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Diastolic heart sound produced by mid-diastolic closure of the mitral valve
Diastolic Heart Sound Produced by Mid-Diastolic Closure of the Mitral Valve
DONALD A. ROTHBAUM, MD’ ROBERT L. DeJOSEPH, MD” MORTON TAVEL. MD, FACC
Mid-diastolic closure of the mftral valve is suggested as the source for an audible diastolic sound In a patient with aortk valve and coronary artery disease. On the apex cardiogram the sound followed the rapid filling wave by 60 msec and preceded the a wave. On the echocardlogram the sound corresponded to premature closure of the mitral valve in mid-diastole. In this case an audible diastolic sound that appeared to originate from mid-diastolic closure of the mitral valve indicated a rapidly increasing left ventricular diastolic pressure wfth severe left ventricular failure. After treatment of the congestive heart failure, the sound diminished in intensity.
Heart sounds are audible vibrations that are probably produced by rapid changes in pressure occurring in association with sudden acceleration or deceleration of blood and of vascular structures such as the heart valves and their attachments, the atria1 and ventricular walls and the blood vesse1s.l Diastolic sounds have been associated with such events as (1) rapid ventricular filling in early diastole (third heart sound, pericardial knock), (2) late ventricular filling with atrial systole (fourth heart sound), (3) sudden checking of opening movement of diseased atrioventricular valve leaflets (opening snap), and (4) movement of a cardiac tumor into the ventricle (tumor p10p).~ This case report suggests mid-diastolic closure of the mitral valve as another source for a diastolic sound. Case Report
From the Krannert Institute of Cardiology, Marion County General Hospital and the Department of Medicine, Indiana University School of Medicine, Indianapolis, Ind. This study was sup ported in part by the Herman C. Krannert Fund. 6. S. Public H&h service Grants HL-06308; HL-05363 and l-k-05749. and the Indiana Heart Association, Indianapolis; lnd. Manuscript accepted December 21.1973. U. S. Public Health Service Trainee in Cardiology. Address for reprints: Donald A. Rothbaum, MD, 1100 West Michigan St., Indiinapolis, Ind. 46202. l
A 49 year old man was referred to the Indiana University Medical Center in May 1973 with aortic stenosis and congestive heart failure. Physical examination disclosed tachypnea, a heart rate of 106 beatslmin and blood pressure of 100/80 mm Hg. Jugular venous pressure was raised 4 cm above the clavicle at 90’ elevation. Carotid pulsations were faint with a slowed upstroke. Scattered rales were present in both lung bases. The heart was enlarged with a diffuse left ventricular impulse. No thrill was present. The first heart sound was soft and followed by an ejection click. The second heart sound was narrowly split. A sharp, high-pitched mid-diastolic sound was loudest at the apex but audible over the entire precordium. A grade 216 systolic ejection murmur was heard in the aortic area; it peaked in mid-systole and radiated into the carotid arteries. No diastolic murmur was heard. The patient’s liver was enlarged, and he had pedal edema. Chest roentgenograms revealed pulmonary vascular congestion, left atria1 and left ventricular enlargement. An electrocardiogram revealed sinus rhythm, frequent premature ventricular contractions, left atria1 enlargement and a qS pattern in leads Vi to Q4 compatible with a diagnosis of old anteroseptal myocardial infarction or severe left ventricular hypertrophy. Graphic tracings: On the fourth hospital day a phonocardiogram, apex cardiogram, carotid pulse tracing and echocardiogram were obtained. It was evident from simultaneous phonocardiographic and apex cardiographic recordings (Fig. 1) that an intense high frequency diastolic sound occurred 60 msec after the end of the rapid filling wave and clearly before the onset of the a wave of the apex cardiogram. From simultaneous phonocardiographic and
September
1974
The American Journal of CARDfOLOGY
Volume 34
367
MID-DIASTOLIC
MITRAL VALVE CLOSURE-ROTHBAUM
ET AL.
tion of the posterior wall of the left ventricle and an old apical transmural myocardial infarction, The resected aortic valve was calcific and stenotic; the mitral valve was anatomically normal. The heart weighed 750 g and manifested left ventricular hypertrophy and dilatation. There was no pericardial disease or cardiac tumor.
