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PubMed1989

Left ventricular hypertrophy in persons age 90 years and older.

Clinical, electrocardiographic and echocardiographic findings of 32 patients age 90 years or older were analyzed to assess the prevalence, characteristics and correlates of left ventricular (LV) hypertrophy. All patients (mean age 92 years, range 90 to 98; 21 women and 11 men) were referred to the echocardiography laboratory with a definite or suspected cardiovascular diagnosis. LV hypertrophy, echocardiographically diagnosed by high LV mass index, was present in 28 patients. The LV mass index ranged from 105 to 215 g/m2 in men and 140 to 262 g/m2 in women. Electrocardiographic evaluation showed LV hypertrophy in only 5 patients. Five patients had low voltage on the electrocardiogram. There was no correlation between the LV mass index and presence of electrocardiographic LV hypertrophy or presence of low voltage on the electrocardiogram. LV hypertrophy was concentric in 19 and eccentric in 9. There was no correlation between types of LV hypertrophy and underlying cardiovascular disease or presence of electrocardiographic LV hypertrophy. It is concluded that LV hypertrophy is frequently present and has a wide range and heterogeneous character in very elderly patients with cardiovascular disease. In the tenth decade of life, echocardiography is a sensitive method for detecting, characterizing and classifying LV hypertrophy, whereas electrocardiography lacks sensitivity in detecting it.

Aged↗
PubMed1991

Congestive heart failure, coronary events and atherothrombotic brain infarction in elderly blacks and whites with systemic hypertension and with and without echocardiographic and electrocardiographic evidence of left ventricular hypertrophy.

Hypertension was present in 50% of 196 blacks and in 36% of 382 whites (p less than 0.001). A prospective study of 84 elderly blacks (70% women) and 326 elderly whites (73% women) with hypertension correlated echocardiographic and electrocardiographic left ventricular (LV) hypertrophy with incidences of congestive heart failure (CHF), coronary events and atherothrombotic brain infarction (ABI). Echocardiographic LV hypertrophy (p less than 0.02) and concentric LV hypertrophy (p less than 0.001) were more prevalent in hypertensive blacks than in hypertensive whites. Hypertensive blacks were younger (78 +/- 9 years) than hypertensive whites (82 +/- 7 years) (p less than 0.001). Other coronary risk factors were similar, except for higher serum triglycerides in whites than in blacks (p less than 0.02). Follow-up was 37 +/- 18 months in blacks and 43 +/- 18 months in whites (p less than 0.01). Incidences of CHF and coronary events were not significantly different in blacks and whites. ABI incidence was 38% in blacks and 21% in whites (p less than 0.005). Multiple logistic regression analysis showed that prior CHF (p = 0.000), concentric LV hypertrophy (p = 0.018) and echocardiographic LV hypertrophy (p = 0.022) were independent risk factors for CHF. Echocardiographic LV hypertrophy (p = 0.001), serum total cholesterol (p = 0.002), concentric LV hypertrophy (p = 0.005) and prior coronary artery disease (p = 0.042) were independent risk factors for coronary events. Prior ABI (p = 0.001), echocardiographic LV hypertrophy (p = 0.001) and electrocardiographic LV hypertrophy (p = 0.034) were independent risk factors for ABI.

Aged↗
PubMed1980

Cardiac hypertrophy: useful adaptation or pathologic process?

An extensive body of evidence supports the concept that cardiac hypertrophy and normal cardiac growth develop in response to increased hemodynamic loading and abnormal systolic and diastolic stresses at the myocardial fiber level. The pattern of hypertrophy reflects the nature of the inciting stress. Experimental studies indicate that if the stress is moderate, gradually applied, and the animal young and healthy, physiologic hypertrophy of muscle with normal contractility develops. In this circumstance, cardiac hypertrophy may be regarded as a useful adaptation to increased hemodynamic loading. When the inciting stress is severe, abruptly applied, or the animal old or debilitated, pathologic hypertrophy develops: in this circumstance, the cardiac muscle produced is abnormal and exhibits depressed contractility. Of particular clinical relevance is the intermediate situation which seems to develop in many patients with chronic left ventricular pressure-overload and perhaps also in left ventricular volume-overload. In this situation, chronic left ventricular pressure or volume overload is initially matched by adequate hypertrophy in the appropriate pattern. Eventually, in some patients, hypertrophy fails to keep pace with the hemodynamic overload so that a systolic stress imbalance occurs at the myocardial fiber level and left ventricular pump failure ensues. If this situation persists uncorrected, it is possible that the increasingly high wall stresses will convert physiologic to pathologic hypertrophy. The task of the clinician is to identify this intermediate stage and to correct the abnormal hemodynamic loading before the transition to pathologic hypertrophy becomes complete.

