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Journal of Hypertension:
doi: 10.1097/HJH.0b013e328360bae9
Editor's Corner

Contributions to management of hypertension from papers in the current issue

Zanchetti, Alberto

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Istituto Auxologico Italiano and Centro Interuniversitario di Fisiologia Clinica e Ipertensione, Università di Milano, Milan, Italy

Correspondence to Professor Alberto Zanchetti, Centro di Fisiologia Clinic e Ipertensione, Università di Milano, Via F. Sforza, 35, 20122 Milan, Italy. Tel: +39 02 50320484; e-mail: alberto.zanchetti@unimi.it/alberto.zanchetti@auxologico.it

There are several aspects of the treatment of hypertension that are approached by papers published in this issue of the Journal of Hypertension. John Chalmers et al. (pp. 1043–1048) report the results of a survey of current hypertension management recommended by national societies affiliated with the International Society of Hypertension. There was a remarkable consistency across countries from different regions and with different levels of income on most aspects of management: methods for blood pressure measurement, changes in life style, choice of antihypertensive agents, and use of combination therapy. All this broadly reflects guideline recommendations. A striking divergence from guidelines was, however, reported by half of the national societies, which did not use the recommended lower threshold and target for treatment in high-risk patients (130/80 rather than 140/90 mmHg). More than a real divergence from guidelines, such as the Joint National Committee 7th report [1] or the European Society of Hypertension (ESH) and European Society of Cardiology 2007 guidelines [2], the more conservative attitude of a large number of the national societies appears to witness the wide influence and acceptance of the ESH reappraisal document [3], which clearly showed the recommendation of a 130/80 mmHg threshold and target for treating high-risk patients (with diabetes, previous stroke, previous coronary disease, chronic kidney disease) was unsupported by trial evidence. The ESH reappraisal paper was published at the end of 2009 [3], and was strengthened in 2010 by the publication of the results of the Action to Control Cardiovascular Risk in Diabetes trial [4] (no significant difference in cardiovascular event incidence in patients with diabetes whose SBP was lowered to a mean of 119 or 133 mmHg). These publications likely influenced the opinions of the societies before these received the survey questionnaire in December 2011. It is pleasing, therefore, to see how promptly evidence-based arguments are shared by scientific societies with clinical influence.

Concern about the use of too low blood pressure targets in high-risk patients, including those with coronary disease, critically discussed in the ESH 2009 reappraisal document [3], is also raised by an important study by Rabkin et al. (pp. 975–982), who have measured DBP beyond a coronary stenosis in a large series of patients with angina pectoris associated with hypertension and/or diabetes. A systemic DBP of 60–65 mmHg was often accompanied by a dramatic reduction in coronary blood flow, sometimes approximating zero. The call to caution resulting from Rabkin et al.'s study is indirectly reinforced by an experimental study by Szymanski et al. (pp. 966–974), showing that rat strains with hypertension or chronic renal disease have an enhanced sensitivity to myocardial ischaemia compared with healthy Wistar rats.

Of course, no current guidelines recommend lowering DBP to levels as low as 60–65 mmHg (evidence from the Hypertension Optimal Treatment [5] and United Kingdom Prospective Diabetes Study trials [6] indicates the optimal target in diabetics is between 80 and 85 mmHg), but the problem may arise in some elderly patients with isolated systolic hypertension and DBP initially very low, in whom attempting to reduce the elevated systolic values may bring diastolic values to a potentially dangerous range. Overwhelming evidence of benefit from treating isolated systolic hypertension in the elderly should not prevent doctors from carefully monitoring symptomatic or electrocardiographic signs of cardiac ischaemia in patients in whom diastolic pressure is or is brought to very low levels. That in hypertension cardiac involvement is widespread and does not involve only the left ventricle, but also right-ventricular hypertrophy often occurs clearly results from an accurate review and meta-analysis published in this issue by Cuspidi et al. on behalf of the Italian Society of Hypertension (pp. 858–865).

