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Bed-Side Biophysical-Semeiotic Diagnosis of Peripheral Arterial Disease, even in early phase.
- Sergio Stagnaro (14 March 2003)
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The context of medical illustrations
- Harold L Behr, 138 Bramley Road, London N14 4HU (16 March 2003)
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MANAGEMENT OF CLAUDICATION IN PRIMARY CARE
- PETER R TAYLOR, RACHEL E BELL, CLINICAL RESEARCH FELLOW (17 March 2003)
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Will 'Best Medical Therapy' ever be good enough?
- Robert E Brightwell (18 March 2003)
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Questionable Conclusions
- Des Spence (20 March 2003)
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The role of the Podiatrist in the management of peripheral arterial disease
- Mairghread J Ellis (20 March 2003)
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Peripheral arterial disease: secondary prevention in hospital patients is the immediate priority
- Simon E Janes, John Walsh, Brian Hopkinson (23 March 2003)
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The role of ozonated autohemotherapy in the management of peripheral arterial disease.
- Leszek Tylicki, Bogdan Biedunkiewicz, specialist internal medicine and nephrology; Tomasz Neweglowski, specialist internal medicine; Boleslaw Rutkowski, professor, specialist internal medicine and nephrology. (26 March 2003)
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Mechanism of action for Ozonated Autohemotherapy
- Trevor G Marshall (28 March 2003)
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Inadequate treatment of peripheral vascular disease
- tazewell banks. MD (1 April 2003)
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Sergio Stagnaro, Specialist in Blood, Gastrointestinal, and Metabolic Diseases. Researcher in Biophysical Semeiotics. Via Erasmo Piaggio 23/8 160037 Riva Trigoso (Genoa) Italy
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Sirs, Based on a 45-year-long clinical experience with Biophysical-Semeiotics, I cannot agree with the statement of the authors of such otherwise interesting article, who write that only a quarter of patients with peripheral arterial disease on clinical examination have symptoms (1). Certainly, this is true just if the doctors ignore Biophysical Semeiotics, as these authors unfortunately do. On the contrary, as I illustrated in the site HONCode 233736, http://digilander.libero.it/semeioticabiofisica, in the Page I hold in www.katamed.it, and in the most visited italian site www.piazzetta.sfera.net, ProfessioneMedica, doctor, expert in the new physical semeiotics, is able to recognize easily at the bed-side both the “arteriosclerotic constitution” and the peripheral arteriopathy, even in its initial phase. In fact, as clinical and experimental evidence suggests (2), partial arterial occlusion brings about immediately microcirculatory activation in related, down-ward, tissues, that doctor can evaluate it in “quantitative” way. Peripheral arterial disease, furthermore, is a marker for systemic atherosclerosis; Biophysical Semeiotics allows doctor to assess the function as well as the structure of macro- and micro-vessels of all biological systems (3, 4, 5). In conclusion, the doctors have to know, all around the world, that “there are thousend suns above the clouds”. (For further information, see the above-cited sites) 1) Burns P., Gough S., BradburyA.W. Management of peripheral arterial disease in primary care. BMJ 2003;326:584-588 ( 15 March ). 2) Stagnaro S., Stagnaro-Neri M., Basi microcircolatorie della semeiotica biofisica. Atti del XVII Cong. Naz. Soc. Ital. Studio Microcircolazione, Firenze ott. 1995, Biblioteca Scient. Scuola Sanità Militare, 1995, 2, 94. 3) Stagnaro-Neri M., Stagnaro S., Deterministic Chaos, Preconditioning and Myocardial Oxygenation evaluated clinically with the aid of Biophysical Semeiotics in the Diagnosis of ischaemic Heart Disease even silent. Acta Med. Medit. 13, 109, 1997. 4) Stagnaro-Neri M., Stagnaro S., Deterministic chaotic biological system: the microcirculatoory bed. Theoretical and practical aspects. Gazz. Med. It. – Arch. Sc. Med. 153, 99, 1994. 5) Stagnaro-Neri M., Stagnaro S., Auscultatory Percussion Evaluation of Arterio-venous Anastomoses Dysfunction in early Arteriosclerosis. Acta Med. Medit. 5, 141, 1989. Competing interests: None declared |
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Harold L Behr, private practice North London Centre for Group Therapy, 138 Bramley Road, London N14 4HU
