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PubMed1984

[Muscular hypertrophy in denervation: report of 2 cases with a histochemical and histometric study of normal and hypertrophic muscles].

Report of two adult males, 31 and 24 years-old, with hypertrophy in their left inferior limb, with denervation in the electromyography. Both patients undergone to a muscle biopsy in the normal and in the enlarged limb, which were processed by histochemistry. The mean muscle fiber diameter, percentage of muscle type fibers and atrophy and hypertrophy factors were calculated, as well as histographic fiber analysis. We found rare atrophic muscle fibers and one of the patients had hypertrophy of type II muscle fiber and the other hypertrophy of both types. The calculation of the atrophy and hypertrophy factors, revealed a predominance of type II fiber hypertrophy in both quadriceps of the two patients and type I hypertrophy in one case. A discussion about the factor responsible by the hypertrophy in denervation is made. The possible etiology of one case was a S1 radiculopathy and in the other, a possible motor neuron disease.

Adult↗
PubMed2005

Podocyte hypertrophy, "adaptation," and "decompensation" associated with glomerular enlargement and glomerulosclerosis in the aging rat: prevention by calorie restriction.

Whether podocyte depletion could cause the glomerulosclerosis of aging in Fischer 344 rats at ages 2, 6, 17, and 24 mo was evaluated. Ad libitum-fed rats developed proteinuria and glomerulosclerosis by 24 mo, whereas calorie-restricted rats did not. No evidence of age-associated progressive linear loss of podocytes from glomeruli was found. Rather, ad libitum-fed rats developed glomerular enlargement over time. To accommodate the increased glomerular volume, podocytes principally underwent hypertrophy, whereas other glomerular cells underwent hyperplasia. Stages of hypertrophy through which podocytes pass en route to podocyte loss and glomerulosclerosis were identified: Stage 1, normal podocyte; stage 2, nonstressed podocyte hypertrophy; stage 3, "adaptive" podocyte hypertrophy manifest by changes in synthesis of structural components (e.g., desmin) but maintenance of normal function; stage 4, "decompensated" podocyte hypertrophy relative to total glomerular volume manifest by reduced production of key machinery necessary for normal podocyte function (e.g., Wilms' tumor 1 protein [WT1], transcription factor pod1, nephrin, glomerular epithelial protein 1, podocalyxin, vascular endothelial growth factor, and alpha5 type IV collagen) and associated with widened foot processes and decreased filter efficiency (proteinuria); and stage 5, podocyte numbers decrease in association with focal segmental glomerulosclerosis. In contrast, in calorie-restricted rats, glomerular enlargement was minor, significant podocyte hypertrophy did not occur, podocyte machinery was unchanged, there was no proteinuria, and glomerulosclerosis did not develop. Glomerular enlargement therefore was associated with podocyte hypertrophy rather than hyperplasia. Hypertrophy above a certain threshold was associated with podocyte stress and then failure, culminating in reduced podocyte numbers in sclerotic glomeruli. This process could be prevented by calorie restriction.

Adaptation, Physiological↗
PubMed2000

Modification of the epidermal growth factor response by ammonia in renal cell hypertrophy.

Epidermal growth factor (EGF) causes proliferation in renal tubular cells but, when it is combined with transforming growth factor-beta1, it causes hypertrophy by a mechanism that requires the activity of the retinoblastoma family of proteins. In contrast, ammonia causes hypertrophy by decreasing lysosomal proteolysis; in some cell types, it also decreases cellular proliferation. These studies were designed to determine whether ammonia, like transforming growth factor-beta1, could convert EGF-induced hyperplasia to hypertrophy. Cultured NRK-52E cells were incubated with EGF and/or ammonia and the protein/DNA ratio was measured, as a marker of hypertrophy. Addition of ammonia to EGF-treated NRK-52E cells converted EGF-induced hyperplasia to hypertrophy, because of a decrease in DNA synthesis. The mechanism involved no change in EGF-induced protein synthesis. Inhibition of lysosomal function with a proton pump inhibitor or lysosomal protease inhibitors also converted the response of EGF-treated cells to hypertrophy. Expression of the human papilloma virus 16 E7 protein (which inactivates all members of the retinoblastoma family) prevented ammonia from converting EGF-induced hyperplasia to hypertrophy. It is concluded that ammonia converts EGF-induced hyperplasia to hypertrophy by a mechanism that involves suppression of lysosomal function and this response can be blocked by inhibiting the activity of the retinoblastoma family of proteins.

