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Discussion of the circus movement. Proof of its occurrence in the clinical auricular flutter
SELECTED
The authors can be diagnosed
Freeman, Arterial
63.5
ABSTRACTS
believe that uncomplicated cases of these two common congenital abnormalities in a large percentage of the cases by observation of the features presented. ZION.
N. E., Leeds, F. H., Disease; Indications
and Gardner, H. E.: and Contraindications.
Sympatheclomy Ann. Surg.
for 126:873
Obliterative (Der.1, 1947.
In the management of obliterative arterial disease of the extremities, sympathcctomy has t\vu functions: first, the ab6lishmenl of vasomotor tone and, second, the abelment of the collateral circulation. The authors point out that the greate,r the &dence of overactivity of the sympathetic nervous system, the better the results following sympathectomy. There are six guiding points which indicate an increase in vasomotor activity in an extremity: (1) coolness; (2) sweating, the combination making for a “cold, clammy foot or hand”; (3) cyanotic mottling of the digits; 14) constriction of the superficial veins; i.5) delayed blanching of the qxtremity on elevation; and (6) the patient’s subject.ive statement of improvement in the extremity following a paravertebral novocaine block. In patients with obliterative arlerial disease, whether it be due to thromboangiitis obliterans or 10 arteriosclerosis, if evidence of a high degree of vasomotor tone is present, then sympathectomy is indicated. Conversely, if little or no evidence of vasomotor activity is present, sympathectomy is not only u~rle~s but may actually prove to be harmful. The authu~-5 citr Atlas’ Ggns which contraindicate sympathectomy: (1) severe extensive al-Lerial occlusion: 11’) rapid blanching on elevation of the extremity; and (3) atrophy of skin ant1 ~ubcut;lneous (issue>. [n ;ttldition to three cases reported by Atlas, the authors reporf four patients who were made worse by sympathectomy. .\I1 had evidence of IO\V vascular tone and should not have been subjected to the operation. The explanation of these observations lies in the fact that there is a dual anatomic slrucLure in the peripheral circulation. First, there is the arteriovenous anastomosis in the form uf the neuromyoarterial ~IOI~LIS, and second, the nutrient capillaries. The former is under the control of the sympathetic nervous system and is important in conservation and release of heat as well as serving as important shunts between the arterial and venous systems. When there is extensive arterial obliterative disease, sympathectomy opens these glomus shunts and indirectly interferes with the circulation through the capillaries, with consequent gangrene of an extremity in some cases. LORD.
Cabrera, E., and Sodi-Pallares, Occurrence in the Clinical (Dec.), 1947.
D. : Discussion of the Auricular Flutter.
Circus Movement. Arch. inst. cardiol.
Proof de Mexico
of Its 17:850
The authors have studied the characteristics and possible modifications of the circus movein clinical auricular flutter. The following conclusions were reached : 1. Rotation of the instantaneous axis is llol in favor of a circus movement in auricular flutter; it is only evidence of the cul-ve described by the vectocardiogram of the flutter which is also present in other cyclic electrical phenomena. 2. Intravenous injection of acetylcholine causes the acceleration of both the auricular ant1 1 he ventricular rates. This can be uscd in the differential diagnosis between auricular flutter and auricular tachycardia because in the latter, acetylcholine either ends the attack or has no effect. 3. Intravenous injection of a large dose of acetylcholine in cases of flutter has never caused an auricular rate similar to that observed in auricular fibrillation, and no irregularity of the auricular waves was observed. 4. The acceleration of flutter caused by acetylcholine supports the theory of a circus movement. 5. The time of activation of the auricles was further studied by simultaneous tracings ol esophageal and precordial leads. While the ventral aspect of the auricular mass was activated from above downward, the dorsal aspect was activated from below upward. This is in favor of the existence of a circus movement. ment
636
AMERICAN
HEART
JOURNAI
6. Rotation of the instantaneous axis and the auricular vectocardiogram suggested in all cases of flutter, except one, that the wave of activation was descending in the anterior part and ascending in the posterior part of the ventricular mass. with
7. The rotation plane of the auricular vectocardiogram the hywthesis of a circus movement around the orifices
was further of both vcnae
found ravae.
in
agreement LlIIYAI)A.
Alzamora Castro, Subendocardic
V. : Corltribu Infarctions.
tion Arch.