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Editor The photograph of a gangrenous toe on your front cover (BMJ 15 March 2003) set me thinking about the psychological impact of medical illustrations. The purpose in publishing the picture was presumably to educate readers on the subject of peripheral arterial disease. However the public nature of front covers means that the photograph was probably glanced at in horrified fascination by a fair number of non-readers of the journal such as relatives at the breakfast table and adjacent commuters on public transport. Illnesses affecting the internal and external aspects of the human body can furnish plenty of graphic images,some of which produce shocking and unpleasant emotional reactions. I am reminded of conversations in doctors' messes where there is a tendency to expatiate on topics which do not go well with efforts to savour a canteen meal. Context is therefore important, and I would like to enter a plea for keeping pictures such as the one referred to inside the the journal instead of on its cover. Harold Behr Child Psychiatrist Competing interests: None declared |
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PETER R TAYLOR, CONSULTANT VASCULAR SURGEON GUY'S & ST. THOMAS' HOSPITAL NHS TRUST, LONDON SE1 7EH, RACHEL E BELL, CLINICAL RESEARCH FELLOW
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Dear Editor, We read the clinical review on the “management of peripheral arterial disease in primary care” with interest (1). The authors take a very narrow view of the meaning of peripheral arterial disease, limiting it to occlusive lower limb disease causing claudication. They mention critical limb ischaemia, abdominal aortic aneurysms and carotid artery symptoms as a reason for referral of patients with claudication to vascular surgeons. We consider that critical limb ischaemia, abdominal aortic aneurysms and carotid artery stenosis are important components of peripheral arterial disease that deserve more than a single sentence. The suggestion, implicit in their article, that abdominal aortic aneurysms can be diagnosed on clinical examination alone is contraindicated by studies showing that ultrasound imaging is much more accurate (2). They also omit popliteal aneurysms as an important cause of intermittent claudication that may not be diagnosed in primary care, and which may require urgent referral to vascular surgeons. We also consider the contention that “only when best medical treatment has been instituted …should endovascular or surgical intervention be considered” is impractical in the majority of patients, as they will continue to smoke. The authors are suggesting a council of perfection that certainly does not pertain to our clinical practice. The title of this article, namely, “management of peripheral arterial disease in primary care” should be changed to “management of claudication in primary care”. We look forward to further articles covering the remaining important topics of peripheral vascular disease. Yours faithfully, Peter R Taylor
Rachel E Bell 1. Burns P, Gough S, Bradbury AW. Management of peripheral arterial disease in primary care. BMJ 2003; 326:584-8 2. Fink HA, Lederle FA, Roth CS, Bowles CA, Nelson DB, Haas MA. The accuracy of physical examination to detect abdominal aortic aneurysm. Archives of Internal Medicine 2000; 160: 833-6 Competing interests: None declared |
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Robert E Brightwell, Research Fellow in Vascular Surgery The Ipswich Hospital NHS Trust, Heath Road, Ipswich, IP4 5PD
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EDITOR, The recently published Clinical Review on the management of peripheral arterial disease (PAD) in primary care was overdue and tackles an important area of practice(1). It seems that despite clear guidelines from the Department of Health(2) this high-risk group of patients continue to receive sub-optimal care. The PARTNERS study demonstrated that this problem is not isolated to this side of the Atlantic: lack of patient and primary care physician awareness of the diagnosis and treatment of PAD was blamed for poor levels of ‘Best Medical Therapy’ (BMT) among this patient group(3). Management of PAD starts with diagnosis, of which gaining an accurate Ankle-Brachial Pressure Index (ABPI) is a large component. It is a cheap test and provides hard evidence of vascular disease. There is also a correlation between low ABPI and overall cardiovascular risk. I was therefore disappointed to see no mention of this in the review article. Work by our unit on a cohort of 500 consecutive patients referred to a vascular clinic by primary care showed a diagnostic accuracy of 70% before and after a directed educational program on the diagnosis and management of PAD – fewer than 5% of referrals included an ABPI. Among our group of 500 patients 38% were not on antiplatelet medication when clinically indicated, likewise only 40% were prescribed lipid-lowering medication where indicated. 