscribed clearly on the Medium-High to High PCG, except the case with an extra- ordinarily loud rumble. The mid-diastolic component was accompanied with the third sound and showed decrescendo character. However, this murmur frequently revealed the change in the configuration from cycle to cycle or from day to day. The atrio-systolic component had no crescendo character even with the and normal P-R interval.

10) Graphic analysis of presystolic component: In respect to the interval between the beginning of P wave and the peak amplitude of presystolic (atrio- systolic) component of this murmur, a comparison was made between 100 cases of pure mitral stenosis and 13 cases with the Austin Flint murmur during sinus rhythm. The peak of amplitude was determined in average in many successive beats, because this point of murmur was frequently variable in com- parison to that of mitral stenosis. In mitral stenosis, the peak amplitude was usually situated just before the first sound except the cases with prolonged

P-R interval. Generally speaking, the longer the P-R interval, the larger the

P-peak amplitude interval (Fig. 1). Such a tendency was similarly observed in cases with the Austin Flint murmur. However, distinct difference was such that the shorter P-peak amplitude interval in cases with the Austin Flint mur- mur. 11) Phonocardiographic findings other than the Austin Flint murmur: All cases had loud blowing regurgitant diastolic murmur of severe degree. 51) Namely, this murmur had a configuration of very short crescendo and relatively short decrescendo, giving scarcely holodiastolic character in many cases. The second heart sound at the base was accentuated in many, but it was not clearly heard at the apex. The first heart sound at the apex was not accentuated in all, but it was muffled in most cases, giving low frequency Vol. 6 No. 4 AUSTIN FLINT MURMUR 297

•œ Aortic insufficiency with Austin Flint murmur

•Z Pure mitral stenosis Fig. 1. Timing of the peak amplitude of the presystolic (atrio-systolic) com- ponent of the Austin Flint murmur. The interval between the beginning of the P wave and the peak amplitude (ordinate) of individual cases was plotted against the P-R interval of the electro- cardiogram (abscissa). See text.

and small amplitude vibration. Aortic ejection sound was not so prominent, and all cases had aortic ejection systolic murmur, which was musical in one. Except 2, this murmur was thought to be functional and was confirmed by autopsy. 12) The Austin Flint murmur in cases of dissecting aortic aneurysm: There was no peculiarity of the apical diastolic rumble of this disease com- pared with that of pure aortic insufficiency. One case had a normal sinus rhythm and the rumble of grade III was mid-diastolic in time, and it was grade IV in another. The latter had atria] fibrillation with complete A-V block and ventricular extrasystole due to digitalis intoxication from the begin- ning of our observation. The murmur of aortic insufficiency was loud in both cases and the murmur of relative aortic stenosis was also loud, accompanying a thrill. B. Patho-anatomical Study 1) Etiology of aortic insufficiency: At autopsy, the etiology of aortic insufficiency was syphilitic in 8 including one of congenital in origin. Rheum- Jap. Heart J. J 298 UEDA, ET AL. uly, 1965 atic etiology was thought in 6 cases. Relative aortic insufficiency was observed in 2 cases of dissecting aneurysm. Two of rheumatic and one of syphilitic cases suffered from subacute bacterial , and one case had bicuspid with rheumatic verrucous valvulitis. 2) Mitral valve: Mitral valve revealed no stenosis even in cases of rheumatic valvulitis, namely, commissural fusion indicating stenosis of mitral orifice was not observed in all cases. However, jet lesions of various degree caused by the aortic regurgitant blood flow were observed in all on the ventric- ular surface of antero-medial (anterior) leaflet of mitral valve. These lesions were of small to large focal endocardial thickenings (fibrosis and elastosis), and sometimes produced cup-shaped lesion which was thought to be the result of oblique regurgitant strikes. No intrusion of the aortic root into the mitral orifice was observed in cases with dissecting aneurysm. 3) Aortic valve: Except 2 with concomitant aortic stenosis, the destruc- tion of aortic valve was moderate to marked in all with organic aortic insuf- ficiency. A half of cases had the destruction of valve leaflet more than 15% compared to the aortic valve orifice, producing severe aortic insufficiency. The destruction of the central closing portion was observed in all cases, and it was the most significant cause of insufficiency in 4 cases. In these and others, there was no tendency that which valve cusp was severely damaged. How- ever, posterior cusp was usually destroyed severely. On the other hand, damage of either left or right cusp was also observed in many cases, and the perforation of both left and right cusps was the dominant lesion in one case. Slight retroversion of right cusp was observed in 3 cases. The destruction of each commissure was moderate or severe in all, and this was observed on the sinistro-posterior commissure in 8, dextro-sinistral in 5, and dextro-posterior in 5 cases, respectively. In 2 cases, one of rheumatic and one of syphilitic, a marked calcification was observed on the left and posterior cusps continuing into the anterior leaflet of mitral valve. Although the jet lesions on the mitral valve above-mentioned were observed in all cases including 2 of dissecting aneurysm, general tendency was that the destruction of sinistro-posterior com- missure usually caused severe jet lesions of mitral valve. 4) Left : All cases except one, 53) showed marked dilatation. In 4 cases, both dilatation and hypertrophy were evident. In all cases, jet lesions were observed on the septal surface and these were evident particularly in cases with the destruction of the central closing portion or of either dextro- posterior or dextro-sinistral commissures. Myocardium revealed moderate to marked degeneration, necrosis or edema on microscopic examination. 5) Weight of heart: Except one above-mentioned, 53)it was more than 500Gm. Vol. 6 No. 4 AUSTIN FLINT MURMUR 299

