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Biomedical subjects

John A Ambrose

Publications and source records attributed to John A Ambrose.

At least 19 recordsLinked to original sources
PubMed2006

Impact of completeness of percutaneous coronary intervention revascularization on long-term outcomes in the stent era.

BACKGROUND: The importance of completeness of revascularization by percutaneous coronary intervention in patients with multivessel disease is unclear in that there is little information on the impact of incomplete revascularization outside of randomized trials. The objective of this study is to compare long-term mortality and subsequent revascularization for percutaneous coronary intervention patients receiving stents who were completely revascularized (CR) with those who were incompletely revascularized (IR). METHODS AND RESULTS: Patients from New York State's Percutaneous Coronary Interventions Reporting System were subdivided into patients who were CR and IR. Then subsets of IR patients were contrasted with CR patients. Differences in long-term survival and subsequent revascularization for CR and IR patients were compared after adjustment for differences in preprocedural risk. A total of 68.9% of all stent patients with multivessel disease who were studied were IR, and 30.1% of all patients had total occlusions and/or > or =2 IR vessels. At baseline, the following patients were at higher risk: those who were older and those with more comorbid conditions, worse ejection fraction, and more renal disease and stroke. After adjustment for these baseline differences, IR patients were significantly more likely to die at any time (adjusted hazard ratio=1.15; 95% confidence interval, 1.01 to 1.30) than CR patients. IR patients with total occlusions and a total of > or =2 IR vessels were at the highest risk compared with CR patients (hazard ratio=1.36; 95% confidence interval, 1.12 to 1.66). CONCLUSIONS: IR with stenting is associated with an adverse impact on long-term mortality, and consideration should be given to either achieving CR, opting for surgery, or monitoring percutaneous coronary intervention patients with IR more closely after discharge.

Adult↗
PubMed2006

A risk score to predict in-hospital mortality for percutaneous coronary interventions.

OBJECTIVES: Our purpose was to develop a risk score to predict in-hospital mortality for percutaneous coronary intervention (PCI) using a statewide population-based PCI registry. BACKGROUND: Risk scores predicting adverse outcomes after PCI have been developed from a single or a small group of hospitals, and their abilities to be generalized to other patient populations might be affected. METHODS: A logistic regression model was developed to predict in-hospital mortality for PCI using data from 46,090 procedures performed in 41 hospitals in the New York State Percutaneous Coronary Intervention Reporting System in 2002. A risk score was derived from this model and was validated using 2003 data from New York. RESULTS: The risk score included nine significant risk factors (age, gender, hemodynamic state, ejection fraction, pre-procedural myocardial infarction, peripheral arterial disease, congestive heart disease, renal failure, and left main disease) that were consistent with other reports. The point values for risk factors range from 1 to 9, and the total risk score ranges from 0 to 40. The observed and recalibrated predicted risks in 2003 were highly correlated for all PCI patients as well as for those in the higher-risk subgroup who suffered myocardial infarctions within 24 h before the procedure. The total risk score for mortality is strongly associated with complication rates and length of stay in the 2003 PCI data. CONCLUSIONS: The risk score accurately predicted in-hospital death for PCI procedures using future New York data. Its performance in other patient populations needs to be further studied.

Aged↗
PubMed2005

Early prognostic usefulness of C-reactive protein added to the Thrombolysis In Myocardial Infarction risk score in acute coronary syndromes.

The aim of the present study was to evaluate whether an elevated plasma C-reactive protein (CRP) level provides any additional prognostic information to the validated Thrombolysis In Myocardial Infarction (TIMI) risk score in patients with acute coronary syndromes. For this purpose, 1,846 consecutive patients with either acute ST-segment elevation myocardial infarction (STEMI; 861 patients) or non-ST-segment elevation acute coronary syndrome (NSTEACS; 985 patients) were included. The incidence of 30-day death and 14-day composite of death, myocardial infarction (or repeat myocardial infarction) and recurrent ischemia was the prespecified primary end point in the STEMI and NSTEACS cohorts, respectively. The incidence of the primary end point was 9.8% and 23.6% in the STEMI and NSTEACS cohorts, respectively. A significantly increased risk of the primary end point was present with an increase in the STEMI and NSTEACS TIMI risk score (p(trend) < 0.001 for the 2 groups). A plasma CRP value of > or = 5 and > or = 3 mg/L (defined by receiver-operating characteristic analysis) was associated with a significantly increased risk of the primary end point in the STEMI and NSTEACS cohorts, respectively (p < 0.001 for the 2 cohorts), and it was true throughout the subgroups of STEMI and NSTEACS TIMI risk scores. In conclusion, an elevated plasma CRP level appears to be a marker that adds prognostic information to the validated STEMI and NSTEACS TIMI risk score. The plasma CRP and TIMI risk score may be used together for enhanced risk stratification in the setting of acute coronary syndromes.

