Pub Date : 2021-10-01DOI: 10.4103/2470-7511.334401
Rachel Parise, S. Ramesh, Manoj Govindarajulu, Amir Ajoolabady, Timothy Moore, M. Dhanasekaran
Viral infections persist globally, among all ages, gender, and ethnicity. Of particular importance is COVID-19, associated with asymptomatic to severe symptoms, including complications/mortality. Cardiovascular disease (CVD) involves heart and blood vessel disorders including coronary heart disease, cerebrovascular disease, peripheral artery disease, thrombosis, and more. CVD associated with severe COVID-19 includes heart failure, coronary artery disease, cardiomyopathy, hypertension, and cerebrovascular disease/stroke. Data were acquired from PubMed, Google Scholar, Centers for Disease Prevention and Control, and Lexi-Comp using the search terms “COVID-19 and cardiovascular pathology;” “COVID-19 induced CVD;” “Viral infection induced CVD;” and “Viral infection induced heart damage.” COVID-19-induced CVD mechanisms include direct viral entry, inflammation, cytokine storm, hypoxia, interferon-mediated immune response, plaque destabilization, stress, and drug-induced causes. Other viral pathologies causing CVD include atherosclerosis, inflammation, cytokine storm, and plaque destabilization. Individual parameters, such as old age, males, and higher body mass index (BMI), are more likely to experience viral-associated complications, possibly explained by patient risk factors or comorbidities. Populations at higher risk include older males with an elevated BMI. Viral mechanisms associated with CVD are similar but differ in disease severity, potentially explained by diverse cytokine profiles where COVID-19 activates different types at higher quantities.
{"title":"COVID-19-induced cardiovascular damage differs from other prevalent viruses","authors":"Rachel Parise, S. Ramesh, Manoj Govindarajulu, Amir Ajoolabady, Timothy Moore, M. Dhanasekaran","doi":"10.4103/2470-7511.334401","DOIUrl":"https://doi.org/10.4103/2470-7511.334401","url":null,"abstract":"Viral infections persist globally, among all ages, gender, and ethnicity. Of particular importance is COVID-19, associated with asymptomatic to severe symptoms, including complications/mortality. Cardiovascular disease (CVD) involves heart and blood vessel disorders including coronary heart disease, cerebrovascular disease, peripheral artery disease, thrombosis, and more. CVD associated with severe COVID-19 includes heart failure, coronary artery disease, cardiomyopathy, hypertension, and cerebrovascular disease/stroke. Data were acquired from PubMed, Google Scholar, Centers for Disease Prevention and Control, and Lexi-Comp using the search terms “COVID-19 and cardiovascular pathology;” “COVID-19 induced CVD;” “Viral infection induced CVD;” and “Viral infection induced heart damage.” COVID-19-induced CVD mechanisms include direct viral entry, inflammation, cytokine storm, hypoxia, interferon-mediated immune response, plaque destabilization, stress, and drug-induced causes. Other viral pathologies causing CVD include atherosclerosis, inflammation, cytokine storm, and plaque destabilization. Individual parameters, such as old age, males, and higher body mass index (BMI), are more likely to experience viral-associated complications, possibly explained by patient risk factors or comorbidities. Populations at higher risk include older males with an elevated BMI. Viral mechanisms associated with CVD are similar but differ in disease severity, potentially explained by diverse cytokine profiles where COVID-19 activates different types at higher quantities.","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"6 1","pages":"231 - 245"},"PeriodicalIF":0.0,"publicationDate":"2021-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42766914","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}
Myocardial ischemia and reperfusion (I/R) lead to an inflammatory response that causes cardiac injury and remodeling. However, increasing evidence suggests this is an over-simplified view. Several proinflammatory cytokines, including tumor necrosis factor-α, interleukin-1α, interleukin-6, macrophage migration inhibitory factor and D-dopachrome tautomerase have been shown to improve cell survival and compensate energy deprivation during I/R. This review summarizes the recent findings that support protective role of proinflammatory cytokines against cardiac injury during acute I/R, as well as therapeutic ramifications of these findings.
