Valentine R J, Kaplan H S, Green R, Jacobsen D W, Myers S I, Clagett G P
Department of Surgery, University of Texas Southwestern Medical Center, Dallas 75235, USA.
J Vasc Surg. 1996 Jan;23(1):53-61, discussion 61-3. doi: 10.1016/s0741-5214(05)80035-7.
Elevated lipoprotein (a) (Lp[a]) lipoprotein, total homocysteine, and hypercoagulable states (HCS) have all been implicated as risk factors for premature-onset atherosclerosis. This study was performed to determine the prevalence of these abnormalities in young men with chronic lower extremity ischemia (peripheral vascular disease [PVD]) and to determine their relative strengths as risk factors for premature peripheral atherosclerosis.
We analyzed 50 young white men (aged 45 years or younger at onset of symptoms) and compared them with 45 age-matched white male control subjects.
Atherosclerotic risk factors were similar in both groups. The mean (+/- SEM) Lp(a) lipoprotein level was 36 +/- 6 mg/dl among the study patients, compared with 14 +/- 2 mg/dl among control subjects (p = 0.02, Mann-Whitney). Twenty (40%) study patients and seven (16%) control subjects had Lp(a) lipoprotein levels of 30 mg/dl or greater (atherosclerotic risk threshold) (p = 0.01, odds ratio = 3.62, confidence interval (CI) 1.4 to 9.5). Positive HCS panels (antiphospholipid antibodies or deficiencies in antithrombin III, protein C, or protein S) were nearly twice as prevalent in study patients (n = 15, 30%) as in controls (n = 8, 18%), but this difference did not achieve statistical significance. The mean total plasma homocysteine level among the study patients was 15.9 +/- 0.9 mumol/L, which was not significantly different from the mean control value of 14.7 +/- 0.7 mumol/L. Lp(a) lipoprotein was related to risk of premature PVD through a linear logistic relationship (p = 0.003, odds ratio per each 1 mg/dl Lp(a) change was 1.03, CI 1.0 to 1.1). Multivariate analysis with stepwise logistic regression selected two variables: Lp(a) lipoprotein > or = 30 mg/dl (p = 0.01, odds ratio = 3.6, CI 1.3 to 9.9) and family history (p = 0.07, odds ratio = 2.2, CI 0.9 to 5.3). Tests of interaction demonstrated no effect between Lp(a) lipoprotein, HCS, and homocysteine.
Lp(a) lipoprotein of 30 mg/dl or greater is an independent risk factor for premature peripheral atherosclerosis in men. None of the other examined variables exhibited a significant association with premature PVD.
脂蛋白（a）[Lp（a）]升高、总同型半胱氨酸以及高凝状态（HCS）均被认为是早发性动脉粥样硬化的危险因素。本研究旨在确定慢性下肢缺血（外周血管疾病[PVD]）年轻男性中这些异常情况的患病率，并确定它们作为早发性外周动脉粥样硬化危险因素的相对强度。
我们分析了50名年轻白人男性（症状出现时年龄为45岁或以下），并将他们与45名年龄匹配的白人男性对照受试者进行比较。
两组的动脉粥样硬化危险因素相似。研究患者的平均（±标准误）Lp（a）脂蛋白水平为36±6mg/dl，而对照受试者为14±2mg/dl（p = 0.02，曼-惠特尼检验）。20名（40%）研究患者和7名（16%）对照受试者的Lp（a）脂蛋白水平达到或高于30mg/dl（动脉粥样硬化风险阈值）（p = 0.01，优势比 = 3.62，置信区间[CI] 1.4至9.5）。阳性HCS指标（抗磷脂抗体或抗凝血酶III、蛋白C或蛋白S缺乏）在研究患者中（n = 15，30%）的患病率几乎是对照组（n = 8，18%）的两倍，但这种差异未达到统计学意义。研究患者的平均血浆总同型半胱氨酸水平为15.9±0.9μmol/L，与对照组的平均水平14.7±0.7μmol/L无显著差异。Lp（a）脂蛋白通过线性逻辑关系与早发性PVD风险相关（p = 0.003，Lp（a）每变化1mg/dl的优势比为1.03，CI 1.0至1.1）。逐步逻辑回归的多变量分析选择了两个变量：Lp（a）脂蛋白≥30mg/dl（p = 0.01，优势比 = 3.6，CI 1.3至9.9）和家族史（p = 0.07，优势比 = 2.2，CI 0.9至5.3）。相互作用检验表明Lp（a）脂蛋白、HCS和同型半胱氨酸之间无相互作用。
Lp（a）脂蛋白水平达到或高于30mg/dl是男性早发性外周动脉粥样硬化的独立危险因素。其他检查变量均未显示与早发性PVD有显著关联。
