Cardiac function in systemic hypertension before and after reversal of left ventricular hypertrophy

AbstractSudden cardiac death (SCD) is most commonly secondary to sustained ventricular arrhythmias (VAs). This review aimed to evaluate if left ventricular hypertrophy (LVH) secondary to systemic hypertension in humans is an isolated risk factor for ventricular arrhythmogenesis. Animal models of hypertensive LVH have shown changes in ion channel function and distribution, gap junction re-distribution and fibrotic deposition. Clinical data has consistently exhibited an increase in prevalence and complexity of non-sustained VAs on electrocardiographic monitoring. However, there is a dearth of trials suggesting progression to sustained VAs and SCD, with extrapolations being confounded by presence of co-existent asymptomatic coronary artery disease (CAD). Putatively, this lack of data may be due to the presence of more homogenous distribution of pathophysiological changes seen in those with hypertensive LVH versus known pro-arrhythmic conditions such as HCM and myocardial infarction. The overall impression is that sustained VAs in the context of hypertensive LVH are most likely to be precipitated by other causes such as CAD or electrolyte disturbance.

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Evaluation of ECG Criteria for Left Ventricular Hypertrophy Before and After Aortic Valve Replacement Using Magnetic Resonance Imaging

Journal of Cardiovascular Magnetic Resonance ◽

10.1081/jcmr-120022262 ◽

2003 ◽

Vol 5 (3) ◽

pp. 465-474 ◽

Cited By ~ 3

Author(s):

Hugo P. Beyerbacht ◽

Jeroen J. Bax ◽

Hildo J. Lamb ◽

Arnoud van der Laarse ◽

Hubert W. Vliegen ◽

...

Keyword(s):

Magnetic Resonance Imaging ◽

Magnetic Resonance ◽

Aortic Valve ◽

Left Ventricular Hypertrophy ◽

Aortic Valve Replacement ◽

Ventricular Hypertrophy ◽

Left Ventricular ◽

Resonance Imaging ◽

Before And After ◽

Ecg Criteria

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Microvascular Dysfunction in Patients with Systemic Hypertension without Left Ventricular Hypertrophy: The Role of Nitric Oxide

Developments in Cardiovascular Medicine - Chest Pain with Normal Coronary Angiograms: Pathogenesis, Diagnosis and Management ◽

10.1007/978-1-4615-5181-2_25 ◽

1999 ◽

pp. 259-267

Author(s):

Julio A. Panza

Keyword(s):

Nitric Oxide ◽

Left Ventricular Hypertrophy ◽

Ventricular Hypertrophy ◽

Microvascular Dysfunction ◽

Left Ventricular ◽

Systemic Hypertension

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Correlations of circulating miR-26b level with left ventricular hypertrophy and cardiac function in elderly patients with hypertension

Pakistan Journal of Medical Sciences ◽

10.12669/pjms.37.4.4048 ◽

2021 ◽

Vol 37 (4) ◽

Author(s):

Jian Fu ◽

Fang Lin ◽

Zhengxia Pan ◽

Chun Wu

Keyword(s):

