Retrieval Of Balloon From Right Coronary Artery Surgically.

BACKGROUND: Angioplasty balloon entrapment remains an infrequent but dangerous obstacle that requires forbearance and pre-built management strategies in order to avoid morbidity or worse, mortality. Here, we discuss an un-expected hurdle of an undeflated stuck balloon with fractured shaft during angioplasty of proximal right coronary artery (RCA) in a 60-year-old male which was attempted percutaneously and redeemed surgically but massive infarction to RCA territory was inevitable.

Reversal of chronic molecular and cellular abnormalities due to heart failure by passive mechanical ventricular containment.

Passive mechanical containment of failing left ventricle (LV) with the Acorn Cardiac Support Device (CSD) was shown to prevent progressive LV dilation in dogs with heart failure (HF) and increase ejection fraction. To examine possible mechanisms for improved LV function with the CSD, we examined the effect of CSD therapy on the expression of cardiac stretch response proteins, myocyte hypertrophy, sarcoplasmic reticulum Ca2+-ATPase activity and uptake, and mRNA gene expression for myosin heavy chain (MHC) isoforms. HF was produced in 12 dogs by intracoronary microembolization. Six dogs were implanted with the CSD and 6 served as concurrent controls. LV tissue from 6 normal dogs was used for comparison. Compared with normal dogs, untreated HF dogs showed reduced cardiomyocyte contraction and relaxation, upregulation of stretch response proteins (p21ras, c-fos, and p38 alpha/beta mitogen-activated protein kinase), increased myocyte hypertrophy, reduced SERCA2a activity with unchanged affinity for calcium, reduced proportion of mRNA gene expression for alpha-MHC, and increased proportion of beta-MHC. Therapy with the CSD was associated with improved cardiomyocyte contraction and relaxation, downregulation of stretch response proteins, attenuation of cardiomyocyte hypertrophy, increased affinity of the pump for calcium, and restoration of alpha- and beta-MHC isoforms ratio. The results suggest that preventing LV dilation and stretch with the CSD promotes downregulation of stretch response proteins, attenuates myocyte hypertrophy and improves SR calcium cycling. These data offer possible mechanisms for improvement of LV function after CSD therapy.

Effects of the AT1-receptor antagonist eprosartan on the progression of left ventricular dysfunction in dogs with heart failure.

1. We examined the effects of eprosartan, an AT(1) receptor antagonist, on the progression of left ventricular (LV) dysfunction and remodelling in dogs with heart failure (HF) produced by intracoronary microembolizations (LV ejection fraction, EF 30 to 40%). 2. Dogs were randomized to 3 months of oral therapy with low-dose eprosartan (600 mg once daily, n=8), high-dose eprosartan (1200 mg once daily, n=8), or placebo (n=8). 3. In the placebo group, LV end-diastolic (EDV) and end-systolic (ESV) volumes increased after 3 months (68+/-7 vs 82+/-9 ml, P<0.004, 43+/-1 vs 58+/-7 ml, P<0.003, respectively), and EF decreased (37+/-1 vs 29+/-1%, P<0.001). In dogs treated with low-dose eprosartan, EF, EDV, and ESV remained unchanged over the course of therapy, whereas in dogs treated with high-dose eprosartan, EF increased (38+/-1 vs 42+/-1%, P<0.004) and ESV decreased (41+/-1 vs 37+/-1 ml, P<0.006), Eprosartan also decreased interstitial fibrosis and cardiomyocyte hypertrophy. 4. We conclude that eprosartan prevents progressive LV dysfunction and attenuates progressive LV remodelling in dogs with moderate HF and may be useful in treating patients with chronic HF.

Reverse remodeling and enhanced adrenergic reserve from passive external support in experimental dilated heart failure.

OBJECTIVES: We sought to test the efficacy of a passive elastic containment device to reverse chronic chamber remodeling and adrenergic down-regulation in the failing heart, yet still maintaining preload reserve. BACKGROUND: Progressive cardiac remodeling due to heart failure is thought to exacerbate underlying myocardial dysfunction. In a pressure-volume analysis, we tested the impact of limiting progressive cardiac dilation by an externally applied passive containment device on both basal and adrenergic-stimulated function in failing canine hearts. METHODS: Ischemic dilated cardiomyopathy was induced by repeated intracoronary microembolizations in six dogs. The animals were studied before and three to six months after surgical implantation of a thin polyester mesh (cardiac support device [CSD]) that surrounded both cardiac ventricles. Pressure-volume relations were measured by a conductance micromanometer catheter. RESULTS: Long-term use of the CSD lowered end-diastolic and end-systolic volumes by -19 +/- 4% and -22 +/- 8%, respectively (both p < 0.0001) and shifted the end-systolic pressure-volume relation to the left (p < 0.01), compatible with reverse remodeling. End-diastolic pressure and chamber diastolic stiffness did not significantly change. The systolic response to dobutamine markedly improved after CSD implantation (55 +/- 8% rise in ejection fraction after CSD vs. -10 +/- 8% before CSD, p < 0.05), in conjunction with a heightened adenylyl cyclase response to isoproterenol. There was no change in the density or affinity of beta-adrenergic receptors. Diastolic compliance was not adversely affected, and preload-recruitable function was preserved with the CSD, consistent with a lack of constriction. CONCLUSIONS: Reverse remodeling with reduced systolic wall stress and improved adrenergic signaling can be achieved by passive external support that does not generate diastolic constriction. This approach may prove useful in the treatment of chronic heart failure.

