Abnormal P‐Wave Terminal Force in Lead V₁ Predicts Left Main and/or Three‐Vessel Disease in Patients with Non–ST‐Segment Elevation Myocardial Infarction P‐Wave Abnormality and Extensive Coronary Artery Disease

To the Editor,

Recently, Li, et al. reported that abnormal P‐wave terminal force in lead V₁ (PtfV₁) on discharge electrocardiogram was associated with an increased risk of long‐term adverse cardiac events in patients with non–ST‐segment elevation acute coronary syndrome.1 They theorized that abnormal PtfV₁ might be associated with irreversible myocardial damage or residual ischemia of nonrevascularized vessels. However, detailed angiographic data were not reported. The extent of coronary artery disease (CAD) has been shown to be associated with worse prognosis in acute coronary syndrome population.2, 3 Therefore, it is of clinical interest to see if abnormal PtfV₁ is associated with the extent of CAD.

We performed a retrospective analysis of 336 patients with non–ST‐segment elevation myocardial infarction (NSTEMI) to clarify the association between abnormal PtfV₁ and the extent of CAD. This study complied with the Declaration of Helsinki and was approved by the institutional review board at our institution. We excluded patients with atrial fibrillation, atrial‐paced rhythm, junctional rhythm, history of coronary artery bypass grafting (CABG), and those with nonobstructive CAD, defined as <50% stenosis. Electrocardiograms on admission were reviewed by two independent physicians. Abnormal PtfV₁ was defined as terminal negative component of P wave that meets both depth ≧1.0 mm and duration ≧40 ms. Left main disease was defined as stenosis ≧50%, and three‐vessel disease was present if there was stenosis ≧70% in all three major epicardial coronary arteries.

Among 336 patients, 104 patients had abnormal PtfV₁. No significant difference was observed in baseline characteristics between those with and without abnormal PtfV₁. Patients with abnormal PtfV₁ had a higher rate of Killip class >1 on admission (28% vs 7%, P < 0.001), and left main and/or three‐vessel disease (LM/3VD) than those without abnormal PtfV₁ (38% vs 25%, P = 0.015). There was a trend toward a higher incidence of in‐hospital CABG in patients with abnormal PtfV₁ (17% vs 11%, P = 0.098). Patients with abnormal PtfV₁ had a higher, albeit statistical insignificant, in‐hospital mortality (2.9% vs 0.9%, P = 0.17).

Our study demonstrated that abnormal PtfV₁ was associated with a higher incidence of LM/3VD in NSTEMI population. Our finding was consistent with a previous study that demonstrated the association between abnormal PtfV₁ and three‐vessel disease in patients with Q‐wave acute myocardial infarction.4 Previous study also has shown that abnormal PtfV₁ is associated with elevated left ventricular end‐diastolic pressure (LVEDP).5 We speculate that extensive CAD in abnormal PtfV₁ group resulted in elevated LVEDP, as indicated by a higher rate of Killip class >1 on admission, which subsequently led to abnormal PtfV₁. The extent of CAD may explain the increased cardiac events associated with abnormal PtfV₁ in Li's study, and it is interesting to know the extent of CAD in their study, which mainly consisted of patients with unstable angina. In conclusion, our study suggested that abnormal PtfV₁ on admission have a predictive value for LM/3VD in patients with NSTEMI.