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PubMed1999

The DD genotype of the angiotensin converting enzyme gene is negatively associated with right ventricular hypertrophy in male patients with chronic obstructive pulmonary disease.

The renin angiotensin system plays an important role in the development of pulmonary artery remodeling and right ventricular hypertrophy in hypoxia-induced pulmonary hypertension as may occur in patients with COPD. Several polymorphisms of genes encoding for components of the renin angiotensin system such as the M235T polymorphism in the angiotensinogen gene, the 287-base-pair insertion (I)/deletion (D) polymorphism at intron 16 of the ACE gene, and the A1166C polymorphism in the angiotensin II type 1 receptor gene have been associated with an increased risk of cardiovascular diseases. With respect to the pulmonary circulation, only limited data exist on possible associations between polymorphisms of these genes and pulmonary hypertension and/or right ventricular hypertrophy. The objective of the present study was to investigate a possible relationship between polymorphisms of the renin angiotensin system and electrocardiographic evidence of right ventricular hypertrophy in patients with COPD. We therefore determined the angiotensinogen (M235T), angiotensin converting enzyme (I/D), and angiotensin II type 1 receptor (A1166C) genotypes in 87 patients with severe COPD and correlated these data with electrocardiographic parameters of right ventricular hypertrophy. Thirty-one patients (36%) of 87 patients with COPD showed electrocardiographic evidence of right ventricular hypertrophy. In the male, but not in the female, subgroup, the angiotensin-converting enzyme DD genotype was negatively associated with electrocardiographic evidence of right ventricular hypertrophy (male: chi2 = 3.8, p = 0.05; female: chi2 = 0.05, p = 0.82). We found no associations between the investigated polymorphisms in the angiotensinogen and angiotensin II type 1 receptor genes and electrocardiographic evidence of right ventricular hypertrophy.

Aged↗
PubMed1988

The role of Haemophilus influenzae in the pathogenesis of tonsillar hypertrophy in children.

The role of specific bacteria in the pathogenesis of tonsillar hypertrophy in children in unknown. To determine the effect of specific bacteria on the presence and nature of tonsillar hypertrophy (measured both clinically and by tonsil weight), quantitative aerobic bacteriology was performed on 54 tonsil-core specimens from 54 children undergoing tonsillectomy for chronic tonsillitis and/or tonsillar hypertrophy. Twelve tonsil-core biopsies from 12 children with no history of tonsil disease served as controls. Haemophilus influenzae (HI), Streptococcus pyogenes (SP), Streptococcus pneumoniae (SPn), and Staphylococcus aureus (SA) were the most common microorganisms cultured from diseased tonsils. Few bacteria were cultured from the cores of controls. HI was cultured as the dominant aerobic bacteria in 15 of 54 tonsils (27%). For HI alone, the number of bacteria/gram tonsil showed a significant positive correlation to tonsil weight (p less than 0.05). Fourteen of 15 (94%) tonsils with HI were found in patients with clinical tonsillar hypertrophy, while only 6 of 10 patients (60%) with SP and SPn had tonsillar hypertrophy. Of the 38 tonsils removed for obstructive symptoms (clinical hypertrophy), 14 of 38 (37%) cultured HI as the dominant microorganisms, whereas only 6 of 38 (16%) cultured SP. Neither the type of HI (b vs. non-b) nor the presence of beta-lactamase production had a significant correlation to tonsil weight, bacterial load or the number of B- or T-cell subsets. The number of T-helper (Th), T-suppressor (Ts) and B-cells (per gram/tonsil) was markedly greater in all diseased tonsils than in controls. For both HI and SP the total number of bacteria/gram tonsil correlated positively to the number of Ts cells (p less than 0.003 and p less than 0.007, respectively). In patients with HI type b (HI-b), the tonsil weight correlated to an increase in Ts and B-cells (p less than 0.004 and p less than 0.007, respectively). An increased presence of the Ts and B-cells in the HI-b tonsils (and not in tonsils with HI non-b) suggests a differential response by the tonsil to these distinct but related bacteria. The above data strongly support an etiological role for HI in the pathogenesis of tonsillar hypertrophy in children. Alterations in the relationship between Th and Ts cells may affect normal B-cell function and be implicated in this phenomenon. Clinical implications for pathogenesis, antimicrobial therapy, and future directions for research are discussed.

