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PubMed1993

Changes in cell length consequent on depolarization in single left ventricular myocytes from guinea-pigs with pressure-overload left ventricular hypertrophy.

Cell length was measured in single guinea-pig left ventricular myocytes by using a high-resolution photodiode array. Step depolarizations from a holding potential of -45 mV were applied using a switch-clamp technique with 2 M KCl microelectrodes, which were devoid of Ca2+ buffering. Comparison was made between myocytes from sham-operated guinea-pigs and guinea-pigs with mild pressure-overload left ventricular hypertrophy induced by infra-renal aortic constriction. The relation between cell shortening and membrane voltage was bell shaped, and a phasic component of shortening was evident at the range of potentials over which the L-type calcium current was activated. Mean cell shortening was increased in the hypertrophy group, and was maximal at +15 mV in both groups (control, 7.6 +/- 0.9 microns, n = 11, hypertrophy 11.0 +/- 1.2 microns, n = 20, p < 0.05). The latency to the onset of contraction was significantly shorter in the hypertrophy myocytes at -25 mV and at potentials positive to +50 mV. The relation between time-to-peak shortening and voltage showed a trend to shorter times in the hypertrophy group. At very positive potentials a slow component of contraction was identified which was relatively larger in the hypertrophy myocytes. This finding is consistent with increased calcium entry via sarcolemmal sodium-calcium exchange in the myocytes from the hypertrophy group.

Action Potentials↗
PubMedDate not supplied

Mouse strain-specific differences in cardiac metabolic enzyme activities observed in a model of isoproterenol-induced cardiac hypertrophy.

1. Alterations in myocardial energy metabolism accompany pressure overload-induced hypertrophy. We previously described a novel model of catecholamine-induced hypertrophy in which A/J mice exhibit more robust cardiac hypertrophy than B6 mice. Accordingly, we assessed the influence of mouse strain on the activities of key myocardial metabolic enzymes and whether there are strain-related metabolic adaptations to short-term, high-dose isoproterenol (ISO) administration. 2. Thirty-nine male mice (19 A/J mice, 20 B6 mice), aged 12-15 weeks, were randomly assigned to receive either ISO (100 mg/kg, s.c.) or vehicle (sterile water) daily for 5 days. On Day 6, all hearts were excised, weighed, freeze clamped and assayed for pyruvate dehydrogenase (PDH), medium chain acyl-CoA dehydrogenase, carnitine palmitoyl transferase I and citrate synthase activities. Plasma fatty acids (FA) were also measured. 3. The ISO-treated A/J mice demonstrated greater percentage increases in gravimetric heart weight/bodyweight ratio than ISO-treated B6 mice (24 vs 3%, respectively; P < 0.001). All enzyme activities were significantly greater in vehicle-treated B6 mice than in A/J mice, illustrating a greater capacity for aerobic metabolism in B6 mice. Administration of ISO reduced PDHa (active form) activity in B6 mice by 47% (P < 0.001), with no significant change seen in A/J mice. Free FA levels were not significantly different between groups; thus, the differences in PDHa were not due to changes in FA. 4. The basal activity of myocardial metabolic enzymes is greater in B6 mice than in A/J mice and ISO alters myocardial PDH activity in a mouse strain-dependent manner. Compared with A/J mice, B6 mice demonstrate less ISO-induced cardiac hypertrophy, but greater activity of key enzymes regulating FA and carbohydrate oxidation, which may protect against the development of hypertrophy. The metabolic adaptations associated with ISO-induced hypertrophy differ from those reported with pressure overload hypertrophy.

Acyl-CoA Dehydrogenase↗
PubMed2005

Gas6 induces Akt/mTOR-mediated mesangial hypertrophy in diabetic nephropathy.

