Interventional cardiologists are held accountable for delay in the door-to-balloon time (DBT) for patients undergoing primary percutaneous coronary intervention in the setting of ST-elevation myocardial infarction (STEMI) even though in the chain of STEMI activation, the interventional cardiologist is the last person that needs to be available to start angiography. The goal of our study is to conduct a thorough analysis of the DBT data to assess time delays by randomly evaluating two consecutive years at the University of Arizona Medical Center (UAMC). We evaluated all available DBT data for STEMIs occurring in the fiscal years of 2011 and 2012 at the UAMC and calculated the time needed for the cardiologist to start the procedure after the patient was ready in the cardiac catheterization laboratory called time to start the procedure (TSP) in addition to other time intervals. Mean TSP time was 4 minutes and 24 seconds, one of the shortest time delays in the chain of STEMI activation and DBT. The median TSP delay was 3 minutes. The longest delay interval was the STEMI team's arrival to with a mean of 17 minutes and 38 seconds. Our data are the first to evaluate delays related to DBT revealing the least delay occurring due to the late arrival of Interventional cardiologists. Our data emphasizes the importance of performing a detailed time analysis of the DBT.
{"title":"Major Delay in Door-to-Ballon Time for Primary Percutaneous Coronary Intervention is Not Related to Interventional Cardiologist's Late Arrival","authors":"M. Movahed, R. Irilouzadian","doi":"10.1055/s-0044-1788279","DOIUrl":"https://doi.org/10.1055/s-0044-1788279","url":null,"abstract":"Interventional cardiologists are held accountable for delay in the door-to-balloon time (DBT) for patients undergoing primary percutaneous coronary intervention in the setting of ST-elevation myocardial infarction (STEMI) even though in the chain of STEMI activation, the interventional cardiologist is the last person that needs to be available to start angiography. The goal of our study is to conduct a thorough analysis of the DBT data to assess time delays by randomly evaluating two consecutive years at the University of Arizona Medical Center (UAMC). We evaluated all available DBT data for STEMIs occurring in the fiscal years of 2011 and 2012 at the UAMC and calculated the time needed for the cardiologist to start the procedure after the patient was ready in the cardiac catheterization laboratory called time to start the procedure (TSP) in addition to other time intervals. Mean TSP time was 4 minutes and 24 seconds, one of the shortest time delays in the chain of STEMI activation and DBT. The median TSP delay was 3 minutes. The longest delay interval was the STEMI team's arrival to with a mean of 17 minutes and 38 seconds. Our data are the first to evaluate delays related to DBT revealing the least delay occurring due to the late arrival of Interventional cardiologists. Our data emphasizes the importance of performing a detailed time analysis of the DBT.","PeriodicalId":506654,"journal":{"name":"International Journal of Angiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141657851","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Hyperhomocysteinemia (HHcy) is an independent risk factor for atherosclerosis. Ischemic stroke and heart disease, coronary heart disease, and cardiovascular disease are events resulting from long-lasting and silent atherosclerosis. This paper deals with the synthesis of homocysteine (Hcy), causes of HHcy, mechanism of HHcy-induced atherosclerosis, and treatment of HHcy. Synthesis and metabolism of Hcy involves demethylation, transmethylation, and transsulfuration, and these processes require vitamin B6 and vitamin B12 folic acid (vitamin B9). Causes of HHcy include deficiency of vitamins B6, B9, and B12, genetic defects, use of smokeless tobacco, cigarette smoking, alcohol consumption, diabetes, rheumatoid arthritis, low thyroid hormone, consumption of caffeine, folic acid antagonist, cholesterol-lowering drugs (niacin), folic acid antagonist (phenytoin), prolonged use of proton pump inhibitors, metformin, and hypertension. HHcy-induced atherosclerosis may be mediated through oxidative stress, decreased availability of nitric oxide (NO), increased expression of monocyte chemoattractant protein-1, smooth muscle cell proliferation, increased thrombogenicity, and induction of arterial connective tissue. HHcy increases the generation of atherogenic biomolecules such as nuclear factor-kappa B, proinflammatory cytokines (IL-1β, IL-6, and IL-8), cell adhesion molecules (intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and E-selection), growth factors (IGF-1 and TGF-β), and monocyte colony-stimulating factor which lead to the development of atherosclerosis. NO which is protective against the development of atherosclerosis is reduced by HHcy. Therapy with folic acid, vitamin B6, and vitamin B12 lowers the levels of Hcy, with folic acid being the most effective. Dietary sources of folic acid, vitamin B6, vitamin B12, omega-3 fatty acid, and green coffee extract reduce Hcy. Abstaining from drinking coffee and alcohol, and smoking also reduces blood levels of Hcy. In conclusion, HHcy induces atherosclerosis by generating atherogenic biomolecules, and treatment of atherosclerosis-induced diseases may be by reducing the levels of Hcy.
