Browsing by Subject "Acute myocardial infarction"

Now showing 1 - 8 of 8
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    Acute myocardial infarction-related mortality among older adults (≥65 years) with malignancy in the U.S. from 1999 to 2020
    (Elsevier, 2025-03-07) Naveed, Muhammad Abdullah; Neppala, Sivaram; Chigurupati, Himaja Dutt; Ali, Ahila; Rehan, Muhammad Omer; Fath, Ayman; Azeem, Bazil; Iqbal, Rabia; Mubeen, Manahil; Naveed, Hamza; Zafar, Muhammad Naveed Uz; Ahmed, Mushood; Rana, Jamal S.; Patel, Brijesh; Medicine, School of Medicine
    Background: Acute Myocardial Infarction (AMI) in malignancy is a global threat, causing significant mortality and economic burden. They share common risk factors, highlighting the urgency of addressing this critical issue. Objective: This study analyzed demographic trends and disparities in mortality rates due to AMI in malignancy among adults aged 65 and older from 1999 to 2020. Methods: We used the CDC WONDER database to analyze Age-adjusted mortality rates (AAMRs) for AMI in malignancy patients (ICD-10 I21, C00-C97) from 1999 to 2020, stratifying by sex, race, geography, and metropolitan status. We calculated Average Annual Percentage Changes (AAPCs) and Annual Percentage Changes (APCs) per 100,000 with 95 % confidence intervals (CI) using Joinpoint regression. Results: Between 1999 and 2020, AMI in malignancy accounted for 172,691 deaths among adults aged ≥65 years, with the majority of deaths occurring in medical facilities (56.9 %). The overall AAMR for AMI in malignancy-related deaths decreased from 30.2 in 1999 to 14.2 in 2020, with an AAPC of -3.90 (p < 0.000001). Men showed higher AAMRs than women (28.6 vs. 12.3), with a more pronounced decrease in men (AAPC: 4.22, p < 0.000001) compared to women (AAPC: 3.78, p < 0.000001). Black individuals have the highest AAMR (22.7), followed by Whites (19.3). Arkansas had the highest AAMR (32.3), while Nevada had the lowest (8.1), with the Northeastern region having the highest regional AAMR (20.2), and nonmetropolitan areas had higher AAMRs. Conclusion: This study reveals significant demographic disparities in mortality rates related to AMI in malignant older adults. These findings emphasize the need for targeted interventions and improved access to care.
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    Association Between Race/Ethnicity and Income on the Likelihood of Coronary Revascularization Among Postmenopausal Women with Acute Myocardial Infarction: Women’s Health Initiative Study
    (Elsevier, 2022) Tertulien, Tarryn; Roberts, Mary B.; Eaton, Charles B.; Cene, Crystal W.; Corbie-Smith, Giselle; Manson, JoAnn E.; Allison, Matthew; Nassir, Rami; Breathett, Khadijah; Medicine, School of Medicine
    Background: Historically, race, income, and gender were associated with likelihood of receipt of coronary revascularization for acute myocardial infarction (AMI). Given public health initiatives such as Healthy People 2010, it is unclear whether race and income remain associated with the likelihood of coronary revascularization among women with AMI. Methods: Using the Women's Health Initiative Study, hazards ratio (HR) of revascularization for AMI was compared for Black and Hispanic women vs White women and among women with annual income <$20,000/year vs ≥$20,000/year over median 9.5 years follow-up(1993-2019). Proportional hazards models were adjusted for demographics, comorbidities, and AMI type. Results were stratified by revascularization type: percutaneous coronary intervention and coronary artery bypass grafting(CABG). Trends by race and income were compared pre- and post-2010 using time-varying analysis. Results: Among 5,284 individuals with AMI (9.5% Black, 2.8% Hispanic, and 87.7% White; 23.2% <$20,000/year), Black race was associated with lower likelihood of receiving revascularization for AMI compared to White race in fully adjusted analyses [HR:0.79(95% Confidence Interval:[CI]0.66,0.95)]. When further stratified by type of revascularization, Black race was associated with lower likelihood of percutaneous coronary intervention for AMI compared to White race [HR:0.72(95% CI:0.59,0.90)] but not for CABG [HR:0.97(95%CI:0.72,1.32)]. Income was associated with lower likelihood of revascularization [HR:0.90(95%CI:0.82,0.99)] for AMI. No differences were observed for other racial/ethnic groups. Time periods (pre/post-2010) were not associated with change in revascularization rates. Conclusion: Black race and income remain associated with lower likelihood of revascularization among patients presenting with AMI. There is a substantial need to disrupt the mechanisms contributing to race, sex, and income disparities in AMI management.
