Letters to the Editor
plasma concentration is ignored. Although the intravenous use of these drugs simplifies this problem somewhat, a large variable, the volume of drug distribution, is unmeasured. There is no reason to believe t h a t the volume of drug distribution is equal between the three clinical classes of p.-tients studied. Indeed, the authors themselves have shown significant difference in blood volume and distribution between the patient groups, suggesting t h a t the volume of drug distribution may also vary. Thus, the drug dose to blood pressure response relationship presented cannot be construed to be equivalent to a drug concentration to response relationship, and thus, conclusions regarding receptor pharmacology become tenuous. Furthermore, to interpret changes in alpha adrenergic receptor pharmacology meaningfully, concentration to response relationships must be c o m p l e t e - t h a t is, curves constructed using drug concentrations resulting in subthreshold to maximal responses must be u s e d - a n d the results should be normalized. Obviously, maximal presser doses of norepinephrine are incompatible with human experimentation; however, short of such data, conclusions, again, are not well founded. Furthermore, in order to compare drug doses which are needed to reach a given response level, t h a t response level must be demonstrated to be within the linear portion of the drug concentration to response relationship. The potential of comparing points at threshold va.lues that are slow rising versus later points which are on the rapid rising, linear portion of the dose response curve invites misinterpretation. The authors' conclusion t h a t a decreased responsiveness to norepinephrine in borderline hypertensive patients suggests the possibility of a change in "the role of availability of receptor sites to the vasoactive agent" may be indeed correct; however, their inferences from this point are incompatible with adrenergic receptor pharmacology. A decrease of available receptor sites implies a competitive or noncompetitive alpha adrenergic receptor antagonist. Alternatively, a physiologic antagonist might give similar results. However, I know of no evidence that shows that norepinephrine can physiologically or pharmacologically antagonize itself. Indeed, if a patient's vascular system were stimulated by pre-existing endogenous norepinephrine as the authors suggest, additional increments of exogenous norepinephrine should give a greater increment of vascular response, since such a system would not be operating on the early threshold portion of the dose response curve but rather on the linear, rapid rising, portion of this relationship. Since the authors' own observations show exactly the opposite, t h a t is, a greater amount of norepinephrine is needed to evoke a similar response, their conclusions seem unsupported by their data. I realize that the above pharmacologic considerations can rarely, if ever, be met in human experimentation. However, in a paper which cites receptor pharmacology and an altered response to vasoactive agents as a prime pathophysiologic determinant in borderline hypertensive patients, I think t h a t it is important that the above concepts be included in the interpretation of the data. Although the authors' interpretations are frequently qualified by the word "suggests," I would prefer their stating clearly where their inferences do and do not meet strict receptor and clinical pharmacologic principles. This information is not always readily available to or remembered by the active clinician. The information, however, is
A m e r i c a n Heart Journal
essential to the proper interpretation of articles dealing with cardiovascular pharmacology as this one does. I would be most interested in the editor's and/or authors' comments in regard to the above critique and in the above concepts of clinical and receptor pharmacology being pub: lished either as the letter above or in terms of an editorial by an expert of your choice.
Kenneth M. Kessler, M.D., Major, MC Formerly, Assistant Chief, General Medicine Service Brooke Army Medical Center Fort Sam Houston, Texas 78234 Present address: Dept of Medicine Temple University Health Sciences Center Philadelphia, Pa. 19140
Autoauscultation in a patient with floppy mitral valve syndrome To the Editor: Laennec ~ named the method of listening with the aid of a stethoscope "mediate" auscultation to distinguish it from "immediate" auscultation which was performed by placing the listener's ear on the body of the patient. "Autoauscultation," an older kind, represents what a person hears of sound emanating from his or her body. Hearing one's heart sounds is a very common experience, which usually occurs while lying in bed on the left side with the chest and the ear on a continuous surface, pillow, or mattress. In some rare instances, patients hear heart murmurs while they are in sitting or standing posture. These murmurs may be transient and usually represent a significant valvular abnormality. In 1880, William Osler published his observations on "a remarkable heart murmur heard at a distance from the chest wall. ''2 The following excerpts from this article are quoted because they describe clinical features which resemble those of our patient. "J. W., aged twelve, a well nourished young girl, was sent to me in May, 1880, by Dr. BuUer,* who had noticed a remark able whistling sound, while examining her eyes. The mothel stated she had been a healthy child though never robust. Had inflammation of the lungs at eighteen months, measles at the age of 3 and scarlet fever, three years age... Auscultation-As she sits upright in the chair the heart sounds at the apex and the base loud and clear; no murmur. When she stands a loud systolic murmur is heard at the apex, high-pitched, somewhat musical, of maximum intensity in fifth interspace; it varies a good deal, being loud for three or four beats, and then faint for one or two succeeding ones, due to the influence of respiration. On removal of the ear from the chest wall, the murmur can be heard at a distance of several inches. It disappeared quite suddenly and could not be detected on most careful examination. She was then asked to run about the room and up and down stairs. On sitting down, after this, the heart's action was very forcible but the heart sounds were clear. The child then suggested that she heard it most frequently when in the stooping posture; and on causing her to lean forward and relax the chest, the murmur was at once heard, and with greatly increased intensity. It was distinctly audible at a distance of three feet two inches by measurement, and could be heard at any point on the chest and on top of the head. Pulse 96. *The first Professor of Ophthalmology at McGill University.
