Right ventricular function after coronary artery bypass graft surgery--a magnetic resonance imaging study.

BACKGROUND: A reduction in right ventricular function commonly occurs in the early postoperative period after coronary artery bypass graft surgery (CABG). We sought to determine the longer-term effect of CABG on right ventricular function. METHODS: Cardiac magnetic resonance imaging was performed before and approximately 3 months after surgery in 28 patients undergoing elective CABG. Right ventricular (RV) ejection fraction was assessed by planimetry of electrocardiographically gated cine images. RESULTS: There was a statistically significant increase in left ventricular ejection fraction from 50% to 58% (P=.003) after CABG. RV ejection fraction also increased from 54% to 60% (P=.002). In patients with lower baseline RV ejection fraction (below the median, < 53%), this parameter improved from 47% to 57% (P<.001). Both on-pump (47% vs. 62%, P=.003) as well as off-pump CABG (47% vs. 55%, P=.009) lead to an improvement in RV function in patients in the initial low RV ejection fraction group. CONCLUSION: Long-term right ventricular function was not adversely affected by CABG. An improvement in RV function occurred after surgery in patients with low baseline RV ejection fraction and was similar in patients who underwent surgery with or without cardiopulmonary bypass.

Mechanism of paradoxical ventricular septal motion after coronary artery bypass grafting.

Paradoxical septal motion is commonly noted on echocardiography after coronary artery bypass grafting (CABG), but its mechanism is unclear. Cardiac magnetic resonance imaging was performed before and 3 months after CABG in 23 patients. On a mid-left ventricular short-axis cine image, the motion of myocardial landmarks during the cardiac cycle was ascertained relative to a stationary anterior reference point. Before CABG, the movement of the ventricular septum in systole was either posterior or neutral (median -2 mm) in 19 patients, whereas after CABG, the septum moved anteriorly in all 23 patients (+4 mm; p<0.001). (A positive sign indicates anterior motion in ventricular systole, and a negative sign denotes posterior motion.) The motion of the right ventricular free wall was reduced after CABG (-5 vs -3 mm; p=0.002), whereas anterior movement of the lateral left ventricular wall in systole increased (+4 vs +9 mm; p<0.001). There was a positive correlation between degree of anterior movement of the ventricular septum and right ventricular ejection fraction (r=0.47, p=0.023). In conclusion, after CABG, the entire left ventricle translocated anteriorly in systole. Despite preserved right ventricular function, there was restricted motion of the right ventricular free wall suggestive of postoperative adhesions. The pattern of movement observed offers a sound explanation for postoperative paradoxical septal motion.

The D-dimer assay: a possible tool in the evaluation of atrial thrombosis.

Atrial fibrillation (AF) is a common arrhythmia seen in clinical practice, and affects more than 4% of the population older than 60 years of age. Peripheral thromboembolism contributes significantly to the observed morbidity and mortality. Symptomatic AF, before cardioversion to normal sinus rhythm, requires either exclusion of atrial thrombi using transesophageal echocardiography (TEE) or the conventional use of three weeks of adequate anticoagulation. The exclusion of atrial thrombi by TEE, a nontomographic technique but comparable with conventional treatment of AF in outcomes, has inherent limitations due to the complex three-dimensional multilobed anatomy of the left atrial appendage, where the majority of atrial thrombi arise. Also, the conventional treatment of three weeks of therapeutic anticoagulation before cardioversion reportedly does not always eliminate atrial thrombi. Plasma D-dimer constitutes an antigen-antibody reaction to the dimeric final degradation product of a mature clot. An elevated fibrin D-dimer has a high sensitivity for intravascular thrombosis and, hence, may improve the evaluation of a patient with AF before cardioversion in addition to a TEE. A case is presented in which a positive D-dimer resulted in performing TEE to document atrial thrombosis and the complications of previous bacterial endocarditis. In the present case, this involved aortic root abscess formation and acute aortic regurgitation because of flailing of the noncoronary cusp that resulted in recurrent pulmonary edema.

Latex D-dimer signal in in situ femoral vein thrombus in swine and effect of minidose exogenous tissue plasminogen activator bolus.

STUDY OBJECTIVES: We created in situ femoral vein thrombi in swine to investigate the response of the latex d-dimer signal to acute in situ venous thrombosis, and to determine the minimum dose of exogenous bolus tissue plasminogen activator (t-PA) required to significantly elevate the d-dimer signal. STUDY DESIGN: We studied seven swine (20 to 22 kg) under pentobarbital anesthesia. A 6-cm segment of the proximal femoral vein was surgically exposed and briefly ligated. Thrombin, 250 U, was then injected into the isolated femoral vein segment to create an in situ clot. After clot formation was documented to be complete between the ligatures, they were then released. D-dimer levels were then measured every 15 min for 1 h before and 1 h after clot formation with ligatures released. Time-response curves to establish timing of peak t-PA effect were performed, and then escalating dose-response curves of d-dimer level to minidose t-PA were plotted. RESULTS: After formation of the clot, the release of ligatures resulted in no change in d-dimer levels over 1 h (p = 0.62) in all swine. When a time-response curve to exogenous t-PA bolus in the presence of femoral clot was plotted, there was a maximal increase in d-dimer signal at 30 min after bolus t-PA administration. The subsequent dose-response curves for escalating fivefold boluses of minidose t-PA showed an increase in d-dimer signal at doses of 0.8 mg (p = 0.03) and 4 mg (p = 0.003). CONCLUSION: We conclude the following: (1) in situ femoral vein clot formation does not elevate d-dimer signal for 1 h after ligature release; (2) minidose t-PA boluses of 0.8 mg and 4 mg significantly elevated the latex d-dimer signal above baseline; and (3) there is a potential role of minidose t-PA in enhancing the d-dimer signal in in situ deep venous thrombosis.