A Prerequisite for Spontaneous Atrial Fibrillation or Flutter in Patients with Acute Myocardial Infarction

Wangden Carson, Yung-Zu Tseng

Cardiovascular Division,Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan

Correspondence: W Carson, Cardiovascular Division, Department of Internal Medicine, National Taiwan University Hospital,
No. 7, Chung-Shan South Road, Taipei, Taiwan 100. E-mail: wcarson72@yahoo.ca

1.  Introduction

There has been no report of any emergency vectorcardiographic study of atrial fibrillation/or flutter, or P loops in patients with acute myocardial infarction in the literature.

2.  Material and Methods

Seventy-three consecutive patients with suspect coronary heart disease enrolled in the serial emergency vectorcardiographic (EVCG) study of acute myocardial infarction. On admission to the Coronary Care Unit through the Emergency Service, each patient was given electrocardiographic and vectorcardiographic examinations, which were repeated at intervals of 24hrs if the patient’s condition were conducive to do so. All the electrocardiograms and vectorcardiograms were recorded by the first author (W.C.) according to orthodox methods [Shine, 1987] of medical research, and read by the other author (Y.T.) without any knowledge of the patients. Patients with later proof without acute myocardial infarction in the hospital will be excluded from the study. The Frank lead vectorcardiographic QRS-loop diagnostic criteria for different locations of myocardial infarction were according to the literature [Carson, 1998].

3.  Results

One hundred and sixty emergency vectorcardiographic tracings were recorded for 55 patients with acute myocardial infarction. Their age was 60 + 8.9 years in this study, and all were male except seven. There were 24 patients with acute anterior myocardial infarction, 22 patients with inferior or infero-posterior, and nine patients with both anterior and inferior infarction according to the vectorcardiographic diagnosis. Twenty-eight (51%) had abnormal inscription direction of the P loop. Seven (13%) among 55 patients developed atrial fibrillation/or flutter. Three of the seven had abnormal inscription direction of the P loop in the first tracing. Six of the seven had abnormal inscription direction of the P loop during the follow-up tracings of acute myocardial infarction. All of the seven had right or left atrium enlargement. They were among 50 patients (91%) with abnormal atrium enlargement of the study group. Four among the seven had slow conduction of the P loop, esp. afferent loop. There were 27 patients (49%) among the total 55 with abnormal slow conduction of the P loop.

4.  Discussion

Abnormal inscription direction (altered activation propagation) could happen in both depolarization and repolarization processes in a diseased heart [Carson et al, 2003]. It is interesting that over half of our patients (51%) had abnormal depolarization of the atria, which is a similar incidence (50%) [Braunwald et al, 1997] of atrial premature contractions in patients after myocardial infarction. An abnormal inscription direction of the P loop indicates minute but undesirable modes of progression in the depolarization process of the atria; such an abnormal P loop as in patients with atrial septal defects can be altered by the transcatheter closure of the defect using the Amplatzer occluder [Carson et al, 2002].

Seven (13%) among 55 patients with acute myocardial infarction developed atrial fibrillation/or flutter. The incidence rate is in accord with the literature (13%) [Goldberg et al, 2002]. Six of the seven had abnormal inscription direction of the P loop during the follow-up period of acute myocardial infarction but only three in the initial tracing. This can be explained by the fact that a 24 hrs per tracing protocol may not ‘catch’ the abnormal activation propagation within the atria, or it has already been abolished by atrial premature contraction or contractions. We have no way of knowing this until the palm-like computer of the timed vectorcardiogram under development is available [Carson, 2001]. Slow conduction of the P loop or atrial enlargement may help in sustaining atrial fibrillation or flutter.

A proposed new theory. Abnormal inscription direction (altered activation propagation) in the depolarization process of the atria could happen in a diseased or healthy heart. The heart will generate an atrial premature contraction (‘physiological’ pacing) or contractions (‘physiological’ overdrive suppression) to abolish the abnormal activation propagation. If it is not successful, the atrial fibrillation or flutter will ensue. With the help of chamber enlargement and/or abnormal conduction within the atria, the abnormal rhythms will be sustained.

Synchronous motors (similar to the right and left atrium) operate as induction motors while being brought up to speed so that they can be synchronized. When synchronized, synchronous motors and generators depend upon their inherent induction characteristics to provide a damping torque which allows them to operate stably without hunting. However, prolonged load current unbalance, caused by unbalanced supply voltage (partial negative sequence), will form reverse-phase rotation (100% negative sequence). This will cause rotating at synchronous speed in the opposite direction of the rotor, will create a torque in the negative direction, which represents a more serious hazard for motors. When negative sequence voltages’ levels reach 4% [Adibi et al, 1999], a motor is finished. Therefore, the premature contraction per se should not be targeted for therapy, whereas the inscription direction abnormalities in the preceding beats should be evaluated seriously.

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