BACKGROUND: We have already reported Gas6 is involved in glomerular hypertrophy observed in diabetic nephropathy. However, the molecular mechanisms involved in glomerular hypertrophy are still unknown, especially in vivo. METHODS: In vivo, diabetes was induced in rats and mice by streptozotocin (STZ) and the activation of the Akt/mTOR pathway in glomeruli was examined. In vitro, mesangial hypertrophy was assessed by [(3)H]leucine incorporation and measuring cell areas. RESULTS: Akt, p70 S6 kinase, and 4E-BP-1 were induced and phosphorylated in rat glomerular lysates after 12 weeks of STZ injection when mesangial and glomerular hypertrophy was observed. We then examined the role of Gas6 by treating STZ-rats with warfarin, and found that warfarin treatment inhibited the phosphorylation of these molecules as well as the hypertrophy. We next examined whether high glucose stimulation can induce the expression of Gas6/Axl in mesangial cells. Stimulation of the cells with 25 mmol/L of glucose increased the expression of Gas6/Axl and mesangial cell size compared with that with 5.6 mmol/L of glucose. This hypertrophic effect was abolished in mesangial cells derived from Gas6 knockout mice. We also found that LY294002 and rapamycin blocked Gas6-induced activation of the Akt/mTOR pathway and mesangial hypertrophy. Furthermore, less phosphorylated Akt-positive or 4E-BP-1-positive areas were found in STZ-treated Gas6 knockout mice than in STZ-treated wild-type mice. CONCLUSION: Our study indicates that the Akt/mTOR pathway is a key signaling cascade in Gas6-mediated mesangial and glomerular hypertrophy and revealed a crucial role of Gas6/Axl and the Akt/mTOR pathway in the development of diabetic nephropathy.

Adaptor Proteins, Signal Transducing↗
PubMed2006

The possible role of caspase-3 in pathological and physiological cardiac hypertrophy in rats.

The present study has been designed to investigate the effect of Ac-DEVD-CHO, a specific caspase-3 inhibitor in partial abdominal aortic constriction for 4 week-induced pathological and chronic swimming training for 8 week-induced physiological cardiac hypertrophy. Ac-DEVD-CHO (2 mg/kg intraperitoneally, day(-1)) treatment was started three days before partial abdominal aortic constriction and chronic swimming test and it was continued for 4 weeks in partial abdominal aortic constriction and 8 weeks in chronic swimming test experimental model. The left ventricular (LV) function and LV hypertrophy were assessed by measuring LV developed pressure, dp/dt(max), dp/dt(min), ratio of LV weight to body weight, LV wall thickness, LV collagen content, protein content and RNA concentration. Further, venous pressure and mean arterial blood pressure were recorded. The partial abdominal aortic constriction but not chronic swimming test produced LV dysfunction by decreasing LV developed pressure, dp/dt(max), dp/dt(min.)and increasing LV collagen content. Further, partial abdominal aortic constriction and chronic swimming test were noted to produce LV hypertrophy by increasing ratio of LV weight to body weight, LV wall thickness, LV protein content and LV RNA concentration. Moreover, in contrast to chronic swimming test, partial abdominal aortic constriction has significantly increased venous pressure and mean arterial blood pressure. The Ac-DEVD-CHO has markedly attenuated partial abdominal aortic constriction-induced LV dysfunction, LV hypertrophy, increase in venous pressure and mean arterial blood pressure. However it did not modulate chronic swimming test-induced LV hypertrophy. These results have implicated caspase-3 in partial abdominal aortic constriction-induced LV dysfunction and pathological cardiac hypertrophy. However, caspase-3 may not be involved in chronic swimming test-induced physiological cardiac hypertrophy.

Animals↗
PubMed1977

Regulation of compensatory kidney hypertrophy by its own products.

1. The ligation of blood vessels of one kidney of adult rats resulted in the compensatory hypertrophy of the other kidney. In most animals the rate of hypertrophy was indistinguishable from that observed after unilateral nephrectomy, but in a few cases the onset was retarded when the renal artery alone had been ligated and the collateral circulation increased.2. When the blood vessels of one kidney of adult rats were ligated and the cortex was excised, the rate of compensatory renal hypertrophy was similar to that observed after unilateral nephrectomy.3. In animals operated for simultaneous partial hepatectomy and unilateral nephrectomy, there was no sign of compensatory renal hypertrophy while the liver was undergoing regeneration. Renal hypertrophy started after 7 days, when about 98% of the amount of liver removed had been regenerated.4. Neither aseptic autolysis of one kidney following suppression of its blood supply, nor unilateral nephrectomy affected the rate of liver regeneration after simultaneous partial hepatectomy.5. Total splenectomy did not affect the rate of compensatory renal hypertrophy following unilateral nephrectomy.6. The heterotopic graft of renal cortical, but not of medullary, cells inhibited compensatory renal hypertrophy in adult rats. The removal of the graft after 14 days was followed by the resumption of compensatory hypertrophy.7. The inhibiting action of fractions of renal cortical extracts fractionated on Sephadex G100 resin and DEAE-52 cellulose were assayed on the ;growth' of renal explants reared in vitro. The final material, though only partially purified, proved to have an inhibiting activity between 250 and 500 times greater than that of the initial extract.8. When injected into unilaterally nephrectomized rats, the partially purified extract from the renal cortex had an inhibiting effect on compensatory renal hypertrophy.9. Immunofluorescence technique showed that the partially purified cortical extract affected the proximal convoluted tubes specifically, irrespective of animal species.

