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Cited by 161Blood Pressure and Hypertension StudiesHeart Rate Variability and Autonomic ControlCardiovascular Function and Risk Factors

Hypertensive left ventricular hypertrophy: relation to peripheral sympathetic drive

Open access
Greenwood, John P, Scott, Eleanor M, Stoker, John B, Mary, David A.S.G·2001·Journal of the American College of Cardiology
DOI 10.1016/s0735-1097(01)01600-x
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Abstract

Objectives This study was designed to examine whether the occurrence of left ventricular hypertrophy (LVH) in moderate to severe essential hypertension (EHT) was associated with alteration in peripheral sympathetic drive.Background In hypertension, LVH is an independent predictor of increased morbidity and mortality. The reported mechanisms leading to LVH remain unclear but include hemodynamic and humoral factors. The sympathetic nervous system may be important, particularly as catecholamines have been shown to have trophic properties. We tested the hypothesis that sympathetic activity measured using microneurography could be different in patients with hypertension depending on the presence of LVH.Methods We examined 28 subjects with moderate to severe EHT (stages 2 to 3; Joint National Committee [JNC]-VI classification). Fourteen had echocardiographic evidence of LVH (EHT + LVH), while the other 14 subjects (EHT) did not. Subjects were matched in terms of age, body mass index and levels of arterial blood pressure. Peripheral muscle sympathetic nerve activity was measured from both multiunit bursts (MSNA) and single unit (s-MSNA) vasoconstrictor impulses via the peroneal nerve.Results The mean frequency of s-MSNA and MSNA was greater in the EHT + LVH group than it was in the EHT group (mean +/- SEM; 75.9 +/- 6.9 impulses/100 beats vs. 52.1 +/- 2.9 impulses/100 beats, p < 0.001 and 64.2 +/- 5.7 bursts/100 beats vs. 48.9 +/- 2.8 bursts/100 beats, p < 0.05).Conclusions These results indicate that, in subjects with moderate to severe hypertension, the presence of LVH is associated with higher sympathetic discharge, evidenced by an increase in unitary firing frequency and also by fiber recruitment.

AI snapshot

Written from the paper’s full text.

TL;DR

In moderate-to-severe essential hypertension, patients with echocardiographic left ventricular hypertrophy had higher resting peripheral sympathetic discharge than matched patients without LVH. The authors conclude that central sympathetic hyperactivity may be a factor in the development of hypertensive LVH.

Key findings

  • Single-unit muscle sympathetic nerve activity (s-MSNA) was greater in EHT + LVH than in EHT without LVH: 75.9 ± 6.9 vs. 52.1 ± 2.9 impulses/100 beats, p < 0.001.
  • Multiunit MSNA was also greater in EHT + LVH: 64.2 ± 5.7 vs. 48.9 ± 2.8 bursts/100 beats, p < 0.05.
  • Per-minute differences did not reach significance: s-MSNA 51.1 ± 5.3 vs. 38.1 ± 2.4 impulses/min (p > 0.05); MSNA 40.6 ± 2.5 vs. 35.5 ± 2.1 bursts/min (p > 0.05).
  • s-MSNA and MSNA per 100 cardiac beats correlated with left ventricular mass index (r = 0.48 and r = 0.46, respectively; p < 0.05).

Methods

  • Cross-sectional study of 28 Caucasian patients with newly diagnosed moderate-to-severe essential hypertension (JNC-VI stages 2–3): 14 with echocardiographic LVH and 14 without LVH, matched for age, body weight, body mass index, and arterial blood pressure.
  • Peripheral muscle sympathetic nerve activity was recorded from the right peroneal nerve using microneurography, measuring both multiunit bursts (MSNA) and single-unit vasoconstrictor impulses (s-MSNA); LVH was assessed by M-mode echocardiography.
  • Two-way ANOVA with Bonferroni post-test comparisons and least-squares linear correlation were used; data are mean ± SEM.

