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Patricia J M Best

Publications and source records attributed to Patricia J M Best.

16 recordsLinked to original sources
PubMed2005

Incidence, retrieval methods, and outcomes of stent loss during percutaneous coronary intervention: a large single-center experience.

Our goal was to examine the incidence and consequences of stent loss during percutaneous coronary intervention (PCI) and the retrieval techniques used. We retrospectively reviewed 11,773 consecutive PCI cases involving stents performed at our institution between January 1994 and March 2004 to identify cases of stent loss. Stent loss occurred in 38 of 11,773 PCI procedures involving stents (0.32%; 95% CI = 0.23-0.44%). Mean age of the patients was 67 +/- 11 years and 82% were men. Stent loss occurred more frequently in lesions with calcification and/or significant proximal angulation. In three patients, the stent was crushed and covered with another stent without attempting retrieval. Stent retrieval was attempted in 35 of 38 cases and was successful in 30 (86%). The following retrieval methods were used (more than one method was used in some cases): advancing a balloon through the stent, inflating the balloon, and withdrawing the stent (45%); twirling two wires around the stent (5%); loop snare (26%); biliary forceps (12%); Cook retained fragment retriever (10%); and basket retrieval device (2%). Patients in whom stent loss occurred had a higher incidence of bleeding requiring transfusion (24% vs. 7%; P < 0.001) and more often required emergency coronary artery bypass surgery (5% vs. 0.4%; P < 0.001). No patients in whom the stent was crushed or deployed in the coronary artery had any major cardiac complication. Stent loss during PCI occurs infrequently. Lost stents can be successfully retrieved in the majority of cases using a variety of retrieval techniques, yet stent loss is associated with an increased risk of complications. Stent deployment or crushing may be a good alternative to retrieval.

Aged↗
PubMed2005

The relation of renal function to ischemic and bleeding outcomes with 2 different glycoprotein IIb/IIIa inhibitors: the do Tirofiban and ReoPro Give Similar Efficacy Outcome (TARGET) trial.

BACKGROUND: Renal function significantly impacts morbidity and mortality after a percutaneous coronary intervention. Platelet glycoprotein (GP) IIb/IIIa inhibitors reduce ischemic complications during percutaneous coronary intervention; little is known of whether their safety and efficacy are influenced by renal function. In particular, whether outcome differences exist between agents that are renally excreted (tirofiban) or not (abciximab) in patients with mild renal impairment is not known. METHODS: The TARGET trial randomized 4623 patients to tirofiban or abciximab. In this analysis, patients were grouped in creatinine clearance quartiles (<70, 70-90, 90-114, >114 mL/min) and analyzed for efficacy and bleeding risk. Univariate and multivariate analyses were performed to identify interactions between GP IIb/IIIa inhibitor used and creatinine clearance with respect to ischemic outcomes and bleeding. RESULTS: Using unadjusted logistic regression tests for trend, 30-day death/myocardial infarction/urgent target vessel revascularization was greater in patients with lower creatinine clearances (7.3%, 8.5%, 5.1%, and 5.8%, P = .005), as were both major and minor bleeding. There was no interaction between assigned GP IIb/IIIa inhibitor, creatinine clearance and ischemic outcome, major bleeding or minor bleeding. CONCLUSIONS: Both ischemic and bleeding complications are highest in the lowest creatinine clearance quartile of patients treated with GP IIb/IIIa inhibitors. Although tirofiban is renally cleared and abciximab is not, there was no interaction between these GP IIb/IIIa inhibitors and creatinine clearance regarding ischemic or bleeding events.

Abciximab↗
PubMed2004

Impact of mild or moderate chronic kidney disease on the frequency of restenosis: results from the PRESTO trial.