Left Ventricular Hypertrophy ◽

Elderly Patients ◽

Cardiac Function ◽

Clinical Data ◽

Ventricular Hypertrophy ◽

Protective Factor ◽

Left Ventricular ◽

Potential Biomarker ◽

Biochemical Indices ◽

Level Group

Objectives: To study the correlations of circulating miR-26b level with left ventricular hypertrophy (LVH) and cardiac function in elderly patients with hypertension. Methods: A total of 132 eligible patients were divided into low and high miR-26b level groups. Their baseline clinical data and biochemical indices were compared. The correlations between miR-26b level and echocardiographic parameters were studied by Pearson’s analysis. Factors affecting LVH were explored by multivariate logistic regression analysis. The role of miR-26b in diagnosing LVH was predicted by receiver operating characteristic curve. Results: The relative expression level of miR-26b was 4.56-16.93, with a median of 7.62. The two groups had similar baseline clinical data and biochemical indices (P>0.05). Compared with high miR-26b level group, interventricular septal thickness (IVST), left ventricular posterior wall thickness (LVPWT), left ventricular mass index (LVMI) and number of LVH cases in low miR-26b level group significantly increased (P<0.05), and mitral ratio of peak early to late diastolic filling velocity (E/A) decreased (P<0.05). Circulating miR-26b level was negatively correlated with IVST, LVPWT and LVMI (P<0.0001), and positively correlated with E/A (P<0.0001). The proportion of cardiac hypofunction cases in low miR-26b level group significantly exceeded that of high miR-26b level group (P<0.05). Age and increased IVST, LVPWT and LVMI were independent risk factors for LVH (P<0.05), and elevated miR-26b level was a protective factor (P<0.05). AUC was 0.836, and the optimal cutoff value was 8.83, with high sensitivity and specificity. Conclusions: MiR-26b level is negatively correlated with LVH and positively correlated with left ventricular diastolic function in elderly hypertensive patients. It is a protective factor for LVH complicated with diastolic dysfunction and a potential biomarker for diagnosis. doi: https://doi.org/10.12669/pjms.37.4.4048 How to cite this:Fu J, Lin F, Pan Z, Wu C. Correlations of circulating miR-26b level with left ventricular hypertrophy and cardiac function in elderly patients with hypertension. Pak J Med Sci. 2021;37(4):---------. doi: https://doi.org/10.12669/pjms.37.4.4048 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Usefulness of Echocardiographie and Electrocardiographic Left Ventricular Hypertrophy in Predicting New Cardiac Events and Atherothrombotic Brain Infarction in Elderly Patients with Systemic Hypertension or Coronary Artery Disease

American Journal of Noninvasive Cardiology ◽

10.1159/000470644 ◽

1989 ◽

Vol 3 (6) ◽

pp. 367-370 ◽

Cited By ~ 13

Author(s):

Wilbert S. Aronow ◽

Mordecai Koenigsberg ◽

Kenneth S. Schwartz

Keyword(s):

Coronary Artery Disease ◽

Coronary Artery ◽

Left Ventricular Hypertrophy ◽

Elderly Patients ◽

Ventricular Hypertrophy ◽

Brain Infarction ◽

Left Ventricular ◽

Systemic Hypertension ◽

Cardiac Events ◽

Artery Disease

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Development of SHR hypertension and cardiac hypertrophy during prolonged beta blockade

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1977.232.6.h639 ◽

1977 ◽

Vol 232 (6) ◽

pp. H639-H644 ◽

Cited By ~ 3

Author(s):

M. A. Pfeffer ◽

J. M. Pfeffer ◽

A. K. Weiss ◽

E. D. Frohlich

Keyword(s):

Left Ventricular Hypertrophy ◽

Arterial Pressure ◽

Adrenergic Receptor ◽

Ventricular Hypertrophy ◽

Tap Water ◽

Left Ventricular ◽

Systemic Hypertension ◽

Beta Blockade ◽

Beta Adrenergic Receptor ◽

Beta Adrenergic

Spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats were treated with beta-adrenergic receptor inhibiting drugs (either propranolol or timolol) from conception until 12 weeks of age to determine if this therapy would alter the development of systemic hypertension or left ventricular hypertrophy. Therapy (propranolol or timolol, 500 mg/liter drinking water) was initiated with breeding parents and continued throughout the pregnancy, nursing, and postweaning periods. Although the heart rates of beta-adrenergic receptor inhibited WKY and SHR rats were consistently reduced with respect to their respective tap-water controls, this therapy did not alter body growth. Hemodynamic studies demonstrated reduced central venous pressure, cardiac index, and maximum acceleration of aortic flow in the beta-adrenergic inhibited rats. In spite of these findings, the arterial pressure of the treated rats and the degree of left ventricular hypertrophy of the SHR were unaltered by treatment. Thus, administration of the beta-adrenergic receptor blocking agents, propranolol or timolol, from conception through the developmental stage of SHR hypertension, failed to alter either the progressive rise in arterial pressure or the development of hypertensive vascular disease and left ventricular hypertrophy.

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