LO
the Study inst. cardiol.
of S-T Cbaryes, de Mexico 17:870
Angina (Dec.),
Yectoris 1947.
and
The authors describe in detail the anatomic, clinical, and electrocardiographic characteristics of a case with extensive suhendocardial infarction involving the entire left ventricle and part of The patient had repeated and almost continuous attacks of precordial pain the right ventricle. during which the electrocardiogram showed downward displacement of the S-T interval in leads where the exploring electrode was near the epicardial surface, and upward displacement in those leads which record the cavity potentials. A clinical diagnosis of a suhendocardial infarction was made. ‘\t necropsy the suhendocardial necrosis was found to he secondary to partial obliteration of the orifices of both coronary arteries caused by syphilitic aortitis. It is not known why a total decrease of the coronary blood flow should cause a selective suhendocardial damage. A hypothetical explanation, based on merhanical factors, is advanced by the authors. The electrocardiographic changes encountered during the attacks of angina pectoris are similar to those reported in the present case. During the pain, a metabolic disturbance, prohahly related to oxygen deficiency, seems to occur; this affects chiefly the deeper or suhendocardial portions of the left ventricle and is accompanied by electrical forces which produce transient electrocardiographic changes. When the circulatory disturbance is severe, prolonged, or repeated, as in this patient, the alterations may reach the stage of necrosis (infarct). Certain clinical syndromes simulating coronary occlusion present electrocardiographic changes similar to those recorded during the attacks of angina pectoris and are probably due to the same basic circulatory changes. These cases have heen classified by the authors as “subenclocardial infarcts” and are characterized electrocardiographically by more or less permanent modifications of the S-T interval. LUISAI)A. Hejtmancik, Special
M. R., Reference
and Herrmann, to Treatment.
G. R.: Texas
Paroxysmal State J. Med.
Ventricular Tacbycardia 53~505 (Dec.), 1947.
With
A series of twenty cases of paroxysmal ventricular tachycardia has been analyzed by the authors. The average age of the patients in the series was 52.8 years, the youngest being 18 and The the oldest, 80 years of age. Coronary artery disease was present in 70 per cent of the cases, No rates of the tachycardia varied between 110 and 220, with an average of 170 per minute. correlation was observed between heart rate and prognosis. Fifteen of the cases were associated with signs of congestive failure. Three patients showed cerebral manifestations; in two these were due to the tachycardia itself, and in one they were secondary to cerebral embolism. One of these had generalized convulsive seizures and another had attacks of syncope. Of two patients with apparently normal hearts, one complained of precordial hurning and the other had no symlrtoms referable to the disorder. In three of the four patients receiving no specific therapy, the disorder persisted until death. Ten of twelve cases reverted to a normal rhythm on quinidine, given orally; the amount required varied from 0.6 Gm. to 5.2 Gm. in twenty-four hours. In one patient with acute myocardial infarction, the rhythm was not abolished by 11.8 Gm. of quinidine, given orally, over a period of The two patients with no demonstrable heart disease were sucfour days, and the patient died. cesafully treated, one with small and one with large oral doses of quinidine. In one patient, whose tachycardia reverted to a normal rhythm with intravenous injection of 16 mg. of morphine, even small doses of quinidine were found to prolong the QRS complex more than 2.5 per cent.
The authors can be diagnosed
Freeman, Arterial
63.5
ABSTRACTS
believe that uncomplicated cases of these two common congenital abnormalities in a large percentage of the cases by observation of the features presented. ZION.
N. E., Leeds, F. H., Disease; Indications
and Gardner, H. E.: and Contraindications.
Sympatheclomy Ann. Surg.
for 126:873
Obliterative (Der.1, 1947.
In the management of obliterative arterial disease of the extremities, sympathcctomy has t\vu functions: first, the ab6lishmenl of vasomotor tone and, second, the abelment of the collateral circulation. The authors point out that the greate,r the &dence of overactivity of the sympathetic nervous system, the better the results following sympathectomy. There are six guiding points which indicate an increase in vasomotor activity in an extremity: (1) coolness; (2) sweating, the combination making for a “cold, clammy foot or hand”; (3) cyanotic mottling of the digits; 14) constriction of the superficial veins; i.5) delayed blanching of the qxtremity on elevation; and (6) the patient’s subject.ive statement of improvement in the extremity following a paravertebral novocaine block. In patients with obliterative arlerial disease, whether it be due to thromboangiitis obliterans or 10 arteriosclerosis, if evidence of a high degree of vasomotor tone is present, then sympathectomy is indicated. Conversely, if little or no evidence of vasomotor activity is present, sympathectomy is not only u~rle~s but may actually prove to be harmful. The authu~-5 citr Atlas’ Ggns which contraindicate sympathectomy: (1) severe extensive al-Lerial occlusion: 11’) rapid blanching on elevation of the extremity; and (3) atrophy of skin ant1 ~ubcut;lneous (issue>. [n ;ttldition to three cases reported by Atlas, the authors reporf four patients who were made worse by sympathectomy. .\I1 had evidence of IO\V vascular tone and should not have been subjected to the operation. The explanation of these observations lies in the fact that there is a dual anatomic slrucLure in the peripheral circulation. First, there is the arteriovenous anastomosis in the form uf the neuromyoarterial ~IOI~LIS, and second, the nutrient capillaries. The former is under the control of the sympathetic nervous system and is important in conservation and release of heat as well as serving as important shunts between the arterial and venous systems. When there is extensive arterial obliterative disease, sympathectomy opens these glomus shunts and indirectly interferes with the circulation through the capillaries, with consequent gangrene of an extremity in some cases. LORD.
Cabrera, E., and Sodi-Pallares, Occurrence in the Clinical (Dec.), 1947.
