Asymmetric Septal Hypertrophy Complicated by Dynamic Left Ventricular Obstruction after Intra-Aortic Balloon Counterpulsation Pl

Intra-aortic balloon pump (IABP) therapy is widely used as hemodynamic support among patients presenting with severe acute myocardial infarction, particularly in the case of cardiogenic shock. Usual complications include limb ischemia and puncture site bleeding. We report the case of a patient with an acute anterior myocardial infarction who showed dynamic left ventricular outflow tract (LVOT) obstruction induced by the intra-aortic counterpulsation. Transthoracic echocardiography (TTE) led to early recognition of this unexpected complication, allowing appropriate therapy to be given. Case Report. A 74-year-old female with a history of hypertension was admitted to our institution for chest pain lasting 6 hours, with electrocardiographic signs of acute anterior myocardial infarction (Figure 1). Physical examination revealed a heart rate of 100 beats/minute and blood pressure of 110/60 mmHg. Intravenous thrombolysis was started, and clinical and electrocardiographic signs of reperfusion occurred 2 hours later. Creatine phosphokinase peaked at 900 UI/L. TTE showed normal left ventricular dimensions but an asymmetric septal hypertrophy of 16 mm, without significant pressure gradient (peak velocity in the LVOT was 1.13 m/second by Doppler). Regional analysis revealed a large akinesis of the anteroapical segment, with compensatory hyperkinesis of the basilar myocardial region. The patient’s estimated ejection fraction was 35%. Slight mitral regurgitation and mitral annulus calcifications were observed, and her pulmonary artery pressure was normal. Twenty-four hours later, the patient became suddenly hypotensive. Electrocardiography showed no recurrent ST-segment elevation in the anterior leads. Immediate cardiac catheterization was performed, and coronary angiography revealed a significant bifurcation lesion in the mid-portion of the left anterior descending (LAD) artery, with TIMI 3 flow. Intra-aortic balloon pump (IABP) placement and intravenous inotropic support with dobutamine 5 g/kg/minute provided improvement of the patient’s hemodynamic status. Six hours later, the patient developed femoral puncture site bleeding requiring blood transfusion. This was nearly concomitant with hemodynamic impairment, and cardiac auscultation revealed intermittent systolic ejection murmur. New TTE was then performed (under dobutamine 5 g/kg/minute and IABP left to 2:1 mode). Continuous-wave Doppler showed a dynamic LVOT obstruction with a late systolic peak gradient reaching 38 mmHg (peak velocity at 3.06 m/second) associated with a typical systolic anterior motion (SAM) of the mitral valve (Figure 2). These pathological findings were only observed when ventricular systole was preceded by balloon counterpulsation. During unassisted systoles, SAM disappeared and the systolic pressure gradient decreased to 14 mmHg (peak velocity at 1.88 m/second) (Figure 2). IABP was then definitively stopped, and all Doppler evidence of LVOT obstruction resolved. Furthermore, counterpulsation interruption was followed by immediate blood pressure improvement to 130/70 mmHg. Dobutamine infusion was progressively discontinued, and intravenous fluid loading was carefully initiated. Thereafter, the patient’s hemodynamic status stabilized and beta-blockers were introduced. On the third day post-infarction, angioplasty of the mid-segment of the LAD artery was successfully performed. Ultimate TTE confirmed the asymmetric septal hypertrophy without LVOT obstruction, even after sublingual nitroglycerin administration. Furthermore, left ventricular function was nearly normalized. The patient was discharged from the hospital on the tenth day post-infarction. Discussion. Aortic counterpulsation lowers myocardial oxygen consumption and allows improvement of cardiac output, diastolic blood pressure and systolic afterload reduction.1 Furthermore, IABP therapy enhances coronary perfusion. Hence, it may be a useful hemodynamic support, particularly after thrombolysis or in patients with cardiogenic shock.^1,2 The most common IABP complications include limb ischemia and puncture site bleeding.³ Dynamic LVOT obstruction after anterior myocardial infarction has been previously described.⁴ This uncommon complication results from compensatory hyperkinesis of normally perfused myocardial segments. Alteration of ventricular geometry may be responsible for an accelerated blood flow in the LVOT.⁴ SAM may be enhanced by mitral annulus calcifications.⁵ Other contributing factors are usually necessary to create dynamic outflow obstruction, such as hypovolemia, hypotension and the use of inotropic agents.⁶ Dynamic outflow obstruction induced by IABP after acute myocardial infarction has rarely been reported.⁶ Ventricular obstruction may appear or worsen with reduction in afterload related to a Venturi-like effect of IABP. In the reported case, the pathological role of IABP was clearly revealed by continuous-wave Doppler which showed intermittent dynamic outflow obstruction and SAM only when ventricular systole was preceded by counterpulsation. To our knowledge, this is the first time that such an alternating hemodynamic state has been documented by Doppler imaging. In our observation, asymmetric septal hypertrophy, hyperkinesis of basilar segments, hypovolemia due to femoral puncture site bleeding and inotropic stimulation by dobutamine have also contributed to worsening of the ventricular obstruction. However, IABP was probably the main and original pathological condition because dynamic LVOT obstruction immediately resolved after IABP discontinuation, despite persistence of other contributing factors. Furthermore, it is worth noting that examining a patient with shock has some value and can be a clue to the diagnosis of ventricular obstruction that can be confirmed by TTE, leading to an appropriate treatment strategy. Thus, when hypotension occurs in the setting of acute anterior myocardial infarction with IABP placement, early recognition of this unusual complication may help to avoid deleterious afterload-reducing therapies.

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