A 46-year-old man with a history of neurosarcoidosis presented to the emergency room with nonradiating, midsternal chest pressure with associated dyspnea lasting for 10 minutes that occurred 1 day before presentation. He was found to be hypotensive; in sinus tachycardia; with a new right bundle-branch block on the ECG, a mildly elevated troponin (1.47 ng/mL), and significantly elevated hepatic transaminases indicative of shock liver; and in acute renal failure. He required large doses of vasopressors and became acutely bradycardic and pulseless. He was resuscitated after 8 minutes of advanced cardiac life support.
A stat transthoracic echocardiogram revealed normal left ventricular function (ejection fraction, 60%) and a moderately to severely enlarged right atrium. The right ventricle was moderately to severely enlarged with severely impaired systolic function that spared the right ventricular apex (see Movies I and II in the online Data Supplement). There was mild tricuspid regurgitation and a systolic pulmonary artery pressure of 60 mm Hg.
He emergently received alteplase through the right internal jugular central venous catheter for presumed massive pulmonary embolism (PE). Within a few hours, his clinical and hemodynamic picture improved dramatically. He was weaned off all vasopressors, and his right bundle-branch block resolved in a few hours. Duplex scan showed lower-extremity deep venous thrombosis in the right popliteal vein and bilateral tibioperoneal veins (Figures 1 through 3⇓⇓). Repeat echocardiogram revealed a decrease in right ventricular and right atrial size with improved right ventricular function and a pulmonary artery pressure of 28 mm Hg.
McConnell’s sign is a distinct echocardiographic finding described in patients with acute PE. There is a distinct regional pattern of right ventricular dysfunction, with akinesia of the mid free wall (centerline excursion, −0.2±0.8 mm; P=0.0001 versus normal) but normal motion at the apex (centerline excursion, 5.7±0.8 mm; P=NS versus normal).1 Three mechanisms have been proposed that may explain these findings. First, in acute PE, the tethering of the right ventricular apex to a contracting and often hyperdynamic left ventricle may account for the preserved wall motion at the apex.1 Second, the right ventricle may be assuming a more spherical shape to equalize regional wall stress when subjected to an abrupt increase in afterload.2,3 Third, there may be localized ischemia of the right ventricular free wall as a result of increased wall stress.1 Overall, echocardiography has a low sensitivity for diagnosing PE; however, the accuracy is much higher in the diagnosis of massive PE.4 Echocardiography may be useful in cases of massive PE in which a rapid presumptive diagnosis is required to justify the use of thrombolytic therapy.5 Regional wall motion abnormalities sparing the right ventricular apex (McConnell’s sign) are particularly suggestive of PE.2
The online-only Data Supplement is available with this article at http://circ.ahajournals.org/cgi/content/full/118/15/e517/DC1.