OBJECTIVES: The goal of this study was to determine if restenosis is increased in mild and moderate chronic kidney disease (CKD) patients after percutaneous coronary intervention (PCI). BACKGROUND: Mortality is increased in CKD after PCI. Restenosis may contribute to increased late mortality. METHODS: We analyzed 11,187 patients with a creatinine <1.8 mg/dl from the Prevention of REStenosis with Tranilast and its Outcomes (PRESTO) trial, grouped by estimated creatinine clearance (CrCl) (<60, 60 to 89, >89 ml/min). The Cox proportional hazards models investigated the association between CrCl group and death, myocardial infarction, and target vessel revascularization (TVR). Generalized estimating equation regression models determined the association between CrCl group and lesion-specific restenosis. RESULTS: At 30 days, there was no difference in myocardial infarction, death, or TVR between the CrCl groups. At nine months, mortality was higher in the lowest CrCl group (2.2%, 1.2%, 0.8%; p < 0.001), which was no longer significant after adjusting for confounding variables. Myocardial infarction and TVR were not different between the groups. In patients undergoing protocol follow-up angiography, restenosis (>/=50%) was not increased with CKD (32%, 32%, 37%; p = 0.02). CONCLUSIONS: Mortality nine months after PCI is mildly increased in mild or moderate CKD patients. However, restenosis is not and does not account for the increased mortality.

Aged↗
PubMed2004

Clopidogrel-associated autoimmune thrombocytopenic purpura.

We report the case of a 51-year-old male who underwent coronary stent placement for the treatment of an acute myocardial infarction. One week later, he developed symptomatic autoimmune thrombocytopenia likely related to clopidogrel use. This was successfully treated with intravenous methylprednisilone and platelet transfusions.

Clopidogrel↗
PubMed2004

Cardiovascular disease and chronic kidney disease: insights and an update.

Despite the high prevalence and significant morbidity and mortality rates of chronic kidney disease (CKD) related to cardiovascular disease, it remains vastly understudied. Most of the current practice recommendations come from small under-powered prospective studies, retrospective reviews, and assuming patients with CKD will similarly benefit from medications and treatments as patients with normal renal function. In addition, because of the previous lack of a consistent definition of CKD and how to measure renal function, definitions of the degree of renal dysfunction have varied widely and compounded the confusion of these data. Remarkably, despite patients with CKD representing the group at highest risk from cardiovascular complications, even greater than patients with diabetes mellitus, there has been a systematic exclusion of patients with CKD from therapeutic trials. This review outlines our current understanding of CKD as a cardiovascular risk factor, treatment options, and the future directions that are needed to treat cardiovascular disease in patients with CKD.

Cardiovascular Diseases↗
PubMed2003

Safety of abciximab in patients with chronic renal insufficiency who are undergoing percutaneous coronary interventions.

BACKGROUND: Patients with chronic renal insufficiency (CRI) have worse outcomes during and after percutaneous coronary interventions (PCI). Abciximab reduces complications, but may cause excessive bleeding in patients with CRI. Therefore, we sought to determine the safety of abciximab in patients with CRI. METHODS: Patients (n = 4158) undergoing PCI at the Mayo Clinic since abciximab became available were analyzed according to their estimated creatinine clearance (> or =70, 50-69, or <50 mL/min) or need for dialysis. Major bleeding was defined as a cerebrovascular bleed or a decrease in the hematocrit level >15%. Minor bleeding was defined as a decrease in the hematocrit level of 10% to 15% with an identifiable site of bleeding. RESULTS: CRI was associated with increased bleeding in patients who received abciximab and patients who did not. However, there was only a trend toward an interaction between creatinine clearance and major bleeding with abciximab (odds ratio [OR], 1.18; P =.06) and no interaction with minor bleeding (OR, 1.01; P =.94) or any bleeding (OR, 1.10; P =.15). CONCLUSION: CRI is associated with an increased risk of bleeding complications after PCI. Although abciximab increases the risk of bleeding in all patients, the increase in relative risk is not significantly greater in patients with CRI. Thus, abciximab may be given safely in patients with CRI who are undergoing PCI.

Abciximab↗
PubMed2003

Endothelin type A receptor antagonism restores myocardial perfusion response to adenosine in experimental hypercholesterolemia.

