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International Journal of Bioelectromagnetism
Vol. 5, No. 1, pp. 229-230, 2003.

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Are Q and Non-Q-Wave Infarcts Two Distinct Entities?

Paul Schweitzer

Beth Israel Medical Center, New York, N.Y., USA


1. Introduction

Rupture of an arteriosclerotic plaque (vulnerable plaques) with superimposed thrombus is the mechanism of acute coronary syndrome (ACS) [Theroux and Fuster]. The manifestations of ACS are Q-wave, non-Q-wave myocardial infarction (MI), unstable angina and sudden cardiac death. The aim of this review is to discuss the evolution of the ECG changes in ACS and the differences between Q and non-Q-wave MI.

2.  Acute Coronary Syndrome

Patients with acute ischemic events are classified into ST segment elevation and non-ST elevation ACS. The initial ECG presentation and the biochemical markers of myocardial necrosis are the two main factors influencing the management of ACS (Newby et al). Because of this newer approach, classification of acute MI into Q and non-Q wave has been challenged. In addition, according to Phibbs et al. myocardial necrosis not only causes abnormal Q waves but also influences the amplitude and the duration of the R waves. This is particularly true for MI localized in the areas depolarized after 40 ms. Furthermore, ST segment elevation ACS is not synonymous with Q wave MI because, opening of an occluded coronary artery might prevent myocardial necrosis or causes only a non-Q-wave MI. Finally, the ECG changes in patients non ST elevation ACS are not uniform and include ST segment depression, T wave inversion, non-specific ST-T wave changes or normal ECG. Because the ECG is not pathognomic for non-Q-wave MI, recent study suggested “ECG criteria are not adequate to define non-ST- segment elevation MI” (Newby et al).

3.  Q-Wave Versus Non-Q-Wave Myocardial Infarction

However, despite the discussed objections, classification of Q and non-Q-wave MI seems to be justified for the following reasons: First, the short and long-term management of Q and non-Q wave MI are different. Second, while the early mortality may be higher or the same in both types of MI, the long-term prognosis is worse in patients with non-Q-wave MI.

In addition to distinct ECG patterns of Q and non-Q-wave MI, there are also important differences in the coronary pathoanatomy. First, the culprit coronary artery can be identified in the majority of patients with Q wave MI and only in 50% or less in those with non-Q-wave MI. Second, in patients with Q-wave MI the thrombus is occlusive and in non-Q-wave MI non-occlusive. Third, the thrombi in Q-wave MI are rich of fibrin and erythrocytes and in non-Q-wave MI, the platelets are the main component of the occlusions (Mizuno et al). Fourth, there is some suggestion that patients with non-Q-wave MI have more advanced coronary artery disease. Fifth, microembolization seems to be an important mechanism of non-Q-wave MI.

Since the eighties, it was also suggested that Q and non-Q-wave MI are two distinct clinical entities. The important clinical differences between Q and non-Q-wave MI are the following. Patients with non-Q- wave MI are older, have higher incidence of previous infarcts, angina pectoris, prior revascularization (CABG, PCI) and peripheral vascular disease. In some studies the 30-days mortality in Q-wave MI was either higher or the same as in non-Q-wave MI while the six months mortality was similar. On the other hand, 1-year survival rate was lower in patients with non-Q-wave than in those with ST segment elevation MI [Armstrong et al., 1998]. Probably the most important difference is the management of Q and non-Q-wave ACS. Patients with ST segment elevation are candidates for thrombolysis while those without ST segment elevation are treated with heparin, IIb/IIIa inhibitors. Because percutaneous coronary intervention may be more effective that pharmacological therapy, it is possible that in the near future both types of ACS will be managed with percutaneous reperfusion. Finally, according to some studies the incidence of non-Q-wave MI is increasing, because reperfusion prevents the development of Q wave MI in patients with ST segment elevation ACS and the use of biochemical markers for the diagnosis of non-Q-wave MI.

 Another important consideration is the role of the ECG for risk stratification and management of non-Q-wave MI. According to the results of the FRISC-II study, patients with ST segment depression benefited from invasive therapy while those with isolated T wave inversion or normal ECG did not. This and other recent findings may challenge the suggestion that the ECG is of limited value in non-Q-wave MI.

4.  Summary

Despite common pathophysiology, there are important differences between Q and non-Q-wave MI, particularly in the coronary circulation, certain clinical parameters and prognosis. However, recent studies suggest that the initial ECG is more important for the management of acute ischemic events while the differentiation between Q and non-Q-wave MI has its role in the long-term care. In patients with non-ST elevation ACS, the initial ECG is helpful to decide between invasive or conservative strategy.

References

Armstrong P.W. Fu Y, Chang W.C. et al. Acute coronary syndrome in the GUSTO-IIb trial: Prognostic insights and impact of recurrent ischemia. Circulation 1998;98:1860-1868

Mizuno K, Satomura K, Miyamoto A. et al.Angioscopic evaluation of coronary artery thrombi in acute coronary syndrome. N Engl J Med 1992;326:287-291

Newby K.L, Alpert JS Ohman E.M. et al. Changing the diagnosis of acute myocardial infarction: Implications for practice and clinical investigations. Am Heart J 2002;144:957-980.

Phibbs B, Marcus F, Marriott H.J.C. et al. Q-wave versus non Q-wave myocardial infarction: A meaningless distinction. J Am Coll Cardiol 1999;33:576-582

Theroux P, Fuster V. Acute coronary syndrome; Unstable angina and non-Q-wave myocardial infarction. Circulation 1998;97:1195-1206

 

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