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Dynamic Left Ventricular Outflow Tract Obstruction in Acute Coronary Syndromes: In Response

      Keegan and colleagues describe a patient who experienced repeated transient episodes of severe hypotension during an attempted angioplasty and stent placement to treat a symptomatic carotid artery stenosis. The authors propose that this patient's hypotension was due to the development of a dynamic LVOT obstruction during the procedure. Although echocardiography was not performed at the time of the patient's symptoms to verify the presence of an LVOT obstruction, some aspects of the patient's presentation are consistent with the presentation of those patients previously described. First, the initial episode of hypotension seemed to resolve after administration of an α-agonist, and hypotension did not recur after the administration of intravenous fluid and β-blocker. In the repeat procedure the patient was treated with a phenylephrine infusion and intermittent esmolol with no recurrence of hypertension. As correctly pointed out by the authors, these measures act to reduce the degree of LVOT obstruction and alleviate hypertension. Second, a transthoracic echocardiogram performed after the patient stabilized showed decreased systolic function with an ejection fraction of 35% with akinesis of the anterior and septal walls from base to apex and no evidence of a dynamic LVOT obstruction. Two days later, the patient underwent coronary angiography during which left ventriculography demonstrated a normal ejection fraction (74%) with no evidence of regional hypokinesis. The patient was shown to have diffuse coronary artery disease and underwent PTCA of the right coronary artery. That the patient's myocardial function recovered within 2 days suggests ischemia as the cause of the LV dysfunction. However, what is not clear is whether the ischemia was a cause of apical akinesis and subsequent basal hyperdynamic function resulting in adynamic LVOT obstruction, or whether an ischemic threshold was achieved during the procedure resulting in a deterioration of global LV function. The second procedure was performed after the patient had undergone PTCA of the right coronary artery as well as with concomitant use of a β-blocker and α-agonist. Thus, it is not clear whether the prevention of a dynamic LVOT obstruction or treatment of the underlying coronary artery disease was responsible for preventing hypotension in the second procedure.
      While the above factors are consistent with the development of a dynamic LVOT obstruction as a cause of the patient's symptoms, some are different from the patient we described. The patient presented had very transient episodes of hypotension which in some instances resolved without intervention. In all the patients presented in our series, the hypotension persisted until measures such as administration of β-blockers or α-agonists and discontinuation of afterload reduction were instituted. Additionally, the echocardiogram performed after the procedure describes akinesis of the septum and anterior wall from apex to base, which raises the question of whether this patient would have been able to develop the basal hyperdynamic function necessary to create an LVOT obstruction.
      Thus, while it can only be speculated that this patient developed a transient dynamic LVOT obstruction as a cause of her symptoms, Keegan and colleagues make some important points. First, the development of a dynamic LVOT obstruction is known to occur in conditions other than acute coronary syndromes and probably occurs more often than is currently appreciated. Studies addressing the frequency with which this phenomenon occurs are currently lacking and should be pursued. Second, when a patient develops sudden hypotension that cannot be readily explained, this phenomenon should be considered as a cause of the patient's symptoms. Finally, this case demonstrates the value of pursuing emergent transthoracic or transesophageal echocardiography in this setting if at all possible, as the diagnosis, with its therapeutic ramifications, can be quickly confirmed or dismissed.

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      • Dynamic Left Ventricular Outflow Tract Obstruction in Acute Coronary Syndromes
        Mayo Clinic ProceedingsVol. 75Issue 2
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          To the Editor: In the September 1999 issue of Mayo Clinic Proceedings, Haley and colleagues1 described 3 patients who had echocardiographically confirmed left ventricular outflow tract (LVOT) obstruction in the absence of baseline hypertrophic cardiomyopathy. All 3 patients had acute myocardial infarction, as well as echocardiographic evidence of regional myocardial akinesia and dyskinesia that caused the LVOT obstruction. In all patients, the obstruction resulted in cardiogenic shock that later responded to therapy appropriate for LVOT obstruction; however, the therapy was not typical for the treatment of isolated myocardial infarction.
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