Child↗
PubMedDate not supplied

A novel cell-based system for evaluating skeletal muscle cell hypertrophy-inducing agents.

Skeletal muscle is a tissue that adapts to increased use by increasing contractile protein gene expression and ultimately skeletal muscle mass (hypertrophy). To identify hypertrophy-inducing agents that may be potentially useful in the treatment of age-related muscle loss (sarcopenia) and to better understand hypertrophy signal transduction pathways, we have created a skeletal muscle cell-based hypertrophy-responsive system. This system was created by permanently modifying the relatively undifferentiated C2C12 cell line so that it contains the beta-myosin heavy chain (beta-MHC) gene promoter and enhancer regions fused to a luciferase reporter gene. This cell line responds, by increasing luciferase expression, to a variety of skeletal muscle hypertrophy-inducing agents, including insulin, insulin-like growth factor I, testosterone, and the beta-adrenergic receptor agonist isoproterenol, in both the undifferentiated and differentiated states. This cell-based system should be useful for identifying novel hypertrophy-inducing agents as well as understanding hypertrophy signal transduction.

Animals↗
PubMed1975

Muscle fiber orientation in normal and hypertrophied hearts.

Muscle fiber orientation in the left ventricular myocardial layer was histometrically estimated in normal, concentric and eccentric hypertrophied hearts. The angle of inclination of muscle fibers from coronal section was largest in the innermost and outermost zones and was progressively diminished toward the middle layer in all the hearts. In the inner layer, the inclination was depressed in eccentric hypertrophy, while there was no difference in fiber orientation in the outer layer. Concentric hypertrophy proved to be an intermediate stage between the normal heart and eccentric hypertrophy, and no opposite behavior was found in the arrangement of heart muscle fibers. The results supported the following view on the mechanism in the activity of hypertrophied hearts. Cardiac hypertrophy is a common accommodation process to increased load, regardless of the difference in the macroscopical shape. In hypertrophy, the ventricular cavity is inevitably enlarged. Consequently, the tension exerted on the ventricular wall on account of intraventricular pressure increases, and the contractile force required from a unit thickness of the ventricular wall is enhanced. The muscle fibers meet this increased demand by starting contraction from an over-stretched state and by ceasing its activity after smaller shortening than in the normal heart.

Cardiomegaly↗
PubMed2006

Proteomic analysis of ovine muscle hypertrophy.

Two-dimensional electrophoresis was used to investigate the effects of a QTL for muscle hypertrophy on sarcoplasmic protein expression in ovine muscles. In the Belgian Texel breed, the QTL for muscle hypertrophy is localized in the myostatin-encoding gene. Based on microsatellite markers flanking the myostatin gene, we compared the hypertrophied genotype with the normal genotype. The average age of the sheep was 3 mo. Among the 4 muscles studied, in the hypertrophied genotype only the vastus medialis was normal, whereas the semimembranosus, tensor fasciae latae, and LM were hypertrophied. In the hypertrophied genotype, these muscles showed upregulation of enzymes involved in glycolytic metabolism together with oxidative metabolism in LM. Certain chaperone proteins, including glutathione S-transferase-Pi, heat shock protein-27, and heat shock cognate-70, were also more highly expressed, probably due to increased use of energetic pathways. Expression of the iron transport protein transferrin was increased. Alpha-1-antitrypsin was the only protein showing a similar pattern of expression (i.e., less expressed) in all 4 muscles of the hypertrophied genotype. It is suggested that transferrin and alpha-1-antitrypsin may interact to reinforce myogenic proliferative signaling.

Animals↗
PubMed1985

Vascular hypertrophy in borderline hypertension: relationship to blood pressure and sympathetic drive.

