Pathophysiology of Hypertensive Heart Disease: Beyond Left Ventricular Hypertrophy

Nwabuo, Chike C.; Vasan, Ramachandran S.

doi:10.1007/s11906-020-1017-9

Cited by 113 publications

(119 citation statements)

References 230 publications

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Section: Discussionmentioning

confidence: 99%

“…The remodeling of the heart due to long term arterial hypertension is a complex process and is not limited to pure anatomical changes [9,27]. Although most research focused on echocardiographic changes in the form of LVH due to hypertensive heart disease, structural and functional adaptions including cardiac fibrosis and alterations of individual cardiac chambers and the arterial system are of rising interest [27]. However, since the diagnosis of cellular changes may require endomyocardial biopsy, TTE as a non-invasive and relatively inexpensive diagnostic method remains of paramount importance in the assessment of myocardial changes due to arterial hypertension [8,9,28,29].…”

Section: Discussionmentioning

confidence: 99%

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Association of Hypertensive Intracerebral Hemorrhage with Left Ventricular Hypertrophy on Transthoracic Echocardiography

Pallesen

Wagner

Lambrou

et al. 2020

JCM

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Introduction: Arterial hypertension is the most frequent cause for spontaneous intracerebral hemorrhage (sICH) and may also cause left ventricular hypertrophy (LVH). We sought to analyze whether hypertensive sICH etiology is associated with LVH. Methods: We analyzed consecutive patients with sICH who were admitted to our tertiary stroke center during a four-year period and underwent transthoracic echocardiography (TTE) as part of the diagnostic work-up. We defined hypertensive sICH as typical localization of hemorrhage in patients with arterial hypertension and no other identified sICH etiology. We defined an increased end-diastolic interventricular septal wall thickness of ≥11 mm on TTE as a surrogate parameter for LVH. Results: Among 395 patients with sICH, 260 patients (65.8%) received TTE as part of their diagnostic work-up. The median age was 71 years (interquartile range (IQR) 17), 160 patients (61.5%) were male, the median baseline National Institute of Health Stroke Scale (NIHSS) score was 8 (IQR 13). Of these, 159 (61.2%) patients had a hypertensive sICH and 156 patients (60%) had LVH. In univariable (113/159 (71.1%) vs. 43/101 (42.6%); odds ratio (OR) 3.31; 95% confidence interval (CI95%) 1.97–5.62); and multivariable (adjusted OR 2.95; CI95% 1.29–6.74) analysis, hypertensive sICH was associated with LVH. Conclusions: In patients with sICH, LVH is associated with hypertensive bleeding etiology. Performing TTE is meaningful for diagnosis of comorbidities and clarification of bleeding etiology in these patients. Future studies should include long-term outcome parameters and assess left ventricular mass as main indicator for LVH.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Association of Hypertensive Intracerebral Hemorrhage with Left Ventricular Hypertrophy on Transthoracic Echocardiography

Pallesen

Wagner

Lambrou

et al. 2020

JCM

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“…With the exception of the Nox4 knockout mice, all angiotensin II-treated animals analyzed in the present study, exhibited significant cardiac hypertrophy, which is a usual outcome of hypertension [35]. Calculating the gain in heart weight, Nox2 knockout mice revealed the highest increase, followed by wildtype mice, Nox1 knockout mice, and Nox4 knockout mice as last.…”

Section: Discussionmentioning

confidence: 49%

The NADPH Oxidase Isoform 1 Contributes to Angiotensin II-Mediated DNA Damage in the Kidney

