and
approached zero. Phase IV proved easier to in pregnant than in non-pregnant women, but, in contrast to their 100% record with phase V, the pairs of observers were able to recognise and agree on phase IV in only 16% of pregnant and 7% of non-pregnant never
recognise
individuals. Since the myth of the unobtainability of phase V has been exposed before,4,5 the continuing use of phase IV in obstetric practice may be related to its greater safety margin-ie, phase IV gives the greater overestimation of the true intra-arterial diastolic pressure (11 mm Hg with phase IV vs 7 mm Hg with phase V)." Other reasons are the fact that phase IV has been used in most published epidemiological and treatment studies, or simply that as neither obstetricians nor midwives make a fetish of accurate blood pressure readingsit scarcely matters which Korotkoff sound is used for the diastolic value. Perhaps the millenium will see obstetricians classifying, treating, and measuring blood pressure in the same way as their colleagues in general medicine. But for the pregnant woman and her child, the devil is not in the detail of how her diastolic blood pressure is measured. As Shennan et al recall, there is even a study8 suggesting that the systolic value is what really matters. PIH may be physiological or pathological. The devil is in the detail of the latter, still usually accorded its most potent, if least accurate, title-pre-eclamptic toxaemia or PET.
Dudley Mathews All Saints 1
2 3
Hospital, Chatham, Kent, UK
Consensus report. National high blood pressure education program working group report on high blood pressure in pregnancy. Am J Obstet Gynecol 1990; 163: 1689-712. Theobald GW. The pregnancy toxaemias or the encymonic atelositeses. London: Henry Kimpton, 1955: 419. Chamberlain GVP, Lewis PJ, de Swiet M, Bulpitt CJ. How obstetricians manage hypertension in pregnancy. BMJ 1978; i: 626-29.
4
5 6
7
8
Perry IJ, Beevers DJ, Luesley DM. Recording diastolic blood pressure in pregnancy. BMJ 1991; 302: 179-80. Brown MA, Whitworth JA. Recording diastolic blood pressure in pregnancy. BMJ 1991; 303: 120-21. Raftery EB, Ward AP. The indirect method of recording blood pressure. Cardiovasc Res 1968; 2: 210-18. Perry IJ, Wilkinson LS, Shinton RA, Beevers DG. Conflicting views on the measurement of blood pressure in pregnancy. Br J Obstet Gynaecol 1991; 98: 241-43. Tervila L, Goecke C, Timonen S. Estimation of gestosis of pregnancy (EPH gestosis). Acta Obstet Gynecol Scand 1973; 52: 235-43.
Origins
of coronary
artery ectasia
Coronary artery ectasia affects about 2% of the general population, but the aetiology of this coronary enlargement is unknown. One possibility is that there is an imbalance between the beneficial effects of nitric oxide (NO) on coronary dilation and the potentially detrimental effects of chronic overstimulation by this endothelium-derived relaxation factor.
patients with angina receive chronic glyceryltrinitrate therapy, yet no one has implicated an increased frequency of ectasia, as one might anticipate since this agent acts via NO stimulation. Perhaps the lack of ectasia is related to the mild doses used and a dosing "holiday". Another possibility is that these patients usually Many
have coronary artery disease, and atherosclerosis blunts the ability of the endothelium to produce adequate NO.