CASE ILLUSTRATION Patient N. T., 58-year-old male with syphilitic aortic insufficiency. He had syphilis while he was young, but no history of . He has complained of occasional shortness of breath since 7 years, from that time our observation and therapy were started. Because of severe dyspnea with orthopnea, palpitation and edema on face and legs, he was hospitalized 2 years prior to his death. Heart rate was 90/min. and regular. Blood pressure was 140/0mm.Hg. The heart was mark- edly enlarged with heaving cardiac apex at the anterior axillary line, where the Austin Flint murmur of grade III was best heard. There were also an aortic systolic ejection murmur of grade II to III and a diastolic regurgitant murmur of grade III at the base. The liver was markedly swollen which was palpable 6cm. below the right costal margin. Slight anemia, increased ESR (30mm./hour), pos- itive serology for syphilis, and slight functional disturbance of liver and kidney

Fig. 2. Phonocardiograms of patient N. T., pure aortic insufficiency . At the apex (upper tracing), diastolic rumble of large amplitude with abrupt beginning during rapid filling phase is inscribed on the Low Frequency (L) phono- cardiogram. This diastolic rumble is essentially mid-diastolic and the presystolic component is inconstant. At least, there is no tendency to presystolic crescendo . Apical first heart sound is of low frequency and relatively small amplitude . The third sound is inscribed at the beginning or just after the diastolic rumble. At the Erb's point (lower tracing), early systolic ejection murmur and diastolic regurgitant murmur with accentuated second sound are inscribed. Both murmurs have fairly high frequency component and well demonstrated on the High Frequency (H) phonocardiogram. Paper speed; 80mm./sec. Jap. Heart J. 300 UEDA, ET AL. July, 1965 were the main laboratory findings. The chest X-ray revealed marked cardiac enlargement and increased peri-bronchial shadow. Electrocardiogram showed left ventricular hypertrophy and left atrial overloading. Phonocardiogram revealed the characteristics of aortic insufficiency with the Austin Flint murmur (Fig. 2). Atrial fibrillation was developed transiently during the course, but the essential graphic findings were not altered, except the disappearance of atrio-systolic com- ponent of the rumble. Autopsy revealed that the heart weighed 710Gm. with marked dilatation and moderate hypertrophy of left ventricle and multi-focal small patchy myocardial fibrosis. The aortic ring was moderately dilated, measured 80mm. in circumference. Aortic cusps showed moderate thickening and shorten- ing, causing aortic incompetence (Fig. 3). A few small jet lesions were observed

