Pub Date : 2022-04-01DOI: 10.1097/CP9.0000000000000011
Hongming Zhu, Jingjing Hu, Z. Dong, Yang Liu, Xiaolei Sun, A. Sun
Abstract Background and purpose: Nitroglycerin tolerance is a common phenomenon in patients with coronary artery disease (CAD). Aldehyde dehydrogenase 2 (ALDH2) is the enzyme that metabolizes nitroglycerin to its active form nitric oxide (NO). Previous studies showed altered nitroglycerin in subjects with ALDH2 mutation, but the functional impact on endothelial cells is not fully understood. Methods: In the first step of in vitro experiments, we examined functional properties of induced pluripotent stem cell-derived CD144+ endothelial cells (iPSC-ECs) that expressed wildtype (WT) vs ALDH2+/− variant. In the second step of human studies, diameter of the left anterior descending (LAD) coronary artery was determined using angiography in 151 adult volunteers (111 with WT ALDH2, 32 with ALDH2+/− and 8 with ALDH2−/− genotype) prior to as well as after intracoronary injection of 200-μg nitroglycerin. Results: Briefly, the ALDH2+/− iPSC-ECs demonstrated impaired low-density lipoprotein (LDL) uptake, proliferation, migration, tube formation, oxidative stress resistance, and viability. In comparison to the WT control, the ALDH2+/− iPSC-ECs had elevated NO production under baseline conditions, but exhibited a delayed NO release after nitroglycerin treatment. Exposure to 10-μg/mL nitroglycerin for 2 h increased NO production in WT iPSC-ECs but 4-h exposure was required to stimulate NO production in the ALDH2+/− iPSC-ECs. In comparison to the WT control, the subjects carrying the ALDH2+/− variants had seemingly larger LAD coronary artery diameter (3.5 and 3.8 mm vs 3.4 mm in the WT control), but attenuated vasodilatory response to nitroglycerin (ALDH2MUT group vs the WT control, 7.1 ± 0.6% vs 10.1 ± 0.8%, P = 0.024). Conclusion: These findings indicated elevated NO production by endothelia cells under basal conditions but attenuated response to nitroglycerin upon ALDH2 mutation.
背景与目的:硝酸甘油耐受是冠状动脉疾病(CAD)患者的常见现象。醛脱氢酶2 (ALDH2)是一种将硝酸甘油代谢为活性形式一氧化氮(NO)的酶。先前的研究表明，ALDH2突变受试者的硝酸甘油发生了改变，但对内皮细胞的功能影响尚不完全清楚。方法:在体外实验的第一步，我们检测了表达野生型(WT)和ALDH2+/−变体的诱导多能干细胞衍生的CD144+内皮细胞(iPSC-ECs)的功能特性。在人体研究的第二步，在冠状动脉内注射200 μg硝酸甘油之前和之后，通过血管造影确定151名成年志愿者(WT ALDH2型111人，ALDH2+/ -型32人，ALDH2 - / -型8人)的左前降支(LAD)冠状动脉直径。结果:简而言之，ALDH2+/−iPSC-ECs表现出低密度脂蛋白(LDL)摄取，增殖，迁移，管形成，氧化应激抗性和活力受损。与WT对照相比，ALDH2+/−iPSC-ECs在基线条件下产生的NO增加，但在硝酸甘油处理后表现出延迟的NO释放。10-μg/mL硝酸甘油暴露2小时可增加WT ipsc - ec中NO的产生，但要刺激ALDH2+/−ipsc - ec中NO的产生，则需要暴露4小时。与WT对照组相比，携带ALDH2+/−变异的受试者LAD冠状动脉直径似乎更大(3.5和3.8 mm vs WT对照组3.4 mm)，但对硝酸甘油的血管舒张反应减弱(ALDH2MUT组vs WT对照组，7.1±0.6% vs 10.1±0.8%，P = 0.024)。结论:这些发现表明内皮细胞在基础条件下产生一氧化氮增加，但在ALDH2突变后对硝酸甘油的反应减弱。
{"title":"ALDH2 mutation results in excessive basal nitric oxide production and a delayed response to nitroglycerin","authors":"Hongming Zhu, Jingjing Hu, Z. Dong, Yang Liu, Xiaolei Sun, A. Sun","doi":"10.1097/CP9.0000000000000011","DOIUrl":"https://doi.org/10.1097/CP9.0000000000000011","url":null,"abstract":"Abstract Background and purpose: Nitroglycerin tolerance is a common phenomenon in patients with coronary artery disease (CAD). Aldehyde dehydrogenase 2 (ALDH2) is the enzyme that metabolizes nitroglycerin to its active form nitric oxide (NO). Previous studies showed altered nitroglycerin in subjects with ALDH2 mutation, but the functional impact on endothelial cells is not fully understood. Methods: In the first step of in vitro experiments, we examined functional properties of induced pluripotent stem cell-derived CD144+ endothelial cells (iPSC-ECs) that expressed wildtype (WT) vs ALDH2+/− variant. In the second step of human studies, diameter of the left anterior descending (LAD) coronary artery was determined using angiography in 151 adult volunteers (111 with WT ALDH2, 32 with ALDH2+/− and 8 with ALDH2−/− genotype) prior to as well as after intracoronary injection of 200-μg nitroglycerin. Results: Briefly, the ALDH2+/− iPSC-ECs demonstrated impaired low-density lipoprotein (LDL) uptake, proliferation, migration, tube formation, oxidative stress resistance, and viability. In comparison to the WT control, the ALDH2+/− iPSC-ECs had elevated NO production under baseline conditions, but exhibited a delayed NO release after nitroglycerin treatment. Exposure to 10-μg/mL nitroglycerin for 2 h increased NO production in WT iPSC-ECs but 4-h exposure was required to stimulate NO production in the ALDH2+/− iPSC-ECs. In comparison to the WT control, the subjects carrying the ALDH2+/− variants had seemingly larger LAD coronary artery diameter (3.5 and 3.8 mm vs 3.4 mm in the WT control), but attenuated vasodilatory response to nitroglycerin (ALDH2MUT group vs the WT control, 7.1 ± 0.6% vs 10.1 ± 0.8%, P = 0.024). Conclusion: These findings indicated elevated NO production by endothelia cells under basal conditions but attenuated response to nitroglycerin upon ALDH2 mutation.","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"7 1","pages":"85 - 91"},"PeriodicalIF":0.0,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47000085","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 : 2022-04-01DOI: 10.1097/CP9.0000000000000006
