scholarly journals Left ventricular hypertrophy in children with blood pressures in the upper quintile of the distribution. The Muscatine Study.

Hypertension ◽  
1981 ◽  
Vol 3 (6) ◽  
pp. 669-675 ◽  
Author(s):  
R M Schieken ◽  
W R Clarke ◽  
R M Lauer
Keyword(s):  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Left Ventricular ◽  
Blood Pressures

A novel therapeutic approach for reversal of left ventricular hypertrophy and blood pressure control in hypertensive patients treated with alpha-methyldopa or propranolol

1985 ◽  
Vol 63 (4) ◽  
pp. 304-308
Author(s):  
P. G. Fernandez ◽  
W. Snedden ◽  
B. K. Kim ◽  
C. C. Lee
Keyword(s):  
Blood Pressure ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Antihypertensive Drugs ◽  
Left Ventricular ◽  
Stepwise Discriminant Analysis ◽  
Therapeutic Effects ◽  
Long Term Effects ◽  
Hypertensive Patients ◽  
Blood Pressures

A recently added goal in the control of primary hypertension is the reversal of left ventricular hypertrophy which may occur early in the disease and which can have serious consequences. We have attempted to define the hemodynamic parameters which distinguish most sensitively between the long-term effects of two antihypertensive drugs, alpha-methyldopa and propranolol, with a view to determining the optimal conditions under which each of the drugs may be used therapeutically. Twenty matched hypertensive patients, all with established left ventricular hypertrophy, were divided at random into two groups who received either alpha-methyldopa or propranolol as monotherapy. Dosage was titrated until blood pressures were normalized (diastolic blood pressure (DBP) ≤ 95 mmHg) (1 mmHg = 133.322 Pa); then therapy was maintained for 48–52 weeks. Supine and erect blood pressures, heart rates, and eight echocardiographic indices were recorded before commencement of therapy and at the 48- to 52-week period. Stepwise discriminant analysis identified erect DBP, erect heart rate, and posterior wall thickness of the left ventricle as being the parameters which distinguished most clearly the therapeutic effects of the chosen drugs. Using these three parameters, all 20 patients were correctly classified into their respective drug groups. We propose that these results may form the basis of a more rational choice of antihypertensive therapy with alpha-methyldopa or propranolol for hypertensive patients based on the initial determination of these three parameters.

β-Adrenergic stimulation causes cardiocyte apoptosis: influence of tachycardia and hypertrophy

1998 ◽  
Vol 275 (3) ◽  
pp. H961-H968 ◽  
Author(s):  
Yukitaka Shizukuda ◽  
Peter M. Buttrick ◽  
David L. Geenen ◽  
Alain C. Borczuk ◽  
Richard N. Kitsis ◽  
...  
Keyword(s):  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Myocardial Damage ◽  
Left Ventricular ◽  
Adrenergic Stimulation ◽  
Aortic Banding ◽  
Abdominal Aortic ◽  
Terminal Deoxynucleotide Transferase ◽  
Blood Pressures ◽  
And Control

To establish whether catecholamines per se in the absence of significant increases in systolic load induce myocardial damage via apoptosis, rats were treated with vehicle or isoproterenol (400 μg ⋅ kg−1 ⋅ h−1). Apoptotic cardiocytes (Apo) were identified in paraffin-embedded sections using terminal deoxynucleotide transferase-mediated dUTP nick end labeling. Results were confirmed using an independent ligase assay. Systolic blood pressures were comparable in isoproterenol-treated and control rats. Twenty-four hours of treatment with isoproterenol resulted in significant numbers of Apo compared with control [7.9 ± 2.5 vs. 0.3 ± 0.3 (SE) cm−2, P < 0.05]. A cohort of animals was subjected to ventricular pacing to induce a tachycardia equivalent to that induced by isoproterenol, and these animals did not show an increase in Apo. The left ventricular hypertrophy induced by 2 wk of abdominal aortic banding also increased Apo (∼7.2-fold); however, 24 h of isoproterenol infusion did not induce additional Apo in these rats. Thus catecholamines, in the absence of altered systolic load, induce Apo which is not mediated solely by tachycardia. Left ventricular hypertrophy secondary to abdominal aortic banding is associated with Apo, but this does not increase sensitivity to isoproterenol-induced Apo.

scholarly journals Office and Home Blood Pressures as Determinants of Electrocardiographic Left Ventricular Hypertrophy Among Black Nigerians Compared With White Flemish

2017 ◽  
Vol 30 (11) ◽  
pp. 1083-1092 ◽  
Author(s):  
Augustine N Odili ◽  
Lutgarde Thijs ◽  
Wen-Yi Yang ◽  
John O Ogedengbe ◽  
Maxwell M Nwegbu ◽  
...  
Keyword(s):  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Left Ventricular ◽  
Blood Pressures

Reversal of Left Ventricular Hypertrophy after Treatment of Hypertension by Atenolol for One Year

1982 ◽  
Vol 63 (s8) ◽  
pp. 367s-369s ◽  
Author(s):  
F. Sau ◽  
A. Cherchi ◽  
C. Seguro
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Essential Hypertension ◽  
Left Ventricle ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Wall Stress ◽  
Left Ventricular ◽  
R Ratio ◽  
Blood Pressures

