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Beriberi heart disease
542
AMERICA&
HEART
JOURNAL
J‘he heart, which was normal grossly, showed small pericardial and also entlocardial collections of lymphocytes and plasma c.ells histologically. The author emphasizes the unusual opportunit? that \vas presented in this case to study the pulmonary lesions of rheumatic fever uncomplicated by secondary infection or by changes secondary to heart disease. He describes rheumatic pneumonitis as a non-suppurative tissue reaction similar to that seen in other organs following hemolytic streptococcic infection of the upper rcspiratory tract; in some instances it was so pronounced as to dominate the clinical picture. Jensen points out the possibilit), of error in diagnosing such a pulmonary involvement as a virus pneumonitis. He recommends more extensive use of the cold pressor and of t hc antistreptolysin tests in differential diagnosis. GOUI.E\.. Hicks,
A. M., Painton, Pneumonia, With Med. 24:775 (May),
J. F., and Hantman, a Discussion of 1946.
the
S.: A Clinical Electrocardiographic
Analysis
of Primary Findings.
.i typical Ann.
Int.
This report is based upon an analysis of 321 cases of atypical pneumonia studied in one of the military hospitals in this country during the recent war. Correlations were established between the incidence of the disease and the age, race, u-eight, length of service, and the season of the year. The clinical features and laborator)findings were reviewed, and the conclusions reached were found to be similar to those expressed in previous reports concerning atypical pneumonia. ‘I‘hc same statement was true of the roentgen patterns and the authors’ comments concerning trcatment of this disease. Electrocardiographic examinations were employed cstensively in sixtythree cases, and twelve of this group showed “electrocardiographic evidence suggestive of myoOnI!, two of these patients presented rlinical evidence cardial and pericardial involvement.” The changes consisted of RS-1‘ segment elevations, Twave suggestive of cardiac abnormality. inversion, a disturbance of A-\’ conduction, or combinations of these. In seven of the cases there was electrocardiographic reversal to normal, whereas the other five showed irreversible changes Sonc of th r cases rame t0 which persisted throughout a three-month period of observation. alltopsy. W~I.:NDKOS. Rlankenhorn, Disease.
M. A., Vilter, C. F., Scheinker, J. A. M. A. 131:717 (June 29),
1. M.,
and
Austin,
R.
S.:
Reriheri
Heart
1946.
These authors report their study of a series of twelve cases which were diagnosed as beriberi heart disease from 1940 to 1945. Five patients died in the hospital; autopsies were performed on three patients. The authors believe that the oriental concept of beriberi heart disease a. characterized by Wenckebach criteria probably has hindered the diagnosis in many instances. This is particularly true in the large group of cases of beriberi heart disease which do not manifest the rapid circulation and which closely resemble other types of degenerative heart disease. The requirements for diagnosis in their series were (1) insufficient evidence of other etiology: (2) three or more months on a thiamine-deficient diet; (3) signs of neuritis or petlagra; (4) enlarged heart with sinus rhythm; (5) dependent edema; (6) elevated venous pressure; (7) minor electrocardiographic changes; (8) recovery with decrease in heart size; or (9) autopsy findings consistent with The chief factor in diagnosis includes the realization that the etiologir beriberi heart disease. The differential diagnosis includes coronary arteriosnature of the heart disease is obscure. clerosis, Fiedter’s myocarditis, and idiopathic hypertrophy. :Zlcoholism accounted for the poor dietaries of eleven patients. The majorit), of diet5 were deficient not only in thiamine, but also in the other water-soluble vitamins, particularl?. .Ilthough the time interval required to produce the degree niacin, riboflavin, and ascorbic acid. of hypovitaminosis sufficient to produce cardiac abnormalities varies considerably in different inIn all twelve cases there was other clinical dividuals, ninety days is the arbitrary point selected. evidence of nutritive failure. There was always some indication of peripheral neuritis or pellagra. In six cases evidence of both disorders was found. Eight of the twelve patients had anemia, which in thrcr
instances
was
normocytir
and
in five
macrocytic
in type.