Adaptation, Physiological↗
PubMed1984

Hypertension and sudden death. Increased ventricular ectopic activity in left ventricular hypertrophy.

The present study was designed to detect and quantify cardiac arrhythmias in hypertensive patients with left ventricular hypertrophy. Continuous ambulatory electrocardiographic tracings and arterial pressure were recorded for 24 hours in 14 normotensive subjects, 10 patients with established essential hypertension without left ventricular hypertrophy, and 16 hypertensive patients with left ventricular hypertrophy by electrocardiographic criteria. Urinary excretion of norepinephrine was simultaneously measured over four successive four-hour and one eight-hour period. Patients with left ventricular hypertrophy had significantly more ventricular (but not atrial) premature contractions than those without left ventricular hypertrophy or than normotensive subjects. Five patients with left ventricular hypertrophy had episodes of more than 30 premature ventricular contractions per minute. Higher-grade ventricular ectopic activity such as coupled premature ventricular contractions was seen in two, and multifocal premature ventricular contractions were seen in three in the group with left ventricular hypertrophy. No difference in urinary catecholamine excretion rates among the three groups was seen. Left ventricular hypertrophy has been shown to be an independent risk factor for sudden death and acute myocardial infarction. Electrocardiographic monitoring of patients with left ventricular hypertrophy allows identification of those who have the highest risk and, therefore, require the most aggressive therapeutic intervention.

Adult↗
PubMedDate not supplied

Heterogeneous signal intensity in magnetic resonance images of hypertrophied left ventricular myocardium.

Left ventricular hypertrophy is associated with decreased longevity and often leads to congestive heart failure. An exploratory study of magnetic resonance imaging in human left ventricular hypertrophy was performed. First, 13 patients with left ventricular hypertrophy and 7 controls of similar ages were studied using electrocardiogramgated end-diastolic images. Visual inspection suggested that low-intensity zones were frequently found within the hypertrophied myocardium. To verify this observation, the images were processed with semi-automatic edge detection and a derivative-based tissue characterization algorithm, yielding tissue heterogeneity indices (THI-A and THI-V) which objectively measured the low-intensity zones. THI-A and THI-V were both significantly greater in left ventricular hypertrophy patients than in controls (THI-A: 0.111 vs 0.038, p = 0.009). THI was also significantly correlated with duration of disease and electrocardiographic abnormalities. To validate these initial findings prospectively, the same quantitative analysis was applied to magnetic resonance images of an additional 20 left ventricular hypertrophy patients and 12 controls from two institutions, using different imaging systems and different acquisition parameters. Again, THI was significantly greater in patients than in controls. Analysis of end-systolic images yielded similar results. In four dogs with left ventricular hypertrophy induced by aortic banding, THI showed a statistically significant increase as left ventricular hypertrophy developed. Hypertrophied myocardium thus shows reproducible differences from normal tissue with magnetic resonance imaging; hence, quantitative magnetic resonance tissue characterization may be useful in assessing pathologic changes in LVH.

Adult↗
PubMed2001

Accentuation of ANP secretion to endothelin-1 in hypertrophied atria.

To investigate modulation of ANP secretion by atrial hypertrophy, the secretion of ANP in response to stretch and endothelin-1 was studied using isolated perfused quiescent atria from rats treated with monocrotaline (MCT). Male Sprague-Dawley rats were given a single subcutaneous injection of 50 mg/kg MCT or saline and were sacrificed at 6 weeks. Rats with right heart hypertrophy showed an increase in ANP mRNA and decrease in tissue concentration of ANP in hypertrophied atria and a marked increase in plasma concentration of ANP. In isolated perfused hypertrophied right atria from MCT rats, changes in atrial volume induced by increased atrial pressure caused proportional increases in mechanically stimulated extracellular fluid (ECF) translocation and stretch-activated ANP secretion. Changes in atrial volume and mechanically stimulated ECF translocation in hypertrophied right atria were not different from those in control right atria. The stretch-activated ANP secretion was suppressed without significant difference in basal ANP secretion, as compared to control right atria. Therefore, the stretch-activated ANP secretion from hypertrophied right atria into the atrial lumen in relation to the ECF translocation (ANP concentration in the interstitium) was lower than that from control atria. A positive correlation between the stretch-activated ANP secretion in relation to the ECF translocation and tissue ANP content was found in control atria but not in hypertrophied atria. Endothelin-1 caused increases in stretch-activated ANP secretion in a dose-dependent manner, which were accentuated in hypertrophied right atria. Therefore, we suggest that atrial hypertrophy causes an attenuated response to stretch and accentuated response to endothelin-1 of ANP secretion.