1. Fifteen patients with essential hypertension, class I, II WHO, nine males and six females, whose mean age was 46 years, were given atenolol, 100 mg a day, for 1 year. 2. After 1 month, compared with control, systolic and diastolic blood pressures, heart rate and cardiac output were reduced, whereas left ventricular end-diastolic dimension and stroke volume were increased and total vascular resistances, wall stress, left ventricular mass and h/diastolic radius (R) ratio were unchanged. 3. After 1 year, compared with control, systolic and diastolic blood pressures, heart rate and cardiac output were still reduced, total vascular resistance and wall stress were unchanged. End-diastolic dimension and stroke volume reverted to previous values; left ventricular mass and h/R ratio were significantly decreased. 4. These results show that left ventricular hypertrophy in essential hypertension can revert after 1 year of treatment with atenolol, at least in relatively young people. Since the left ventricle wall stress was not changed after atenolol, the regression of left ventricle hypertrophy seems prevalently to be related to the decrease of adrenergic activity of the heart.

scholarly journals Changes in Biomarker Profile and Left Ventricular Hypertrophy Regression: Results from the Frequent Hemodialysis Network Trials

2018 ◽  
Vol 47 (3) ◽  
pp. 208-217 ◽  
Author(s):  
Christopher T. Chan ◽  
George A. Kaysen ◽  
Gerald J. Beck ◽  
Minwei Li ◽  
Joan Lo ◽  
...  
Keyword(s):  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Left Ventricular ◽  
Tissue Inhibitors Of Metalloproteinase ◽  
Observational Cohort ◽  
Blood Pressures ◽  
Cardiovascular Biomarker ◽  
More Frequent Hemodialysis ◽  
Post Hoc ◽  
Frequent Hemodialysis

Background: Regression of left ventricular hypertrophy (LVH) is feasible with more frequent hemodialysis (HD). We aimed to ascertain pathways associated with regression of left ventricular mass (LVM) in patients enrolled in the Frequent HD Network (FHN) trials. Methods: This was a post hoc observational cohort study. We hypothesized LVH regression with frequent HD was associated with a different cardiovascular biomarker profile. Regressors were defined as patients who achieved a reduction of more than 10% in LVM at 12 months. Progressors were defined as patients who had a minimum of 10% increase in LVM at 12 months. Results: Among 332 randomized patients, 243 had biomarker data available. Of these, 121 patients did not progress or regress, 77 were regressors, and 45 were progressors. Mean LVM change differed between regressors and progressors by –65.6 (–74.0 to –57.2) g, p < 0.001. Regressors had a median (interquartile range) increase in dialysis frequency (from 3.0 [3.0–3.0] to 4.9 [3–5.7] per week, p = 0.001) and reductions in pre-dialysis systolic (from 149.0 [136.0–162.0] to 136.0 [123.0–152.0] mm Hg, p < 0.001) and diastolic (from 83.0 [71.0–91.0] to 76.0 [68.0–84.0] mm Hg, p < 0.001) blood pressures. Klotho levels increased in regressors versus progressors (76.9 [10.5–143.3] pg/mL, p = 0.024). Tissue inhibitors of metalloproteinase (TIMP)-2 levels fell in regressors compared to progressors (–7,853 [–14,653 to –1,052] pg/mL, p = 0.024). TIMP-1 and log (brain natriuretic ­peptide [BNP]) levels also tended to fall in regressors. Changes in LVM correlated inversely with changes in klotho (r = –0.24, p = 0.014). ­Conclusions: Markers of collagen turnover and changes in klotho levels are potential novel pathways associated with regression of LVH in the dialysis population, which will require further prospective validation.

Left Ventricular Hypertrophy

2014 ◽  
Vol 19 (2) ◽  
pp. 11-15
Author(s):  
Steven L. Demeter
Keyword(s):  
Risk Factors ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Left Ventricular Mass Index ◽  
Medical Science ◽  
Careful Analysis ◽  
Left Ventricular ◽  
Hypertensive Disease ◽  
Accurate Analysis ◽  
Clear Explanation

Abstract The fourth, fifth, and sixth editions of the AMA Guides to the Evaluation of Permanent Impairment (AMA Guides) use left ventricular hypertrophy (LVH) as a variable to determine impairment caused by hypertensive disease. The issue of LVH, as assessed echocardiographically, is a prime example of medical science being at odds with legal jurisprudence. Some legislatures have allowed any cause of LVH in a hypertensive individual to be an allowed manifestation of hypertensive changes. This situation has arisen because a physician can never say that no component of LVH was not caused by the hypertension, even in an individual with a cardiomyopathy or valvular disorder. This article recommends that evaluators consider three points: if the cause of the LVH is hypertension, is the examinee at maximum medical improvement; is the LVH caused by hypertension or another factor; and, if apportionment is allowed, then a careful analysis of the risk factors for other disorders associated with LVH is necessary. The left ventricular mass index should be present in the echocardiogram report and can guide the interpretation of the alleged LVH; if not present, it should be requested because it facilitates a more accurate analysis. Further, if the cause of the LVH is more likely independent of the hypertension, then careful reasoning and an explanation should be included in the impairment report. If hypertension is only a partial cause, a reasoned analysis and clear explanation of the apportionment are required.

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