Limitations

  • The paper states that human autonomic studies are constrained by limited techniques for directly quantifying sympathetic activity; microneurography records from a peripheral nerve, and reflex sympathetic activation is heterogeneous, though this study was performed at rest.
  • The paper states that this was a cross-sectional study, so it implies association but gives no direct evidence of causality, and that many additional factors are important in LVH development.
  • Evident from the text: the sample was small (28 patients), 6 of 14 EHT + LVH patients were already on antihypertensive therapy before the study (omitted only on the study day), and there was some overlap in left ventricular mass between groups.

Model-written summary. Check it against the paper before relying on it.

Integrity signals

Registry

Crossref · 10.1016/s0735-1097(01)01600-x

Cites

43 of 43 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Claims the paper makes

0 of 51 cited sources checked · 0 supported · 0 flagged

  • Findingown data
    § Results

    The mean frequency of MSNA per minute was not significantly different between the EHT+LVH and EHT groups.

    “The group mean frequency of MSNA in EHT + LVH versus EHT was 40.6 ± 2.5 bursts/min versus 35.5 ± 2.1 bursts/min (p > 0.05) and 64.2 ± 5.7 bursts/100 beats versus 48.9 ± 2.8 bursts/100 beats (p < 0.05).”
    Quote in the paperNot a substantial claim
  • Findingown data
    § Results

    Posterior wall thickness was greater in the EHT+LVH group than in the EHT group.

    “Respectively, for the EHT + LVH and the EHT groups, posterior wall thickness was 13 ± 0.8 mm and 10 ± 0.3 mm (p < 0.05); interventricular septal thickness was 12 ± 0.8 mm and 10 ± 0.3 mm (p > 0.05), and end-diastolic volumes were 124 ± 12.4 ml and 127 ± 15.8 ml (p > 0.8).”
    Quote in the paperSubstantial claim
  • Findingown data
    § Results

    Left ventricular mass index was greater in the EHT+LVH group than in the EHT group.

    “The estimated LVM in the EHT + LVH group was 301 ± 26.6 g and in the EHT group was 215 ± 19 g (p < 0.05), and the values for LVMI when indexed by body surface area were 155 ± 13 g/m2and 113 ± 10.9 g/m2for the two groups, respectively (p < 0.05).”
    Quote in the paperSubstantial claim
  • Findingown data
    § RESULTS

    In patients with moderate to severe essential hypertension, the mean frequency of single-unit muscle sympathetic nerve activity (s-MSNA) per 100 cardiac beats is greater in those with left ventricular hypertrophy (LVH) than in those without LVH.

    “The mean frequency of s-MSNA and MSNA was greater in the EHT + LVH group than it was in the EHT group (mean ± SEM; 75.9 ± 6.9 impulses/100 beats vs. 52.1 ± 2.9 impulses/100 beats, p < 0.001 and 64.2 ± 5.7 bursts/100 beats vs. 48.9 ± 2.8 bursts/100 beats, p < 0.05).”
    • Also stated in: § Results · plain
      “The group mean frequency of s-MSNA in EHT + LVH versus EHT was 51.1 ± 5.3 impulses/min versus 38.1 ± 2.4 impulses/min (p > 0.05) and 75.9 ± 6.9 impulses/100 beats versus 52.1 ± 2.9 impulses/100 beats (p < 0.001).”
    • Also stated in: § Discussion · plain
      “In this study, the resting mean discharge frequency of s-MSNA per 100 cardiac beats in the patients with EHT + LVH was significantly greater (by about 46%) than that in the EHT group.”
    Quote in the paperSubstantial claim
  • Findingown data
    § Results

    Within each group, there was no significant correlation between resting sympathetic discharge (s-MSNA or MSNA) and resting arterial blood pressure or heart rate.

    “However, there was no significant correlation within any group (consistently r< 0.38, p > 0.09) between resting sympathetic discharge (s-MSNA or MSNA) and the levels of resting arterial blood pressure (systolic, diastolic or mean pressure) or heart rate.”
    Quote in the paperNot a substantial claim
  • May combine two claims. 21
  • Classified as probably not a substantial claim. 15

  • May combine two claims.

