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Featured researches published by Satyendra Giri.


American Journal of Cardiology | 1999

Functional assessment with electrocardiographic gated single-photon emission computed tomography improves the ability of technetium-99m sestamibi myocardial perfusion imaging to predict myocardial viability in patients undergoing revascularization.

Michael G. Levine; Carol C McGill; Alan W. Ahlberg; Michael P. White; Satyendra Giri; Babar Shareef; David D. Waters; Gary V. Heller

This study evaluates the use of electrocardiographic (ECG) gated single-photon emission computed tomographic (SPECT) myocardial perfusion imaging for the prediction of viability in patients undergoing revascularization, who have coronary disease and left ventricular dysfunction. Fifty patients underwent technectium-99m (Tc-99m) sestamibi ECG gated SPECT imaging preoperatively at rest and 1 week after revascularization, whereas 36 (72%) also underwent imaging 6 weeks after revascularization. Images were interpreted by the consensus of 3 experienced readers without knowledge of patient identity or time of imaging (pre- or postrevascularization) for perfusion and wall motion using a 17-segment model. Results of perfusion alone were compared with perfusion and wall motion combined. One hundred five coronary artery territories were revascularized, 96 of which were viable and 9 nonviable. Perfusion alone predicted 87 to be viable and 18 nonviable (sensitivity 86%, specificity 55%, positive predictive value 95%, negative predictive value 28%, and overall accuracy 85%). Perfusion and wall motion combined identified 95 territories to be viable (sensitivity 95%; p <0.025; specificity 55%, positive predictive value 96%, negative predictive value 50%, and overall accuracy 91%; p <0.05). Thus, Tc-99m sestamibi ECG gated SPECT myocardial perfusion imaging at rest allows assessment of both perfusion and wall motion, which significantly improves the sensitivity and overall accuracy for determination of viability in comparison with perfusion alone.


Atherosclerosis | 1998

Oral estrogen improves serum lipids, homocysteine and fibrinolysis in elderly men

Satyendra Giri; Paul D. Thompson; Pamela Taxel; John H. Contois; James D. Otvos; Robert Allen; Gordon Ens; Alan H.B. Wu; David D. Waters

The effects of estrogen on cardiovascular risk factors have been less well defined in men than in women. We measured lipid and lipoprotein concentrations, lipoprotein particle size distributions, lipoprotein (a), homocysteine, and markers of thrombosis and fibrinolysis in 18 [corrected] healthy elderly men (age 74 +/- 3 years, mean +/- S.D.) before and after 9 weeks of treatment with 0.5, 1 or 2 mg/day of oral micronized 17beta-estradiol. LDL-C (-6%), apo B (-9%), triglyceride (-5%), and homocysteine (-11%) concentrations decreased with estradiol, whereas HDL-C (+14%) increased. Intermediate-size VLDL subclass concentrations were lowered and LDL and HDL subclass levels altered in such a way as to cause average LDL and HDL particle size to increase. Lipoprotein (a) did not change. Fibrinogen (-13%) and plasminogen activator inhibitor-1 (PAI-1) concentrations (-26%) decreased, but there were no changes in thrombotic markers including thrombin-antithrombin III complex, prothrombin fragment 1.2, D-dimer, antithrombin activity, protein-C and S and von Willebrand factor antigen. Breast tenderness occurred in four men and heartburn in five but did not require discontinuation of treatment. We conclude that oral estrogen in men reduces homocysteine, fibrinogen, and PAI-1 concentrations and favorably influences VLDL, LDL and HDL subclass levels without increasing markers of thrombotic risk.


Journal of Nuclear Cardiology | 1999

Comparison of acute rest myocardial perfusion imaging and serum markers of myocardial injury in patients with chest pain syndromes

Maria D. Duca; Satyendra Giri; Alan H.B. Wu; R. Scott Morris; G. Cyr; Alan W. Ahlberg; Michael P. White; David D. Waters; Gary V. Heller