50.4% had a resting blood pressure greater than 140/85mmHg. We diagnosed 1.8% of patients referred to the clinic as newly diabetic. There is clearly a long way to go if primary care is going to be responsible solely for the medical management of PAD. Perhaps, for now at least, specialists in vascular disease could supervise primary care until uptake of BMT is widespread. This is a system that our unit has employed for the past 4 years with great success. In the controlled clinic environment we can tackle all the common risk factors and consider the more esoteric variety, such as hyperhomocysteinaemia, that were not mentioned in the review article. 1) Burns P, Gough S, Bradbury AW. Management of peripheral arterial disease in primary care. BMJ 2003;326:584-8 2) Department of Health. National Service Framework for Coronary Heart Disease. London:DoH, 2000 3) Hirsch AT, Criqui MH et al. Peripheral arterial disease detection, awareness, and treatment in primary care. JAMA 2001;286:1317- 1324 Competing interests: None declared |
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Des Spence, GP Glasgow
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"Controlling hypertension and diabetes reduces invasive intervention" in peripheral vascular disease (PVD). Front page of the BMJ. I have read this review and but could not come to the same conclusion. The paper suggests that "best medical practice" would be an ACE, a Statin, tight glyceamic control, tight BP control and antiplatelet medication. It also states that 20% of the population over 65 ( although I see no reference for this figure) have peripheral vascular disease which would follow that this population be on this “best medical treatment”. I could find no reference to a specific trial looking at patients with PVD and all these conclusion are inferred from other patient groups.. Importantly also this was written for primary care but had no authors from primary care. Other issues to consider. UKPDS did not show that tight glyceamic treatment reduced macro vascular events [1]. In the Heart Protection Study the annualised NNTS to prevent death was 500 and to prevent a vascular event 100 [2]. Yet in the ALLHATT study looking at similar population no benefit from Pravasatin was found [3]. I am unaware of outcome evidence for the treatment hypertension in PVD. In the HOPE study[4] had annualised NNTs for death of 250 and all end points of 125 but this is countered in the ALLHAT study looking at Lisinopril [3]. This paper infers that 20% ( perhaps higher)of patient over 65 should be on a polypharmcy to prevent peripheral vascular disease but has no specific evidence to back up it claims. The statement "Controlling hypertension and diabetes reduces invasive intervention" in peripheral vascular disease is unsupported by the evidence presented. The only interventions with evidence are smoking cessation and exercise but were given little priority in this article. Finally the last paragraph reads PVD primary care clinics “ would likely be cost neutral, or even beneficial , in the medium term and long term through the prevention of expensive vascular events such as stroke and amputation” . This is simply unsubstantiated by any of the evidence provided with no attempt at a cost analysis PVD should merely be seen and yet another risk factor ischeamic heart disease. 1. Seeing what you want to see in randomised controlled trials: versions and perversions of UKPDS data James McCormack, Trisha Greenhalgh, BMJ 2000;320:1720-1723 ( 24 June ) 2. Heart Protection Study Collaborative Group. MRC/BHF heart protection study of cholesterol lowering with simvastatin in 20 536 high- risk individuals: a randomised placebo-controlled trial. Lancet 2002;360:7 -22. 3. ALLHAT Officers and Coordinators for the ALLHAT Collaborative Research Group. JAMA, 2002, 288(23): 2981-2997. 4. Heart Outcomes Prevention Evaluation Study Investigators. Effects of an angiotensin converting enzyme inhibitor, ramipril, on cardiovascular events in high risk patients. N Engl J Med 2000;342:145-53. Competing interests: None declared |
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Mairghread J Ellis, Part time lecturer, subject area of Podiatry Queen Margaret University College, Edinburgh, EH6 8HF