Animals↗
PubMed1995

Heart rate variability in left ventricular hypertrophy.

BACKGROUND: Electrocardiographic left ventricular hypertrophy and strain are associated with increased cardiac morbidity and mortality. Impaired cardiac autonomic function, assessed non-invasively by spontaneous heart rate variability on Holter monitoring, is associated with an increased risk of sudden death after myocardial infarction. AIM: To study the effect of left ventricular hypertrophy on heart rate variability. PATIENTS: 36 controls and 154 patients with left ventricular hypertrophy (94 with hypertension and 60 with aortic valve disease). SETTING: Tertiary referral centre. METHODS: Heart rate variability was measured on 24 h Holter recordings by non-spectral methods. Left ventricular mass index and fractional shortening were measured by echocardiography. RESULTS: Patients with left ventricular hypertrophy had a higher left ventricular mass index (P < 0.001) and reduced heart rate variability (P < 0.001) compared with those of the controls. A continuous inverse relation was apparent between heart rate variability and left ventricular mass index (r = -0.478, P < 0.001). Heart rate variability was not affected by age, the presence of coronary artery disease in patients with left ventricular hypertrophy, or beta blocker treatment for hypertension. Multivariate analysis showed that left ventricular mass index is the most important determinant of heart rate variability. CONCLUSION: Heart rate variability is significantly reduced in patients with left ventricular hypertrophy secondary to hypertension or aortic valve disease. A continuous inverse relation exists between heart rate variability and left ventricular mass index. Impaired cardiac autonomic function in left ventricular hypertrophy may contribute to the mechanism of sudden death.

Aortic Valve Stenosis↗
PubMed1998

Hypertrophied bronchial artery at thin-section CT in patients with bronchiectasis: correlation with CT angiographic findings.

PURPOSE: To evaluate hypertrophied bronchial arteries on thin-section computed tomographic (CT) scans in patients with bronchiectasis by using CT angiographic correlation. MATERIALS AND METHODS: Spiral CT angiography was performed prospectively in 14 patients (eight men, six women; age range, 34-71 years) with bronchiectasis who were suspected of having bronchial arterial hypertrophy at thin-section CT (performed without contrast medium). The inclusion criteria were tubular (in six patients) or nodular (in 14 patients) areas of soft-tissue attenuation that had an appearance unlike that of lymph nodes at thin-section CT and that were within the mediastinum and around the central airway. These findings were subsequently correlated with the spiral CT angiographic findings. RESULTS: At comparative analysis of thin-section CT scans and CT angiograms, seven of the eight (88%) tubular lesions and 19 of the 36 (53%) nodular lesions in the mediastinal soft tissue were proved to be hypertrophied bronchial arteries. All of the six (100%) tubular and 19 of the 21 (90%) nodular lesions around the walls of the main (primary) and lobar bronchi were hypertrophied bronchial arteries. In eight (57%) patients, CT angiograms showed 11 intraluminal protrusions caused by hypertrophied bronchial arteries in the main bronchi, lobar bronchi, or both. CONCLUSION: Nodular and tubular structures in the mediastinum and around the central airway on thin-section CT scans in the patients with bronchiectasis are suggestive of hypertrophied bronchial arteries. Recognition of the hypertrophied bronchial artery can be critical for the bronchoscopist.

Adult↗
PubMed1996

Role of microtubules in myocyte contractile dysfunction during cardiac hypertrophy in the rat.

