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PubMed2002

The importance of blood pressure variability in rat aortic and left ventricular hypertrophy produced by sinoaortic denervation.

OBJECTIVE: The main objective was to examine the role of hemodynamics in rat aortic and left ventricular hypertrophy produced by sinoaortic denervation (SAD). DESIGN AND METHODS: Rats were examined at different times after SAD or sham operation (Sham). Hemodynamics were recorded continuously in conscious unrestrained rats. The time course of hemodynamic changes and cardiovascular hypertrophy was observed and linear regression analysis was performed to study the role of hemodynamics in SAD-induced aortic and left ventricular hypertrophy. Long-term mortality, water and food intake, and body weight were also determined after operation. RESULTS: High mortality (40%), dramatic reduction of water and food intake, and weight loss occurred within 1 week after SAD. Chronic SAD rats exhibited a marked increase in blood pressure variability (BPV), with no change in the average level of blood pressure (BP), as compared with the Sham control rats. Increased BPV was higher at 2 weeks (about threefold) than 16 weeks (about twofold) after SAD. Aortic hypertrophy existed in all three kinds of examined rats: 2-, 10- and 16-week SAD rats. Left ventricular hypertrophy was found only in 10- and 16-week SAD rats. Both aortic hypertrophy and left ventricular hypertrophy were significantly and positively correlated with BPV, but not with BP level. CONCLUSION: Persistent high BPV following SAD can lead to aortic and left ventricular hypertrophy. The aorta is more sensitive to increased BPV than the heart.

Animals↗
PubMed1997

The link among nitric oxide synthase activity, endothelial function, and aortic and ventricular hypertrophy in hypertension.

The adaptive changes that occur in the left ventricle (LV) and vessels in response to hypertension, namely, muscle hypertrophy/hyperplasia, endothelial dysfunction, and extracellular matrix increase, do not depend solely on blood pressure elevation. These changes are in fact, maladaptive since they are forerunners of cardiac failure, stroke, and renal failure. Nitric oxide, an endogenous vasodilator and inhibitor of vascular smooth muscle cell growth, is synthesized in the endothelium by constitutive nitric oxide synthase (cNOS). We investigated the relationships among LV and aortic cNOS activity (conversion of [14C] L-arginine to [14C] L-citrulline), with LV hypertrophy (LV weight/body weight), and (2) aortic hypertrophy (aortic weight/ length) in spontaneously hypertensive rats (SHR) and Dahl salt-sensitive (DS) rats matched for blood pressure (219 +/- 12 versus 211 +/- 7 mm Hg, P = NS) and age. Compared with their normotensive counterparts, aortic cNOS activity was increased 106% in SHR but reduced by 73% in DS rats. The correlation between blood pressure and aortic cNOS activity was positive (r = .74, P < .01) in SHR and negative (r = -.82, P < .01) in DS rats, LV cNOS activity was increased 73% in SHR compared with normotensive Wistar-Kyoto rats (P < .01). On the other hand, LV cNOS activity was not increased in hypertensive DS rats compared with normotensive DS rats. In SHR, aortic hypertrophy did not increase significantly and LV hypertrophy increased only 15%, whereas in hypertensive DS rats the aorta and LV hypertrophied 36% and 88%, respectively (both P < .01). Moreover, in DS rats there was a negative correlation between cNOS activity and aortic hypertrophy (r = -.70, P < .01). In DS rats, antihypertensive therapy consisting of an angiotensin-converting enzyme inhibitor, perindopril, and a diuretic, indapamide, normalized blood pressure, aortic cNOS activity, and LV hypertrophy and reduced aortic hypertrophy. Our studies imply that upregulation of vascular cNOS activity has a protective cardiovascular homeostatic role in hypertension. Clinically, the variable end-organ disease observed in individuals with similar severity of hypertension may be explained, at least in part, by genetically conditioned differences in vascular cNOS activity in response to hypertension.

Animals↗
PubMed2002

Hypertrophy after free vascularized fibular transfer to the lower limb.