Alkalies↗
PubMed2006

Left ventricular hypertrophy in hypertensive obese women.

OBJECTIVE: Left ventricular hypertrophy (LVH) is an independent predictor of cardiovascular and general mortality. Both arterial hypertension and obesity cause changes in structure and function of the left ventricle. Given the rising global epidemic of obesity, it is likely that adverse health consequences of excess adiposity will escalate in the future. The aim of this investigation was to assess the relation and predictive value of obesity on the occurrence of left ventricular hypertrophy in hypertensive middle-aged women. METHODS AND RESULTS: Investigation was conducted on a sample of 64 middle-aged women, diagnosed with arterial hypertension and treated longer than 10 years in the absence of other chronic diseases or heart failure. Based on anthropometric parameters, 14 women (21.9%) had a body mass index (BMI) within the normal range, 17 (26.6%) were overweight, and 33 (52.5%) were obese. Left ventricular hypertrophy was assessed by electrocardiographic and echocardiographic criteria. The influence of anthropometric parameters on left ventricular hypertrophy and patterns in left ventricular geometry was assessed using multivariate regression analyses. The prevalence of LV hypertrophy was 7.1% among normal-weight hypertensive women, 41.2% among overweight and 66.7% among obese women. Compared to normal-weight women, overweight and obese hypertensive subjects had higher mean values of all ECG and echo parameters. The strong correlation between anthropometric and left ventricular parameters was observed. Multivariate analysis showed that percent of body fat (OR = 1.226; 95% CI 1.011-1.486) was the only independent predictor of left ventricular hypertrophy. Being overweight was identified as predictor for the development of eccentric LV hypertrophy (OR = 31.824; 95% CI 1.225-826.850), and for concentric left ventricular remodelling (OR = 20.755; 95% CI 1.119-385.029). CONCLUSIONS: Heart abnormalities occurring in arterial hypertension in conjunction with overweight/obesity include left ventricular hypertrophy and structural changes in the left ventricle. These findings support weight control and the regulation of blood pressure for the prevention of left heart abnormalities.

Body Mass Index↗
PubMed2003

Estrogen and enalapril attenuate the development of right ventricular hypertrophy induced by monocrotaline in ovariectomized rats.

The present study evaluated the importance of ovarian functions and the renin-angiotensin system in the progression of the right ventricular (RV) hypertrophy. Female Sprague-Dawley rats were bilaterally ovariectomized (Ovx) and injected with monocrotaline (MCT, 60 mg/kg, sc). Four weeks after MCT-treatment, only the male and Ovx female rats showed marked RV hypertrophy. The hypertrophied RV of the male-MCT and Ovx-MCT rats exhibited remarkably elevated renin mRNA levels. Gene expression levels of angiotensinogen, TGF-beta1, and endothelin-1 in the hypertrophied RV also increased, but to the less degree than did the renin mRNA. To investigate beneficial effects of estrogen or enalapril on progression of the pulmonary hypertension and RV hypertrophy, histological changes of the lung and heart were examined. Sham-MCT female rats showed histological changes indicating pulmonary hypertension without RV hypertrophy. In contrast, Ovx-MCT rats showed marked RV hypertrophy with pathological changes, denoting severe pulmonary and myocardial injuries. Estrogen-or enalapril-treated Ovx-MCT rats did not show RV hypertrophy, and showed remarkably ameliorated ultrastructural changes in the lung and RV. These results from this rat model suggest that both estrogen and inhibition of the renin-angiotensin system have protective functions against the development of the pulmonary hypertension and cardiac remodeling.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1992

The prognostic role of left ventricular hypertrophy in patients with or without coronary artery disease.