Animals↗
PubMed1984

Development and regression of left ventricular hypertrophy.

Left ventricular hypertrophy is an important adaptive response to chronic pressure or volume overload of the left ventricle. The different types and the pathophysiologic mechanisms of the development of left ventricular hypertrophy in various disease states are reviewed. Detection of left ventricular hypertrophy may be accomplished by electrocardiography and cardiac angiography. Echocardiography, however, is the most accurate noninvasive method to detect the presence and estimate the severity of increased left ventricular mass. The clinical significance of left ventricular hypertrophy and its prognostic implications in several cardiac diseases associated with hypertrophy are discussed. The critical transition stage from adaptive, compensatory and reversible left ventricular hypertrophy to "pathologic" hypertrophy with impaired left ventricular contractility and irreversible myocardial damage is yet unknown. Recent data are presented that provide evidence of regression of left ventricular hypertrophy after medical treatment of patients with hypertension and after aortic valve replacement in patients with aortic valve disease. The clinical importance of regression of hypertrophy and its effects on long-term prognosis remain to be determined.

Animals↗
PubMed1986

Accuracy of computerized electrocardiographic identification of left ventricular hypertrophy as determined by echocardiographic measurements of left ventricular mass: evaluation of a widely used computer program.

The Hewlett-Packard 1000 electrocardiographic management system employs a user-interactive computer with revisable software. The diagnostic accuracy of this system in predicting left ventricular hypertrophy has been evaluated by comparing computer-predicted with anatomic left ventricular hypertrophy. The latter was defined as a left ventricular mass greater than 247 g as determined by M-mode echocardiography within 1 week of the computerized electrocardiogram. In this study, the Hewlett-Packard system was evaluated in 134 consecutive patients having anatomic left ventricular hypertrophy and 157 similarly studied patients with a normal left ventricular mass. By means of various combinations of voltage criteria, ST-T wave changes, abnormal QRS duration or ventricular activation time, left atrial enlargement and left axis deviation, the computer correctly identified 43 of 134 patients with left ventricular hypertrophy (sensitivity 32%); left ventricular hypertrophy was suggested or identified in an additional 18 patients with a normal left ventricular mass (specificity 89%). Graded probability statements (that is, the "strength" of the left ventricular hypertrophy diagnosis) increased with ventricular mass not only in patients with anatomic left ventricular hypertrophy but also in the patients with a "false positive" computerized electrocardiogram. Overall diagnostic accuracy was improved only in men by adjusting the definition of left ventricular hypertrophy for sex (at least 300 g for men and 220 g for women). Diagnostic accuracy was significantly better in patients 65 years of age and younger than in older patients (p = 0.007). It is concluded that the overall performance of this computer program (version ECLSB6) requires modification to improve its accuracy in identifying left ventricular hypertrophy.

Age Factors↗
PubMed2006

Prevention and reversal of cardiac hypertrophy by soluble epoxide hydrolase inhibitors.

Sustained cardiac hypertrophy represents one of the most common causes leading to cardiac failure. There is emerging evidence to implicate the involvement of NF-kappaB in the development of cardiac hypertrophy. However, several critical questions remain unanswered. We tested the use of soluble epoxide hydrolase (sEH) inhibitors as a means to enhance the biological activities of epoxyeicosatrienoic acids (EETs) to treat cardiac hypertrophy. sEH catalyzes the conversion of EETs to form the corresponding dihydroxyeicosatrienoic acids. Previous data have suggested that EETs may inhibit the activation of NF-kappaB-mediated gene transcription. We directly demonstrate the beneficial effects of several potent sEH inhibitors (sEHIs) in cardiac hypertrophy. Specifically, we show that sEHIs can prevent the development of cardiac hypertrophy using a murine model of pressure-induced cardiac hypertrophy. In addition, sEHIs reverse the preestablished cardiac hypertrophy caused by chronic pressure overload. We further demonstrate that these compounds potently block the NF-kappaB activation in cardiac myocytes. Moreover, by using in vivo electrophysiologic recordings, our study shows a beneficial effect of the compounds in the prevention of cardiac arrhythmias that occur in association with cardiac hypertrophy. We conclude that the use of sEHIs to increase the level of the endogenous lipid epoxides such as EETs may represent a viable and completely unexplored avenue to reduce cardiac hypertrophy by blocking NF-kappaB activation.

