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clinical investigations in critical care: Jae-Hyeong Park, Soo-Jin Kang, Jae-Kwan Song, Hyun Kuk Kim, Chae Man Lim, Duk-Hyun Kang, and Younsuck Koh Left Ventricular Apical Ballooning Due to Severe Physical Stress in Patients Admitted to the Medical ICU Chest 2005; 128: 296-302 [Abstract] [Full text] [PDF]

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Left Ventricular Apical Ballooning In Patients Admitted To Medical ICU

Sandeep Arora   (24 July 2005)

Left Ventricular Apical Ballooning In Patients Admitted To Medical ICU 24 July 2005
Sandeep Arora Western Pennsylvania Hospital/Temple University Program Send letter to journal: Re: Left Ventricular Apical Ballooning In Patients Admitted To Medical ICU sandeeparora24{at}hotmail.com Sandeep Arora	To the Editor: We read the article by Park et al 'Left ventricular Apical ballooning due to severe physical stress in patients admitted to medical ICU' (Chest 2005 128: 296-302) with great interest. However we disagree with the methodology, interpretation and implication of some of their findings. Authors in the present study have defined Left ventricular apical ballooning (LVAB) as 'symmetric severe hypokinesia or akinesia of the left ventricular wall, except for the basal part of the left ventricle, with a reduced ejection fraction' based on echocardiography. They excluded patients with previous ischemic heart disease and have pointed out that echocardiography can easily differentiate between LVAB and anterior wall MI. Reversible segmental cardiac contraction abnormalities have been well described in critically ill patients without significant coronary artery disease(1). Regional wall motion abnormalities seen in these patients resemble those of LVAB. However we strongly believe that it is difficult to attribute these contractile abnormalities to non-ischemic causes in the absence of coronary angiography. Though involvement of both anterior and inferior-apical segmental areas in LVAB does not correlate with any single epicardial artery distribution, involvement of multiple arteries and/or their branches, coronary vasospasm or microvascular ischemia may have similar picture. Though authors have admitted that mechanical ventilation in critically ill patients did not allow them to do coronary angiography or stress myocardial perfusion scan, none of the survivors of LVAB who recovered from the condition underwent angiography on follow up. Angiography is still the 'gold standard' to diagnose coronary artery disease in any patient and echocardiography can not reliably exclude it based on contractile patterns. LVAB is a newly recognized entity and its incidence, pathophysiology and prognosis are still under investigation. Using echocardiogram to diagnose this entity may result in more uncertainty and potentially undermine the importance of recognizing much more prevalent ischemic heart disease. Authors have reported the incidence of LVAB to be 26% in critically ill ICU patients which seems to be much higher than expected by previous experience and by historical controls. One of the reasons could be a cut off value of LVEF of 50% which is an arbitrary value and is probably too high, especially in this group of patients. Also, sepsis by itself can lead to myocardial injury, elevation in cardiac enzymes and regional wall motion abnormalities(2). Multiple pathophysiological mechanism are implicated for sepsis induced myocardial dysfunction including cytokines (IL-6, IL-1, TNF-alfa, lipopolysaccharides), nitric oxide mediated apoptosis, increased intracellular adhesion molecules 1, tissue hypoxia, reperfusion injury and excessive catecholamines. Typically, LVAB has been described as sudden onset chest pain in previously healthy individuals and it is unclear that patients with sepsis induced myocardial dysfunction should be labeled as LVAB. Lastly, none of the patient in the present study underwent endomyocardial biopsy or cardiac MRI to exclude regional myocarditis which may be a confounding variable in critically ill and septic patients. Thus the true incidence of the disease can not be correctly estimated by the above results. Authors have raised a concern that LVAB may be associated with poor prognosis and have concluded that routine echocardiographic screening may be the only effective method of detecting this 'potentially fatal disease'. Though mean 2- month survival rate was lower in patients with LVAB, multivariate analysis showed that development of LVAB was not related with increased mortality. Multiple previous studies have shown excellent prognosis in these patients (except for rare complications). Considering the reversible nature of this disease, LVAB by itself should not be implicated for poor prognosis in these patients. Moreover, management of patients with LVAB is essentially supportive. Thus routine screening for LVAB in critically ill patients by echocardiography will have little influence on their management and outcomes. On the other hand it is important to realize that these patients are prone to develop LVAB as it may avoid unnecessary invasive procedures especially in the setting of EKG changes/elevated cardiac enzymes. Almost all previous case series of patients with LVAB, including a series of 3 patients in our Institute (unpublished data) have defined LVAB in presence of normal coronaries on angiography (3,4,5). Though diagnostic criteria for LVAB have not been clearly established, most authors agree that a significant coronary artery disease should be excluded in order to make a diagnosis. Mayo clinic have proposed clinical criteria for LVAB which require absence of obstructive coronary disease by angiography as one of four essential criteria(6). We strongly believe that echocardiography is not sufficient to diagnose this entity in absence of other supportive and/or confirmatory tests. Also the incidence of the disease and its prognostic value can not be truly estimated by above study. Lastly, in view of excellent prognosis and absence of specific therapeutic modalities, routine screening for LVAB is not recommended at this point. The results of the above study and its clinical implications should therefore be interpreted with great caution. References: 1. Sharkey SW, Shear W, Hodges M, Herzog CA. Reversible myocardial contraction abnormalities in patients with an acute noncardiac illness. Chest 1998;114:98-105. 2. Mehta NJ, Khan IA, Gupta V, Jani K et al. Cardiac troponin I predicts myocardial dysfunction and adverse outcome in septic shock. Int J Cardiol. 2004;95(1):13-17 3. Wittstein IS, Thiemann DR, Lima JAC, Baughman KL et al. Neurohumoral features of myocardial stunning due to sudden emotional stress. N Eng J Med. 2005;352(6):539-548. 4. Sharkey SW, Lesser JR, Zenovich AG, Maron MS et al. Acute and reversible cardiomyopathyprovoked by stress in women from the United States. Circulation, 2005;111:472-479. 5. Tsuchihashi K, Ueshima K, Uchida T, Oh-mura N et al. Transient left ventricular apical ballooning without coronary artery stenosis: A novel heart syndrome mimicking acute myocardial infarction. J Am Coll Cardiol 2110;38:11-8. 6. Bybee KA, Kara T, Prasad A, Lerman A et al. Systematic review: Transient left ventricular apical ballooning: A syndrome that mimics ST- segment myocardial infarction. Ann Intern Med 2004;141:858-865.