Hypoproteinemia
was
ron-
sI~LECTEI~
.5-K<
ABSTRACTS
‘Ten of the patients during life showed clinical and roentsistently observed in these patients. Dependent edema was present in eleven of t hc twelve genologic evidence of cardiac enlargement. Serial electrocardiograms were patients, and elevated venous pressure was observed in nine. The most common abnormalities made in ten of the twelve cases and all showed abnormalities. observed were low voltage and minor alterations in the T w-al-es. WThen beriberi heart disease was suspected, the patient was put on a strict regimen which included rest in bed and a diet very low in thiamine. The control period was continued as long as the patient’s condition permitted. Large doses of thiamine were then given intravenously. Most cases which showed improvement did so gradually; only one showed dramatic improvement Three of tive patients who received digitalis apparently benein a period of twenty-four. hours. fited from this drug. There is some uncertainty as to the origin of the dictum that digitalis is of no aid in this condition and that if the heart responds well to this drug the cfiagnosis of beriberi is eliminated. While alterations in the myocardium in beriberi heart disease have been described and Three of their studied repeatedly for many decades, no pathognomic picture has been revealed. cases which came to necropsy showed degenerative changes of the heart muscle and interstitial edema. These observations were considered consistent with but not diagnostic of beriberi heart disease. In two instances in which the nervous system was examined, definite lesions in the tentral, peripheral. and autonomic nervous systems were revealed. hLI.KT. Nathanson,
Med.
M.
77:491
H.:
Hyperactive
(May).
1946.
Cardioinhihitory
Carotid
Sinus
Reflex.
=\rch,
lnt.
This report was based on a study of 115 patients showing hyperactive carotid sinus reflexes. The carotid sinus was considered hyperative when it fulfilled the following criteria: (1) a cardiac standstill of at least five seconds; (2) cardiac inhibition induced by simple pressure on the carotid sinus without massage of sinus; (3) standstill of equal intensity elicited on several tests. The youngest patient was 30 and the oldest in the group was 81 years of age; the average age was 58.9 years. Of the 115 patients, seventy-seven (67 per cent) presented no symptoms suggestive of carotid sinus syndrome. In ten cases, manifestations of the carotid sinus syndrome were the chief complaints. Attacks ,of syncope were experienced by only six patients. Symptoms resembling those of carotid sinus syndrome were presented by fifteen patients, but some mechanism other than the hyperactive carotid sinus reflex could be demonstrated as a basis for the attacks. In five of these patients, there was a true vertigo with nausea and tinnitus, indicative of Meniere’s syndrome. The sensations following pressure on the carotid sinus had no similarity to the sensations at the time of the spontaneous attacks. In four patients, the symptoms of faintness and dizziness were associated with attacks of paroxysmal tachycardia. A definite distinction is made between the hyperactive carotid sinus reflex which designated a hyperactive response to stimulation of the carotid sinus and the carotid sinus syndrome which designated a clinical condition. The author explains the presence of symptoms in some and the absence of symptoms in others with similar degrees of sensitivity to a difference in individual response to cerebral ischemia. This author also made an attempt to determine the site of the hyperactive cardioinhibitory reflex. Pressure over the carotid sinus was shown by Hering to elicit two independent effects: (I) a cardioinhibitory effect and (2) a vasodepressor effect. The former may be abolished by atropine, permitting observations of the vasodepressor effect. Blood pressure readings were taken during stimulation of the carotid sinus, before and after administration of atropine. It was observed that there was definite lowering of the blood pressure following carotid sinus stimulation He therefore concludes that either the vagus center in the medulla in the atropinized patient. or some portion of the efferent path in the vagus nerve must be considered responsible for the hyperactive response. This observation is of practical importance because denervation of the carotid sinus would not insure a consistent and permanent cure if the hypersensitivity was predominantly in the vagus nerve. BELLET.