X. Zhuang, S. Luo, Huizhi Fan, Jin-Jin Zhang, Hua Chen, Ping-ping Yan, Liwen Bao
Abstract A 26-year-old young man presented with paroxysmal chest pain and systemic edema that started 2 years earlier and worsened during the past 2 months. Echocardiogram indicated total heart enlargement as well as severe left and right ventricular systolic dysfunction. MRI revealed atrophy of most muscles in the thigh and calf on both sides. EMG suggested myogenic damage to myoelectrical changes and early recruitment changes. A diagnosis of Duchenne muscular dystrophy (DMD) was established on biopsy and genetic testing showing deletion of exons 45 and 49 of the dystrophin gene. He had no family history of major cardiovascular diseases. The patient disclosed later that muscle weakening started at 7 years of age. Symptoms improved after treatment with a variety of agents to manage heart failure and complications, and was discharged. He survived for 2 years, during which the general condition and heart failure deteriorated progressively. In summary, skeletal muscle weakness is typically the first sign of DMD, but heart involvement is commonly seen later. With the current treatment options, prognosis is poor. Gene therapy might be warranted.
{"title":"Duchenne muscular dystrophy and dilated cardiomyopathy with deletion of exon 45 and 49","authors":"X. Zhuang, S. Luo, Huizhi Fan, Jin-Jin Zhang, Hua Chen, Ping-ping Yan, Liwen Bao","doi":"10.1097/CP9.0000000000000006","DOIUrl":"https://doi.org/10.1097/CP9.0000000000000006","url":null,"abstract":"Abstract A 26-year-old young man presented with paroxysmal chest pain and systemic edema that started 2 years earlier and worsened during the past 2 months. Echocardiogram indicated total heart enlargement as well as severe left and right ventricular systolic dysfunction. MRI revealed atrophy of most muscles in the thigh and calf on both sides. EMG suggested myogenic damage to myoelectrical changes and early recruitment changes. A diagnosis of Duchenne muscular dystrophy (DMD) was established on biopsy and genetic testing showing deletion of exons 45 and 49 of the dystrophin gene. He had no family history of major cardiovascular diseases. The patient disclosed later that muscle weakening started at 7 years of age. Symptoms improved after treatment with a variety of agents to manage heart failure and complications, and was discharged. He survived for 2 years, during which the general condition and heart failure deteriorated progressively. In summary, skeletal muscle weakness is typically the first sign of DMD, but heart involvement is commonly seen later. With the current treatment options, prognosis is poor. Gene therapy might be warranted.","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"7 1","pages":"97 - 101"},"PeriodicalIF":0.0,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43784092","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 : 2022-04-01DOI: 10.1097/cp9.0000000000000017
Jaqui Walker
Professor Junbo Ge welcomed speakers and attendees both present (25, 600) and virtual (120,000) to the International Aspirin Foundation (IAF) Symposium at the Oriental Congress of Cardiology (OCC). He introduced aspirin as the cornerstone of antiplatelet therapy with evidence for its efficacy and safety in cardiovascular disease (CVD) prevention accumulating since the 1970s. Aspirin works by irreversibly inactivating the cyclooxygenase (COX) activity of the ubiquitous bifunctional enzyme, prostaglandin (PG)G/H-synthase, which catalyzes the conversion of arachidonic acid to PGG 2 (through its COX activity) and PGH 2 (through its peroxidase activity) 1 . PGH 2 is a common intermediate in the biosynthesis of different prostanoids (e.g., PGE 2 , thromboxane [TX] A 2 and prostacyclin [PGI 2 ]), through the action of tissue-specific isomerases and synthases. three clinical case studies to illustrate his perspectives on aspirin’s role in the prevention of cardiovascular events using data from both primary and secondary prevention trials. For secondary prevention of CVD, in those with known atherosclerotic disease prior myocardial infarction the that risk of in serious thrombotic atrial clear benefits for low-dose aspirin. Two of Professor Gaziano’s case studies illustrated the types of people benefiting from aspirin for the secondary prevention of CVD. There are over 13.7 million new strokes worldwide each year, with individuals having a lifetime risk of 20%. TIA and minor stroke comprise 70% of all acute cerebrovascular events and often herald an impending major stroke, with seven-day risk of major stroke as high as 10% 1,2 . However, urgent medical assessment and treatment are very effective in preventing early recurrent major stroke. The EXPRESS study showed urgent investigation/treatment