{"title":"Atherogenic Effect of Homocysteine, a Biomarker of Inflammation and Its Treatment","authors":"K. Prasad","doi":"10.1055/s-0044-1788280","DOIUrl":"https://doi.org/10.1055/s-0044-1788280","url":null,"abstract":"Hyperhomocysteinemia (HHcy) is an independent risk factor for atherosclerosis. Ischemic stroke and heart disease, coronary heart disease, and cardiovascular disease are events resulting from long-lasting and silent atherosclerosis. This paper deals with the synthesis of homocysteine (Hcy), causes of HHcy, mechanism of HHcy-induced atherosclerosis, and treatment of HHcy. Synthesis and metabolism of Hcy involves demethylation, transmethylation, and transsulfuration, and these processes require vitamin B6 and vitamin B12 folic acid (vitamin B9). Causes of HHcy include deficiency of vitamins B6, B9, and B12, genetic defects, use of smokeless tobacco, cigarette smoking, alcohol consumption, diabetes, rheumatoid arthritis, low thyroid hormone, consumption of caffeine, folic acid antagonist, cholesterol-lowering drugs (niacin), folic acid antagonist (phenytoin), prolonged use of proton pump inhibitors, metformin, and hypertension. HHcy-induced atherosclerosis may be mediated through oxidative stress, decreased availability of nitric oxide (NO), increased expression of monocyte chemoattractant protein-1, smooth muscle cell proliferation, increased thrombogenicity, and induction of arterial connective tissue. HHcy increases the generation of atherogenic biomolecules such as nuclear factor-kappa B, proinflammatory cytokines (IL-1β, IL-6, and IL-8), cell adhesion molecules (intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and E-selection), growth factors (IGF-1 and TGF-β), and monocyte colony-stimulating factor which lead to the development of atherosclerosis. NO which is protective against the development of atherosclerosis is reduced by HHcy. Therapy with folic acid, vitamin B6, and vitamin B12 lowers the levels of Hcy, with folic acid being the most effective. Dietary sources of folic acid, vitamin B6, vitamin B12, omega-3 fatty acid, and green coffee extract reduce Hcy. Abstaining from drinking coffee and alcohol, and smoking also reduces blood levels of Hcy. In conclusion, HHcy induces atherosclerosis by generating atherogenic biomolecules, and treatment of atherosclerosis-induced diseases may be by reducing the levels of Hcy.","PeriodicalId":506654,"journal":{"name":"International Journal of Angiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141666547","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Sahar Mahani, Michael V DiCaro, Nadia Tak, Sigurd Hartnett, Tillman Cyrus, Tahir Tak
Venous thromboembolism (VTE) is the third most common cause of death worldwide even though incidence rates differ globally. Western nations report 1 to 2 cases per 1,000 person-years, while Eastern countries exhibit lower rates (<1 per 1,000 person-years). This comprehensive review delves into diverse VTE risk factors including gender, diabetes, obesity, smoking, genetic mutations, hormonal influences, travel, infections, trauma, and cancer. Notably, VTE incidence is highest in certain cancers (such as pancreatic, liver, and non-small-cell lung cancers) and lowest in others (such as breast, melanoma, and prostate cancers). The extensive review provides essential information about prevalent factors and explores potential molecular mechanism contributing to VTE.