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I am somewhat disappointed to see no mention made of the role of the podiatrist in the management of individuals with peripheral arterial disease. It is a large part of the scope of practice of both the community and hospital based podiatrist to assess, monitor and manage the patient with peripheral arterial disease, with or without diabetes mellitus. The podiatrist also has a huge part to play in patient education and health promotion. Assessment of vascular status by means of doppler ultrasound and ABPI measurement is a regular part of our practice, as is neurologicla assessment, especially in individuals with diabetes mellitus. The podiatrist, as part of the multidisciplinary primary care team plays a significant role in maximising the viability of extremely vulnerable lower limbs. SIGN guideline 55 (management of diabetes, section 7) highlights the role of podiatry in enabling individuals with peripheral arterial disease to optimise their mobility, thus individually being the least burden to the finite resources of the NHS. Competing interests: None declared |
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Simon E Janes, PRHO Queen's Medical Centre, Nottingham, John Walsh, Brian Hopkinson
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Sir, In their review on medical management of peripheral arterial disease, Burns et al recommend that surgical intervention should be postponed until best medical treatment has been effectively implemented(1), much of which could take place in primary care. However, despite a high prevalence of peripheral arterial disease in the community, awareness of the condition and implementation of appropriate primary care is low(2). Hence hospital physicians have a crucial role and patients admitted for surgical intervention represent an important target for secondary prevention. Recent evidence has shown that patients undergoing surgical intervention received poor prior secondary prevention but had significant reductions in death, myocardial infarction and stroke when secondary prevention measures were initiated post-operatively(3). This prompted us to prospectively audit local secondary prevention in patients with peripheral arterial disease requiring surgical intervention in a tertiary referral centre. Forty-eight patients (29 male, median age 76.5 years) were assessed. Sixteen (33%) were diabetic. Anti-platelet agents were used in 23 (48%) and only one quarter received angiotensin converting enzyme inhibitors. Untreated hypercholesterolaemia was present in 18 (37%) patients and a further 9 patients (19%) were treated with statins. Eight patients (17%) had untreated systolic hypertension. Use of anti-platelet agents and angiotensin converting enzyme inhibitors was significantly higher in the diabetic group when compared to those with no history of diabetes, P= 0.04 and 0.04 respectively. Documentation of smoking history was concerning: there was no record present in 11 (23%)patients. A systematic review for the Health Education Authority graded accurate recording of smoking history as category “A” evidence in their recommendations to the National Health Service strategy for treating tobacco dependence(4). Clearly we are missing this essential first step to identifying patients who may benefit from opportunistic advice and support. Application of secondary prevention is poor in hospital patients with peripheral arterial disease, and this group should be our first priority. In the long term greater awareness and treatment by general practitioners will reduce the development of atherosclerosis and need for surgical intervention in patients with peripheral arterial disease. Simon Janes, surgical PRHO, Queen’s Medical Centre, Nottingham John Walsh, Consultant cardiologist, department of cardiovascular medicine, Queen’s Medical Centre, Nottingham Brian Hopkinson, Professor of Vascular surgery, academic division of vascular surgery, Queen’s Medical Centre, Nottingham Conflict of interests: none declared 1. Burns P, Gough S, Bradbury A. Management of peripheral arterial disease in primary care. BMJ 2003; 326: 584-588 2. Hirsch AT, Criqui MH, Treat-Jacobson D, Regensteiner JG, et al. Peripheral arterial disease detection, awareness and treatment in primary care. JAMA 2001; 286:1317-1324 3. Mukherjee D, Lingham P, Chetcuti S, Grossman PM, Moscucci M, Luciano AE, Eagle KA. Missed opportunities to treat atherosclerosis in patients undergoing peripheral vascular interventions: insights from the University of Michigan Perippheral Vascular Disease Quality Improvement Initiative (PVD-QI2). Circulation 2002; 106: 1909-1912 4. West R, Mc Neill A, Raw M. Smoking cessation guidelines for health professionals: an update. Thorax 2000; 55: 987-999 Competing interests: None declared |
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Leszek Tylicki, MD, PhD; specialist internal medicine Department of Nephrology, Medical University of Gdansk. 80-211 Gdansk. Debinki 7. Poland., Bogdan Biedunkiewicz, specialist internal medicine and nephrology; Tomasz Neweglowski, specialist internal medicine; Boleslaw Rutkowski, professor, specialist internal medicine and nephrology.