after TIA and minor stroke reduced the 90-day risk of major recurrent stroke by about 80% - one of the most effective interventions in medicine 3,4 . This benefit was achieved by changing care from non-urgent general practice prescribing to urgent assessment and treatment using existing medications. Other studies show similar feasibility and results 5 . However, the EXPRESS Study intervention was multifactorial, including aspirin, other antiplatelet drugs in high-risk patients, BP-lowering drugs and statins, and it was uncertain which component had reduced stroke risk. Aspirin was given to all patients, but the effect of aspirin on recurrent stroke risk had long been considered modest, based on trials in acute major stroke and in long-term prevention after TIA/minor stroke. By detailed re-analysis of individual patient data from these trials, it was shown the acute benefits of aspirin in TIA/minor stroke had been considerably underestimated, showing that aspirin alone reduced 90-day risk of disabling recurrent stroke by 80% and of all stroke by 60% 6 . Despite patients given benefits of aspirin. this, Professor Rothwell has with guideline writers recommend low-dose
{"title":"Low-dose aspirin for the prevention of atherothrombosis across the cardiovascular risk continuum","authors":"Jaqui Walker","doi":"10.1097/cp9.0000000000000017","DOIUrl":"https://doi.org/10.1097/cp9.0000000000000017","url":null,"abstract":"Professor Junbo Ge welcomed speakers and attendees both present (25, 600) and virtual (120,000) to the International Aspirin Foundation (IAF) Symposium at the Oriental Congress of Cardiology (OCC). He introduced aspirin as the cornerstone of antiplatelet therapy with evidence for its efficacy and safety in cardiovascular disease (CVD) prevention accumulating since the 1970s. Aspirin works by irreversibly inactivating the cyclooxygenase (COX) activity of the ubiquitous bifunctional enzyme, prostaglandin (PG)G/H-synthase, which catalyzes the conversion of arachidonic acid to PGG 2 (through its COX activity) and PGH 2 (through its peroxidase activity) 1 . PGH 2 is a common intermediate in the biosynthesis of different prostanoids (e.g., PGE 2 , thromboxane [TX] A 2 and prostacyclin [PGI 2 ]), through the action of tissue-specific isomerases and synthases. three clinical case studies to illustrate his perspectives on aspirin’s role in the prevention of cardiovascular events using data from both primary and secondary prevention trials. For secondary prevention of CVD, in those with known atherosclerotic disease prior myocardial infarction the that risk of in serious thrombotic atrial clear benefits for low-dose aspirin. Two of Professor Gaziano’s case studies illustrated the types of people benefiting from aspirin for the secondary prevention of CVD. There are over 13.7 million new strokes worldwide each year, with individuals having a lifetime risk of 20%. TIA and minor stroke comprise 70% of all acute cerebrovascular events and often herald an impending major stroke, with seven-day risk of major stroke as high as 10% 1,2 . However, urgent medical assessment and treatment are very effective in preventing early recurrent major stroke. The EXPRESS study showed urgent investigation/treatment after TIA and minor stroke reduced the 90-day risk of major recurrent stroke by about 80% - one of the most effective interventions in medicine 3,4 . This benefit was achieved by changing care from non-urgent general practice prescribing to urgent assessment and treatment using existing medications. Other studies show similar feasibility and results 5 . However, the EXPRESS Study intervention was multifactorial, including aspirin, other antiplatelet drugs in high-risk patients, BP-lowering drugs and statins, and it was uncertain which component had reduced stroke risk. Aspirin was given to all patients, but the effect of aspirin on recurrent stroke risk had long been considered modest, based on trials in acute major stroke and in long-term prevention after TIA/minor stroke. By detailed re-analysis of individual patient data from these trials, it was shown the acute benefits of aspirin in TIA/minor stroke had been considerably underestimated, showing that aspirin alone reduced 90-day risk of disabling recurrent stroke by 80% and of all stroke by 60% 6 . Despite patients given benefits of aspirin. this, Professor Rothwell has with guideline writers recommend low-dose ","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42428058","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 : 2022-04-01DOI: 10.1097/CP9.0000000000000012
L. Qi, Shu-Lian Zhao, Jiyan Chen, Mei Zhang, Xiaodong Li, Yugang Dong, Xiaomei Guo, Kaikai Huang, Fang Wang, Y. Huo, J. Ge