While borderline hypertension increases the chance for cardiovascular disease, most with borderline hypertension will not experience problems. Thus, the risk of intervening probably outweighs benefit for the majority. However, those with target organ damage are probably at higher risk and might benefit from more aggressive management. Therefore, we assessed vascular hypertrophy and average home blood pressures in patients with borderline hypertension which might be of value in therapeutic planning. Minimum forearm vascular resistance (mFAVR) was used as an index of vascular hypertrophy. Comparing ten normotensive controls to twenty individuals with borderline hypertension revealed a significant difference in mFAVR (1.7 +/- 0.06 vs 2.1 +/- 0.1, p less than .05). There were obvious differences in blood pressure between normotensives and borderlines which contributed to differences in mFAVR. However, within the group with borderline hypertension, no relationship was apparent between mean blood pressure and mFAVR, r = 0.13, NS. Among the borderline hypertensives, baseline plasma norepinephrine correlated with mFAVR, r = 0.48, p less than .05, suggesting that the sympathetic nervous system contributes to vascular hypertrophy in this group. In a separate group of individuals with nine normotensives and nine borderline hypertensives we wished to find if average home blood pressure would correlate better with mFAVR than a single laboratory measurement. While both the home (r = 0.56, p less than .05) and laboratory (r = 0.66, p less than .01) MBP correlated significantly with mFAVR, the data did not confirm the hypothesis that the average home blood pressures would better predict the degree of vascular hypertrophy. These data show that a substantial proportion of patients with borderline hypertension have evidence for vascular hypertrophy, sympathetic drive might contribute to vascular hypertrophy in borderline hypertension, average home blood pressures did not aid in separating those with and without evidence for vascular hypertrophy.

Adult↗
PubMed1993

Differential sensitivity of rat uterine growth and epithelium hypertrophy to estrogens and antiestrogens.

Triphenylethylene antiestrogens are considered weak estrogen agonists based on their limited ability to induce estrogen responses, in particular uterine growth. We compared the uterotrophic activity of naturally occurring and synthetic estrogens with that of antiestrogens by quantitating uterine wet weight and hypertrophy in the uterine luminal and glandular epithelium. Immature rats received five daily injections of either an estrogen (17 beta-estradiol [E2], diethylstilbestrol [DES], or ethynyl estradiol [EE]) or an antiestrogen (tamoxifen [TAM], monohydroxytamoxifen [OH-TAM], or clomiphene citrate [CC]) (0.001-100 micrograms/rat/day) subcutaneously in sesame oil and were sacrificed approximately 2 hr after the last injection. Both DES and EE increased uterine weight at doses between 0.01-100 micrograms/rat/day; E2 was about 10-fold less potent. The antiestrogens increased uterine weight only slightly. DES, EE, and the three antiestrogens each increased luminal epithelium hypertrophy to over 3-fold above that in controls. While the potencies of these synthetic compounds differed (DES = EE > OH-TAM > TAM = CC), each hypertrophic response occurred over two log doses, and the response curves displayed identical slopes. E2, however, required a range of four log doses to achieve the same degree of luminal epithelium hypertrophy. The three antiestrogens elicited glandular epithelium hypertrophy up to 2-fold above controls at the same doses that induced luminal epithelium hypertrophy; the order of potency was OH-TAM > TAM = CC. However, the three estrogens increased glandular epithelium hypertrophy only marginally. Thus, under dosing conditions commonly used to assess uterotrophic activity, these "antiestrogens" are complete, albeit less potent, estrogen agonists in the luminal epithelium and, unlike estrogens, induce hypertrophy in the glandular epithelium.

Animals↗
PubMed1991

[Influence of tonsillar hypertrophy to physical growth and diseases of the nose and ear in school-age children].

The authors investigated the influence of facial tonsillar hypertrophy to physical growth, and diseases of the nose and the ear for 7190 pupils of elementary schools in nine different areas in Japan. Tonsillar hypertrophy seemed to prevent physical growth of pupils of lower grades. In pupils without tonsillar hypertrophy, the number of pupils suffering from rhinitis gradually decreased from 16.9% in the first grade to 8% in the sixth degree. On the other hand, the number of pupils suffering from rhinitis remained to be large, ranging between 20.5% and 29.7% in the group of tonsillar hypertrophy. The number of pupils with hearing loss were much more in the group of tonsillar hypertrophy. Since an only available diagnostic mean of ear disease was an otoscopic examination, a significant number of pupils with serous otitis media may be labeled as hearing loss. For this reason, tonsillar hypertrophy possibly affected the number of pupils with hearing loss. There were no apparent relations between tonsillar hypertrophy and allergic rhinitis, chronic paranasal sinusitis and chronic otitis media.

