Rationale and design of a multicentre, randomized, placebo-controlled trial of mirabegron, a Beta3-adrenergic receptor agonist on left ventricular mass and diastolic function in patients with structural heart disease Beta3-left ventricular hypertrophy (Be

Electrocardiographic criteria for left ventricular hypertrophy (L VH) were examined in 84 unselected pediatric patients with rheumatic heart disease. There were 47 male and 3 7 female patients, ranging in age from 6 to 19 years. Electrocardiographic L VH was detected m 41 patients (48.8%), i.e. in 55.3% (26/47) of boys and in 36.6% (15/41) of girls. Echocardiographically determined L VH was present in 42 cases (50%) if left ventricular mass (L VM) was indexed for height, or 47 cases (56%) if L VM was indexed for body surface area (BSA). The overall sensitivity of height-indexed electrocardiographic diagnosis of LVH was 71.4% (95% confidence interval= 57.7% to 85.1%), while its sensitivity was 73.8% (95% confidence interval= 60.0% to 87.0%). For BSA indexed echocardiographic LVH, the sensitivity was 68.1% (95% confidence interval = 54.8 to 81.4%) and the specificity was 75.7% (95% confidence interval = 61.9% to 89.5%). When sex-adjustment was examined, there was no increase of sensitivity of electrocardiographic LVH. Sensitivity of the electrocardiogram for LVH increased when age-adjustment was examined with 13 years of age as a cut-off point, both for height indexed and BSA-indexed echocardiographic LVH. Reasons/or the difference between these findings and the findings in adult patients (remarkably low sensitivity and very high specificity of ECG L VH) were discussed. Electrocardiogram was a moderate diagnostic modality in the detection of L VH in our pediatric patients with rheumatic heart disease. Sex did not influence the sensitivity of ECG L VH, but older age group tended to increase its sensitivity.

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HEART RATE VARIABILITY AND LEFT VENTRICULAR DIASTOLIC FUNCTION IN PATIENTS WITH BORDERLINE HYPERTENSION WITH AND WITHOUT LEFT VENTRICULAR HYPERTROPHY

Clinical and Experimental Hypertension ◽

10.1081/ceh-100001199 ◽

2001 ◽

Vol 23 (1-2) ◽

pp. 77-87 ◽

Cited By ~ 14

Author(s):

Gianpiero Martini ◽

Franco Rabbia ◽

Lucetta Gastaldi ◽

Piero Riva ◽

Maria Pia Sibona ◽

...

Keyword(s):

Heart Rate ◽

Heart Rate Variability ◽

Left Ventricular Hypertrophy ◽

Diastolic Function ◽

Ventricular Hypertrophy ◽

Left Ventricular Diastolic Function ◽

Left Ventricular ◽

Ventricular Diastolic Function ◽

Borderline Hypertension

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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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