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Supplemental Digital Content is available in the text, Rationale: Pulmonary embolism (PE) is a common diagnostic consideration for patients who present to the emergency department (ED) with chest pain, dyspnea, or both. In addition, PE has a very high mortality in patients who are hemodynamically unstable. An electrocardiography, bedside transthoracic echocardiogram, and computed tomography pulmonary angiogram are usually performed to confirm the diagnosis. Patient concerns: A 53-year-old man was admitted to the cardiology clinic with complaints of dyspnea, chest pain, and general weakness after walking. He had a history of hypertension and smoking. Diagnosis: During synchronous recording of echocardiographic images, a large mobile thrombus detached from the right atrium, and first embolized to the right ventricle and then to the main pulmonary artery from the right heart chambers. Soon after, shortness of breath developed which clinically worsened the patient. Transthoracic echocardiogram which demonstrated the thrombus in the pulmonary artery or right heart chambers was suspected of causing acute massive PE. Interventions: The patient was transferred to Critical Care Unit for monitoring; 100 mg of alteplase was initiated immediately and alleviated the hemodynamic instability within 2 hours of intravenous administration. Outcomes: To the best of our knowledge, this is the first synchronous echocardiographic recording showing the embolization of a thrombus from the right atrium, first to the right ventricle and then to the main pulmonary artery. Lessons: Transthoracic echocardiography provides a safe, rapid, and noninvasive diagnostic tool for evaluation of suspected massive PE. Thrombolytic therapy is useful for treating acute massive PE that leads to hemodynamic instability.

In mitral stenosis (MS) patients, resting hemodynamic data do not always correlate with symptom severity. Stress tests may be carried out in these patients, but the mechanisms of different hemodynamic and clinical responses to stress are not clearly established. The study aim was to evaluate hemodynamic changes that correlate with dyspnea development during dobutamine infusion (DI) in patients with MS, and to assess determinants of transmitral gradient response.Forty-five consecutive mild or moderately symptomatic patients (36 women, nine men; mean age 44 +/- 10 years; range: 26-66 years), in NYHA class II and with MS (mean mitral valve area (MVA) 1.6 +/- 0.1 cm2; range: 1.5-1.9 cm2) were evaluated with dobutamine stress echocardiography.During DI, dyspnea developed in 12 patients, and 33 patients remained asymptomatic. During infusion, both mean transmitral gradient (6 +/- 3 versus 11 +/- 6 mmHg, p = 0.01) and pulmonary artery systolic pressure (PASP) (13 +/- 4 versus 21 +/- 3 mmHg, p0.001) were significantly increased in patients who developed dyspnea compared to others. Hence, a subgroup of patients with more serious MS was identified using the hemodynamic response to dobutamine. Based on these clinical and hemodynamic results, management was changed in 12 patients (27%); five underwent percutaneous mitral balloon commissurotomy and seven received intensive medical treatment. In all patients, PASP at rest (p = 0.001), MVA (p0.0001) and subvalvular mitral score (p = 0.004), which is indicative of mitral valve damage, were significantly correlated with mean mitral valve gradient response.These results suggest that patients in whom dyspnea is provoked during DI show a greater increase in hemodynamic parameters than patients in whom provocation does not occur. The mean mitral valve gradient-response correlates with baseline pulmonary artery pressure, MVA and subvalvular echo score, and may be predicted by these parameters. Association between dyspnea and presence of severe mitral valve hemodynamics showed a high sensitivity and negative and positive predictive value. It is possible that dyspnea may be of value in identifying those patients with significant mitral valve obstruction.