{"title":"Venous Thromboembolism: Current Insights and Future Directions","authors":"Sahar Mahani, Michael V DiCaro, Nadia Tak, Sigurd Hartnett, Tillman Cyrus, Tahir Tak","doi":"10.1055/s-0044-1787652","DOIUrl":"https://doi.org/10.1055/s-0044-1787652","url":null,"abstract":"Venous thromboembolism (VTE) is the third most common cause of death worldwide even though incidence rates differ globally. Western nations report 1 to 2 cases per 1,000 person-years, while Eastern countries exhibit lower rates (<1 per 1,000 person-years). This comprehensive review delves into diverse VTE risk factors including gender, diabetes, obesity, smoking, genetic mutations, hormonal influences, travel, infections, trauma, and cancer. Notably, VTE incidence is highest in certain cancers (such as pancreatic, liver, and non-small-cell lung cancers) and lowest in others (such as breast, melanoma, and prostate cancers). The extensive review provides essential information about prevalent factors and explores potential molecular mechanism contributing to VTE.","PeriodicalId":506654,"journal":{"name":"International Journal of Angiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141666762","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
S. T. Raza, A. Eba, Irshad A. Wani, Sanchita Srivastava, F. Mahdi
Abstract Coronary artery disease (CAD) is one of the most common cardiovascular diseases (CVDs), being the foremost reason for mortality and disability globally. It is a cascade of polygenic architecture of various disorders as a resultant of complexities between various genetic factors and environmental factors. The aim of the present study was to investigate whether the ET1 and APE1 gene polymorphism is associated with the susceptibility to CAD. This study was approved by the Ethical Review Committee of Era Medical College and Hospital. Three milliliters of venous blood sample was collected in ethylenediaminetetraacetic acid-coated vials, and genomic DNA was isolated by using the standard phenol-chloroform extraction method for restriction fragment length polymorphism-polymerase chain reaction study. The APE1 gene AA, AG, GG, and AG + GG genotypes frequencies were 13.91, 40.87, 45.22, and 86.99% in CAD cases and 13, 50, 37, and 87% in controls, respectively. The ET1 gene GG, GT, TT, GT + TT genotypes frequencies were 6.67, 37.5, 55.8, and 93.34% in CAD cases and 6.67, 25.33, 68, and 93.34% in controls. The ET1 and APE1 gene polymorphisms were not significantly associated with the risk of CAD.
{"title":"Association of ET1 and APE1 Genes Polymorphism with Coronary Artery Disease","authors":"S. T. Raza, A. Eba, Irshad A. Wani, Sanchita Srivastava, F. Mahdi","doi":"10.1055/s-0044-1788069","DOIUrl":"https://doi.org/10.1055/s-0044-1788069","url":null,"abstract":"Abstract Coronary artery disease (CAD) is one of the most common cardiovascular diseases (CVDs), being the foremost reason for mortality and disability globally. It is a cascade of polygenic architecture of various disorders as a resultant of complexities between various genetic factors and environmental factors. The aim of the present study was to investigate whether the ET1 and APE1 gene polymorphism is associated with the susceptibility to CAD. This study was approved by the Ethical Review Committee of Era Medical College and Hospital. Three milliliters of venous blood sample was collected in ethylenediaminetetraacetic acid-coated vials, and genomic DNA was isolated by using the standard phenol-chloroform extraction method for restriction fragment length polymorphism-polymerase chain reaction study. The APE1 gene AA, AG, GG, and AG + GG genotypes frequencies were 13.91, 40.87, 45.22, and 86.99% in CAD cases and 13, 50, 37, and 87% in controls, respectively. The ET1 gene GG, GT, TT, GT + TT genotypes frequencies were 6.67, 37.5, 55.8, and 93.34% in CAD cases and 6.67, 25.33, 68, and 93.34% in controls. The ET1 and APE1 gene polymorphisms were not significantly associated with the risk of CAD.","PeriodicalId":506654,"journal":{"name":"International Journal of Angiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141677821","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jordan Schneider, Alejandro Alvarez-Betancourt, Joshua Elbaz, P. Wenn, A. Makaryus, R. Zeltser
Abstract Hypertension (HTN) is a major cardiovascular risk factor and a significant contributor to disease burden in the United States. Despite therapeutic advances, gaps remain between clinical trials and practice. This study aims to bridge those gaps by evaluating antihypertensive strategies. This was a retrospective analysis of HTN patients seen at a hospital clinic from 2016 to 2022 with 3- and 12-month follow-up appointments. Demographics, history, blood pressure (BP), and medication regimen were recorded. Treatment strategies were categorized as follows: adding medication (AM), increasing dosage (ID), switching medications (SM), dropped medications (DrM), or no change (NC). Changes in systolic blood pressure (SBP) were compared using linear regressions to assess the efficacy of HTN management. Of 873 patient charts reviewed, 332 patients were included. The AM group had an adjusted ∆SBP of −11 mm Hg at 3 months ( p < 0.001) and −9 mm Hg at 12 months ( p = 0.006). The ID group had an ∆SBP of −8.5 mm Hg at 3 months ( p = 0.074) and −7 mm Hg at 12 months ( p = 0.3). ∆SBP between the AM and ID groups was not statistically significant ( p = 0.8). SM was associated with an ∆SBP of −3 mm Hg at 3 months ( p = 0.6) and −3 mm Hg at 12 months ( p = 0.7). There are meaningful differences in SBP reduction between antihypertensive medication adjustment strategies. AM had the greatest effect on lowering SBP, with ID having a slightly lesser effect. The difference in ∆SBP between the AM versus ID groups was not significant. While further study with a larger dataset is warranted, our findings highlight trends in the efficacy of HTN management strategies to help guide therapeutic regimens.
