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Biomedical subjects

Deepak L Bhatt

Publications and source records attributed to Deepak L Bhatt.

At least 37 records · Page 2Linked to original sources
PubMed2006

Bare metal stent restenosis is not a benign clinical entity.

BACKGROUND: Restenosis after percutaneous coronary intervention (PCI) has been thought to present in a stable manner as exertional angina. However, the presentation of in-stent restenosis (ISR) is not well-studied. We hypothesized that a substantial proportion of bare metal ISR presents as acute coronary syndromes. We aimed to characterize the severity of the clinical presentation of ISR. METHODS: We searched our PCI database for all cases of PCI for bare metal ISR occurring between May 1999 and September 2003. Multivessel interventions were excluded. In-stent restenosis presentation was classified into three categories: (1) myocardial infarction (MI), (2) unstable angina requiring hospitalization before angiography, and (3) exertional angina. Routine angiographic screening after initial stent placement was not performed, so ISR episodes were clinical, rather than angiographic, ISR. RESULTS: We identified 1186 cases of bare metal ISR in 984 patients. Median age was 63, 72% were male, and 36% had diabetes. Of the ISR episodes, 9.5% presented as acute MI (7.3% as non-ST-segment elevation MI and 2.2% as ST-segment elevation MI), 26.4% as unstable angina requiring hospitalization before angiography, and 64.1% as exertional angina. CONCLUSIONS: More than one third of bare metal ISR episodes presented as MI or unstable angina requiring hospitalization. The acuity of the clinical presentation of bare metal ISR appears to be more severe than has been previously thought. Aggressive efforts, such as drug-eluting stents to decrease the incidence of unstable angina due to bare metal ISR, are warranted.

Acute Disease↗
PubMed2006

The REduction of Atherothrombosis for Continued Health (REACH) Registry: an international, prospective, observational investigation in subjects at risk for atherothrombotic events-study design.

BACKGROUND: The risk of atherothrombosis is a large health care burden worldwide. With its global prevalence, there is a need to understand all the associated risk factors, both old and new, and their interdependencies in the development of this complex disease leading to myocardial infarction, ischemic stroke, and vascular death and, thus, the major cause of mortality throughout the world. METHODS: The REACH Registry sought to compile an international data set to extend our knowledge of atherothrombotic risk factors and ischemic events in the outpatient setting. The Registry will recruit approximately 68,000 outpatients in 44 countries across 6 major regions (Latin America, North America, Europe, Asia, the Middle East, and Australia) from >5000 physician outpatient practices. Patients aged > or =45 years with at least 3 atherothrombotic risk factors or documented cerebrovascular, coronary artery, or peripheral arterial disease will be enrolled. Medical history, risk factors, demographic information, and management will be collected at baseline, and clinical events that occur during the follow-up period of up to 2 years in duration will be recorded. CONCLUSION: The REACH Registry offers an opportunity to provide a better understanding of the prevalence and clinical consequences of atherothrombosis in the outpatient setting in a wide range of patients from different parts of the world.

Comorbidity↗
PubMed2006

Lack of effect of enteric coating on aspirin-induced inhibition of platelet aggregation in healthy volunteers.

BACKGROUND: Aspirin inhibits platelet aggregation and is widely used in the treatment of cardiovascular disease. Some individuals are less responsive to aspirin's antiplatelet effect, a phenomenon termed aspirin resistance. It is not known whether the antiplatelet effect is fully preserved with the enteric-coated (EC) formulation. METHODS: We performed a prospective randomized trial of 50 healthy volunteers using a crossover design to compare the EC with the standard aspirin formulations. The subjects received a 7-day course of each aspirin formulation (81-mg) (Bayer Corporation, Morristown, NJ) separated by a 3-week washout period. Platelet function was measured before and after each course using optical aggregometry (with arachidonic acid and adenosine diphosphate as agonists) and a point-of-care platelet assay. RESULTS: The assays were reproducible, and the variation in baseline platelet function was small to moderate between the subjects. There was no difference in the extent of platelet inhibition between the EC and standard formulations with any of the 3 assays. With the point-of-care platelet assay, the mean aspirin effect favoring the standard formulation (more aggregation inhibition) compared with the EC formulation was 1.6% +/- 15.8% (P = .60 for difference between the formulations). The corresponding optical aggregometry values were -3.4% +/- 39.5% (P = .97) and -1.4% +/- 16.6% (P = .75) for arachidonic acid and adenosine diphosphate, respectively. CONCLUSIONS: Compared with standard aspirin, EC aspirin appears to exhibit similar inhibition of platelet aggregation in healthy volunteers. Furthermore, point-of-care platelet assessment correlated well with the gold standard of laboratory-based optical platelet aggregometry.