We have shown that increased microtubules cause myocyte contractile dysfunction in feline right ventricular pressure-overload hypertrophy. To investigate the association between the progression of cardiac hypertrophy and microtubules and to delineate the role of microtubules in contractile defects in hypertrophied myocytes, we assessed the amounts of free and polymerized tubulin proteins, using Western blot analysis and immunofluorescence micrograph, and evaluated the sarcomere mechanics of myocytes isolated from rats with pressure-overload left ventricular (LV) hypertrophy. Total and polymerized tubulins were progressively and persistently increased in LV after the imposition of pressure overload. The increase in microtubules was associated with the development and progression of hypertrophy and not the immediate response to the stress loading to the myocardium. The contractile function of hypertrophied myocytes was depressed in parallel with the increase in microtubules. Depolymerization of microtubules normalized the initially depressed LV myocyte contractile function. Thus the progressive increase of microtubule density during LV hypertrophy due to persistent pressure overloading to the myocardium may cause the consequent myocyte contractile dysfunction.

Animals↗
PubMed1994

Modulation of IGF mRNA abundance during stretch-induced skeletal muscle hypertrophy and regression.

Increased load on a muscle (synergistic overload or stretch) results in muscle hypertrophy. The expression of insulin-like growth factor I (IGF-I) mRNA in rat skeletal muscle is increased during synergistic overload-induced hypertrophy. Although it has also been established that fasting animals lose muscle protein, it has been shown that compensatory muscle hypertrophy occurs in adult fasting rats that are undergoing a net loss of body weight. The purpose of this investigation was to determine whether a relationship exists between IGF-I mRNA levels and muscle growth and regression. This was accomplished by examining whether IGF-I mRNA levels were altered during muscle hypertrophy after stretch and regression and the effect of fasting on IGF-I mRNA levels during stretch-induced hypertrophy. Patagialis (PAT) muscle weights increased 13 and 44% at 2 and 11 days of stretch, respectively. However, after removal of the stretch stimulus on day 11, PAT weights began to decrease, reaching control weights by 18 days. During the first time point (2 days), PAT muscle IGF-I mRNA remained constant. IGF-I mRNA abundance was threefold greater than contralateral control levels by 11 days of stretch. IGF-I mRNA levels decreased but remained significantly above control levels throughout the regression of hypertrophy (13, 18, and 25 days). Fasting did not alter PAT muscle response to stretch. After 11 days of stretch, PAT muscle weight increased 60% compared with contralateral control muscles and IGF-I mRNA levels increased three-fold. This study supports a role for IGF-I in muscle hypertrophy but not muscle atrophy.

Animals↗
PubMed1978

Effect of compensatory hypertrophy studied in individual motor units in medial gastrocnemius muscle of the cat.

1. Compensatory hypertrophy of the medial gastrocnemius (MG) muscle was produced by denervating or removing its synergists (i.e., the lateral gastrocnemius, soleus, and plantaris muscles) in adult cats. Following survival times of 14-32 wk, intracellular recording and stimulation techniques were used to study the motor-unit population in MG. The data obtained were compared with results from MG motor units in normal unoperated cats of the same body size and weight. 2. Using criteria employed for normal motor units, the units in hypertrophic MG muscles were readily classified into the same groups (types FF, F(int), FR, and S) as in normal MG. There was no detectable difference in the distribution of motor-unit types after hypertrophy. 3. When compared with a normal motor-unit sample, there was a large increase in mean tetanic tension, but no significant change in twitch tension, for each motor-unit type in the hypertrophied muscles. The most marked increase was found among the fatigue-resistant type S and type FR motor units. There was no alteration of twitch contraction times or fatigue resistance in any unit type after hypertrophy. 4. For each motor-unit type, the mean homonymous (MG) group Ia EPSP amplitude was the same in normal and hypertrophic MG populations. There was, however, a significant increase in the average conduction velocity of MG motor axons in the animals with uncomplicated MG synergist removal and maximal MG hypertrophy. 5. On the basis of histochemical staining, muscle fibers from comparable sections of hypertrophic and contralateral (unoperated) MG muscles were presumptively identified as belonging to FF, FR, or S units. There was no significant difference between hypertrophic and contralateral MG muscles in the percentage of each fiber type, although there was some variability in muscle composition from one cat to another. One muscle pair was studied in detail for fiber cross-sectional area. In this cat, with marked hypertrophy by muscle weight, there was a modest increase in the mean fiber areas of histochemical S and FR muscle fibers, but no evident change in FF fibers, on the hypertrophic side. 6. MG motor units were examined in several cats in which synergist removal resulted in scarring and marked limitation of passive ankle mobility, and no evident weight gain in MG. Motor units of all types in these animals showed a decrease in twitch tension and in mean twitch/tetanus ratios, with little alteration in mean tetanic tensions. 7. The main effect of compensatory hypertrophy under the present conditions was a large increase in tetanic tension output from individual motor units due, at least in part, to an increase in fiber cross-sectional area. There was no evidence indicating any "conversion" of motor units or of their muscle fibers from one type to another.