Body Constitution↗
PubMed2001

[The role of AT1 receptor and cyclin kinase inhibitor p27 protein in angiotensin II-induced hypertrophy of mesangial cell].

OBJECTIVE: To investigate the role of p27 and AT1 receptor in the hypertrophy of mesangial cell (MC) induced by angiotensin II (Ang II). METHODS: p27 protein of MC lysate was detected with Western blotting analysis. The degree of cultured MC hypertrophy was estimated through [3H] thymidine incorporation and [3H] leucine incorporation. The effect of reducing p27 expression on cell hypertrophy was analysed with p27 antisense oligodeoxynucleotide (ODN) phosphorothioate. The extracellular matrix (ECM) protein (type IV collagen and fibronectin) of MC lysate was examined with ELISA. RESULTS: Ang II stimulated p27 expression of MC cultured in normal glucose DMEM. MC stimulated by Ang II revealed hypertrophy as well as increased [3H] leucine incorporation, decreased [3H] thymidine incorporation and increased ECM. p27 antisense ODN transfection abolished the effect of Ang II mentioned above. Losartan lowered p27 level of MC stimulated by Ang II and attenuated MC hypertrophy induced by Ang II; meanwhile [3H] leucine incorporation and ECM level decreased, [3H] thymidine incorporation increased. The effect of Losartan was dose-dependent. CONCLUSION: Ang II induced MC hypertrophy by increasing p27 protein level through AT1 receptor. Because the cell cycle is controlled by the interplay between the positive and negative cell cycle regulatory proteins (CCRP), further research is needed to study the expression of the positive and negative CCRP in MC in order to understand better the role of CCRP in MC hypertrophy induced by Ang II.

Angiotensin II↗
PubMed2002

Captopril fails to reverse hypertrophy of the left ventricle induced by aortic insufficiency in rabbits.

Angiotensin converting enzyme (ACE) inhibition has been reported to induce regression of hypertrophy in several models of hemodynamic pressure overload. The aim of the present study was to determine whether the ACE inhibitor captopril can reduce hypertrophy of the left ventricle induced by a chronic volume overload and modify collagen composition of the hypertrophied myocardium. Rabbits with four months lasting aortic insufficiency were divided into two groups: treated with captopril (20 mg/kg/day) for five weeks and treated with placebo. The respective control groups were represented by sham-operated animals. Aortic insufficiency induced a decrease of diastolic pressure, an increase of systolic and pulse pressure, hypertrophy of the left and right ventricle, and an increase of hydroxyproline content in the left ventricle without a change of hydroxyproline concentrations in either ventricle. Captopril treatment further enhanced pulse pressure by decreasing diastolic blood pressure. Hypertrophy of the left ventricle, hydroxyproline content and concentration in both ventricles were unaffected by captopril treatment. It is concluded that ACE inhibition did not reverse the left ventricular hypertrophy developed as a result of overload induced by aortic insufficiency. We suggest that mechanisms different from activation of the renin-angiotensin system may play a decisive role in the maintenance of hypertrophy in this particular model of volume hemodynamic overload.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1980

Protein turnover during skeletal muscle hypertrophy.

Skeletal muscle hypertrophy has been investigated in several models including denervation, increased work induced by tenotomy of a synergist, and the addition of weights to the wing of a chicken. The stimulus for growth probably involves passive stretch along with increased tension development induced by the stretch reflex in innervated muscles. In early studies of hypertrophy of rat soleus and plantaris muscles, turnover measurements were interpreted as indicating increased protein synthesis and decreased degradation as the mechanism for the hypertrophy. However, these conclusions are probably unjustified. In particular it has been shown that there is a marked increase in reutilization and isotope recycling in muscle during hypertrophy. Several studies indicate that both protein synthesis and degradation are increased during hypertrophy. This has been shown in the transient hypertrophy of the denervated hemidiaphragm. During hypertrophy of the innervated anterior latissimus dorsi of chickens, there are increases in protein synthesis and degradation to the extent that as much as two-thirds of the total increase in synthesis may be associated with increased turnover or "wastage" and only one-third with growth.