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    Electroanatomic Remodeling of the Left Stellate Ganglion After Myocardial Infarction
    (Elsevier, 2012) Han, Seongwook; Kobayashi, Kenzaburo; Joung, Boyoung; Piccirillo, Gianfranco; Maruyama, Mitsunori; Vinters, Harry V.; March, Keith; Lin, Shien-Fong; Shen, Changyu; Fishbein, Michael C.; Chen, Peng-Sheng; Chen, Lan S.; Medicine, School of Medicine
    Objectives: The purpose of this study was to evaluate the changes of left stellate ganglionic nerve activity (SGNA) and left thoracic vagal nerve activity (VNA) after acute myocardial infarction (MI). Background: Whether MI results in remodeling of extracardiac nerve activity remains unclear. Methods: We implanted radiotransmitters to record the SGNA, VNA, and electrocardiogram in 9 ambulatory dogs. After baseline monitoring, MI was created by 1-h balloon occlusion of the coronary arteries. The dogs were then continuously monitored for 2 months. Both stellate ganglia were stained for growth-associated protein 43 and synaptophysin. The stellate ganglia from 5 normal dogs were used as control. Results: MI increased 24-h integrated SGNA from 7.44 ± 7.19 Ln(Vs)/day at baseline to 8.09 ± 7.75 Ln(Vs)/day after the MI (p < 0.05). The 24-h integrated VNA before and after the MI was 5.29 ± 5.04 Ln(Vs)/day and 5.58 ± 5.15 Ln(Vs)/day, respectively (p < 0.05). A significant 24-h circadian variation was noted for the SGNA (p < 0.05) but not the VNA. The SGNA/VNA ratio also showed significant circadian variation. The nerve densities from the left SG were 63,218 ± 34,719 μm(2)/mm(2) and 20,623 ± 4,926 μm(2)/mm(2) for growth-associated protein 43 (p < 0.05) and were 32,116 ± 8,190 μm(2)/mm(2)and 16,326 ± 4,679 μm(2)/mm(2) for synaptophysin (p < 0.05) in MI and control groups, respectively. The right SG also showed increased nerve density after MI (p < 0.05). Conclusions: MI results in persistent increase in the synaptic density of bilateral stellate ganglia and is associated with increased SGNA and VNA. There is a circadian variation of the SGNA/VNA ratio. These data indicate significant remodeling of the extracardiac autonomic nerve activity and structures after MI.
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    Endothelial Colony Forming Cells (ECFCs): Identification, Specification and Modulation in Cardiovascular Diseases
    (2009-12) Huang, Lan; Pescovitz, Mark D.; Quilliam, Lawrence A.; Ingram, David A., Jr.; Pescovitz, Mark D.
    A hierarchy of endothelial colony forming cells (ECFCs) with different levels of proliferative potential has been identified in human circulating blood and blood vessels. High proliferative potential ECFCs (HPP-ECFCs) display properties (robust proliferative potential in vitro and vessel-forming ability in vivo) consistent with stem/progenitor cells for the endothelial lineage. Corneal endothelial cells (CECs) are different from circulating and resident vascular endothelial cells (ECs). Whereas systemic vascular endothelium slowly proliferates throughout life, CECs fail to proliferate in situ and merely expand in size to accommodate areas of CEC loss due to injury or senescence. However, we have identified an entire hierarchy of ECFC resident in bovine CECs. Thus, this study provides a new conceptual framework for defining corneal endothelial progenitor cell potential. The identification of persistent corneal HPP-ECFCs in adult subjects might contribute to regenerative medicine in corneal transplantation. While human cord blood derived ECFCs are able to form vessels in vivo, it is unknown whether they are committed to an arterial or venous fate. We have demonstrated that human cord blood derived ECFCs heterogeneously express gene transcripts normally restricted to arterial or venous endothelium. They can be induced to display an arterial gene expression pattern after vascular endothelial growth factor 165 (VEGF165) or Notch ligand Dll1 (Delta1ext-IgG) stimulation in vitro. However, the in vitro Dll1 primed ECFCs fail to display significant skewing toward arterial EC phenotype and function in vivo upon implantation, suggesting that in vitro priming is not sufficient for in vivo specification. Future studies will determine whether ECFCs are amenable to specification in vivo by altering the properties of the implantation microenvironment. There is emerging evidence suggesting that the concentration of circulating ECFCs is closely related to the adverse progression of cardiovascular disorders. In a pig model of acute myocardial ischemia (AMI), we have demonstrated that AMI rapidly mobilizes ECFCs into the circulation, with a significant shift toward HPP-ECFCs. The exact role of the mobilized HPP-ECFCs in homing and participation in repair of the ischemic tissue remains unknown. In summary, these studies contribute to an improved understanding of ECFCs and suggest several possible therapeutic applications of ECFCs.