Adult↗
PubMed2006

Prevalence, predictors, and outcomes of patients with non-ST-segment elevation myocardial infarction and insignificant coronary artery disease: results from the Can Rapid risk stratification of Unstable angina patients Suppress ADverse outcomes with Early implementation of the ACC/AHA Guidelines (CRUSADE) initiative.

BACKGROUND: Unlike ST-segment elevation myocardial infarction, the degree of stenosis and physiology of ischemia varies in patients with non-ST-segment elevation myocardial infarction (NSTEMI). The prevalence, predictors, and outcomes of patients with NSTEMI who lack significant epicardial coronary artery disease (CAD) in routine clinical practice remain poorly characterized. We sought to determine the prevalence, predictors, and outcomes of patients with NSTEMI and insignificant CAD. METHODS: We analyzed 38301 patients with NSTEMI in the CRUSADE quality improvement initiative who underwent cardiac catheterization to determine the prevalence and factors associated with insignificant CAD (all coronary stenoses <50%) and inhospital outcomes for patients with and without CAD. A multivariable model was used to determine the factors associated with insignificant CAD. RESULTS: A total of 3306 (8.6%) of 38301 patients had insignificant CAD. The strongest multivariable predictors of insignificant CAD were female sex (odds ratio 2.8, 95% CI 2.6-3.1), younger age (odds ratio per 10-year decrease 1.5, 95% CI 1.5-1.6), and lack of current/recent smoking (odds ratio 1.9, 95% CI 1.7-2.0). Inhospital rates of death were 0.65% for patients with insignificant CAD compared with 2.36% for patients with CAD (P < .0001). CONCLUSION: Insignificant CAD is present in 9% of patients with NSTEMI and is associated with a low incidence of adverse outcomes. The strongest predictors of insignificant CAD are female sex and younger age. These findings underscore the need for research to understand the pathophysiology of myocardial infarction in this population.

Acute Disease↗
PubMed2006

Paradoxical rebound platelet activation after painkillers cessation: missing risk for vascular events?

BACKGROUND: Several reliable reports strongly indicate that the use of nonsteroidal anti-inflammatory drugs (NSAIDs) and cyclooxygenase-2 (COX-2) inhibitors is associated with an increased risk of cardiovascular events. Considering the key role of platelets in coronary atherosclerosis and the fact that antiplatelet therapy with aspirin (and more recently, clopidogrel) has been associated with reduced vascular mortality, we sought to determine the effect of therapy and withdrawal of NSAIDs and COX-2 inhibitors on platelet activity. METHODS: Platelet characteristics from 34 aspirin-naive volunteers who were receiving NSAIDs and COX-2 inhibitors were compared with 138 drug-free controls. Platelets were assessed twice at baseline (at least 1 month of NSAIDs and COX-2 inhibitors) and after a 14-day washout. We used adenosine diphosphate-induced conventional aggregometry, the point-of-care Ultegra analyzer (Ultegra Accumetrics, San Diego, Calif), and whole blood flow cytometry. RESULTS: Platelet activity during therapy with NSAIDs and COX-2 inhibitors was similar and unremarkable between groups. However, there was a highly significant increase of platelet activity as assessed by conventional aggregometry (P=.0003), Ultegra analyzer readings (P=.03), and expression of GPIIb/IIIa (P=.02), P-selectin (P=.03), and platelet endothelial cell adhesion molecule-1 (P=.001) after withdrawal from NSAIDs and COX-2 inhibitors. CONCLUSIONS: These data suggest that drug cessation, rather than continuous therapy with NSAIDs and COX-2 inhibitors, may be associated with rebound platelet activation, which may predispose one to a higher risk of vascular events. This hypothesis requires intensive testing in crossover randomized studies and may justify more aggressive antiplatelet regimens in patients after discontinuation of therapy with NSAIDs and COX-2 inhibitors.