AMERICA&
HEART
JOURNAL
J‘he heart, which was normal grossly, showed small pericardial and also entlocardial collections of lymphocytes and plasma c.ells histologically. The author emphasizes the unusual opportunit? that \vas presented in this case to study the pulmonary lesions of rheumatic fever uncomplicated by secondary infection or by changes secondary to heart disease. He describes rheumatic pneumonitis as a non-suppurative tissue reaction similar to that seen in other organs following hemolytic streptococcic infection of the upper rcspiratory tract; in some instances it was so pronounced as to dominate the clinical picture. Jensen points out the possibilit), of error in diagnosing such a pulmonary involvement as a virus pneumonitis. He recommends more extensive use of the cold pressor and of t hc antistreptolysin tests in differential diagnosis. GOUI.E\.. Hicks,
A. M., Painton, Pneumonia, With Med. 24:775 (May),
J. F., and Hantman, a Discussion of 1946.
the
S.: A Clinical Electrocardiographic
Analysis
of Primary Findings.
.i typical Ann.
Int.
This report is based upon an analysis of 321 cases of atypical pneumonia studied in one of the military hospitals in this country during the recent war. Correlations were established between the incidence of the disease and the age, race, u-eight, length of service, and the season of the year. The clinical features and laborator)findings were reviewed, and the conclusions reached were found to be similar to those expressed in previous reports concerning atypical pneumonia. ‘I‘hc same statement was true of the roentgen patterns and the authors’ comments concerning trcatment of this disease. Electrocardiographic examinations were employed cstensively in sixtythree cases, and twelve of this group showed “electrocardiographic evidence suggestive of myoOnI!, two of these patients presented rlinical evidence cardial and pericardial involvement.” The changes consisted of RS-1‘ segment elevations, Twave suggestive of cardiac abnormality. inversion, a disturbance of A-\’ conduction, or combinations of these. In seven of the cases there was electrocardiographic reversal to normal, whereas the other five showed irreversible changes Sonc of th r cases rame t0 which persisted throughout a three-month period of observation. alltopsy. W~I.:NDKOS. Rlankenhorn, Disease.
M. A., Vilter, C. F., Scheinker, J. A. M. A. 131:717 (June 29),
1. M.,
and
Austin,
R.
S.:
Reriheri
Heart
1946.
These authors report their study of a series of twelve cases which were diagnosed as beriberi heart disease from 1940 to 1945. Five patients died in the hospital; autopsies were performed on three patients. The authors believe that the oriental concept of beriberi heart disease a. characterized by Wenckebach criteria probably has hindered the diagnosis in many instances. This is particularly true in the large group of cases of beriberi heart disease which do not manifest the rapid circulation and which closely resemble other types of degenerative heart disease. The requirements for diagnosis in their series were (1) insufficient evidence of other etiology: (2) three or more months on a thiamine-deficient diet; (3) signs of neuritis or petlagra; (4) enlarged heart with sinus rhythm; (5) dependent edema; (6) elevated venous pressure; (7) minor electrocardiographic changes; (8) recovery with decrease in heart size; or (9) autopsy findings consistent with The chief factor in diagnosis includes the realization that the etiologir beriberi heart disease. The differential diagnosis includes coronary arteriosnature of the heart disease is obscure. clerosis, Fiedter’s myocarditis, and idiopathic hypertrophy. :Zlcoholism accounted for the poor dietaries of eleven patients. The majorit), of diet5 were deficient not only in thiamine, but also in the other water-soluble vitamins, particularl?. .Ilthough the time interval required to produce the degree niacin, riboflavin, and ascorbic acid. of hypovitaminosis sufficient to produce cardiac abnormalities varies considerably in different inIn all twelve cases there was other clinical dividuals, ninety days is the arbitrary point selected. evidence of nutritive failure. There was always some indication of peripheral neuritis or pellagra. In six cases evidence of both disorders was found. Eight of the twelve patients had anemia, which in thrcr
instances
was
normocytir
and
in five
macrocytic
in type.