This study included 25 patients with lower limb tumors who had reconstruction by vascularized fibula osteoseptocutaneous flap performed at least 24 months before the end of the study. Hypertrophy of the transplanted fibula was estimated on serial radiographs by a modification of the formula of De Boer and Wood (J Bone Joint Surg [Br] 71:374-378, 1989). A significant graft was observed in 90% of the patients at an average follow-up of 27 months (range, 30-200%). The time to graft union (start of partial weight-bearing) positively correlated with the time to significant graft hypertrophy (r = 0.9, P < 0.01). The final amount of graft hypertrophy was affected by the age of the patient (P < 0.01) and the length of follow-up (P < 0.05). Graft hypertrophy progressed at an average rate of 3.3% per month (range, 2.3-4.9%) until the end of the 30th month; thereafter, little or no increase in graft hypertrophy was observed. The rate of graft hypertrophy showed two significant peaks at 6-12 months (P < 0.001) and at 18-24 months (P < 0.05). Patients younger than age 20 years showed faster hypertrophy, with a peak at the 12th month. Hypertrophy progressed faster in patients who received chemotherapy until the 12th month, and then declined sharply compared to those who did not receive chemotherapy.

Adolescent↗
PubMed1998

Action potential prolongation and potassium currents in left-ventricular myocytes isolated from hypertrophied rabbit hearts.

We have studied the action potential characteristics and potassium currents in single left ventricular myocytes isolated from control and hypertrophied rabbit hearts. Left-ventricular hypertrophy (LVH) was induced following perinephritis-induced hypertension. Control animals underwent a sham operation. Animals were killed at 10 weeks post-operation. Left-ventricular myocytes were isolated by an enzyme dissociation technique. Action potential duration (APD) at 50 and 90% repolarisation was prolonged in myocytes obtained from hypertrophied compared to control hearts over the range of stimulation frequencies (0.1-1.5 Hz). This prolongation in APD was more pronounced in epicardial compared to endocardial myocytes. Steady-state ionic current, measured at the end of voltage clamp steps of 3-s duration, stepping at intervals of 10 mV, from a holding potential of -40 mV, was similar in control and hypertrophied myocytes. However, when normalised for capacitative cell surface area, steady-state current was significantly smaller in hypertrophied myocytes over the voltage range -40 to -60 mV and at potentials greater than +10 mV. Inward rectifier potassium current (IKl), identified as the barium chloride (0.1 mM)-sensitive current, contributed to the steady state current at negative potentials. Normalised IKl was significantly smaller in hypertrophied compared to control myocytes at potentials negative to -60 mV. Peak transient outward potassium current (Ito) density was reduced in hypertrophied compared to control myocytes at 0 and +10 mV, from a holding potential -80 mV (12.9 +/- 2.3 v 24.9 +/- 3.9 microA cm2, at +10 mV, P < 0.05). Steady-state inactivation of Ito was similar in control and hypertrophied myocytes. In conclusion, LVH induced by perinephritis hypertension in the rabbit is associated with a prolongation in APD. Reductions in IKl, sustained outward current and Ito may contribute to the prolongation in APD.

Action Potentials↗
PubMed2001

Reduced ryanodine receptor to dihydropyridine receptor ratio may underlie slowed contraction in a rabbit model of left ventricular cardiac hypertrophy.

Cardiac hypertrophy is associated with contractile dysfunction, a feature of which is a slowing of the time to reach peak contraction. We have examined the main mechanisms involved in the initiation of contraction and investigated if their functions are changed during cardiac hypertrophy. Cardiac hypertrophy was induced by constriction of the ascending aorta in the rabbit. After 6 weeks left ventricular myocytes were isolated or left ventricular and septal mixed membrane preparations were produced for electrophysiological and radioligand binding studies, respectively. Aortic constriction resulted in a 24% and 23% increase in heart weight to body weight ratio and cell capacitance, respectively. Action potential duration and time-to-reach 50% and 90% peak contraction (TTP(50)and TTP(90), respectively) were significantly prolonged in myocytes from hypertrophied hearts. The prolongation of TTP(50)and TTP(90)could not be explained by altered peak calcium current density or SR calcium content which were unchanged in hypertrophy. Radioligand binding studies performed on tissue preparations from the same hearts, revealed a 34% reduction in ryanodine receptor (RYR) density with no change in dihydropyridine receptor (DHPR) density. This resulted in a reduction in the ratio of RYR to DHPR from 4.4:1 to 3.3:1 in hypertrophy. Ryanodine receptor Ca(2+)-sensitivity was unchanged between sham operated and hypertrophied groups. A reduction in the ratio of RYRs to DHPRs may result in a degree of "functional uncoupling" causing defective release of Ca(2+)from the SR. These findings may underlie the slowed TTP of myocyte contraction in hypertrophy.

