The DOI matches its Crossref record; 42 of the 43 references it cites were found in a registry or an index; 2 of the 51 sources its claims cite were checked for support.
Hypertensive left ventricular hypertrophy: relation to peripheral sympathetic drive
Open accessAbstract
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.
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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.
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Claims the paper makes
23 Not checked yet · 12 Own interpretation · 12 Own result · 10 Own method · 3 No basis given · 1 Partly supported · accuracy not yet measured
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Therefore, the increased activity in EHT + LVH was not attributable to antihypertensive treatment and, in fact, was still apparent despite the use of agents”
What the sources say
- Not checked yetcites [29] Greenwood, 1998, Effect of atenolol therapy on peripheral sympathetic nerve discharge in essential hypertension, J Hypertens
- Partly supportedcites [30] Wallin, 1984, Sympathetic outflow to muscles during treatment of hypertension with metoprolol, Hypertension sourceExperimental — accuracy not yet measured
The Abstract reports that long-term metoprolol treatment reduced muscle sympathetic nerve activity in patients with essential hypertension, supporting the inference that this treatment would not explain an increase. The paper does not study the EHT + LVH subgroup or establish that antihypertensive treatment generally could not account for its increased activity. (LLM, conf=0.84)
- Not checked yetcites [31] Grassi, 1998, Effect of chronic angiotensin converting enzyme inhibition on sympathetic nerve traffic and baroreflex control of the circulation in essential hypertension, J Hypertens source
- Partly supportedcites [32] Matsukawa, 1993, Elevated sympathetic nerve activity in patients with accelerated essential hypertension, J Clin Invest sourceExperimental — accuracy not yet measured
The Discussion (p. 3) reports elevated basal sympathetic activity in accelerated hypertension, and the Methods (p. 2) say antihypertensive drugs were stopped before measurement. The paper does not identify an EHT + LVH group, and its measurements do not show that elevated activity remained apparent while patients were taking antihypertensive agents. (LLM, conf=0.87)
plain- Asserted: passes — The authors put it forward as true.
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A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“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).”
plain- Asserted: passes — The authors put it forward as true.
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A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“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).”
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“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).”
hedged- Asserted: passes — The authors put it forward as true.
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A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“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.”
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Also stated in: § Results · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“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.”
plain- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“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 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).”
- Also stated in: § Discussion · plain
“Assessment from multiunit MSNA bursts revealed that the EHT + LVH group still had about 31% greater sympathetic activity than the EHT group.”
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Also stated in: § Results · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“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).”
plain- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“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).”
plain- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“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).”
hedged- Asserted: passes — The authors put it forward as true.
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- It may state two separate claims as one. 21
- Probably not a substantial claim. 15
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“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).”
plaincorrelational- Asserted: passes — The authors put it forward as true.
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A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“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).”
plaincorrelational- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“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).”
What the sources say
- Not checked yetcites [15] Grassi, 1998, Baroreflex control of sympathetic nerve activity in essential and secondary hypertension, Hypertension source
- Not checked yetcites [16] Greenwood, 1999, Single unit sympathetic discharge, Circulation source
- Not checked yetcites [25] Yamada, 1989, Age-related changes in muscle sympathetic nerve activity in essential hypertension, Hypertension source
- Not checked yetcites [26] Matsukawa, 1991, Reduced baroreflex changes in muscle sympathetic nerve activity during blood pressure elevation in essential hypertension, J Hypertens source
- Not checked yetcites [28] Miyajima, 1991, Muscle sympathetic nerve activity in renovascular hypertension and primary aldosteronism, Hypertension source
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“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.”
boostedcorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
- Also stated in: § Conclusions · boosted
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“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.”
plainn = 14- Asserted: passes — The authors put it forward as true.
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- Also stated in: § Methods · plain
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Second, increased MSNA represents central activation as well as reflex-based increases (fiber recruitment) in sympathetic activity.”
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“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.”
plaindirect- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“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).”
What the sources say
- Not checked yetcites [1] Levy, 1990, Prognostic implications of echocardiographically determined left ventricular mass in the Framingham Heart study, N Engl J Med source
- Not checked yetcites [2] Koren, 1991, Relation of left ventricular mass and geometry to morbidity and mortality in uncomplicated essential hypertension, Ann Intern Med source
- Not checked yetcites [3] Kannel, 1992, Left ventricular hypertrophy as a risk factor in arterial hypertension, Eur Heart J source
- Not checked yetcites [4] Gueyffier, 1999, Identification of risk factors in hypertensive patients, Circulation source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Microneurography is a well-established technique that has been used successfully in the assessment of peripheral sympathetic activity (14).”
What the sources say
- Not checked yetcites [14] Wallin, 1993, Assessment of sympathetic mechanisms for recordings of postganglionic efferent nerve traffic
boosted- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“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).”