Hypoproteinemia
was
ron-
sI~LECTEI~
.5-K<
ABSTRACTS
‘Ten of the patients during life showed clinical and roentsistently observed in these patients. Dependent edema was present in eleven of t hc twelve genologic evidence of cardiac enlargement. Serial electrocardiograms were patients, and elevated venous pressure was observed in nine. The most common abnormalities made in ten of the twelve cases and all showed abnormalities. observed were low voltage and minor alterations in the T w-al-es. WThen beriberi heart disease was suspected, the patient was put on a strict regimen which included rest in bed and a diet very low in thiamine. The control period was continued as long as the patient’s condition permitted. Large doses of thiamine were then given intravenously. Most cases which showed improvement did so gradually; only one showed dramatic improvement Three of tive patients who received digitalis apparently benein a period of twenty-four. hours. fited from this drug. There is some uncertainty as to the origin of the dictum that digitalis is of no aid in this condition and that if the heart responds well to this drug the cfiagnosis of beriberi is eliminated. While alterations in the myocardium in beriberi heart disease have been described and Three of their studied repeatedly for many decades, no pathognomic picture has been revealed. cases which came to necropsy showed degenerative changes of the heart muscle and interstitial edema. These observations were considered consistent with but not diagnostic of beriberi heart disease. In two instances in which the nervous system was examined, definite lesions in the tentral, peripheral. and autonomic nervous systems were revealed. hLI.KT. Nathanson,
Med.
M.
77:491
H.:
Hyperactive
(May).
1946.
Cardioinhihitory
Carotid
Sinus
Reflex.
=\rch,
lnt.
This report was based on a study of 115 patients showing hyperactive carotid sinus reflexes. The carotid sinus was considered hyperative when it fulfilled the following criteria: (1) a cardiac standstill of at least five seconds; (2) cardiac inhibition induced by simple pressure on the carotid sinus without massage of sinus; (3) standstill of equal intensity elicited on several tests. The youngest patient was 30 and the oldest in the group was 81 years of age; the average age was 58.9 years. Of the 115 patients, seventy-seven (67 per cent) presented no symptoms suggestive of carotid sinus syndrome. In ten cases, manifestations of the carotid sinus syndrome were the chief complaints. Attacks ,of syncope were experienced by only six patients. Symptoms resembling those of carotid sinus syndrome were presented by fifteen patients, but some mechanism other than the hyperactive carotid sinus reflex could be demonstrated as a basis for the attacks. In five of these patients, there was a true vertigo with nausea and tinnitus, indicative of Meniere’s syndrome. The sensations following pressure on the carotid sinus had no similarity to the sensations at the time of the spontaneous attacks. In four patients, the symptoms of faintness and dizziness were associated with attacks of paroxysmal tachycardia. A definite distinction is made between the hyperactive carotid sinus reflex which designated a hyperactive response to stimulation of the carotid sinus and the carotid sinus syndrome which designated a clinical condition. The author explains the presence of symptoms in some and the absence of symptoms in others with similar degrees of sensitivity to a difference in individual response to cerebral ischemia. This author also made an attempt to determine the site of the hyperactive cardioinhibitory reflex. Pressure over the carotid sinus was shown by Hering to elicit two independent effects: (I) a cardioinhibitory effect and (2) a vasodepressor effect. The former may be abolished by atropine, permitting observations of the vasodepressor effect. Blood pressure readings were taken during stimulation of the carotid sinus, before and after administration of atropine. It was observed that there was definite lowering of the blood pressure following carotid sinus stimulation He therefore concludes that either the vagus center in the medulla in the atropinized patient. or some portion of the efferent path in the vagus nerve must be considered responsible for the hyperactive response. This observation is of practical importance because denervation of the carotid sinus would not insure a consistent and permanent cure if the hypersensitivity was predominantly in the vagus nerve. BELLET.