Discussion
FIGURE 1. Simultaneous electrocardiographic lead II (ECG), phonocardiogram from the pulmonic area (PA), phonocardiogram from the apex (AX), and apex cardiogram (ACG). The phonocardiiram at the apex demonstrates a loud, high-pitched middllstolic sound (MDS) which follows the peak of the rapid filling wave (RFW) and the apex cardiogram by 60 msec and precedes the atrial filling wave (a). In addition, a third heart sound (Ss) is recorded by the phonocardiogram at the peak of the rapid filling wave. The first heart sound (S1) is followed by a loud ejection click (X) and a systolic ejection murmur (SEM). Two components of the second heart sound (Ss) are present. Paper speed is 100 mm/set. Band pass filters were 120 to 500 Hz; attenuation was 6 decibels/octave.
echocardiographic tracings (Fig. 2), it appeared that the diastolic sound corresponded with mid-diastolic closure of the mitral valve. Cardiac catheterization: On the 8th hospital day cardiac catheterization was performed, left atria1 and left ventricular pressures were obtained by the transseptal technique. Pertinent data included the following pressures (measured in millimeters of mercury): pulmonary arterial 73133, mean 50; left atria1 a .wave 40, v wave 50, mean 37; left ventricular systolic 140, initial diastolic 20, end-diastolic 38; ascending aortic 100/74, mean 89. Cardiac output was 3.6 liters/min, cardiac index 1.9 liters/min per m2 and pulmonary vascular resistance 3.6 units. There was a 40 mm Hg gradient across the aortic valve, and review of cineangiograms indicated grade 3/4 aortic insufficiency.3 Coronary cineangiographic studies revealed total occlusion of the left anterior descending and right coronary arteries. The temporal relation of the mid-diastolic sound to the left atria1 and ventricular pressures is illustrated in Figure 3. Pathologic findings: On the 18th hospital day, the patient underwent aortic valve replacement and saphenous vein coronary bypass. Twelve hours after operation, ventricular fibrillation developed and he could not be resuscitated. At autopsy, there was severe atherosclerotic narrowing of the left anterior descending and right coronary arteries. There was a recent extensive subendocardial infarc-
366
September
1974
The American Journal of CARDfGLGGY
In our patient the diastolic sound apparently did not originate from the usual sources. Its occurrence 60 msec after the peak of the rapid filling wave of the apex cardiogram was too late to consider it a third heart sound. Moreover, a faint third heart sound was recorded before this sound (Fig. 1). Since the diastolic sound preceded the a wave of the apex cardiogram, it could not have been a fourth heart sound. Finally, there was no postmortem evidence of a cardiac tumor or pericardial constriction to account for the abnormal sound. Mid-diasto!ic closure of mitral valve: The most plausible explanation is that the abnormal sound arose from mid-diastolic closure of the mitral valve. As shown by Pridie et a1.,4 a rapid early increase in the left ventricular diastolic pressure with .aortic insufficiency results in a characteristic pattern of mitral valve motion. The echocardiographic tracings in our patient revealed a similar pattern of mid-diastolic closure of the mitral valve. After the mitral valve leaflets separated in early diastole, they suddenly moved toward each other in mid-diastole at a time corresponding to that of the diastolic sound (Fig. 2). After this convergent movement, the valve leaflets separated only minimally during atria1 systole. The first heart sound has been shown to coincide temporally with completion of closure of the mitral valve although valve closure actually occurs 20 to 40 msec after the crossing point of the atria1 and ventricular pressures.5 The mid-diastolic sound in our patient may have had an analogous origin. The superimposed, nonsimultaneous left atria1 and left ventricular pressures in Figure 3 illustrate important temporal features of this sound. Timed from the electrocardiogram, the mid-diastolic sound would occur during the period when the diastolic left ventricular pressure was -rapidly increasing. At this time atria1 systole would have just begun. The a wave of the left ventricular pressure tracing (coinciding with the atrial a wave) is actually the second small end-diastolic deflection, not the mid-diastolic pressure peak (Fig. 3). The very small a wave in the left ventricular pressure tracing is compatible with the failure to record distinct mitral valve,reopening with atria1 systole in the echocardiogram (Fig. 2). In addition, the first heart sound (Si) was quite faint in the phonocardiographic tracing (Fig. 1). This finding is consistent with the observation that when mitral valve closure occurred in mid-diastole, the mitral valve component of the first heart sound was lost and the resultant first heart sound was soft.s7 Clinical implication: One of the factors influenc-
Volume 34
MID-DIASTOLIC
MITRAL VALVE
CLOSURE-ROTHBAUM
ET AL.
