Early Atrial Arrhythmias in Acute Myocardial Infarction* Role of the Sinus Node Artery Michael Kyriakidis, M.D., F.C.C.P.; john Barbetseas, M.D.; Athanassios Antonopoulos, M.D.; Charalambos Skouros, M.D.; Costas Tentolouris, M.D.; and Pavlos Toutouzas, M.D. We studied atrial arrhythmias during the first 12 h of admission to the hospital in 266 consecutive patients with acute myocardial infarction who subsequently underwent coronary angiography. Ten patients developed atrial fibrillation, one atrial Rutter, and one supraventricular tachycardia. Another five developed sinus dysrhythmias. All of the above patients had an acute inferior myocardial infarction, and in 10 of the 12 patients with supraventricular arrhythmias and in four of five with sinus dysrhythmias,
the origin of the sinus node artery started just after an occluded right coronary or left circumftex artery or was involved in the occlusion. Thus, ischemia of the sinus node due to coronary occlusion proximal to the origin of the sinus node artery was a likely cause of these arrhythmias.
arrhythmias have been reported in as many as 20 percent of cases of acute myocardial infarction. 1 They are most common in the later stages of myocardial infarction as a complication of pericarditis 2 -"~ In the early stages, they are rare, or heart failure. and the pathogenesis is uncertain. 5 ·6 The underlying cause of the arrhythmias is ischemia, but the precise mechanism and the extent remain controversial. In the present prospective clinical angiographic study of 266 consecutive patients with acute myocardial infarction, we attempted to correlate serious atrial arrhythmias during the first 12 h of admission with the ischemia produced by interruption of the blood Row in the arteries supplying the atrium, in particular the sinus node artery.
was 2.2 h. All patients were in sinus rhythm. Patients with clinical evidence of left ventricular failure, defined as pulmonary edema, significant crepitations, gallop rhythm, and low output state, were excluded from the study because of the possibility of dysrhythmias as a result of hemodynamic changes. Of the 266 patients without contraindications to thrombolysis, 197 received thrombolytic therapy on arrival in the coronary care unit, started in less than 6 h of the onset of symptoms of the acute event. The patients were also treated with morphine for severe chest pain, intravenous nitroglycerin if their systolic blood pressure was above 100 mm Hg, and lignocaine intravenously if they developed several ventricular ectopic or other ventricular arrhythmias. Twelve patients with hypotension received intravenous dobutamine, and six patients with severe sinus hradycanlia ret.-eived atropine intravenously. No patient received digoxin with the exception of those patients who developed atrial fibrillation up until they were restored to sinus rhythm. All patients were monitored carefully for electrolyte abnormalities, particularly hypokalemia. A total of 130 patients had an anterior infarction and the remaining 136 had an inferior infarction on ECG traces. The artery of infarction and the site of the oc'Clusion were easily recognized in 119 patients. In the remaining 17 patients with inferior myocanlial infarction and severe stenoses or occlusions in both right coronary artery and left circumftex, the artery of infarction and the site of the occlusion were identified by conmary angiographic criteria of an uk-erated atheromatous plaque. The regional pattern of left ventricular dysfunction on contrast ventriculography, as well as by ECG criteria, viz inferior myocanlial infarction due to left circumftex occlusion, unlike that due to right coronary artery occlusion, produced ST elevation in leads 1 and aVL.
~rial
METHODS
Study Patients
We studied 266 t:onsecutive patients who were admitted to the mnmary care unit of the Hippokration Hospital, Athens, with definite Q wave myocardial infarction. Subsequently, all underwent mnmary arteriography from one to eight weeks after the acute event. The gnmp was mmprised of249 men and 17 women, ranging in age from 32 to 72 years, with a mean of 53± 9.1 years. Coronary arteriography was performed hy the Judkins technique using standard projections. All patients were monitored fi1r canliac arrhythmias from their arrival in the mronary care unit. The tracings were displayed on a to a t.-enter monitor at the bedside monitor (Hellige) L~mnected nurses' station. The cardiac rhythm of all patients was continually and carefully observed on the center monitor by experient.-ed staff nurses and the duty cardiologist. Each arrhythmia was reconled u~th the aid of a 60-s memory loop. Additionally, any rhythm disturbances alerted the monitor alarm and were recorded on electrocardiographic paper. On admission In the hospital, mean time after onset of symptoms *From the Cardiac Department, Hippokration Hospital, University of Athens, Greece. Manuscript received June 13; revision accepted September 26. Reprint requests: Dr. Kyriakidis, 139-143 Kuraiskou Street, Piraeus, Greece 185 35
944
(Cheat 1992; 101:944-47) S-A= sinoatrial
RESULTS
Ten patients developed atrial fibrillation, one atrial Rutter, and one paroxysmal atrial tachycardia, in the first 12 h after admission. The duration of these arrhythmias was less than 1 h in eight patients, while the remaining four developed atrial fibrillation which lasted up to 3 h. None of these had a history of paroxysmal atrial fibrillation or supraventricular tachycardia before the acute myocardial infarction. All 12 patients had an acute inferior myocardial infarction, Early Atrial Arrhylhmias in Acute Ml (Kyrlalddis
et al}
Table 1-Angiographic and Electrocardiographic Data of lbtients with Atrial Tachyarrhythmia
Patientst
RCA
LCx
*1 2 3
+ + + + + + + + +
+
t4 5 6
7
8 9 10 11 12
+ +
+
+
+ + + + + +
LAD
+ + + + + + +
SN Artery
AVN Artery
Initial ECG Rhythm
+ + + + + + + + + +
+ + + + + + + (L) + + + + +
SR. AVB SR SR SR, AVB SR SR , AVB SR, AVB SR. AVB SR SR, AVB SR SR
(L)
(L) (L)
*RCA , ri~ht
the origin of the sinus node artery started just after an occluded right coronary or left circumftex artery or was involved in the occlusion. Thus, ischemia of the sinus node due to coronary occlusion proximal to the origin of the sinus node artery was a likely cause of these arrhythmias.