Aged↗
PubMed2005

Volume-outcome relationships for percutaneous coronary interventions in the stent era.

BACKGROUND: Most studies that are the basis of recommended volume thresholds for percutaneous coronary interventions (PCIs) predate the routine use of stent placement. METHODS AND RESULTS: Data from New York's Percutaneous Coronary Interventions Reporting System in 1998 to 2000 (n=107 713) were used to examine the impact of annual hospital volume and annual operator volume on in-hospital mortality, same-day coronary artery bypass graft (CABG) surgery, and same-stay CABG surgery after adjustment for differences in patients' severity of illness. For a hospital-volume threshold of 400, the odds ratios for low-volume hospitals versus high-volume hospitals were 1.98 (95% CI, 1.17, 3.35) for in-hospital mortality, 2.07 (95% CI, 1.36, 3.15) for same-day CABG surgery, and 1.51 (95% CI, 1.03, 2.21) for same-stay CABG surgery. For an operator-volume threshold of 75, the odds ratios for low-volume versus high-volume operators were 1.65 (95% CI, 1.05, 2.60) for same-day CABG surgery and 1.55 (95% CI, 1.10, 2.18) for same-stay CABG surgery. Operator volume was not significantly associated with mortality. Also, for hospital volumes below 400 and operator volumes below 75, the respective odds of mortality, same-day CABG surgery, and same-stay CABG surgery were 5.92, 4.02, and 3.92 times the odds for hospital volumes of 400 or higher and operator volumes of 75 or higher. CONCLUSIONS: Higher-volume operators and hospitals continue to experience lower risk-adjusted PCI outcome rates.

Angioplasty, Balloon, Coronary↗
PubMed2005

Classification of systemic therapies for potential stabilization of the vulnerable plaque to prevent acute myocardial infarction.

In this editorial, a classification of systemic therapies for potential plaque stabilization of vulnerable plaque to prevent acute myocardial infarction is proposed based on both biologic plausibility (a potential mechanism to explain the effect) and clinical evidence (i.e., whether the agent reduced acute myocardial infarction in well-designed clinical trials). All therapies possess biologic plausibility but are classified into groups I to IV based on clinical data.

Coronary Artery Disease↗
PubMed2005

Preprocedural plasma C-reactive protein levels, postprocedural creatine kinase-MB release, and long-term prognosis after successful coronary stenting (four-year results from the GENERATION study).

Increased creatine kinase-MB isoenzymes after coronary stenting are common, and many studies have suggested an association of this increase with an adverse long-term prognosis. How such postprocedural creatine kinase-MB release affects long-term prognosis remains unclear. Whether any actual causal relation exists remains unanswered.

Aged↗
PubMed2005

Proton pump inhibitors for patients with coronary artery disease associated with reduced chest pain, emergency department visits, and hospitalizations.

BACKGROUND: Patients with coronary artery disease (CAD) presenting to an emergency department (ED) with chest pain are likely to undergo hospitalization as clinicians attempt to elucidate the etiology. HYPOTHESIS: We hypothesized that proton pump inhibitor (PPI) therapy is associated with reduced chest pain events and evaluations in patients with CAD. METHODS: A patient population from a veterans medical center with documented CAD was identified retrospectively, and chest pain episodes, ED visits, and hospitalizations for chest pain were prospectively followed over 2 years. Comparison of patient outcomes between PPI (+PPI) and nonuse of PPI therapy (-PPI) was determined. RESULTS: Of 415 male patients, average age 73.4 years, 23% utilized a PPI and 77% did not. Proton pump inhibitor therapy was associated with reduced chest pain episodes (11.8 vs. 26.2%, p = 0.002), ED visits (12.3 vs. 24.3%, p = 0.044), and hospitalizations (12.8 vs. 23.9%, p = 0.086). Relative reductions were 55, 49, and 46%, respectively, after 2 years. Numbers of adverse events were also decreased in the +PPI group of patients: 70% fewer occurrences of chest pain (p = 0.002, relative risk [RR] = 3.3), 55% fewer ED visits (p = 0.049, RR = 2.2), and 53% fewer hospitalizations (p = 0.064, RR = 2.1). By multivariate analysis, PPI therapy independently predicted reduced prevalence of patients experiencing chest pain, ED visits, or hospitalizations (odds ratio [OR] = 0.09 [0.04-0.21]; 0.15 [0.06-0.40]; 0.14 [0.05-0.40]; all p < 0.001). CONCLUSIONS: Proton pump inhibitor therapy for male patients with CAD from a veterans medical center was associated with reduced prevalence of chest pain, ED visits, and hospitalizations for chest pain and reduced incidence of these events.

