Stefanadis C, Tsiamis E, Vlachopoulos C, Stratos C, Toutouzas K, Pitsavos C, Marakas S, Boudoulas H, Toutouzas P
Department of Cardiology, Hippokration Hospital, University of Athens, Greece.
Circulation. 1997 Jan 7;95(1):31-8. doi: 10.1161/01.cir.95.1.31.
Smoking is a major risk factor for cardiovascular morbidity and mortality. Because previous studies have shown that smoking affects vasomotor response, we hypothesized that smoking may also acutely alter aortic elastic properties.
We studied 40 male current and long-term smokers who underwent diagnostic cardiac catheterization for chest-pain evaluation. Twenty subjects (age, 48 +/- 2 years, mean +/- SEM) were randomly assigned to smoking and 20 (age, 47 +/- 2 years) to sham smoking studies. Aortic elastic properties were studied with the determination of the aortic pressure-diameter relation before smoking, every minute for the first 5 minutes after the initiation of smoking or sham smoking, and every 5 minutes for the following 15 minutes. Instantaneous diameter of the thoracic aorta was measured with a special ultrasonic dimension catheter developed in our laboratory and previously validated. Instantaneous aortic pressure was measured at the same site as was diameter with a Millar micromanometer. Smoking was associated with significant changes in the aortic pressure-diameter relation that denote deterioration of the elastic properties and were maintained during the whole study period: the slope of the pressure-diameter loop became steeper (baseline, 35.43 +/- 1.38; minute 1, 45.26 +/- 1.65; peak at minute 10, 46.36 +/- 1.69 mm Hg/mm; P < .001) and aortic distensibility decreased (baseline, 2.08 +/- 0.12; minute 1, 1.60 +/- 0.08; nadir at minute 5, 1.54 +/- 0.07 x 10(-6) cm2.dyne-1; P < .001). In contrast, no changes in aortic elasticity indexes were observed with sham smoking.
Smoking is associated with an acute deterioration of aortic elastic properties. This effect of smoking may contribute to the unfavorable consequences of smoking on the cardiovascular system.
吸烟是心血管疾病发病和死亡的主要危险因素。由于先前的研究表明吸烟会影响血管舒缩反应,我们推测吸烟可能也会急性改变主动脉弹性特性。
我们研究了40名因胸痛评估而接受诊断性心导管检查的男性现吸烟者和长期吸烟者。20名受试者(年龄48±2岁,均值±标准误)被随机分配到吸烟组,20名(年龄47±2岁)被分配到假吸烟组进行研究。在吸烟前、开始吸烟或假吸烟后的前5分钟每分钟以及随后15分钟每5分钟测定主动脉压力-直径关系,以此研究主动脉弹性特性。使用我们实验室研制并经先前验证的特殊超声尺寸导管测量胸主动脉的瞬时直径。使用Millar微测压计在与测量直径相同的部位测量主动脉瞬时压力。吸烟与主动脉压力-直径关系的显著变化相关,这表明弹性特性恶化,且在整个研究期间持续存在:压力-直径环的斜率变得更陡(基线时为35.43±1.38;第1分钟时为45.26±1.65;第10分钟时达到峰值,为46.36±1.69 mmHg/mm;P<0.001),主动脉扩张性降低(基线时为2.08±0.12;第1分钟时为1.60±0.08;第5分钟时降至最低点,为1.54±0.07×10⁻⁶ cm²·dyne⁻¹;P<0.001)。相比之下,假吸烟未观察到主动脉弹性指标的变化。
吸烟与主动脉弹性特性的急性恶化相关。吸烟的这种作用可能导致吸烟对心血管系统产生不良后果。