{"title":"Comparative Efficacy of Hypertension Management Strategies","authors":"Jordan Schneider, Alejandro Alvarez-Betancourt, Joshua Elbaz, P. Wenn, A. Makaryus, R. Zeltser","doi":"10.1055/s-0044-1788068","DOIUrl":"https://doi.org/10.1055/s-0044-1788068","url":null,"abstract":"Abstract Hypertension (HTN) is a major cardiovascular risk factor and a significant contributor to disease burden in the United States. Despite therapeutic advances, gaps remain between clinical trials and practice. This study aims to bridge those gaps by evaluating antihypertensive strategies. This was a retrospective analysis of HTN patients seen at a hospital clinic from 2016 to 2022 with 3- and 12-month follow-up appointments. Demographics, history, blood pressure (BP), and medication regimen were recorded. Treatment strategies were categorized as follows: adding medication (AM), increasing dosage (ID), switching medications (SM), dropped medications (DrM), or no change (NC). Changes in systolic blood pressure (SBP) were compared using linear regressions to assess the efficacy of HTN management. Of 873 patient charts reviewed, 332 patients were included. The AM group had an adjusted ∆SBP of −11 mm Hg at 3 months ( p < 0.001) and −9 mm Hg at 12 months ( p = 0.006). The ID group had an ∆SBP of −8.5 mm Hg at 3 months ( p = 0.074) and −7 mm Hg at 12 months ( p = 0.3). ∆SBP between the AM and ID groups was not statistically significant ( p = 0.8). SM was associated with an ∆SBP of −3 mm Hg at 3 months ( p = 0.6) and −3 mm Hg at 12 months ( p = 0.7). There are meaningful differences in SBP reduction between antihypertensive medication adjustment strategies. AM had the greatest effect on lowering SBP, with ID having a slightly lesser effect. The difference in ∆SBP between the AM versus ID groups was not significant. While further study with a larger dataset is warranted, our findings highlight trends in the efficacy of HTN management strategies to help guide therapeutic regimens.","PeriodicalId":506654,"journal":{"name":"International Journal of Angiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141680669","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ashok Akula, Heidi R. Grafft, Nadia Tak, Douglas A. Haberman, Tahir Tak
The aim was to explore the effectiveness of enhanced external counterpulsation (EECP) therapy in patients with severe angina pectoris/ chronic heart failure symptoms, who were not suitable candidates for invasive treatment. This retrospective study employed a comprehensive methodology that includes individualized treatment, continuous monitoring, and thorough pre- and postprogram evaluations to assess the efficacy of EECP therapy. The standard protocol involved 35 one-hour treatments, with flexibility for extensions based on therapeutic progress. When pre- and posttreatment results were analyzed, EECP improved the original functional class compared with pretreatment. The mean difference in the functional class was 1.32 (0.92), p < 0.0001. Six-minute walk (6MW) distance improved from 383.6 m (110.24) to 423.1 m (121.50) with mean difference of 37.1 (44.99), p < 0.0001. Duke Activity Status Index (DASI) score improved from 3.9 (2.75) to 6.0 (4.17) with mean difference of 2.16 (3.8), p < 0.0001. Training metabolic equivalents (METs) improved from 3.0 (0.74) to 4.0 (1.57) with mean difference of 1.04 (1.2), p < 0.0001. Weekly anginal events decreased from 13.1 (13.19) to 3.2 (7.38) with mean difference of –9.78 (11.7), p < 0.0001. EECP resulted in improvement of angina pectoris functional class, the 6MW distance, reduction in the number of hospitalizations in first year posttreatment, a significant decrease in sublingual nitroglycerin use, improvement of systolic and diastolic blood pressure, and improvement of DASI score.
