Residual Vein Thrombosis Echogenicity Is Associated to the Risk of DVT Recurrence: A Cohort Study.

Although deep vein thrombosis (DVT) recurrence is a common late complication of the disease, there are few predictive markers to risk-stratify patients long-term after the thrombotic event. The accuracy of residual vein thrombosis (RVT) in this context is controversial, possibly due to a lack of a standardized methodology. The objective of the study was to evaluate the accuracy of RVT echogenicity as a predictive marker of late DVT recurrence. To evaluate the accuracy of RVT echogenicity as a predictive marker of late DVT recurrence. This prospective study included patients with history of DVT in the past 33 months. Ultrasound examination was performed to detect the presence of RVT, and its echogenicity was determined by calculating the grayscale median (GSM) of the images. Blood samplings were taken for plasma D-dimer levels. Patients were followed-up for 28 months and the primary end point was DVT recurrence. Deep vein thrombosis recurrence was confirmed or excluded by ultrasound during the follow-up. Fifty-six patients were included, of which 10 presented DVT recurrence during the follow-up. D-dimer levels above 630 ng/mL conferred higher risk for recurrence with a negative predictive value of 94%. The absence of RVT was a protective marker for recurrence with a negative predictive value of 100%. Also, the presence of hypoechoic RVT, determined by GSM values below 24, positively predicted 75% of DVT recurrences. Our results suggest that the persistence of RVT and, particularly, the presence of hypoechoic thrombi (GSM < 24) are predictive markers of the risk of DVT recurrence. Residual vein thrombosis echogenicity, by GSM analysis, could represent a new strategy for the evaluation of recurrence risk in patients with DVT.

Severe postthrombotic syndrome is associated with characteristic sonographic pattern of the residual thrombosis.

Postthrombotic syndrome (PTS) may affect 50% of patients with deep venous thrombosis, 5-10% of them may present severe manifestations. The causes for PTS development and severity have not been well established. This study evaluated whether PTS may be associated with the presence, and echogenicity, of the residual vein thrombosis (RVT). We included patients with a history of deep venous thrombosis in the past 58 months. These patients were further evaluated for PTS diagnosis, clinical comorbidities, plasma levels of D-dimer, serum levels of C-reactive protein and for the presence of RVT. Particularly, RVT was detected by ultrasound examination and the residual thrombi echogenicity was determined by grayscale median (GSM). Fifty-six patients were included, of which 41 presented PTS. Mild PTS was detected in 23 patients, moderate PTS in 11 and severe PTS in seven patients. Patients with severe PTS showed higher body mass index, higher abdominal circumference and higher C-reactive protein levels when compared with the other patients (P = 0.007, P = 0.002, P = 0.02, respectively). The ultrasound-generated GSM was significantly lower in patients with severe PTS compared with patients with mild-moderate PTS or no PTS (median = 24, 35 and 41, respectively; P = 0.04). A GSM value less than 25, which was consistent with a hypoechoic RVT, was the best cut-off value to discriminate patients with severe PTS from those with mild or moderate PTS and those without PTS. RVT is a common finding among patients with PTS and the echogenicity of the RVT may impact the severity of PTS.

Relação entre reduçäo volumétrica do ventrículo esquerdo e incremento do prolapso da valva mitral: um estudo experimental em cäes / Experimental Study on the Relationship Between Reduction of Left Ventricular Volume and Increment of Mitral Valve Prolapse

PURPOSE--To verify whether accentuated reductions of left ventricular volume lead to mitral valve prolapse. METHODS--Seven mongrel dogs were bled through the internal jugular vein, the systolic systemic pressure being kept between 100 and 140 mmHg by means of continuous infusion of dopamine; the inferior vena cava vein, in tree other dogs, was partially obstructed for 4 to 6 seconds; epicardial echocardiography was carried out in all cases. RESULTS--Reductions of volemia were about 50 per cent of the estimated total blood volume. Systolic internal diameter of left ventricle decreased about 25 per cent and systolic ostial diameter, about 12.5 per cent . Three out of seven died suddenly from arrhythmia before one has reached a significant decrease in total blood volume; one showed momentary mitral valve prolapse, during a period of hypotension; however, this prolapse disappeared completely when systemic blood pressure was restored by increasing the dopamine dosage; one dog had slight systolic displacement of the anterior cusp toward left atrium (0.5mm) and the last two showed no change; one out of 3 dogs submitted to partial constriction of inferior vena cava had systolic displacement of anterior cusp of 1mm; in one case there was an equivalent degree of displacement of the anterior cusp toward the left ventricle and in the last one no change was detected. In all dogs there was a change in the dynamics of mitral valve closure: with accentuated reduction of left ventricular volume the posterior cusp became less mobile, the anterior cusp being the principal responsible for the systolic ostial occlusion. CONCLUSION--Accentuated reduction of dog's left ventricular volume does not, necessarily, cause mitral valve prolapse but only slight displacement of the anterior cusp toward the left atrium in some animals or no displacement at all

Objetivo - Verificar se diminuições acentuadas do volume ventricular esquerdo provocam o aparecimento de abaulamento sistólicos da valva mitral. Métodos - Sete cães foram submetidos a lenta sangria pela veia jugular interna (20 a 30min), mantendose os níveis sistólicos entre 100 e 140mmHg através da infusão contínua de dopamina; 3 cães foram submetidos a veno-constricções parciais e momentâneas (5-6s) da veia cava inferior; foi feita exploração ecocardiográfica epicárdica com transdutor de 5mHz em todos os casos. Resultados - Provocou-se redução da volemia estimada dos animais de até 50%, ocorrendo uma diminuição média do diâmetro ostial sistólico de 12,5% e redução média do diâmetro sistólico esquerdo de 25%. Tres dos 7 cães submetidos a sangria apresentaram arritmia grave e morreram antes de se conseguir uma diminuição apreciável do volume ventricular esquerdo; 1 exibiu momentâneo abaulamento sistólico mitral durante período de hipotensão que desapareceu com a elevação dos niíveis pressóricos por aumento da dose de dopamina e a despeito de se continuar a redução do volume ventricular pelo sangramento; 1 mostrou discreto deslocamento da cúspide anterior (0,5mm); os 2 últimos deste grupo não exibiram qualquer movimento da valva mitral em direção ao átrio esquerdo; dos 3 animais em constricção parcial da veia cava inferior, detectamos, em 1 deles, abaulamento sistólico da cúspide anterior de 1mm; em outro, a cúspide anterior exibiu um deslocamento de 1mm em direção ao ventrículo esquerdo, nada sendo observado no último animal. Em todos os 7 cães notou-se mudança da dinâmica do fechamento da valva mitral: com redução volumétrica do ventrículo esquerdo, a cúspide posterior passou a se mostrar menos móvel, cabendo à anterior o principal papel na oclusão do óstio atrioventricular. Conclusão - Reduções acentuadas do volume ventricular esquerdo produzidas por sangramento e por veno-constricção parcial da veia cava inferior não levam, necessariamente, a abaulamentos da valva mitral. Nossos achados contrapõem-se à admitida relação en tre incremento do prolapso da valva mitral e manobras clínicas que provocam redução do volume ventricular esquerdo