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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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    Intracoronary and retrograde coronary venous myocardial delivery of adipose-derived stem cells in swine infarction lead to transient myocardial trapping with predominant pulmonary redistribution
    (Wiley, 2014-01) Jun Hong, Soon; Hou, Dongming; Brinton, Todd J.; Johnstone, Brian; Feng, Dongni; Rogers, Pamela; Fearon, William F.; Yock, Paul; March, Keith L.; Department of Medicine, IU School of Medicine
    OBJECTIVES: To examine the comparative fate of adipose-derived stem cells (ASCs) as well as their impact on coronary microcirculation following either retrograde coronary venous (RCV) or arterial delivery. BACKGROUND: Local delivery of ASCs to the heart has been proposed as a practical approach to limiting the extent of myocardial infarction. Mouse models of mesenchymal stem cell effects on the heart have also demonstrated significant benefits from systemic (intravenous) delivery, prompting a question about the advantage of local delivery. There has been no study addressing the extent of myocardial vs. systemic disposition of ASCs in large animal models following local delivery to the myocardium. METHODS: In an initial experiment, dose-dependent effects of ASC delivery on coronary circulation in normal swine were evaluated to establish a tolerable ASC dosing range for intracoronary (IC) delivery. In a set of subsequent experiments, an anterior acute myocardial infarction (AMI) was created by balloon occlusion of the proximal left anterior descending (LAD) artery, followed by either IC or RCV infusion of 10(7) (111)Indium-labeled autologous ASCs 6 days following AMI. Indices of microcirculatory resistance (IMR) and coronary flow reserve (CFR) were measured before sacrifices to collect tissues for analysis at 1 or 24 hr after cell delivery. RESULTS: IC delivery of porcine ASCs to normal myocardium was well tolerated up to a cumulative dose of 14 × 10(6) cells (approximately 0.5 × 10(6) cells/kg). There was evidence suggesting microcirculatory trapping of ASC: at unit doses of 50 × 10(6) ASCs, IMR and CFR were found to be persistently altered in the target LAD distribution at 7 days following delivery, whereas at 10 × 10(6) ASCs, only CFR was altered. In the context of recent MI, a significantly higher percentage of ASCs was retained at 1 hr with IC delivery compared with RCV delivery (57.2 ± 12.7% vs. 17.9 ± 1.6%, P = 0.037) but this initial difference was not apparent at 24 hr (22.6 ± 5.5% vs. 18.7 ± 8.6%; P = 0.722). In both approaches, most ASC redistributed to the pulmonary circulation by 24 hr postdelivery. There were no significant differences in CFR or IMR following ASC delivery to infarcted tissue by either route. CONCLUSIONS: Selective intravascular delivery of ASC by coronary arterial and venous routes leads to similarly limited myocardial cell retention with predominant redistribution of cells to the lungs. IC arterial delivery of ASC leads to only transiently greater myocardial retention, which is accompanied by obstruction of normal regions of coronary microcirculation at higher doses. The predominant intrapulmonary localization of cells following local delivery via both methods prompts the notion that systemic delivery of ASC might provide similarly beneficial outcomes while avoiding risks of inadvertent microcirculatory compromise.
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    Myocardial Infarction and the Fine Balance of Iron
    (Elsevier, 2021-07-26) Dharmakumar, Rohan; Nair, Anand R.; Kumar, Andreas; Francis, Joseph; Medicine, School of Medicine
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    Retrospective assessment of at-risk myocardium in reperfused acute myocardial infarction patients using contrast‐enhanced balanced steady‐state free‐precession cardiovascular magnetic resonance at 3T with SPECT validation
    (Elsevier, 2021-03-15) Sun, Zheng; Zhang, Qiuhang; Zhao, Huan; Yan, Chengxi; Yang, Hsin‑Jung; Li, Debiao; Li, Kuncheng; Liu, Zhi; Yang, Qi; Dharmakumar, Rohan; Medicine, School of Medicine
    Background: Contrast-enhanced (CE) steady-state free precession (SSFP) CMR at 1.5T has been shown to be a valuable alternative to T2-based methods for the detection and quantifications of area-at-risk (AAR) in acute myocardial infarction (AMI) patients. However, CE-SSFP's capacity for assessment of AAR at 3T has not been investigated. We examined the clinical utility of CE-SSFP and T2-STIR for the retrospective assessment of AAR at 3T with single-photon-emission-computed tomography (SPECT) validation. Materials and methods: A total of 60 AMI patients (ST-elevation AMI, n = 44; non-ST-elevation AMI, n = 16) were recruited into the CMR study between 3 and 7 days post revascularization. All patients underwent T2-STIR, CE-bSSFP and late-gadolinium-enhancement CMR. For validation, SPECT images were acquired in a subgroup of patients (n = 30). Results: In 53 of 60 patients (88 %), T2-STIR was of diagnostic quality compared with 54 of 60 (90 %) with CE-SSFP. In a head-to-head per-slice comparison (n = 365), there was no difference in AAR quantified using T2-STIR and CE-SSFP (R2 = 0.92, p < 0.001; bias:-0.4 ± 0.8 cm2, p = 0.46). On a per-patient basis, there was good agreement between CE-SSFP (n = 29) and SPECT (R2 = 0.86, p < 0.001; bias: - 1.3 ± 7.8 %LV, p = 0.39) for AAR determination. T2-STIR also showed good agreement with SPECT for AAR measurement (R2 = 0.81, p < 0.001, bias: 0.5 ± 11.1 %LV, p = 0.81). There was also a strong agreement between CE-SSFP and T2-STIR with respect to the assessment of AAR on per-patient analysis (R2 = 0.84, p < 0.001, bias: - 2.1 ± 10.1 %LV, p = 0.31). Conclusions: At 3T, both CE-SSFP and T2-STIR can retrospectively quantify the at-risk myocardium with high accuracy.