Evidence supporting a new rate threshold for multifocal atrial tachycardia.

BACKGROUND: Exacerbation of chronic obstructive pulmonary disease (COPD) is overwhelmingly represented among patients presenting with multifocal atrial tachycardia (MAT) and has been used as a paradigm for such patients. The quasidiagnostic tachycardia threshold for MAT is conventionally set at 100 beats/min. Nevertheless, this threshold has not been demonstrated to be optimal. HYPOTHESIS: Using COPD as a paradigm for MAT, clinical experience led to the hypothesis that MAT with a tachycardia threshold < 100 beats/min could be more closely associated with COPD exacerbation. METHODS AND RESULTS: We reviewed 60 consecutive patients with multifocal atrial arrhythmia (MAA) at any heart rate and found a better association between the incidence of COPD exacerbations and MAT using a tachycardia threshold of 90 beats/min (p = 0.00036) than when using a threshold of 100 beats/min (p = 0.515). CONCLUSION: The rate threshold of MAT should be reduced from 100 to 90 beats/min.

Acute right atrial strain: regression in normal as well as abnormal P-wave amplitudes with treatment of obstructive pulmonary disease.

OBJECTIVE: To evaluate right atrial (RA) "strain" as reflected by changes in P-wave amplitude and vector in patients with COPD immediately before and immediately after beginning treatment of exacerbations. BACKGROUND: P-pulmonale (frequently temporary, reflecting acute RA strain) occurs under a variety of circumstances, including COPD. Emergency room (ED) ECGs in patients with acute exacerbations of COPD have suggested that P-pulmonale (P waves > or = 2.5 in leads II, III, and aVF) tends to resolve subsequent to acute treatment. RA strain is defined as a response to RA stress (probably transient pressure rise and/or acute RA enlargement) in patients with COPD. Since P-pulmonale occurs in a small minority of patients with COPD, we investigated dynamic changes in size and mean vector (axis) of all frontal plane P waves in the ED vs the immediate subsequent ward ECG in patients with acute exacerbations of COPD. METHODS: We prospectively compared P-wave amplitude in the ED with the first in-patient ECG in 50 consecutive patients with acute exacerbations of COPD and in 20 consecutive nonpulmonary control patients, analyzing only ECGs showing sinus rhythm and in which P waves were clearly recorded. Despite using a calibrated magnifying graticule, it was difficult to interpret a dynamic change if the initial ED ECG had P-wave amplitude < 1.5 mm in leads II and aVF. We selected lead II because it usually has the largest frontal plane P waves and also aVF to reflect the relative verticality of the mean P vector (axis). We performed a matched-pair analysis to compare the equality of means. RESULTS: Of the patients with COPD, only seven patients (14%) had classical P-pulmonale on the ED ECG. Forty-eight of 50 consecutive patients (96%) demonstrated a decrease in P-wave amplitude between ED and subsequent ward ECGs. Two patients showed no change. The mean differences of P-wave amplitude between ED and ward ECGs in lead II was 0.78 mm, and that in lead aVF was 0.8 mm. The difference of the mean P-axis between ED and ward ECGs was - 5.24 degrees (p < 0.0001 for all three measurements). There was no P-wave amplitude change in the control group between ED and ward ECGs. CONCLUSIONS: P-wave amplitude in patients with COPD decreases once an acute exacerbation subsides. Thus, P-wave amplitude and vector are dynamic and could reflect reduced RA strain. We question the traditional (1935) absolute cutoff of 2.5 mm for P-pulmonale as of limited value due to insensitivity, hence inappropriate for what this investigation demonstrates to be a continuous variable.

Widely split P waves in the presence of interatrial block.

Interatrial block (IAB; P wave>or=110 milliseconds), conduction delay between the atria, is highly prevalent and is associated with atrial tachyarrhythmias, left atrial electromechanical dysfunction, as well as a potential risk for systemic embolism. However, much is still yet to be known of IAB's exact pathophysiology and how it may manifest in relation to medical disease. We present an unusual case of widely split P waves in the presence of IAB in a severely ill patient.