Animals↗
PubMed2006

Microarray analysis of Akt1 activation in transgenic mouse hearts reveals transcript expression profiles associated with compensatory hypertrophy and failure.

To investigate molecular mechanisms involved in the development of cardiac hypertrophy and heart failure, we developed a tetracycline-regulated transgenic system to conditionally switch a constitutively active form of the Akt1 protein kinase on or off in the adult heart. Short-term activation (2 wk) of Akt1 resulted in completely reversible hypertrophy with maintained contractility. In contrast, chronic Akt1 activation (6 wk) induced extensive cardiac hypertrophy, severe contractile dysfunction, and massive interstitial fibrosis. The focus of this study was to create a transcript expression profile of the heart as it undergoes reversible Akt1-mediated hypertrophy and during the transition from compensated hypertrophy to heart failure. Heart tissue was analyzed before transgene induction, 2 wk after transgene induction, 2 wk of transgene induction followed by 2 days of repression, 6 wk after transgene induction, and 6 wk of transgene induction followed by 2 wk of repression. Acute overexpression of Akt1 (2 wk) leads to changes in the expression of 826 transcripts relative to noninduced hearts, whereas chronic induction (6 wk) led to changes in the expression of 1,611, of which 65% represented transcripts that were regulated during the pathological phase of heart growth. Another set of genes identified was uniquely regulated during heart regression but not growth, indicating that nonoverlapping transcription programs participate in the processes of cardiac hypertrophy and atrophy. These data define the gene regulatory programs downstream of Akt that control heart size and contribute to the transition from compensatory hypertrophy to heart failure.

Animals↗
PubMed2005

Connective tissue growth factor-mediated angiotensin II-induced hypertrophy of proximal tubular cells.

BACKGROUND: Cellular hypertrophy is an early, important pathological feature of renal diseases such as diabetic nephropathy and remnant kidney. Recent studies have demonstrated that angiotensin II (AngII) plays a key role in mediating cell hypertrophy. The aim of our work was to explore the role of connective tissue growth factor (CTGF) in mediating AngII-induced tubular cell hypertrophy in vivoandin vitro. METHODS: In an in vivo study, male Sprague-Dawley rats were randomly divided into three groups: control rats, diabetic rats and diabetic rats treated with irbesartan (IRB). The index of kidney hypertrophy (kidney weight/body weight, KW/BW), glomerular tuft area (AG), glomerular tuft volume (VG) and proximal tubular area (AT) were determined. Renal expression for CTGF was detected by immunohistochemical staining. In an in vitro study, the influence of CTGF antisense oligonucleotide (CTGF AS) on AngII-induced CTGF expression and cell hypertrophy was also investigated. RESULTS: In an in vivo study, diabetic rats showed a significant increase of KW/BW, AG, VG, and AT from week 1 onwards compared to normal control, which could be significantly inhibited by using IRB. Furthermore, there was a significantly increasing expression of CTGF in both glomeruli and tubuli in diabetic rats compared to control, and the extent of CTGF expression closely correlated with the severity of renal hypertrophy. Treatment with IRB could markedly inhibit the renal expression of CTGF. In an in vitro study, AngII stimulated the expression of CTGF mRNA and CTGF protein. AngII significantly increased the total protein content in HK2 cells, which was markedly inhibited by co-treatment with CTGF AS. The average cellular diameter determined by scanning electronic microscope showed that the increase of cell size induced by AngII could be significantly inhibited by CTGF AS. Furthermore, flow cytometer study showed that AngII arrested the cell cycle in the G0-G1 phase, which was significantly reversed by treatment with CTGF AS. CONCLUSION: Our data provide both in vivo and in vitroevidence that CTGF is involved in mediating AngII-induced renal hypertrophy.