Aged↗
PubMed2005

Sirolimus- and taxol-eluting stents differ towards intimal hyperplasia and re-endothelialization.

Restenosis is a direct result of vessel injury, local inflammation, and remodeling following balloon angioplasty and coronary stenting resulting in luminal narrowing. The process involves a complex interplay of released growth factors that stimulate smooth muscle cells (SMCs) to migrate and proliferate, as well as activating endothelial cells (ECs) at injury sites. The latter re-establishes the luminal endothelial monolayer that keeps a barrier to circulating cells from underlying extracellular matrix and SMCs. Understanding the cellular mechanisms of intimal hyperplasia and re-endothelialization is important in that uncontrolled cellular processes account for coronary luminal narrowing, leading to the recurrence of clinical symptoms, hospitalizations, and repeat interventions. The evolution of drug-eluting stents that inhibit intimal hyperplasia has revolutionized percutaneous coronary interventions in that potential late luminal narrowing is attenuated. Sirolimus and paclitaxel are two medications utilized for their efficacy at inhibiting intimal hyperplasia and subsequent clinical events. The effects of these drugs on EC biology have not been well investigated. This article discusses basic cellular processes of vessel repair after balloon angioplasty and stenting, and focuses on the differential molecular mechanisms of sirolimus and paclitaxel towards proliferation and migration. These drugs inhibit both SMC and EC proliferation, but by different mechanisms, and paclitaxel inhibits EC migration, whereas sirolimus does not. Their discriminating effects towards re-endothelialization may clinically differentiate these two drugs. Inhibiting re-endothelialization may translate into more adverse clinical events.

Antineoplastic Agents, Phytogenic↗
PubMed2004

The pathophysiology of cigarette smoking and cardiovascular disease: an update.

Cigarette smoking (CS) continues to be a major health hazard, and it contributes significantly to cardiovascular morbidity and mortality. Cigarette smoking impacts all phases of atherosclerosis from endothelial dysfunction to acute clinical events, the latter being largely thrombotic. Both active and passive (environmental) cigarette smoke exposure predispose to cardiovascular events. Whether there is a distinct direct dose-dependent correlation between cigarette smoke exposure and risk is debatable, as some recent experimental clinical studies have shown a non-linear relation to cigarette smoke exposure. The exact toxic components of cigarette smoke and the mechanisms involved in CS-related cardiovascular dysfunction are largely unknown, but CS increases inflammation, thrombosis, and oxidation of low-density lipoprotein cholesterol. Recent experimental and clinical data support the hypothesis that cigarette smoke exposure increases oxidative stress as a potential mechanism for initiating cardiovascular dysfunction.

Arteriosclerosis↗
PubMed2004

Predictors of troponin elevation after percutaneous coronary intervention.

The predictors of troponin release after percutaneous coronary intervention were prospectively assessed in 405 consecutive patients. Troponin release occurred frequently (27%) and was associated with complications during the procedure, including sapheneous vein graft interventions, multistent use, glycoprotein IIb/IIIa use, and a history of hypercholesterolemia.

Angioplasty, Balloon, Coronary↗
PubMed2004

Value of low-dose dobutamine addition to routine dual isotope gated SPECT myocardial imaging in patients with healed myocardial infarction or abnormal wall thickening by echocardiogram.