FIGURE 2. Simultaneous retouched phonocardiogram (APEX) at the apex and echocardiogram. The mld-diastollc sound (MDS) appears to correspond to mid-diistolic closure of the anterior (AN) and posterior (PM/) mitral valve leaflets. The first (S,) and second (Ss) heart sounds are noted on the phonocardiogram, and the interventricular septum (IVS) and posterior left ventricular wall (PLV) are noted on the echocardiogram (ECHO). The left ventricle is dilated. The interventricuhr septum is flat and posterior left ventricular wall motion is diminished. Paper speed is 50 mm/set; time lines are at 200 msec intervals.
ing the amplitude of the high frequency components of the first heart sound is the rate of increase of left ventricular pressure.7*8 On the fourth hospital day, when the patient had severe congestive heart failure, the mid-diastolic sound was loud and high-pitchedmore like a first heart sound than a gallop. In addition to premature mitral valve closure, the echocardiographic findings revealed left ventricular dilatation, diminished posterior left ventricular wall motion and a flat interventricular septum (Fig. 2). These echocardiographic findings are all consistent with severely impaired left ventricular function, particularly in the presence of aortic regurgitation. Although grade 314 aortic regurgitation was disclosed by the cineangiographic studies, 3 the progressive opacification of the left ventricle during several cardiac cycles was the result of the combination of a small regurgitant jet and a diminished stroke volume. Consistent with the angiographic observation was the failure to detect a diastolic decrescendo murmur by either auscultation or phonocardiography. In this case moderate aortic regurgitation into a poorly compliant left ventricle resulted in a sufficiently rapid increase in left ventricular diastolic pressure to cause premature mitral valve closure and a mid-diastolic sound. The presence of a mid-diastolic sound of audible intensity probably reflected severe left ventricular decompensation rather than a large amount of aortic regurgitation. After
140
120
k L
u
a :
40
/ 20
FIGU :. Simultaneous electrocardiogram (ECG) and left ventricuiar pressure tracing (LV) with superimposed, nonsimultaneous left atrial pressure tracing (LA). The temporal relation of the mtddiastolic sound (MDS) to the electrocardiogram and pressure tracings is illustrated. The middlastollc sound occurs while left ventricular diastolic pressure is rapidly increasing and left atrial systole has just begun. The a wave of the left ventricular pressure (A) is barely evident. Paper speed is 100 mm/set, time lines are at 200 msec intervals. Time delay through the catheter manometer system is 5 msecs
September 1974
The Amerkan Journal of CARDIGLGGY
Volume 34
369
MID-DIASTOLIC
MITRAL VALVE
CLOSURE-ROTHBAUM
ET AL.
treatment of congestive heart failure, the patient’s mid-diastolic sound decreased in intensity. The change in the sound probably indicated a decrease in the rate of rise of left ventricular diastolic pressure and an improvement in left ventricular function.
These observations raise the possibility that diastolic sounds other than gallop sounds may signify the presence of congestive heart failure. Their frequency and clinical and prognostic significance remain to be determined.
References 1. Rushmer RF: Cardiovascular Dynamics, third ediiion. Philadelphia, WB Saunders, 1970. p 301-313 2. Tavel ME: Clinical Phonocardiography and External Pulse Recording, second edition. Chicago, Year Book Medical Publishers, 1972, p go-105 3. Cohn LH, Maeon DT, Roes J Jr, et al: Preoperative assessment of aortic regurgitation in patients with mitral valve disease. Am J Cardiil 19:177-182, 1967 4. Pridle RB, Benham R, Oakley CM Echocardiiraphy of the mitral valve in aortic valve disease. Br Heart J 33:296-304, 1971 5. Lanlado S, Yeltln EL, Mllter H, et al: Temporal relation of the first heart sound to closure of the mitral valve. Circulation 47:10061014, 1973
370
Soptomber
1974
The Amerkan Jcumel ot CARMOLDGY
6. Meadows WR, Van Praagh S, lndrelka Y, et al: Premature mitral valve closure: a hemodynamic explanation for absence of the first sound in aortic insufficiency. Circulation 28:251-258, 1963 7. Shah PM, Kramer DH, Gramlak R: Influence of the timing of atrial systole on mitral valve closure and on the first heart sound in man. Am J Cardiol 26:231-237, 1970 8. Sakamoto T, Kusukawa R, MacCanon DM, et al: Hemodynamic determinants of the amplitude of the first heart sound. Circ Res 16:45-57, 1965 9. Tavel ME, Felgenbaum H, Stelnmetz EF: The apexcardiogram and its relationship to hemodynamic events within the left heart. Br Heart J 27:829-839, 1965
Votume 34
DONALD A. ROTHBAUM, MD’ ROBERT L. DeJOSEPH, MD” MORTON TAVEL. MD, FACC
Mid-diastolic closure of the mftral valve is suggested as the source for an audible diastolic sound In a patient with aortk valve and coronary artery disease. On the apex cardiogram the sound followed the rapid filling wave by 60 msec and preceded the a wave. On the echocardlogram the sound corresponded to premature closure of the mitral valve in mid-diastole. In this case an audible diastolic sound that appeared to originate from mid-diastolic closure of the mitral valve indicated a rapidly increasing left ventricular diastolic pressure wfth severe left ventricular failure. After treatment of the congestive heart failure, the sound diminished in intensity.