Angiotensin II↗
PubMed1994

Induction of myocardial insulin-like growth factor-I gene expression in left ventricular hypertrophy.

BACKGROUND: Left ventricular hypertrophy is a generalized adaptation to increased afterload, but the growth factors mediating this response have not been identified. To explore whether the hypertrophic response was associated with changes in local insulin-like growth factor-I (IGF-I) gene regulation, we examined the induction of the cardiac IGF-I gene in three models of systolic hypertension and resultant hypertrophy. METHODS AND RESULTS: The model systems were suprarenal aortic constriction, uninephrectomized spontaneously hypertensive rats (SHR), and uninephrectomized, deoxycorticosterone-treated, saline-fed rats (DOCA salt). Systolic blood pressure reached hypertensive levels at 3 to 4 weeks in all three systems. A differential increase in ventricular weight to body weight (hypertrophy) occurred at 3 weeks in the SHR and aortic constriction models and at 4 weeks in the DOCA salt model. Ventricular IGF-I mRNA was detected by solution hybridization/RNase protection assay. IGF-I mRNA levels increased in all three systems coincident with the onset of hypertension and the development of ventricular hypertrophy. Maximum induction was 10-fold over control at 5 weeks in the aortic constriction model, 8-fold at 3 weeks in the SHR, and 6-fold at 6 weeks in the DOCA salt model. IGF-I mRNA levels returned to control values by the end of the experimental period despite continued hypertension and hypertrophy in all three systems. In contrast, ventricular c-myc mRNA content increased twofold to threefold at 1 week and returned to control levels by 2 weeks. Ventricular IGF-I receptor mRNA levels were unchanged over the time course studied. The increased ventricular IGF-I mRNA content was reflected in an increased ventricular IGF-I protein content, as determined both by radioimmunoassay and immunofluorescence histochemistry. CONCLUSIONS: We conclude that (1) hypertension induces significant increases in cardiac IGF-I mRNA and protein that occur coordinately with its onset and early in the development of hypertrophy, (2) IGF-I mRNA levels normalize as the hypertrophic response is established, (3) in comparison to IGF-I, both c-myc and IGF-I receptor genes are differentially controlled in experimental hypertension. These findings suggest that IGF-I may participate in initiating ventricular hypertrophy in response to altered loading conditions. The consistency of these findings in models of high-, moderate-, and low-renin hypertension suggests that they occur independently of the systemic renin-angiotensin endocrine axis.

Animals↗
PubMed2006

Longitudinal mitral annulus velocities are reduced in hypertensive subjects with or without left ventricle hypertrophy.

Normotensive and hypertensive subjects with and without left ventricular (LV) hypertrophy (LV mass index [LVMI] >51 g/m(2.7)) were examined by conventional echocardiography and tissue Doppler imaging of mitral annulus motion. The subgroups included nonobese normotensive subjects (n=16; age 51+/-9 years; 11 female; systolic blood pressure [SBP] 109+/-11 mm Hg, body mass index [BMI] 24+/-2.7 kg/m2; LVMI 32+/-5.5 g/m(2.7)), nonobese hypertensive subjects without LV hypertrophy (n=16; age 54+/-12 years; 12 female; SBP 166+/-15 mm Hg; BMI 25+/-2.7 kg/m2; LVMI 42+/-5.5 g/m(2.7)), and hypertensive subjects with LV hypertrophy (n=22; age 56+/-10 years; 10 female; SBP 181+/-19 mm Hg; BMI 26+/-2.3 kg/m2; LVMI 69+/-16 g/m(2.7)). Ejection fraction was comparable among the subgroups, but midwall fractional shortening was reduced in hypertensive subjects with LV hypertrophy (approximately 26%). Isovolumic relaxation time was increased in subjects with LV hypertrophy, whereas mitral wave A velocity was increased in hypertensive subjects with and without LV hypertrophy. Tissue Doppler imaging mitral annulus systolic (SM) and diastolic (EM) velocities were reduced in subjects with and without LV hypertrophy compared with normotensive subjects. There was a positive correlation between SM and EM (r=0.68; P<0.0001) and negative correlations between these 2 variables and LVMI (SM, r=-0.41; P=0.002; EM, r=-0.56; P<0.0001). Thus, reductions in mitral annulus systolic and diastolic velocities parallel increases in LV mass in hypertensive subjects, beginning at LV mass within the clinically defined normal values.