Abstract Background and purpose: Hybutimibe is proved to be safe in healthy adults by a phase I study. A multi-center, randomized, double-blind phase II clinical trial evaluated its effectiveness and safety of Hybutimibe in the treatment of primary hypercholesterolemia. Methods: A total of 244 patients between August 2014 and August 2015, with primary hypercholesterolemia from 15 centers in China were enrolled and randomly assigned to receive placebo, ezetimibe, or hybutimibe 5, 10, or 20 mg/day in a 1:1:1:1:1 ratio. The primary outcome was evaluated from the change rate of low-density lipoprotein cholesterol (LDL-C) at week 8 from baseline, whereas secondary outcomes were evaluated from the change rates of LDL-C, TC, TG, HDL-C, non-HDL-C, APO-B, APO-A1 at weeks 1, 2, 4, and 8 from baseline. Results: After 8 weeks of treatment, the average decrease rate of LDL-C was −20.01% for ezetimibe, −10.84% (95% CI: −14.67, −7.00) for hybutimibe 5 mg/day, −17.06% (95% CI: −20.83, −13.29) for hybutimibe 10 mg/day, and −17.04% (95% CI: −20.30, −13.79) for hybutimibe 20 mg/day, respectively. The change rates of TC, non-HDL-C, and APO-B levels were significantly improved in all treatments compared with placebo (P < 0.05), whereas changes in the above lipid profiles of hybutimibe 20 mg/day were similar with ezetimibe. In terms of safety, the most common adverse events were elevation in ALT, gastrointestinal reaction, dizziness, and headache. Conclusions: This clinical study found that hybutimibe with the least dose of 5 mg/day effectively improved the LDL-C, TC, non-HDL-C, and APO-B levels in patients with primary hyperlipidemia with good tolerance and safety with no significant effect on TG levels.
{"title":"Efficacy and safety of hybutimibe on primary hypercholesterolemia: a randomized, double-blinded, placebo and positive–controlled, parallel phase II study","authors":"L. Qi, Shu-Lian Zhao, Jiyan Chen, Mei Zhang, Xiaodong Li, Yugang Dong, Xiaomei Guo, Kaikai Huang, Fang Wang, Y. Huo, J. Ge","doi":"10.1097/CP9.0000000000000012","DOIUrl":"https://doi.org/10.1097/CP9.0000000000000012","url":null,"abstract":"Abstract Background and purpose: Hybutimibe is proved to be safe in healthy adults by a phase I study. A multi-center, randomized, double-blind phase II clinical trial evaluated its effectiveness and safety of Hybutimibe in the treatment of primary hypercholesterolemia. Methods: A total of 244 patients between August 2014 and August 2015, with primary hypercholesterolemia from 15 centers in China were enrolled and randomly assigned to receive placebo, ezetimibe, or hybutimibe 5, 10, or 20 mg/day in a 1:1:1:1:1 ratio. The primary outcome was evaluated from the change rate of low-density lipoprotein cholesterol (LDL-C) at week 8 from baseline, whereas secondary outcomes were evaluated from the change rates of LDL-C, TC, TG, HDL-C, non-HDL-C, APO-B, APO-A1 at weeks 1, 2, 4, and 8 from baseline. Results: After 8 weeks of treatment, the average decrease rate of LDL-C was −20.01% for ezetimibe, −10.84% (95% CI: −14.67, −7.00) for hybutimibe 5 mg/day, −17.06% (95% CI: −20.83, −13.29) for hybutimibe 10 mg/day, and −17.04% (95% CI: −20.30, −13.79) for hybutimibe 20 mg/day, respectively. The change rates of TC, non-HDL-C, and APO-B levels were significantly improved in all treatments compared with placebo (P < 0.05), whereas changes in the above lipid profiles of hybutimibe 20 mg/day were similar with ezetimibe. In terms of safety, the most common adverse events were elevation in ALT, gastrointestinal reaction, dizziness, and headache. Conclusions: This clinical study found that hybutimibe with the least dose of 5 mg/day effectively improved the LDL-C, TC, non-HDL-C, and APO-B levels in patients with primary hyperlipidemia with good tolerance and safety with no significant effect on TG levels.","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"7 1","pages":"77 - 84"},"PeriodicalIF":0.0,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41895719","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 : 2022-04-01DOI: 10.1097/CP9.0000000000000013
Jianjun Li
Familial hypercholesterolemia (FH) is one of the most common genetic disorders characterized by a predominant elevation in plasma low-density lipoprotein (LDL) cholesterol (LDL-C) concentration and higher incidence of premature atherosclerotic cardiovascular disease (ASCVD). It has been reported that the long-term coronary artery disease (CAD) and ASCVD risk in the US adults with the FH phenotype are up to approximately five-fold higher than that in the general population.[1] It has also been estimated that there is an important longterm burden of ASCVD in phenotypic but undiagnosed FH patients in the US, with the acceleration of CAD risk by 20–30years.[1] In recent years, the features of underdiagnosis and under-treatment of FH patients has attained an intensive attention worldwide.[2] This increased risk is age dependent, with the highest relative risk in younger index ages. Notably, several atherosclerosisrelated international academic organizations or societies have issued statements or guidelines consequently, which call for the actions to improve the diagnosis and treatment of this unique, treatable disease globally.