Fig. 3. Autopsy specimen from patient N. T. Several small jet lesions are demonstrated by large arrow. These are located on the ventricular surface of anterior leaflet of mitral valve. A few cup-shaped jet lesions are seen just below the dextro-sinistral commissure (small arrow). Aorta shows moderate atherosclerosis accompanied by syphilitic aortitis. Aortic ring is moderately dilated, and left ventricle shows marked dilatation and moderate hyper- trophy. on the upper portion of ventricular surface of the anterior mitral leaflet as well as the upper part of ventricular septum. Marked edema, degeneration and patchy fibrosis were observed in myocardium. Patient K. M., 19-year-old male with congenital syphilitic aortic insufficiency. His parents had syphilis. Since past 1 year, he has complained of cough with bloody sputum, dyspnea, palpitation and edema. Digitalis and diuretics administration resulted in remarkable improvement. On admission, generalized edema, jugular venous engorgement, marked sweating, cyanosis and orthopnea were noticed. Si- nus tachycardia was marked, and cardiac impulse was broad and heaving, best palpable at the anterior axillary line. Blood pressure was 152/0mm.Hg. On auscultation, apical first heart sound was soft and occasionally musical. The second heart sound was also muffled and inseparable from the diastolic blowing murmur. Apical second sound was not clearly heard. Simultaneous auscultation with carotid palpation revealed a very loud (grade V) low-pitched and occasion- ally musical diastolic murmur with a thrill, loudest at the apex. This rumble was well transmitted to the entire precordium and superimposed on a diastolic blowing murmur at the lower left sternal border, where the latter had the point of maximum intensity (grade IV). No mitral opening snap was audible. Systolic ejection murmur was not so loud. Aschner's test failed to give a slow heart rate and the amyl nitrite Vol. 6 No. 4 AUSTIN FLINT MURMUR 301 inhalation also had no effect on the murmur, probably because of marked congestive heart failure. Following intensive digitalization with diuretics, atrial fibrillation developed, and the blowing diastolic murmur decreased in intensity (grade III). However, the mid-diastolic rumble with a thrill showed no appreciable change. Again, amyl nitrite inhalation as well as intravenous administration of methoxamine gave no significant changes in cardiac murmur, though aortic regurgitant murmur

Fig. 4. Phonocardiogram of patient K, M. during a period of sinus rhythm. Aortic diastolic blowing murmur with accentuated second sound is well in- scribed at the lower left sternal border (upper 2 tracings). There is also an ejection systolic murmur of small amplitude. At the apex (lower 2 tracings), a mid-diastolic murmur of somewhat musical quality of large amplitude is well demonstrated on Low Frequency phonocardiogram. This murmur is located after P wave of electro- cardiogram because of tachycardia, but there is no crescendo configuration towards the diminished first sound. Note the murmur of same configuration also seen on the Low Frequency phonocardiogram at lower left sternal border. Low frequency cardiogram shown in the middle was taken from the same area of the lower 2 tracings. Paper speed; 100mm./sec. Jap. Heart J. 302 UEDA, ET AL. July, 1965

Fig. 5. Phonocardiogram of patient K. M. during a period of atrial fibrillation. These tracings well demonstrate the change in the Austin Flint murmur in case with atrial fibrillation. Apical tracings (upper 2 tracings) show the low fre- quency rumble and high frequency blow, and the former is well ceased during mid- diastole with long diastole. This rumble is also seen on the Low Frequency phono- cardiogram from the Erb's point, where the blowing diastolic murmur is best recorded. The musicality of the Austin Flint murmur is lost on this occasion. was slightly increased concomitant with the blood pressure elevation by methoxamine from 166/0 to 198/0. Moist rales, ascites and liver swelling were not improved by therapy. Chest X-ray showed marked cardiac enlargement to both sides, and the electrocardiogram showed left ventricular hypertrophy. Phonocardiogram was shown in Figs. 4 and 5. This patient died suddenly and autopsy revealed cardiac enlargement weighing 730Gm. Both ventricles were dilated with slight hypertrophy. Fibrous fusion was observed between posterior and left aortic cusps accompanied with fibrous contraction of left cusp and slight retroversion of right cusp, causing a marked aortic insufficiency (Fig. 6). In addition to several small jet lesions on Vol. 6 No. 4 AUSTIN FLINT MURMUR 303

Fig. 6. Autopsy specimen from patient K. M.