Experimental hypercholesterolemia is characterized by increased endothelin-1 (ET-1) activity and is associated with an attenuated myocardial perfusion response and an inappropriate increase in coronary microvascular permeability during episodes of increased myocardial demand. This study was designed to determine the effect of chronic selective ET type A (ET(A)) receptor antagonism on coronary vascular response to simulated cardiac stress in experimental hypercholesterolemia. Twenty-one pigs were randomized to three groups: normal diet (N), high-cholesterol diet (HC), and HC diet plus ABT-627, a selective ET(A) receptor antagonist, (HC+ABT-627). After 12 weeks, cardiac electron beam computed tomography (EBCT) was performed before and during intravenous infusion of adenosine, and myocardial perfusion (ml/min per g) and coronary microvascular permeability index (arbitrary units) were calculated. Basal myocardial perfusion was similar in all groups (N: 0.91+/-0.10; HC: 0.95+/-0.08; HC+ABT-627: 1.03+/-0.09; P=0.64). Adenosine infusion led to a significant increase in myocardial perfusion in the N (1.32+/-0.15; P<0.001) but not in the HC (0.95+/-0.07) group. However, in the HC+ABT-627 group, adenosine also significantly increased myocardial perfusion (1.33+/-0.12; P=0.001). Basal permeability index did not differ between the groups (N: 1.56+/-0.13; HC: 1.34+/-0.19; HC+ABT-627: 1.62+/-0.10; P=0.38). Adenosine infusion significantly increased permeability index in HC pigs (2.29+/-0.22; P<0.001) but not in N (1.71+/-0.21) and HC+ABT-627 (1.82+/-0.08) pigs. We conclude that chronic selective ET(A) receptor antagonism preserves myocardial perfusion response and coronary microvascular integrity during episodes of increased myocardial demand in experimental hypercholesterolemia, indicating an important role for the endogenous endothelin system in this disorder.

Adenosine↗
PubMed2002

Dendroaspis natriuretic peptide relaxes isolated human arteries and veins.

BACKGROUND: Dendroaspis natriuretic peptide (DNP) is the newest member of the natriuretic peptide family and is a circulating peptide in humans. The effects of DNP on the human vasculature are unknown. Since other natriuretic peptides are known to cause vasorelaxation, we determined the response to DNP on human blood vessels in vitro. We also investigated the mechanism of DNP mediated vasorelaxation. METHODS: Rings of human internal mammary artery and saphenous vein were suspended in an organ bath. The response to cumulative concentrations of DNP was obtained. Inhibiting agents were used to determine the mechanism of this vasorelaxation. RESULTS: DNP caused dose-dependent relaxation, with a greater effect on the internal mammary arteries (relaxation from 10(-7) mol/l DNP: 80.6+/-4.1%) than the saphenous veins (33.4+/-4.1%). At 10(-7) mol/l, DNP resulted in less arterial relaxation compared with atrial and C-type natriuretic peptides and similar relaxation to brain natriuretic peptide. In veins, DNP caused the greatest relaxation of the natriuretic peptides. DNP increased tissue cyclic guanosine monophosphate (cGMP) determined by radioimmunoassay by over 7-fold. Barium chloride and indomethacin attenuated DNP mediated vasorelaxation. However, glibenclamide, charydotoxin, apamin, tetraethyl-ammonium chloride and diisothiocyanato-stilbene-2,2'-disulfonic acid did not. DNP mediated vasorelaxation was mildly attenuated with removal of the endothelium. DNP immunoreactivity was identified in both arteries and veins. CONCLUSIONS: The current study demonstrates that DNP is an endogenous human natriuretic peptide that relaxes human arteries more than veins. Furthermore, DNP mediated vasorelaxation involves the inward rectifying potassium channels, prostaglandins, and cGMP. This newest member of the natriuretic peptide family may have an important physiologic role in the human vasculature.

Chloride Channels↗
PubMed2002

The impact of renal insufficiency on clinical outcomes in patients undergoing percutaneous coronary interventions.

