"The year of the Carotid": what I've learned (so far...).
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Blood Vessel Prosthesis Implantation↗
Biomedical subjects
Barry F Uretsky
Publications and source records attributed to Barry F Uretsky.
The 2005 National Meeting at Ponte Vedra: a great meeting and a very good sign for the future.
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Cardiac Surgical Procedures↗
Society planning and consensus-building in 2005: where have we been? Where should we go next?
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Consensus↗
Left main coronary artery thrombus: a case series with different outcomes.
Left main coronary artery (LMCA) thrombosis with acute myocardial infarction is an uncommon condition with an extremely high mortality. The small number of reported cases prevents the development of an evidence-based approach. Hence there are no clear-cut guidelines describing the best management approach for this condition. We describe our experience with six patients who presented with LMCA thrombosis and discuss the epidemiology, etiology and management options available for this high-risk subgroup.
Aged↗
Early post-thrombolysis catheterisation may be preferable to a conservative strategy for people with ST-elevation myocardial infarction. Commentary 1.
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Comment↗
Gadodiamide-based coronary angiography in a patient with severe renal insufficiency.
The risk of contrast-induced nephropathy (CIN) is extremely high in patients with preexisting renal insufficiency. Gadolinium-based coronary angiography has been proposed as an approach to prevent CIN in this high risk subgroup. We report the use of gadodiamide-based coronary angiography in a patient with severe renal insufficiency and in vitro comparisons of combinations of iodinated contrast with gadodiamide and saline.
Contrast Media↗
Administration of vascular endothelial growth factor adjunctive to fetal cardiomyocyte transplantation and improvement of cardiac function in the rat model.
BACKGROUND: The functional impact of cellular transplantation and the potential role of the addition of angiogenic factors for survival of engrafts remain controversial. METHODS: Vascular endothelial growth factor (VEGF) (25 ng/mL) was added to cultured fetal cardiomyocytes labeled with bromodeoxyuridine (BrDU), which was injected into the border zones of myocardial infarction 4 weeks after coronary occlusion in rat hearts. Group 1 (n = 12) received cells plus VEGF protein (100 ng), group 2 (n = 12) received cells without VEGF, group 3 (n = 10) received VEGF without cells, and group 4 (n = 12) received pure culture medium. Cardiac function was then assessed by transthoracic two-dimensional echocardiography and Langendorff perfusion system. In situ hybridization for Y chromosomes of transplanted cells, detection of BrDU-labeled cells, and platelet/endothelial cell adhesion molecule-1 (PECAM-1) staining for endothelial cells was performed. RESULTS: Echocardiography revealed smaller end-diastolic left ventricular dimensions in transplanted hearts in group 1 (0.83 +/- 0.13 cm 4 weeks after coronary occlusion before transplantation and 0.69 +/- 0.14 cm 2 months after transplantation, P < .05) and in group 2 (0.88 +/- 0.09 cm after coronary occlusion before transplantation and 0.76 +/- 0.08 cm 2 months after transplant), and increases in fractional shortening (34.2% +/- 8.53% before transplant and 45.3% +/- 10.9% after [P < .05] in group 1; 26.9% +/- 6.02% before transplant and 37.15% +/-8.08% after [P < .005] in group 2), whereas groups 3 and 4 showed a decrease in fractional shortening. Transplanted hearts developed higher pressures at rest (group 1, 96.8 +/- 20.8 mm Hg; group 2, 98.6 +/- 21.9 mm Hg) compared with controls (group 4, 70.9 +/- 25 mm Hg) (P < .05) and during inotropic stimulation (group 1, 111 +/- 19.5 mm Hg and group 2, 113.3 +/- 32.6 vs group 4, 80.7 +/- 31.6 mm Hg, P < .05). Histologic analysis demonstrated the presence of transplanted cells in border zones of infarcted host myocardium with neovascularization in all transplanted hearts. CONCLUSION: Transplantation of fetal cardiomyocytes results in improvement of left ventricular function. The addition of VEGF does not contribute to further improvement of left ventricular function and angiogenesis in the present model.
Animals↗
Carvedilol improves myocardial contractility compared with metoprolol in patients with chronic hibernating myocardium after revascularization.