Animals↗
PubMed2001

Enhanced gene expression of renin-angiotensin system, TGF-beta1, endothelin-1 and nitric oxide synthase in right-ventricular hypertrophy.

It has been suggested that various vasoactive substances and growth factors are involved in left-ventricular myocardial hypertrophy and failure. However, limited data are available on the role of humoral factors involved in right-ventricular (RV) hypertrophy. To examine implications of humoral factors involved in the development of RV hypertrophy, altered mRNA expressions of the renin-angiotensin system (RAS), transforming growth factor (TGF)- beta1, endothelin-1 and nitric oxide synthase (NOS) were investigated in monocrotaline (MCT)-induced pulmonary hypertensive rats. Male Sprague-Dawley rats were treated with MCT (60 mg x kg(-1), s.c.) to induce a selective RV hypertrophy. Three or 6 weeks later, the heart was removed to determine the tissue gene expressions in the right and left ventricles (LV) by reverse transcription-polymerase chain reaction due to the relatively low mRNA expression levels of the RAS components in the ventricle (n= 6 in each group). MCT-treated rats showed a selective RV hypertrophy at weeks 3 and 6 of MCT treatment (the ratios of RV/body weight were 1.5- and 2.2-fold higher than the controls, respectively). Levels of renin and angiotensinogen mRNAs in the hypertrophied RV were significantly increased at both weeks 3 and 6 of MCT treatment. The angiotensin-converting enzyme mRNA level also increased approximately 2-fold at week 3. In contrast, RAS component mRNAs in the LV were not significantly altered by MCT treatment, except for a 1.8-fold increase of angiotensinogen mRNA at week 3. The expression of Ang II receptors, either AT1A or AT1B, was not significantly altered by MCT treatment. Furthermore, MCT treatment significantly increased TGF- beta1 mRNA levels in the RV at weeks 3 and 6, while it did not significantly affect them in the LV. Endothelin-1 mRNA expression was significantly higher in the RV at week 3, but was normalized at week 6 of MCT treatment. The gene expression of the endothelial constitutive isoform of NOS was increased in the RV at weeks 3 and 6, but not in the LV. Elevated gene expression of local RAS, along with TGF- beta1 and endothelin-1 in the present study may contribute to the development of RV hypertrophy. On the contrary, an enhanced ecNOS expression may be a mechanism counteracting the hypertrophy.

Animals↗
PubMed1993

Effect of decentralization or contralateral ganglionectomy on obstruction-induced hypertrophy of rat urinary bladder muscle and pelvic ganglion.

After urethral obstruction the musculature of the rat urinary bladder undergoes extensive hypertrophy, irrespective of whether its innervation is intact or whether one of the two pelvic ganglia has been decentralized or excised. Even the excision of both ganglia does not inhibit muscle hypertrophy. The presence of nerves is not a prerequisite for the muscle growth to occur. The stimulus for growth resides in the bladder itself, and the present and previous observations are in agreement with the notion that the distension of the muscle is a primary stimulus for muscle growth. With bladder hypertrophy, the pelvic ganglion neurons undergo hypertrophy, even when they are devoid of their preganglionic input. Synaptic connection with the preganglionic fibres and stimuli from the spinal cord are not prerequisites for neuronal hypertrophy. However, the hypertrophy is less marked in the decentralized ganglion neurons than in the neurons of the contralateral intact ganglion. With bladder hypertrophy and contralateral ganglionectomy, the neuronal hypertrophy is greater than with either procedure alone, suggesting that the two forms of neuronal growth stimulation can be added to each other.

Animals↗
PubMed1999

Altered phosphorylation of sarcoplasmic reticulum contributes to the diminished contractile response to isoproterenol in hypertrophied rat hearts.

