Blood pressure lowering effects of non-surgical and non-pharmacological procedures for medullary vascular decompression.
The notion that the central nervous system participates in the development, maintenance and progression of the essential hypertensive state dates back to almost a century ago and throughout the years it has received a consistent number of experimental and clinical supports. These include the evidence that central neural factors participate at the short- and long-term blood pressure control and that abnormalities in neurogenic modulation of cardiovascular function characterize the early as well as the more established forms of the essential hypertensive state.1
*Further support for the so-called ‘neurogenic hypothesis’ of hypertension comes from the evidence of a close link between some hypertensive states and neurovascular compression of the rostral ventrolateral medulla oblongata,
that is, an area of the central nervous system with an important efferent pathway of the sympathetic nervous system.2, 3, 4, 5 This association is strengthened by the evidence that in different experimental animal models electrical, chemical or mechanical stimulation of the ventricular medulla triggers a transient pressor response.6, 7 It is also strengthened by the finding that in subgroups of patients with severe and/or resistant hypertension microsurgical decompression at the level of the rostral ventrolateral medulla substantially improves blood pressure control, leading to a long-term blood pressure normalization in a moderate number of patients.3, 8, 9, 10 The favorable hemodynamic outcome of the surgical intervention is likely to be triggered by a sympathetic deactivation, as several indirect and/or direct markers of adrenergic neural drive, such as plasma and urinary noradrenaline, low-frequency/high-frequency spectral power ratio as well as efferent postganglionic sympathetic nerve firing rate, have all shown a consistent and rather homogeneous reduction of adrenergic cardiovascular drive following surgical decompression.10, 11
In the present issue of the Journal of Human Hypertension, Bakris et al.12adds a new piece of information to the above-mentioned findings,
*by providing evidence on the favorable blood pressure lowering effects of chiropractic procedures capable of correcting a misalignment of the Atlas vertebra, thus inducing medullary vascular decompression.
According to a double-blind, placebo-controlled study design, hypertensive patients with documented evidence of Atlas vertebral misalignment were randomized either to a chiropractic vertebral realignment procedure or to a sham intervention.
*The primary efficacy end point of the study was represented by the effects of the approach on sphygmomanometric systolic and diastolic blood pressure values, which were reduced at the end of the 8-week follow-up period by about 14 and 8 mm Hg, respectively (placebo-corrected values).12
The intriguing findings provided by Bakris et al. in this pilot study raise a number of questions that hopefully will be matter of future investigations. First, how are the blood pressure lowering effects of the chiropractic procedure satisfactorily documented in the present study? Second, do the consistent short-term blood pressure lowering effects of the intervention persist over the long-term period? (* That depends on chronicity and articular decay) Third, does the lack of effect on the intervention of heart rate rule out any participation of sympathetic neural mechanisms to blood pressure reduction?
*Fourth, is the procedure associated with additional favorable cardiovascular effects, such as end organ damage regression? (interesting; subluxation degeneration with end organ disease or the regression there of)
*Finally, do the results of the present study imply that a misalignment of the Atlas vertebra represents a risk factor for development of hypertension and do chiropractic procedures stand as a new antihypertensive therapeutic approach?
A study limitation is represented by the fact that the assessment of the blood pressure lowering effects of the intervention was based on clinical blood pressure measurements, which in a trial testing the effectiveness of a hypertensive intervention is known to encompass various limitations.13 An important factor is the lack of information on the ability of the approach to lower blood pressure in daily-life conditions, that is, during a 24-h period. A further ‘intrinsic weakness’ of the study refers to the lack of information on the blood pressure lowering effects of the chiropractic intervention in the long-term period (months and years), as it has been carried out for the evaluation of the antihypertensive effects of surgical microvascular decompression.10 As far as heart rate as marker of adrenergic function is concerned, the lack of any change of this variable following the intervention does not necessarily imply that the chiropractic procedure has no sympatholytic effects. This is because heart rate is a poor and insensitive marker of sympathetic function, poorly correlating with more robust humoral or neurophysiological indices of adrenergic cardiovascular drive, such as plasma noradrenaline or muscle sympathetic nerve firing rate.14, 15Other relationships to adrenergic function, such as age, heredity, concomitant drug therapies and so on, will also need to be considered in any study.16, 17, 18
*In conclusion, the study by Bakris et al. provides new information regarding the favorable blood pressure lowering effects of chiropractic induced medullary microvascular decompression.