OBJECTIVE: To examine the association between echocardiographically determined left ventricular hypertrophy and mortality in patients with and without coronary artery disease. DESIGN: Cohort study with a mean follow-up period of 4 years. SETTING: An inner-city public hospital in Chicago. PATIENTS: A cohort of 785 patients, most of whom were black and had hypertension. INTERVENTIONS: Coronary arteriography for presumed coronary artery disease and echocardiography. MAIN OUTCOME MEASURE: All-cause and cardiac mortality. RESULTS: Left ventricular hypertrophy, based on left ventricular mass corrected for body surface area, was present in 194 of 381 patients (51%) with coronary artery disease and in 162 of 404 patients (40%) without coronary artery disease. Patients with left ventricular hypertrophy had worse survival than those without hypertrophy in both the group with coronary artery disease and the group without coronary artery disease. After adjustment was made for age at baseline, sex, and hypertension, the relative risk for death from any cause in patients with hypertrophy compared with patients without hypertrophy was 2.14 (95% CI, 1.24 to 3.68) among those with coronary artery disease and 4.14 (CI, 1.77 to 9.71) among those without coronary artery disease. CONCLUSIONS: Echocardiographically determined left ventricular hypertrophy is an important prognostic marker in patients with or without coronary artery disease. The effect of reversing ventricular hypertrophy in patients with and without coronary disease deserves further study.

Adult↗
PubMed2000

Dispersion of ventricular repolarization and ventricular fibrillation in left ventricular hypertrophy: influence of selective potassium channel blockers.

This study tested the hypothesis that combination ion channel blockers of the transient outward current (I(to)) and the rapid component of the delayed rectifying current (I(Kr)) would produce greater prolongation of the ventricular action potential duration (APD) and increased dispersion of the APD in hypertrophied hearts compared with control hearts. Isolated rabbit hearts were studied 48 +/- 5 days postabdominal aortic banding. Left ventricular endocardial and epicardial APDs were significantly greater at baseline in the hypertrophied group than in controls (P <.05). The magnitude of APD prolongation induced by the I(to) blocker 4-aminopyridine (4-AP) and combination 4-AP and the I(Kr) blocker dofetilide was greater in the hypertrophied hearts than in the normal hearts (P <.01). Mean APD dispersion was significantly greater in the hypertrophied group than in the control hearts at baseline (P <.05). 4-AP increased APD dispersion by a similar magnitude in the hypertrophied hearts (10 +/- 10 ms) and the control hearts (8 +/- 8 ms, P = NS), whereas the combination 4-AP and dofetilide increased APD dispersion by a greater magnitude in the hypertrophied hearts (41 +/- 28 ms) than the control hearts (21 +/- 11 ms, P <.05). Ventricular fibrillation occurred spontaneously in four hypertrophied hearts (40%) during combination drug perfusion and in none of the control hearts (P <.05). Thus, combination I(to) and I(Kr) blockers cause greater prolongation APD and increased APD dispersion in left ventricular hypertrophy, and this is associated with the development of ventricular fibrillation.

4-Aminopyridine↗
PubMed2002

[QT dispersion and characteristics of left ventricular hypertrophy in primary hypertension].

UNLABELLED: The aim of the study was to evaluate the QT dispersion and the severity of arrhythmias in hypertensive patients according to the asymmetry of the left ventricular hypertrophy. The study group consisted of 47 hypertensive patients. In 24 of them the left ventricular hypertrophy was symmetrical (group I) and in 23--asymmetrical (group II). For the evaluation of the left ventricular hypertrophy its thickness was analyzed in 13 segments. The ratio between the maximum and minimum thickness from any location was determined as the asymmetry index (AI). The value of this index 1,3 distinguished between patients with the symmetrical and asymmetrical left ventricular hypertrophy. 20 healthy subjects were examined as a control group (group III). All subjects underwent physical examination, the standard 12-lead electrocardiogram (ECG), twenty-four hour Holter recording and echocardiography. All the results for the QT dispersion (QTd, QTdc, QTdR) were highest in group II, lower in patients from group I and the lowest were observed in the control group. The differences in all parameters between group I and II were statistically significant: for QTd--V p < 0.01, QTdc--p < 0.05, QTdR--p < 0.05. The differences between groups II and III as well as I and III were statistically significant for all QT dispersion parameters: for QTd--p < 0.001 and p < 0.01 respectively, QTdc--p < 0.001, QTdR--p < 0.001 for both groups. We have observed a very distinct positive correlation between the asymmetry index and QTd, QTdc, QTdR (p < 0.001). These values correlated also, but less distinctly with the left ventricular mass index--LVMI (p < 0.05). The frequency and severity of ventricular ectopic beats did not differ significantly between group I and II. The results obtained indicate the lack of connection between the frequency of ventricular premature complexes and (1) all QT dispersion parameters, (2) LVMI, (3) AI. Supraventricular premature complexes occurred significantly more frequently in patients with the asymmetrical left ventricular hypertrophy compared to the group with the regular left ventricular hypertrophy (p < 0.05) and control group (p < 0.01). CONCLUSIONS: The left ventricular hypertrophy in primary hypertension may increase the QT dispersion. It seems that asymmetry of the left ventricular hypertrophy reinforces this increase. The increased QT dispersion in primary hypertension does not influence significantly the occurrence of ventricular arrhythmias.