Animals↗
PubMed2000

Expression profiling reveals distinct sets of genes altered during induction and regression of cardiac hypertrophy.

Although cardiac hypertrophy has been the subject of intensive investigation, regression of hypertrophy has been significantly less studied, precluding large-scale analysis of the relationship between these processes. In the present study, using pharmacological models of cardiac hypertrophy in mice, expression profiling was performed with fragments of more than 4,000 genes to characterize and contrast expression changes during induction and regression of hypertrophy. Administration of angiotensin II and isoproterenol by osmotic minipump produced increases in heart weight (15 and 45%, respectively) that returned to preinduction size after drug withdrawal. From multiple expression analyses of left ventricular RNA isolated at daily time-points during cardiac hypertrophy and regression, we identified sets of genes whose expression was altered at specific stages of this process. While confirming the participation of 25 genes or pathways previously shown to be altered by hypertrophy, a larger set of 30 genes was identified whose expression had not previously been associated with cardiac hypertrophy or regression. Of the 55 genes that showed reproducible changes during the time course of induction and regression, 32 genes were altered only during induction, and 8 were altered only during regression. This study identified both known and novel genes whose expression is affected at different stages of cardiac hypertrophy and regression and demonstrates that cardiac remodeling during regression utilizes a set of genes that are distinct from those used during induction of hypertrophy.

Angiotensin II↗
PubMed2006

Cardiac hypertrophy: a risk factor for QT-prolongation and cardiac sudden death.

Cardiac hypertrophy was viewed as a compensatory response to hemodynamic stress. However, cumulative evidence obtained from studies using more advanced technologies in human patients and animal models suggests that cardiac hypertrophy is a maladaptive process of the heart in response to intrinsic and extrinsic stimuli. Although hypertrophy can normalize wall tension, it is a risk factor for QT-prolongation and cardiac sudden death. Studies using molecular biology techniques such as transgenic and knockout mice have revealed many important molecules that are involved in the development of heart hypertrophy and have demonstrated signaling pathways leading to the pathogenesis. With the same approach, the consequence of heart hypertrophy has been examined. The significance of hypertrophy in the development of overt heart failure has been demonstrated and several critical molecular pathways involved in the process were revealed. A comprehensive understanding of the threats of heart hypertrophy to patients has helped to develop novel treatment strategies. The recognition of hypertrophy as a major risk factor for QT-prolongation and cardiac sudden death is an important advance in cardiac medicine. Cellular and molecular mechanisms of this risk aspect are currently under extensively exploring. These studies would lead to more comprehensive approaches to prevention of potential life threatening arrhythmia and cardiac sudden death. The adaptation of new approaches such as functional genomics and proteomics will further advance our knowledge of heart hypertrophy.

Adaptation, Physiological↗
PubMed1988

The effects of pressure-induced cardiac hypertrophy on the functional capacity of the coronary circulation.

Pressure-induced cardiac hypertrophy has many effects on the functional capacity of the coronary circulation. Many studies have been performed in both animal and humans and the major findings are as follows: 1. Most types of myocardial hypertrophy are associated with the decrement in coronary vasodilator reserve; 2. The magnitude of the decrement in coronary reserve in myocardial hypertrophy is usually much more prominent in patients with myocardial hypertrophy than in animal models; 3. Left ventricular hypertrophy secondary to systemic hypertension is associated with altered autoregulation of myocardial perfusion; 4. The perfusion abnormalities associated with hypertension and left ventricular hypertrophy are affected by various factors such as age of onset, ventricular involvement, and the stimulus for hypertrophy; 5. Left ventricular hypertrophy secondary to renal hypertension markedly augments the adverse effects of coronary occlusion. In this setting, coronary occlusion is associated with a three-fold increase in the incidence of lethal ventricular arrhythmias and a 35% increase in infarct size. Thus, pressure-induced hypertrophy profoundly alters the coronary circulation.

Angina Pectoris↗
PubMed1982

Effect of volume-overload hypertrophy on the coronary circulation awake dogs.