What the sources say
- Not checked yetcites [15] Grassi, 1998, Baroreflex control of sympathetic nerve activity in essential and secondary hypertension, Hypertension source
- Not checked yetcites [25] Yamada, 1989, Age-related changes in muscle sympathetic nerve activity in essential hypertension, Hypertension source
- Not checked yetcites [26] Matsukawa, 1991, Reduced baroreflex changes in muscle sympathetic nerve activity during blood pressure elevation in essential hypertension, J Hypertens source
- Not checked yetcites [27] Floras, 1993, Sympathoneural and haemodynamic characteristics of young subjects with mild essential hypertension, J Hypertens source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: fails — The paper’s conclusions may not depend on it.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“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).”
What the sources say
- Not checked yetcites [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 yetcites [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 yetcites [7] Duprez, 1993, Influence of arterial blood pressure and aldosterone on left ventricular hypertrophy in moderate essential hypertension, Am J Cardiol source
- Not checked yetcites [8] Harrap, 1996, Plasma angiotensin II, predisposition to hypertension, and left ventricular size in healthy young adults, Circulation source
- Not checked yetcites [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 yetcites [10] Julius, 1998, Effect of sympathetic overactivity on cardiovascular prognosis in hypertension, Eur Heart J
plainconditional- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“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.”
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
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It may state two separate claims as one.
In the paper
“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).”
What the sources say
- Not checked yetcites [16] Greenwood, 1999, Single unit sympathetic discharge, Circulation source
plain- Asserted: passes — The authors put it forward as true.
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What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“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.”
plaincorrelational- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“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).”
What the sources say
plaincorrelational- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“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.”
What the sources say
plain- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“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.”
What the sources say
- Not checked yetcites [29] Greenwood, 1998, Effect of atenolol therapy on peripheral sympathetic nerve discharge in essential hypertension, J Hypertens
- Not checked yetcites [30] Wallin, 1984, Sympathetic outflow to muscles during treatment of hypertension with metoprolol, Hypertension source
hedgedconditional- Asserted: passes — The authors put it forward as true.
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What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“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.).”
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“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).”
What the sources say
- Not checked yetcites [24] Sundlöf, 1977, The variability of muscle nerve sympathetic activity in resting recumbent man, J Physiol (Lond) source
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“The study group was recruited from among 34 patients; in 6 patients it was not possible to obtain stable microneurographic data.”
plainn = 6- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“First, blood pressure classification differed between the studies, the former using an arbitrary classification and the latter using the JNC-VI classification (21).”
What the sources say
- Not checked yetcites [21] 1997, The sixth report of the Joint National Committee on prevention, detection, evaluation, and treatment of high blood pressure, Arch Intern Med source
plain- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Thus, using a combination of single and multiunit assessment may have allowed further characterization of the hypertensive subjects.”
hedgedconditional- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. It may be too vague to check against evidence.
None of the sources cited for this claim have been checked yet.
In the paper
“In support of this, catecholamines have been shown experimentally to have trophic properties on cardiac myocytes (35)and in the intact animal heart (36).”
What the sources say
- Not checked yetcites [35] Simpson, 1983, Norepinephrine-stimulated hypertrophy of cultured rat myocardial cells is an alpha-1 adrenergic response, J Clin Invest source
- Not checked yetcites [36] Sen, 1986, Cardiovascular hypertrophy in spontaneously hypertensive rats, J Hypertens
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“and that increased sympathetic drive enhances vascular hypertrophy (10).”
What the sources say
- Not checked yetcites [10] Julius, 1998, Effect of sympathetic overactivity on cardiovascular prognosis in hypertension, Eur Heart J
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
None of the sources cited for this claim have been checked yet.
In the paper
“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).”
What the sources say
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Although microneurography has been considered the only technique available to “directly” record sympathetic activity in human subjects, recordings are made from a peripheral nerve.”
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“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.”
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“The fundamental problem of all studies of human autonomic control is the constraint imposed by the limited techniques available to actually quantify sympathetic activity.”
plain- Asserted: passes — The authors put it forward as true.
- Checkable: fails — It may be too vague to check against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. It may be too vague to check against evidence. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“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.”
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
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.”
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?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“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]
Experimental — accuracy not yet measuredIn the citing paper
“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]
In the citing paper
“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]
Citations
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Cited by
Sorted by citations
The Autonomic Nervous System and Hypertension
Mancia, G., & Grassi, G. (2014) · Circulation Research · doi:10.1161/circresaha.114.302524 · Cited by 627
The Sympathetic Nervous System Alterations in Human Hypertension
Grassi, G., Mark, A., & Esler, M. (2015) · Circulation Research · doi:10.1161/circresaha.116.303604 · Cited by 616
Relation Between Cardiac Sympathetic Activity and Hypertensive Left Ventricular Hypertrophy
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Assessment of Sympathetic Cardiovascular Drive in Human Hypertension
Grassi, G. M. (2009) · Hypertension · doi:10.1161/hypertensionaha.108.119883 · Cited by 340
Impact of Type 2 Diabetes Mellitus on Sympathetic Neural Mechanisms in Hypertension
Huggett, R. J., Scott, E. M., Gilbey, S. G., Stoker, J. B., Mackintosh, A. F., & Mary, D. A. S. G. (2003) · Circulation · doi:10.1161/01.cir.0000103123.66264.fe · Cited by 305
Self-citation
Metadata
- 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
- 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)
- 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
- bronze
- doi.org
- 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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