3) Discussion:
In hyperthyroidism the increased serum concentration of T3 up-regulates
several cardiac-specific genes enhancing contractility, improving
cardiac relaxation, lowering SVR, increasing blood volume, and elevating
baseline heart rate (1). In the setting of prolonged, severe
hyperthyroidism, sustained tachycardia impairs left ventricular
contractility and increases atrial-filling pressures leading to heart
failure. Ultimately, an untreated high-output state may lead to
ventricular dilatation and persistent tachycardia resulting in
cardiogenic shock (2). 6% of patients with thyrotoxicosis develop
symptoms of heart failure, but less than 1% develop a dilated
cardiomyopathy and impaired systolic function (3). Of these patients
with impaired systolic function cardiogenic shock is rare, but with
mortality rates that approach 30% (4).
The above case illustrates how rapid recognition of the severity of
illness accompanied by aggressive management with mechanical circulatory
support can result in a good outcome and avoid serious comorbidities. On
presentation our patient appeared relatively stable, which is likely due
to his young age and ability to significantly increase his SVR despite a
thyrotoxic state. However when his SVR dropped, his poor cardiac output
led to rapid clinical decline and laboratory evidence of multi-organ
hypo-perfusion. While it is not possible to delineate whether his
ventricular dysfunction was due to prolonged tachyarrhythmia or
thyrotoxicosis, this difference did not affect management as he required
support while the underlying disorder was treated.
The combination of his deteriorating clinical status, laboratory data
and the abnormal echocardiogram, led us to proceed with invasive
hemodynamics. In the lab, there was clear evidence of severely impaired
left ventricular function by CPO. Several hemodynamic measurements
including PAPi, RA:PCWP ratio, and RVSWI were indicative of severe right
ventricular dysfunction (table II). Previous studies to evaluate the
most effective management of bi-ventricular failure have yielded mixed
results (5). Given the limited options for medical therapy, the use of
acute mechanical circulatory support has grown as Impella, TandemHeart,
and VA-ECMO have been used with increased frequency over the last 15
years (6).
The decision to place an impella CP was made based on what we identified
as a reversible cause of cardiogenic shock. The use of impella over ECMO
was based on the concept of ventricular unloading to allow the ventricle
time to recover as the underlying cause of heart failure was treated.
Following placement of the impella CP the patient was monitored in the
cath lab to see if the right ventricular function improved with
off-loading of the left ventricle. This resulted in a slight improvement
of his PAPi and RVSWI, however both were still severely reduced and his
RA:PCWP ratio was unchanged and severely elevated. Prior studies have
indicated that a reduced RVSWI is an independent predictor for
biventricular support requirement in patient undergoing LVAD placement
(7) and that an increased RA:PCWP ratio is associated with reduced RV
function and adverse outcomes in advanced heart failure (8). Given this
previous data, combined with hemodynamic findings and minimal clinical
improvement, we determined that RV support, in addition to LV support,
was necessary to allow for treatment of his underlying disorder. Prior
evidence indicates that biventricular impella (Bi-Pella) is a feasible
approach that improves cardiac output and may be associated with
improved outcomes in patients with bi-ventricular failure (9). Thus
following the Recover Right Trial, an RP impella was placed (10) which
showed an improvement in his PAPi and RA:PCWP ratio, (table II), and
more importantly a significant improvement in his mental status.
What followed was rapid improvement in his overall clinical status.
Multi-organ failure was reversed within 48 hours of mechanical support
and the need for other advanced supportive care was avoided. By 48 hours
there was significant improvement in bi-ventricular function. With
resolution of clinical cardiogenic shock and evidence of hemolysis
(table I) the RP impella was discontinued. Following this the hemolysis
improved and the impella CP was discontinued shortly thereafter.
This case illustrates that the use of Bi-Pella may have a significant
impact on mortality in patients with acute, reversible causes of
cardiogenic shock. The short-term use of the support device likely
limited our device related complications to mild hemolysis and
thrombocytopenia. In this situation the benefits of left and right
ventricular offloading significantly outweighed device complications.
This leads us to believe that Bi-Pella has a “sweet spot” for duration
of support where a mortality benefit can be gleaned. Further studies
should be done to determine the balance between duration of support and
degree of ventricular recovery that will have the greatest benefit in
patient care.
One limitation in our case is that for our cardiac output we utilized
the Fick equation with nomogram-derived estimates of O2 consumption. In
a thyrotoxic state this may underestimate true O2 consumption and lead
to an underestimation of cardiac output and an overestimation of SVR.
However, the patient had severe tricuspid regurgitation by
echocardiogram and in his clinically low-flow state thermodilution
likely would yield similar limitations. Second, given his degree of
illness, full hemodynamics were not performed at every stage, but only
as necessary to direct management.