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The effect of atherosclerosis on NO production was recently shown by Quyyumi et a1.2 They found that coronary vascular dilation in response to acetylcholine is predominantly caused by increased production of NO and that, despite the absence of angiographic evidence of atherosclerosis, patients with at least one known risk factor for coronary artery disease had reduced resting and stimulated bioavailability of NO from the coronary circulation. A paradoxical vasoconstriction has been seen in atherosclerotic vessels stimulated with acetylcholine; this may be related to the normal relation between NO-induced vasodilation and endothelin-induced vasoconstriction. When the reduced bioavailable NO is stimulated by acetylcholine, the contrasting action of endothelin becomes dominant and vasoconstriction could result. Several observations may help us to understand the aetiology of ectasia. England4 found an increased frequency or "clustering" of ectasia in a retrospective review of young men surviving a myocardial infarction in rural Australia. These individuals were farmers who had been exposed to herbicide sprays. Common components of most herbicides include 2,4-D (dichlorophenoxyacetic
acid), 2,4,5-T (trichlorophenoxyacetic acid), or an acetylcholinesterase inhibitor. Extended exposure to these agents might lead to chronically raised concentrations of acetylcholine in the coronary interstitium. A possible mechanism is that 2,4-D and 2,4,5-T herbicides increase acids) acetylcholine (containing acetic concentrations through competitive inhibition by directly increasing the end products of acetylcholine breakdown, choline and acetic acid. Herbicides containing inhibitors would acetylcholinesterase directly increase the concentrations of acetylcholine. Acetylcholine is a potent stimulator of NO,’ so, herbicides might be responsible for locally increased NO concentrations. NO stimulates the relaxation of vascular smooth muscle via the guanylate cyclase pathway and release of calcium from the endoplasmic reticulum. Whether a chronic relaxation stimulus could lead to coronary artery ectasia is unknown. However, there is indirect evidence that chronic vascular relaxation may lead to a clinical syndrome similar to that seen in ectasia. Munitions workers in Wisconsin who were exposed to nitrites chronically had arterial spasm, myocardial infarctions, and an out-of-proportion incidence of sudden death, but no evidence of coronary stenosis at angiography.6 A 15-fold increase in mortality was found in this population of workers.The researchers proposed that chronic nitrite exposure caused hyaline degeneration of the coronary artery intima and media, and this could certainly result in abnormal coronary dilation. 1% of patients who had clinical, electrocardiographic, and biochemically proven myocardial infarctions had normal "large" coronary arteries.8 It is possible that these enlarged, non-stenotic, dilated coronary arteries were in fact ectatic. England9 referred to "isolated investigations in Vietnam veterans with coronary artery ectasia", and it is, noteworthy that agent orange, a herbicide used in Vietnam, contains 2,4,5-T. England also referred to evidence provided by Kelly et al, who had earlier shown a medial fibrinoid necrosis of the coronary arteries in dogs exposed to herbicide sprays. An increased incidence of
acetylcholine production.
virtually eliminating the association as the representative of Ontario’s 23 000 physicians. The Bill itself is one of the most authoritarian pieces of legislation ever introduced by a provincial or federal government, yet it almost slipped through the legislature, without an opportunity for adequate hearings and debate until the scheme was discovered, exposed, and emphatically denounced by the political opposition. Ontario’s previous left-leaning New Democratic Party (NDP) government, despite its open criticism of physicians, managed to negotiate a rather comprehensive
Vincent L Sorrell, Michael J Davis, Alfred A Bove
agreement with the OMA. This agreement covered issues
coronary heart disease has been reported in chemical workers exposed to 2,4,5-T in factory accidents. 10 Certain particulate concentrations (mostly nitrate aerosols) are related to increased mortality. The most of this increased cause common mortality is which accounts for a 1-4% overall cardiovascular disease, increase (the same incidence of ectasia in the "
population)."
The common thread is clearly the potential stimulation of NO via chronic nitrite exposure or indirectly via
East Carolina University School of Medicine, Greenville, NC; University of Texas Medical Branch of Galveston, Galveston, TX; and Temple University Hospital, Philadelphia, PA, USA 1
Hartnell GG, Parnell BM, Pridie RB. Coronary artery ectasia: its prevalence and clinical significance in 4993 patients. Br Heart J 1985; 54: 392-95.