    Findingown data
    § Results

    There was a significant positive correlation between both s-MSNA and MSNA quantified per 100 cardiac beats and left ventricular mass index.

    “there was a significant correlation between both s-MSNA and MSNA (quantified per 100 cardiac beats) and LVMI (always p < 0.05; r= 0.48 and r= 0.46, respectively).”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Findingown data
    § Results

    There was a significant positive correlation between resting s-MSNA and MSNA and age across subjects.

    “As expected, there was a significant positive correlation (r) for resting s-MSNA and MSNA with the subjects age (rat least 0.42 and at most 0.59; p < 0.0002).”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Findingcitation
    § Discussion

    The results obtained from MSNA recordings in this study were similar to those previously published in age-comparable hypertensive subjects.

    “The results obtained from MSNA recordings in this study were similar to those previously published in age-comparable hypertensive subjects (15,16,25,26,28).”
    Quote in the paperNot a substantial claim0 of 5 sources checked
    • cites [15] Grassi, 1998, Baroreflex control of sympathetic nerve activity in essential and secondary hypertension, Hypertension source

      Not checked in the free run.

    • cites [16] Greenwood, 1999, Single unit sympathetic discharge, Circulation source

      Not checked in the free run.

    • cites [25] Yamada, 1989, Age-related changes in muscle sympathetic nerve activity in essential hypertension, Hypertension source

      Not checked in the free run.

    • cites [26] Matsukawa, 1991, Reduced baroreflex changes in muscle sympathetic nerve activity during blood pressure elevation in essential hypertension, J Hypertens source

      Not checked in the free run.

    • cites [28] Miyajima, 1991, Muscle sympathetic nerve activity in renovascular hypertension and primary aldosteronism, Hypertension source

      Not checked in the free run.

  • May combine two claims.

    Findingown data
    § Discussion

    In patients with moderate to severe essential hypertension, the presence of left ventricular hypertrophy is associated with higher resting sympathetic discharge, evidenced by both an increase in unitary firing frequency and by fiber recruitment, compared with subjects without left ventricular hypertrophy.

    “The results of this investigation suggest that the occurrence of LVH in EHT is associated with an increase in magnitude of the sympathetic hyperactivity compared with that in subjects without LVH.”
    • Also stated in: § Conclusions · boosted
      “This is the first evidence that, in patients with moderate to severe EHT, the presence of LVH is associated with higher resting sympathetic discharge, evidenced by both an increase in unitary firing frequency and by fiber recruitment.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Study design and conductown data
    § Results

    There was no significant difference in age, body weight, body mass index, heart rate or arterial blood pressure between the EHT+LVH and EHT groups.

    “There was no significant difference in age, body weight, body mass index, heart rate or arterial blood pressure between the groups.”
    • Also stated in: § Methods · plain
      “these were matched in terms of age, body weight, body mass index and levels of arterial blood pressure.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Interpretationreasoning
    § Discussion

    Increased MSNA represents central activation as well as reflex-based increases (fiber recruitment) in sympathetic activity.

    “Second, increased MSNA represents central activation as well as reflex-based increases (fiber recruitment) in sympathetic activity.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Interpretationown data
    § Discussion

    The relative sympathetic hyperactivity in EHT+LVH reflected an increased central output at rest and was not caused by differences in arterial blood pressure, age or body weight.

    “This relative sympathetic hyperactivity reflected an increased central output at rest and was not caused by differences in arterial blood pressure, age or body weight.”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation
    § CONCLUSIONS

    In patients with hypertension, the occurrence of LVH has been associated with an increase in mortality from all cardiovascular causes.

    “In patients with hypertension, the occurrence of left ventricular hypertrophy (LVH) has been associated with an increase in mortality from all cardiovascular causes (1–4).”
    Quote in the paperNot a substantial claim0 of 4 sources checked
    • cites [1] Levy, 1990, Prognostic implications of echocardiographically determined left ventricular mass in the Framingham Heart study, N Engl J Med source

      Not checked in the free run.