{"title":"Enhanced External Counterpulsation Outcomes Study: Retrospective Analyses of Data Obtained from Patients at a Single Medical Center in United States","authors":"Ashok Akula, Heidi R. Grafft, Nadia Tak, Douglas A. Haberman, Tahir Tak","doi":"10.1055/s-0044-1782657","DOIUrl":"https://doi.org/10.1055/s-0044-1782657","url":null,"abstract":"The aim was to explore the effectiveness of enhanced external counterpulsation (EECP) therapy in patients with severe angina pectoris/ chronic heart failure symptoms, who were not suitable candidates for invasive treatment. This retrospective study employed a comprehensive methodology that includes individualized treatment, continuous monitoring, and thorough pre- and postprogram evaluations to assess the efficacy of EECP therapy. The standard protocol involved 35 one-hour treatments, with flexibility for extensions based on therapeutic progress. When pre- and posttreatment results were analyzed, EECP improved the original functional class compared with pretreatment. The mean difference in the functional class was 1.32 (0.92), p < 0.0001. Six-minute walk (6MW) distance improved from 383.6 m (110.24) to 423.1 m (121.50) with mean difference of 37.1 (44.99), p < 0.0001. Duke Activity Status Index (DASI) score improved from 3.9 (2.75) to 6.0 (4.17) with mean difference of 2.16 (3.8), p < 0.0001. Training metabolic equivalents (METs) improved from 3.0 (0.74) to 4.0 (1.57) with mean difference of 1.04 (1.2), p < 0.0001. Weekly anginal events decreased from 13.1 (13.19) to 3.2 (7.38) with mean difference of –9.78 (11.7), p < 0.0001. EECP resulted in improvement of angina pectoris functional class, the 6MW distance, reduction in the number of hospitalizations in first year posttreatment, a significant decrease in sublingual nitroglycerin use, improvement of systolic and diastolic blood pressure, and improvement of DASI score.","PeriodicalId":506654,"journal":{"name":"International Journal of Angiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140361275","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pulmonary embolism (PE) is a common disease associated with significant morbidity and mortality. Despite the familiarity with this disease, the best treatment remains undefined. Traditionally, treatment of PE has involved a choice of anticoagulation, thrombolysis, or surgery. However, the debate over pharmacologic versus mechanical treatment of acute PE reared up again with the advent of user-friendly mechanical and aspiration thrombectomy technologies. This is especially true for submassive PE, which is an area for potential growth both for understanding the pathophysiology of the disease process and management. Multiple devices are available for treatment of PE. Understanding the risks and benefits of each device is paramount in the complex management of PE.
肺栓塞（PE）是一种常见疾病，发病率和死亡率都很高。尽管人们对这种疾病非常熟悉，但最佳治疗方法仍未确定。传统上，肺栓塞的治疗方法包括抗凝、溶栓或手术。然而，随着便于使用的机械和抽吸式血栓切除技术的出现，关于急性 PE 的药物治疗与机械治疗的争论再次出现。这对亚浸润性 PE 尤为如此，无论是在了解疾病过程的病理生理学方面，还是在治疗方面，这都是一个潜在的增长领域。目前有多种设备可用于治疗 PE。了解每种设备的风险和益处对于复杂的 PE 治疗至关重要。
{"title":"Risks and Benefits of Device-Assisted Treatment of Pulmonary Embolism","authors":"Sofia Kim, Michael Kim, Arber Kodra","doi":"10.1055/s-0044-1782535","DOIUrl":"https://doi.org/10.1055/s-0044-1782535","url":null,"abstract":"Pulmonary embolism (PE) is a common disease associated with significant morbidity and mortality. Despite the familiarity with this disease, the best treatment remains undefined. Traditionally, treatment of PE has involved a choice of anticoagulation, thrombolysis, or surgery. However, the debate over pharmacologic versus mechanical treatment of acute PE reared up again with the advent of user-friendly mechanical and aspiration thrombectomy technologies. This is especially true for submassive PE, which is an area for potential growth both for understanding the pathophysiology of the disease process and management. Multiple devices are available for treatment of PE. Understanding the risks and benefits of each device is paramount in the complex management of PE.","PeriodicalId":506654,"journal":{"name":"International Journal of Angiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140380626","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Sandy Goyette, Tulika Mishra, Farah Raza, Zahra Naqvi, Sarah Khan, Abrar Khan, Pamphil Igman, M. S. Bhat