This figure demonstrates a well-developed jet lesion on the ventricular surface of anterior leaflet of mitral valve (long arrow). This lesion is cup-shaped and

2.0•~1.0•~0.2cm. in size, and faced to the sinistro-posterior commissure of aortic valve, which is severely destroyed. On the septal surface of left ventricle, several small jet lesions are also seen below the right cusp (short arrow).

the ventricular septum, a cup-shaped jet lesion of 2.0•~1.0•~0.2cm. in size was observed on the ventricular surface of anterior mitral leaflet just beneath the destroyed sinistro-

posterior commissure of aortic valve. Otherwise, the mitral valve was completely intact. Histological examination revealed paramount miliary gummata with case- ous tissue containing giant cells in the aortic valve cusps as well as their marginal zone to the aorta. Patient M. N., 29-year-old female with aortic insufficiency due to possible rheu- matic valvulitis and subacute bacterial endocarditis. This case had loud Austin Flint murmur, and the diastolic blowing murmur was replaced by loud musical murmur (seagull cry) during hospital course. The heart weighed only 290Gm. and had no evidence of marked left ventricular dilatation on the clinical and other examination. The details of this case was presented separately. 53) Patient A. S., 25-year-old male with dissecting aortic aneurysm. He had no history of rheumatic fever or syphilis. At his age of 12, exertional palpitation

and easy fatiguability appeared and cardiomegaly was noticed at that time . Two years ago, and dyspnea occurred suddenly, which subsided at rest. No treatment was done until 2 months ago, when dyspnea re-appeared. Cyanosis and edema were gradually developed, with which headache, nausea and back pain were accompanied. Digitalis was administered, which caused marked arrhythmia, and he was hospitalized. On admission, marked orthopnea and generalized edema were noticed. Pulse was regular and the rate was 40/min ., but atrial fibrillation with complete A-V block and bigeminy was established by phonocardiographic

and electrocardiographic examinations. Blood pressure was 150/40-0mm .Hg on the right arm and lower extremities, whereas it was 90/30 on the left arm . Broad and heaving cardiac apex was displaced to the left mid-axillary line . A blowing diastolic murmur of grade III was best heard in the 3rd intercostal space at the right sternal border. A diastolic rumble of grade IV with protodiastolic accentua- tion was best heard at the apex, but it was transmitted widely and well recorded

to the right side of the sternum (Fig. 7). Frequently, the rumble was musical . Ejection systolic murmur was also noticed with a thrill on the neck . The first sound was rather faint, the second sound showed paradoxical splitting. The phonocar- diogram was repeatedly taken, and Fig. 7 illustrates 2 kinds of diastolic murmur Jap. Heart J. J 304 UEDA, ET AL. uly, 1965 Vol. 6 No. 4 AUSTIN FLINT MURMUR 305

Fig. 8. Autopsy specimen from patient A. S. The upper half of this figure demonstrates severe dissecting aneurysm and subsequent dilatation of aortic valve ring (130mm. in circumference), which caused severe aortic insufficiency. Slight fibrous thickening and contraction of the closing edge of the cusps are shown. Arrow indicates jet lesions on the ventricular surface of the anterior leaflet of mitral valve. There is no appreciable intrusion of the aortic root into the mitral orifice. Probe at the upper right corner indicates the aperture of real anrta. when bigeminy disappeared. Moist rales were over the lower lung fields. The venous pressure was 150mm. H2O on admission and later 240mm. H2O. Serology for rheumatic fever and syphilis was negative. Chest X-ray revealed marked cardiac enlargement (cardio-thoracic ratio: 74 %) and enormously elongated and dilated aortic arch. Pulmonary markings were moderately increased. Left ventricular hypertrophy was evident on the electrocardiogram. The oxygen inhalation and diuretics caused marked improvement and bigeminy disappeared thereafter. However, left hemiparesis and severe abdominal pain accompanied by Cheyne-Stokes' respiration developed suddenly, and he died soon later. At autopsy, markedly enlarged heart weighed 730Gm. The left ventricle showed marked dilatation and slight hypertrophy. Both atria and right ventricle also revealed moderate dilatation. Severe dissecting aneurysm involving ascending aorta and right carotid and left subclavian was noticed. Three cm. distal to the aortic ring, a narrow aorta passed about 9cm. through the aneurysm (Fig. 8). Scant thrombi were found on the aneurysmal wall consisting of tunica media. Severe aortic insufficiency was caused by the marked dilatation of the aortic valve ring (130mm. in circumference), but the aortic valve itself showed only slight fibrous thickening and contraction of the closing edge without commissural fusion. Several jet lesions were observed on the septal surface and the ventricular surface of anterior mitral leaflet. Both mitral and tricuspid valve rings showed marked dilatation, 135 and 140mm. in circumference, respectively. Acute infarction of left kidney due to massive embolism of left renal artery was noticed. Softening of slight degree was observed in the right cerebral insula.

