Browsing by Author "Sinha, Anjan"

Now showing 1 - 6 of 6
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    A Vascular Plug for Persistent Shock Following Transcatheter Mitral Valve Replacement
    (Elsevier, 2024-09-04) Torabi, Asad J.; Patel, Purva; Reborido, Natalia; Morris, Michelle C.; Everett, Jeffrey; Sinha, Anjan; Medicine, School of Medicine
    A 78-year-old woman with severe bioprosthetic mitral valve degeneration underwent successful transcatheter mitral valve replacement with a valve-in-valve procedure. This case postprocedure was complicated by cardiogenic shock from left ventricular perforation and underscores the importance of the accurate assessment and treatment of patients following transcatheter valvular procedures.
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    Factor XIII Val34Leu polymorphism and recurrent myocardial infarction in patients with coronary artery disease
    (Springer, 2014-10) Kreutz, Rolf P.; Bitar, Abbas; Owens, Janelle; Desta, Zeruesenay; Breall, Jeffrey A.; von der Lohe, Elisabeth; Sinha, Anjan; Vatta, Matteo; Nystrom, Perry; Flockhart, David A.; Department of Medicine, IU School of Medicine
    Factor XIII (FXIII) is necessary for cross linking of fibrin strands and generation of stable fibrin clot. FXIII Val34Leu is a common genetic single nucleotide polymorphism that has been associated with accelerated fibrin stabilization and reduced rate of fibrinolysis. The contribution of Val34Leu to long term risk of recurrent myocardial infarction (MI) in patients with coronary stenting has not been conclusively established. The objective of the study was to examine the effects of Val34Leu on fibrin generation, platelet aggregation, and long term clinical outcomes in patients with coronary artery disease treated with dual antiplatelet therapy. Patients with angiographically documented coronary artery disease who were treated with aspirin and clopidogrel were enrolled (n = 211). Light transmittance aggregometry and plasma fibrin clot formation using thrombelastography (TEG) were determined. Genotyping of Val34Leu was performed using Taqman assay. Clinical events during follow up were recorded. Homozygous carriers of 34Leu variant had significantly shorter fibrin clot formation time as compared to wild type individuals (TEG K: 1.27 ± 0.3 vs. 1.68 ± 1.1 min, p = 0.011). The Val34Leu variant was associated with gene dose dependent increased risk of MI (log rank, p = 0.002) or occurrence of composite of MI and CV death (log rank, p = 0.005) with highest event rates observed in homozygous carriers of 34Leu. In summary, FXIII Val34Leu polymorphism was associated with increased rate of fibrin stabilization in homozygous carriers of the variant and may increase risk of recurrent MI and death in patients with angiographically established coronary artery disease treated with dual antiplatelet therapy.
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    Fibrin clot strength measured by thrombelastography and outcomes after percutaneous coronary intervention
    (Thieme, 2017-01-26) Kreutz, Rolf P.; Schmeisser, Glen; Maatman, Benjamin; Schaffter, Andrea; Sinha, Anjan; von der Lohe, Elisabeth; Breall, Jeffrey A.; Medicine, School of Medicine
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    Fulminant myocarditis: COVID or not COVID? Reinfection or co-infection?
    (Future Medicine, 2021) Yeleti, Ramya; Guglin, Maya; Saleem, Kashif; Adigopula, Sasikanth V.; Sinha, Anjan; Upadhyay, Smrity; Everett, Jeffrey E.; Ballut, Kareem; Uppuluri, Sarada; Rao, Roopa A.; Medicine, School of Medicine
    We describe a unique case of fulminant myocarditis in a patient with presumed SARS-CoV-2 reinfection. Patient had initial infection 4 months backand had COVID-19 antibody at the time of presentation. Endomyocardial biopsy showed lymphocytic myocarditis, that is usually seen in viral myocarditis. The molecular diagnostic testing of the endomyocardial biopsy for cardiotropic viruses was positive for Parvovirus and negative for SARS-CoV-2. Authors highly suspect co-infection of SARS-CoV-2 and Parvovirus, that possibly triggered the immune cascade resulting in fulminant myocarditis. Patient was hemodynamically unstable with ventricular tachycardia and was supported on VA ECMO and Impella CP. There was impressive recovery of left ventricular function within 48 hours, leading to decannulation of VA ECMO in 72 h. This unique case was written by the survivor herself.