    • cites [2] Koren, 1991, Relation of left ventricular mass and geometry to morbidity and mortality in uncomplicated essential hypertension, Ann Intern Med source

      Not checked in the free run.

    • cites [3] Kannel, 1992, Left ventricular hypertrophy as a risk factor in arterial hypertension, Eur Heart J source

      Not checked in the free run.

    • cites [4] Gueyffier, 1999, Identification of risk factors in hypertensive patients, Circulation source

      Not checked in the free run.

  • Classified as probably not a substantial claim. May combine two claims.

    Premisecitation
    § Discussion

    Microneurography is a well-established technique that has been used successfully in the assessment of peripheral sympathetic activity.

    “Microneurography is a well-established technique that has been used successfully in the assessment of peripheral sympathetic activity (14).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [14] Wallin, 1993, Assessment of sympathetic mechanisms for recordings of postganglionic efferent nerve traffic

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation
    § Discussion

    Patients with hypertension have a greater frequency of MSNA bursts than properly matched normotensive subjects.

    “Despite the difficulty of establishing that every unit within a burst has a vasoconstrictor role, there is a wealth of evidence to suggest that patients with hypertension have a greater frequency of MSNA bursts than properly matched normotensive subjects (15,25–27).”
    Quote in the paperNot a substantial claim0 of 4 sources checked
    • cites [15] Grassi, 1998, Baroreflex control of sympathetic nerve activity in essential and secondary hypertension, Hypertension source

      Not checked in the free run.

    • cites [25] Yamada, 1989, Age-related changes in muscle sympathetic nerve activity in essential hypertension, Hypertension source

      Not checked in the free run.

    • cites [26] Matsukawa, 1991, Reduced baroreflex changes in muscle sympathetic nerve activity during blood pressure elevation in essential hypertension, J Hypertens source

      Not checked in the free run.

    • cites [27] Floras, 1993, Sympathoneural and haemodynamic characteristics of young subjects with mild essential hypertension, J Hypertens source

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation
    § CONCLUSIONS

    The development of LVH has been attributed to many factors, including raised arterial pressure levels and growth-promoting substances such as angiotensin II, insulin-like growth factor-1 and circulating catecholamines.

    “The development of LVH has been attributed to many factors, including raised arterial pressure levels (resulting in increased myocardial workload) and growth-promoting substances such as angiotensin II, insulin-like growth factor-1 and circulating catecholamines (5–10).”
    Quote in the paperNot a substantial claim0 of 6 sources checked
    • cites [5] Lauer, 1991, Influence of contemporary versus 30-year blood pressure levels on left ventricular mass and geometry, J Am Coll Cardiol source

      Not checked in the free run.

    • cites [6] Bauwens, 1991, Influence of the arterial blood pressure and nonhemodynamic factors on left ventricular hypertrophy in moderate essential hypertension, Am J Cardiol source

      Not checked in the free run.

    • cites [7] Duprez, 1993, Influence of arterial blood pressure and aldosterone on left ventricular hypertrophy in moderate essential hypertension, Am J Cardiol source

      Not checked in the free run.

    • cites [8] Harrap, 1996, Plasma angiotensin II, predisposition to hypertension, and left ventricular size in healthy young adults, Circulation source

      Not checked in the free run.

    • cites [9] Verdecchia, 1999, Circulating insulin and insulin growth factor-1 are independent determinants of left ventricular mass and geometry in essential hypertension, Circulation source

      Not checked in the free run.

    • cites [10] Julius, 1998, Effect of sympathetic overactivity on cardiovascular prognosis in hypertension, Eur Heart J

      Not checked in the free run.

  • May combine two claims.

    Interpretationown data
    § CONCLUSIONS

    In subjects with moderate to severe hypertension, the presence of LVH is associated with higher sympathetic discharge, evidenced by an increase in unitary firing frequency and also by fiber recruitment.