Before recommending this therapeutic strategy in the current clinical practice, however, it seems reasonable to wait for the results of large-scale clinical trials aimed at defining the long-term effects of the intention on clinic and ambulatory blood pressure as well as on some surrogate end points, such as cardiac and vascular target organ damage.
References
Grassi G. Role of the sympathetic nervous system in human hypertension. J Hypertens 1998; 16: 1979–1987.
Fein FM, Frishman W. Neurogenic hypertension related to vascular compression of the lateral medulla. Neurosurgery 1980; 6: 615–622.
Jannetta PJ, Segal R, Wolfson Jr SD. Neurogenic hypertension: etiology and surgical treatment. I: observation in 53 patients. Am Surg 1985; 201: 391–398.
Morimoto S, Sasaki S, Miky S, Kawa T, Itoh H, Nakata T et al. Pulsatile compression of the rostral ventrolateral medulla in hypertension. Hypertension 1997; 29(Part 2): 514–518.
Nicholas JS, D’Agostino SJ, Patel SJ. Arterial compression of the retrolineary sulcus of the ventrolateral medulla in essential hypertension and diabetes. Hypertension 2005; 46(Part 2): 982–985.
Jannetta PJ, Segal R, Wolfson SK, Dujovny M, Semba A. Neurogenic hypertension: etiology and surgical treatment: II: observations in an experimental nonhuman primate model. Am Surg 1985; 201: 253–261.
Morimoto S, Sasaki S, Shigejuki M, Kawa T, Nakamura K, Ischita Tet al. Pressor response to compression of the ventrolateral medulla mediated by glutamate receptors. Hypertension 1999; 33: 1207–1213.
Geiger H, Naraghi R, Schobel HP, Frank H, Sterzel R, Fahlbusch R. Decrease of blood pressure by ventrolateral medullary decompression in essential hypertension. Lancet 1998; 352: 446–449.
Levy EI, Clyde B, McLaughlin MR, Jannetta PJ. Microvascular decompression of the left lateral medulla oblongata for severe refractory neurogenic hypertension. Neurosurgery 1998; 43: 1–6.
Frank H, Schobel HP, Heusser K, Geiger H, Fahlbusch R, Naraghi R. Long-term results after microvascular decompression in essential hypertension. Stroke 2001; 32: 2950–2955.
Morimoto S, Susaki S, Takeda K, Furuya S, Naruse S, Matsumoto Ket al. Decreases in blood pressure and sympathetic nerve activity by microvascular decompression of the rostral ventrolateral medulla in essential hypertension. Stroke 1999; 30: 1707–1710.
Bakris G, Dickholtz M, Meyer PM, Kravits G, Avery E, Miller M et al. Atlas vertebra realignment and achievement of arterial pressure goal in hypertensive patients: a pilot study. J Hum Hypertens 2007 [E-pub ahead of print: 25 January 2007; doi:10.1038/sj.jhh.1002133].
Mancia G, Parati G. Guiding antihypertensive treatment decisions using ambulatory blood pressure monitoring. Curr Hypertens Rep2006; 8: 330–337.
Grassi G, Esler M. How to assess sympathetic activity in humans. J Hypertens 1999; 17: 719–734.
Grassi G, Vailati S, Bertinieri G, Seravalle G, Stella ML, Dell’Oro Ret al. Heart rate as a marker of sympathetic overactivity. J Hypertens 1998; 16: 1635–1639.
Konrady AO, Kasherininov YR, Shavarov AA, Shavarova EK, Vachrameeva NV, Krutikov AN et al. How can we block sympathetic overactivity? Effects of rilmenidine and atenolol in overweight hypertensive patients. J Hum Hypertens 2006; 20(6): 398–406.
Kennedy BP, Rao F, Botiglieri T, Sharma S, Lillie EO, Ziegler MG et al. Contributions of the sympathetic nervous system, glutathione, body mass and gender to blood pressure increase with normal aging: influence of heredity. J Hum Hypertens 2005; 19(12): 951–969.
Amador N, Encarnacion JJ, Guizar JM, Rodriguez L, Lopez M. Effect of losartan and spironolactone on left ventricular mass and heart sympathetic activity in prehypertensive obese subjects: a 16-week randomized trial. J Hum Hypertens 2005; 19(4): 277–283.