Hemostatic alterations associated with supraceliac aortic cross-clamping.

PURPOSE: The causative role of consumptive coagulopathy in the development of bleeding complications after supraceliac (SC) aortic cross-clamping (AXC) has been challenged by recent reports that ascribe this coagulopathy to primary fibrinolysis. This theory is made on the basis of evidence that tissue plasminogen activator (t-PA) antigen (Ag) levels increase after SC AXC. However, t-PA Ag levels reflect both active and inactive (bound to serum t-PA inhibitors) forms of serum t-PA, and elevations confirm the presence of fibrinolysis only in conjunction with an increase in t-PA activity. METHODS: To investigate the etiology of this coagulopathy, we submitted eight pigs to SC AXC and six pigs to infrarenal (IR) AXC for 30 minutes. Blood was drawn from the portal vein, the hepatic vein, and the carotid artery before AXC, just before unclamping, and 5, 30, and 60 minutes after unclamping. Prothrombin time (PT), partial thromboplastin time (PTT), fibrinogen (FBG), platelets (PLT), thrombin-antithrombin complexes (TAT), t-PA Ag, t-PA activity, plasminogen activator inhibitor-1 (PAI-1), and alpha2-antiplasmin (AP) activities were measured. Statistical analysis was performed by using repeated measures analysis of variance and t tests RESULTS: The PT did not differ between the two groups at any point. After unclamping, in the SC group there was a drop in PLT levels (P =.005), a decrease in FBG levels (P <.001), and a trend toward PTT prolongation (P =.06) compared with baseline. In contrast, there were no changes in PTT, PLT levels, or FBG levels in the IR group. TAT, a serum marker of thrombin generation, increased with SC AXC (P =.04), remained elevated 5 minutes after unclamping (P =.08), and returned to normal 30 minutes after unclamping. In contrast, TAT levels did not change in the IR control group. In the SC AXC group, the TAT levels did not differ between the three test sites at any time. SC AXC was associated with an increase in t-PA Ag just before unclamping (P <.001) and 5 minutes after unclamping (P =.002), but IR AXC was not. t-PA activity levels decreased in both experimental groups 30 and 60 minutes after unclamping. Levels of alpha2-AP activity decreased to a similar degree in both groups after unclamping when compared with baseline CONCLUSION: Thirty minutes of SC AXC results in intravascular thrombosis that cannot be localized to the ischemic visceral circulation. This intravascular thrombosis is associated with consumption of clotting factors. Thirty minutes of SC AXC causes an activation of fibrinolytic pathways that does not result in a hyperfibrinolytic state. An increase in t-PA Ag without a rise in t-PA activity does not represent true fibrinolysis, but rather an increase in the bound, inactive forms of serum t-PA. Both IR and SC AXC result in decreased fibrinolytic activity ("fibrinolytic shutdown") after release of the aortic clamp.

Effects of long-term monotherapy with metoprolol CR/XL on the progression of left ventricular dysfunction and remodeling in dogs with chronic heart failure.

We examined the effects of long-term monotherapy with the beta-blocker, metoprolol controlled release/extended release (CR/XL), on the progression of LV dysfunction as well as on global and cellular remodeling in dogs with heart failure (HF). Chronic HF was produced by intracoronary microembolizations that were discontinued when LV ejection fraction (EF) was between 30% and 40%. Dogs were randomized to 3 months oral monotherapy with metoprolol CR/XL (100 mg once daily, n = 7) or no therapy at all (control, n = 7). In control dogs, EF decreased from 38 +/- 1% to 31 +/- 2% (p = 0.002), and LV end-systolic volume (ESV) and LV end-diastolic volume (EDV) increased (37 +/- 2 vs 45 +/- 2 ml, p = 0.001; 59 +/- 3 vs 65 +/- 3 ml, p = 0.001; respectively) during the 3 month follow-up period. In dogs treated with metoprolol CR/XL, EF increased after 3 months from 36 +/- 1% to 43 +/- 1% (p = 0.001), and ESV decreased (42 +/- 2 vs 38 +/- 2 ml, p = 0.003), whereas EDV remained unchanged. Compared to controls, treatment with metoprolol CR/XL showed 46% reduction in replacement fibrosis, 54% reduction in interstitial fibrosis and 20% reduction in myocyte cross-sectional area, a measure of myocyte hypertrophy. These findings indicate that metoprolol CR/XL improves LV function and attenuates progressive global and cellular LV remodeling in dogs with HF. The benefits are fully attributable to beta-blockade alone as no other adjunctive therapy was used.