Adult↗
PubMed1975

Mechanism of work-induced hypertrophy of skeletal muscle.

Skeletal muscle can undergo rapid growth in response to a sudden increase in work load. For example, the rat soleus muscle increases in weight by 40% within six days after the tendon of the synergistic gastrocnemius is sectioned. Such growth of the overworked muscle involves an enlargement of muscle fibers and occasional longitudinal splitting. Hypertrophy leads to greater maximal tension development, although decreased contraction time and reduced contractility have also been reported. Unlike normal developmental growth, work-induced hypertrophy can be induced in hypophysectomized or diabetic animals. This process thus appears independent of growth hormone and insulin as well as testosterone and thyroid hormones. Hypertrophy of the soleus can also be induced in fasting animals, in which there is a generalized muscle wasting. Thus muscular activity takes precedence over endocrine influences on muscle size. The increase in muscle weight reflects an increase in protein, especially sarcoplasmic protein, and results from greater protein synthesis and reduced protein breakdown. Within several hours after operation, the hypertrophying soleus shows more rapid uptake of certain amino acids and synthesis of phosphatidyl-inositol. By 8 hours, protein synthesis is enhanced. RNA synthesis also increases, and hypertrophy can be prevented with actinomycin D. Nuclear DNA synthesis also increases on the second day after operation and leads to a greater DNA content. The significance of the increased RNA and DNA synthesis is not clear, since most of it occurs in interstitial and satellite cells. The proliferation of the non-muscle cells seems linked to the growth of the muscle fibers; in addition, factors causing muscle atrophy (e.g. denervation) decrease DNA synthesis by such cells. In order to define more precisely the early events in hypertrophy, the effects of contractile activity were studied in rat muscles in vitro. Electrical stimulation enhanced active transport of certain amino acids within an hour, and the magnitude of this effect depended on the amount of contractile activity. Stimulation or passive stretch of the soleus or diaphragm also retarded protein degradation. Presumably these effects of mechanical activity contribute to the changes occuring during hypertrophy in vivo. However, under the same conditions, or even after more prolonged stimulation, no change in rates of protein synthesis was detected. These findings with passive tension in vitro are particularly interesting, since passive stretch has been reported to retard atrophy or to induce hypertrophy of denervated muscle in vivo. It is suggested that increased tension development (either passive or active) is the critical event in initiating compensatory growth.

Adaptation, Physiological↗
PubMed1992

The magnitude of left ventricular myocardial hypertrophy related to the degree of its dysfunction in patients with dilated cardiomyopathy (DCM).

The aim of the study was to analyze the relationship between the magnitude of left ventricular (LV) hypertrophy and selected haemodynamic parameters reflecting LV systolic and diastolic function. The "hypertrophy-function" relationship was evaluated in 22 patients with dilated cardiomyopathy (DCM) and in patients with left ventricular dilatation resulting from volume overload due to valve disease (DVOL). The parametres of systolic and diastolic left ventricular function were obtained from right- and left-heart catheterization and quantitative angiocardiography, DCM patients were divided into subgroups depending on the magnitude of hypertrophy and degree of dilatation: Ia- moderate hypertrophy (100 g/m2 < LVMI < 175 g/m2). Ib- massive hypertrophy (LVMI > 175 g/m2); IIa- mass/volume ratio (M/V) < 1.1, and IIb - M/V > 1.1. It was found that the magnitude of myocardial hypertrophy and the M/V ratio do not affect the degree of systolic and diastolic dysfunction in patients with DCM. Myocardial hypertrophy accompanying dilatation due to DCM and DVOL showed very similar progression of impairment of isovolumetric systole and relaxation. Significant differences in EF, LVMDP and LVEDP may result from a different degree of total LV volume stiffness as a consequence of various mechanisms of hypertrophy in DCM and DVOL.