The large number of our readers concerned with resistant or uncontrolled hypertension may read with interest a paper by Oudman et al. (pp. 1025–1031) showing that high serum levels of creatine kinase is associated with higher prevalence of hypertension and hypertension treatment failure. The authors hypothesize that creatine kinase may increase blood pressure through greater sodium retention and cardiovascular contractility.

The emerging problem of hypertension in developing countries is the topic of an epidemiological study from Kenya (van de Vijver et al., pp. 1018–1024) indicating that in slums in Nairobi, hypertension is associated with very low rates of awareness, treatment and control. However, an optimistic message is that, once people are aware of their hypertension, most seek treatment, and therefore the best gain in treatment can be made by raising awareness. The paper is commented by Etyang et al. who underline that studying determinants and control of hypertension in previously neglected settings such as slums may yield results that are widely applicable worldwide (pp. 877–879). Another optimistic message comes from a large prospective study investigating the effect of hypertension on hospitalization risk and medical expenditure in Japan (Nakamura et al., pp. 1032–1042), showing that untreated grade 3 hypertension led to more frequent hospitalization and higher expenditure compared with optimal blood pressure. The impact of a higher risk of hospitalization on healthcare cost is commented by Waeber and Feihl (pp. 880–881) in an accompanying editorial. Finally, Schaefer et al. (pp. 993–1000) report the results of administering the angiotensin receptor blocker, valsartan, to small children (aged 6 months to 5 years) with hypertension.

Prevention largely depends on capacities of predicting. A group of papers in this issue of the journal are devoted to prediction of hypertension. Almoosawi et al. (pp. 882–892), analysing data from the prospective 1946 British birth cohort, find that the time-of-day of energy intake influences development of subsequent hypertension, with greater energy intake late in the evening being associated with higher hypertension prevalence, incidence and greater increases in blood pressure. The implications of these findings are discussed in an editorial by Ferreira and Huijberts in the context of the function of an endogenous circadian clock (pp. 866–869). They also warn that more research is needed before the popular advice ‘eat breakfast like a king, lunch like a prince, and dinner like a pauper’ is accepted or rejected. Always in terms of prediction, in a large community-based sample of elderly in Uppsala, impairment of carefully measured endothelial function did not predict development of hypertension or blood pressure increase (Lytsy et al., pp. 936–939). In a paediatric primary care setting, BMI, waist circumference-to-height ratio and low exercise were confirmed as factors related to risk of hypertension and prehypertension (Giussani et al., pp. 983–992).

As to risk of diabetes, the Framingham Offspring Study is the source of data analysed by De Miguel-Yanes et al. (pp. 1001–1009) to investigate possible interactions between genetic factors related to beta-cell frailty and hypertension in their associations with change over time in fasting glucose and onset of type 2 diabetes mellitus: although both genetic factors and hypertension played a significant role, no interaction was found.

The risk of all-cause mortality has been explored by Bursztyn and Ben-Dov (pp. 900–905) in relation to salt sensitivity. The authors have made recourse to surrogate measurements of salt sensitivity derived from ambulatory blood pressure monitoring, and based on the extent of dipping and the mean 24-h heart rate. Assuming salt sensitivity is accurately signalled by low dipping and high heart rate, they found 20-year all-cause mortality to be associated with salt sensitivity in men but not in women. Relation of ambulatory blood pressure indices with salt sensitivity are commented in an accompanying editorial by Castiglioni et al., who remark that ambulatory blood pressure-derived sodium sensitivity may become a relatively simple tool in clinical practice once it is validated through comparison with classic salt loading studies (pp. 870–873).

Assessing changes in large artery functional properties with age and hypertension continues to be of primary interest in research and clinical examination. Two important methodological studies on pulse wave velocity measurement are published in the current issue of the Journal. Levi-Marpillat et al. (pp. 940–945) report it is crucial to use a sliding calliper to assess the carotid–femoral distance, while using a flexible tape leads to overestimations depending on BMI. In a carefully controlled study, Bossuyt et al. (pp. 946–951) have compared the real travelled carotid–femoral distance, as measured on MRI, with the distance obtained with a tape. They conclude that the travelled path is slightly longer at the right than at the left body side and the straight MRI distance tends to perform better than tape measure distance, thus supporting the recommendation to measure pulse wave velocity at the right body side using a calliper.