Adult↗
PubMed2006

Late thrombosis of drug-eluting stents: a meta-analysis of randomized clinical trials.

PURPOSE: Drug-eluting stents are commonly used for percutaneous coronary intervention. Despite excellent clinical efficacy, the association between drug-eluting stents and the risk for late thrombosis remains imprecisely defined. METHODS: We performed a meta-analysis on 14 contemporary clinical trials that randomized 6675 patients to drug-eluting stents (paclitaxel or sirolimus) compared with bare metal stents. Eight of these trials have reported more than a year of clinical follow-up. RESULTS: The incidence of very late thrombosis (>1 year after the index procedure) was 5.0 events per 1000 drug-eluting stent patients, with no events in bare metal stent patients (risk ratio [RR]=5.02, 95% confidence interval [CI], 1.29 to 19.52, P=.02). Among sirolimus trials, the incidence of very late thrombosis was 3.6 events per 1000 sirolimus stent patients, with no events in bare metal stent patients (RR=3.99, 95% CI, .45 to 35.62, P=.22). The median time of late sirolimus stent thrombosis was 15.5 months, whereas with bare metal stents it was 4 months. Among paclitaxel trials, the incidence of very late thrombosis was 5.9 events per 1000 paclitaxel stent patients, with no events in bare metal stent patients (RR=5.72, 95% CI, 1.08 to 32.45, P=.049). The median time of late paclitaxel stent thrombosis was 18 months, whereas it was 3.5 months in bare metal stent patients. CONCLUSIONS: Although the incidence of very late stent thrombosis more than 1 year after coronary revascularization is low, drug-eluting stents appear to increase the risk for late thrombosis. Although more of this risk was seen with paclitaxel stents, it remains possible that sirolimus stents similarly increase the risk for late thrombosis compared with bare metal stents.

Coronary Disease↗
PubMed2006

Antithrombotic therapy for percutaneous coronary intervention.

This article outlines the antiplatelet and antithrombotic therapy used in contemporary percutaneous coronary interventions. It is a comprehensive review of past and present pharmacologic agents and includes a discussion of the more promising potential future therapies. The clinical trials that provide the basis for the current standard of care are provided, as are ongoing trials that will likely shape the future standard. This article is not intended to provide a detailed discussion of precise mechanistic or structural features of each agent but to serve as a practical clinical guide to the interventionalist when choosing specific pharmacotherapies for specific patients in the catheterization laboratory.

Angioplasty, Balloon, Coronary↗
PubMed2006

Using statins to treat inflammation in acute coronary syndromes: Are we there yet?

Inflammation and oxidative damage play direct roles in coronary artery disease. C-reactive protein (CRP) is currently the best available marker of inflammation, and statins can potentially reduce coronary inflammation. Until now, CRP testing has been somewhat controversial in the context of cardiovascular disease, as has statin treatment specifically to treat inflammation. However, three recent studies showed that early and aggressive treatment with statins reduces future cardiovascular and cerebrovascular events in patients with acute coronary syndromes; another study showed that aggressive statin treatment leads to regression of stable coronary artery disease. In all the studies, the benefit correlated with reductions in CRP.

Acute Disease↗
PubMed2006

Treatment disparities in the care of patients with and without diabetes presenting with non-ST-segment elevation acute coronary syndromes.