BACKGROUND: We tested the hypothesis of whether carvedilol delays morphologic degeneration and improves functional outcome compared with metoprolol tartrate in patients with hibernating myocardium undergoing surgical revascularization. We have previously shown that patients with chronic hibernating myocardium undergo progressive cellular degeneration and fibrosis. METHODS: Twenty patients with multivessel coronary artery disease revascularization and hibernating myocardium as assessed by technetium-99m perfusion scintigraphy and fluorine-18-fluorodeoxyglucose positron emission tomography were randomized to receive either carvedilol or metoprolol tartrate for at least 2 months before surgery, and this was continued for 7 months postoperatively. Left ventricular ejection fraction and regional wall motion abnormalities were assessed by left ventriculography at baseline and 7 months postoperatively. Intraoperative transmural needle biopsy samples were obtained for microscopic analysis. RESULTS: Postoperatively, the ejection fraction increased from 31% +/- 5% to 44% +/- 4% (P < .005) in the carvedilol group (n = 10), and from 30% +/- 6% to 40% +/- 6% in the metoprolol tartrate group (P < .05 vs preoperatively and vs carvedilol). Wall motion abnormalities in the carvedilol group improved from -2.1 +/- 0.4 to -0.6 +/- 0.5 (P < .05) and from -2.3 +/- 0.5 to -1.6 +/- 0.6 in the metoprolol tartrate group (P < .05 vs preoperatively and vs carvedilol). Microscopic analysis after 72 +/- 18 days of either treatment showed mild cardiomyocyte degeneration and moderate-to-severe fibrosis (28% +/- 7%) in the carvedilol group compared with moderate cardiomyocyte degeneration and moderate-to-severe fibrosis (33% +/- 6%) in the metoprolol tartrate group. Apoptosis, as assessed by the terminal deoxynucleotidyl transferase nick end labeling method, was observed in only 1 patient in each group. CONCLUSIONS: Carvedilol treatment of hibernating myocardium results in improved functional recovery after revascularization compared with metoprolol tartrate, and this might partially be related to reduced cardiomyocyte degeneration.
Adrenergic beta-Antagonists↗
The renal patient with coronary artery disease: current concepts and dilemmas.
The patient with chronic kidney disease and coronary artery disease (CAD) presents special challenges. This report reviews the scope of the challenge, the hostile internal milieu predisposing to CAD and cardiac events, management issues, unresolved dilemmas, and the need for randomized trials to allow for evidence-based treatment.
Angioplasty, Balloon, Coronary↗
Acute coronary syndrome induced by intravenous ephedrine in pregnant woman with normal coronaries.
Intravenous ephedrine administered during a C-section was observed to cause an acute coronary syndrome in a pregnant woman with normal coronaries. The patient developed sub-sternal chest pain, was noted to have 10 beats of non-sustained ventricular tachycardia, ST abnormalities were observed on her ECG and cardiac enzymes were elevated. The patient had normal coronary arteries by angiogram and during a one-year period of follow up no further cardiac events occurred.
Acute Disease↗
Covered stent septal ablation for hypertrophic obstruction cardiomyopathy.
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Cardiomyopathy, Hypertrophic↗
Effect of rosiglitazone on restenosis after coronary stenting in patients with type 2 diabetes.
BACKGROUND: Thiazolidinediones have been shown to have an antiproliferative vascular effect in experimental models. We sought to study the effect of rosiglitazone on in-stent restenosis in patients with established type 2 diabetes. METHODS: Patients with treated type 2 diabetes (mean duration 5.5 +/- 7.5 years) referred for coronary stenting were randomized in a double-blind fashion to receive oral rosiglitazone or placebo for 6 months. Quantitative coronary angiography and intravascular ultrasound data were obtained at baseline and follow-up. Plasma plasminogen activator inhibitor-1 levels were prospectively measured. RESULTS: Sixteen patients were enrolled. There were no significant differences in follow-up in-stent luminal diameter stenosis measured by quantitative coronary angiography or in-stent luminal area stenosis and neointimal volume index obtained by intravascular ultrasound, nor were there any differences in plasma plasminogen activator inhibitor-1 levels after long-term use despite improvement in diabetes control and insulin sensitivity. CONCLUSIONS: Rosiglitazone, given at the time of stent implantation in treated diabetics, did not reduce in-stent restenosis in this small series. The vascular biological effects of this agent await further clarification in humans and evaluation in larger clinical trials.
Administration, Oral↗
A novel minimal-invasive model of chronic myocardial infarction in swine.
BACKGROUND: Most animal studies on myocardial infarction (MI) have used open-chest models with direct surgical coronary artery ligation, which imply local as well as generalized side effects of major surgery. Some closed-chest models of MI have been established, mainly using catheterization techniques with coronary artery embolization, balloon occlusion, and intracoronary injection of thrombogenic agents. The aim of this study was to develop a closed-chest technique of chronic coronary artery occlusion at a selected location with subsequent thrombus formation without use of balloon inflation or thrombotic chemical agents. METHODS AND RESULTS: A coronary angiography via the carotid artery was performed using a 7 F guiding catheter in 21 pigs. After insertion of a percutaneous transluminal coronary angioplasty (PTCA) guide wire into the distal coronary artery, a vessel-size adapted flexible foreign body comprising an open-cell sponge was advanced into the coronary artery via the guide wire by a non-inflated PTCA balloon. Five min after removal of the guide wire and the balloon catheter, total coronary artery occlusion was documented by angiography. Retrograde thrombosis of the coronary artery occurred in three animals. After one week, total vessel occlusion at the previously selected location was visualized by coronary angiography in animals that had survived. Macroscopic analysis demonstrated the foreign body with subsequent thrombus formation in the coronary artery and distal MI. Post-mortem histological analysis revealed myocardial necrosis and granulocyte infiltration at the margin of the infarction, without damage to remote myocardium. CONCLUSIONS: This new easy-to-perform closed-chest technique provides reproducible chronic coronary artery occlusion at a selected location with subsequent MI. It avoids major surgery and thoracotomy and does not require balloon inflation or intracoronary injection of thrombotic or chemical agents.