2(}9
Letters to the Editor
Fig. 1. Quantitative symbol phonocardiogram (QSPcg) depicts the normal pattern of heart sounds with respect to loudness, duration and quality. The late, cresendo, coarse systolic m u r m u r was the first clue to the diagnosis of floppy mitral valve syndrome. Auscultation at the apex with the patient standing, then bent forward touching her toes with her fingers, then again in the standing position, seems to have elicited a quite loud musical cresendo systolic m u r m u r which however was not loud enough to be audible by the patient who did not hear any m u r m u r during the entire study. The exercise consisted of 40 mountings of the two-step in 90 seconds, raising the heart rate to about 150 per minute. A significant, somewhat superficial and musical m u r m u r appeared 30 seconds after exercise and grew a little louder until the second milmte when no m u r m u r but the early systolic "click" (a short sound), which appeared at 30 seconds, persisted. This too, disappeared in the third minute when the late short crescendo-systolic murmur reappeared. But this too disappeared in the fourth minute, leaving only the normal first and second sounds. When the patient was examined again on February 10, 1975, the only abnormal feature was a faint, short early click about half as loud as the one heard on J a n u a r y 8th. These observations emphasize the wide, unpredictable variability of the systolic click and m u r m u r which point to the diagnosis of a floppy mitral valve. The QSPcg, written while listening, contains precise details, some of which could not be found in an electrophonocardiogram (EPcg), e.g., the superficial musical quality of the systolic murmur, the distinction between the coarse quality of the crescendo m u r m u r before exercise, and the blowing quality immediately after exercise. On the other hand, the electrophonocardiogram (EPcg) would permit precise measurement of the time interval between the first sound and the click. (Diagram adapted and modified from Segall, Harold N., in Encyclopedia of Cardiology, Luisada, A. A., ed., New York, 1959, McGraw-Hill Book Company, Inc., Vo|. 1, p. 3lO5.)
270
February, 1976, Vol. 91, No. 2
Letters to the Editor
Fig. 2. Lead II, recorded after exercise, reveals occasional ventricular ectopic beats.
On May 28th, she was shown at the Medico-Chirurgical Society of Montreal and most of the members heard the murmur. A day or two before the meeting, I called at her mother's house and satisfied myself of its presence though it was very variable. On July 13, I saw her again at her home and failed after prolonged examination to hear the murmur. She stated that she had not heard it herself for some time." When he examined her on July 21, he did hear the murmur and added t h a t . . . "There was no constancy in the variations. The rhythm is distinctly systolic, the first sound of the heart is not effaced by it though not so sharp as in its absence. During an examination extending over twenty minutes, the murmur was present four or five times and for a brief interval only, less than a minute each time." It is tempting to continue quoting Osler's remarks and his discussion of the literature, which he ends with the following, "I am not prepared to suggest an explana: tion of the cause of the murmur in this instance" and he adds t h a t his patient was "delicately built and nervous." The person who reported Osler,s presentation of the case at the Medico-Chirurgical Society of Montreal* wrote the following: "Dr. Osler cannot account for the murmur, but thinks, perhaps, it arises from an unusually flexible chest and pressure thus exerted on the pulmonary artery and aorta. Dr. Rosst suggested that it might possibly be exPlained by the existence of some loosely pedunculated body hanging inside the heart in such a way that, only in certain positions, it would *An error has crept into the records of the date of this meeting: Osler gives May 28, 1880; this report uses April 30th. tDr. George Ross.
