目的:探讨急性ST段抬高型心肌梗死(STEMI)患者低密度脂蛋白胆固醇(LDL-C)/高密度脂蛋白胆固醇(HDL-C)比值(LHR)与其院内主要不良心血管事件(MACE)的相关性及其在临床中的应用价值。方法:收集发病12h内就诊的481例STEMI住院患者的临床资...目的:探讨急性ST段抬高型心肌梗死(STEMI)患者低密度脂蛋白胆固醇(LDL-C)/高密度脂蛋白胆固醇(HDL-C)比值(LHR)与其院内主要不良心血管事件(MACE)的相关性及其在临床中的应用价值。方法:收集发病12h内就诊的481例STEMI住院患者的临床资料及MACE发生情况,根据LHR的中位数(2.9)将患者分为低LHR组(LHR≤2.9,n=223)和高LHR组(LHR>2.9,n=258)。分析LHR与STEMI患者院内MACE的相关性。结果:高LHR组患者院内MACE比例均高于低LHR组[恶性室性心律失常:29(11.2%) VS 9(4.0%),P=0.004;高度房室传导阻滞:22(8.5%) VS 6(2.7%),P=0.006;心源性休克+死亡:29(11.2%) VS 7(3.1%),P=0.001]。恶性室性心律失常、心源性休克+死亡患者LHR差异有统计学意义(P均<0.05)。Pearson相关分析显示,除高度房室传导阻滞(r=0.060,P>0.05)外,LHR与恶性室性心律失常(r=0.121)、心源性休克和死亡(r=0.115)均显著相关(P<0.05)。多因素Logistic回归分析显示,LHR、空腹血糖是STEMI患者发生院内MACE的独立危险因素(P均<0.05)。ROC曲线显示LHR预测STEMI患者院内MACE的曲线下面积为0.606(95%CI:0.544~0.668),cut-off值为2.854,敏感度为80.6%,特异度为52.1%;LHR>2.854时STEMI住院患者很可能会发生MACE。结论:STEMI患者LHR升高与恶性室性心律失常、心源性休克及死亡发生呈正相关。LHR是STEMI患者发生MACE的独立危险因素,对恶性室性心律失常、心源性休克及死亡发生有一定的预测价值。展开更多
Acute myocardial infarction is a deadly disease, and in the Indian context, it occurs at a younger age, even below the age of 40 years, and sometimes even below 30 years. These young MI patients have high mortality ra...Acute myocardial infarction is a deadly disease, and in the Indian context, it occurs at a younger age, even below the age of 40 years, and sometimes even below 30 years. These young MI patients have high mortality rates, and many of them are not able to reach the hospital. The pathophysiology of AMI is very well understood. AMI is a multifactorial disease and has several risk factors, like dyslipidemia, diabetes, hypertension, smoking, diet, etc. However, low-density lipoprotein cholesterol (LDL-C) has a very strong causal relationship with atherosclerosis. Reducing LDL-C to <70 results in the arrest of the progression of atherosclerosis, and slashing its level to below 50 produces the regression of atherosclerosis. The cumulative exposure of LDL-C to the arterial wall is a very strong determinant of atherosclerosis and the development of AMI. The coronary heart disease (CHD) threshold target of LDL-C for the development of AMI is roughly 7000 mg/year. If LDL-C is 100 mg/dL from an early age, the CHD threshold target for the development of AMI will reach 70 years of age. However, if LDL-C target is <70 mg/dL from an early age, the patients will reach the CHD threshold of LDL-C at the age of 100 years. Based on the current science, this is an emerging concept to postpone AMI by several years, even up to 100 years. The goal of LDL-C <70 mg/dL can be achieved by available oral or injectable drugs. Gene editing with CRISPR technology is emerging as a very exciting modality for lowering LDL-C to a very low level for the rest of life.展开更多
文摘目的:探讨急性ST段抬高型心肌梗死(STEMI)患者低密度脂蛋白胆固醇(LDL-C)/高密度脂蛋白胆固醇(HDL-C)比值(LHR)与其院内主要不良心血管事件(MACE)的相关性及其在临床中的应用价值。方法:收集发病12h内就诊的481例STEMI住院患者的临床资料及MACE发生情况,根据LHR的中位数(2.9)将患者分为低LHR组(LHR≤2.9,n=223)和高LHR组(LHR>2.9,n=258)。分析LHR与STEMI患者院内MACE的相关性。结果:高LHR组患者院内MACE比例均高于低LHR组[恶性室性心律失常:29(11.2%) VS 9(4.0%),P=0.004;高度房室传导阻滞:22(8.5%) VS 6(2.7%),P=0.006;心源性休克+死亡:29(11.2%) VS 7(3.1%),P=0.001]。恶性室性心律失常、心源性休克+死亡患者LHR差异有统计学意义(P均<0.05)。Pearson相关分析显示,除高度房室传导阻滞(r=0.060,P>0.05)外,LHR与恶性室性心律失常(r=0.121)、心源性休克和死亡(r=0.115)均显著相关(P<0.05)。多因素Logistic回归分析显示,LHR、空腹血糖是STEMI患者发生院内MACE的独立危险因素(P均<0.05)。ROC曲线显示LHR预测STEMI患者院内MACE的曲线下面积为0.606(95%CI:0.544~0.668),cut-off值为2.854,敏感度为80.6%,特异度为52.1%;LHR>2.854时STEMI住院患者很可能会发生MACE。结论:STEMI患者LHR升高与恶性室性心律失常、心源性休克及死亡发生呈正相关。LHR是STEMI患者发生MACE的独立危险因素,对恶性室性心律失常、心源性休克及死亡发生有一定的预测价值。
文摘Acute myocardial infarction is a deadly disease, and in the Indian context, it occurs at a younger age, even below the age of 40 years, and sometimes even below 30 years. These young MI patients have high mortality rates, and many of them are not able to reach the hospital. The pathophysiology of AMI is very well understood. AMI is a multifactorial disease and has several risk factors, like dyslipidemia, diabetes, hypertension, smoking, diet, etc. However, low-density lipoprotein cholesterol (LDL-C) has a very strong causal relationship with atherosclerosis. Reducing LDL-C to <70 results in the arrest of the progression of atherosclerosis, and slashing its level to below 50 produces the regression of atherosclerosis. The cumulative exposure of LDL-C to the arterial wall is a very strong determinant of atherosclerosis and the development of AMI. The coronary heart disease (CHD) threshold target of LDL-C for the development of AMI is roughly 7000 mg/year. If LDL-C is 100 mg/dL from an early age, the CHD threshold target for the development of AMI will reach 70 years of age. However, if LDL-C target is <70 mg/dL from an early age, the patients will reach the CHD threshold of LDL-C at the age of 100 years. Based on the current science, this is an emerging concept to postpone AMI by several years, even up to 100 years. The goal of LDL-C <70 mg/dL can be achieved by available oral or injectable drugs. Gene editing with CRISPR technology is emerging as a very exciting modality for lowering LDL-C to a very low level for the rest of life.