    “These results indicate that, in subjects with moderate to severe hypertension, the presence of LVH is associated with higher sympathetic discharge, evidenced by an increase in unitary firing frequency and also by fiber recruitment.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Premisecitation
    § Discussion

    In patients with moderate to severe hypertension, sympathetic output was lower or equal compared with matched groups with milder hypertension, depending on whether single units or multiunits were examined.

    “More recently, we have shown that patients with moderate to severe hypertension had either lower or equal sympathetic output compared with matched groups with milder hypertension, depending on whether single units or multiunits were examined (16).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [16] Greenwood, 1999, Single unit sympathetic discharge, Circulation source

      Not checked in the free run.

  • Classified as probably not a substantial claim. May combine two claims.

    Study design and conductreasoning
    § Discussion

    This was a cross-sectional study, which implies an association but gives no direct evidence of causality.

    “One final point to remember is that this was a cross-sectional study, which, although it implies an association, gives no direct evidence of causality.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Premisecitation
    § Discussion

    The onset of hypertension is associated with sympathetic hyperactivity, while eventually the severity of hypertension is maintained, in part, by the occurrence of end-organ structural changes.

    “These findings have provided support to the theory that the onset of hypertension is associated with sympathetic hyperactivity, while, eventually, the severity of hypertension is maintained, in part, by the occurrence of end-organ structural changes (11,34).”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [11] Julius, 1996, Sympathetic overactivity in hypertension. A moving target, Am J Hypertens source

      Not checked in the free run.

    • cites [34] Folkow, 1982, Physiological aspect of primary hypertension, Physiol Rev source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation
    § Discussion

    In the former study, subjects with severe hypertension had a high left ventricular mass index, whereas in the latter study left ventricular hypertrophy was excluded.

    “Finally, and perhaps most importantly, subjects with severe hypertension in the former study had a high LVMI, whereas, in the latter study, LVH was excluded.”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [15] Grassi, 1998, Baroreflex control of sympathetic nerve activity in essential and secondary hypertension, Hypertension source

      Not checked in the free run.

    • cites [16] Greenwood, 1999, Single unit sympathetic discharge, Circulation source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation
    § Discussion

    Chronic administration of atenolol or metoprolol may have either no effect on or reduce the resting mean frequency of sympathetic discharge in essential hypertension.

    “However, chronic administration, as in this study, with agents such as atenolol (29)and metoprolol (30)may, respectively, have either no effect on or reduce the resting mean frequency of sympathetic discharge in EHT.”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [29] Greenwood, 1998, Effect of atenolol therapy on peripheral sympathetic nerve discharge in essential hypertension, J Hypertens

      Not checked in the free run.

    • cites [30] Wallin, 1984, Sympathetic outflow to muscles during treatment of hypertension with metoprolol, Hypertension source

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Study design and conductnone given
    § Methods

    Data analysis was performed off-line by a single experienced operator without knowledge of the patient diagnosis.

    “Without knowledge of the patient diagnosis, data analysis was performed off-line by a single experienced operator using signal-processing software (FASTDAQ, Lectromed UK Ltd.).”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation
    § Methods

    Neural activity was expressed both per minute and per 100 cardiac beats because there is a complex relationship between heart rate and sympathetic discharge frequency, and the latter expression avoids interference by the length of the cardiac cycle.

    “Neural activity was expressed both per min and per 100 cardiac beats as it is understood that there is a complex relationship between heart rate and sympathetic discharge frequency, and the latter expression avoids any interference by the length of the cardiac cycle (24).”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [24] Sundlöf, 1977, The variability of muscle nerve sympathetic activity in resting recumbent man, J Physiol (Lond) source

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Study design and conductnone given
    § Methods

    The study group was recruited from among 34 patients; in 6 patients it was not possible to obtain stable microneurographic data.

    “The study group was recruited from among 34 patients; in 6 patients it was not possible to obtain stable microneurographic data.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Premisecitation
    § Discussion

    Blood pressure classification differed between the two studies, the former using an arbitrary classification and the latter using the JNC-VI classification.