American Heart Journal
Fig. 3. In the dorsal recumbent posture, the interval between the beginning of the first sound and of t h e click varies between 200 and 210 msec: In the sitting posture, it varies between 240 and 260 msec. The amplitude of the sound waves do not precisely reflect the relative loudness of the sounds heard with the stethoscope, as depicted in the quantitative symbol phonocardiogram (QSPcg). Clinical auscultation affords a clearer distinction between the late, crescendo systolic murmur and the second sound than the electrophonocardiogram (EPcg).
271
Letters to the Editor
fall into the blood current and develop a m u r m u r . . . The President* rather favoured the idea that it was most likely due to bending of the costal cartilages and pressure on the pulmonary artery. ''~ Our patient, V. R. (ECG #64,496), a young woman of 23, heard a peculiar noise emanating from inside her chest at the age of twelve. She remembers that one day when at home, seated and in the company of several friends, she became aware of a peculiar "squeaking, grating noise," a rhythmically recurring noise emanating from her chest. She could listen to the conversation while hearing this noise which "soon" disappeared. 1' During the next ten years it recurred "occasionally." At the age of eighteen, she consulted a physician because she noticed irregularity in her heart beating. The physician reassured her and recommended abstinence from tea and coffee. She has never smoked cigarettes or any type of tobacco. The irregularity continued to recur and in addition the noise began to appear with gradually increasing frequency. During the past year or so, she heard the noise once in many weeks, then the intervals shortened to about two weeks, then several times a week and more recently she has been hearing it several times a day. She has n~ver heard it while in bed or otherwise recumbent. In search of some correlation with a particular activity she has noticed that it tends to come on when she is standing in the kitchen and vigorously stirring a mixture of food she is preparing. Emotional excitement also tends to elicit the noise. It is invariably regular in rhythm. Sometimes it stops for only a few beats then starts again and continues for some minutes when it stops and becomes audible again only the next day, or several days later. She feels the cardiac irregularity independently of the noise. When she consulted Dr. Lawrence Battersby recently, he heard the noise, the first physician who did hear it, and he referred her to us for further study. About two months previously, she asked her boyfriend to place his ear on her chest when she was aware of the noise and he confirmed that it accompanied each heart beat. Both parents, her brother, and sister, are in good health. Having in mind a recent experience with twin males aged 65, both of whom have the floppy mitral valve syndrome and each of whom has one son who also has this condition, we invited her parents and siblings to be examined. They declined, apparently without regrets. She has not had any major illness in the past. She did have measles and chicken pox as a child and influenza at nineteen. She works as a clerk in the library of an industrial firm. Physical examination: A slender, delicate, young woman of 28; weight 91 pounds, height 63 inches. Nothing could be found to suggest Marfan syndrome. No abnormalities could be detected until the heart murmurs were heard. The pattern of heart, sounds, the heart murmurs, and Korotkoff sounds are described more precisely, more completely in greater detail by the quantitative symbol phonocardiogram (QSPcg) in Fig. 1 than any description in language could achieve.:~"~The electrophonocardiogram (EPcg) in Fig. 2 confirms variations in time relationship of the click. The electrocardiogram (Fig. 3) presents only normal *Dr. H. Howard. Dr. R. P. Howard, Osler's teacher, was present at the meeting; no discussion by him is recorded.