Adolescent↗
PubMed2004

[Reactive oxygen species mediate cultured neonatal rat cardiac myocyte hypertrophy induced by endothelin-1].

The effects of endothelin-1 (ET-1) and other drugs on the reactive oxygen species (ROS) generation and cardiomyocyte hypertrophy were examined in experiments on the cultured neonatal rat cardiomyocytes. The role of ROS on neonatal rat cardiomyocyte hypertrophy induced by ET-1 was studied and the relationship of PKC activation and ROS generation was investigated. The level of intracellular ROS was measured by the ROS-specific probe 2',7'-dichlorofluorescin diacetate (DCF-DA). Cardiomyocyte hypertrophy was determined by the RNA content, the total protein of cells and the cell surface area. The results are as follows. The fluorescence intensity of intracellular DCF-DA increased by 77% in cultured neonatal rat cardiac myocytes treated with ET-1 (10 nmol/L) vs control group. Compared with control group, the fluorescence intensity of intracellular PI, protein content and cell surface area increased by 128%, 87% and 151% respectively (all P<0.01) in cardiac myocytes treated with ET-1 (10 nmol/L). ABT-627, CC, or CAT inhibited the ET-1-induced increase in fluorescence intensity of intracellular DCF-DA by 62%,60% and 51% respectively (all P<0.01), and also attenuated the cardiac hypertrophy. The fluorescence intensity of intracellular DCF-DA increased by 74% (P<0.01) in myocytes treated with PMA (1 micromol/L) vs control group. Therefore, in the course of cardiomyocyte hypertrophy, ET-1 increases intracellular ROS in the cultured neonatal rat cardiac myocytes and inhibits cardiomyocyte hypertrophy induced by ROS. The ET(A) and PKC activation mediate the ROS production and cardiomyocyte hypertrophy induced by ET-1. ROS is necessary in the ET-1-induced cardiomyocyte hypertrophy.

Animals↗
PubMed2004

Influence of ACE I/D genotypes on left ventricular hypertrophy in aortic stenosis: gender-related differences.

BACKGROUND AND AIM OF THE STUDY: Factors responsible for cardiac hypertrophy in patients with aortic stenosis (AS) are not well defined. The study aim was to examine the relationship between angiotensin-converting enzyme (ACE) I/D polymorphism and the degree of cardiac hypertrophy in patients with AS. METHODS: A total of 392 white patients (159 women, 233 men; age range: 32-82 years) with AS was analyzed, with clinical data, echocardiographic parameters and ACE I/D polymorphism being assessed. RESULTS: Left ventricular mass index (LVMI) and wall thickness (LVWT) were greater in men than in women (226 +/- 66 versus 200 +/- 68 g/m2, p <0.0001; and 28.4 +/- 4.5 versus 27.3 +/- 4.1 mm, p = 0.02, respectively). In all patients, LVMI was significantly correlated with the maximal aortic gradient, ejection fraction and gender, whereas LVWT was dependent upon maximal aortic gradient, ejection fraction, gender and history of hypertension. In women, cardiac hypertrophy increased with age. Hypertrophy in women aged <66 years correlated with an absence of the DD genotype. In men, a reverse correlation of both LVMI and LVWT with age was observed (higher in younger patients). The presence of a DD genotype in men seemed to have a significant impact on the degree of cardiac hypertrophy. CONCLUSION: The degree of left ventricular hypertrophy in patients with AS was higher in men than in women. ACE I/D polymorphism appeared to have a modulating impact on cardiac hypertrophy in patients with AS, notably those aged <66 years. A higher degree of cardiac hypertrophy was seen in men with the DD genotype, and in women without the DD genotype.