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    Prediction of Ischemic Events after Percutaneous Coronary Intervention: Thrombelastography Profiles and Factor XIIIa Activity
    (Thieme Medical Publishers, 2018-04) Kreutz, Rolf P.; Schmeisser, Glen; Schaffter, Andrea; Kanuri, Sri; Owens, Janelle; Maatman, Benjamin; Sinha, Anjan; Lohe, Elisabeth von der; Breall, Jeffrey A.; Medicine, School of Medicine
    Background: High plasma fibrin clot strength (MA) measured by thrombelastography (TEG) is associated with increased risk of cardiac events after percutaneous coronary interventions (PCIs). Factor XIIIa (FXIIIa) cross-links soluble fibrin, shortens clot formation time (TEG-K), and increases final clot strength (MA). Methods: We analyzed platelet-poor plasma from patients with previous PCI. Kaolin-activated TEG (R, K, MA) in citrate platelet-poor plasma and FXIIIa were measured (n = 257). Combined primary endpoint was defined as recurrent myocardial infarction (MI) or cardiovascular death (CVD). Relationship of FXIIIa and TEG measurements on cardiac risk was explored. Results: FXIIIa correlated with TEG-MA (p = 0.002) and inversely with TEG-K (p < 0.001). High MA (≥35.35 mm; p = 0.001), low K (<1.15 min; p = 0.038), and elevated FXIIIa (≥83.51%; p = 0.011) were associated with increased risk of CVD or MI. Inclusion of FXIIIa activity and low TEG-K in risk scores did not improve risk prediction as compared with high TEG-MA alone. Conclusion: FXIIIa is associated with higher plasma TEG-MA and low TEG-K. High FXIIIa activity is associated with a modest increase in cardiovascular risk after PCI, but is less sensitive and specific than TEG-MA. Addition of FXIIIa does not provide additional risk stratification beyond risk associated with high fibrin clot strength phenotype measured by TEG.
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    Simultaneous administration of high-dose atorvastatin and clopidogrel does not interfere with platelet inhibition during percutaneous coronary intervention
    (Dove Medical Press, 2016) Kreutz, Rolf P.; Breall, Jeffrey A.; Sinha, Anjan; von der Lohe, Elisabeth; Kovacs, Richard J.; Flockhart, David A.; Department of Medicine, IU School of Medicine
    BACKGROUND: Reloading with high-dose atorvastatin shortly before percutaneous coronary interventions (PCIs) has been proposed as a strategy to reduce periprocedural myonecrosis. There has been a concern that statins that are metabolized by cytochrome P450 3A4 may interfere with clopidogrel metabolism at high doses. The impact of simultaneous administration of high doses of atorvastatin and clopidogrel on the efficacy of platelet inhibition has not been established. METHODS: Subjects (n=60) were randomized to receive atorvastatin 80 mg together with clopidogrel 600 mg loading dose (n=28) versus clopidogrel 600 mg alone (n=32) at the time of PCI. Platelet aggregation was measured at baseline, 4 hours after clopidogrel loading dose, and 16-24 hours after clopidogrel loading dose by light transmittance aggregometry using adenosine diphosphate as agonist. RESULTS: Platelet aggregation was similar at baseline in both the atorvastatin and the control groups (adenosine diphosphate 10 µM: 57%±19% vs 61%±21%; P=0.52). There was no significant difference in platelet aggregation between the atorvastatin and the control groups at 4 hours (37%±18% vs 39%±21%; P=0.72) and 16-24 hours post-clopidogrel loading dose (35%±17% vs 37%±18%; P=0.75). No significant difference in incidence of periprocedural myonecrosis was observed between the atorvastatin and control groups (odds ratio: 1.02; 95% confidence interval 0.37-2.8). CONCLUSION: High-dose atorvastatin given simultaneously with clopidogrel loading dose at the time of PCI does not significantly alter platelet inhibition by clopidogrel. Statin reloading with high doses of atorvastatin at the time of PCI appears to be safe without adverse effects on platelet inhibition by clopidogrel (ClinicalTrials.gov: NCT00979940).