272
features before exercise but after forty mountings of the twostep exercise test, two ventricular premature beats were recorded. X-ray film of the chest revealed no abnormalities. The following report was received from Dr. F. Winsberg of the Montreal General Hospital about the ultrasound study. "Echocardiogram shows a classic midsystolic buckling of the mitral valve. This is the sort of prolapse which produces the midsystolic click-late systolic murmur pattern. There is no evidence of chamber enlargement." Eighty-five years separate Osler's observations from ours. His vivid description strongly favors the view that his patient had a floppy mitral valve. Had he remained in Montreal during the next 39 years of his life, we might have had an interesting follow-up report on t h a t patient. At present, the technique of echocardiography makes possible a good correlation between the physical signs and the diagnosis of the anatomical and physiological anomaly. From the experience with other patients, notably with one of the twins mentioned above, we have learned that wide variations in the pattern of sounds and murmurs occur in some cases. The transient character of the typical signs accounts for the fact t h a t when our patient was examined annually at school and before going to camp, no physician noted a significant abnormality until Dr. Lawrence Battersby happened to listen when the systolic click and murmur did appear. The autoauscultation feature makes the clinical story of this patient of special interest. Osler's case of 95 years ago gains in significance in the light of current use of echocardiography. Our speculations about the cardiodynamics which result in the absence, the appearance, disappearance, and reappearance of the click and murmur in so wide a variety of loudnesses, durations, and qualities would resemble in accuracy the speculations of Osler, Ross, and Howard, about the origin of the murmur. The author wishes to express his cordial thanks to Dr. Lawrence Battersby, who introduced the patient to him, and to Dr. F. Winsberg who did the echocardiogram.
Harold N. SegaU, M.D. Department of Medicine McGill University and The Montreal General and Jewish General Hospitals Montreal, Quebec, Canada
REFERENCES
1. Laennec, R. T. H.: Trait~ de l'auscultation m~diate et des maladies des poumons et du coeur, 4th ed., J. S. Claude, Paris, 1837 vol. 1, 10. 2. Osler, W.: On a remarkable heart murmur, heard at a distance from the chest wall, Med. Times and Gaz. Lond., ii, 432-433, 1880. Patient presented, Medico Chirurgical Society of Montreal April 30, 1880. Reported in Can. Med. Surg. J. Vl11:518-519, 1879-1880. 3. Segall, H. N.: Use of written symbols to describe cardiovascular sounds and murmurs, in Encyclopedia of Cardiology, Luisada, A. A., ed., McGraw-Hill Book Company, Inc., vol. 2, p. 3-105, 1959. 4. Segall, H. N.: Evolution of graphic symbols for cardiovascular sounds and murmurs, Br. Heart J. 24:1, 1962.
February, 1976, Vol. 91, No. 2
plasma concentration is ignored. Although the intravenous use of these drugs simplifies this problem somewhat, a large variable, the volume of drug distribution, is unmeasured. There is no reason to believe t h a t the volume of drug distribution is equal between the three clinical classes of p.-tients studied. Indeed, the authors themselves have shown significant difference in blood volume and distribution between the patient groups, suggesting t h a t the volume of drug distribution may also vary. Thus, the drug dose to blood pressure response relationship presented cannot be construed to be equivalent to a drug concentration to response relationship, and thus, conclusions regarding receptor pharmacology become tenuous. Furthermore, to interpret changes in alpha adrenergic receptor pharmacology meaningfully, concentration to response relationships must be c o m p l e t e - t h a t is, curves constructed using drug concentrations resulting in subthreshold to maximal responses must be u s e d - a n d the results should be normalized. Obviously, maximal presser doses of norepinephrine are incompatible with human experimentation; however, short of such data, conclusions, again, are not well founded. Furthermore, in order to compare drug doses which are needed to reach a given response level, t h a t response level must be demonstrated to be within the linear portion of the drug concentration to response relationship. The potential of comparing points at threshold va.lues that are slow rising versus later points which are on the rapid rising, linear portion of the dose response curve invites misinterpretation. The authors' conclusion t h a t a decreased responsiveness to norepinephrine in borderline hypertensive patients suggests the possibility of a change in "the role of availability of receptor sites to the vasoactive agent" may be indeed correct; however, their inferences from this point are incompatible with adrenergic receptor pharmacology. A decrease of available receptor sites implies a competitive or noncompetitive alpha adrenergic receptor antagonist. Alternatively, a physiologic antagonist might give similar results. However, I know of no evidence that shows that norepinephrine can physiologically or pharmacologically antagonize itself. Indeed, if a patient's vascular system were stimulated by pre-existing endogenous norepinephrine as the authors suggest, additional increments of exogenous norepinephrine should give a greater increment of vascular response, since such a system would not be operating on the early threshold portion of the dose response curve but rather on the linear, rapid rising, portion of this relationship. Since the authors' own observations show exactly the opposite, t h a t is, a greater amount of norepinephrine is needed to evoke a similar response, their conclusions seem unsupported by their data. I realize that the above pharmacologic considerations can rarely, if ever, be met in human experimentation. However, in a paper which cites receptor pharmacology and an altered response to vasoactive agents as a prime pathophysiologic determinant in borderline hypertensive patients, I think t h a t it is important that the above concepts be included in the interpretation of the data. Although the authors' interpretations are frequently qualified by the word "suggests," I would prefer their stating clearly where their inferences do and do not meet strict receptor and clinical pharmacologic principles. This information is not always readily available to or remembered by the active clinician. The information, however, is
A m e r i c a n Heart Journal
essential to the proper interpretation of articles dealing with cardiovascular pharmacology as this one does. I would be most interested in the editor's and/or authors' comments in regard to the above critique and in the above concepts of clinical and receptor pharmacology being pub: lished either as the letter above or in terms of an editorial by an expert of your choice.