DISCUSSION

Since the description of Flint in 1862, there has been much difference in opinion as to the frequency, the character and the cause of the Austin Flint murmur. Jap. Heart J. J 306 UEDA, ET AL. uly, 1965

A. Frequency and Definition of the Austin Flint Murmur

Apart from the cases of the auscultatory illusion illustrated by Luisada,25) the real incidence of the Austin Flint murmur has been a subject of much of the controversy. It has been regarded as a relatively infrequent phenomenon by Flint 1)-5) and many authors. Of these, Weber 35) stated that there is no case with •gpresystolic•hmurmur in pure aortic insufficiency. On the contrary,

Guiteras, 7) Thayer, 14) Herrmann22) and Ravin 39) have an opinion that it is not infrequent. Here, a question may arise as to the •gpresystolic•h blubbering mitral direct murmur of Flint. 1)-5)

Since the first phonocardiographic observation of the Austin Flint murmur by Weiss and Joachim, 16) the •gpresystolic•h nature of this murmur has been thought that it may be really mid-diastolic and presystolic (atrio-systolic) murmurs. Indeed, the description of Flint 1) was •gthe aortic regurgitant is the only true diastolic murmur,•h and •gthe mitral direct is a presystolic mur- mur.•h Moreover, he described that •gthe aortic regurgitant murmur accom- panies and follows the second sound of the heart,•h and •gthe mitral direct commences after the second sound.•h It is obvious, therefore, that the •gpre- systolic•h murmur of Flint's designation is such that this murmur begins during rapid inflow phase of the left ventricle, then includes both mid-diastolic and presystolic (atrio-systolic) murmurs. This is further confirmed by the fact that, on his contemporary, there was no clear-cut description of mid-diastolic murmur of •gtrue•h mitral stenosis, but this murmur, combined with the true , was called as •gpresystolic•h in timing. The rarity of the Austin Flint murmur will be accepted, if one adheres to the classical designa- tion just like as Weber, 35) Evans 48) and others. Thus the incidence of this murmur will become changed, and it is worth-while to note that the severe aortic insufficiency which results in death is always accompanied by the Austin

Flint murmur as shown in this report. Actually, the phonocardiographic examination reveals frequently a mid-diastolic and presystolic murmur in many cases of moderate and severe isolated aortic insufficiency. 42), 56), 59) Simultaneous recording of both blowing and rumbling murmurs is of great significance to detect the difference in various characteristics of these 2 murmurs as shown in Figs. 4, 5 and 7.