D. : Discussion of the Auricular Flutter.
Circus Movement. Arch. inst. cardiol.
Proof de Mexico
of Its 17:850
The authors have studied the characteristics and possible modifications of the circus movein clinical auricular flutter. The following conclusions were reached : 1. Rotation of the instantaneous axis is llol in favor of a circus movement in auricular flutter; it is only evidence of the cul-ve described by the vectocardiogram of the flutter which is also present in other cyclic electrical phenomena. 2. Intravenous injection of acetylcholine causes the acceleration of both the auricular ant1 1 he ventricular rates. This can be uscd in the differential diagnosis between auricular flutter and auricular tachycardia because in the latter, acetylcholine either ends the attack or has no effect. 3. Intravenous injection of a large dose of acetylcholine in cases of flutter has never caused an auricular rate similar to that observed in auricular fibrillation, and no irregularity of the auricular waves was observed. 4. The acceleration of flutter caused by acetylcholine supports the theory of a circus movement. 5. The time of activation of the auricles was further studied by simultaneous tracings ol esophageal and precordial leads. While the ventral aspect of the auricular mass was activated from above downward, the dorsal aspect was activated from below upward. This is in favor of the existence of a circus movement. ment
636
AMERICAN
HEART
JOURNAI
6. Rotation of the instantaneous axis and the auricular vectocardiogram suggested in all cases of flutter, except one, that the wave of activation was descending in the anterior part and ascending in the posterior part of the ventricular mass. with
7. The rotation plane of the auricular vectocardiogram the hywthesis of a circus movement around the orifices
was further of both vcnae
found ravae.
in
agreement LlIIYAI)A.
Alzamora Castro, Subendocardic
V. : Corltribu Infarctions.
tion Arch.
LO
the Study inst. cardiol.
of S-T Cbaryes, de Mexico 17:870
Angina (Dec.),
Yectoris 1947.
and
The authors describe in detail the anatomic, clinical, and electrocardiographic characteristics of a case with extensive suhendocardial infarction involving the entire left ventricle and part of The patient had repeated and almost continuous attacks of precordial pain the right ventricle. during which the electrocardiogram showed downward displacement of the S-T interval in leads where the exploring electrode was near the epicardial surface, and upward displacement in those leads which record the cavity potentials. A clinical diagnosis of a suhendocardial infarction was made. ‘\t necropsy the suhendocardial necrosis was found to he secondary to partial obliteration of the orifices of both coronary arteries caused by syphilitic aortitis. It is not known why a total decrease of the coronary blood flow should cause a selective suhendocardial damage. A hypothetical explanation, based on merhanical factors, is advanced by the authors. The electrocardiographic changes encountered during the attacks of angina pectoris are similar to those reported in the present case. During the pain, a metabolic disturbance, prohahly related to oxygen deficiency, seems to occur; this affects chiefly the deeper or suhendocardial portions of the left ventricle and is accompanied by electrical forces which produce transient electrocardiographic changes. When the circulatory disturbance is severe, prolonged, or repeated, as in this patient, the alterations may reach the stage of necrosis (infarct). Certain clinical syndromes simulating coronary occlusion present electrocardiographic changes similar to those recorded during the attacks of angina pectoris and are probably due to the same basic circulatory changes. These cases have heen classified by the authors as “subenclocardial infarcts” and are characterized electrocardiographically by more or less permanent modifications of the S-T interval. LUISAI)A. Hejtmancik, Special
M. R., Reference
and Herrmann, to Treatment.
G. R.: Texas
Paroxysmal State J. Med.
Ventricular Tacbycardia 53~505 (Dec.), 1947.
With
A series of twenty cases of paroxysmal ventricular tachycardia has been analyzed by the authors. The average age of the patients in the series was 52.8 years, the youngest being 18 and The the oldest, 80 years of age. Coronary artery disease was present in 70 per cent of the cases, No rates of the tachycardia varied between 110 and 220, with an average of 170 per minute. correlation was observed between heart rate and prognosis. Fifteen of the cases were associated with signs of congestive failure. Three patients showed cerebral manifestations; in two these were due to the tachycardia itself, and in one they were secondary to cerebral embolism. One of these had generalized convulsive seizures and another had attacks of syncope. Of two patients with apparently normal hearts, one complained of precordial hurning and the other had no symlrtoms referable to the disorder. In three of the four patients receiving no specific therapy, the disorder persisted until death. Ten of twelve cases reverted to a normal rhythm on quinidine, given orally; the amount required varied from 0.6 Gm. to 5.2 Gm. in twenty-four hours. In one patient with acute myocardial infarction, the rhythm was not abolished by 11.8 Gm. of quinidine, given orally, over a period of The two patients with no demonstrable heart disease were sucfour days, and the patient died. cesafully treated, one with small and one with large oral doses of quinidine. In one patient, whose tachycardia reverted to a normal rhythm with intravenous injection of 16 mg. of morphine, even small doses of quinidine were found to prolong the QRS complex more than 2.5 per cent.