Adult↗
PubMed1988

Evaluation of medial hypertrophy in resistance vessels of spontaneously hypertensive rats.

The role of smooth muscle cell hypertrophy, hyperploidy, and hyperplasia in medial hypertrophy of mesenteric resistance vessels of 107- to 111-day-old spontaneously hypertensive rats (SHR) was examined using a combination of morphometric, biochemical, and immunological techniques. Mesenteric arteries were classified on the basis of branching order for comparative purposes. Branch level I vessels were those that directly enter the jejunal wall, while Branches II to IV represented more proximal vessels; Branch IV vessels were those that branch from the superior mesenteric artery. Medial hypertrophy was assessed in perfusion-fixed vessels by morphometric evaluation of medial cross-sectional area and smooth muscle content. Medial cross-sectional area and smooth muscle content were significantly increased in larger (Branches III and IV) but not smaller (Branches I and II) mesenteric resistance vessels of SHR compared with control normotensive Wistar-Kyoto rats (WKY). Smooth muscle cell hypertrophy and hyperploidy were evaluated in isolated cells obtained by enzymatic dissociation of mesenteric resistance vessels. Approximately 80% of the cells in these preparations were identified as smooth muscle cells using a smooth muscle-specific isoactin antibody. Feulgen-DNA microdensitometric evaluation of isolated cells showed that polyploid cells were present in mesenteric resistance vessels but at very low frequencies, and no differences were apparent between SHR and WKY. Likewise, no differences in cellular protein content or relative smooth muscle cell size (i.e., area profile) were observed between cells obtained from SHR and WKY vessels. These results demonstrate that the increase in medial smooth muscle content observed in larger mesenteric resistance vessels of SHR cannot be accounted for by smooth muscle hypertrophy and hyperploidy, inferring that hyperplasia must be present. Results indicate that studies of the initiating mechanisms for medial smooth muscle hypertrophy in SHR resistance vessels, at least relatively early in hypertension, should focus on examination of factors that induce true cellular proliferation rather than hypertrophy and hyperploidy.

Animals↗
PubMed1996

Time-voltage area of the QRS for the identification of left ventricular hypertrophy.

Standard electrocardiographic criteria have exhibited poor sensitivity for left ventricular hypertrophy at acceptable levels of specificity and perform less well in women than men, even when sex-specific criteria are used. The time-voltage integral of the horizontal plane vector QRS complex can improve identification of hypertrophy in men, but performance of this approach in women and the effect of sex-specific criteria on accuracy have not been examined. To evaluate the accuracy of the time-voltage integral of the QRS complex for the identification of left ventricular hypertrophy in women and to examine the effect of sex-and non-sex-specific criteria on test performance, we obtained standard 12-lead and orthogonal-lead signal-averaged electrocardiograms and echocardiograms in 175 control subjects without hypertrophy (43 women and 132 men) and 75 patients with hypertrophy (26 women and 49 men) defined by echocardiographic criteria (indexed left ventricular mass > 110 g/m2 in women and > 125 g/m2 in men). Voltage of the QRS complex was integrated over the total QRS duration in leads X and Z for calculation of the time-voltage integral of the horizontal plane vector complex. With the use of a partition of 99.2 microV.s with a specificity of 98% in the entire normal group, sensitivity of the horizontal plane vector integral was significantly lower in women than men (31% versus 71%, P < .001). In contrast, use of sex-specific partitions of 75.4 microV.s in women and 99.2 microV.s in men with matched 98% specificity significantly improved sensitivity in women to 81% (P < .001), with no change in sensitivity in men (71%). Comparison of receiver operating characteristic curves with the use of sex-specific criteria demonstrated no significant difference in overall performance of the horizontal plane vector integral between men and women. The 81% and 71% sensitivities of the sex-specific horizontal plane vector integral were significantly greater than the 27% to 58% sensitivities of sex-specific 12-lead electrocardiographic criteria in this population. Thus, sex-specific criteria significantly improve performance of the time-voltage integral of the QRS for the identification of left ventricular hypertrophy in women, with no loss of accuracy in men. Use of the time-voltage integral can improve the accuracy of the electrocardiogram for the identification of left ventricular hypertrophy in both women and men.

