Letters to the Editor
Hypertension: how low to go?
- Alasdair Livingston, John H. Hill, Dr Suzanne Hill
- Aust Prescr 2003;26:99-102
- 1 October 2003
- DOI: 10.18773/austprescr.2003.073
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Editor, – Articles which challenge accepted orthodoxy are usually good reading, and Suzanne Hill's article on hypertension (Aust Prescr 2003;26:53-5) is no exception. A number of interesting points emerge from her critique of the HOT study.
I take it that Table 1 deals with the whole population studied, including the 20% who were no longer using felodipine by the end of the study. The reason for cessation was not given in the study, but if it was due to adverse effects (few people enjoy having swollen legs) the results do not flatter felodipine as a first-choice drug.
Although the risk reductions shown in Table 1 all fail to reach statistical significance, seven out of nine favour the target groups with higher diastolic blood pressure. It is very hard indeed to see how they can be interpreted as showing 'the benefits of lowering the diastolic blood pressure down to 82.6 mmHg'. Dr Hill rightly rejects that conclusion.
Perhaps the study can be classified with the many which assess the effect of a single treatment regimen on a single selection of end-points (or surrogate end-points). The authors of such studies seem to forget that it is possible to die of something other than the disorder they are investigating. Indeed, the more proficient we become at preventing death from the big killers, the more of us will be left to die of something more painful, prolonged and expensive, such as cancer or dementia. Dr Hill rightly remarks that we should discuss quality issues with our patients, and not merely try to preserve them from this or that disease. In other words, we should treat patients, not statistics.
Dr Hill tells us that the diabetic sub-group definitely benefited from a more intensive effort to reduce their diastolic blood pressure. That means that the non-diabetic sub-group contributed more than their fair share to the non-benefit (or harm). It would be interesting to know if any of the comparisons in the non-diabetic sub-group showed significant harm.
Half the study population was given aspirin and the other half placebo. It would be useful to know if aspirin, used as primary prevention, contributed in any way to the good or bad effects, and if so in combination with which antihypertensives.
Bringing down the blood pressure with a calcium channel blocker may not be the same as bringing it down with (say) an ACE inhibitor. It is risky, therefore, to infer from the HOT study (or any other) that setting a target blood pressure, and achieving it by any means is a good or bad idea.
Editor, – The hypertension article in Australian Prescriber (Aust Prescr 2003;26:53-5) reports the HOT study in which the emphasis is on the diastolic blood pressure whereas a recent report, of the Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure in the USA, emphasises the systolic blood pressure. I understand current thinking is that emphasis should be on the systolic blood pressure as, if the systolic blood pressure is the aim of treatment the diastolic blood pressure will be satisfactory. Emphasis on diastolic blood pressure can leave the patient with a systolic blood pressure which is at a dangerous level.
John H. Hill
Dr Suzanne Hill, the author of the article, comments:
Dr Livingston identifies a number of interesting points around the interpretation of data from blood pressure trials. One of the difficulties about writing review articles in this area at the moment is that the literature is moving very quickly, with the recent publication of two more large clinical trials (Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) and the Second Australian National Blood Pressure Study (ANBP2)) as well as the publication of meta-analyses.1
Specific issues raised by Dr Livingston that I am not able to address include the question of whether there was particular harm in the sub-group of patients without diabetes. This is not reported in the original paper. The question of the role of aspirin would also have to be addressed by further analyses of the data, and indeed this is being addressed by ongoing studies2looking at the combinations of treatment for cardiovascular disease. The question of class effects and therapeutic group effects is a topical area and may need to be addressed by an article that more comprehensively reviews the current 'state of play' in thinking about treatment of hypertension.
Dr Hill noted the question of identifying risk based on systolic blood pressure versus diastolic blood pressure. This was not a question addressed by the HOT study, as he rightly identifies, and the answer would require a comprehensive review of current blood pressure literature to address completely.