    “First, blood pressure classification differed between the studies, the former using an arbitrary classification and the latter using the JNC-VI classification (21).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [21] 1997, The sixth report of the Joint National Committee on prevention, detection, evaluation, and treatment of high blood pressure, Arch Intern Med source

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S2 (checkable).

    Interpretationreasoning
    § Discussion

    Using a combination of single and multiunit assessment may have allowed further characterization of the hypertensive subjects.

    “Thus, using a combination of single and multiunit assessment may have allowed further characterization of the hypertensive subjects.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Premisecitation
    § Discussion

    Catecholamines have trophic properties on cardiac myocytes and in the intact animal heart.

    “In support of this, catecholamines have been shown experimentally to have trophic properties on cardiac myocytes (35)and in the intact animal heart (36).”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [35] Simpson, 1983, Norepinephrine-stimulated hypertrophy of cultured rat myocardial cells is an alpha-1 adrenergic response, J Clin Invest source

      Not checked in the free run.

    • cites [36] Sen, 1986, Cardiovascular hypertrophy in spontaneously hypertensive rats, J Hypertens

      Not checked in the free run.

  • Classified as probably not a substantial claim.

    Premisecitation
    § CONCLUSIONS

    Increased sympathetic drive enhances vascular hypertrophy.

    “and that increased sympathetic drive enhances vascular hypertrophy (10).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [10] Julius, 1998, Effect of sympathetic overactivity on cardiovascular prognosis in hypertension, Eur Heart J

      Not checked in the free run.

  • Classified as probably not a substantial claim. May combine two claims.

    Study design and conductcitation
    § Methods

    Only vasoconstrictor activity was accepted and examined, with acceptance criteria being appropriate responses to spontaneous changes in arterial blood pressure, the Valsalva maneuver and isometric hand-grip exercise.

    “Only vasoconstrictor activity was accepted and examined, the criteria of acceptance being appropriate responses to spontaneous changes in arterial blood pressure, the Valsalva maneuver and isometric hand-grip exercise, as previously described (16,17).”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [16] Greenwood, 1999, Single unit sympathetic discharge, Circulation source

      Not checked in the free run.

    • cites [17] Macefield, 1994, The discharge behaviour of single vasoconstrictor motoneurones in human muscle nerves, J Physiol (Lond) source

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Study design and conductnone given
    § Discussion

    Microneurography recordings are made from a peripheral nerve, although microneurography has been considered the only technique available to directly record sympathetic activity in human subjects.

    “Although microneurography has been considered the only technique available to “directly” record sympathetic activity in human subjects, recordings are made from a peripheral nerve.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Interpretationown data
    § Discussion

    Even if the EHT group had some degree of LVH, it remains valid that the EHT+LVH group with a greater degree of LVH have greater sympathetic activation.

    “However, even if we hypothesize that the EHT group had some degree of LVH (to explain the overlap), it remains valid that the EHT + LVH group with a greater degree of LVH have greater sympathetic activation.”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S2 (checkable), S3 (load-bearing), S4 (based).

    Study design and conductnone given
    § Discussion

    The fundamental problem of all studies of human autonomic control is the constraint imposed by the limited techniques available to actually quantify sympathetic activity.

    “The fundamental problem of all studies of human autonomic control is the constraint imposed by the limited techniques available to actually quantify sympathetic activity.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Study design and conductnone given
    § Discussion

    Recording neural activity from a single sympathetic unit allows further insight into central command and a true assessment of central sympathetic discharge frequency.

    “Secondly, we have shown that the ability to record neural activity from a single sympathetic unit allows further insight into central command, as it allows a true assessment of central sympathetic discharge frequency.”
    Quote in the paperSubstantial claim
29 of 29

  • The paper relies on this without support.

    Catecholamines have trophic properties.

    “particularly as catecholamines have been shown to have trophic properties.”

  • The paper relies on this without support.

    The reasons why not all hypertensive subjects develop LVH remain undetermined.

    “However, not all subjects go on to develop LVH, and the reasons for this remain undetermined.”

  • The paper relies on this without support.