Adult↗
PubMed1980

Compensatory hypertrophy of the residual small intestine after partial enterectomy. A neurohumoral feedback?

Experiments were designed to test, using 76 pigs, 1) whether a humoral factor inducing compensatory hypertrophy is released after partial enterectomy or not, and 2) whether visceral sensitivity conducted to the central nervous system by the route of the vagus plays a role in the compensatory hypertrophy or not. Vascular parabiosis was established between pigs paired for an identical blood group and histocompatibility. A continuous blood cross circulation was maintained for 410 h either between two normal pigs or between a normal and a jejunectomized (30 per cent) pig. Their growth and food intake, and the tissue weight of their small intestine were checked. Both the jejunectomized pigs and their unoperated partners showed a significant hypertrophy of the small intestine, whether residual or intact, as compared to intact pigs cross circulated between them. The hypertrophy observed in the unoperated partners of the jejunectomized pigs was not the result of any hyperphagia. There was thus a true humoral mediation of the compensatory hypertrophy. Vagal deafferentation, i.e. a selective surgical suppression of the vagal afferent (sensory) pathways originating below the diaphragm, was performed in jejunectomized pigs. Their performances and small intestine morphology (whole tissue weight and dry weight of the mucosa) were compared to those measured in jejunectomized but vagally intact pigs. The dry weight of the mucosa of the residual small intestine in resected pigs was restored (after 28 days) at a value similar to that measured for the intact small intestine in controls. Opposite to that, the dry weight of the mucosa of the residual intestine of resected + deafferented pigs was significantly lower, due to the absence of any compensatory hypertrophy. This difference did not result from any change in the food intake level. Therefore it was concluded that vagal afferences from the digestive tract are necessary in eliciting the compensatory hypertrophy. From these results and some recent bibliographical data, it is tentatively concluded that compensatory hypertrophy of the residual small intestine after partial enterectomy might be mediated through a neuro-humoral feedback whose afferent way would be the vagal sensory pathway, and efferent way would be a hormonal one monitored by the hypothalamo-hypophyseal axis.

Adaptation, Physiological↗
PubMed1995

The electrophysiology of rabbit hearts with left ventricular hypertrophy under normal and ischaemic conditions.

OBJECTIVES: To examine the cardiac electrophysiological effects of left ventricular hypertrophy (LVH) and to determine whether any observed differences are modified by global zero-flow ischaemia. METHODS: LVH was induced by perinephritic hypertension in New Zealand White rabbits. Transmembrane action potential recordings were made using conventional floating glass microelectrodes and effective refractory periods (ERP) determined by programmed stimulation in isolated arterially perfused interventricular septa during normal perfusion and a 30-min period of global ischaemia. The electrophysiological data were pooled into 6-min periods during ischaemia. RESULTS: The post-operative blood pressure was 76(2) mmHg (mean(s.e.m.)) and 113(2) mmHg (P < 0.0005) in the sham and perinephritic rabbits respectively. The left ventricular to body weight ratio was 0.27(0.01) g kg-1 in the sham and 0.36(0.02) g kg-1 in the perinephritic group (P < 0.005) representing 33% hypertrophy. In the isolated septa, prior to ischaemia, the hypertrophied group exhibited significant prolongations in action potential duration to 50% and 90% repolarisation (APD50, APD90) and ERP of 20%, 12% and 19% respectively (P < 0.005) without any differences in resting membrane potential (Em), upstroke velocity (dV/dtmax) or amplitude (APA) of the action potential. During ischaemia Em, APA and dV/dtmax progressively decreased to a similar extent in both groups. Ischaemia resulted in shortenings in APD50, APD90 and ERP in the hypertrophy group of 122(9) ms, 131(8) ms and 99 (6) ms respectively which were greater than those observed in the control group (84 (7) ms, 115 (7) ms and 50 (13) ms, P < 0.05). These differences resulted in loss of the preischaemic prolongation of repolarisation and refractoriness in the hypertrophy group. CONCLUSIONS: There was enhanced shortening of APD and ventricular refractoriness in hypertrophied muscle during global ischaemia. This could increase the dispersion of repolarization and refractoriness between normal and ischaemic hypertrophied muscle during regional ischaemia which may explain the increased susceptibility of hypertrophied hearts to arrhythmias.

