We thank all of the correspondents for their interest in our review. Ibanez and colleagues report that intravascular ultrasonography detected plaque rupture in the left anterior descending coronary arteries of 5 patients presenting with transient left ventricular apical ballooning (1). These patients had coronary arteries that appeared normal on angiography and a large recurrent distal segment of the left anterior descending coronary artery. These findings are interesting but seem an unlikely pathophysiologic explanation for most cases of transient left ventricular apical ballooning. First, angiographically detectable intracoronary thrombus in the left anterior descending coronary artery would be expected more frequently if plaque rupture were the primary mechanism of the syndrome. Second, abnormal coronary blood flow has been documented in all 3 major epicardial coronary arteries during the acute presentation phase of the syndrome (2, 3). Third, patients presenting with transient left ventricular apical ballooning commonly do not have long recurrent distal left anterior descending coronary arteries and indeed manifest wall-motion abnormalities beyond that of a single epicardial coronary artery distribution. Fourth, this mechanism would not explain the strong predominance of transient left ventricular apical ballooning among women. Last, we have observed acute transient right ventricular systolic dysfunction in many patients presenting with transient left ventricular apical ballooning, which could not be explained by isolated transient occlusion of the left anterior descending coronary artery. It is our feeling that transient left ventricular apical ballooning should be considered an acute cardiac syndrome, rather than an acute coronary syndrome, until additional investigative data elucidating the pathophysiologic mechanisms underlying the disorder are available.

In listing exclusion criteria as a part of the diagnostic criteria for transient left ventricular apical ballooning, our intent was to exclude distinct conditions that could potentially present in a similar manner. Tachycardia-mediated left ventricular dysfunction rarely presents as an acute cardiac syndrome and lacks the characteristic distribution of wall-motion abnormalities seen with transient left ventricular apical ballooning. Therefore, we do not feel it is necessary to include this entity as an exclusion criterion, as suggested by Drs. Dehnavi and van der Wall.

Drs. Ako, Honda, and Fitzgerald suggest that head trauma and intracranial bleeding should not be exclusion criteria for the clinical diagnosis of transient left ventricular apical ballooning. Significant head trauma and intracranial bleeding may indeed be associated with reversible apical left ventricular dysfunction; however, the reported distribution of wall-motion abnormalities in consecutive patients with brain injury differs. For example, one study suggests that basal hypokinesis with preservation of apical function is the most common finding in these patients (4). At this point, it is unclear whether left ventricular dysfunction associated with brain injury and transient left ventricular apical ballooning share similar pathophysiologic mechanisms.

The mechanisms responsible for transient left ventricular apical ballooning remain ill-defined, and further research is needed. Collaborative investigative efforts, including the development of a transient left ventricular apical ballooning registry, would probably expedite our understanding of this underrecognized syndrome.