JMS Pearce
Hull, England

Marcus Tullius Cicero (106 BC–43 BC), statesman, scholar, and philosopher once said: If no use is made of the labours of past ages, the world must remain always in the infancy of knowledge. It may therefore be worthwhile to recollect the aspects of hypertension highlighted by the famously protracted saga of the 1950–1960 era often referred to as the “Pickering-Platt debate.”¹

Medical opinion has wavered over many decades about the questions: what is abnormally high blood pressure? And, what does it signify? These vital questions were unanswerable until blood pressure (BP) could be accurately measured. Karl Samuel Ritter Von Basch first measured human blood pressure in 1881. He invented the sphygmomanometer, a compressible rubber bulb filled with water, squeezed to obliterate the pulse, and connected to a mercury column, which showed the pressure required. In 1896, Scipione Riva-Rocci (1863–1937) improved the device with an inflatable cuff. The technique was refined by the surgeon Nikolai Korotkoff (1874–1920), who in 1905 distinguished systolic and diastolic blood pressures corresponding to the auscultated “Korotkoff sounds” when the inflated cuff was released.

The Pickering–Platt debate

Lord Robert Platt (1900–1978) was the Professor of Medicine, a nephrologist in Manchester, and president of the Royal College of Physicians. Sir George Pickering FRS (1904–1980) was an outstanding clinical scientist at St. Mary’s Hospital who in 1956 moved to Oxford as Regius Professor of Medicine.

Platt had published “Hereditary hypertension” in the Quarterly Journal of Medicine in 1947, regarding it as a distinct disease. The first of Pickering’s investigations appeared in Clinical Science where though acknowledging genetic factors he argued that essential hypertension represented a quantitative and not a qualitative deviation from normal.² Pickering believed that blood pressure was a continuous, unimodally distributed physiological trait:

It would seem, in fact, that the term essential hypertension represents no more than that section of the population in which the arterial pressure exceeds an arbitrary value and in which no other disease is found to account for the arterial pressures observed. According to where we draw the line, so we can make essential hypertension as common or as rare as we wish.^3,4

“Hypertension is,” wrote Pickering in 1974, “… as I pointed out in 1955, a new type of disease in which the deviation from the norm is one of degree and not of kind. It is a quantitative disease.”

By contrast, Sir Robert Platt repugned this concept, arguing that the high blood pressure values distinguished a discrete group that represented hypertension as a disease. He postulated (but did not claim to prove) that the disease might be caused by a gene behaving as a Mendelian dominant characteristic. Within a population, a hypertensive group could be distinguished from the normotensive remainder—a bimodal distribution.

This concept of essential hypertension as an inherited tendency to develop high blood-pressure in middle life presumes that there are two populations, one in which blood-pressure rises significantly in middle age, often reaching heights at which it seriously contributes to mortality, and another population in which the blood-pressure rises only very little if at all with increasing years.⁵

These opposing concepts for many years appeared in The Lancet and elsewhere with controversial views that influenced clinical practice and theoretical notions both of definition and classification. Essentially, the two schools were based on different methods: Platt’s on clinical illnesses seen in a hospital environment, Pickering’s on surveillance medicine in the healthy community. Both recognized the cardiovascular risks of high blood pressure.

Since then, epidemiological evidence is consistent with unimodally distributed blood pressure; it also supports Pickering’s claim that there is benefit in lowering blood pressure in anyone at sufficient cardiovascular risk.⁶ What constitutes sufficient cardiovascular risk is less well defined. The Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7) in 2003 identified a group with BPs of 120–139 mm Hg systolic and 80–89 mm Hg diastolic as having “prehypertension.” However, the therapeutic assertion of Law et al. 6 that (emphasis mine) “Our results indicate the importance of lowering blood pressure in everyone over a certain age, rather than measuring it in everyone and treating it in some” is at least as debatable as the “Pickering-Platt debate.”⁷

Though not fully resolved, the Pickering-Platt argument subsided in the mid-1960s, when both proponents slightly resiled from their original opinions. Platt edged away from his single gene hypothesis, while Pickering conceded that the bell-shaped curve may accommodate pathologies caused by single gene mutations.⁸ Recently discovered somatic variants in genomic studies have identified more than 500 blood pressure relevant gene loci, but each gene exerts only a small effect on blood pressure, which lends limited support to Platt’s assertion.

Robert Platt was created Baronet in 1959 and became a Life Peer as Baron Platt of Grindleford in 1967. Sir George Pickering’s list of honorary degrees was “too lengthy to be included in entirety” in his Munk’s Roll entry; he was knighted in 1957 and in 1960 was elected a Fellow of the Royal Society.

***

Sir George Pickering’s son Thomas G. Pickering— a distinguished clinical investigator at Cornell University, Mount Sinai, and Columbia University— independently introduced ambulatory BP measurement (ABPM).⁹ He demonstrated white‐coat hypertension in patients whose BP is elevated in a clinic, but not during ambulatory measurement in the course of varying daily activities; he also identified masked hypertension (reverse white‐coat hypertension) in patients normotensive in a doctor’s clinic but who had an elevated ABPM. The extent of the clinical risks of these variants has still not been wholly resolved.⁷

References

1. Swales JD. (Editor) Platt versus Pickering. An Episode in Recent Medical History. London: Keynes Press, 1985.
2. Hamilton M, Pickering GW, Fraser Roberts JA, Sowry GSC. The aetiology of essential hypertension: 4. The role of inheritance. Clinical Science 1954;13:273-304.
3. Oldham PD, Pickering G, Fraser Roberts J A, Sowry GSC. The nature of essential hypertension. Lancet 1960;275:170.
4. Pickering G. Hypertension: Causes, Consequences and Management. London: Churchill Livingstone, 1974.
5. Platt R. The nature of essential hypertension. Lancet 1959;274:1092.
6. Law MR, Morris JK, Wald NJ. Use of blood pressure lowering drugs in the prevention of cardiovascular disease: meta-analysis of 147 randomised trials in the context of expectations from prospective epidemiological studies. British Medical Journal 2009;19:338:b1665.
7. Pickering, TG. Lowering the Thresholds of Disease—Are Any of Us Still Healthy? The Journal of Clinical Hypertension 2004;6:672-4.
8. Timmermann C. A Matter of Degree: The Normalisation of Hypertension, circa 1940–2000. In: Waltraud Ernst (ed.), Histories of the Normal and the Abnormal. London: Routledge, 2006; 245-61.
9. O’Brien E. First Thomas Pickering memorial lecture: ambulatory blood pressure measurement is essential for the management of hypertension. J Clin Hypertens (Greenwich). 2012;(12):836-47.