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Paroxysmal ventricular tachycardia with special reference to treatment
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.
After reversion of the tachycardia to a normal rhythm, twelve patients were maintained on quinidine sulfate, orally, in doses of from 0.6 to 1.0 Gm. daily. In ten cases paroxysmal centricular tachycardia did not recur on this maintenance regime. However, four of these patients died within one week, in spite of the qstablished and maintained normal rhythm. Two patients, in critical condition following myocardial infarction, were given quinidine intravwously. One had not responded to intravenous dosages of morphine of 11, 11, and 32 mg., and oral quinidine totalling 2, 5, and 3.3 Gm. on three successive days. This patient reverted to normal rhythm after 1.7 Gm. of quinidine sulfate was given by slow intravenous drip. Another patient, who was admitted in shock, showed no change in rhythm after being given 0.6 Gm. of quinidine sulfate intravenously in 10 C.C. of distilled water and died in about one hour. One patient under treatment for subacute bacterial endocarditis was given 1.0 Gm. of quinidine sulfate intravenously in divided doses over a period of twelve hours, and then reverted to normal rhythm after 1.2 mg. of Cedilanid was administered intravenously. The intravenous injection of 16 mg. of morphine sulfate resulted in immediate cessation of the abnormal rhythm in one patient with myocardial infarction. In another patient, the ventricular tachycardia reverted to sinus rhythm on carotid sinus pressure six minutes after 4.5 mg. of morphine sulfate had been given intravenously, the disturbance having been unaffected previously by repeated carotid sinus stimulation and 32 mg. of morphine.
BEILET.
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.
After reversion of the tachycardia to a normal rhythm, twelve patients were maintained on quinidine sulfate, orally, in doses of from 0.6 to 1.0 Gm. daily. In ten cases paroxysmal centricular tachycardia did not recur on this maintenance regime. However, four of these patients died within one week, in spite of the qstablished and maintained normal rhythm. Two patients, in critical condition following myocardial infarction, were given quinidine intravwously. One had not responded to intravenous dosages of morphine of 11, 11, and 32 mg., and oral quinidine totalling 2, 5, and 3.3 Gm. on three successive days. This patient reverted to normal rhythm after 1.7 Gm. of quinidine sulfate was given by slow intravenous drip. Another patient, who was admitted in shock, showed no change in rhythm after being given 0.6 Gm. of quinidine sulfate intravenously in 10 C.C. of distilled water and died in about one hour. One patient under treatment for subacute bacterial endocarditis was given 1.0 Gm. of quinidine sulfate intravenously in divided doses over a period of twelve hours, and then reverted to normal rhythm after 1.2 mg. of Cedilanid was administered intravenously. The intravenous injection of 16 mg. of morphine sulfate resulted in immediate cessation of the abnormal rhythm in one patient with myocardial infarction. In another patient, the ventricular tachycardia reverted to sinus rhythm on carotid sinus pressure six minutes after 4.5 mg. of morphine sulfate had been given intravenously, the disturbance having been unaffected previously by repeated carotid sinus stimulation and 32 mg. of morphine.
BEILET.