Analysis of Variance↗
PubMed1996

Association of carotid atherosclerosis with electrocardiographic myocardial ischemia and left ventricular hypertrophy.

Patients with carotid atherosclerosis have an increased risk of coronary events and an increased prevalence of echocardiographic left ventricular hypertrophy. However, little is known regarding the association between electrocardiographic abnormalities and carotid atherosclerosis. The relationship of electrocardiographic evidence of myocardial ischemia and left ventricular hypertrophy to the presence of carotid atherosclerosis was prospectively studied in 349 asymptomatic subjects who underwent echocardiography and carotid ultrasonography. Myocardial ischemia on the electrocardiogram was defined by the presence of localized T-wave inversions, and electrocardiographic hypertrophy was defined by the product of Cornell voltage and QRS duration. Carotid atherosclerosis was present in 21% (72/ 349) of subjects and was associated with older age, higher systolic and pulse pressures, and greater left ventricular mass. Both ischemia and hypertrophy on the electrocardiogram were strongly associated with carotid plaque. Carotid atherosclerosis was more than three times more prevalent in subjects with electrocardiographic ischemia (69% [11/16] versus 18% [61/333], P < .0001) or electrocardiographic left ventricular hypertrophy (78% [7/9] versus 19% [65/340], P = .0003) than in subjects without these findings. Logistic regression analysis, including standard risk factors, revealed that both ischemia and hypertrophy on the electrocardiogram remained significant independent predictors of the presence of carotid atherosclerosis, along with age and echocardiographic left ventricular mass. These findings suggest that the associations of ischemia and left ventricular hypertrophy with carotid atherosclerosis may contribute to the increased incidence of coronary events in patients with carotid atherosclerosis.

Adult↗
PubMed1998

Opposite effects of remodeling and hypertrophy on arterial compliance in hypertension.

Sustained hypertension is associated with a reduction in large artery compliance. However, we previously showed that, at the site of the radial artery, a distal muscular artery, the compliance of hypertensive patients was not significantly different from those of normotensive controls when the two groups were studied at their respective mean arterial pressures, despite increased wall thickness in hypertensives. To determine whether this paradoxical finding could be related to a specific pattern of geometrical changes, we studied arterial compliance in never-treated hypertensive patients characterized either by radial artery hypertrophy or remodeling, and compared them to normotensive controls. By analogy with Devereux's classification for left ventricular hypertrophy, we defined remodeling as an increased thickness to radius ratio (h/r) and a normal vascular mass (VM), and arterial hypertrophy as an increased VM irrespective of the values of h/r. Internal diameter and wall thickness were measured at the site of the radial artery using a high resolution echo-tracking system. The lumen cross-section-pressure curve was determined from the two simultaneous and continuous recordings of arterial diameter and blood pressure. Then, the cross-sectional compliance (CC)-pressure curve was calculated. Isobaric compliance was calculated at 100 mm Hg. Thresholds for h/r and VM were determined according to gender as the 95th percentile of a group of 100 normotensive subjects. The group of hypertensive patients included 58 patients with hypertrophy (h/r: 0.25+/-0.04; VM: 31+/-6 mg/cm; mean+/-SD) and 25 patients with remodeling (h/r: 0.29+/-0.06; VM: 20+/-4 mg/cm) and was compared to a group of 50 age- and gender-matched normotensives (h/r: 0.16+/-0.02; VM: 17+/-4 mg/cm). Compared to normotensives, isobaric compliance of the radial artery was increased in hypertensive patients with hypertrophy (HH) whereas it was not different in hypertensive patients with remodeling (RH). These results indicate that compliance is dependent on hypertrophy or remodeling pattern and suggest that in the face of hypertension, only arterial hypertrophy is an adaptive process leading to normal operating compliance through an increased isobaric compliance.

Blood Pressure↗