[3–6] In the Asia Pacific region, FH is estimated to affect at least 15 million people.[7] Among them, China alone may account for more than half of the FH patients as it is the world’s most populous country. The general knowledge regarding FH is not very unfamiliar for medical professionals. Premature ASCVD is a great concern in FH patients due to the extremely high plasma LDL-C concentration. If homozygous FH (HoFH) is left untreated, tendon xanthomas may usually be detected.[2] Since the 1950s, FH patients have been divided into heterozygous FH (HeFH) and HoFH, and diagnosing HeFH and HoFH based on the phenotypic features of ASCVD or xanthomas has frequently been difficult without the DNA analysis of FH genes.[3] With the development of genetic testing technology, multiple studies revealed that a severe defect in the ability to bind and internalize LDL particles was caused by mutations in both alleles of the
{"title":"Familial hypercholesterolemia in China requires greater efforts","authors":"Jianjun Li","doi":"10.1097/CP9.0000000000000013","DOIUrl":"https://doi.org/10.1097/CP9.0000000000000013","url":null,"abstract":"Familial hypercholesterolemia (FH) is one of the most common genetic disorders characterized by a predominant elevation in plasma low-density lipoprotein (LDL) cholesterol (LDL-C) concentration and higher incidence of premature atherosclerotic cardiovascular disease (ASCVD). It has been reported that the long-term coronary artery disease (CAD) and ASCVD risk in the US adults with the FH phenotype are up to approximately five-fold higher than that in the general population.[1] It has also been estimated that there is an important longterm burden of ASCVD in phenotypic but undiagnosed FH patients in the US, with the acceleration of CAD risk by 20–30years.[1] In recent years, the features of underdiagnosis and under-treatment of FH patients has attained an intensive attention worldwide.[2] This increased risk is age dependent, with the highest relative risk in younger index ages. Notably, several atherosclerosisrelated international academic organizations or societies have issued statements or guidelines consequently, which call for the actions to improve the diagnosis and treatment of this unique, treatable disease globally.[3–6] In the Asia Pacific region, FH is estimated to affect at least 15 million people.[7] Among them, China alone may account for more than half of the FH patients as it is the world’s most populous country. The general knowledge regarding FH is not very unfamiliar for medical professionals. Premature ASCVD is a great concern in FH patients due to the extremely high plasma LDL-C concentration. If homozygous FH (HoFH) is left untreated, tendon xanthomas may usually be detected.[2] Since the 1950s, FH patients have been divided into heterozygous FH (HeFH) and HoFH, and diagnosing HeFH and HoFH based on the phenotypic features of ASCVD or xanthomas has frequently been difficult without the DNA analysis of FH genes.[3] With the development of genetic testing technology, multiple studies revealed that a severe defect in the ability to bind and internalize LDL particles was caused by mutations in both alleles of the","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"7 1","pages":"61 - 63"},"PeriodicalIF":0.0,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44149927","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 : 2022-04-01DOI: 10.1097/CP9.0000000000000015
Chen Luo, Zhenyue Chen
Abstract Several large prospective cohort studies demonstrated an association between higher cardiovascular disease (CVD) risk with low blood level of omega-3 fatty acids as well as low Omega-3 Index [<4% eicosapentaenoic acid (EPA)+ docosahexaenoic acid (DHA) to total fatty acids in red blood cell membrane]. However, randomized controlled trials of omega-3 fatty acids as either primary or secondary prevention have yielded controversial results. In this review, we summarize the evidence that supports or argues against the use omega-3 fatty acids, with a focus on the underlying mechanisms for the observed discrepancies (eg, differences in dosage, comparators and EPA levels or Omega-3 Index). Omega-3 Index is an independent risk factor for cardiovascular risk. The baseline Omega-3 Index can be used as a reference for whether and how much fish oil should be supplemented. To some degree, it can be used to explain why there are so much inconsistencies in clinical trials. Omega-3 Index could be a promising treatment target in clinical practice and in public health settings although there are still some barriers. This review summarizes current evidences from both epidemiological studies and randomized controlled trials of omega-3 fatty acids as primary and secondary prevention of CVD, and aims to provide a comprehensive overview of fish oil supplements on risk for CVD, and Omega-3 Index as a tool to identify subjects at high risk as well as a treatment target in CVD prevention.