2
3
4 5 6
7 8
9
10 11
Quyyumi AA, Dakak N, Andrews NP, et al. Nitric oxide activity in the human coronary circulation. Impact on risk factors for coronary atherosclerosis. J Clin Invest 1995; 95: 1747-55. Ludmer PL, Selwyn AP, Shook TL, et al. Paradoxical vasoconstriction induced by acetylcholine in atherosclerotic coronary arteries. N Engl J Med 1986; 315: 1046-51. England JF. Herbicides and coronary artery ectasia. Med J Aust 1981; ii: 140. Vanhoutte PM. Endothelium and control of vascular function. Hypertension 1989; 13: 658-67. Lange RL, Reid MS, Tresch DD, Keelan MH, Bernhard VM, Coolidge G. Nonatheromatous ischemic heart disease following withdrawal from chronic industrial nitroglycerin exposure. Circulation 1972; 46: 666-78. Carmichael P, Lieben J. Sudden death in explosives workers. Arch Environ Health 1963; 7: 424-39. Proudfit WL, Shirley EK, Sones MF. Selective cine coronary arteriography: correlation with clinical findings in 1000 patients. Circulation 1966; 33: 901. England JF. Herbicides and coronary artery ectasia. Med J Aust 1981; 68: 260. International Agency for Research on Cancer. Lyon: IARC, 1978 (June); no 78: 001: 7-49. Dockery DW, Pope CA. Respiratory effects of particles: health effect studies. Annu Rev Public Health 1994; 15: 113-32.
Government assault
on
Canada’s
physicians Canadian physicians are facing unprecedented assaults by their provincial governments, which are having to cope with diminishing federal transfer payments while trying to control provincial debts and deficits. At the same time there seems to be a blunted federal and provincial commitment to universal health care.’I Although disapproving comments about physicians are nothing new, negative media coverage and attacks by governments were never before directed to the jugular of the association of physicians or the position of professional doctors in society. Recent proposed healthcare cutbacks in Alberta would have substantially decreased physician payments, but confrontations with the government led to some softening of the strongly negative position held by the premier towards Alberta’s doctors and even a semblance of armistice. Meanwhile, current events in Ontario have surpassed any attacks by other provincial governments. As part of a recently introduced Omnibus Bill, the Ontario government has sought to dismember the Ontario Medical Association (OMA). The Bill provides for sector by sector negotiations within the profession, thereby
relating to billings, licensure, human resource planning, and deployment and set up a shared infrastructure for tackling important issues. As part of the negotiated ceiling on billing, the profession achieved copayment for escalations in malpractice insurance to compensate for substantial lost income, an especially important feature for some of the riskier medical specialties. Even so, most Ontario physicians probably welcomed the election in June, 1995, of the Progressive Conservative government to replace the perceived antimedical NDP bias. During their term of office, the NDP unilaterally negated collective agreements with the public sector, which included many healthcare workers, as a means of reducing costs while minimising redundancies. Physicians’ fees were clawed-back, and many within the profession felt that the conservatives would be more sympathetic towards them. The OMA seemed to start well, by offering to renegotiate the existing bilateral agreement and suggesting that extra-billing, which had resulted in the unsuccessful physicians’ strike in 1986, be reintroduced and that the government consider the introduction of private medicine in parallel to the public system into the
province. The OMA and the profession were therefore astounded by a blatantly antimedical broadside, delivered by the Minister of Health, as the sweeping provisions of the Omnibus Bill were introduced at public hearings. The Minister accused the profession of financially motivated systematic fraud as well as substantial clinically unnecessary overutilisation. The result is a proposed law with powers for government representatives to gain access to medical records without patient or physician consent and without a warrant-a level of intrusion that is hitherto unprecedented in Canada. Moreover, the Minister raised the spectre of dismembering the OMA as the official representative body of the medical profession, reducing it to an agency of advocacy rather than an important partner in healthcare planning. The medical profession were accused of "disengagement" from the healthcare system, despite ample evidence of physicians’ tireless commitment and participation in hospital committees, district health councils, and community, government, and volunteer agency sponsored initiatives that require medical input. The Bill also gives unilateral power to the government to deny billing numbers, essential for practice in the public system, to physicians who choose not to go to underserviced areas or to certain medical specialists who do not have hospital privileges, even though many specialists-eg, psychiatrists and dermatologists-do not need direct hospital connections to practise their specialty. Funding for physicians and methods of payment will be determined unilaterally by the Ministry of Health,
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