Animals↗
Simvastatin-induced myocardial protection against ischemia-reperfusion injury is mediated by activation of ATP-sensitive K+ channels.
OBJECTIVES: Previous studies have suggested that the 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors attenuate ischemia-reperfusion injury. We investigated whether pretreatment with simvastatin reduces myocardial infarct size and whether glyburide, a non-selective inhibitor of the ATP-sensitive K channels, abrogates this infarct size-limiting effect. METHODS: Sprague-Dawley rats were treated with either simvastatin (20 mg/kg per day) or saline alone for 3 days. Additional groups of rats were treated as above and on the fourth day they received intravenous glyburide (0.3 mg/kg). All rats underwent 30 min of coronary artery occlusion followed by 180 min of reperfusion. Ischemic myocardium at risk was assessed with blue dye and infarct size with triphenyltetrazolium chloride. RESULTS: Infarct size, expressed as a percentage of the myocardium at risk, was significantly smaller in the simvastatin group (n = 8, 20.8 +/- 3.4%) than in the placebo group (n = 6, 40.1 +/- 2.7%) (P = 0.001). Glyburide abolished the protective effect of simvastatin with infarct size being 34.2 +/- 6.9% and 29.7 +/- 3.9% of the area at risk in the simvastatin group (n = 7) and placebo (n = 7) group, respectively (P = 0.58). CONCLUSIONS: Simvastatin significantly reduced myocardial infarct size. The protective effect was completely abrogated by glyburide, strongly suggesting that this protective effect is mediated via activation of the ATP-sensitive K channels.
ATP-Binding Cassette Transporters↗
Monocyte chemoattractant protein 1-induced monocyte infiltration produces angiogenesis but not arteriogenesis in chronically infarcted myocardium.
BACKGROUND: Monocyte chemoattractant protein 1 (MCP-1) stimulates the invasion of monocytes into ischemic tissue with concomitant adhesion to endothelial cells. Monocyte stimulation has been shown to be involved in the induction of arteriogenesis, which is the development of functional arterioles resulting in improvement of perfusion. However, angiogenesis (newly developed capillaries contribute to improved tissue perfusion) in several models has not resulted in any improvement in blood flow. OBJECTIVE: The effects of MCP-1 on potential angiogenesis and arteriogenesis as well as changes in left ventricular function were tested in a chronic infarct model in rat hearts. METHODS: Anesthetized rats were subjected to open-chest ligation of the left coronary artery with subsequent myocardial infarction. After 6 weeks, animals were randomized to receive either MCP-1 (3 microL in 0.15 mL NaCl, group 1, n = 9) or saline (0.15 mL, group 2, n = 9), which was injected into the myocardium at the border zones of the infarcts. For assessment of left ventricular dimensions and global cardiac function, transthoracic two-dimensional echocardiography was performed at baseline, 6 weeks after myocardial infarction, and 4 weeks after MCP-1 or saline injection, by use of a 12-MHz pediatric transducer. For light microscopic analysis, myocardial tissue was stained with Elastica-van-Giesson and von Willebrand factor for blood vessels and endothelial cells, respectively. In a subset of animals, hearts were excised 24 hours after MCP-1 administration (n = 4) or saline administration (n = 4) for assessment of monocyte infiltration by immunohistologic staining of the CD31 antigen. RESULTS: Left ventricular dimensions and ejection fraction changed after coronary occlusion (from 60.4% +/- 2.85% to 24.8% +/- 5.01% ejection fraction in group 1, and from 58.4% +/-2.06% to 26.3% +/- 4.3% ejection fraction in group 2 at 6 weeks, P < .005) without any further change 4 weeks after treatment (ejection fraction in group 1, 26.3% +/- 2.7%, ejection fraction in group 2, 25.0% +/- 5.18%). The MCP-1 group resulted in 390.6 +/- 10.36 endothelial cells compared with 285.2 +/- 13.56 in group 2 (P < .005) at the injection site. Monocyte infiltration was observed at the MCP-1 injection site with an increase in capillary growth (angiogenesis). However, there was no difference in the number of arteriolar structures between animals treated with MCP-1 and saline animals (group 1, 19.0 +/- 1.52 vs group 2, 16.4 +/- 0.68, P > .05). CONCLUSION: A single intramyocardial injection of MCP-1 into the infarct border zone resulted in neo-angiogenesis and monocyte infiltration but not arteriogenesis in the rat heart. There was no functional change of chronically infarcted myocardium in the present model.