Animals↗
PubMed1995

Insulin-like growth factor binding proteins in arterial hypertension: relationship to left ventricular hypertrophy.

OBJECTIVE: It was reported previously that circulating insulin-like growth factor I levels are abnormally elevated in patients with essential hypertension and left ventricular hypertrophy. Tissue availability of the factor depends on the distribution of the circulating bound factor between its high- and low-molecular mass binding proteins, only the latter being able to cross the endothelium. The aim of this study was to investigate whether the presence of the different serum binding proteins is altered in patients with essential hypertension and left ventricular hypertrophy. DESIGN: The study was performed in 30 never-treated patients with essential hypertension and 30 age- and sex-matched normotensive subjects. Patients were separated into two groups according to the presence or the absence of echocardiographically determined left ventricular hypertrophy. METHODS: Plasma insulin-like growth factor I levels were determined by specific radioimmunoassay. The different molecular forms of its serum binding proteins were analysed by Western blotting using [125I]-labelled insulin-like growth factor I. A densitometric scanning of the blots was performed to analyse the quantitative relationships between the different forms of binding proteins. RESULTS: Insulin-like growth factor I levels were significantly higher in the hypertensive patients with than in the hypertensive patients without left ventricular hypertrophy or in the normotensive subjects. Compared with the normotensive subjects, both hypertensive patients subgroups exhibited increased high-molecular mass binding protein type 3 and decreased low-molecular mass binding proteins types 1 and 2. However, changes in the binding proteins were more marked in the hypertensive patients without than in the hypertensive patients with left ventricular hypertrophy. Accordingly, the ratio of low- to high-molecular mass binding proteins (an index of insulin-like growth factor I bioavailability) was higher in the hypertensive patients with than in the hypertensive patients without left ventricular hypertrophy. CONCLUSIONS: These results show that the distribution of the molecular forms of serum insulin-like growth factor binding proteins is altered in patients with essential hypertension, independently of insulin-like growth factor I levels. This suggests that regulation of the binding proteins is abnormal in essential hypertension. Whether the tissue availability of circulating insulin-like growth factor I is higher in hypertensive patients with than in hypertensive patients without left ventricular hypertrophy merits further investigation.

Adult↗
PubMed1995

Renal epithelial cell hyperplasia and hypertrophy.

Renal epithelial cells that are part of an intact tubule epithelium divide at a very slow rate. However, in response to physiological signals or pathological processes, their rate of growth can rapidly increase. In these situations, the growth response can be hyperplasic (an increase in cell number) and/or hypertrophic (an increase in cell size). This article reviews our current understanding of the signaling pathways involved in renal epithelial cell hyperplasia and hypertrophy. Hyperplasia involves an initiating mitogenic stimulus, followed by the synthesis of a number of proteins that regulate a cascade of events governing progression through each of the phases of the cell cycle (G1, S, G2, and M phases). Renal epithelial cell hypertrophy can occur by cell cycle-dependent or -independent mechanisms. Cell cycle-dependent hypertrophy involves signals that cause cells to enter the first phase of the cell cycle (G1), but become arrested before leaving this phase. The consequence of these two sequential events is cell growth without DNA replication and, thus, cell hypertrophy. pRB plays a key role is the development of this form of hypertrophy. Cell cycle-independent hypertrophy probably involves inhibition of pH-sensitive lysosomal enzymes, leading to decreased protein degradation, and consequently an increase in cell protein content and cell hypertrophy.

Animals↗
PubMed1995

Depressed transient outward current in single hypertrophied cardiomyocytes isolated from the right ventricle of ferret heart.