B. Auscultatory and Phonocardiographic Features of the Austin Flint

Murmur

The Austin Flint murmur has been thought by White 20), 31) and others that it is indistinguishable from that of organic mitral stenosis. Some authors 14), 23), 34), 39), 42), 47), 54) pointed out the difference in respect to the dimin- ished first sound, accentuated third sound, absence of opening snap and other graphic characteristics, with which the present results were consistent. How- Vol. 6 No. 4 AUSTIN FLINT MURMUR 307 ever, the absence of either accentuated first sound or opening snap do not necessarily exclude the organic mitral stenosis in severe case with aortic in- sufficiency. The mitral opening snap may be completely covered by the loud aortic regurgitant murmur. On the other hand, the mitral opening sound 52) may be observed on the phonocardiogram in cases of pure aortic insufficiency. Combined mitral stenosis and aortic insufficiencymay not show the accentuated first sound, whereas severe aortic insufficiency may show the normal first sound.55) Moreover, Q-first sound interval in severe aortic insufficiency with decompensation may be prolonged beyond the normal range 51)just like as that of mitral stenosis. Therefore, the points described previously are not necessarily sufficient to make the differentiation between 2 conditions, the one is aortic insufficiency with the Austin Flint murmur, the other is aortic in- sufficiency combined with mitral stenosis. The presystolic (atrio-systolic) component of the Austin Flint murmur was not regarded by Segal42) as the essential part of this murmur. Actually, the presystolic component was not observed in 2 cases with sinus rhythm. In others, however, this component revealed some peculiarities on the graphic configuration. Though, except a case recorded by Weiss and Joachim, 16)the short interval between the beginning of the P wave and the peak amplitude of this component has not been described yet, this character of the Austin Flint murmur may be one of the most important phonocardiographic findings. Ueda et al. 47)described such a murmur, usually following the atrial sound, in cases of myocardial disease of various origin, and explained it as a reflection of an elevated left ventricular end-diastolic pressure without significant atrio- ventricular pressure gradient during this phase. Actually, 5 cases with the Austin Flint murmur showed the atrial sound with the presystolic murmur . The difference in the presystolic murmurs between mitral stenosis and aortic insufficiency is obviously the reflection of the presence or absence of the atrio- systolic left atrial-left ventricular pressure gradient . Such an atrial sound is usually intensified or newly evoked by amyl nitrite inhalation 56)with diminu- tion or transient disappearance of the presystolic as well as mid-diastolic com- ponent of the Austin Flint murmur. 56)-58) Currens et al. 33)also demonstrated a case in which protoveratrine caused the disappearance of the Austin Flint murmur. On the contrary, methoxamine usually causes the intensification of this murmur. 59) Though severe cardiac failure seen in cases with marked aortic insufficiencymay eliminate the effect of these drugs as shown in patient K.M., these functional phonocardiography will be the best differential method in most cases. Wide area of transmission of the Austin Flint murmur was first described by Luisada. 28),34) In aortic insufficiency, the enlarged left ventricle occupies Jap. Heart J. 308 UEDA, ET AL. July, 1965 the large area just behind the precordium, and this fact may be responsible for the wide transmission. However, the mode of transmission will not be accurately assessed by simple auscultation because of the superimposition of the aortic diastolic murmur. In this situation, the phonocardiogram usually reveals both diastolic murmurs as shown in figures illustrated.

C. Clinical Features

Though the purpose of this study is primarily in the phonocardiographic and patho-anatomical study, the differential clues of the Austin Flint murmur listed by Segal 42) should also be considered. Striking things are the atrial fibrillation and hemoptysis seen in some cases with the Austin Flint murmur.

Indeed, these cases were diagnosed by some as having organic mitral stenosis before admission or during hospital course. Although most of Segal's criteria are statistically true, the application of these clues to the individual patient should be made carefully.

D. Mechanism of Production of the Austin Flint Murmur

The mechanism proposed for the production of the Austin Flint murmur may be categorised into 4 assumptions with minor variations.

Originally, Flint 1) suggested the left ventricular dilatation as a cause of this murmur, and subsequently this hypothesis was supported by several

authors. 15), 20),25) Flint assumed the rapid distension of enlarged left ventricle will cause the coaptation of the mitral valve by floating up just before the atrial contraction. Guiteras 7) had a view that not only floating up but also driving of the anterior mitral leaflet upward should be present to produce the actual

mitral obstruction. The possibility of this hypothesis will be demonstrated

below. These authors as well as Broadbent 13) and Da Costa 15) assumed the vibration of mitral leaflet itself. The present study did not reveal any patho-

logical evidence that the mitral valve itself does vibrate to produce the Austin

Flint murmur as suggested by several authors. 1), 13), 15), 22), 33) However, it may

be reasonable to accept the hypothesis that the mitral valve itself may occa-

sionally vibrate and produce a •gmusical•h quality of this murmur as shown in

our illustration. In this situation, the calcification of the left and posterior

cusps of the aortic valve which continues to the anterior mitral curtain may

contribute to the musicality of this murmur.

On the other hand, relative mitral stenosis conditioned by the dispropor- tion of the normal mitral orifice to the large left ventricle was regarded as a

cause of this murmur by White 20), 30) and Luisada. 25), 28), 34), 44) The fact that the same condition will give a similar diastolic murmur without aortic in- sufficiency may further confirm this hypothesis. 25), 10), 40), 43), 47), 54) However, such a murmur is usually faint, and is overlooked by simple auscultation. 35) In our experience, the left ventricular dilatation without a diastolic rumble is Vol. 6 No. 4 AUSTIN FLINT MURMUR 309

much more common.47) Furthermore, this hypothesis cannot explain the

Austin Flint murmur seen in a small heart. 33), 53)