{"title":"Is Omega-3 Index necessary for fish oil supplements for CVD risk prevention?","authors":"Chen Luo, Zhenyue Chen","doi":"10.1097/CP9.0000000000000015","DOIUrl":"https://doi.org/10.1097/CP9.0000000000000015","url":null,"abstract":"Abstract Several large prospective cohort studies demonstrated an association between higher cardiovascular disease (CVD) risk with low blood level of omega-3 fatty acids as well as low Omega-3 Index [<4% eicosapentaenoic acid (EPA)+ docosahexaenoic acid (DHA) to total fatty acids in red blood cell membrane]. However, randomized controlled trials of omega-3 fatty acids as either primary or secondary prevention have yielded controversial results. In this review, we summarize the evidence that supports or argues against the use omega-3 fatty acids, with a focus on the underlying mechanisms for the observed discrepancies (eg, differences in dosage, comparators and EPA levels or Omega-3 Index). Omega-3 Index is an independent risk factor for cardiovascular risk. The baseline Omega-3 Index can be used as a reference for whether and how much fish oil should be supplemented. To some degree, it can be used to explain why there are so much inconsistencies in clinical trials. Omega-3 Index could be a promising treatment target in clinical practice and in public health settings although there are still some barriers. This review summarizes current evidences from both epidemiological studies and randomized controlled trials of omega-3 fatty acids as primary and secondary prevention of CVD, and aims to provide a comprehensive overview of fish oil supplements on risk for CVD, and Omega-3 Index as a tool to identify subjects at high risk as well as a treatment target in CVD prevention.","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"7 1","pages":"70 - 76"},"PeriodicalIF":0.0,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46445527","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 : 2022-04-01DOI: 10.1097/CP9.0000000000000016
Bei Liu, Shujuan Yang, Lixia Yang, Bin Zhang, R. Guo
Abstract Background and purpose: Poor ST-segment resolution (STR) is strongly associated with poor prognosis in patients with ST segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PPCI). previous studies suggested higher HCY level in the people who live in high altitudes, so a retrospective analysis is conducted to examine the potential relationship between elevated serum HCY and poor STR after PPCI at high altitudes. Methods: This retrospective analysis included 308 high-altitude dwelling patients (1800-2200 meters elevation from the sea level) undergoing PPCI for STEMI during a period from September 2021 to March 2022. Clinical data were collected and statistically analyzed. Results: In comparison to the patients with normal plasma homocysteine (≤15 mmol/L; n = 155), patients with elevated homocysteine (>15 mmol/L) had higher percentage of men (92.81% vs. 80.00%; p = 0.001) and smoker (79.08% vs. 63.87%; p = 0.003), but no difference in other key baseline characteristics. The rate of complete ST-segment resolution after PPCI (≥ 70%) was 83.23% in the control group and 49.67% in the elevated HCY group (p ≤ 0.001). In multivariable regression analysis, poor ST-segment resolution (<70%) was independently associated with longer pain-to-balloon time (OR 0.832; 95%CI: 0.775–0.894), lower uric acid (OR 1.003; 95%CI: 1.000-1.005), and elevated HCY (OR 0.957 vs. normal HCY; 95%CI: 0.937–0.977). Conclusion: Elevated plasma HCY level was associated with poor ST segment resolution in patients undergoing PPCI STEMI at high altitude.