{"title":"Cardiac protective effects of proinflammatory cytokines during ischemia-reperfusion","authors":"Li-Sha Li, Hong Wu, Shu-Xia Wang, Sui-xin Liu, Le-Qing Lin, Da-Ke Qi","doi":"10.4103/2470-7511.334402","DOIUrl":"https://doi.org/10.4103/2470-7511.334402","url":null,"abstract":"Myocardial ischemia and reperfusion (I/R) lead to an inflammatory response that causes cardiac injury and remodeling. However, increasing evidence suggests this is an over-simplified view. Several proinflammatory cytokines, including tumor necrosis factor-α, interleukin-1α, interleukin-6, macrophage migration inhibitory factor and D-dopachrome tautomerase have been shown to improve cell survival and compensate energy deprivation during I/R. This review summarizes the recent findings that support protective role of proinflammatory cytokines against cardiac injury during acute I/R, as well as therapeutic ramifications of these findings.","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"6 1","pages":"246 - 255"},"PeriodicalIF":0.0,"publicationDate":"2021-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43302434","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}
Pub Date : 2021-10-01DOI: 10.4103/2470-7511.334403
Donghui Zhao, Sidney Smith Jr
Acute coronary syndrome (ACS) is a severe clinical manifestation of ischemic heart disease with a high risk of death. The quality of care provided by the health system and medical providers to patients with ACS in daily clinical practice determines the likelihood of desired health outcomes or prognosis. This review provides an overview of several key issues in the quality of care for ACS, including how to measure the quality of care for ACS and the main strategies to improve the quality of care for ACS patients in both the acute and chronic phases. Efforts to improve the quality of care for ACS through specific programs in Western countries and in China are also described.
{"title":"Quality of Care for Patients with Acute Coronary Syndrome","authors":"Donghui Zhao, Sidney Smith Jr","doi":"10.4103/2470-7511.334403","DOIUrl":"https://doi.org/10.4103/2470-7511.334403","url":null,"abstract":"Acute coronary syndrome (ACS) is a severe clinical manifestation of ischemic heart disease with a high risk of death. The quality of care provided by the health system and medical providers to patients with ACS in daily clinical practice determines the likelihood of desired health outcomes or prognosis. This review provides an overview of several key issues in the quality of care for ACS, including how to measure the quality of care for ACS and the main strategies to improve the quality of care for ACS patients in both the acute and chronic phases. Efforts to improve the quality of care for ACS through specific programs in Western countries and in China are also described.","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"6 1","pages":"202 - 209"},"PeriodicalIF":0.0,"publicationDate":"2021-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46928291","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}
Pub Date : 2021-10-01DOI: 10.4103/2470-7511.334399
D. Yan, Yongming Zhang, Yu-hua Ji, Tao Wang, Xiao-Xing Xiong, Heng Zhao
Backgrounds: Whether there are distinctive macrophage functional phenotypes of M1 versus M2 has been debated. We re-examined them by studying M1/M2 gene and protein expressions in cultured BV2 microglial cells and their effects on stroke outcomes in vivo. Methods: BV2 microglia cells were cultured and polarized with lipopolysaccharide (LPS) and interleukin-4 (IL-4) to produce M (LPS) and M (IL-4) phenotypes, which were originally defined as M1 and M2 phenotypes, respectively. Typical M1 and M2 gene or protein expression patterns were analyzed in M (LPS) and M (IL-4) phenotypes and their distinctive effects on stroke outcomes were compared. Results: M (LPS) and M (IL-4) had distinctive morphologies. M (IL-4) had significantly higher gene expressions of the typical M2 markers and other anti-inflammatory genes, while M (LPS) had higher gene expression of typical M1 markers and other pro-inflammatory genes. Nevertheless, M2 gene expressions were also enhanced in M (LPS), and M1 gene expressions were increased in M (IL-4), although with relatively lower levels. Adoptive transfer of M (IL-4) reduced infarction and improved neurological scores, while M (LPS) macrophages generated the opposite effect. Fluorescence activated cell sorting (FACS) and confocal studies suggest that M (IL-4) inhibited, while M (LPS) promoted the infiltration of monocyte-derived macrophages and iNOS-positive cells. Conclusions: M (LPS) and M (IL-4) from cultured BV2 cells indeed are distinctive functional phenotypes, but it is inaccurate to simply classify them into M1 and M2 phenotypes based on a few typical gene and protein markers.