Kenneth M. Kessler, M.D., Major, MC Formerly, Assistant Chief, General Medicine Service Brooke Army Medical Center Fort Sam Houston, Texas 78234 Present address: Dept of Medicine Temple University Health Sciences Center Philadelphia, Pa. 19140
Autoauscultation in a patient with floppy mitral valve syndrome To the Editor: Laennec ~ named the method of listening with the aid of a stethoscope "mediate" auscultation to distinguish it from "immediate" auscultation which was performed by placing the listener's ear on the body of the patient. "Autoauscultation," an older kind, represents what a person hears of sound emanating from his or her body. Hearing one's heart sounds is a very common experience, which usually occurs while lying in bed on the left side with the chest and the ear on a continuous surface, pillow, or mattress. In some rare instances, patients hear heart murmurs while they are in sitting or standing posture. These murmurs may be transient and usually represent a significant valvular abnormality. In 1880, William Osler published his observations on "a remarkable heart murmur heard at a distance from the chest wall. ''2 The following excerpts from this article are quoted because they describe clinical features which resemble those of our patient. "J. W., aged twelve, a well nourished young girl, was sent to me in May, 1880, by Dr. BuUer,* who had noticed a remark able whistling sound, while examining her eyes. The mothel stated she had been a healthy child though never robust. Had inflammation of the lungs at eighteen months, measles at the age of 3 and scarlet fever, three years age... Auscultation-As she sits upright in the chair the heart sounds at the apex and the base loud and clear; no murmur. When she stands a loud systolic murmur is heard at the apex, high-pitched, somewhat musical, of maximum intensity in fifth interspace; it varies a good deal, being loud for three or four beats, and then faint for one or two succeeding ones, due to the influence of respiration. On removal of the ear from the chest wall, the murmur can be heard at a distance of several inches. It disappeared quite suddenly and could not be detected on most careful examination. She was then asked to run about the room and up and down stairs. On sitting down, after this, the heart's action was very forcible but the heart sounds were clear. The child then suggested that she heard it most frequently when in the stooping posture; and on causing her to lean forward and relax the chest, the murmur was at once heard, and with greatly increased intensity. It was distinctly audible at a distance of three feet two inches by measurement, and could be heard at any point on the chest and on top of the head. Pulse 96. *The first Professor of Ophthalmology at McGill University.
2(}9
Letters to the Editor
Fig. 1. Quantitative symbol phonocardiogram (QSPcg) depicts the normal pattern of heart sounds with respect to loudness, duration and quality. The late, cresendo, coarse systolic m u r m u r was the first clue to the diagnosis of floppy mitral valve syndrome. Auscultation at the apex with the patient standing, then bent forward touching her toes with her fingers, then again in the standing position, seems to have elicited a quite loud musical cresendo systolic m u r m u r which however was not loud enough to be audible by the patient who did not hear any m u r m u r during the entire study. The exercise consisted of 40 mountings of the two-step in 90 seconds, raising the heart rate to about 150 per minute. A significant, somewhat superficial and musical m u r m u r appeared 30 seconds after exercise and grew a little louder until the second milmte when no m u r m u r but the early systolic "click" (a short sound), which appeared at 30 seconds, persisted. This too, disappeared in the third minute when the late short crescendo-systolic murmur reappeared. But this too disappeared in the fourth minute, leaving only the normal first and second sounds. When the patient was examined again on February 10, 1975, the only abnormal feature was a faint, short early click about half as loud as the one heard on J a n u a r y 8th. These observations emphasize the wide, unpredictable variability of the systolic click and m u r m u r which point to the diagnosis of a floppy mitral valve. The QSPcg, written while listening, contains precise details, some of which could not be found in an electrophonocardiogram (EPcg), e.g., the superficial musical quality of the systolic murmur, the distinction between the coarse quality of the crescendo m u r m u r before exercise, and the blowing quality immediately after exercise. On the other hand, the electrophonocardiogram (EPcg) would permit precise measurement of the time interval between the first sound and the click. (Diagram adapted and modified from Segall, Harold N., in Encyclopedia of Cardiology, Luisada, A. A., ed., New York, 1959, McGraw-Hill Book Company, Inc., Vo|. 1, p. 3lO5.)