{"title":"Elevated plasma homocysteine level is associated with poor ST-segment resolution in patients with ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention at high altitude","authors":"Bei Liu, Shujuan Yang, Lixia Yang, Bin Zhang, R. Guo","doi":"10.1097/CP9.0000000000000016","DOIUrl":"https://doi.org/10.1097/CP9.0000000000000016","url":null,"abstract":"Abstract Background and purpose: Poor ST-segment resolution (STR) is strongly associated with poor prognosis in patients with ST segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PPCI). previous studies suggested higher HCY level in the people who live in high altitudes, so a retrospective analysis is conducted to examine the potential relationship between elevated serum HCY and poor STR after PPCI at high altitudes. Methods: This retrospective analysis included 308 high-altitude dwelling patients (1800-2200 meters elevation from the sea level) undergoing PPCI for STEMI during a period from September 2021 to March 2022. Clinical data were collected and statistically analyzed. Results: In comparison to the patients with normal plasma homocysteine (≤15 mmol/L; n = 155), patients with elevated homocysteine (>15 mmol/L) had higher percentage of men (92.81% vs. 80.00%; p = 0.001) and smoker (79.08% vs. 63.87%; p = 0.003), but no difference in other key baseline characteristics. The rate of complete ST-segment resolution after PPCI (≥ 70%) was 83.23% in the control group and 49.67% in the elevated HCY group (p ≤ 0.001). In multivariable regression analysis, poor ST-segment resolution (<70%) was independently associated with longer pain-to-balloon time (OR 0.832; 95%CI: 0.775–0.894), lower uric acid (OR 1.003; 95%CI: 1.000-1.005), and elevated HCY (OR 0.957 vs. normal HCY; 95%CI: 0.937–0.977). Conclusion: Elevated plasma HCY level was associated with poor ST segment resolution in patients undergoing PPCI STEMI at high altitude.","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"7 1","pages":"92 - 96"},"PeriodicalIF":0.0,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48473235","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 : 2022-03-01DOI: 10.1097/CP9.0000000000000007
E. Ruffino, M. Gori, E. D’Elia, E. Sciatti, V. Shi, M. Senni
Abstract Heart failure with reduced ejection fraction (HFrEF) is a common disease requiring multi-drug therapy. Moreover, it is associated with a poor prognosis, with increasing prevalence in the community. In the last decade, two major drug classes were introduced to the heart failure (HF) specialist's arsenal: angiotensin receptor neprilysin inhibitors (ARNIs) and sodium-glucose-cotransporter 2 inhibitors (SGLT2is). The current paradigm of sequential drug therapy is changing, favoring a multi-drug combination therapy upfront, including four “pillar” classes: beta-blockers, mineralcorticoid receptor antagonists (MRAs), ARNIs, and SGLT-2is. Recent putative placebo analyses of large-scale randomized clinical trials compared a combination of all four drug classes with a standard of care and was in favor of the multi-drug combination revealing a hazard ratio for cardiovascular (CV) death and HF hospitalization of 0.5 and 0.32, respectively. We reviewed the approval landmark trials for the four drug classes and have subincluded a short comment about the implications and impact of each study in clinical practice. Moreover, we present more detailed trials concerning the use of these drugs in different settings (eg, acute phase, in-hospital, and outpatient) and more data about the clinical, biochemical, functional, and echographic remodeling effects of the molecules. The results of the meta-analyses and putative placebo analyses in the literature we reviewed suggest the benefit of offering all the best therapy available upfront. This approach ensures maximal life expectancy gain, especially in younger patients, and cuts the costs of rehospitalizations. Thus, this review underlines the importance of the four-drug approach to HFrEF therapy, as recently stated in the ESC guidelines.