We tested the hypothesis that changes in phosphorylation of the sarcoplasmic reticulum (SR) protein, phospholamban (PIB) and myofibrillar proteins troponin I (TnI) and C protein are responsible for the decreased relaxant response to isoproterenol in cardiac hypertrophy and failure induced by ascending aortic banding in rats. In isolated perfused heart preparations under maximal isoproterenol stimulation, the capacity for in vitro cAMP-dependent phosphorylation of PIB was significantly increased at the compensatory stage of hypertrophy (126-130%, P<0.001), but decreased with failure (70-76%, P<0.001). Phosphorylation of TnI also decreased in the failing hearts, however to a lesser extent (80-83%, P<0.05). No significant hypertrophy-related difference was evident in isoproterenol-induced phosphorylation of C protein. The relative tissue level of PIB was increased (150-168%, P<0.001) in hypertrophied and decreased (71-83.8%, P<0.05) in failing hearts compared with the respective age-matched sham-operated controls (100%). As a percentage above baseline, the maximal isoproterenol-induced increase in the EC50 of the SR Ca2+ pump in response to phosphorylation of PIB was 38.5+/-1.1% for sham-operated rats, and 26.0+/-3.8% and 15.4+/-4.2% for hypertrophied and failing hearts respectively. As a consequence, linear correlation was observed between the maximal increase in EC50 and the maximal rate of relaxation [(-dP/dt)/DevP] upon isoproterenol stimulation, declining with progressive hypertrophy to failure. These data suggest that hypertrophy-induced alterations in PIB phosphorylation and protein level contribute to the diminished relaxant response of the hypertrophied and failing heart to adrenergic agonists.

Animals↗
PubMed1999

Lack of lymphoid cell apoptosis in the pathogenesis of tonsillar hypertrophy as compared to recurrent tonsillitis.

UNLABELLED: The pathogenic mechanism of tonsillar hypertrophy is unknown and lacks a proper infectious or immunological explanation. Epidemiological studies point to polluted environments as the main cause of tonsillar hypertrophy in the adaptation of the juvenile organism. Tonsils and adenoids of 67 children aged 2-16 years (mean 5.9 years) were divided into three groups: recurrent tonsillitis (n = 21), recurrent tonsillitis with tonsillar hypertrophy (n = 21) and tonsillar hypertrophy without history of tonsillitis (n = 25). The following biological markers were studied: anti-streptolysin O antibody and anti-deoxy ribonuclease B antibody serology, microbiology and cell count of granulocytes in tonsils and adenoids as well as lymphocyte subsets and "ex vivo" endonuclease activity in tonsils. Anti-streptolysin O antibody and anti-deoxyribonuclease B antibody titres were significantly raised in recurrent tonsillitis. Positive bacterial cultures for Streptococcus pyogenes were rare in cases of tonsillar hypertrophy. T-lymphocytes counts were lower and the proportion of basophils was higher in hypertrophic tonsils than in recurrent tonsillitis. Two parameters of apoptosis were studied; the activation of endonuclease, inducing breakdown of DNA resulting in cell death, and the sensitivity to thapsigargin, known to trigger the cleavage of DNA by apoptotic endonuclease. In children with tonsillar hypertrophy both parameters were decreased contrasting with those with recurrent tonsillitis where apoptosis is increased. It may be speculated that the increase of basophils in children with tonsillar hypertrophy results in increased release of interleukin-4, which could prevent lymphoid apoptosis and lead to cell proliferation in tonsillar tissue. CONCLUSION: Whereas recurrent tonsillitis is characterised by apoptotic death of lymphoid tissue, tonsillar hypertrophy is caused by environmental pollution agents that trigger the chronic inflammatory process without apoptotic cell death.

Apoptosis↗
PubMed2000

Genetic contributions to left ventricular hypertrophy.

Left ventricular (LV) hypertrophy is a common condition that profoundly affects morbidity and mortality from cardiovascular diseases, including myocardial infarction, congestive heart failure, and stroke. Noninvasive imaging methods have greatly expanded our ability to evaluate cardiac structural and functional characteristics, and enhanced our understanding of the natural history of LV hypertrophy. The etiology of LV hypertrophy is likely due to the effects of multiple genes interacting with other genes and the environment. Although hypertension is recognized as a strong determinant of LV hypertrophy, blood pressure explains only a limited amount of the interindividual variation in LV mass. Moreover, LV hypertrophy occurs in the absence of hypertension, and in some cases precedes its development. Genes encoding proteins involved in the structure of the LV, as well as genes encoding cell signal transduction, hormones, growth factors, calcium homeostasis, and blood pressure, are likely candidates for the development of common forms of LV hypertrophy. An overview of the epidemiology and pathophysiology of LV hypertrophy and dysfunction is provided, in addition to evidence of the genetic basis for LV hypertrophy.

Black People↗
PubMed2004

Genes for left ventricular hypertrophy.

