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Contrast-induced nephropathy (CIN) is the third most common cause of hospital-acquired renal failure after acute ischemic stroke and hypovolemia ([@ref1], [@ref2]). Comorbid medical conditions such as diabetes mellitus, hypertension, heart failure, peripheral vascular disease, a history of contrast exposure and congestive heart failure are risk factors for CIN ([@ref3]-[@ref5]).
Cardiac stress can be defined as increased risk of adverse cardiovascular or cerebrovascular events when myocardial ischemia is associated with the primary procedure or contrast agent ([@ref6]). CIN occurs either as a primary or indirect complication of cardiac stress. The most common mechanism of renal damage is tubular ischemia. Direct toxicity may be evident in the form of impairment of renal function. Other contributory factors are decreased renal blood flow, activation of the renin-angiotensin system and release of arachidonic acid metabolites, which in turn activate kinin and 5-lipoxygenase pathways ([@ref6]).
Reports have shown that some noninvasive electrocardiographic markers, such as QT dispersion (QTD), QTc dispersion (QTcd), T wave peak-to-end interval dispersion (Tp-e), standard deviation of ST-segment duration (STD-SDS), and Tp-e/QT ratio (Tp-e/QT) can be used to identify risk of myocardial ischemia or cardiac ischemia. In patients with acute myocardial infarction, QT dispersion (QTd) and Tp-e (Tpe) can predict future cardiovascular events ([@ref7]). Noninvasive electrocardiographic markers can also be useful in the detection of myocardial ischemia in patients with chronic heart failure.
Ricci-Cherto et al. demonstrated that noninvasive QTcd is a highly sensitive marker of myocardial ischemia in patients with chronic congestive heart failure. They also showed that an increased QTcd and QTcd/QT ratio during exercise can be helpful in the detection of myocardial ischemia in these patients ([@ref8]).
Our aim was to determine whether Tpe and 0b46394aab
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