- Email: [email protected]
THIAZIDE OR BETA-BLOCKER FOR HYPERTENSION
1383
(insignificantly different from placebo) must
also be
tract operations. This is a high exclusion rate, and we ought to be told the fate of these patients. Platt and his colleagues reached a very important conclusion-that patients in the unsealed junction group had a significantly greater chance of dying than did those in the sealed junction group. Was this indeed due to the greater incidence of urinary infection in the "unsealed"group? Table in in their paper shows that in patients not given an antibiotic 15/108 in the unsealed group compared with 4/112 in sealed group died, but 9 of the 15 deaths were in patients whose urine was uninfected. Fisher’s exact test comparing 0/11 with 6/29 gives p=0 . 124. Platt et al wrote that "most of the excess mortality among the uninfected patients was attributable to patients who had either 104 cfu/ml during catheterisation, or who were found to be infected after the catheter course ended". Please may we have figures in support of this statement? I thank Platt and his colleagues for drawing attention to the importance of maintaining a closed urine drainage system. Should we now go a step further and incorporate an antiseptic in the collecting bag, or a valve into the system similar to the one which is proving effective in patients after percutaneous transhepatic catheterisation of the obstructed biliary system?1
Medical Department, ICI Pharmaceuticals Division, Macclesfield, Cheshire
P. M. DAWES
Scarborough Hospital,
Dudley Road Hospital, Birmingham B 18 7QH
D. G. BEEVERS
North Yorkshire YO12
A. V. POLLOCK
6QL
for
a
major cause
concern.
Dollery5
Furthermore, recently suggested that "there is no evidence that thiazides have a specific beneficial effect on atheroma, and there has been some speculation that their effect may be adverse" whereas by contrast "there have also been suggestions that beta-adrenergic blockade may reduce the incidence of myocardial infarction in treated hypertensive patients."6The beneficial effect of beta-blockers in reducing cardiovascular complications more than other agents has been further prospective trials are underway to resolve this point.4.9 Thus it may be wrong to draw conclusions on the long-term treatment of hypertension from pooled systolic blood pressure results in a mixed-race short-term trial. On the basis of total cost, efficacy (particularly in White patients), and prevention of the sequelae of high blood pressure, it is difficult to justify the preference of thiazide to propranolol for sole therapy of
substantiated, 7 8 and
hypertension.
PRIMARY PREVENTION OF HYPERTENSION THIAZIDE OR BETA-BLOCKER FOR HYPERTENSION
SIR,—From
the
results
of the
Veterans
Administration
Cooperative Study Group’s trial )2,3 Dr Burris (April 16, p 870) compares routine antihypertensive treatment with propranolol and thiazide diuretics on the basis of efficacy and cost. However, he omits to consider the additional expense of repeated biochemical measurements and potassium supplements in the cost of diuretic treatment, does not mention that nearly 60% of the patients in the trial were Black (and it is generally considered that beta-blockers are less effective in Black patients), and does not consider the effects of long-term treatment on prognosis. Serum potassium fell below 3 - 5 mmol/1 in 41% of the patients treated with hydrochlorothiazide,3prompting the trial group to suggest that if the work "showing an increase in ventricular ectopic activity associated with hypokalemia is confirmed, then it would seem to be necessary to pay considerably more attention to even trivial decrements in serum potassium". Thus, regular measurement of serum potassium and administration of potassium supplements or expensive potassium-retaining agents would be required for many patients. In contrast beta-blockers cause no fall in serum potassium. Regarding efficacy, in the long-term follow-up, the reductions in diastolic blood pressure with propranolol were 11.5 5 mm Hg (White patients), 11.3 mm Hg (Blacks) and with hydrochlorothiazide 12.0mm Hg (Whites) and 14.0mm Hg
(Blacks). In the dose-finding study propranolol reduced diastolic blood pressure in White patients to a significantly greater extent (12-66 mm Hg) than did hydrochlorothiazide (10.9 mm Hg) whereas in both parts of the study hydrochlorothiazide produced greater reductions in systolic pressure, particularly in Black patients. It is difficult to conclude that thiazide is clinically more effective than propranolol, especially in White patients. The finding, in the MRC trial of mild of impotence in 22’ 6% of thiazide treated cases compared with 13-2% of beta-blocker cases
hypertension,
1. Blenkharn 2
JI, McPherson GAD, Blumgart LH. An improvement system for external biliary drainage. Lancet 1981; ii 781-82 Veterans Administration Cooperative Study Group on Antihypertensive Agents.
Comparison of propranolol and hydrochlorothiazide for the initial treatment of hypertension I: Results of short-term titration with emphasis on racial differences in response. JAMA 3
hypertension II: Results of long-term therapy. JAMA 1982; 248: 2004-11. Working Party on Mild to Moderate Hypertension. Adverse reactions to bendrofluazide and propranolol in the treatment of mild hypertension. Lancet 1981, ii: 539-43.