Heart sounds are audible vibrations that are probably produced by rapid changes in pressure occurring in association with sudden acceleration or deceleration of blood and of vascular structures such as the heart valves and their attachments, the atria1 and ventricular walls and the blood vesse1s.l Diastolic sounds have been associated with such events as (1) rapid ventricular filling in early diastole (third heart sound, pericardial knock), (2) late ventricular filling with atrial systole (fourth heart sound), (3) sudden checking of opening movement of diseased atrioventricular valve leaflets (opening snap), and (4) movement of a cardiac tumor into the ventricle (tumor p10p).~ This case report suggests mid-diastolic closure of the mitral valve as another source for a diastolic sound. Case Report
From the Krannert Institute of Cardiology, Marion County General Hospital and the Department of Medicine, Indiana University School of Medicine, Indianapolis, Ind. This study was sup ported in part by the Herman C. Krannert Fund. 6. S. Public H&h service Grants HL-06308; HL-05363 and l-k-05749. and the Indiana Heart Association, Indianapolis; lnd. Manuscript accepted December 21.1973. U. S. Public Health Service Trainee in Cardiology. Address for reprints: Donald A. Rothbaum, MD, 1100 West Michigan St., Indiinapolis, Ind. 46202. l
A 49 year old man was referred to the Indiana University Medical Center in May 1973 with aortic stenosis and congestive heart failure. Physical examination disclosed tachypnea, a heart rate of 106 beatslmin and blood pressure of 100/80 mm Hg. Jugular venous pressure was raised 4 cm above the clavicle at 90’ elevation. Carotid pulsations were faint with a slowed upstroke. Scattered rales were present in both lung bases. The heart was enlarged with a diffuse left ventricular impulse. No thrill was present. The first heart sound was soft and followed by an ejection click. The second heart sound was narrowly split. A sharp, high-pitched mid-diastolic sound was loudest at the apex but audible over the entire precordium. A grade 216 systolic ejection murmur was heard in the aortic area; it peaked in mid-systole and radiated into the carotid arteries. No diastolic murmur was heard. The patient’s liver was enlarged, and he had pedal edema. Chest roentgenograms revealed pulmonary vascular congestion, left atria1 and left ventricular enlargement. An electrocardiogram revealed sinus rhythm, frequent premature ventricular contractions, left atria1 enlargement and a qS pattern in leads Vi to Q4 compatible with a diagnosis of old anteroseptal myocardial infarction or severe left ventricular hypertrophy. Graphic tracings: On the fourth hospital day a phonocardiogram, apex cardiogram, carotid pulse tracing and echocardiogram were obtained. It was evident from simultaneous phonocardiographic and apex cardiographic recordings (Fig. 1) that an intense high frequency diastolic sound occurred 60 msec after the end of the rapid filling wave and clearly before the onset of the a wave of the apex cardiogram. From simultaneous phonocardiographic and
September
1974
The American Journal of CARDfOLOGY
Volume 34
367
MID-DIASTOLIC
MITRAL VALVE CLOSURE-ROTHBAUM
ET AL.
tion of the posterior wall of the left ventricle and an old apical transmural myocardial infarction, The resected aortic valve was calcific and stenotic; the mitral valve was anatomically normal. The heart weighed 750 g and manifested left ventricular hypertrophy and dilatation. There was no pericardial disease or cardiac tumor.