Correlation of increased arterial stiffness with various risk factors has been investigated in two studies. Teoh et al. (pp. 1010–1017) report that central obesity in people with type 2 diabetes is associated with increased arterial stiffness, the association being independent of conventional risk factors for central obesity. Van Dijk et al. (pp. 952–959) have found homocysteine to be strongly associated with pulse wave velocity particularly in older persons, and suggest increased aortic stiffness may account for the strong association between homocysteine and cardiovascular mortality in the elderly. This suggestion is critically discussed in an editorial by Delles, who remarks that what is suggested by this study is not that homocysteine is a marker of risk in the very elderly, but that damage accumulates over a long period of time until it can be assessed with relatively crude techniques such as PWV (pp. 874–876). Also a review article by Safar and Nilsson (pp. 848–857) is devoted to central artery stiffening, vascular aging and cardiovascular risk in the elderly.

Microvascular disease is the object of a study by Downie et al. (pp. 960–965) comparing the traditional Keith, Wagner and Barker classification of hypertensive retinopathy with a new simplified classification. The new classification was found both reliable and repeatable, with the advantage of allowing the correlation of retinal microvascular signs to incident cardiovascular risk.

Four other studies in this issue of the journal concern different areas of hypertension research. Michal et al. (pp. 893–899) have approached the debated problem of the relationship between hypertension and depression by the analysis of a large cross-sectional population from the Gutenberg Health Study, and report that multiple pathways of opposite directions appear to link depressive symptoms with blood pressure, hypertension and antihypertensive medications. Tikkakoski et al. (pp. 906–915) have compared haemodynamics in hypertensive and normotensive individuals at rest and during passive head-up tilt, and remark that not only supine haemodynamics, but also responses to tilt differ between normotension and hypertension. Blanco-Rivero et al. (pp. 916–926) report interesting experiments about the effects of aerobic exercise in rats on contractile responses in the mesenteric artery implying increased neuronal nitric oxide release and bioavailability. Finally, Crespo et al. (pp. 927–935) report their studies on congenic rat strains exploring the genetics of hypertensive diastolic heart failure.

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ACKNOWLEDGEMENTS

Conflicts of interest

There is no conflict of interest.

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REFERENCES

1. Chobanian AV, Bakris GL, Black HR, Cushman WC, Green LA, Izzo VL Jr, et al. Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure. Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Hypertension 2003; 42:1206–1252.

2. Mancia G, De Backer G, Dominiczak A, Cifkova R, Fagard R, Germano G, et al. 2007 Guidelines for the Management of Arterial Hypertension. The Task Force for the Management of Arterial Hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC). J Hypertens 2007; 25:1105–1187.

3. Mancia G, Laurent S, Agabiti-Rosei E, Ambrosioni E, Bunier M, Caulfield MJ, et al. Reappraisal of the European guidelines on hypertension management: a European Society of Hypertension Task Force document. J Hypertens 2009; 27:2121–2158.

4. The ACCORD Study Group. Effects of intensive blood pressure control in type 2 diabetes mellitus. N Engl J Med 2010; 362:1575–1585.

5. Hansson L, Zanchetti A, Carruthers SG, Dahlöf B, Elmfeldt D, Julius S, et al. Effects of intensive blood pressure lowering and low dose aspirin in patients with hypertension: principal results of the Hypertension Optimal Treatment (HOT) randomized trial. Lancet 1998; 351:1755–1762.

6. UK Prospective Diabetes Study Group. Tight blood pressure control and risk of macrovascular and microvascular complications in type 2 diabetes: IKPDS 38. BMJ 1998; 317:703–713.

© 2013 Lippincott Williams & Wilkins, Inc.

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