The differential for hemodynamic compromise is broad and can include etiologies such as hypovolemia, sepsis, etc. In the setting of an acute myocardial infarction, this differential should be expanded to include post-catheterization complications (i.e. acute blood loss such as a retroperitoneal bleed or cardiac tamponade) and mechanical complications (i.e. ventricular free wall rupture, papillary muscle rupture, ventricular septal rupture). Our case highlights a less common etiology, but just as important to consider: dynamic LVOTO. Emphasis should be placed on dynamic LVOTO, implying that the obstruction is secondary to a variety of acute factors, as opposed to a chronic or congenital process (such as hypertrophic obstructive cardiomyopathy).
Factors that can contribute to dynamic LVOTO include [ref 1]:
- Basal hypercontractility (especially in the setting of underlying left ventricular hypertrophy).
- Apical dysfunction (such as seen in an anterior myocardial infarction or Takotsubo's cardiomyopathy).
- Reduced left ventricular chamber size (as seen in hypovolemia).
- SAM of the anterior mitral leaflet: a Venturi effect can occur, where a high velocity flow through a narrowed LVOT can move the mitral valve leaflet anteriorly towards the septum.
Management relies on interventions that increase the left ventricular filling/cavity size and reduce basal hypercontractility. Some options include:
- Stopping inotropic medications and cautiously applying beta-blockers: Reduces basal hypercontractility and reduces heart rate, which can increase left ventricular filling and size.
- Fluid resuscitation: Increases left ventricular filling and size.
- Afterload augmentation: Decreases the hyperdynamic motion of the basal wall segment [ref 2]. This can be accomplished by avoidance of agents that can decrease afterload (vasodilators or intra-aortic balloon pumps), as well as the use of alpha-agonists (e.g. phenylephrine).
- Coronary revascularization: May reduce apical dysfunction (and compensatory basal hypercontractility).
Note that some of these options may appear counterintuitive in the setting of hypotension (i.e. beta-blockers) or an acute myocardial infarction (i.e. afterload augmentation), but can actually lead to decreased LVOTO and consequently improved hemodynamics. The risks and benefits of each intervention must be weighed separately for each individual patient scenario.
Hemodynamic instability following an acute myocardial infarction (AMI) is a medical emergency, which must be dealt with immediately. While LV dysfunction is the most common cause of cardiogenic shock, appropriately treated with inotropes, afterload reduction, and IABP, one must be vigilant for mechanical complications of AMI (ruptured papillary muscle, ventricular septal defect, LV pseudoaneurysm and rupture), which need to be treated surgically. This case illustrated an unusual cause of post-AMI hypotension, in which the usual treatments for LV dysfunction are precisely the wrong approach. Here, a distal LAD MI produced apical dysfunction resulting in compensatory basilar hyperkinesis. An underlying upper septal hypertrophy (1.8 cm) predisposed the patient for systolic anterior motion (SAM) of the mitral valve, resulting in LVOTO, further exacerbated by IABP and vasodilators. This dynamic LVOTO can cause a loud systolic murmur, which might be mistaken for severe MR or VSD. To avoid this, one needs an awareness of this entity and a carefully done echocardiogram to demonstrate the SAM and document the LVOT gradient. Once recognized, the exacerbating factors should be reversed (weaning the IABP, vasodilators and any inotropes, administering volume) and beta blockers administered cautiously, while carefully observing the hemodynamics. As in this case, most patients will see improvement in their blood pressure and cardiac output.
- Chockalingam et al. Dynamic left ventricular outflow tract obstruction in acute myocardial infarction with shock: cause, effect and coincidence. Circulation. 2007 Jul 31;116(5);e110-3.
- Matyal et al. Anterior myocardial infarction with dynamic left ventricular outflow tract obstruction. Ann Thorac Surg. 2011 Mar;91(3);e39-40.