OBJECTIVE: The objective of this study was to characterize treatment patterns among patients with diabetes presenting with non-ST-segment elevation (NSTE) acute coronary syndromes (ACSs). RESEARCH DESIGN AND METHODS: We compared adherence to treatment recommendations from the American College of Cardiology (ACC)/American Heart Association (AHA) guidelines for NSTE ACS among 46,410 patients from 413 U.S. hospitals that were included in the Can Risk Stratification of Unstable Angina Patients Suppress Adverse Outcomes with Early Implementation of the ACC/AHA Guidelines (CRUSADE) quality improvement initiative. Patients were stratified as nondiabetic, non-insulin-dependent diabetic (type 2 diabetic), and insulin-treated diabetic. RESULTS: Insulin-treated diabetic patients were less likely than nondiabetic patients to receive aspirin (adjusted odds ratio 0.83 [95% CI 0.74-0.93]), beta-blockers (0.89 [0.83-0.96]), heparin (0.90 [0.83-0.98]), and glycoprotein IIb/IIIa inhibitors (0.86 [0.79-0.93]). Type 2 diabetic patients were treated similarly to nondiabetic patients. After adjustment for differences in clinical characteristics, insulin-treated diabetic patients were significantly less likely than nondiabetic patients to receive cardiac catheterization within 48 h of presentation (0.80 [0.74-0.86]) or percutaneous coronary intervention (0.87 [0.82-0.94]). Compared with nondiabetic patients, insulin-treated diabetic and type 2 diabetic patients were more likely to undergo coronary artery bypass grafting (1.34 [1.21-1.49] and 1.35 [1.26-1.44]). In-hospital mortality rates were higher in insulin-treated diabetic (6.8%) and type 2 diabetic (5.4%) than in nondiabetic (4.4%) patients. CONCLUSIONS: Diabetic patients have a higher risk of mortality than nondiabetic patients, yet physicians adhere to the ACC/AHA NSTE ACS guidelines less often when treating diabetic patients, particularly insulin-treated diabetic patients. Increased use of guideline-recommended therapies and early invasive management strategies in diabetic patients may improve their outcomes.

Acute Disease↗
PubMed2005

Aspirin and clopidogrel resistance: an emerging clinical entity.

Antiplatelet therapy is a cornerstone of cardiovascular medicine. Aspirin and clopidogrel have emerged as critical therapies in the treatment of cardiovascular disease. Despite their efficacy, patients on these medications continue to suffer complications. Millions of patients are currently on low-dose antiplatelet therapy but it is unknown how many of these patients are under-treated or on the wrong medication. Aspirin and clopidogrel resistance are emerging clinical entities with potentially severe consequences such as recurrent myocardial infarction, stroke, or death. The mechanism of resistance remains incompletely defined, but there are specific clinical, cellular, and genetic factors that influence therapeutic failure. These factors range from physicians who fail to prescribe these medications despite appropriate indications to polymorphisms of platelet membrane glycoproteins. Rapid and accurate diagnosis of antiplatelet resistance also remains an issue as new bedside tests are developed. By understanding the mechanism of therapeutic failure and by improving the diagnosis of this clinical entity, a new era of individualized antiplatelet therapy may arise with routine measurements of platelet activity in the same way that cholesterol, blood pressure, and blood sugar are followed, thus improving the care for millions of people.

Aged↗
PubMed2005

Chronic obstructive pulmonary disease as a predictor of mortality in patients undergoing percutaneous coronary intervention.

Previous studies have shown that patients with chronic obstructive pulmonary disease (COPD) who undergo surgical revascularization have higher in-hospital mortality rates. Limited data are available on the outcomes of patients with COPD undergoing percutaneous coronary intervention (PCI). Our study evaluated the association between COPD and in-hospital and long-term mortality in patients undergoing PCI. We studied 10,994 patients who underwent PCI from 1997 to 2003 at our institution (1,117 with and 9,877 without COPD). A patient was considered to have COPD if it was listed as a co-morbid condition in our database. The primary end point was all-cause mortality. Cox logistic regression models were used to determine whether COPD was an independent predictor of all-cause mortality after PCI. The mean age of the study population was 64 years, and 70.2% were men. Significantly more patients with COPD died in hospital (2.9% vs 1.2%, p <0.0001). The median follow-up was 33 months; 89.6% of patients without COPD versus 75.6% of patients with COPD (log-rank 280, degree of freedom 1, p <0.0001) were alive at the end of the follow-up. After adjusting for other variables known to increase mortality, COPD was a significant independent predictor of in-hospital death (odds ratio 2.51, 95% confidence interval 1.45 to 4.35, p = 0.001) and long-term mortality (hazard ratio 2.16, 95% confidence interval 1.81 to 2.56, p <0.0001) after PCI. In conclusion, patients with a history of COPD have higher in-hospital and long-term mortality rates than those without COPD after PCI.