Action Potentials↗
PubMed1993

[Ventricular arrhythmia and sudden cardiac death: the significance of left ventricular hypertrophy as risk factor].

Left ventricular hypertrophy is a frequent and early manifestation of cardiac structural adaptation in patients with essential hypertension. Prospective studies have clearly demonstrated that left ventricular hypertrophy represents a risk factor for cardiovascular morbidity and mortality, including sudden cardiac death. The increased risk is independent of the impact of high blood pressure and other risk factors on the cardiovascular system. Various clinical studies noted increased prevalence and severity of premature ventricular beats in hypertensive patients with left ventricular hypertrophy. Hypertrophy of myocardial cells, dilation of the left ventricle, increased stress of subendocardial myocardium and impaired coronary reserve are discussed as a possible pathogenetic link between myocardial hypertrophy and ventricular arrhythmias. Therapeutically, the primary goal for ventricular arrhythmias in hypertensive patients with left ventricular hypertrophy is regression of left ventricular mass. For this purpose, centrally sympatholytic agents, angiotensin converting enzyme inhibitors, betablockers and calcium antagonists have been found to be effective. Recently we observed that a reduction of left ventricular hypertrophy was associated with a decreased prevalence and severity of ventricular arrhythmias. Nevertheless, prospective studies are required to demonstrate whether reduction of severe ventricular arrhythmias helps to prevent sudden cardiac death due to left ventricular hypertrophy in hypertension.

Antihypertensive Agents↗
PubMed1994

[A study on glomerular hypertrophy in various renal disease].

We studied the contributions of glomerular hypertrophy in renal disease. The patients were 20 cases of IgA nephropathy with prolonged proteinuria, 13 cases of Alport syndrome and 12 cases of focal glomerular sclerosis (FGS). All patients had a normal creatinine level on renal biopsy. We determined the mean glomerular tuft area in the equatorial region of five glomeruli that showed no sclerotic change in each patient using an image analyzer and compared the value with the mean value in normal controls. Glomerular hypertrophy was defined as a value over the mean glomerular tuft area +1SD of normal controls. Glomerular hypertrophy was found in 14 IgA nephropathy cases (70.0%), 4 Alport syndrome cases (30.7%) and 8 FGS cases (66.7%). The incidence of glomerular hypertrophy was significantly higher in IgA nephropathy than in Alport syndrome and FGS showed a higher tendency compared with Alport syndrome. Of the patients with renal insufficiency, 4 of 6 IgA nephropathy cases (66.6%), 0 of 5 Alport syndrome cases (0%) and 1 of 3 FGS cases (33.3%) showed glomerular hypertrophy, IgA nephropathy patients showed the highest incidence of glomerular hypertrophy. The interval between the final biopsy and renal insufficiency showed no significant difference in this study. In IgA nephropathy, obsolescent glomeruli were significantly increased in the group in which the glomerular tuft area was over the mean +2SD compared with the group with an area less than the mean +2SD. FGS cases showed no relationship between the ratio of obsolescent glomeruli to whole glomeruli and glomerular hypertrophy. This study suggested that glomerular hypertrophy may cause declining renal function in IgA nephropathy, but not in Alport syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1994

Juxtaglomerular cell hypertrophy and hyperplasia induced in rhesus monkeys by angiotensin II receptor antagonists.