BackgroundNewer diagnostic modalities such as serum markers and acute rest myocardial perfusion imaging (MPI) have been evaluated diagnostically in patients with chest pain in the emergency department (ED), but never concurrently. We compared these two modalities in distinguishing patients in the ED with symptomatic myocardial ischemia from those with non-cardiac causes.MethodsSerum markers and acute technetium-99m sestamibi/tetrofosmin rest MPI were obtained in 75 patients admitted to the ED with chest pain and nondiagnostic electrocardiograms. Venous samples were drawn at admission and 8 to 24 hours later for total creatine kinase, CK-MB fraction, troponin T, troponin I, and myoglobin. Three nuclear cardiologists performed blinded image interpretation. Coronary artery disease (CAD) was confirmed either by diagnostic testing or by the occurrence of myocardial infarction (MI).ResultsAcute rest MPI results were abnormal in all 9 patients with MI. An additional 26 patients had objective evidence of CAD confirmed by diagnostic testing. The sensitivity of acute rest MPI for objective evidence of CAD was 73%. Serum troponin T and troponin I were highly specific for acute MI but had low sensitivity at presentation. Individual serum markers had very low sensitivity for symptomatic myocardial ischemia alone. In the multivariate regression model, only acute rest MPI and diabetes were independently predictive of CAD.ConclusionAt the time of presentation and 8 to 24 hours later, acute rest MPI has a better sensitivity and similar specificity for patients with objective evidence of CAD when compared with serum markers.


The Annals of Thoracic Surgery | 2002

A comparison of two individual amiodarone regimens to placebo in open heart surgery patients.

C Michael White; Satyendra Giri; James P. Tsikouris; Alisha Dunn; Kathy Felton; Prabashni Reddy; Jeffrey Kluger

BACKGROUND This study compares the ability of two oral amiodarone regimens to reduce the risk of atrial fibrillation (AF) as compared with the placebo among elderly open heart surgery (OHS) patients receiving beta blockade. METHODS This is a randomized, double-blinded, placebo-controlled trial of 220 patients undergoing OHS. Patients (average age, 73 years) received 7 g of oral amiodarone more than 10 days starting 5 days before OHS (slow load; n = 56), a 6 g oral amiodarone regimen more than 6 days starting 1 day before OHS (fast load; n = 64), or matching placebo in one of the two previously mentioned regimens (n = 100). RESULTS Patients receiving the slow load amiodarone regimen had a significant reduction in the risk of AF (48.4%; p = 0.013), AF lasting more than 24 hours (76.5%; p = 0.003), symptomatic AF (90.0%; p = 0.002), and recurrent AF (64.5%; p = 0.025) as compared with the placebo. Patients receiving the fast load amiodarone regimen had significant reductions in the risk of AF lasting more than 24 hours (52.6%; p = 0.038) and symptomatic AF (65.0%; p = 0.024), but the incidence of any AF or any recurrence of AF only showed a trend toward significance (34.0% and 45.5%; p = 0.054 and 0.09, respectively). CONCLUSIONS Oral amiodarone in a slow loading regimen provides significant suppression of all AF factors and can be used when a patient has started it at least 5 days before OHS. If a patient has less than 5 days before OHS, the fast loading regimen is an efficacious alternative as it provides significant benefits in preventing AF from lasting more than 24 hours and for preventing symptomatic AF. Both regimens were well tolerated and safe in elderly patients receiving beta blockade according to the hospitals standard protocol.


Atherosclerosis | 2002

The effects of hydroxy-methyl-glutaryl co-enzyme A reductase inhibitors on platelet thrombus formation

Paul D. Thompson; Niall M. Moyna; C Michael White; Kelly M Weber; Satyendra Giri; David D. Waters

BACKGROUND Hydroxy-methyl-glutaryl co-enzyme A reductase inhibitors (HMG CoA RIs) markedly improve the lipid profile of patients with hypercholesterolemia, but the magnitude and time course of the effect of these drugs on other risk factors for atherosclerosis are not well defined. METHODS We employed a random assignment, double-blind design to compare the effect of 8 weeks of HMG CoA RI therapy with either pravastatin (40 mg QD; n=12) or simvastatin (20 mg QD; n=12) with placebo (n=13) on serum lipids, platelet thrombus formation (PTF), and markers of inflammation and thrombosis in patients with coronary artery disease. PTF was measured using a validated ex vivo perfusion chamber system. RESULTS Total and LDL cholesterol decreased 20.3 +/- 12.7% and 31.4 +/- 16.5% in the HMG CoA RI group and were unchanged with placebo (P<0.01). Triglycerides also decreased 15.3 +/- 22.5% with HMG CoA RI therapy, but increased 8.4 +/- 30.0% with placebo (P=0.01). PTF increased 54.1 +/- 89.0% with placebo and decreased 8.0 +/- 46.82% with HMG CoA RI treatment (P<0.01). CONCLUSIONS HMG CoA RI therapy with pravastatin or simvastatin reduces PTF after only 8 weeks of therapy. Such lipid effects may contribute to the prompt reduction in cardiovascular events noted in some clinical trials.