Aged↗
PubMed2005

Effects of clopidogrel and aspirin in combination versus aspirin alone on platelet activation and major receptor expression in patients after recent ischemic stroke: for the Plavix Use for Treatment of Stroke (PLUTO-Stroke) trial.

BACKGROUND AND PURPOSE: Clopidogrel is widely used in patients after recent ischemic stroke; however, its ability to yield additional antiplatelet protection on top of aspirin has never been explored in a controlled study. To determine whether clopidogrel with aspirin (C+ASA) will produce more potent platelet inhibition than aspirin alone (ASA) in patients after ischemic stroke, we conducted the Plavix Use for Treatment of Stroke trial. METHODS: Seventy patients after ischemic stroke were randomly assigned to C+ASA or ASA groups. Platelet studies included aggregometry; cartridge-based analyzers; expression of PECAM-1, P-selectin, GP IIb/IIIa (antigen and activity), vitronectin receptor, and formation of platelet-leukocyte microparticles by flow cytometry. Platelet tests were performed at baseline and after 30 days after randomization. RESULTS: There were no deaths, hospitalizations, or serious adverse events. There were no differences in the baseline platelet characteristics between C+ASA and ASA groups, or significant changes in platelet parameters in the ASA group, except diminished collagen-induced aggregation (P=0.001). In contrast, therapy with C+ASA resulted in a significant inhibition of platelet activity assessed by ADP- (P=0.00001) and collagen-induced (P=0.02) aggregation; closure time prolongation (P=0.03), and reduction of platelet activation units with Ultegra (P=0.00001); expression of PECAM-1 (P=0.01), and GP IIb/IIIa activity with PAC-1 (P=0.02) when compared with ASA group. Therapy with C+ASA also resulted in the reduced formation of platelet-leukocyte microparticles (P=0.02). CONCLUSIONS: Treatment with C+ASA for 1 month provides significantly greater inhibition of platelet activity than ASA alone in patients after recent ischemic stroke in the frame of the small randomized trial.

Aged↗
PubMed2005

Comparison of results of carotid stenting followed by open heart surgery versus combined carotid endarterectomy and open heart surgery (coronary bypass with or without another procedure).

We compared a novel strategy of carotid stenting (CS) followed by open heart surgery (OHS) to the combined carotid endarterectomy (CEA) and the OHS approach in patients requiring coronary and carotid revascularization. Between 1997 and 2002, CS as a prelude to OHS was performed in 56 patients, and 111 patients underwent combined CEA+OHS. Adverse events included stroke, myocardial infarction (MI), death, and their combinations. At baseline, the CS+OHS group had more unstable/severe angina (52% vs 27%, p = 0.002), severe left ventricular dysfunction (20% vs 9%, p = 0.05), symptomatic carotid disease (46% vs 23%, p = 0.002), and the need for repeat OHS (32% vs 9%, p = 0.0002). Severe contralateral carotid disease was more prevalent in the CEA+OHS group (28% vs 11%, p = 0.01). At 30 days, CS+OHS patients had a significantly lower incidence of stroke or MI (5% vs 19%, p = 0.02). A propensity score was created for each patient to account for baseline differences. In a final logistic regression model that included the propensity score, CS+OHS was associated with a trend toward reduced stroke or MI (odds ratio 0.26, 95% confidence interval 0.06 to 1.09, p = 0.06) and reduced death, stroke, or MI (odds ratio 0.40, 95% confidence interval 0.12 to 1.27, p = 0.12). In conclusion, despite a higher baseline risk profile, patients who underwent CS+OHS had significantly fewer adverse events than those undergoing CEA+OHS. CS may be a safer carotid revascularization option for this challenging patient population.

Aged↗