Download Acute Mitral Regurgitation: Another Great Masquerader?

Acute Mitral Regurgitation: Another Great Masquerader?
Rinjal Brahmbhatt MD, Jacqueline Kehler MD, and Jonathan Keevil MD
University of Wisconsin School of Medicine and Public Health
Diagnosis of Acute MR
Dyspnea and a Murmur
Transthoracic Echocardiography (TTE)
 Demonstrates valve disruption and provide semi-quantitative
measure of regurgitation severity
 Limited sensitivity: misses up to 25% of MR seen on TTE
 Only finding may be hyperdynamic left ventricular function
Case
 87 YOF with a history of HTN and osteoporosis was admitted to
the hospital with acute-onset SOB both at rest and with exertion that
began the day prior to admission and was associated with chest
tightness, fatigue, and orthopnea
 No f/c, cough, wheezing, hemoptysis, lower extremity edema,
weight gain, or PND
 Possible sick contacts at her assisted living facility
 Recently traveled to Missouri
 No hx of known lung disease, pets, occupational exposures, TB
risk factors, hx of VTE, or hx of tobacco use
 Home medications: acetominophen prn, calcium, vitamin D, and
lisinopril-HCTZ
 Vitals: 36.8, 142/65, 121, 23, 96% on CPAP
 Exam was remarkable only for a 2/6 holosystolic murmur heard
best at the apex with radiation to the axilla.
Significant Labs
WBC 15.1
BUN 25
BNP 430
D-dimer 2.4
Transesophageal Echocardiography (TEE)
 Obtain if TTE is not diagnostic and patient has acute heart
failure and hyperdynamic left ventricular function on TTE
 Provides more detailed information about anatomic etiology
 Is favored for surgical planning
Treatment
 Typically a bridge to emergent surgical repair or replacement
Figure 1. CXR with asymmetric opacities, right > left.
Cr 1.05
Troponin <0.02
ABG 7.38/39/279/23 on 100% FiO2
Figure 2. Chest CTA with predominantly RUL abnormalities:
ground glass opacities, intralobular septal thickening,
consolidation.
Figure 3. TEE showing mitral valve with flailed leaflet.
 If hypotensive, ionotropic agents and an intra-aortic balloon
pump may be required in addition to nitroprusside
ECG Sinus tachycardia, no ischemic changes
LUPV
Imaging
 CXR showed asymmetric opacities, right > left (Figure 1).
 Chest CT angiogram showed predominantly right upper lobe
abnormalities with ground glass opacities, intralobular septal
thickening, and consolidation (Figure 2).
Clinical Course
 Despite IV diuresis for suspected decompensated HF and empiric
broad-spectrum antibiotics for a possible atypical pneumonia, she
did not improve.
 Given the new murmur on exam, a TTE was obtained and showed
no wall motion abnormalities, hyperdynamic LV with EF 80%, MV
prolapse of the anterior leaflet without regurgitation, grade 2 diastolic
dysfunction, normal RV size and function, and PASP of 40 mmHg.
 A follow-up TEE showed severe MR directed eccentrically (which
explained the lack of TTE findings) and posteriorly with severe flail
motion of the anterior leaflet due to chord rupture (Figure 3).
 As evidenced by Doppler images, the regurgitant jet generated more
significant flow reversal in the right pulmonary vein than it did in the
left, which could explain the unilateral findings on chest imaging
(Figures 4 & 5).
 Due to advanced age and comorbidities, our patient chose medical
management with afterload reduction rather than surgical valve
repair.
Differential Diagnosis of Unilateral
Pulmonary Infiltrates
Cardiac
 Acute MR
 Acute MI without
MR
 L sided HF (rare)
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Pulmonary
 Pneumonia
 Aspiration
 Acute pneumonitis
 Malignancy
 Re-expansion
pulmonary edema after
thoracentesis
 Bronchial obstruction
 Nitroprusside to reduce afterload, improve left ventricular
forward flow, and reduce pulmonary vascular congestion
 Pulmonary
vein obstruction
 ARDS
 Alveolar
hemorrhage
 Lung
infarction
RUPV
Conclusions
 Asymmetric or unilateral pulmonary edema is a rare cause of
focal abnormalities on chest imaging and is frequently mistaken
for more common conditions such as infection or malignancy.
 The asymmetry of pulmonary infiltrates in MR is due to the
asymmetrical jet of mitral regurgitation causing a selective
increase in R upper pulmonary vein pressure and consequently, a
greater degree of R-sided pulmonary edema.
Low Flow Reversal
 There are clinically important limitations in relying on TTE to
diagnose acute MR. In a patient with symptoms suggestive of
acute heart failure and hyperdynamic LV function on TTE, acute
MR should be considered and a TEE should be obtained.
Flow Reversal
Figure 4. TEE showing Left Upper Pulmonary Vein (LUPV) and minimal
systolic flow reversal on Doppler.
Causes of Acute MR
 MI
 Papillar muscle rupture
 Infective endocarditis
 Blunt chest trauma
 Acute rheumatic fever
 Myxomatous degeneration as in Marfan s
 HOCM
 Atrial myxoma
 Idiopathic chordae tendinaeae rupture due to spontaneous
rupture
 Sepsis
 Intramural amyloidosis
 Coronary vasospasm
Figure 5. TEE showing Right Upper Pulmonary Vein (RUPV) and systolic
flow reversal on Doppler.
 This case highlights the importance of recognizing the variation
in clinical manifestations of acute mitral regurgitation.
 Physicians should include acute valvular regurgitation in the
differential diagnosis of any patient presenting with pulmonary
manifestations, even with focal findings on chest imaging.
Clinical Presentation of
Acute MR
 Sudden, rapid onset of pulmonary edema
 Hypotension +/- cardiogenic shock
 Acute right-sided heart failure
 SOB, DOE, fatigue, weakness
 Exam with tachycardia, peripheral vasoconstriction with thready
pulses, pallor, diaphoresis, elevated JVD
 If TR has developed, there may be a RV lift
 Soft, low-pitched systolic murmur along the left sternal border that
may radiate to the back
 S3, loud P2 may be present
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