Discussion
FIGURE 1. Simultaneous electrocardiographic lead II (ECG), phonocardiogram from the pulmonic area (PA), phonocardiogram from the apex (AX), and apex cardiogram (ACG). The phonocardiiram at the apex demonstrates a loud, high-pitched middllstolic sound (MDS) which follows the peak of the rapid filling wave (RFW) and the apex cardiogram by 60 msec and precedes the atrial filling wave (a). In addition, a third heart sound (Ss) is recorded by the phonocardiogram at the peak of the rapid filling wave. The first heart sound (S1) is followed by a loud ejection click (X) and a systolic ejection murmur (SEM). Two components of the second heart sound (Ss) are present. Paper speed is 100 mm/set. Band pass filters were 120 to 500 Hz; attenuation was 6 decibels/octave.
echocardiographic tracings (Fig. 2), it appeared that the diastolic sound corresponded with mid-diastolic closure of the mitral valve. Cardiac catheterization: On the 8th hospital day cardiac catheterization was performed, left atria1 and left ventricular pressures were obtained by the transseptal technique. Pertinent data included the following pressures (measured in millimeters of mercury): pulmonary arterial 73133, mean 50; left atria1 a .wave 40, v wave 50, mean 37; left ventricular systolic 140, initial diastolic 20, end-diastolic 38; ascending aortic 100/74, mean 89. Cardiac output was 3.6 liters/min, cardiac index 1.9 liters/min per m2 and pulmonary vascular resistance 3.6 units. There was a 40 mm Hg gradient across the aortic valve, and review of cineangiograms indicated grade 3/4 aortic insufficiency.3 Coronary cineangiographic studies revealed total occlusion of the left anterior descending and right coronary arteries. The temporal relation of the mid-diastolic sound to the left atria1 and ventricular pressures is illustrated in Figure 3. Pathologic findings: On the 18th hospital day, the patient underwent aortic valve replacement and saphenous vein coronary bypass. Twelve hours after operation, ventricular fibrillation developed and he could not be resuscitated. At autopsy, there was severe atherosclerotic narrowing of the left anterior descending and right coronary arteries. There was a recent extensive subendocardial infarc-
366
September
1974
The American Journal of CARDfGLGGY
In our patient the diastolic sound apparently did not originate from the usual sources. Its occurrence 60 msec after the peak of the rapid filling wave of the apex cardiogram was too late to consider it a third heart sound. Moreover, a faint third heart sound was recorded before this sound (Fig. 1). Since the diastolic sound preceded the a wave of the apex cardiogram, it could not have been a fourth heart sound. Finally, there was no postmortem evidence of a cardiac tumor or pericardial constriction to account for the abnormal sound. Mid-diasto!ic closure of mitral valve: The most plausible explanation is that the abnormal sound arose from mid-diastolic closure of the mitral valve. As shown by Pridie et a1.,4 a rapid early increase in the left ventricular diastolic pressure with .aortic insufficiency results in a characteristic pattern of mitral valve motion. The echocardiographic tracings in our patient revealed a similar pattern of mid-diastolic closure of the mitral valve. After the mitral valve leaflets separated in early diastole, they suddenly moved toward each other in mid-diastole at a time corresponding to that of the diastolic sound (Fig. 2). After this convergent movement, the valve leaflets separated only minimally during atria1 systole. The first heart sound has been shown to coincide temporally with completion of closure of the mitral valve although valve closure actually occurs 20 to 40 msec after the crossing point of the atria1 and ventricular pressures.5 The mid-diastolic sound in our patient may have had an analogous origin. The superimposed, nonsimultaneous left atria1 and left ventricular pressures in Figure 3 illustrate important temporal features of this sound. Timed from the electrocardiogram, the mid-diastolic sound would occur during the period when the diastolic left ventricular pressure was -rapidly increasing. At this time atria1 systole would have just begun. The a wave of the left ventricular pressure tracing (coinciding with the atrial a wave) is actually the second small end-diastolic deflection, not the mid-diastolic pressure peak (Fig. 3). The very small a wave in the left ventricular pressure tracing is compatible with the failure to record distinct mitral valve,reopening with atria1 systole in the echocardiogram (Fig. 2). In addition, the first heart sound (Si) was quite faint in the phonocardiographic tracing (Fig. 1). This finding is consistent with the observation that when mitral valve closure occurred in mid-diastole, the mitral valve component of the first heart sound was lost and the resultant first heart sound was soft.s7 Clinical implication: One of the factors influenc-
Volume 34
MID-DIASTOLIC
MITRAL VALVE
CLOSURE-ROTHBAUM
ET AL.