T he other cause of relative mitral stenosis is the presence of relative

(functional) mitral insufficiency which may be associated with marked left ventricular dilatation. 20) Just as the case of organic mitral insufficiency, 60),61)

or of ventricular septal defect or patent ductus arteriosus, 62), 63) the augmented

mitral flow during rapid filling phase may cause a diastolic rumble in severe

cases with relative insufficiency. The blood flow propelled from hypertrophied

and dilated left into the hypotonic left ventricle was regarded by Phear 12)

as an important cause of this murmur. The third sound and the mid-diastolic

accentuation of the Austin Flint murmur may explain a part of the mechanism

involved. However, again, the same objection mentioned above will be

proposed for this hypothesis. The third hypothesis was originally proposed by Hirschfeld er, 18) who

suggested that the Austin Flint murmur will be caused by elevated left ventric-

ular diastolic pressure which cause the functional mitral obstruction. The

observation that this murmur is frequently associated with left ventricular

Failure 21), 38) supports this hypothesis, and the plausible explanation will be

obtained based on the recent hemodynamic studies of severe aortic insuf-

ficiency. 64), 65) However, same degree of the elevated diastolic pressure is also

observed without an appreciable diastolic rumble in cases of myocardial in-

farction and other lesions. Therefore, left heart failure will not be regarded

as a sole determinant of this murmur. Simultaneous phonocardiographic and

hemodynamic study may reveal the real significance of this hypothesis in

Future.

Finally, the most probable assumption was proposed based on the well-

grounded patho-anatomical observations. Herrmann 22) observed that, both experimentally and clinically, the lesion of •gposterior•h aortic cusp predisposed

the development of the Austin Flint murmur. In this situation, Herrmann

thought that, just like as Guiteras, 7) regurgitant stream drives the anterior mitral

curtain to produce a functional mitral stenosis. On the other hand, Gouley 24)

emphasized the characteristic deformity of the •gright•h aortic cusp, a concave,

cup-shaped deficiency of the inner portion of the cusp, which necessitates the

regurgitant blood towards the lower portion of anterior leaflet of mitral valve

to cause a functional mitral stenosis. Unfortunately enough, however, their

clinical observations were not ascertained by the graphic method, and a clinico-

pathological study using a phonocardiography made by Currens et al. 33) did not solve the controversial observations above-mentioned. Though the jet

lesions on the ventricular surface of the anterior mitral leaflet is the result of t he aortic regurgitant flow, 24), 66) this is a sole common pathological finding Jap. Heart J. J 310 UEDA, ET AL. uly, 1965 seen in cases of the Austin Flint murmur. In cases of severe insufficiency, a large volume of regurgitant flow takes place during isometric relaxation and rapid filling phases, 67)so that the anterior mitral leaflet should be forced to drive upwards to close the mitral orifice, just as the explanation of Guiteras. 7) In this situation, the damage of the sinistro-posterior commissure may play an important role because the jet regurgitation is apt to direct towards the anterior mitral leaflet. However, such a jet seemed to take place in any kinds of destruc- tion of valve or commissure in severe cases of aortic insufficiency seen in this study. Therefore, the conclusion of this study is that, though our series of material is not so large, the jet stream to the anterior leaflet of mitral valve is the primary cause of this functional mitral stenosis, whereas the site of damage of the aortic valve discussed in the previous works has only accessory importance. The loud Austin Flint murmur seen in cases of dissecting aortic aneurysm may con- firm our hypothesis.

SUMMARY AND CONCLUSIONS

Based on 15 autopsy cases including 13 of isolated aortic insufficiency and 2 of dissecting aortic aneurysm, the phonocardiogram of the Austin Flint murmur was analysed and the patho-anatomical determinant was investigated. The Austin Flint murmur was not infrequent in cases of severe aortic insufficiency, and the phonocardiogram as well as the auscultation revealed this murmur in all 15 cases. This murmur was composed of both mid-diastolic and presystolic (atrio-systolic) components of low-pitched vibration. The former was the essential component, which was following the third heart sound and had a decrescendo configuration. The latter showed little tendency of presystolic crescendo, and was not the essential component in some cases. The earlier appearance of the peak amplitude of the atrio-systolic component was illustrated and the importance of this graphic characteristic to differential diagnosis from organic mitral stenosis was suggested. Based on the patho-anatomy, the possibility of several assumptions ad- vocated as to the cause of the Austin Flint murmur was discussed. In this respect, the importance of aortic regurgitant jet on the ventricular surface of the anterior leaflet of the mitral valve was stressed as a cause of this particular functional mitral stenosis.

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