Woden Valley Hospital, Canberra, ACT 2606, Australia
TREVOR C. BEARD
OXYGEN FOR MULTIPLE SCLEROSIS p 1161) will find in "Greenfield"1 an description of fat embolism of the central nervous system in man which is very different from the neuropathological description which James submits as evidence for his theories. Fat embolism produces headaches and drowsiness; these are not features of multiple sclerosis (MS). Fat embolism is often fatal but MS is not, despite very large lesions. In the embolic process petechial haemorrhages are widespread in the white-matter, as are ring-andball haemorrhages; the capillary walls show focal necrosis and in the grey-matter necrotic areas with loss of nerve cells are found; and
SIR,—Dr James (May 21,
accurate
5
Dollery CT. Hypertension and new antihypertensive drugs: Clinical perspectives. Fed
Proc 1983; 42: 207-10. 6. Stewart IMcD G. Beta-adrenoceptor blockade and the incidence of myocardial infarction during treatment of severe hypertension. Br J Clin Pharmacol 1982; 13: 91-93.
DG, Johnston JH, Larkin H, Davies P. Clinical evidence that &bgr; adrenoceptor more cardiovascular complications than other antihypertensive drugs Drugs 1983; 25 (suppl 2): 326-30. Trafford JAP, Horn CR, O’Neal H, McGonigle R, Halford-Maw L, Evans R Five year follow-up of effects of treatment in mild and moderate hypertension. Br Med J 1981,
7. Beevers
blockers prevent
1982, 248: 1996-2003.
Veterans Administration Cooperative Study Group on Antihypertensive Agents. Comparison of propranolol and hydrochlorothiazide for the initial treatment of
4. MRC
SIR,—Dr MacGregor (April 2, p 750) notes that the most precise epidemiological data will never prove the sodium-hypertension hypothesis, but apparently the intervention studies needed for a definitive test will have to wait indefinitely, for "ethical and practical reasons". The hypothesis can be tested amongst the families of patients adopting a natural (unsalted) diet as a treatment for hypertension. In communities where suitable food is readily available, it seems both ethical and practical to recommend the whole family to eat it. Catering is easier, and children are probably protected from expressing their genetic potential for hypertension. In cases of dietary remission, such as MacGregor himselfhas reported, it might seem unethical not to try to involve the family. The hypothesis can be tested by showing whether many of the nonhypertensive family members who share meals with a spouse or parent dieting for hypertension remain normal, over a period in which blood pressures rise in a matched reference population on a higher sodium intake.
8
282: 1111-13
L, Berglund G, Elmfeldt O, Wedel H Beta-blockers hypertension Prev Med 1981; 10: 38-43. Greenfield JG. Neuropathology London: Edward Arnold, 1958:
9. Wilhelmsen 1.
versus
95.
saluretics in
(insignificantly different from placebo) must
also be
tract operations. This is a high exclusion rate, and we ought to be told the fate of these patients. Platt and his colleagues reached a very important conclusion-that patients in the unsealed junction group had a significantly greater chance of dying than did those in the sealed junction group. Was this indeed due to the greater incidence of urinary infection in the "unsealed"group? Table in in their paper shows that in patients not given an antibiotic 15/108 in the unsealed group compared with 4/112 in sealed group died, but 9 of the 15 deaths were in patients whose urine was uninfected. Fisher’s exact test comparing 0/11 with 6/29 gives p=0 . 124. Platt et al wrote that "most of the excess mortality among the uninfected patients was attributable to patients who had either 104 cfu/ml during catheterisation, or who were found to be infected after the catheter course ended". Please may we have figures in support of this statement? I thank Platt and his colleagues for drawing attention to the importance of maintaining a closed urine drainage system. Should we now go a step further and incorporate an antiseptic in the collecting bag, or a valve into the system similar to the one which is proving effective in patients after percutaneous transhepatic catheterisation of the obstructed biliary system?1
Medical Department, ICI Pharmaceuticals Division, Macclesfield, Cheshire
P. M. DAWES
Scarborough Hospital,
Dudley Road Hospital, Birmingham B 18 7QH
D. G. BEEVERS
North Yorkshire YO12
A. V. POLLOCK
6QL
for
a
major cause
concern.
Dollery5
Furthermore, recently suggested that "there is no evidence that thiazides have a specific beneficial effect on atheroma, and there has been some speculation that their effect may be adverse" whereas by contrast "there have also been suggestions that beta-adrenergic blockade may reduce the incidence of myocardial infarction in treated hypertensive patients."6The beneficial effect of beta-blockers in reducing cardiovascular complications more than other agents has been further prospective trials are underway to resolve this point.4.9 Thus it may be wrong to draw conclusions on the long-term treatment of hypertension from pooled systolic blood pressure results in a mixed-race short-term trial. On the basis of total cost, efficacy (particularly in White patients), and prevention of the sequelae of high blood pressure, it is difficult to justify the preference of thiazide to propranolol for sole therapy of
substantiated, 7 8 and
hypertension.