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EDITORS: Burns et al. (1) reviewed the current knowledge on the management of peripheral arterial disease (PAD). They did not even mentioned ozonated autohemotherapy (O3-AHT), the therapeutic modality used in symptomatic treatment of lower limbs ischemia in some countries from several decades. In this method, a known volume of blood is exposed ex vivo to an oxygen-ozone mixture with strict ozone concentration, afterwards reinfused back to the patient. Given the fact that ozone, a strong oxidant may be toxic, this medical approach has encountered skepticism, if not outright objection in a big part of medical community. In-depth studies of Bocci and coworkers, performed in the last decade helped to improve the understanding of biological mechanism of ozone activity. They gave also precise recommendations on the use of O3-AHT in PAD, and established the range of ozone concentrations in which it does not induce oxidative cell damage (2). The other important issue is the clinical effectiveness of O3-AHT. Despite the some uncontrolled reports showing clinical improvement after O3-AHT in patients with symptomatic PAD, a strict evidence was not provided to date (3). To shed light on this point, we performed a prospective, placebo-controlled study to evaluate the impact of O3-AHT on the walking distance in patients on maintenance HD with PAD (II-III stage according to Fontain) (4). 10 subjects received 9 sessions of O3-AHT with ozone concentration of 50 ìg/ml and 9 sessions of oxygen autohemotherapy as a control in a cross-over, single-blind manner. Intermittent claudication distance was measured using a march test on a treadmill. Significant prolongation in walking distance after O3-AHT was found, as compared to the baseline (by 30.5%) and to the oxygen control (by 22.7%) [p<0.04 and p<0.02]. Thus, we demonstrated, to our best knowledge for the first time in a placebo-controlled manner, that O3-AHT may attenuate clinical symptoms of lower limbs ischemia. The rationale for these beneficial effects may come from several possible mechanisms of ozone activity leading to an improvement of blood flow in hypoxic areas. These include a decrease in blood viscosity and coagulation, vasorelaxation and alterations in prostanoids production. The influence of ozone on the increase of 2,3-diphosphoglycerate levels, responsible for enhanced oxygen delivery to ischemic tissues has also been postulated but not substantiated in all studies (2,3). Despite our encouraging results, a wide use of O3-AHT should be preceded by large- scale clinical trials, which could finally confirm or deny the effectiveness of this modality. Leszek Tylicki, Bogdan Biedunkiewicz, Tomasz Neweglowski, Boleslaw
Rutkowski
REFERENCES 1. Burns P, Gough S, Bradbury A. Management of peripheral arterial disease in primary care. BMJ 2003; 326: 584-588. 2. Bocci V: Biological and clinical effects of ozone. Has ozone therapy a future in medicine? Br J Biomed Sci 1999; 56: 270-279. 3. Tylicki L, Nieweglowski T, Biedunkiewicz B, Burakowski S, Rutkowski B: Beneficial clinical effects of ozonated autohemotherapy in chronically dialyzed patients with atherosclerotic ischemia of the lower limbs. Int J Artif Organs 2001; 24: 79-82. 4. Biedunkiewicz B, Tylicki L, Nieweglowski T, Burakowski S, Chamienia A, Debska-Slizien A, Rutkowski B: Beneficial effects of ozonated autohemotherapy in hemodialyzed patients with atherosclerotic ischemia of lower limbs. Nephrol Dial Tansplant 2002; 17(Suppl. 12): 260(abstract). Competing interests: None declared |
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Trevor G Marshall, Research Director Sarcinfo, Thousand Oaks, California 91360-1122