Literature reveals two kinds of menstruation-related anginas—cardiac syndrome X (CSX) and catamenial angina. CSX generally occurs in perimenopausal or postmenopausal women; catamenial angina affects females from puberty to menopause with existing/preexisting or predisposed to coronary artery disease. CSX involves recurring anginal-type retrosternal chest pains during exercise or rest with no significant findings on angiogram. Catamenial angina is menstruation-associated recurrent nonexertional left-sided chest pain alongside diaphoresis, hot flushes, and persistent lethargy. Pathophysiology of both anginas revolve around decreased levels of estrogen. Estrogen is known to act via genomic and nongenomic pathways on cardiomyocytes, endothelial cells, and smooth muscle cells to exert its cardioprotective effect. These cardioprotective effects could be lost during the postovulation phase and at the end of menstruation as well as during perimenopause or menopause owing to the decreased levels of estrogen. Evaluation should begin with a history and physical examination and focus on noninvasive tests such as exercise tolerance test, electrocardiogram, and echocardiogram. Reducing symptoms that cause discomfort and improving quality of life should be the main goal in management. Nitrates along with β blockers and analgesics for pain are the main pharmacologic modalities. Exercise training, smoking cessation, weight loss, and dietary changes are nonpharmacological modalities. Proper awareness and effective communication with patients or caregivers can lead to early diagnosis and treatment initiation.
{"title":"Menstruation-Related Angina—The Wee Hours","authors":"Sandy Goyette, Tulika Mishra, Farah Raza, Zahra Naqvi, Sarah Khan, Abrar Khan, Pamphil Igman, M. S. Bhat","doi":"10.1055/s-0044-1782602","DOIUrl":"https://doi.org/10.1055/s-0044-1782602","url":null,"abstract":"Literature reveals two kinds of menstruation-related anginas—cardiac syndrome X (CSX) and catamenial angina. CSX generally occurs in perimenopausal or postmenopausal women; catamenial angina affects females from puberty to menopause with existing/preexisting or predisposed to coronary artery disease. CSX involves recurring anginal-type retrosternal chest pains during exercise or rest with no significant findings on angiogram. Catamenial angina is menstruation-associated recurrent nonexertional left-sided chest pain alongside diaphoresis, hot flushes, and persistent lethargy. Pathophysiology of both anginas revolve around decreased levels of estrogen. Estrogen is known to act via genomic and nongenomic pathways on cardiomyocytes, endothelial cells, and smooth muscle cells to exert its cardioprotective effect. These cardioprotective effects could be lost during the postovulation phase and at the end of menstruation as well as during perimenopause or menopause owing to the decreased levels of estrogen. Evaluation should begin with a history and physical examination and focus on noninvasive tests such as exercise tolerance test, electrocardiogram, and echocardiogram. Reducing symptoms that cause discomfort and improving quality of life should be the main goal in management. Nitrates along with β blockers and analgesics for pain are the main pharmacologic modalities. Exercise training, smoking cessation, weight loss, and dietary changes are nonpharmacological modalities. Proper awareness and effective communication with patients or caregivers can lead to early diagnosis and treatment initiation.","PeriodicalId":506654,"journal":{"name":"International Journal of Angiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140240356","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
In efforts to decrease the mortality on the waiting list for lung transplantation, alternatives to increase the donor pool have been explored. Caution must be used when accepting donor lungs with pulmonary embolism (PE), as prior evidence has shown mixed results after transplantation of donor lungs with PE. However, the mere diagnosis of PE on imaging should not be the sole reason for the exclusion of these donors for transplant, and they should be reviewed as any other donor. A comprehensive evaluation should be performed for every donor, with a special focus on abnormalities of gas exchange and gross pathologic characteristics during procurement.