Current Opinion in Cardiology | 1996

Pathophysiology and initial management of the acute coronary syndromes.

Satyendra Giri; David D. Waters

Acute coronary syndromes are responsible for more than half a million hospital admissions each year in the United States alone. Plaque rupture is the precipitating pathophysiologic event. The degree of narrowing of plaques that rupture is not necessarily severe, in the range of 30% to 70% diameter stenosis. Plaques containing large lipid pools with only thin fibrous caps are most at risk. The site of rupture is most often at the shoulder of the plaque, where stress is highest. Clusters of macrophages are often seen at these points. Most plaque ruptures heal without causing symptoms, perhaps leaving a narrowing somewhat more severe than before. Plaque ruptures that expose larger areas of thrombogenic intramural debris to flowing blood in areas of high turbulence are most likely to provoke more extensive thrombosis. Risk factors, particularly smoking and hypercholesterolemia, cause increased thrombin deposition at the site of deep arterial injury. Thrombin deposition causes local coronary vasoconstriction that may contribute to the development of ischemia. Whether plaque rupture with thrombosis causes infarction, unstable angina, or no symptoms at all depends on the site of the lesion, its severity, and whether the jeopardized myocardium is served by collaterals. Aspirin, heparin, and, potentially, the newer agents provide benefit in each of the acute coronary syndromes.


Pharmacotherapy | 2002

An Economic Analysis of Amiodarone versus Placebo for the Prevention of Atrial Fibrillation After Open Heart Surgery

Prabashni Reddy; Alisha Dunn; C Michael White; James P. Tsikouris; Satyendra Giri; Jeffrey Kluger

Study Objective. To determine if the additional costs of oral amiodarone in patients undergoing open heart surgery would be offset by reductions in the frequency of atrial fibrillation.


Journal of the American College of Cardiology | 2003

First-pass magnetic resonance imaging myocardial perfusion can determine microvascular dysfunction in acute myocardial infarction: Validation against angiographic thrombolysis in myocardial infarction frame count and myocardial blush score

Raymond Y. Kwong; Robert D. Winslow; Jennifer Blount; Minang Turakhia; Scott D. Solomon; E. Kent Yucel; Satyendra Giri

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Annals of Noninvasive Electrocardiology | 2002

The immediate and short-term effect of successful percutaneous coronary intervention on repolarization in acute myocardial infarction patients.

Dalia Giedrimiene; Satyendra Giri; C Michael White; Evaldas Giedrirnas; Jeffrey Kluger

Objectives: The primary objective was to assess the immediate and short‐term impact of successful percutaneous coronary intervention (PCI) on QT dispersion (QT disp) and corrected QT dispersion (QTc disp). Secondarily, the impact of PCI on QT and QTc disp within different infarct‐related arteries and the impact of successful PCI in these different arteries were evaluated.


Archive | 1998

Pathophysiology of Acute Coronary Syndromes

Satyendra Giri; David D. Waters; Alan H.B. Wu

Acute coronary syndromes encompass a spectrum of symptomatic manifestations of ischemic heart disease, including unstable angina (UA)*, and non-Q-wave and Q-wave acute myocardial infarction (AMI). The syndrome of warning chest pain preceding the event was first described in 1912 by Herrick (1). His suspicion of acute coronary occlu-sion resulting from evolving coronary thrombus as a cause of this chest pain syndrome was further substantiated in 1930s (2). Subsequently, the now near universally accepted term “unstable angina” was coined in 1971 (3). Since then, descriptive classifications of UA have been proposed, and their prognostic value in managing acute coronary syndromes has been substantiated (4-6).

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David D. Waters

San Francisco General Hospital

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Alan H.B. Wu

University of California

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C Michael White

University of Connecticut

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Jeffrey Kluger

University of Connecticut

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Andrew C. Eisenhauer

Brigham and Women's Hospital

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Gary V. Heller

Morristown Medical Center

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