OBJECTIVE: The aim of this study was to investigate transient outward potassium current (Ito) changes as a basis for the prolongation of the action potential associated with cardiac hypertrophy. METHODS: Right ventricular hypertrophy was induced by chronic pulmonary artery constriction in adult male ferrets. After 4-6 weeks, hearts were excised and single myocytes were isolated from the right ventricles of banded and sham-operated (control) animals by enzymatic dissociation. Ito was recorded by means of the whole cell patch clamp technique. RESULTS: Heart weight:body weight ratio and cell membrane capacitance, as indications of hypertrophy, were increased by 17% (P < 0.05) and 32% (P < 0.01) respectively in the banded group. Analysis of Ito showed that in hypertrophied myocytes compared to normal controls: (1) the density of current was significantly reduced; (2) both the time to peak and the time constant of inactivation were increased; (3) the voltage-dependent steady-state availability was not changed, with similar potentials for half activation (30.4 +/- 6.8 mV in control and 33.9 +/- 8.5 mV in hypertrophied cells) and half inactivation (-12.3 +/- 3.3 mV in control and -11.4 +/- 2.7 mV in hypertrophied cells); (4) the time constant for recovery from inactivation was significantly increased regardless of the holding potentials (-50 mV, -70 mV or -90 mV). CONCLUSIONS: Alterations of the transient outward potassium current with respect to its density, kinetics and recovery from inactivation can explain the prolongation of the action potential in myocytes isolated from pressure-overload hypertrophied heart and may thus be an important step in such cardiac adaptation.

Action Potentials↗
PubMed1995

Wall stress induced arrhythmia is enhanced by low potassium and early left ventricular hypertrophy in the working rat heart.

OBJECTIVE: The aim was to investigate the effect of lowering external potassium on the sensitivity of the normal and hypertrophied rat heart to arrhythmias induced by increases in ventricular wall stress. METHODS: The isolated working heart model was used to compare hypertrophied hearts from the spontaneously hypertensive rat (SHR) with hearts from normotensive control rats (NCR) from the Wistar and Wistar-Kyoto strains. Young animals [131.5(SEM 0.64) days] were used to ensure uncomplicated left ventricular hypertrophy. Arrhythmias were induced by 20 s increases in ventricular wall stress. The ECG was recorded and the arrhythmic response of each heart was compared during perfusion with Tyrode solutions containing [K] 6, 4.8, 3.6, and 2.4 mM. RESULTS: Hypertrophied SHR hearts showed a significantly greater arrhythmic response than control hearts at all levels of afterload increase when perfused with [K] 3.6 and 2.4 mM (t test P < 0.05 and P < 0.01). Both the number and complexity of arrhythmias were increased in the SHR hearts; ventricular tachycardia occurred in 10/12 compared with 4/12 control hearts whereas ventricular fibrillation occurred in 5/12 hearts but in none of the control hearts. CONCLUSIONS: At higher levels of [K] the sensitivity of SHR and normal hearts to wall stress induced arrhythmias is similar. However, as [K] is lowered to 3.6 mM or below, hypertrophied hearts show a greatly enhanced response to increases in ventricular wall stress. They develop a larger number of ventricular ectopics and more complex ventricular arrhythmias when compared to normal hearts. This may be of relevance to arrhythmic sudden death in hypertensive patients in whom left ventricular hypertrophy, potassium depletion, and blood pressure lability is common. Excessive fluctuations in systolic pressure and therefore ventricular wall stress could provide a powerful arrhythmic stimulus in hypertensive patients with left ventricular hypertrophy, even before ischaemia, cardiac failure, or extensive extracellular fibrosis have developed.

Animals↗
PubMed1994

[When is echography necessary in the diagnosis of pylorus hypertrophy in young children?].