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re: The role of ozonated autohemotherapy in the management of peripheral arterial disease I was fascinated with the study reported by Tylicki, even allowing for the limited sample size. I wanted to suggest another etiology which might explain the observed results. Brown et al [1], recently used Lida Mattman's advanced staining techniques [2] to identify Cell Wall Deficient (antibiotic resistant) Bacteria circulating in the blood of 37% to 63% of 150 Control subjects. It could be expected that such blood-borne CWD bacteria might succumb to ozonated autohemotherapy. Our studies have focused on patients with an immune dysfunction which makes them particularly susceptible to such bacteria [3], but the same CWD bacteria might also be responsible for initiating the localized Th1 inflammatory reactions in patients susceptible to Peripheral Arterial Disease. We have found that Angiotensin II Receptor Blockers have an immediate anti-inflammatory effect in Th1 mediated immune disease, and have proposed a working description of the endocrine biochemistry which links the RAS and immune inflammation [4]. A quick test to exclude CWD Bacterial etiology would be to administer Minocycline or Doxycycline 100mg qod for 2-4 weeks and then re-evaluate the walking distances (please remember that these antibiotics can temporarily induce a severe Jarisch-Herxheimer Reaction in individuals with Rheumatic or immune dysfunction [5]). 1. Brown ST, Brett I, Almenoff PL, Lesser M, Terrin M, Teirstein AS: Recovery of cell wall-deficient organisms from blood does not distinguish between patients with sarcoidosis and control subjects. Chest 2003 Feb; 123(2): 413-7 [Abstract] 2. Mattman L: Cell Wall Deficient Forms: Stealth Pathogens. 2nd Edition: CRC Press; 1992, ISBN 0849344050 3. Marshall TG: Brown, et al, ACCESS Study finds Bacterial Pathogens in Sarcoidosis Patients.[Electronic Letter] Chest 12 Feb 2003; Available from URL http://www.chestjournal.org/cgi/eletters/123/2/413#96, Accessed 12 Feb 2003 4. Marshall TG, Marshall FE: The Science Points to Angiotensin II and 1,25-Dihydroxyvitamin D. [Electronic Letter] Chest 6 Feb 2003; Available from URL http://www.chestjournal.org/cgi/eletters/123/1/18#95, Accessed 27 Mar 2003 5. Marshall TG: Adverse Reactions to Doxycycline, Minocycline, are
often Jarisch-Herxheimer Reaction. [Rapid Response]
BMJ 24 March 2003; Available from URL
http://bmj.com/cgi/eletters/326/7390/613#30713
Accessed 24 Mar 2003
Competing interests: None declared |
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tazewell banks. MD, Professor of Medicine Howard Medical School, 20060
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Your review failed to emphasize aggressive treatment of the lipids as the most effective tool for this disease. A.There are over 20 articles which emphasis that the
percent reduction in LDL is far more effective than the absolute goal
level {e.g. AHA goals of 100mg/dl]. Remember the Heart Protection Study in
Lancet last year? 21% had LDLs below 83mg/dl at the beginning.
B. We've known since the early 1970s that atherosclerosis is caused primarily by our diets and can be reversed by diet[primarily in monkeys then] but by Dean Ornish back in the early 1990s]. C. It's irrational to advise an alcoholic cirrhotic to reduce his alcohol by a third or to have a lung patient reduce his cigarettss by a third. It's just as dumb to advise atherosclerotic patients to follow the NCEP 2 diet [lowers cholesterol <10%]. They should be introduced to Ornish <10% fat vegetarian diets and placed on large enough statins [with/without other lipid lowering drugs] to get at least an overall 50% LDL reduction. The excuse that "my patients won't stay on those diets" is the same excuse given over 20-30 years ago by many doctors who didn't advise patients to stop smoking. D. Alerting patients to the observation that this disease is stabilizable and even regressable would imrove compliance. E. The failure to use aggressive diets and antilipid drugs and diets is the main reason why at least 80% of ASHD deaths occur in patients who were known to have the disease [but were inadequately treated]. It's also the reason that post myocardial infraction medicare patients in Canada have the same 34% one year mortality as in the US even though we do >8 times more arteriograms, angioplasties and coronary surgery in the first 30 days than in Canada. Competing interests: None declared |
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