{"title":"Re-visit the concept of M1 versus M2 phenotypes of BV2 microglia and test their effects on stroke outcome in mice","authors":"D. Yan, Yongming Zhang, Yu-hua Ji, Tao Wang, Xiao-Xing Xiong, Heng Zhao","doi":"10.4103/2470-7511.334399","DOIUrl":"https://doi.org/10.4103/2470-7511.334399","url":null,"abstract":"Backgrounds: Whether there are distinctive macrophage functional phenotypes of M1 versus M2 has been debated. We re-examined them by studying M1/M2 gene and protein expressions in cultured BV2 microglial cells and their effects on stroke outcomes in vivo. Methods: BV2 microglia cells were cultured and polarized with lipopolysaccharide (LPS) and interleukin-4 (IL-4) to produce M (LPS) and M (IL-4) phenotypes, which were originally defined as M1 and M2 phenotypes, respectively. Typical M1 and M2 gene or protein expression patterns were analyzed in M (LPS) and M (IL-4) phenotypes and their distinctive effects on stroke outcomes were compared. Results: M (LPS) and M (IL-4) had distinctive morphologies. M (IL-4) had significantly higher gene expressions of the typical M2 markers and other anti-inflammatory genes, while M (LPS) had higher gene expression of typical M1 markers and other pro-inflammatory genes. Nevertheless, M2 gene expressions were also enhanced in M (LPS), and M1 gene expressions were increased in M (IL-4), although with relatively lower levels. Adoptive transfer of M (IL-4) reduced infarction and improved neurological scores, while M (LPS) macrophages generated the opposite effect. Fluorescence activated cell sorting (FACS) and confocal studies suggest that M (IL-4) inhibited, while M (LPS) promoted the infiltration of monocyte-derived macrophages and iNOS-positive cells. Conclusions: M (LPS) and M (IL-4) from cultured BV2 cells indeed are distinctive functional phenotypes, but it is inaccurate to simply classify them into M1 and M2 phenotypes based on a few typical gene and protein markers.","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"6 1","pages":"264 - 273"},"PeriodicalIF":0.0,"publicationDate":"2021-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47752503","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}
Pub Date : 2021-10-01DOI: 10.4103/2470-7511.334400
C. Tam, C. Siu, H. Tse
The coronavirus disease-2019 (COVID-19) pandemic has brought unprecedented changes to our world and health-care system. Its high virulence and infectiousness directly infect people's respiratory system and indirectly disrupt our health-care infrastructure. In particular, ST elevation myocardial infarction (STEMI) is a clinical emergency emphasizes on the establishment of care system to minimize delay to reperfusion. As such, the impact of COVID-19 on STEMI care, ranging from disease severity, patient delay, diagnostic difficulty, triage to selection of reperfusion strategy and postoperative care, is immense. Importantly, not only we have to save our patients, but we must also need to protect all health-care workers and prevent environmental contamination. Otherwise, in-hospital transmission can quickly evolve into nosocomial outbreak with staff infection and quarantine which lead to health-care system collapse. In this article, we will discuss the challenges in various aspects of STEMI management during COVID-19, as well as the mitigation measures we can take to optimize outcome and our future.