BACKGROUND: Juxtaglomerular (JG) cell hypertrophy and hyperplasia were investigated in rhesus monkeys given angiotensin II (AII) AT1 receptor antagonists L-158,338 and DUP 753 (MK-0954, losartan). EXPERIMENTAL DESIGN: In 2 initial studies, L-158,338 was given orally at 10, 30, and 90 mg/kg/day for 3 or 14 weeks. To investigate the observed JG hypertrophy and hyperplasia, in a third 5-week experiment L-158,338 was given alone at 90 mg/kg/day, or with physiologic saline supplementation at 25 ml/kg/day, or coadministered with the angiotensin converting enzyme inhibitor enalapril at 10 mg/kg/day. Physiologic saline was given to attempt to suppress renin release through volume expansion and/or sodium retention. Enalapril was given to lower plasma AII levels and observe whether JG cell hypertrophy and hyperplasia were increased or decreased. For comparison, DUP 753 was given at 90 and 300 mg/kg/day. Plasma renin activity and AII concentration were measured in this study. RESULTS: Dose- and time-dependent increases in JG cell hypertrophy and hyperplasia were seen in the 2 initial experiment. In the third experiment, plasma renin activity and AII concentration were increased 3-fold and 6-fold over pretest values by L-158,338 at 90 mg/kg/day for 5 weeks. Saline supplementation had no effect on these parameters but diminished the group mean severity grade for JG hypertrophy and hyperplasia from 1.5 to 1.0. Enalapril coadministration had no effect on plasma renin activity, whereas it blunted the plasma AII increase caused by L-158,338 and increased the group mean grade to 2.5. DUP 753 at 300 mg/kg/day produced similar increases in plasma renin activity and AII concentration but only resulted in grade 1 JG cell hypertrophy and hyperplasia. CONCLUSIONS: L-158,338-induced JG cell hypertrophy and hyperplasia is an exaggerated pharmacologic response that can be modulated by saline supplementation and angiotensin converting enzyme inhibition. These results suggest that decreased renal perfusion or altered sodium homeostasis and plasma AII concentration are important variables that contribute to AT1 receptor blockade to induce JG cell hypertrophy and hyperplasia.

Angiotensin II↗
PubMedDate not supplied

[Relation of electrocardiographic features and distribution of hypertrophy in hypertrophic non-obstructive cardiomyopathy during childhood].

The relationship between the electrocardiographic features and the distribution of ventricular hypertrophy in pediatric patients with hypertrophic non-obstructive cardiomyopathy (HNCM) aged from 6 to 16 years (mean 11.6 years) was studied during a period of 6 months to 10 years (mean 3.9 years). Hypertrophy in the three segments (anterior septum, lateral free wall, posterior free wall) of the left ventricle in 17 patients with HNCM was evaluated by two-dimensional echocardiography (short-axis cross section of the left ventricle) at the end-diastolic period. The 17 patients were divided into four groups according to the echocardiographic findings as follows: Group A: hypertrophy in the ventricular anterior septum with or without posterior septum (eight patients). Group B: hypertrophy in both the ventricular septum and lateral left ventricular free wall (three patients). Group C: hypertrophy in the lateral left ventricular free wall (three patients). Group D: hypertrophy in the posterior left ventricular free wall with or without posterior septum (three patients). The incidence of electrocardiographic abnormalities in each group was analyzed using serial standard 12-lead electrocardiography. Electrocardiographic abnormalities and the distribution of the ventricular hypertrophy were related as follows: Lateral free wall: increased SV1 + RV6 (p < 0.05), ST-T change in leads V5.6 (p < 0.01). Posterior free wall: ST-T change in leads II.aVF (p < 0.05). Electrocardiographic abnormalities in HNCM patients in the hypertrophy were: Group A: abnormal Q waves in leads II.III.aVF (75%) and V5.6 (50%), high voltage R waves in leads II.III.aVF (25%) and V1 (38%), low voltage R waves in leads V2.3 (13%) and V5.6 (38%), and ST-T changes in leads I.aVL (25%), II.aVF (13%) and V2-4 (50%). Group B: abnormal Q waves in leads II.III.aVF (33%), high voltage R wave in lead V1 (33%), increased SV1 + RV6 (67%), low voltage R waves in leads V2.3 (33%) and V5.6 (33%), and ST-T changes in leads I.aVL (33%), II.aVF (33%), V2-4 (67%) and V5.6 (67%). Group C: abnormal Q waves in leads I.aVL (33%) and V5.6 (33%), high voltage R waves in leads II.III.aVF (33%), V1 (67%) and V5.6 (33%), increased SV1 + RV6 (67%), low voltage R waves in leads V5.6 (33%) and ST-T changes in leads II.aVF (33%), V2-4 (33%) and V5.6 (67%).

Adolescent↗