270
February, 1976, Vol. 91, No. 2
Letters to the Editor
Fig. 2. Lead II, recorded after exercise, reveals occasional ventricular ectopic beats.
On May 28th, she was shown at the Medico-Chirurgical Society of Montreal and most of the members heard the murmur. A day or two before the meeting, I called at her mother's house and satisfied myself of its presence though it was very variable. On July 13, I saw her again at her home and failed after prolonged examination to hear the murmur. She stated that she had not heard it herself for some time." When he examined her on July 21, he did hear the murmur and added t h a t . . . "There was no constancy in the variations. The rhythm is distinctly systolic, the first sound of the heart is not effaced by it though not so sharp as in its absence. During an examination extending over twenty minutes, the murmur was present four or five times and for a brief interval only, less than a minute each time." It is tempting to continue quoting Osler's remarks and his discussion of the literature, which he ends with the following, "I am not prepared to suggest an explana: tion of the cause of the murmur in this instance" and he adds t h a t his patient was "delicately built and nervous." The person who reported Osler,s presentation of the case at the Medico-Chirurgical Society of Montreal* wrote the following: "Dr. Osler cannot account for the murmur, but thinks, perhaps, it arises from an unusually flexible chest and pressure thus exerted on the pulmonary artery and aorta. Dr. Rosst suggested that it might possibly be exPlained by the existence of some loosely pedunculated body hanging inside the heart in such a way that, only in certain positions, it would *An error has crept into the records of the date of this meeting: Osler gives May 28, 1880; this report uses April 30th. tDr. George Ross.
American Heart Journal
Fig. 3. In the dorsal recumbent posture, the interval between the beginning of the first sound and of t h e click varies between 200 and 210 msec: In the sitting posture, it varies between 240 and 260 msec. The amplitude of the sound waves do not precisely reflect the relative loudness of the sounds heard with the stethoscope, as depicted in the quantitative symbol phonocardiogram (QSPcg). Clinical auscultation affords a clearer distinction between the late, crescendo systolic murmur and the second sound than the electrophonocardiogram (EPcg).
271
Letters to the Editor
fall into the blood current and develop a m u r m u r . . . The President* rather favoured the idea that it was most likely due to bending of the costal cartilages and pressure on the pulmonary artery. ''~ Our patient, V. R. (ECG #64,496), a young woman of 23, heard a peculiar noise emanating from inside her chest at the age of twelve. She remembers that one day when at home, seated and in the company of several friends, she became aware of a peculiar "squeaking, grating noise," a rhythmically recurring noise emanating from her chest. She could listen to the conversation while hearing this noise which "soon" disappeared. 1' During the next ten years it recurred "occasionally." At the age of eighteen, she consulted a physician because she noticed irregularity in her heart beating. The physician reassured her and recommended abstinence from tea and coffee. She has never smoked cigarettes or any type of tobacco. The irregularity continued to recur and in addition the noise began to appear with gradually increasing frequency. During the past year or so, she heard the noise once in many weeks, then the intervals shortened to about two weeks, then several times a week and more recently she has been hearing it several times a day. She has n~ver heard it while in bed or otherwise recumbent. In search of some correlation with a particular activity she has noticed that it tends to come on when she is standing in the kitchen and vigorously stirring a mixture of food she is preparing. Emotional excitement also tends to elicit the noise. It is invariably regular in rhythm. Sometimes it stops for only a few beats then starts again and continues for some minutes when it stops and becomes audible again only the next day, or several days later. She feels the cardiac irregularity independently of the noise. When she consulted Dr. Lawrence Battersby recently, he heard the noise, the first physician who did hear it, and he referred her to us for