OBJECTIVE: To determine if ultrasonography is necessary for the diagnosis of pyloric hypertrophy in children and if in (clinical) doubt the ultrasonographic diagnosis of 'pylori hypertrophy' may constitute the indication for operation. SETTING: Leiden University Hospital and Amsterdam Centre for Paediatric Surgery. DESIGN: Retrospective study. METHOD: In the period 1985-1990, 83 children younger than 4 months were operated on for pyloric hypertrophy (group I; 73 of them had been examined by ultrasonography), while 15 underwent sonography because of suspicion of pyloric hypertrophy (group II), without operation. An attempt was made to find clinical and laboratory data that might be an indication of pyloric hypertrophy, and render supplementary ultrasonography unnecessary. RESULTS: In group I, the combination of projectile vomiting, discernible gastric peristalsis after test meal and metabolic alkalosis was present in 34%, while a tumour in the upper abdomen was palpated in 25%; neither finding was present in group II. The sensitivity of one-time ultrasonography was 74%, that including follow-up examination in case of doubt, 82%. The predictive value of an ultrasonographic result positive for 'pyloric hypertrophy' was 98%, that of a negative finding 52%, the accuracy was 84%. CONCLUSION: In children younger than 4 months with the combination of projectile vomiting, gastric peristalsis after test meal and metabolic alkalosis, or with a palpable swelling in the upper abdomen, no ultrasonography is necessary to make the diagnosis of 'pyloric hypertrophy'. In case of clinical doubt, the indication for operation may be based on the result of ultrasonography.

Humans↗
PubMed1993

[Antihypertensive treatment and left ventricular hypertrophy].

Left ventricular hypertrophy in arterial hypertension can be considered as an adaptive response of the heart to the increased afterload, in order to reduce wall stress; however, cardiac hypertrophy can also represent the first step toward a pathological process that leads to the development of congestive heart failure. Epidemiological studies have documented that left ventricular hypertrophy in essential hypertension represents an independent risk factor for cardiovascular morbidity and mortality. The possibility of reversing, or even preventing, left ventricular hypertrophy through a reduction in elevated blood pressure values and modification of some other pathogenetic factors should represent a major therapeutic need in the treatment of hypertensive patients. It has been demonstrated that different classes of antihypertensive drugs do not have the same effect in reducing left ventricular mass, probably because beyond control of blood pressure, the pharmacological interference with adrenergic system, the renin-angiotensin-aldosterone system or other growth factors can influence the development and the reduction of cardiac hypertrophy. Two recent meta-analyses of the principal regression studies have shown that ACE-inhibitors, followed by calcium antagonists and drugs capable of reducing sympathetic nervous system activity, are more effective in decreasing left ventricular mass. The results of experimental and clinical studies have demonstrated that the reversal of cardiac hypertrophy is associated with an improvement of the functional consequences of an increased left ventricular mass. Further studies are needed in order to verify whether the reversal of left ventricular hypertrophy per se increases survival in essential hypertensive patients.

Adaptation, Physiological↗
PubMed1993

The importance of the renin-angiotensin system in reversal of left ventricular hypertrophy.

BACKGROUND: The renin-angiotensin system has an important effect on the development of cardiac hypertrophy and the regulation of left ventricular function, in particular by promoting cardiac interstitial fibrosis. EFFECT OF ANGIOTENSIN CONVERTING ENZYME (ACE) INHIBITORS: In both experimental and human studies, ACE inhibitors have shown a clear tendency to perform better than other types of antihypertensive therapy in reversing cardiac structural changes. A recent meta-analysis of 109 studies showed that ACE inhibitors were more effective than beta-blockers, calcium antagonists and diuretics in reducing left ventricular mass. Furthermore, cardiac hypertrophy was reversed to a significantly greater extent with enalapril than hydrochlorothiazide in a long-term study of previously untreated men. Multivariate analyses of the results from that study showed that the reversal of cardiac hypertrophy was independently related to the blockade of the circulating renin-angiotensin system. Furthermore, experimental studies have shown that ACE inhibition can induce reversal of left ventricular hypertrophy even without a fall in blood pressure. EFFECT OF LOSARTAN: The novel angiotensin II blocker losartan has, like ACE inhibitors, shown significant effects on cardiovascular structure in animal models. CONCLUSIONS: Blockade of the renin-angiotensin system with ACE inhibitors seems to have independent significance for the reversal of cardiac hypertrophy. However, we still do not know whether it is the attenuation of angiotensin II (locally or systemically), apart from a fall in blood pressure, that is the most important effect of ACE inhibition. Therefore, results from future studies on the ability of angiotensin II antagonists to affect left ventricular hypertrophy, in comparison with ACE inhibitors, are awaited with great interest, especially regarding the differential effects on myocyte hypertrophy and interstitial fibrosis.

Angiotensin II↗