Left ventricular (LV) hypertrophy is very common, particularly among hypertensives. The presence of LV hypertrophy profoundly affects morbidity and mortality from cardiovascular diseases and stroke, and is now recognized as the most important predictor of chronic heart failure. Hypertension, obesity, and diabetes are important determinants of LV hypertrophy, but they fail to identify many individuals with the condition, suggesting that other factors, likely genetic in origin, play a role. Although much research has been undertaken to understand the causes of hypertrophy and the medical treatments that can lead to its regression, much remains unknown about its genetic basis. LV hypertrophy is considered a complex genetic disease, likely representing an interaction of several genes with the environment. The heritability of LV mass, measured as a quantitative trait, falls between 0.3 and 0.7 in different populations, suggesting it has a familial component. Genes encoding proteins involved in LV structure, as well as genes encoding cell signal transduction, hormones, growth factors, calcium homeostasis, substrate metabolism, and blood pressure are likely candidates for the development of common forms of LV hypertrophy. An overview of the pathophysiology of LV hypertrophy and dysfunction is provided, in addition to evidence of the genetic basis for LV hypertrophy in humans and animal models.

Genetic Predisposition to Disease↗
PubMed1991

Reversal of cardiac and vascular hypertrophy by antihypertensive therapy.

Cardiovascular hypertrophy, such as left ventricular hypertrophy, and arteriolar hypertrophic changes are common in established hypertension. Left ventricular hypertrophy, in particular, markedly increases the risk of cardiovascular complications and death. The ability of an antihypertensive agent to reverse hypertrophic changes could, therefore, be greatly advantageous. Clinical studies with beta-blockers have shown them able to substantially reduce left ventricular hypertrophy. For reversal of arteriolar hypertrophy, vasodilatory beta-blockers have been shown to be preferable to ordinary beta-blockers, possibly because vasodilation reduces vascular smooth-muscle tone, which may facilitate reversal of hypertrophy. Theoretically, a vasodilatory beta-blocker, such as celiprolol, would therefore appear to offer advantages because of its ability to reverse left ventricular and arteriolar hypertrophy in addition to its antihypertensive action. The practical and clinical effects of cardiovascular hypertrophy reversal remain to be fully evaluated; however, it is logical to assume that they would be of considerable benefit to the hypertensive patient.

Arteries↗
PubMed1994

Echocardiographic evidence of left ventricular hypertrophy in a general aged population.

The purpose of this study was to measure the frequency of left ventricular (LV) hypertrophy in old age. Random subjects born in 1904, 1909, and 1914 (n = 501), and 76 born in 1920 to 1935 were studied. All subjects underwent clinical and echocardiographic investigation. An electrocardiogram was obtained in 449 subjects. Complete data for calculation of LV mass corrected for body size were available in 422 of the studied subjects (73%). LV hypertrophy was defined as calculated LV mass exceeding either an internal standard of the Helsinki Aging Study, earlier published limits from the Framingham Heart Study, or criteria from Devereux et al. LV wall thickness and mass were positively related to age. Hypertrophy was present in both sexes, the rate even exceeding 70% in the oldest cohort aged 85 to 86 years using the Framingham and Devereux limits. LV hypertrophy (LV mass exceeding defined limits after correction for body height) was significantly and independently related to age, systolic blood pressure, body mass index, and mitral regurgitation. A sustained apex beat, third heart sound, and electrocardiographic changes were significantly more frequent in the group with echocardiographic hypertrophy, although with considerable overlapping. The fourth heart sound was unrelated to hypertrophy. Use of age-independent criteria result in an extremely high prevalence of LV hypertrophy in old age. This is partly due to age-related diseases increasing LV mass, but also partly to an independent effect of age. The usefulness of clinical signs for detecting LV hypertrophy is limited in old age.

Aged↗
PubMed1994

Comparison of diastolic left ventricular filling and cardiac dysrhythmias in hypertensive patients with and without isolated septal hypertrophy.