Animals↗
Distal myocardial protection during percutaneous coronary intervention with an intracoronary beta-blocker.
BACKGROUND: Experimental studies have demonstrated that intravenous beta-blocker administration before coronary artery occlusion significantly reduces myocardial injury. Clinical studies have shown that intracoronary (IC) propranolol administration before percutaneous coronary intervention (PCI) delays myocardial ischemia. The present study tested the hypothesis that IC propranolol treatment protects ischemic myocardium from myocardial damage and reduces the incidence of myocardial infarction (MI) and short-term adverse outcomes after PCI. METHODS AND RESULTS: Patients undergoing PCI (n=150) were randomly assigned in a double-blind fashion to receive IC propranolol (n=75) or placebo (n=75). Study drug was delivered before first balloon inflation via an intracoronary catheter with the tip distal to the coronary lesion. Biochemical markers were evaluated through the first 24 hours and clinical outcomes to 30 days. Evidence of MI with creatine kinase-MB elevation after PCI was seen in 36% of placebo and 17% of propranolol patients (P=0.01). Troponin T elevation was seen in 33% of placebo and 13% of propranolol patients (P=0.005). At 30 days, the composite end point of death, postprocedural MI, non-Q-wave MI after PCI hospitalization, or urgent target-lesion revascularization occurred in 40% of placebo versus 18% of propranolol patients (hazard ratio 2.14, 95% CI 1.24 to 3.71, P=0.004). CONCLUSIONS: IC administration of propranolol protects the myocardium during PCI, significantly reducing the incidence of MI and improving short-term clinical outcomes.
Adrenergic beta-Antagonists↗
Reduction of infarct size by short-term pretreatment with atorvastatin.
Previous studies have suggested that the 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors attenuate ischemia-reperfusion injury by increasing the activity of endothelial nitric oxide synthase (eNOS). We assessed whether short-term treatment with atorvastatin reduces myocardial infarct size in the rat. Rats (male Sprague-Dawley) received atorvastatin 2 mg/kg per day (n = 9), 10 mg/kg per day (n = 8), or 75 mg/kg per day (n = 11), or placebo (n = 11) by gastric gavage for 3 days. Two additional groups received atorvastatin 10 mg/kg (n = 7) or placebo (n = 7) for 3 days and the nonselective nitric oxide synthase inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME), 15 mg/kg intravenously 15 min before surgery. All rats underwent 30 min of coronary artery occlusion followed by 180 min of reperfusion. Ischemic myocardium at risk was assessed with blue dye and infarct size by triphenyltetrazolium chloride. Ischemic myocardium at risk was comparable among groups. Infarct size, expressed as a percentage of the myocardium at risk, was significantly smaller in the atorvastatin 75 mg/kg group (22.6 +/- 2.8%; p = 0.035 vs. placebo) and atorvastatin 10 mg/kg (20.3 +/- 3.8%; p = 0.022 vs. placebo) compared with placebo (37.5 +/- 4.3%). The effect of atorvastatin 2 mg/kg was of smaller magnitude and did not reach statistical significance (infarct size 30.6 +/- 4.2% of the myocardium at risk). L-NAME abolished the protective effect of atorvastatin 10 mg/kg per day. Infarct size was 43.0 +/- 4.1% in the atorvastatin group and 39.4 +/- 3.3% in the placebo group (p = 0.503). In conclusion, short-term (3 days) atorvastatin (10-75 mg/kg/d) significantly reduced myocardial infarct size. The protective effect was completely abolished by L-NAME, strongly suggesting that this protective effect is mediated via the nitric oxide synthase pathway.
Animals↗
Ventricular free wall rupture following acute myocardial infarction.
SUMMARY: Ventricular free wall rupture remains a dreaded complication of acute myocardial infarction. A dramatic fatal presentation is not universal and if recognized early, especially in its sub-acute form, a therapeutic intervention may be lifesaving. Changing trends in its natural history and the previously described pathological subtypes have emerged since the advent of thrombolysis. Although frequently unpredictable, certain clinical, echocardiographic and electrocardiographic signs should suggest the diagnosis. Moreover, knowledge of predisposing risk factors and a high index of suspicion are helpful in early recognition of this complication. In recent years, several different therapeutic approaches have been described including percutaneous seals and surgical mechanical closure of ventricular free wall rupture. In this review, we sought to highlight established and debatable aspects of this pathology to hopefully enhance prompt diagnosis and treatment by all clinicians caring for patients suffering acute myocardial infarction.
Aneurysm, False↗