arrhythmias have been reported in as many as 20 percent of cases of acute myocardial infarction. 1 They are most common in the later stages of myocardial infarction as a complication of pericarditis 2 -"~ In the early stages, they are rare, or heart failure. and the pathogenesis is uncertain. 5 ·6 The underlying cause of the arrhythmias is ischemia, but the precise mechanism and the extent remain controversial. In the present prospective clinical angiographic study of 266 consecutive patients with acute myocardial infarction, we attempted to correlate serious atrial arrhythmias during the first 12 h of admission with the ischemia produced by interruption of the blood Row in the arteries supplying the atrium, in particular the sinus node artery.
was 2.2 h. All patients were in sinus rhythm. Patients with clinical evidence of left ventricular failure, defined as pulmonary edema, significant crepitations, gallop rhythm, and low output state, were excluded from the study because of the possibility of dysrhythmias as a result of hemodynamic changes. Of the 266 patients without contraindications to thrombolysis, 197 received thrombolytic therapy on arrival in the coronary care unit, started in less than 6 h of the onset of symptoms of the acute event. The patients were also treated with morphine for severe chest pain, intravenous nitroglycerin if their systolic blood pressure was above 100 mm Hg, and lignocaine intravenously if they developed several ventricular ectopic or other ventricular arrhythmias. Twelve patients with hypotension received intravenous dobutamine, and six patients with severe sinus hradycanlia ret.-eived atropine intravenously. No patient received digoxin with the exception of those patients who developed atrial fibrillation up until they were restored to sinus rhythm. All patients were monitored carefully for electrolyte abnormalities, particularly hypokalemia. A total of 130 patients had an anterior infarction and the remaining 136 had an inferior infarction on ECG traces. The artery of infarction and the site of the oc'Clusion were easily recognized in 119 patients. In the remaining 17 patients with inferior myocanlial infarction and severe stenoses or occlusions in both right coronary artery and left circumftex, the artery of infarction and the site of the occlusion were identified by conmary angiographic criteria of an uk-erated atheromatous plaque. The regional pattern of left ventricular dysfunction on contrast ventriculography, as well as by ECG criteria, viz inferior myocanlial infarction due to left circumftex occlusion, unlike that due to right coronary artery occlusion, produced ST elevation in leads 1 and aVL.
~rial
METHODS
Study Patients
We studied 266 t:onsecutive patients who were admitted to the mnmary care unit of the Hippokration Hospital, Athens, with definite Q wave myocardial infarction. Subsequently, all underwent mnmary arteriography from one to eight weeks after the acute event. The gnmp was mmprised of249 men and 17 women, ranging in age from 32 to 72 years, with a mean of 53± 9.1 years. Coronary arteriography was performed hy the Judkins technique using standard projections. All patients were monitored fi1r canliac arrhythmias from their arrival in the mronary care unit. The tracings were displayed on a to a t.-enter monitor at the bedside monitor (Hellige) L~mnected nurses' station. The cardiac rhythm of all patients was continually and carefully observed on the center monitor by experient.-ed staff nurses and the duty cardiologist. Each arrhythmia was reconled u~th the aid of a 60-s memory loop. Additionally, any rhythm disturbances alerted the monitor alarm and were recorded on electrocardiographic paper. On admission In the hospital, mean time after onset of symptoms *From the Cardiac Department, Hippokration Hospital, University of Athens, Greece. Manuscript received June 13; revision accepted September 26. Reprint requests: Dr. Kyriakidis, 139-143 Kuraiskou Street, Piraeus, Greece 185 35
944
(Cheat 1992; 101:944-47) S-A= sinoatrial
RESULTS
Ten patients developed atrial fibrillation, one atrial Rutter, and one paroxysmal atrial tachycardia, in the first 12 h after admission. The duration of these arrhythmias was less than 1 h in eight patients, while the remaining four developed atrial fibrillation which lasted up to 3 h. None of these had a history of paroxysmal atrial fibrillation or supraventricular tachycardia before the acute myocardial infarction. All 12 patients had an acute inferior myocardial infarction, Early Atrial Arrhylhmias in Acute Ml (Kyrlalddis
et al}
Table 1-Angiographic and Electrocardiographic Data of lbtients with Atrial Tachyarrhythmia
Patientst
RCA
LCx
*1 2 3
+ + + + + + + + +
+
t4 5 6
7
8 9 10 11 12
+ +
+
+
+ + + + + +
LAD
+ + + + + + +
SN Artery
AVN Artery
Initial ECG Rhythm
+ + + + + + + + + +
+ + + + + + + (L) + + + + +
SR. AVB SR SR SR, AVB SR SR , AVB SR, AVB SR. AVB SR SR, AVB SR SR
(L)
(L) (L)
*RCA , ri~ht
