Case Study: An 85 Year-Old Male with Hemodynamic Decompensation After an Acute Myocardial Infarction
Case presentation - May 2013
Manju Pai MD, Cardiology Fellow, Cleveland Clinic
An 85 year-old male presented to the Cleveland Clinic emergency department via ambulance for complaint of lightheadedness, weakness, and the setting in of chest pain.
Past medical history
His past medical history was significant for coronary artery disease, hypertension, hyperlipidemia, stage IV chronic kidney disease with a baseline creatinine of approximately 2.0mg/dL, and a history of a remote cerebral vascular accident.
Hospital course prior to presentation to Cleveland Clinic
At approximately 5 a.m., the patient awoke to use the bathroom. Upon arising from bed, he noted extreme lightheadedness and weakness, at which time the daughter called emergency medical services (EMS). Notable findings upon EMS arrival were complaints of chest pain and a blood pressure of 80/40mmHg. A telemetry strip was obtained, which raised concern for an ST-elevation MI. He was given aspirin 325mg and two doses of sublingual nitroglycerin. His chest pain subsequently resolved and he was transferred urgently to Cleveland Clinic.
Initial hospital course at Cleveland Clinic
Click on images for a larger view
Figure 1: Coronary angiography demonstrating total occlusion in the mid-segment of the left anterior descending artery [arrow].
Upon arrival to the Emergency Department, a 12-lead EKG was immediately obtained, which was highly suggestive for an acute anterior myocardial infarction. Blood pressure had improved upon arrival (111/60mmHg), with a pulse of 84. He was alert, oriented and mentating well; physical exam was otherwise unremarkable, including cardiac and pulmonary exams. The patient was placed on intravenous unfractionated heparin, administered a 600mg loading dose of clopidogrel and triaged urgently to the catheterization lab. Before transfer, patient suffered a cardiac arrest, due to his rhythm degenerating into pulseless ventricular tachycardia. He required CPR, epinephrine, amiodarone and two rounds of defibrillation, returning to spontaneous circulation after approximately four minutes. During this event, the patient was intubated for airway control and placed on mechanical ventilation.
When stable, the patient was urgently brought to the cardiac catheterization laboratory. An intra-aortic balloon pump was placed (due to his earlier hemodynamic instability) and left heart catheterization was undertaken.
Significant findings included: a focal 80% stenosis of the proximal left anterior descending artery, followed by a total occlusion in the middle-third of the artery (Figure 1); diffuse 30-40% stenoses of the proximal left circumflex artery; a focal 80% stenosis of a large obtuse marginal branch; and a total occlusion of the proximal right coronary artery, which was supplied by bridging and left-to-right collaterals.
It was felt that the patient's acute clinical picture was explained by the occlusion of the left anterior descending artery. A single bare metal stent was placed in the proximal-to-middle segment of the artery, with successful revascularization of the vessel.
The patient was then transferred to the cardiac intensive care unit. The intra-aortic balloon pump continued to be in place (at 1:1 counterpulsation), in addition to intravenous vasodilating agents (sodium nitroprusside, nitroglycerin). While hemodynamics were initially stable, the patient soon decompensated, with poor augmentation with the balloon pump (mean augmentation BPs ~50-60mmHg), low intracardiac pressures (PA 20/10 mmHg; PCWP 7 mmHg) and low cardiac indices (CO/CI: 3.0/1.6).
A transthoracic echocardiogram was subsequently obtained to further elucidate the change in clinical status. Significant findings included an ejection fraction of 40% with an apical wall motion abnormality; hyperdynamic basal segments with septal hypertrophy; a small left ventricular cavity size; anterior motion of the anterior mitral valve during systole causing obstruction of the left ventricular outflow tract (Figures 2, 3; Videos 1, 2) with flow acceleration starting in the mid-left ventricular cavity and a resting gradient of 55-60mmHg in the LVOT (Figures 4-6).
Figure 2: Parasternal long axis view during systole demonstrating 1) near obliteration of the left ventricular cavity size and 2) anterior displacement of the anterior mitral valve leaflet [arrow] causing left ventricular outflow tract obstruction.
LA: Left atrium, LV: Left Ventricle, *: Left Ventricular Outflow Tract, Ao: Aorta, RV: Right Ventricle
Figure 3: Apical 4-chamber view during systole demonstrating anterior displacement of the anterior mitral valve leaflet [arrow] causing left ventricular outflow tract obstruction.
LA: Left atrium, LV: Left Ventricle, *: Left Ventricular Outflow Tract, RA: Right Atrium, RV: Right Ventricle
Figures 4-6: Gradient measurements in the left ventricular cavity, in the mid segment, basal segment and LVOT, respectively. Note that the resting gradient increases as the LVOT is approached.
The etiology for the patient's current hemodynamic instability was felt to be secondary to a dynamic left ventricular outflow tract obstruction (LVOTO). This was due to a variety of factors, all leading to a decrease in the left ventricular outflow tract cross-sectional area, with resultant decreased forward perfusion: 1) an anterior infarction with a compensatory hyperdynamic basal wall; 2) hypovolemia leading to an underfilled and small left ventricular cavity size; and 3) decreased afterload (due to the intra-aortic balloon pump and intravenous vasodilators), which allowed for more dynamic basal wall movement.
Given these findings, our patient was subsequently managed by a combination of intravenous saline resuscitation, down-titration of intravenous vasodilators, weaning of the intra-aortic balloon pump and slow initiation of beta-blockers. With these interventions, his hemodynamics improved dramatically.
A transthoracic echocardiogram was repeated four days after initial presentation (and after removal of the intra-aortic balloon pump). Significant findings included improved myocardial function after revascularization (EF of 54% with an improvement in the prior anterior wall motion abnormality), an increase in the left ventricular cavity size and resolution of systolic anterior motion (SAM) of the anterior mitral leaflet. These changes led to an increase in the left ventricular outflow tract cross-sectional area, with resolution of the dynamic LVOTO (Figures 7, 8; Videos 3,4). Additionally, pre and post images of the decrease in LVOT gradient are shown in Figures 9 and 10, with color doppler in Videos 5 and 6.
Figures 7, 8: Parasternal long axis and apical 4-chamber views during systole. Note 1) improved function of the anterior wall evidenced by wall thickening, 2) improved left ventricular cavity size, 3) resolution of systolic anterior motion of the anterior mitral valve [arrow] and 4) an increase in the left ventricular outflow tract cross-sectional area.
RA: Right Atrium, RV: Right Ventricle, LA: Left Atrium, LV: Left Ventricle, *: Left Ventricular Outflow Tract
Figures 9, 10: Pre and post images of the dynamic LVOT gradient, taken in the apical view.
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.
Non-critical demographic information has been changed to protect the anonymity of the individual and no association with any actual patient is intended or should be inferred.
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