    It remains unknown whether hypertensive patients who have developed LVH have altered sympathetic drive compared with those without LVH who have similar blood pressure levels.

    “Thus, it remains unknown whether hypertensive patients who have developed LVH have altered sympathetic drive compared with those without LVH who have similar blood pressure levels.”
3 of 3

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Microneurographic studies almost universally show that sympathetic nerve traffic is potentiated in established hypertension in middle age and in elderly as well as young patients.

    “As far as the second issue is concerned, microneurographic studies almost universally shown that sympathetic nerve traffic is potentiated in established hypertension in middle age and in elderly as well as young patients38–46.”

    From The Sympathetic Nervous System Alterations in Human Hypertension (2015) · cites this paper as [40]

  • Adrenergic neural factors may contribute to the development and progression of target organ damage, as documented by pronounced increases in sympathetic nerve traffic and cardiac norepinephrine spillover rate in patients with hypertension complicated by left ventricular hypertrophy or left ventricular diastolic dysfunction.

    “Adrenergic neural factors may also contribute to the development and progression of target organ damage, as documented by the pronounced increase in sympathetic nerve traffic and cardiac norepinephrine spillover rate in patients in which hypertension is complicated by left ventricular hypertrophy or left ventricular diastolic dysfunction40,42,44,45.”

    From The Sympathetic Nervous System Alterations in Human Hypertension (2015) · cites this paper as [40]

  • The sympathetic neural outflow is commonly activated also to the heart and skeletal muscle vasculature, but renal sympathetic activation is central to hypertension pathogenesis.

    “The sympathetic neural outflow is commonly activated also to the heart, shown with selective cardiac norepinephrine spillover measurements28, and to the skeletal muscle vasculature, demonstrated with microneurographic nerve traffic recording32,33,38–46, but it is the renal sympathetic activation which is central to hypertension pathogenesis96–97.”

    From The Sympathetic Nervous System Alterations in Human Hypertension (2015) · cites this paper as [40]

Cites

Flagged first, then by citations

Research works printed but not linked: 2

  1. Esler, 1990, Increased regional sympathetic nervous activity in human hypertension, J Hypertens, 8, S53
  2. Greenwood, 1998, Effect of atenolol therapy on peripheral sympathetic nerve discharge in essential hypertension, J Hypertens, 16, S240

Cited by

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Related

Authors
Greenwood, J. P., Scott, E. M., Stoker, J. B., & Mary, D. A. S. G.
Affiliations
St James's University Hospital (GB)
Corresponding author
Greenwood, John P
ORCID
Venue
Journal of the American College of Cardiology
Publisher
Elsevier BV
Published
2001-11
Volume
38
Issue
6
Pages
1711-1717
ISSN
0735-1097 (ISSN-L)
DOI
10.1016/s0735-1097(01)01600-x
OpenAlex
W2063781207
Cited by
161
References
43
Citations by year
2026: 1 · 2025: 2 · 2024: 2 · 2023: 5 · 2022: 4 · 2021: 2 · 2020: 2 · 2019: 2 · 2018: 7 · 2017: 3 · 2016: 15 · 2015: 6 · 2014: 5 · 2013: 20 · 2012: 25
FWCI
5.84
Type
journal article
Language
en
Open access
Licence
Locations
  • Journal of the American College of Cardiology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Blood Pressure and Hypertension Studies
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Heart Rate Variability and Autonomic Control
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Function and Risk Factors
Keywords
left ventricular hypertrophy, essential hypertension, peripheral sympathetic nervous system, muscle sympathetic nerve activity, sympathetic nerve discharge, catecholamines, peroneal nerve, fiber recruitment
MeSH terms
Action Potentials, Analysis of Variance, Humans, Hypertension, Sympathetic Nervous System, Vasoconstriction, Least-Squares Analysis, Case-Control Studies, Hypertrophy, Left Ventricular

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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Claims read by deepseek-v4.1-flash under definition version 3 (extract-v3) on 2026-10-10.

Classified by jev-1.13-20260917 (gold-guideline-v0.2) on 2026-10-10.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

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