Analysis of coagulation changes associated with supraceliac aortic crossclamping using thromboelastography.

INTRODUCTION: The etiology of the coagulation changes seen with supraceliac (SC) aortic crossclamping (AXC) remains controversial; both primary fibrinolysis and clotting factor consumption have been implicated. The cause of these changes was investigated with thromboelastography (TEG), a test that measures the viscoelastic properties of thrombus to dynamically assess coagulation and fibrinolysis. METHODS: Eight pigs underwent SC AXC for 30 min; 5 pigs undergoing 30 min of infrarenal (IR) aortic clamping served as controls. Blood was drawn before AXC, before unclamping, and 5 and 60 min after unclamping. Thromboelastography and standard coagulation tests [prothrombin time (PT), partial thromboplastin time (PTT), fibrinogen, and platelet count] were performed. Measured TEG parameters included fibrinolytic index (a measure of fibrinolysis), r value (a reflection of intrinsic coagulation cascade activity), and the alpha angle and K values (measures of the speed of solid clot formation). Repeated measures ANOVA and t test were used for statistical analysis. RESULTS: There was no difference in the fibrinolytic index at any time point between the two groups. Increased activity of the intrinsic coagulation cascade during SC clamping was reflected by a lower R value just before unclamping (12.6 +/- 3.0 vs 20.0 +/- 3.0, P = 0.048) compared to IR AXC. Decreased speed of solid clot formation was noted 5 min after unclamping in the SC group but not the IR group [as defined by an increased K value (ANOVA, P = 0.010) and a decreased alpha angle value (ANOVA, P = 0.005)]. Fibrinogen levels were lower in the SC than in the IR group 5 (P = 0.013) and 60 min after unclamping (P = 0.02), but PT, PTT, and platelets did not differ between the groups at any time points. CONCLUSIONS: Thirty minutes of SC AXC does not result in fibrinolysis. There is increased clotting activity during SC clamping followed by decreased speed of clot formation and decreased fibrinogen levels after unclamping. These changes are consistent with clotting factor consumption.

Acute ventricular reduction with the acorn cardiac support device: effect on progressive left ventricular dysfunction and dilation in dogs with chronic heart failure.

BACKGROUND AND AIM: Surgical resection of myocardium that acutely reduces left ventricular (LV) volume in patients with advanced heart failure (HF), the so-called "Batista Operation," remains controversial. We examined the effects of acute LV reduction with the Acorn Cardiac Support Device (CSD) in dogs with HF (LV ejection fraction < 30%). METHODS: HF was produced in 15 dogs by intracoronary microembolization. In nine dogs, intravenous dobutamine was administered to reduce LV end-diastolic dimension (LVEDD) by 10%-25%. While on dobutamine infusion, the CSD, a preformed knitted polyester device, was surgically placed around the ventricles, anchored to the arteriovenous (AV) groove, and tailored anteriorly to fit snugly over the ventricles. Dogs were then weaned off dobutamine. RESULTS: On average, the procedure reduced LVEDD by 7 +/- 1 mm (range 5-12 mm). Of the nine dogs, two died before completion of the study and seven survived for the entire period. Six dogs did not undergo device placement and served as controls. All were followed for 3 months prior to sacrifice. In controls, LV end-diastolic volume increased after 3 months (66 +/- 5 mL vs 77 +/- 6 mL; p = 0.007), while in CSD-treated dogs (n = 7), it decreased (80 +/- 5 mL vs 60 +/- 3 mL; p = 0.002). In controls, LV ejection fraction (EF) decreased after 3 months (27 +/- 1% vs 23 +/- 1%; p = 0.001) but was unchanged in CSD-treated dogs (25 +/- 1% vs 26 +/- 1%; p = 0.66). Compared to controls, CSD-treated dogs showed improved LV diastolic dysfunction and chamber sphericity, decreased wall stress, and no functional mitral regurgitation (MR). CONCLUSION: In dogs with advanced HF, acute LV reduction with the Acorn CSD prevents progressive global LV dilatation and ameliorates functional MR.

Passive epicardial containment prevents ventricular remodeling in heart failure.

BACKGROUND: We examined the effects of passive containment of the cardiac ventricles with a surgically placed epicardial prosthetic wrap on indexes of left ventricular (LV) remodeling in dogs with heart failure. METHODS: Heart failure (LV ejection fraction 30% to 40%) was produced in 12 dogs by intracoronary microembolization. Six dogs underwent mid-sternotomy and pericardiotomy with placement of a preformed-knitted polyester device (Acorn Cardiac Support Device [CSD], Acorn Cardiovascular, Inc, St. Paul, MN) snugly around the ventricles and anchored to the atrioventricular groove. Six dogs did not undergo surgery and served as controls. Dogs were followed for 3 months prior to sacrifice. RESULTS: In controls, LV end-diastolic volume increased after 3 months (67 +/- 12 versus 83 +/- 8 ml; p = 0.04), while in CSD-treated dogs, it decreased (68 +/- 10 versus 61 +/- 10 ml; p = 0.002). CSD-containment of LV size was associated with increased LV systolic fractional area of shortening, while in controls, fractional area of shortening decreased. CSD-treated dogs also showed amelioration of myocyte hypertrophy and attenuation of interstitial fibrosis compared to controls. CONCLUSIONS: In dogs with heart failure, passive epicardial containment of the ventricles with the Acorn CSD ameliorates LV remodeling and improves LV systolic function.