{"title":"Challenges in management of ST elevation myocardial infarction during COVID-19 pandemic","authors":"C. Tam, C. Siu, H. Tse","doi":"10.4103/2470-7511.334400","DOIUrl":"https://doi.org/10.4103/2470-7511.334400","url":null,"abstract":"The coronavirus disease-2019 (COVID-19) pandemic has brought unprecedented changes to our world and health-care system. Its high virulence and infectiousness directly infect people's respiratory system and indirectly disrupt our health-care infrastructure. In particular, ST elevation myocardial infarction (STEMI) is a clinical emergency emphasizes on the establishment of care system to minimize delay to reperfusion. As such, the impact of COVID-19 on STEMI care, ranging from disease severity, patient delay, diagnostic difficulty, triage to selection of reperfusion strategy and postoperative care, is immense. Importantly, not only we have to save our patients, but we must also need to protect all health-care workers and prevent environmental contamination. Otherwise, in-hospital transmission can quickly evolve into nosocomial outbreak with staff infection and quarantine which lead to health-care system collapse. In this article, we will discuss the challenges in various aspects of STEMI management during COVID-19, as well as the mitigation measures we can take to optimize outcome and our future.","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"6 1","pages":"218 - 230"},"PeriodicalIF":0.0,"publicationDate":"2021-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47272021","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}
Pub Date : 2021-10-01Epub Date: 2021-12-30DOI: 10.4103/2470-7511.334404
Jun Ren
{"title":"Cardiovascular medicine in the era of COVID-19 pandemics.","authors":"Jun Ren","doi":"10.4103/2470-7511.334404","DOIUrl":"10.4103/2470-7511.334404","url":null,"abstract":"","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"6 1","pages":"199-201"},"PeriodicalIF":0.0,"publicationDate":"2021-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8951666/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46144437","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-10-01DOI: 10.4103/2470-7511.334397
Jia Guang-Hong, J. Sowers
The global coronavirus disease-19 (COVID-19) pandemic, caused by severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2), has created an unprecedented, global public health crisis. Epidemiological studies showed that hypertension is a frequent comorbidity, as well as an independent prognostic risk factor in patients with COVID-19. Angiotensin-converting enzyme-2 (ACE-2) is a receptor for SARS-CoV-2, and thus essential for viral entry into human cells. This review summarizes the recent findings of epidemiology of hypertension in COVID-19 patients and highlights the critical role of ACE2. We also review the impact of endothelial dysfunction, inflammation, and arterial stiffness in promoting hypertension and cardiovascular disease in COVID-19 patients. This review also discusses therapeutic strategies for managing hypertension in patients with COVID-19, with particular emphasis on ACE inhibitors, angiotensin receptor blockers, and calcium channel blockers.
{"title":"Management of hypertension in patients with COVID-19: Implication of angiotensin-converting enzyme 2","authors":"Jia Guang-Hong, J. Sowers","doi":"10.4103/2470-7511.334397","DOIUrl":"https://doi.org/10.4103/2470-7511.334397","url":null,"abstract":"The global coronavirus disease-19 (COVID-19) pandemic, caused by severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2), has created an unprecedented, global public health crisis. Epidemiological studies showed that hypertension is a frequent comorbidity, as well as an independent prognostic risk factor in patients with COVID-19. Angiotensin-converting enzyme-2 (ACE-2) is a receptor for SARS-CoV-2, and thus essential for viral entry into human cells. This review summarizes the recent findings of epidemiology of hypertension in COVID-19 patients and highlights the critical role of ACE2. We also review the impact of endothelial dysfunction, inflammation, and arterial stiffness in promoting hypertension and cardiovascular disease in COVID-19 patients. This review also discusses therapeutic strategies for managing hypertension in patients with COVID-19, with particular emphasis on ACE inhibitors, angiotensin receptor blockers, and calcium channel blockers.","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"6 1","pages":"210 - 217"},"PeriodicalIF":0.0,"publicationDate":"2021-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49137076","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}
Pub Date : 2021-07-01DOI: 10.4103/2470-7511.327241
Lifan Yang, W. Pan, L. Guan, Xiao-chun Zhang, Lei Zhang, Shasha Chen, Daxin Zhou, J. Ge
Objectives: Patients undergoing trans-carotid transcatheter aortic valve replacement (TC-TAVR) are more likely to suffer from a stroke because of cerebral blood hypoperfusion and blood occlusion caused by the introducer sheath compared with the trans-femoral (TF) approach. The present study aimed to compare the incidence of stroke between the TC and TF approaches and explore the causes of stroke after TAVR. Methods: We retrospectively reviewed the medical records of 414 consecutive patients with severe aortic valve stenosis who underwent TC- or TF-TAVR at our center from October 2010 to November 2019; these patients were included in this observational study. The clinical data, such as the incidence of stroke, were compared between TC- and TF-TAVR patients. The correlation between carotid artery blood block interval (CABBI) and neurological events was also analyzed. The study was approved by the Ethics Committee of Zhongshan Hospital of Fudan University (approval No. YL2014-32). Results: Patients undergoing TC-TAVR had a significantly higher incidence of stroke than those undergoing TF-TAVR (12.5% vs. 0, P < 0.001), whereas the baseline data and the incidence of other complications did not differ significantly between the patients undergoing TC- and TF-TAVR (P > 0.05). Moreover, in TC-TAVR patients, the average CABBI of stroke was significantly longer than that of nonstroke patients (61.7 ± 20.7 min vs. 25.1 ± 1.6 min, P = 0.001). The number of patients with CABBI >30 min in the stroke group was greater than that in the nonstroke group (P < 0.001). Conclusions: In the absence of the cerebral and carotid artery evaluation before TAVR, surgeons should take into consideration the time of CABBI <30 min to avoid the possibility of stroke.