Although many patients with hypertension develop isolated septal hypertrophy (ISH) rather than concentric or eccentric left ventricular (LV) hypertrophy, limited data are available on cardiac structure, function, and arrhythmias in hypertensive patients with ISH. Clinical features, hemodynamics, M-mode echocardiograms, and 24-hour electrocardiographic recordings were evaluated in 21 healthy normotensive subjects, 23 hypertensive patients without LV hypertrophy, 31 hypertensive patients with concentric LV hypertrophy, and 23 hypertensive patients with ISH to determine the prevalence and complexity of cardiac arrhythmias and diastolic LV filling abnormalities. Age, sex, race, obesity indexes, preload, ejection fraction, and LV contractility were similar in all 4 groups, and arterial pressure and afterload were statistically similar in the 3 hypertensive groups. Left atrial emptying index (p < 0.01) and peak LV filling rate (p < 0.01), 2 indexes of diastolic LV filling, were significantly reduced in the 3 hypertensive groups compared with the normotensive group. The duration of rapid LV filling, however, was significantly prolonged only in hypertensive patients with concentric LV hypertrophy and ISH (p < 0.05) but not in hypertensive patients without LV hypertrophy. The prevalence (p < 0.001) and complexity (p < 0.001) of ventricular ectopic activity was also significantly increased to a similar degree in hypertensive patients with concentric LV hypertrophy and in those with ISH compared with normotensive subjects or hypertensive patients without LV hypertrophy. The prevalence and complexity of atrial ectopic activity was only increased significantly (p < 0.001) in those with ISH.

Adult↗
PubMed1996

Coronary artery dimensions in primary and secondary left ventricular hypertrophy.

BACKGROUND: Coronary artery enlargement has been previously described in left ventricular hypertrophy. OBJECTIVES: We sought to assess coronary artery dimensions and their relation to left ventricular muscle mass in primary and secondary hypertrophy. METHODS: Cross-sectional area of the left and right coronary arteries was determined by quantitative coronary angiography in 52 patients: 12 control subjects and 40 patients (13 with hypertrophic cardiomyopathy, 12 with dilated cardiomyopathy and 15 with aortic valve disease). As a measure of left ventricular hypertrophy, angiographic left ventricular mass and equatorial cross-sectional muscle area were determined. RESULTS: Cross-sectional area of both the left and right coronary arteries is increased in left ventricular hypertrophy (p < 0.05 vs. values in control subjects). There is a curvilinear relation between left coronary artery size and left ventricular muscle mass (r = 0.76) or cross-sectional muscle area (r = 0.75). However, normalization of coronary cross-sectional area for left ventricular muscle mass or muscle area shows insufficient enlargement of the coronary arteries in both primary and secondary hypertrophy. CONCLUSIONS: 1) Coronary artery size increases as left ventricular mass increases in both primary and secondary hypertrophy. 2) The enlargement of left coronary cross-sectional area is independent of the cause of the increase in left ventricular mass. 3) The size of the coronary arteries is inappropriate with regard to left ventricular hypertrophy. Thus, the stimulus for growth of the coronary arteries is not influenced by the underlying disease but appears to depend on the degree of left ventricular hypertrophy.

Adult↗
PubMed2005

Significance and relation between magnitude of left ventricular hypertrophy and heart failure symptoms in hypertrophic cardiomyopathy.

In hypertrophic cardiomyopathy (HC), an important subgroup of patients develop progressive and disabling symptoms that are related to heart failure and death. Although a direct relation has been demonstrated between left ventricular (LV) wall thickness and likelihood of sudden and unexpected death (usually in patients who are asymptomatic or mildly symptomatic), it is unresolved whether magnitude of hypertrophy is similarly associated with severity of heart failure. To determine the relation of LV wall thickness to heart failure symptoms in HC, 700 consecutive patients who had HC were assessed by 2-dimensional echocardiography. The relation between maximum level of heart failure symptoms by New York Heart Association functional class and maximum LV wall thickness was not linear but rather parabolic. Therefore, marked symptoms were most commonly associated with moderate degrees of LV hypertrophy (wall thickness 16 to 24 mm; 27%) but less frequently with extreme hypertrophy (>/=30 mm 13%) or mild hypertrophy (</=15 mm; 19%, p = 0.0001). Mean New York Heart Association functional class showed a similar pattern with respect to moderate hypertrophy (1.9 +/- 0.8), mild hypertrophy (1.6 +/- 0.9), and extreme hypertrophy (1.6 +/- 0.7, p = 0.005). Multivariable regression analysis showed the parabolic relation between heart failure symptoms and magnitude of LV hypertrophy to be independent of other hypertrophic cardiomyopathy related clinical variables. In conclusion, no direct relation was evident between symptoms of heart failure and magnitude of LV wall thickness, with implications for the natural history of HC.

Adolescent↗
PubMed2006

Beta2-adrenergic receptor polymorphisms and treatment-induced regression of left ventricular hypertrophy in hypertension.

