Sodium, Left Ventricular Mass, and Arterial Hypertension

Simone, Giovanni de; Marco, Marina De

doi:10.1161/hypertensionaha.111.176271

Cited by 7 publications

(4 citation statements)

References 14 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These findings are made even more relevant because the rate of BP control at the time of follow‐up was excellent (62%), as compared to baseline (n=360 or 42%, P <0.0001), and greater than generally reported in the literature . The discrepancy between BP control and persistence of initial values of LVMi is consistent with a number of previous findings, suggesting that the paradigm of BP‐LVH as cause effect relation should be revised to recognize the role of potentially interfering parameters . Increased LVM has been shown to precede development of arterial hypertension in a number of clinical and epidemiological studies, a finding that supports a reverse‐causation speculation and helps explain why therapeutic intervention may control BP (the effect), and much less LVM (one of the potential determinants under this scenario).…”

Section: Discussionsupporting

confidence: 85%

“…28 The discrepancy between BP control and persistence of initial values of LVMi is consistent with a number of previous findings, suggesting that the paradigm of BP-LVH as cause effect relation should be revised to recognize the role of potentially interfering parameters. 29 Increased LVM has been shown to precede development of arterial hypertension in a number of clinical and epidemiological studies, [30][31][32][33] a finding that supports a reverse-causation speculation 29,34 and helps explain why therapeutic intervention may control BP (the effect), and much less LVM (one of the potential determinants under this scenario). Unfortunately a more extensive analysis of the potential effect of therapy could not be done because only the association with the initial treatment could be analyzed leaving a lack of information on variation of treatment during the follow-up.…”

Section: Discussionmentioning

confidence: 92%

See 1 more Smart Citation

Lack of Reduction of Left Ventricular Mass in Treated Hypertension: The Strong Heart Study

Simone

Devereux

Izzo

et al. 2013

JAHA

Self Cite

View full text Add to dashboard Cite

BackgroundHypertensive left ventricular mass (LVM) is expected to decrease during antihypertensive therapy, based on results of clinical trials.Methods and ResultsWe assessed 4‐year change of echocardiographic LVM in 851 hypertensive free‐living participants of the Strong Heart Study (57% women, 81% treated). Variations of 5% or more of the initial systolic blood pressure (SBP) and LVM were categorized for analysis. At baseline, 23% of men and 36% of women exhibited LV hypertrophy (LVH, P<0.0001). At the follow‐up, 3% of men and 10% of women had regression of LVH (P<0.0001 between genders); 14% of men and 15% of women, free of baseline LVH, developed LVH. There was an increase in LVM over time, more in men than in women (P<0.001). Participants whose LVM did not decrease had similar baseline SBP and diastolic BP, but higher body mass index (BMI), waist/hip ratio, heart rate (all P<0.008), and urinary albumin/creatinine excretion (P<0.001) than those whose LVM decreased. After adjusting for field center, initial LVM index, target BP, and kinship degree, lack of decrease in LVM was predicted by higher baseline BMI and urinary albumin/creatinine excretion, independently of classes of antihypertensive medications, and significant effects of older age, male gender, and percentage increase in BP over time. Similar findings were obtained in the subpopulation (n=526) with normal BP at follow‐up.ConclusionsIn a free‐living population, higher BMI is associated with less reduction of hypertensive LVH; lack of reduction of LVM is independent of BP control and of types of antihypertensive treatment, but is associated with renal damage.

show abstract

Section: Discussionsupporting

confidence: 85%

Section: Discussionmentioning

confidence: 92%

Lack of Reduction of Left Ventricular Mass in Treated Hypertension: The Strong Heart Study

Simone

Devereux

Izzo

et al. 2013

JAHA

Self Cite

View full text Add to dashboard Cite

show abstract

“…(c) Chlorthalidone and triamterene/HCTZ are superior to HCTZ for reducing CVEs and CHF . (d) Reducing sodium reduces LVM, and chlorthalidone and PSD/HCTZ combinations reduce sodium more than HCTZ (Supplement 1 in ), (e) Preserving potassium reduces LVM, and PSD/HCTZ combinations are of course superior to HCTZ for preserving potassium …”