further study. About two months previously, she asked her boyfriend to place his ear on her chest when she was aware of the noise and he confirmed that it accompanied each heart beat. Both parents, her brother, and sister, are in good health. Having in mind a recent experience with twin males aged 65, both of whom have the floppy mitral valve syndrome and each of whom has one son who also has this condition, we invited her parents and siblings to be examined. They declined, apparently without regrets. She has not had any major illness in the past. She did have measles and chicken pox as a child and influenza at nineteen. She works as a clerk in the library of an industrial firm. Physical examination: A slender, delicate, young woman of 28; weight 91 pounds, height 63 inches. Nothing could be found to suggest Marfan syndrome. No abnormalities could be detected until the heart murmurs were heard. The pattern of heart, sounds, the heart murmurs, and Korotkoff sounds are described more precisely, more completely in greater detail by the quantitative symbol phonocardiogram (QSPcg) in Fig. 1 than any description in language could achieve.:~"~The electrophonocardiogram (EPcg) in Fig. 2 confirms variations in time relationship of the click. The electrocardiogram (Fig. 3) presents only normal *Dr. H. Howard. Dr. R. P. Howard, Osler's teacher, was present at the meeting; no discussion by him is recorded.
272
features before exercise but after forty mountings of the twostep exercise test, two ventricular premature beats were recorded. X-ray film of the chest revealed no abnormalities. The following report was received from Dr. F. Winsberg of the Montreal General Hospital about the ultrasound study. "Echocardiogram shows a classic midsystolic buckling of the mitral valve. This is the sort of prolapse which produces the midsystolic click-late systolic murmur pattern. There is no evidence of chamber enlargement." Eighty-five years separate Osler's observations from ours. His vivid description strongly favors the view that his patient had a floppy mitral valve. Had he remained in Montreal during the next 39 years of his life, we might have had an interesting follow-up report on t h a t patient. At present, the technique of echocardiography makes possible a good correlation between the physical signs and the diagnosis of the anatomical and physiological anomaly. From the experience with other patients, notably with one of the twins mentioned above, we have learned that wide variations in the pattern of sounds and murmurs occur in some cases. The transient character of the typical signs accounts for the fact t h a t when our patient was examined annually at school and before going to camp, no physician noted a significant abnormality until Dr. Lawrence Battersby happened to listen when the systolic click and murmur did appear. The autoauscultation feature makes the clinical story of this patient of special interest. Osler's case of 95 years ago gains in significance in the light of current use of echocardiography. Our speculations about the cardiodynamics which result in the absence, the appearance, disappearance, and reappearance of the click and murmur in so wide a variety of loudnesses, durations, and qualities would resemble in accuracy the speculations of Osler, Ross, and Howard, about the origin of the murmur. The author wishes to express his cordial thanks to Dr. Lawrence Battersby, who introduced the patient to him, and to Dr. F. Winsberg who did the echocardiogram.
Harold N. SegaU, M.D. Department of Medicine McGill University and The Montreal General and Jewish General Hospitals Montreal, Quebec, Canada
REFERENCES
1. Laennec, R. T. H.: Trait~ de l'auscultation m~diate et des maladies des poumons et du coeur, 4th ed., J. S. Claude, Paris, 1837 vol. 1, 10. 2. Osler, W.: On a remarkable heart murmur, heard at a distance from the chest wall, Med. Times and Gaz. Lond., ii, 432-433, 1880. Patient presented, Medico Chirurgical Society of Montreal April 30, 1880. Reported in Can. Med. Surg. J. Vl11:518-519, 1879-1880. 3. Segall, H. N.: Use of written symbols to describe cardiovascular sounds and murmurs, in Encyclopedia of Cardiology, Luisada, A. A., ed., McGraw-Hill Book Company, Inc., vol. 2, p. 3-105, 1959. 4. Segall, H. N.: Evolution of graphic symbols for cardiovascular sounds and murmurs, Br. Heart J. 24:1, 1962.
February, 1976, Vol. 91, No. 2