OBJECTIVES: Although blood pressure is considered the major determinant of left ventricular hypertrophy in hypertension, genetic variability is increasingly being considered among the factors influencing this complication. beta(2)-Adrenergic receptors (beta(2)ARs) are up-regulated in hypertension and largely polymorphic within the human population. Recently, we have shown that the Glu27 beta(2)AR variant is strongly associated with cardiac hypertrophy in hypertension. The objective of this study is to verify whether this polymorphism also affects hypertrophy regression in response to antihypertensive therapy. METHODS: In a prospective follow-up study we screened 970 hypertensive patients of Caucasian descent for the Gly16Arg, Gln27Glu, and Thr164Ile beta(2)AR polymorphisms and left ventricular echocardiographic hypertrophy and assigned selected patients to enalapril or atenolol to assess left ventricular hypertrophy regression after 2-year follow-up. Results were stratified according to treatment and the Glu27Gln polymorphism of the beta(2)AR. In cells with stable overexpression of the Glu27 or Gln27 variant of beta(2)AR, we also explored the implications of this polymorphism on hypertrophy-related intracellular signal transduction. RESULTS: Among hypertensive patients, the Gly16 allele was found in 63% of patients and the Glu27 allele was found in 40.6%. Both polymorphisms were in linkage disequilibrium, as expected. Four hundred forty-one hypertrophic hypertensive patients completed the 2-year follow-up. At baseline, patients carrying at least 1 allele of the Glu27 variant presented with a larger cardiac size despite similar blood pressure levels (142.9 +/- 22.5 g/m(2) in Glu27 carriers versus 138.2 +/- 18.4 g/m(2) in Gln27 carriers, P < .02). Blood pressure normalization was achieved by both drugs. At follow-up, compared with the Gln27 patients, the Glu27 patients showed a larger reduction in hypertrophy when treated with enalapril (percent change in left ventricular mass, -6.3% +/- 7.7% in Glu27 carriers versus -2.18% +/- 7.9% in Gln27 carriers; P < .05) but not with atenolol therapy (-2.8% +/- 8.9% in Glu27 carriers versus -2.4% +/- 8.8% in Gln27 carriers, P = not significant). In in vitro studies the activation of p38 and extracellular signal-regulated kinase (ERK-) 1/2 (data not shown) and the activity of the atrial natriuretic factor (ANF) promoter after isoproterenol (INN, isoprenaline) stimulation were larger in Glu27 beta(2)AR overexpressing cells than in Gln27 beta(2)AR overexpressing cells (fold difference compared with unstimulated cells, 9.7 +/- 2.9 for Glu27 beta(2)AR versus 4.2 +/- 0.3 for Gln27 beta(2)AR; P < .05). CONCLUSIONS: The Glu27 variant of beta(2)AR enhances hypertension-induced left ventricular hypertrophy. In these patients angiotensin-converting enzyme inhibitors are more efficient than beta-blockers in reducing cardiac size.

Antihypertensive Agents↗
PubMed2003

Cardiac hypertrophy in aryl hydrocarbon receptor null mice is correlated with elevated angiotensin II, endothelin-1, and mean arterial blood pressure.

The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor that mediates toxicity of xenobiotics, such as 2,3,7,8-tetrachlorodibenzo-p-dioxin. Genetic deletion of the AhR leads to cardiac hypertrophy, suggesting a role for the AhR in cardiovascular physiology and disease; however, the pathways involved in the development of cardiac hypertrophy have not been determined. Thus, we investigated the role of (1) pressure overload using indwelling catheters and (2) vasoactive peptides endothelin-1 (ET-1) and angiotensin II (Ang II), assessed by RIA, in the progression of cardiac hypertrophy in AhR-null mice. Histochemical analysis, expression of cardiac hypertrophy marker genes, and echocardiography were used to assess the degree of cardiac hypertrophy. AhR-null mice developed elevated mean arterial pressures (MAP) by 5 months, which was associated with a two- and ninefold increase in plasma ET-1 and Ang II, respectively, compared to wild-type. Captopril-treatment (4 mg/kg) of AhR-null mice from 2 to 5 months of age significantly decreased MAP and plasma Ang II, but did not affect ET-1. Further, captopril improved cardiac function and reduced cardiac hypertrophy as evidenced by reduction in left ventricle mass, left ventricle internal dimension, and molecular cardiac hypertrophy markers. Captopril also decreased fibrosis of the heart and kidney. These findings show that pressure overload is associated with elevated ET-1 and hypertrophic growth of the heart and that cardiac hypertrophy is mediated, in part, by Ang II.

Angiotensin II↗