FIGURE 2. Simultaneous retouched phonocardiogram (APEX) at the apex and echocardiogram. The mld-diastollc sound (MDS) appears to correspond to mid-diistolic closure of the anterior (AN) and posterior (PM/) mitral valve leaflets. The first (S,) and second (Ss) heart sounds are noted on the phonocardiogram, and the interventricular septum (IVS) and posterior left ventricular wall (PLV) are noted on the echocardiogram (ECHO). The left ventricle is dilated. The interventricuhr septum is flat and posterior left ventricular wall motion is diminished. Paper speed is 50 mm/set; time lines are at 200 msec intervals.
ing the amplitude of the high frequency components of the first heart sound is the rate of increase of left ventricular pressure.7*8 On the fourth hospital day, when the patient had severe congestive heart failure, the mid-diastolic sound was loud and high-pitchedmore like a first heart sound than a gallop. In addition to premature mitral valve closure, the echocardiographic findings revealed left ventricular dilatation, diminished posterior left ventricular wall motion and a flat interventricular septum (Fig. 2). These echocardiographic findings are all consistent with severely impaired left ventricular function, particularly in the presence of aortic regurgitation. Although grade 314 aortic regurgitation was disclosed by the cineangiographic studies, 3 the progressive opacification of the left ventricle during several cardiac cycles was the result of the combination of a small regurgitant jet and a diminished stroke volume. Consistent with the angiographic observation was the failure to detect a diastolic decrescendo murmur by either auscultation or phonocardiography. In this case moderate aortic regurgitation into a poorly compliant left ventricle resulted in a sufficiently rapid increase in left ventricular diastolic pressure to cause premature mitral valve closure and a mid-diastolic sound. The presence of a mid-diastolic sound of audible intensity probably reflected severe left ventricular decompensation rather than a large amount of aortic regurgitation. After
140
120
k L
u
a :
40
/ 20
FIGU :. Simultaneous electrocardiogram (ECG) and left ventricuiar pressure tracing (LV) with superimposed, nonsimultaneous left atrial pressure tracing (LA). The temporal relation of the mtddiastolic sound (MDS) to the electrocardiogram and pressure tracings is illustrated. The middlastollc sound occurs while left ventricular diastolic pressure is rapidly increasing and left atrial systole has just begun. The a wave of the left ventricular pressure (A) is barely evident. Paper speed is 100 mm/set, time lines are at 200 msec intervals. Time delay through the catheter manometer system is 5 msecs
September 1974
The Amerkan Journal of CARDIGLGGY
Volume 34
369
MID-DIASTOLIC
MITRAL VALVE
CLOSURE-ROTHBAUM
ET AL.
treatment of congestive heart failure, the patient’s mid-diastolic sound decreased in intensity. The change in the sound probably indicated a decrease in the rate of rise of left ventricular diastolic pressure and an improvement in left ventricular function.
These observations raise the possibility that diastolic sounds other than gallop sounds may signify the presence of congestive heart failure. Their frequency and clinical and prognostic significance remain to be determined.
References 1. Rushmer RF: Cardiovascular Dynamics, third ediiion. Philadelphia, WB Saunders, 1970. p 301-313 2. Tavel ME: Clinical Phonocardiography and External Pulse Recording, second edition. Chicago, Year Book Medical Publishers, 1972, p go-105 3. Cohn LH, Maeon DT, Roes J Jr, et al: Preoperative assessment of aortic regurgitation in patients with mitral valve disease. Am J Cardiil 19:177-182, 1967 4. Pridle RB, Benham R, Oakley CM Echocardiiraphy of the mitral valve in aortic valve disease. Br Heart J 33:296-304, 1971 5. Lanlado S, Yeltln EL, Mllter H, et al: Temporal relation of the first heart sound to closure of the mitral valve. Circulation 47:10061014, 1973
370
Soptomber
1974
The Amerkan Jcumel ot CARMOLDGY
6. Meadows WR, Van Praagh S, lndrelka Y, et al: Premature mitral valve closure: a hemodynamic explanation for absence of the first sound in aortic insufficiency. Circulation 28:251-258, 1963 7. Shah PM, Kramer DH, Gramlak R: Influence of the timing of atrial systole on mitral valve closure and on the first heart sound in man. Am J Cardiol 26:231-237, 1970 8. Sakamoto T, Kusukawa R, MacCanon DM, et al: Hemodynamic determinants of the amplitude of the first heart sound. Circ Res 16:45-57, 1965 9. Tavel ME, Felgenbaum H, Stelnmetz EF: The apexcardiogram and its relationship to hemodynamic events within the left heart. Br Heart J 27:829-839, 1965
Votume 34