OBJECTIVES: We sought to determine the effect of varying degrees of renal insufficiency on death and cardiac events during and after a percutaneous coronary intervention (PCI). BACKGROUND: Patients with end-stage renal disease have a high mortality from coronary artery disease. Little is known about the impact of mild and moderate renal insufficiency on clinical outcomes after PCI. METHODS: Cardiac mortality and all-cause mortality were determined for 5,327 patients undergoing PCI from January 1, 1994, to August 31, 1999, at the Mayo Clinic, based on the estimated creatinine clearance or whether the patient was on dialysis. RESULTS: In-hospital mortality was significantly associated with renal insufficiency (p = 0.001). Even after successful PCI, one-year mortality was 1.5% when the creatinine clearance was > or =70 ml/min (n = 2,558), 3.6% when it was 50 to 69 ml/min (n = 1,458), 7.8% when it was 30 to 49 ml/min (n = 828) and 18.3% when it was < 30 ml/min (n = 141). The 18.3% mortality rate for the group with < 30 ml/min creatinine clearance was similar to the 19.9% mortality rate in patients on dialysis (n = 46). The mortality risk was largely independent of all other factors. CONCLUSIONS: Renal insufficiency is a strong predictor of death and subsequent cardiac events in a dose-dependent fashion during and after PCI. Patients with renal insufficiency have more baseline cardiovascular risk factors, but renal insufficiency is associated with an increased risk of death and other adverse cardiovascular events, independent of all other measured variables.

Aged↗
PubMed2002

Nuclear factor-kappaB immunoreactivity is present in human coronary plaque and enhanced in patients with unstable angina pectoris.

BACKGROUND: Nuclear factor-kappaB (NF-kappaB) is a transcription factor which plays a coordinating role in inflammation and cellular proliferation and is thought to be involved in the pathogenesis of atherosclerosis. Its role in unstable coronary plaque in humans is unknown. METHODS AND RESULTS: Coronary atherectomy plaque was obtained via directional coronary atherectomy from 32 patients [16 with unstable angina pectoris (UAP) and 16 with stable angina pectoris (SAP)]. The predominant pathology in UAP consisted of richly cellular areas with atheromatous gruel or loose intimal proliferative tissue within a myxoid matrix (P<0.05 compared with SAP). By contrast, SAP plaques showed more dense fibrosis (P<0.01 compared with UAP). Sections were then stained with a monoclonal antibody to the activated p65 subunit of NF-kappaB and this staining was present in 31/32 specimens, localized to smooth muscle cells, macrophages and foam cells. Staining was then graded semiquantitatively by three independent observers. Immunostaining grades for activated NF-kappaB were significantly higher in UAP compared with SAP (2.60+/-0.1 vs. 1.98+/-0.18; P<0.01). CONCLUSIONS: NF-kappaB immunoreactivity is present in coronary atherosclerotic plaque and is increased among patients with unstable coronary syndromes. These data support a role for NF-kappaB in the pathogenesis of acute coronary syndromes in humans.

Adult↗
PubMed2002

Vascular responses in vivo to 8-epi PGF(2alpha) in normal and hypercholesterolemic pigs.

Hypercholesterolemia (HC) is characterized by increased circulating 8-epi-prostaglandin-F(2alpha) (isoprostane), a vasoconstrictor, marker, and mediator of increased oxidative stress, whose vascular effects might be augmented in HC. Anesthetized pigs were studied in vivo with electron beam computed tomography after a 12-wk normal (n = 8) or HC (n = 8) diet. Mean arterial pressure (MAP), single-kidney perfusion, and glomerular filtration rate (GFR) were quantified before and during unilateral intrarenal infusions of U46619 (10 ng x kg(-1) x min(-1)) or isoprostane (1 microg x kg(-1) x min(-1)). Basal renal perfusion and function were similar, and isoprostane infusion elevated its systemic levels similarly in normal and HC (333 +/- 89 vs. 366 +/- 48 pg/ml, respectively, P < 0.01 vs. baseline). Both drugs markedly and comparably decreased cortical perfusion and GFR in both groups, whereas medullary perfusion decreased significantly only in HC. Moreover, MAP increased significantly only in HC (+9 +/- 3 and +11 +/- 3 mmHg, respectively, P<or= 0.05). Hence, in HC, renal functional responses to high-dose isoprostane are largely similar to normal, but the systemic circulation exhibits augmented sensitivity to pathophysiological levels of isoprostane and U46619, which may potentially play a role in development of hypertension and vascular injury associated with increased oxidative stress.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