PRIMARY PREVENTION OF HYPERTENSION THIAZIDE OR BETA-BLOCKER FOR HYPERTENSION
SIR,—From
the
results
of the
Veterans
Administration
Cooperative Study Group’s trial )2,3 Dr Burris (April 16, p 870) compares routine antihypertensive treatment with propranolol and thiazide diuretics on the basis of efficacy and cost. However, he omits to consider the additional expense of repeated biochemical measurements and potassium supplements in the cost of diuretic treatment, does not mention that nearly 60% of the patients in the trial were Black (and it is generally considered that beta-blockers are less effective in Black patients), and does not consider the effects of long-term treatment on prognosis. Serum potassium fell below 3 - 5 mmol/1 in 41% of the patients treated with hydrochlorothiazide,3prompting the trial group to suggest that if the work "showing an increase in ventricular ectopic activity associated with hypokalemia is confirmed, then it would seem to be necessary to pay considerably more attention to even trivial decrements in serum potassium". Thus, regular measurement of serum potassium and administration of potassium supplements or expensive potassium-retaining agents would be required for many patients. In contrast beta-blockers cause no fall in serum potassium. Regarding efficacy, in the long-term follow-up, the reductions in diastolic blood pressure with propranolol were 11.5 5 mm Hg (White patients), 11.3 mm Hg (Blacks) and with hydrochlorothiazide 12.0mm Hg (Whites) and 14.0mm Hg
(Blacks). In the dose-finding study propranolol reduced diastolic blood pressure in White patients to a significantly greater extent (12-66 mm Hg) than did hydrochlorothiazide (10.9 mm Hg) whereas in both parts of the study hydrochlorothiazide produced greater reductions in systolic pressure, particularly in Black patients. It is difficult to conclude that thiazide is clinically more effective than propranolol, especially in White patients. The finding, in the MRC trial of mild of impotence in 22’ 6% of thiazide treated cases compared with 13-2% of beta-blocker cases
hypertension,
1. Blenkharn 2
JI, McPherson GAD, Blumgart LH. An improvement system for external biliary drainage. Lancet 1981; ii 781-82 Veterans Administration Cooperative Study Group on Antihypertensive Agents.
Comparison of propranolol and hydrochlorothiazide for the initial treatment of hypertension I: Results of short-term titration with emphasis on racial differences in response. JAMA 3
hypertension II: Results of long-term therapy. JAMA 1982; 248: 2004-11. Working Party on Mild to Moderate Hypertension. Adverse reactions to bendrofluazide and propranolol in the treatment of mild hypertension. Lancet 1981, ii: 539-43.
Woden Valley Hospital, Canberra, ACT 2606, Australia
TREVOR C. BEARD
OXYGEN FOR MULTIPLE SCLEROSIS p 1161) will find in "Greenfield"1 an description of fat embolism of the central nervous system in man which is very different from the neuropathological description which James submits as evidence for his theories. Fat embolism produces headaches and drowsiness; these are not features of multiple sclerosis (MS). Fat embolism is often fatal but MS is not, despite very large lesions. In the embolic process petechial haemorrhages are widespread in the white-matter, as are ring-andball haemorrhages; the capillary walls show focal necrosis and in the grey-matter necrotic areas with loss of nerve cells are found; and
SIR,—Dr James (May 21,
accurate
5
Dollery CT. Hypertension and new antihypertensive drugs: Clinical perspectives. Fed
Proc 1983; 42: 207-10. 6. Stewart IMcD G. Beta-adrenoceptor blockade and the incidence of myocardial infarction during treatment of severe hypertension. Br J Clin Pharmacol 1982; 13: 91-93.
DG, Johnston JH, Larkin H, Davies P. Clinical evidence that &bgr; adrenoceptor more cardiovascular complications than other antihypertensive drugs Drugs 1983; 25 (suppl 2): 326-30. Trafford JAP, Horn CR, O’Neal H, McGonigle R, Halford-Maw L, Evans R Five year follow-up of effects of treatment in mild and moderate hypertension. Br Med J 1981,
7. Beevers
blockers prevent
1982, 248: 1996-2003.
Veterans Administration Cooperative Study Group on Antihypertensive Agents. Comparison of propranolol and hydrochlorothiazide for the initial treatment of
4. MRC
SIR,—Dr MacGregor (April 2, p 750) notes that the most precise epidemiological data will never prove the sodium-hypertension hypothesis, but apparently the intervention studies needed for a definitive test will have to wait indefinitely, for "ethical and practical reasons". The hypothesis can be tested amongst the families of patients adopting a natural (unsalted) diet as a treatment for hypertension. In communities where suitable food is readily available, it seems both ethical and practical to recommend the whole family to eat it. Catering is easier, and children are probably protected from expressing their genetic potential for hypertension. In cases of dietary remission, such as MacGregor himselfhas reported, it might seem unethical not to try to involve the family. The hypothesis can be tested by showing whether many of the nonhypertensive family members who share meals with a spouse or parent dieting for hypertension remain normal, over a period in which blood pressures rise in a matched reference population on a higher sodium intake.
8
282: 1111-13
L, Berglund G, Elmfeldt O, Wedel H Beta-blockers hypertension Prev Med 1981; 10: 38-43. Greenfield JG. Neuropathology London: Edward Arnold, 1958:
9. Wilhelmsen 1.
versus
95.
saluretics in