{"title":"Four aces of heart failure therapy: systematic review of established and emerging therapies for heart failure with reduced ejection fraction","authors":"E. Ruffino, M. Gori, E. D’Elia, E. Sciatti, V. Shi, M. Senni","doi":"10.1097/CP9.0000000000000007","DOIUrl":"https://doi.org/10.1097/CP9.0000000000000007","url":null,"abstract":"Abstract Heart failure with reduced ejection fraction (HFrEF) is a common disease requiring multi-drug therapy. Moreover, it is associated with a poor prognosis, with increasing prevalence in the community. In the last decade, two major drug classes were introduced to the heart failure (HF) specialist's arsenal: angiotensin receptor neprilysin inhibitors (ARNIs) and sodium-glucose-cotransporter 2 inhibitors (SGLT2is). The current paradigm of sequential drug therapy is changing, favoring a multi-drug combination therapy upfront, including four “pillar” classes: beta-blockers, mineralcorticoid receptor antagonists (MRAs), ARNIs, and SGLT-2is. Recent putative placebo analyses of large-scale randomized clinical trials compared a combination of all four drug classes with a standard of care and was in favor of the multi-drug combination revealing a hazard ratio for cardiovascular (CV) death and HF hospitalization of 0.5 and 0.32, respectively. We reviewed the approval landmark trials for the four drug classes and have subincluded a short comment about the implications and impact of each study in clinical practice. Moreover, we present more detailed trials concerning the use of these drugs in different settings (eg, acute phase, in-hospital, and outpatient) and more data about the clinical, biochemical, functional, and echographic remodeling effects of the molecules. The results of the meta-analyses and putative placebo analyses in the literature we reviewed suggest the benefit of offering all the best therapy available upfront. This approach ensures maximal life expectancy gain, especially in younger patients, and cuts the costs of rehospitalizations. Thus, this review underlines the importance of the four-drug approach to HFrEF therapy, as recently stated in the ESC guidelines.","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"7 1","pages":"20 - 28"},"PeriodicalIF":0.0,"publicationDate":"2022-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48294937","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 : 2022-03-01DOI: 10.1097/CP9.0000000000000003
Yawei Yang, Jun Yuan, Jing-Fen Xing, M. Fan
Abstract Background: Left ventricular noncompaction (LVNC) is a rare type of cardiomyopathy. The core clinical feature is heart failure that responds poorly to treatments. Case presentation: A 58-year-old woman received various treatments (including metoprolol, benazepril, torasemide, spirolactone, and digoxin) for 4 years for LVNC, but responded poorly. Upon presentation, transthoracic echocardiogram (ECHO) showed 26% left ventricular ejection fraction (LVEF) and class IV diastolic dysfunction. Upon cardiac magnetic resonance imaging (CMRI), the ratio of noncompacted versus compacted myocardium was 3.9. She received guideline-recommended treatments that included sacubitril-valsartan (100 mg/day) in addition to β-blocker, torasemide, spirolactone, digoxin, and isosorbide. Symptoms and signs improved rapidly, and she was discharged 1 week later. Sacubitril-valsartan dosage was adjusted to 200 mg/day 4 weeks later. She remained in relatively good health thereafter. At the last follow-up 16 months later, LVEF was 51% on ECHO. CMRI showed the significantly reduced ratio of 2.8 in noncompacted versus compacted myocardium. Conclusions: Sacubitril-valsartan therapy may result in reverse remodeling and improve long-term outcomes in LVNC patients.
{"title":"Sacubitril-valsartan therapy in a patient with heart failure due to isolated left ventricular noncompaction: a case report and literature review","authors":"Yawei Yang, Jun Yuan, Jing-Fen Xing, M. Fan","doi":"10.1097/CP9.0000000000000003","DOIUrl":"https://doi.org/10.1097/CP9.0000000000000003","url":null,"abstract":"Abstract Background: Left ventricular noncompaction (LVNC) is a rare type of cardiomyopathy. The core clinical feature is heart failure that responds poorly to treatments. Case presentation: A 58-year-old woman received various treatments (including metoprolol, benazepril, torasemide, spirolactone, and digoxin) for 4 years for LVNC, but responded poorly. Upon presentation, transthoracic echocardiogram (ECHO) showed 26% left ventricular ejection fraction (LVEF) and class IV diastolic dysfunction. Upon cardiac magnetic resonance imaging (CMRI), the ratio of noncompacted versus compacted myocardium was 3.9. She received guideline-recommended treatments that included sacubitril-valsartan (100 mg/day) in addition to β-blocker, torasemide, spirolactone, digoxin, and isosorbide. Symptoms and signs improved rapidly, and she was discharged 1 week later. Sacubitril-valsartan dosage was adjusted to 200 mg/day 4 weeks later. She remained in relatively good health thereafter. At the last follow-up 16 months later, LVEF was 51% on ECHO. CMRI showed the significantly reduced ratio of 2.8 in noncompacted versus compacted myocardium. Conclusions: Sacubitril-valsartan therapy may result in reverse remodeling and improve long-term outcomes in LVNC patients.","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"7 1","pages":"56 - 59"},"PeriodicalIF":0.0,"publicationDate":"2022-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41676095","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 : 2022-03-01DOI: 10.1097/cp9.0000000000000005
Y. Dai, J. Ge
{"title":"Managing residual inflammatory risk in atherosclerotic cardiovascular disease: another piece of the puzzle?","authors":"Y. Dai, J. Ge","doi":"10.1097/cp9.0000000000000005","DOIUrl":"https://doi.org/10.1097/cp9.0000000000000005","url":null,"abstract":"","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43142371","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}
京公网安备 11010802042870号
京ICP备2023020795号-1
扫码关注我们
求助内容：
应助结果提醒方式：