Smoking and vascular surgery
Smoking and vascular surgery
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DOI：
10.1002/bjs.1800680902
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发表时间：
1981-09
影响因子：
9.6
通讯作者：
Martin Thomas
中科院分区：
文献类型：
--
作者：
Martin Thomas
“香烟会严重损害您的健康”。自第二次世界大战以来，这一警告的证据不断增加 (1 -3)。在外科门诊就诊的周围血管疾病患者中吸烟者的比例远高于一般人群，并且男性患者中吸烟者的比例很少低于 90% (4-9)。虽然英国总人口中 60% 的男性和 40% 的女性吸烟 (1)，但不同国家的情况有所不同 (1012)；在澳大利亚，40% 的男性和 30% 的女性吸烟 (13)。吸烟与周围血管疾病之间的这种持续联系并不能证明吸烟会导致这种疾病，甚至也不能证明吸烟会导致这种疾病。为了确定吸烟是否确实是血管疾病发生的危险因素，需要进行长期的前瞻性研究。第一项此类研究于 1949 年在马萨诸塞州弗雷明汉开展，旨在评估冠心病的危险因素 (1 4,15)。后来，该简报扩展到包括脑部和外周疾病，并且每两年对 5209 名受试者进行一次检查。在 16 年的随访期间，有五个因素被证明是动脉粥样硬化的明确前兆，无论是在大脑、心脏还是腿部 (1 5) 。这些是：高血压、血清胆固醇升高至 7.7 mmol/l 以上、葡萄糖不耐症、心电图显示左心室肥大和吸烟。有趣的是，这些因素在不同部位的动脉粥样硬化发展中的重要性不同。当高血压占主导地位时，吸烟作为间歇性跛行的危险因素比中风更重要 (15)。另一项针对瑞士巴斯克 6400 人的研究也表明，吸烟是间歇性跛行的高危因素 (16)。牛津大学对间歇性跛行危险因素的一项研究发现，吸烟是最重要的因素 (17)。数据还估计，45岁以上、每天吸烟超过15支的人患间歇性跛行的风险几乎是不吸烟者的9倍。此外，有人提出，除了吸烟之外，相关的危险因素，包括收缩压或舒张压升高、血清甘油三酯升高和血清尿酸升高，会产生乘数效应，其中 3 个或更多这些因素的存在会使跛行的风险增加 20 倍以上。吸烟与动脉粥样硬化之间的关系很复杂，并非简单的因果关系。由于动脉粥样硬化在烟草出现之前就已存在，因此毫无疑问，古代文明就曾遭受过这种疾病的困扰。在打开著名的希伯来法老法老梅内夫塔 (Menephtah) 的包裹后，这一点首次被曝光，其主动脉的一块被送往伦敦的沙托克 (Shattock)，在皇家医学会揭示典型的晚期动脉粥样硬化之前，那里展示了良好的显微镜切片 (1 8)。对美国人和日本人的动脉疾病死亡率进行比较后发现，美国人的死亡率是日本人的七倍 (19)，尽管日本人的烟瘾较大 (10)。这种相关性的缺乏也适用于间歇性跛行。在发达国家，约 2% 的 45 岁以上人群 (1-7) 和约 7% 的退休年龄人群 (16) 患有间歇性跛行，而 50% 的人口 (2) 和超过 90% 的跛行者吸烟。因此，吸烟不太可能是动脉粥样硬化的引发因素，但更有可能加速现有疾病的进展。在出现周围血管疾病的症状（例如间歇性跛行）后，患者甚至医生有时会认为损害已经造成，因此戒烟没有什么意义，尽管早期研究表明戒烟可以降低截肢率并延长预期寿命（20,21）。牛津大学的另一项研究对跛行患者进行了长达 8 年的随访 (22)。那些减少或戒烟的患者预后明显改善；在研究期间，他们的静息痛发作次数、动脉手术次数、截肢次数和死亡次数均减少。 520例周围神经病患者截肢率
‘CIGARETTES can seriously damage your health’. Evidence for this warning has been accruing inexorably since the Second World War (1 -3). The percentage of smokers amongst patients with peripheral vascular disease attending surgical clinics is much higher than in the general population and the proportion is seldom less than 90 per cent in male patients (4-9). While 60 per cent of men and 40 per cent of women in the general population smoke in the UK (1) this varies in different countries (1012); in Australia 40 per cent of men and 30 per cent of women smoke (13). This constant association between tobacco smoking and peripheral vascular disease does not constitute proof that smoking causes the disease, nor even that it predisposes to the disease. To ascertain whether smoking is truly a risk factor in the development of vascular disease, long term prospective studies are required. The first such study was set up in Framingham, Massachusetts, in 1949, to assess risk factors for coronary heart disease (1 4,15). Later, the brief was extended to include cerebral and peripheral disease and 5209 subjects have been examined bi-annually. In a follow-up period of 16 years five factors were shown to be definite precursors to atherosclerosis, whether in the brain, heart or legs (1 5) . These were: hypertension, serum cholesterol raised above 7.7 mmol/l, glucose intolerance, left ventricular hypertrophy on ECG and smoking. Interestingly, these factors varied in importance in the development of atherosclerosis a t different sites. Smoking was relatively more important as a risk factor for intermittent claudication than for stroke, when hypertension was predominant (15). Another study of 6400 people in Bask, Switzerland, also showed that smoking was a high-risk factor for intermittent claudication (16). In an Oxford study of the risk factors for intermittent claudication, smoking was found to be the most important factor (17). I t was also estimated from the data that the risk of developing intermittent claudication in people over 45 years of age, who smoked in excess of 15 cigarettes a day, was almost nine times that of non-smokers. Furthermore, it was suggested that associated risk factors, which included raised systolic or diastolic blood pressure, raised serum triglyceride and a raised serum urate in addition to smoking, exerted a multiplicative effect in that the presence of 3 or more of them increased the risk of claudication by more than 20 times. The relationship between smoking and atherosclerosis is complex and not simply cause and effect. Since atheroma existed in the world before the advent of tobacco there is no doubt that ancient civilizations were afflicted with the disease. This first came to light after the unwrapping of Menephtah, the reputed Pharoah of the Hebrew exodus, a piece of whose aorta was sent to Shattock in London where good microscopic sections exhibited before the Royal Society of Medicine revealed typical advanced atherosclerosis (1 8). A comparison of the mortality rates from arterial disease between Americans and Japanese showed the former to be seven times as great (19), even though the Japanese are the heavier smokers (10). This lack of correlation also applies to intermittent claudication. In developed countries intermittent claudication occurs in about 2 per cent of people over 45 years (1 7) and about 7 per cent of those at the age of retirement (16), whilst 50 per cent of the population (2) and over 90 per cent of claudicants smoke. Smoking is therefore unlikely to be an initiating factor of atherosclerosis, but more probably accelerates progression of established disease. Having developed symptoms of peripheral vascular disease, such as intermittent claudication, patients and even doctors sometimes argue that the damage has already been done and there is therefore little point in giving up smoking, although early studies suggested that cessation of smoking carried a lower amputation rate and increased life expectancy (20,21). In another study from Oxford claudicants were followed up for 8 years (22). Those patients who reduced or stopped smoking had a much improved prognosis; they suffered fewer episodes of rest pain, less arterial surgery, fewer amputations and fewer died over the period studied. The amputation rate of 520 patients with peripheral