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Abstract & Commentary
Synopsis: Despite similar repiratory variations in the mitral E velocity, COPD patients demonstrate greater changes in SVC systolic forward flow velocity, which is not observed in constrictive pericarditis patients.
Source: Boonyaratavej S, et al. J Am Coll Cardiol 1998;32:2043-2048.
Constrictive pericarditis (cp) and chronic obstructive pulmonary disease (COPD) can have the same clinical presentation and diseases such as tuberculosis can be associated with both. Boonyaratavej and associates from the Mayo Clinic hypothesized that since the exaggerated respiratory variation in mitral inflow velocities is due to increased intrathoracic pressure swings in COPD as opposed to a disassociation of intrathoracic and intrapericardial pressures in CP, superior vena cava (SVC) flow velocity would be different in the two conditions. Thus, they studied 20 patients with COPD vs. 20 patients with surgically proven CP by Doppler echocardiography. Respiratory variation in mitral E wave velocity was similar in both groups (41 vs 46%). However, in CP patients, the E/A ratio was higher throughout the respiratory cycle compared to COPD patients, due mainly to a lower A velocity and a somewhat higher E velocity in the CP patients. Also, deceleration of E was lower in the CP patients, as was SVC inspiratory systolic forward flow velocity (36 ± 9 vs 73 ± 22 cm/s; P < 0.0001). Consequently, there was much less respiratory variation in SVC systolic forward flow velocity in CP patients (4 ± 3 vs 40 ± 19 cm/s: P < 0.0001), with only one COPD patient who overlapped with the values in the CP patients. Boonyaratavej et al conclude that despite similar respiratory variations in the mitral E velocity, CP patients show a more restricted mitral E pattern than do COPD patients, but COPD patients demonstrate much greater changes in SVC systolic forward flow velocity, which is not observed in CP patients.
Comment by Michael H. Crawford, MD
Patients with COPD and CP can both present with dyspnea, Kussmauls sign, signs of right heart failure, and increased respiratory variation in mitral E wave velocities. Other diseases can also augment respiratory mitral Doppler E wave velocity changes, such as cardiac tamponade or acute right ventricular dilation due to infarction or pulmonary embolism. Usually, clinical features and echo findings, such as pericardial effusion and dilated right ventricle, can distinguish the latter conditions, but COPD can be a challenge clinically and on echocardiography. Thus, the observation that SVC systolic forward flow velocity changes with respiration are discriminative is useful. However, SVC recordings require right supradavicular fossa or suprasternal notch windows that may not be used frequently in many adult echo laboratories.
With obstructive airway disease, intrathoracic pressure swings are increased by augmented diaphragmatic action to attempt to move air. These pressure swings are readily transmitted to the SVC and left atrium, markedly altering flow velocities in these areas. In CP, normal intrathoracic inspiratory pressure drops are not transmitted to the heart chambers, resulting in lower pressure gradients from the pulmonary veins to the left heart—exaggerating the swings in mitral flow velocity but not the SVC. In severe COPD, diaphragmatic movement can be reduced due to lung hyperinflation and the change in SVC flow reduced. This was the explanation for the one patient in the study with COPD whose SVC velocity changes with inspiration were similar to the CP group.
Although this appears to be a useful Doppler echocardiographic finding that should be sought in all patients suspected of having CP, a few cautions are in order. As mentioned, severe lung hyperinflation can cause a false positive SVC velocity sign suggesting CP. Also, it is conceivable that severe tricuspid regurgitation could reduce SVC systolic forward flow velocities, giving the false impression of CP. Severe tricuspid regurgitation could be due to unrecognized right ventricular infarction or pulmonary emboli, which could augment the respiratory variation in mitral E velocities as well. Thus, in the final analysis, the diagnosis of CP rests on detecting thickened pericardium and this is best accomplished by MRI. However, SVC flow velocity measures are an important new screening tool that all echocardiography laboratories should gear up to do well.