Cardiac dysfunction is common in ICU patients and is a poor prognostic factor [1,2]. Acute myocardial infarction (AMI) is commonly diagnosed in ICU patients and cardiospecific proteins are detected in up to 47% of these patients. An AMI diagnosis is often based only on detection of cardiospecific proteins in plasma and/or ECG and echocardiographic findings. Angiographic evidence is rarely present [2]. Furthermore, reported plasma troponin levels are often mildly to moderately elevated, a laboratory finding that is consistent not only with a small or moderately sized AMI but also with stress-induced cardiomyopathy (SIC). It is thus possible that many or perhaps most cases of myocardial infarction diagnosed in the ICU may in fact be SIC. SICwas first described in 1990 but is nowan increasingly recognized acute cardiac syndrome and an important differential diagnosis in patients presenting with chest pain [3]. SIC is characterized by severe regional myocardial hypokinesia or akinesia, often but not always involving apical segments, in the absence of an explanatory coronary lesion [4]. Although the pathomechanisms behind SIC is believed to differ substantially from that of AMI the two conditions appear clinically similar and cannot, as yet, be differentiated by non-invasive modalities [5]. However, plasma troponin levels are typically mildly to moderately elevated in SIC and extreme values are rare. SIC is typically preceded by an emotional or somatic stressor and although the pathophysiology of SIC is poorly understood, there exist strong evidence for an important role of catecholamine overstimulation [5]. Among the evidence indicating catecholamines in the pathogenesis of SIC are the observations that plasma levels of epinephrine and norepinephrine are severely elevated in SIC patients, also compared to AMI patients, and several reports where iatrogenously administered beta-adrenergic agonists have triggered SIC or worsened the patients' condition [5,6]. Furthermore, we have shown that i.p. administration of isoprenaline, a nonselective β-adrenoreceptor agonist, induces SIC-like left ventricular apical akinesia in rats [7]. We believe that there is reason to believe that SIC may be particularly prevalent among patients admitted because of severe non-cardiac disease, conditions associated with internal somatic stress and a strong adrenergic drive. A recent report showed that N20% of patients admitted to an intensive care unit (ICU) displayed SIC-like left ventricular apical ballooning. Development of SIC-like cardiac dysfunction was particularly likely in sepsis, a condition associated with a profound endogenous stress response [1]. Considering the liberal use of inotropic support in ICU patients, including catecholamine, detection of SIC patients in this setting may be of particular importance and may merit re-evaluation of treatment strategies [6,8]. Cardiac output is often inadequate in ICUpatients despite optimization of filling pressures and afterload. These patients therefore require additional support tomaintain adequate tissue perfusion. Typical regimens include positive inotropes and/or vasopressor substances, manyofwhich are catecholamines.Webelieve that further stimulation of adrenergic signaling pathways may exacerbate cardiac dysfunction in somepatients andmay lead toparadoxical deterioration of these patients condition (Fig.1). In patients suffering from severe heart failure inotropic support by the β-adrenoreceptor agonist dobutamine was associated with a near statistically significantly increased mortality compared to placebo [8]. We believe that suspicion of stress-induced cardiac dysfunction should deter the anesthesiologist towards switching to non-catecholamine vasopressors. Similarly, non-catecholamine vasopressors may also be preferable in these patients. We propose that many so-called AMIs detected in the ICU may in fact be SIC and in many cases these SICs may have been caused or exacerbated by iatrogenously administered inotropic agents, especially β-adrenoreceptor agonist. Non-catecholamine inotropes and/or vasopressors or mechanical assist may be preferable in patients at risk of developing SIC. Until SIC is better understood and these patients can be identified we argue for judicious use of catecholamine inotropes and liberal use of mechanical assist, particularly in patients displaying signs of cardiac dysfunction or injury.
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