There is overlap in myocardial viability detection by thallium-201 uptake and contractile reserve (CR) using low-dose dobutamine (LDD). The dual isotope protocol was modified in this study by acquiring thallium-201 images using LDD to enhance viability detection in addition to coronary flow reserve assessment. One hundred twenty-four patients with coronary disease underwent gated single-photon emission computed tomographic thallium-201 imaging at rest with LDD (10 microg/kg/min) during acquisition followed by stress technetium-99m sestamibi myocardial perfusion (MP) imaging with dobutamine, adenosine, or treadmill exercise. F-18-fluorodeoxyglucose (FDG) positron emission tomography was obtained in 41 patients. Myocardial perfusion (MP) imaging was divided into normal, fixed, and ischemic segments, and subclassified by wall motion and/or thickening changes between 1-hour poststress and LDD into normal, fixed, or improved dysfunctional segments (CR present). Mean left ventricular ejection fraction was 39% at 1 hour after stress and 47% with LDD (p <0.001). In dysfunctional myocardium, CR was significantly higher (p <0.001) in ischemic (233 of 368) and fixed segments (150 of 335) than in normal MP segments (43 of 220). Combined MP and CR analysis showed higher accuracy and negative predictive value in identifying FDG-viable myocardium than either method alone, whereas a high positive predictive value was maintained, similar to both markers. Quantitative analysis showed significant increased wall motion and thickening with LDD compared with 1 hour after stress, which was highest in ischemic segments and lowest in fixed segments. Thus, LDD dual isotope is a practical protocol that improves viability detection by simultaneous MP and CR analysis in addition to coronary flow reserve assessment in 1 study. Moreover, it requires no extra imaging time or radioactivity than the routine protocol.

Aged↗
PubMed2004

Luminal recovery from six to twelve months after implantation of "thicker strut" coronary stents.

A group of 50 patients with 51 de novo lesions treated with thicker strut stents (strut thickness >100 microm) was angiographically evaluated at baseline, after stenting, and at 6 and 12 months. Minimal luminal diameter (MLD) significantly increased from 6 to 12 months (6 months: 1.72 +/- 0.50 mm vs 12 months: 1.81 +/- 0.47 mm; p <0.01). The binary restenosis (diameter stenosis >50%) rate was 17% at 6 months and 11% at 12 months (p = NS). At multivariate analysis, lumen loss at 6 months (p = 0.018) and deployment pressure (p = 0.041) independently predicted the changes in MLD between 6 and 12 months.

Coronary Angiography↗
PubMed2003

Reactive oxygen species are involved in smoking-induced dysfunction of nitric oxide biosynthesis and upregulation of endothelial nitric oxide synthase: an in vitro demonstration in human coronary artery endothelial cells.

BACKGROUND: Our group has previously shown that human umbilical vein endothelial cells exposed to smokers' serum decreased nitric oxide (NO) production and endothelial nitric oxide synthase (eNOS) activity in the presence of increased eNOS expression. In the present study, we examined whether these observations extended to human coronary artery endothelial cells (HCAECs). In addition, the role of reactive oxygen species in the observed alterations was examined. METHODS AND RESULTS: HCAECs were incubated with serum from 10 nonsmokers and 15 smokers for 12 hours with or without the addition of either polyethylene glycol-superoxide dismutase (PEG-SOD, 300 U/mL), PEG-SOD+PEG-catalase (1000 U/mL), chelerythrine (3 micromol/L), or tetrahydrobiopterin (20 micromol/L). At the end of incubation, NO, eNOS protein, and eNOS activity were measured from the same culture. HCAECs incubated with smokers' serum alone showed significantly lower NO production (P<0.05) and eNOS activity (P<0.005) but higher eNOS expression (P<0.005) compared with nonsmokers. In smokers, addition of PEG-SOD, PEG-SOD+PEG-catalase, or tetrahydrobiopterin significantly (P<0.05) improved NO levels and eNOS activity. Interestingly, in the same smokers, a significant decrease in eNOS expression was only seen with the addition of PEG-SOD+PEG-catalase (P<0.05) and treatment with PEG-SOD alone insignificantly increased eNOS expression. CONCLUSIONS: The present study indicates that in vitro, HCAECs show similar changes in NO biosynthesis as human umbilical vein endothelial cells when exposed to smokers' serum and also confirms that oxidative stress plays a central role in smoking-mediated dysfunction of NO biosynthesis in endothelial cells. Furthermore, these data support other studies suggesting a role for hydrogen peroxide in the upregulation of eNOS.

Adult↗