目的:与经股动脉(TF)入路相比，经颈动脉经导管主动脉瓣置换术(TC-TAVR)患者更容易发生脑卒中，因为引入器鞘引起的脑血灌注不足和血液闭塞。本研究旨在比较TAVR入路与TF入路的卒中发生率，并探讨TAVR后卒中的原因。方法:回顾性分析2010年10月至2019年11月在本中心连续接受TC或TF-TAVR治疗的414例严重主动脉瓣狭窄患者的病历;这些患者被纳入这项观察性研究。比较TC- tavr和TF-TAVR患者的临床资料，如卒中发生率。分析颈动脉血阻断间隔(CABBI)与神经事件的相关性。本研究已获复旦大学中山医院伦理委员会批准(批准号:YL2014-32)。结果:TC- tavr患者卒中发生率明显高于TF-TAVR患者(12.5% vs. 0, P < 0.001)，而TC- tavr和TF-TAVR患者的基线数据和其他并发症发生率无显著差异(P < 0.05)。此外，TC-TAVR患者卒中的平均CABBI明显长于非卒中患者(61.7±20.7 min vs. 25.1±1.6 min, P = 0.001)。卒中组bbb30 min发生CABBI的患者数大于非卒中组(P < 0.001)。结论:在TAVR术前未进行脑动脉和颈动脉评估的情况下，外科医生应考虑CABBI时间< 30min，以避免发生脑卒中的可能性。
{"title":"Association between stroke and carotid artery blood block interval in trans-carotid transcatheter aortic valve replacement: A retrospective observational study","authors":"Lifan Yang, W. Pan, L. Guan, Xiao-chun Zhang, Lei Zhang, Shasha Chen, Daxin Zhou, J. Ge","doi":"10.4103/2470-7511.327241","DOIUrl":"https://doi.org/10.4103/2470-7511.327241","url":null,"abstract":"Objectives: Patients undergoing trans-carotid transcatheter aortic valve replacement (TC-TAVR) are more likely to suffer from a stroke because of cerebral blood hypoperfusion and blood occlusion caused by the introducer sheath compared with the trans-femoral (TF) approach. The present study aimed to compare the incidence of stroke between the TC and TF approaches and explore the causes of stroke after TAVR. Methods: We retrospectively reviewed the medical records of 414 consecutive patients with severe aortic valve stenosis who underwent TC- or TF-TAVR at our center from October 2010 to November 2019; these patients were included in this observational study. The clinical data, such as the incidence of stroke, were compared between TC- and TF-TAVR patients. The correlation between carotid artery blood block interval (CABBI) and neurological events was also analyzed. The study was approved by the Ethics Committee of Zhongshan Hospital of Fudan University (approval No. YL2014-32). Results: Patients undergoing TC-TAVR had a significantly higher incidence of stroke than those undergoing TF-TAVR (12.5% vs. 0, P < 0.001), whereas the baseline data and the incidence of other complications did not differ significantly between the patients undergoing TC- and TF-TAVR (P > 0.05). Moreover, in TC-TAVR patients, the average CABBI of stroke was significantly longer than that of nonstroke patients (61.7 ± 20.7 min vs. 25.1 ± 1.6 min, P = 0.001). The number of patients with CABBI >30 min in the stroke group was greater than that in the nonstroke group (P < 0.001). Conclusions: In the absence of the cerebral and carotid artery evaluation before TAVR, surgeons should take into consideration the time of CABBI <30 min to avoid the possibility of stroke.","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"6 1","pages":"181 - 186"},"PeriodicalIF":0.0,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45770779","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}
Pub Date : 2021-07-01DOI: 10.4103/2470-7511.327240
Hui-Wen Zhang, Yuan-Lin Guo, Cheng-gang Zhu, N. Wu, Ying Gao, Q. Dong, Jing Sun, Jian‐Jun Li
Background and Objectives: Patients with nonobstructive coronary artery disease (NOCAD) have an increased risk of cardiovascular events (CVEs) compared to that in individuals with normal or near-normal coronary arteries (NNCAs) and even a similar risk to that in individuals with obstructive coronary artery disease (OCAD). However, the predictors for a worse outcome in patients with NOCAD are not fully determined. This study aimed to investigate the association of high-sensitive C-reactive protein (hs-CRP) and CVEs in patients with NOCAD. Materials and Methods: In total, 4662 patients with coronary artery angiography were enrolled and followed up for CVE. Patients were classified as having NNCA (<20% stenosis, n = 698, 15.0%), NOCAD (20%–49% stenosis, n = 639, 14.3%), and OCAD (≥50% stenosis, n = 3325, 70.7%) and then further subdivided into three groups based on their baseline hs-CRP level (<1, 1–3, and >3 mg/L). Proportional hazards models were used to assess the risk of CVEs. Results: Over an average 13403 person-year follow-up, 338 patients experienced CVEs. Patients with NOCAD and OCAD had a higher rate of CVE than those with NNCA (P < 0.05). The CVE risk was significantly higher in NOCAD (hazard ratio [HR]: 2.31, 95% confidence interval [CI]: 1.30–4.01, P = 0.004) and OCAD (HR: 3.09, 95% CI: 1.88–5.07, P < 0.001) patients than in NNCA patients. Moreover, elevated hs-CRP levels were associated with an incremental rate of CVE (P < 0.05). Conclusions: Patients with NOCAD had worse outcomes and elevated hs-CRP levels were positively associated with CVEs, which potentially helps assess risk in NOCAD patients.
{"title":"The relationship between c-reactive protein and cardiovascular events in patients with obstructive and nonobstructive coronary artery disease","authors":"Hui-Wen Zhang, Yuan-Lin Guo, Cheng-gang Zhu, N. Wu, Ying Gao, Q. Dong, Jing Sun, Jian‐Jun Li","doi":"10.4103/2470-7511.327240","DOIUrl":"https://doi.org/10.4103/2470-7511.327240","url":null,"abstract":"Background and Objectives: Patients with nonobstructive coronary artery disease (NOCAD) have an increased risk of cardiovascular events (CVEs) compared to that in individuals with normal or near-normal coronary arteries (NNCAs) and even a similar risk to that in individuals with obstructive coronary artery disease (OCAD). However, the predictors for a worse outcome in patients with NOCAD are not fully determined. This study aimed to investigate the association of high-sensitive C-reactive protein (hs-CRP) and CVEs in patients with NOCAD. Materials and Methods: In total, 4662 patients with coronary artery angiography were enrolled and followed up for CVE. Patients were classified as having NNCA (<20% stenosis, n = 698, 15.0%), NOCAD (20%–49% stenosis, n = 639, 14.3%), and OCAD (≥50% stenosis, n = 3325, 70.7%) and then further subdivided into three groups based on their baseline hs-CRP level (<1, 1–3, and >3 mg/L). Proportional hazards models were used to assess the risk of CVEs. Results: Over an average 13403 person-year follow-up, 338 patients experienced CVEs. Patients with NOCAD and OCAD had a higher rate of CVE than those with NNCA (P < 0.05). The CVE risk was significantly higher in NOCAD (hazard ratio [HR]: 2.31, 95% confidence interval [CI]: 1.30–4.01, P = 0.004) and OCAD (HR: 3.09, 95% CI: 1.88–5.07, P < 0.001) patients than in NNCA patients. Moreover, elevated hs-CRP levels were associated with an incremental rate of CVE (P < 0.05). Conclusions: Patients with NOCAD had worse outcomes and elevated hs-CRP levels were positively associated with CVEs, which potentially helps assess risk in NOCAD patients.","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"6 1","pages":"166 - 173"},"PeriodicalIF":0.0,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46761473","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}
Background and Objectives: Sodium-glucose co-transporter 2 inhibitors (SGLT2is) significantly reduce the risk of cardiovascular events in patients with type 2 diabetes mellitus (T2DM). However, the effectiveness of SGLT2is in heart failure (HF) treatment has not yet been established. The aim of this meta-analysis was to assess the efficacy and safety of SGLT2is in HF treatment by focusing on cardiovascular death (CVD), hospitalization for HF (HHF), and a composite of CVD and HHF. Methods: We searched literature sources in PubMed, EMBASE, and Cochrane Library up until December 20, 2020. Only randomized controlled trials were included in this meta-analysis. We compared the treatment and placebo groups in terms of their associated risks of CVD and HHF and their safety endpoints. The