Tariq Cheema

Consequences of Venous Thromboembolism, Including Chronic Thromboembolic Pulmonary Hypertension

Venous thromboembolism includes both deep vein thrombosis and pulmonary embolism. They pose a significant risk for morbidity and mortality. In an appropriate clinical setting, invasive interventions, including administration of thrombolytics, anticoagulation, and placement of vena cava filter, are warranted. Bleeding, postthrombotic syndrome, recurrence, and filter-associated complications are few of the complications of this disease. More recently, chronic thromboembolic pulmonary hypertension has gained clinical interest in patients with pulmonary embolism and has warranted close follow-up.

Controversies in Venous Thromboembolism

Numerous controversies exist in the diagnosis of venous thromboembolism despite all the guidelines that are currently available. Screening of malignancy in venous thromboembolism has been a debated issue, as it has not been shown to change mortality. Calf vein thrombosis is also a controversial topic, but evidence points to risk stratifying those patients. Overdiagnosis, most notably from the finding of subsegmental pulmonary embolism, ultimately requires evaluating the risk and benefit for each patient. In addition, treatment of upper extremity deep vein thrombosis is a challenging scenario that is quite common in clinical practice. Finally, postthrombotic syndrome may be reduced by graduated compression stockings, but their use has not been validated for preventive use at this time and is still being discussed.

McConnell’s sign unveiled

Summary McConnell’s sign is well described in echocardiography as a harbinger of severe RV failure and more extensive arterial thrombus burden but its mechanical basis has never been satifactorily defined despite multiple current theories. CMR RF tissue-tagging now unveils the mechanism. Background Evidence of echocardiographic RV ‘strain’ in the setting of a large, clinically important, often devasting pulmonary embolism (PE) is defined by the presence of paradoxical, often hyperdynamic RV apical contraction in the setting of severely dysfunctional RV function; so denoted ‘McConnell’ ss ign’. Despite its original observation by its namesake in 1996, it has neither been observed via CMR nor more importantly, while many theories exist, mechanistically explained. Hypothesis We hypothesize that McConnell’s sign (MS) is observable utilizing CMR and can be explained via CMR deformational analysis. Methods Modestly stable patients who had CT confirmed large (>one pulmonary branch obstruction and/or saddle PE) were evaluated via echocardiography and CMR. CMR radio-frequency tissue tagging was performed to determine midwall intramyocardial deformation patterns with superimposition of quiver plot technique to define direction and amplitude of myocardial displacements assuming homogenous tissue strain (%S). Results