为了降低肺移植等待名单上的死亡率，人们一直在探索增加供体库的替代方法。在接受患有肺栓塞（PE）的供肺时必须谨慎，因为之前的证据显示，患有肺栓塞的供肺在移植后的结果好坏参半。然而，不能仅凭影像学诊断出 PE 就将这些供体排除在移植之外，而应像对待其他供体一样对他们进行审查。应对每一位捐献者进行全面评估，重点关注气体交换异常和采集过程中的重大病理特征。
{"title":"Pulmonary Embolism in Donor Lungs—Incidence and Management","authors":"Juliano Lentz Carvalho, Suresh Keshavamurthy","doi":"10.1055/s-0044-1782536","DOIUrl":"https://doi.org/10.1055/s-0044-1782536","url":null,"abstract":"In efforts to decrease the mortality on the waiting list for lung transplantation, alternatives to increase the donor pool have been explored. Caution must be used when accepting donor lungs with pulmonary embolism (PE), as prior evidence has shown mixed results after transplantation of donor lungs with PE. However, the mere diagnosis of PE on imaging should not be the sole reason for the exclusion of these donors for transplant, and they should be reviewed as any other donor. A comprehensive evaluation should be performed for every donor, with a special focus on abnormalities of gas exchange and gross pathologic characteristics during procurement.","PeriodicalId":506654,"journal":{"name":"International Journal of Angiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140238906","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Yu Qiu, Meiying Yang, Xinting Che, Xinming Yu, Kangkang Zhi
Deep vein thrombosis (DVT) is a common postoperative complication of orthopaedic surgery with a complex pathogenesis mechanism. The effect of the miR-2467-3p/acting-binding LIM protein 1 (ABLIM1) axis on thrombus formation and human vascular endothelial cells (HUVECs) progression was evaluated aiming to identify a novel potential biomarker of DVT. DVT rat models were established by inferior vena cava stenosis. The expression of the miR-2467-3p/ABLIM1 axis was analyzed by PCR. HUVECs were induced with oxidative low-density lipoprotein (ox-LDL). Cell growth and motility were assessed by cell counting kit 8 (CCK8) and Transwell assay. The inflammation and oxidative stress were estimated by proinflammatory cytokines and generation of MDA and reactive oxygen species (ROS). ABLIM1 was downregulated in DVT rats. Overexpressing ABLIM1 could suppress the formation of thrombosis and alleviate inflammation and oxidative stress. In HUVECs, ox-LDL induced significantly increased miR-2467-3p and decreased ABLIM1, and miR-2467-3p could negatively regulate ABLIM1. The knockdown of miR-2467-3p could alleviate the inhibited cell growth and motility by ox-LDL, and the inflammation and oxidative stress were also attenuated. While silencing could reverse the effect of miR-2467-3p on ox-LDL-induced HUVECs. The miR-2467-3p/ABLIM1 axis regulates the occurrence and development of DVT through modulating HUVECs inflammation and oxidative stress.
{"title":"miR-2467-3p/ABLIM1 Axis Mediates the Formation and Progression of Deep Vein Thrombosis by Regulating Inflammation and Oxidative Stress","authors":"Yu Qiu, Meiying Yang, Xinting Che, Xinming Yu, Kangkang Zhi","doi":"10.1055/s-0044-1779663","DOIUrl":"https://doi.org/10.1055/s-0044-1779663","url":null,"abstract":"Deep vein thrombosis (DVT) is a common postoperative complication of orthopaedic surgery with a complex pathogenesis mechanism. The effect of the miR-2467-3p/acting-binding LIM protein 1 (ABLIM1) axis on thrombus formation and human vascular endothelial cells (HUVECs) progression was evaluated aiming to identify a novel potential biomarker of DVT. DVT rat models were established by inferior vena cava stenosis. The expression of the miR-2467-3p/ABLIM1 axis was analyzed by PCR. HUVECs were induced with oxidative low-density lipoprotein (ox-LDL). Cell growth and motility were assessed by cell counting kit 8 (CCK8) and Transwell assay. The inflammation and oxidative stress were estimated by proinflammatory cytokines and generation of MDA and reactive oxygen species (ROS). ABLIM1 was downregulated in DVT rats. Overexpressing ABLIM1 could suppress the formation of thrombosis and alleviate inflammation and oxidative stress. In HUVECs, ox-LDL induced significantly increased miR-2467-3p and decreased ABLIM1, and miR-2467-3p could negatively regulate ABLIM1. The knockdown of miR-2467-3p could alleviate the inhibited cell growth and motility by ox-LDL, and the inflammation and oxidative stress were also attenuated. While silencing could reverse the effect of miR-2467-3p on ox-LDL-induced HUVECs. The miR-2467-3p/ABLIM1 axis regulates the occurrence and development of DVT through modulating HUVECs inflammation and oxidative stress.","PeriodicalId":506654,"journal":{"name":"International Journal of Angiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140442780","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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