Cochrane tool for assessing risk of bias in randomized trials was applied. Results: The 10 selected studies included 17,043 HF patients and dapagliflozin, empagliflozin, canagliflozin, ertugliflozin, and sotagliflozin as experimental arms. At least 4 included studies were with high quality. For CVD, HHF, and their composite, the pooled risk ratio estimates were 0.87 (95% confidence interval [CI], 0.78–0.96; P = 0.004), 0.70 (95% CI, 0.65–0.76; P < 0.001), and 0.76 (95% CI, 0.71–0.81; P < 0.001), respectively. The incidence of volume depletion, hypoglycemia events, fractures, acute renal injury, and urogenital tract infection was not significantly higher in the SGLT2i group than in the placebo group. Stratified analyses showed similar efficacy and safety results for HF patients with T2DM, those without T2DM, and those being treated with different types of SGLT2is. Conclusions: This meta-analysis demonstrated that various SGLT2is significantly decreased the risks of CVD and HHF in HF patients with and without T2DM. It also showed that clinical administration of SGLT2is was relatively safe in terms of the aforementioned risk factors. SGLT2is might embrace broader clinical application in future HF treatment.
{"title":"Efficacy and safety of sodium-glucose co-transporter 2 inhibitors in heart failure patients: A systematic review and meta-analysis of randomized controlled trials","authors":"Yucheng Wang, Ming-hui Li, Ying Yu, Hui Shi, Ruizhen Chen","doi":"10.4103/2470-7511.327238","DOIUrl":"https://doi.org/10.4103/2470-7511.327238","url":null,"abstract":"Background and Objectives: Sodium-glucose co-transporter 2 inhibitors (SGLT2is) significantly reduce the risk of cardiovascular events in patients with type 2 diabetes mellitus (T2DM). However, the effectiveness of SGLT2is in heart failure (HF) treatment has not yet been established. The aim of this meta-analysis was to assess the efficacy and safety of SGLT2is in HF treatment by focusing on cardiovascular death (CVD), hospitalization for HF (HHF), and a composite of CVD and HHF. Methods: We searched literature sources in PubMed, EMBASE, and Cochrane Library up until December 20, 2020. Only randomized controlled trials were included in this meta-analysis. We compared the treatment and placebo groups in terms of their associated risks of CVD and HHF and their safety endpoints. The Cochrane tool for assessing risk of bias in randomized trials was applied. Results: The 10 selected studies included 17,043 HF patients and dapagliflozin, empagliflozin, canagliflozin, ertugliflozin, and sotagliflozin as experimental arms. At least 4 included studies were with high quality. For CVD, HHF, and their composite, the pooled risk ratio estimates were 0.87 (95% confidence interval [CI], 0.78–0.96; P = 0.004), 0.70 (95% CI, 0.65–0.76; P < 0.001), and 0.76 (95% CI, 0.71–0.81; P < 0.001), respectively. The incidence of volume depletion, hypoglycemia events, fractures, acute renal injury, and urogenital tract infection was not significantly higher in the SGLT2i group than in the placebo group. Stratified analyses showed similar efficacy and safety results for HF patients with T2DM, those without T2DM, and those being treated with different types of SGLT2is. Conclusions: This meta-analysis demonstrated that various SGLT2is significantly decreased the risks of CVD and HHF in HF patients with and without T2DM. It also showed that clinical administration of SGLT2is was relatively safe in terms of the aforementioned risk factors. SGLT2is might embrace broader clinical application in future HF treatment.","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"6 1","pages":"156 - 165"},"PeriodicalIF":0.0,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43848324","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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