Section: Introductionmentioning

confidence: 99%

“…[14][15][16][17] (c) Chlorthalidone and triamterene/HCTZ are superior to HCTZ for reducing CVEs and CHF. 12,18,19 (d) Reducing sodium reduces LVM, [20][21][22][23][24][25][26][27][28] and chlorthalidone and PSD/HCTZ combinations reduce sodium more than HCTZ (Supplement 1 in Appendix S1), [29][30][31] (e) Preserving potassium reduces LVM, [20][21][22][32][33][34] and PSD/ HCTZ combinations are of course superior to HCTZ for preserving potassium. 35,36 To test the hypothesis that this set of diuretics is superior to HCTZ for reducing LVM, a systematic review and network metaanalyses of randomized trials were conducted.…”

mentioning

confidence: 99%

Hydrochlorothiazide vs chlorthalidone, indapamide, and potassium‐sparing/hydrochlorothiazide diuretics for reducing left ventricular hypertrophy: A systematic review and meta‐analysis

Roush

Abdelfattah

Song

et al. 2018

J of Clinical Hypertension

View full text Add to dashboard Cite

Left ventricular hypertrophy develops in 36%‐41% of hypertensive patients and independently predicts cardiovascular events and total mortality. Moreover, drug‐induced reduction in left ventricular mass (LVM) correlates with improved prognosis. The optimal thiazide‐type diuretic for reducing LVM is unknown. Evidence regarding potency, cardiovascular events, sodium, and potassium suggested the hypothesis that “CHIP” diuretics (CHlorthalidone, Indapamide, and Potassium‐sparing diuretic/hydrochlorothiazide [PSD/HCTZ]) would reduce LVM more than HCTZ. Systematic searches of five databases were conducted. Among the 38 randomized trials, a 1% reduction in systolic blood pressure (SBP) predicted a 1% reduction in LVM, P = 0.00001. CHIP‐HCTZ differences in reducing LVM differed across trials (ie, heterogeneity), making interpretation uncertain. However, among the 28 double‐blind trials, heterogeneity was undetectable, and HCTZ reduced LVM (percent reduction [95% CI]) by −7.3 (−10.4, −4.2), P < 0.0001. CHIP diuretics surpassed HCTZ in reducing LVM: chlorthalidone −8.2 (−14.7, −1.6), P = 0.015; indapamide −7.5 (−12.7, −2.3), P = 0.005; and all CHIP diuretics combined −7.7 (−12.2, −3.1), P < 0.001. The comparison of PSD/HCTZ with HCTZ had low statistical power but favored PSD/HCTZ: −6.0 (−14.1, +2.1), P = 0.149. Thus, compared to HCTZ, CHIP diuretics had twice the effect on LVM. CHIP diuretics did not surpass HCTZ in reducing systolic or diastolic blood pressure: −0.3 (−5.0, +4.3) and −1.6 (−5.6, +2.4), respectively. The strength of evidence that CHIP diuretics surpass HCTZ for reducing LVM was high (GRADE criteria). In conclusion, these novel results have demonstrated that CHIP diuretics reduce LVM 2‐fold more than HCTZ among hypertensive patients. Although generally related to LVM, blood pressure fails to explain the superiority of CHIP diuretics for reducing LVM.

show abstract

High salt intake as a multifaceted cardiovascular disease: new support from cellular and molecular evidence

2015

View full text Add to dashboard Cite

Scientists worldwide have disseminated the idea that increased dietary salt increases blood pressure. Currently, salt intake in the general population is ten times higher than that consumed in the past and at least two times higher than the current recommendation. Indeed, a salt-rich diet increases cardiovascular morbidity and mortality. For a long time, however, the deleterious effects associated with high salt consumption were only related to the effect of salt on blood pressure. Currently, several other effects have been reported. In some cases, the deleterious effects of high salt consumption are independently associated with other common risk factors. In this article, we gather data on the effects of increased salt intake on the cardiovascular system, from infancy to adulthood, to describe the route by which increased salt intake leads to cardiovascular diseases. We have reviewed the cellular and molecular mechanisms through which a high intake of salt acts on the cardiovascular system to lead to the progressive failure of a healthy heart.

show abstract

Sodium, Left Ventricular Mass, and Arterial Hypertension

Cited by 7 publications

References 14 publications

Lack of Reduction of Left Ventricular Mass in Treated Hypertension: The Strong Heart Study

Lack of Reduction of Left Ventricular Mass in Treated Hypertension: The Strong Heart Study

Hydrochlorothiazide vs chlorthalidone, indapamide, and potassium‐sparing/hydrochlorothiazide diuretics for reducing left ventricular hypertrophy: A systematic review and meta‐analysis

High salt intake as a multifaceted cardiovascular disease: new support from cellular and molecular evidence

Contact Info

Product

Resources

About