et al. 2020

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In higher concentrations, the blood pressure regulating hormone angiotensin II leads to vasoconstriction, hypertension, and oxidative stress by activating NADPH oxidases which are a major enzymatic source of reactive oxygen species (ROS). With the help of knockout animals, the impact of the three predominant NADPH oxidases present in the kidney, i.e., Nox1, Nox2 and Nox4 on angiotensin II-induced oxidative damage was studied. Male wildtype (WT) C57BL/6 mice, Nox1-, Nox2- and Nox4-deficient mice were equipped with osmotic minipumps, delivering either vehicle (PBS) or angiotensin II, for 28 days. Angiotensin II increased blood pressure and urinary albumin levels significantly in all treated mouse strains. In Nox1 knockout mice these increases were significantly lower than in WT, or Nox2 knockout mice. In WT mice, angiotensin II also raised systemic oxidative stress, ROS formation and DNA lesions in the kidney. A local significantly increased ROS production was also found in Nox2 and Nox4 knockout mice but not in Nox1 knockout mice who further had significantly lower systemic oxidative stress and DNA damage than WT animals. Nox2 and Nox4 knockout mice had increased basal DNA damage, concealing possible angiotensin II-induced increases. In conclusion, in the kidney, Nox1 seemed to play a role in angiotensin II-induced DNA damage.

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“…The pathophysiological arguments that can support this association are as follows: It is now recognized that LVH is mediated not only by mechanical stress from pressure overload, but also by various neurohormonal substances and metabolic abnormalities that independently exert trophic effects on cardiomyocytes and the extracellular matrix [28,62]. This is substantiated by the high prevalence of LVH in normotensive type 2 diabetics [63,64].…”

Section: Discussionmentioning

confidence: 99%

Association between insulin resistance and left ventricular hypertrophy in sub-saharan hypertensive black patients with preserved ejection fraction: A case control study

Phanzu

Aliocha

Eleuthère

et al. 2020

Preprint

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Background:Conflicting information exists regarding the association between insulin resistance (IR) and left ventricular hypertrophy (LVH).We described the associations between parameters of obesity, fasting insulinemia, HOMAIR with LVH in black patients with essential hypertension.Materials and Methods:A case-control study was conducted at the Centre Médical de Kinshasa (CMK), the Democratic Republic of the Congo, between January and December 2019. Cases and controls were hypertensive patients with and without LVH, respectively. The relationship between obesity indices, physical inactivity, parameters of glucose metabolisme and lipid disorders and LVH were assessed using linear and logistic regression analyses in simple and univariate exploratory analysis, respectively. When differences were observed between LVH and the independent variables, the effect of potential confounders was studied by adjustment in multiple linear regression and in conditional logistic regression in multivariate analysis. The coefficients of determinations (R2), the adjusted ORs and their 95% CI were calculated to determine the association between the LVH and the independent variablesResults:Eighty-eight cases (52 men) were compared to 132 controls (81 men). Nineteen percent of left ventricular mass (LVM) variation (19%) was predicted by age, 31.3% by the duration of hypertension, 44.4% by BMI, 42.5% by WC, 20% by glycemia, 44.8% by insulinemia and 43.7% by HOMAIR. In multiple linear regression analysis, duration of hypertension, Body Mass Index (BMI), insulinemia and HOMAIR explained 68.3% of the variability in the increase in LVM. In the logisitic model obesity multiplied the risk of LVH by 3 (aOR: 2.8, 95% CI (1.06-7.4), p = 0.038), IR by 8 (aOR: 8.4, 95: (3.7-15.7), p <0.001).Conclusion:Obesity and IR appear to be the main predictors of LVH. The comprehensive management of cardiovascular risk factors should be emphasized with particular attention to obesity and insulin resistance. A prospective black sub-saharan population based study with serial imaging remain essential to better understand subclinical LV deterioration over time and to confirm the role of insulin resistance in black sub-saharan hypertensives.

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Pathophysiology of Hypertensive Heart Disease: Beyond Left Ventricular Hypertrophy

Cited by 113 publications

References 230 publications

Association of Hypertensive Intracerebral Hemorrhage with Left Ventricular Hypertrophy on Transthoracic Echocardiography

Association of Hypertensive Intracerebral Hemorrhage with Left Ventricular Hypertrophy on Transthoracic Echocardiography

The NADPH Oxidase Isoform 1 Contributes to Angiotensin II-Mediated DNA Damage in the Kidney

Association between insulin resistance and left ventricular hypertrophy in sub-saharan hypertensive black patients with preserved ejection fraction: A case control study

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