Inadequate coronary reserve is present in left ventricular hypertrophy secondary to hypertension. Since this abnormality might be due in part to vascular hypertrophy of coronary resistance vessels in response to chronic hypertension, we studied a model of ventricular hypertrophy without hypertension. Volume-overload hypertrophy was produced by creating complete heart block in mongrel dogs; 6 to 7 weeks later the dogs were studied in the awake state. The thirteen dogs with chronic heart block had a 49% increase (P less than 0.05) in left ventricular mass compared with eight control dogs. The major findings in this study were: 1) at rest, coronary blood flow (microsphere technique) per unit weight of left ventricle was not increased in dogs with hypertrophy; and 2) the minimal coronary vascular resistance per unit weight of left ventricle calculated during iv adenosine infusion at a rate that produced maximal vasodilatation was not significantly higher in dogs with left ventricular hypertrophy than in controls (16.4 +/- 1.0 vs 14.7 +/- 1.5 kPa . litre-1 . min . 100 g, respectively). Minimal coronary vascular resistance of the entire left ventricle was significantly less in dogs with hypertrophy than controls (13.0 +/- 0.8 vs 17.3 +/- 1.7 kPa . litre-1 . min, respectively). This data suggests that vascular hypertrophy of coronary resistance vessels related to chronic hypertension may be the cause of the increased minimal coronary vascular resistance seen in dogs with pressure-overload left ventricular hypertrophy.

Adenosine↗
PubMed1991

Effect of left ventricular hypertrophy secondary to systemic hypertension on left coronary artery flow dynamics.

STUDY OBJECTIVE: The aim was to clarify the characteristics of the phasic blood velocity pattern and their possible causes in left ventricular hypertrophy secondary to systemic hypertension. DESIGN: Measurements of blood velocities in the left anterior descending coronary artery were made with a 20 MHz Doppler catheter with a top mounted annular crystal. All patients had normal coronary arteriograms. PATIENTS: 23 hypertensive patients [systolic/diastolic pressure: 181(SD 15)/100(4) mm Hg)] with left ventricular hypertrophy, and 13 atypical chest pain patients without left ventricular hypertrophy or any abnormal haemodynamic findings (normal controls) entered the study. MEASUREMENTS AND MAIN RESULTS: The left anterior descending coronary artery blood velocity waveform in pressure overloaded left ventricular hypertrophy was characterised by delayed early diastolic inflow. The diastolic rise time of coronary flow (TDR), ie, the time from the beginning of diastole to peak velocity, was higher in patients with hypertensive left ventricular hypertrophy than in normal controls, at 145(56) v 66(15) ms, p less than 0.001. In patients with hypertensive left ventricular hypertrophy, TDR correlated well with the degree of hypertrophy (r = 0.83, p less than 0.01) and also with peak left ventricular systolic pressure (r = 0.62, p less than 0.01). The coronary flow reserve, calculated from the ratio of the diastolic mean velocity after intracoronary injection of papaverine to the resting flow velocity, decreased with prolongation of TDR (r = 0.58, p less than 0.02). CONCLUSIONS: (1) Impairment of early diastolic coronary arterial inflow is the most remarkable characteristic in pressure overloaded left ventricular hypertrophy; (2) preceding systolic vascular compression and impaired left ventricular relaxation correlate with the delayed early diastolic inflow; (3) the delayed inflow is an important possible cause of the decreased coronary flow reserve in the hypertensive left ventricular hypertrophy.

Adult↗
PubMed1988

Regression of myocardial and coronary vascular hypertrophy in hypertensive heart disease.

In essential hypertension, ventricular function is determined primarily by the degree of hypertrophy (myocardial factor) and by the organic complications in the coronary artery (coronary factor). Ventricular function is inversely correlated with ventricular size and systolic wall stress, inasmuch as ventricular function diminishes when these two variables increase. Coronary reserve is reduced even in hypertensive hypertrophy without evidence of coronary artery disease. MVO2 per mass unit is directly correlated with systolic wall stress per cross-sectional area of the left ventricular wall. It is concluded that the appropriateness of left ventricular hypertrophy, as a result of mass-to-volume ratio and stress, is a major determinant of left ventricular performance, of coronary blood flow, and of myocardial oxygen consumption. Pharmacotherapeutical means of reversing cardiac hypertrophy (prazosin, clonidine, enalapril, and nifedipine) were analyzed in concentrically, as well as eccentrically, hypertrophied left ventricles. Regression of cardiac hypertrophy, i.e., therapeutic intervention on a critical precursor of hypertensive congestive heart failure, can be obtained by various antihypertensive agents. Prazosin, calcium channel blockers, and angiotensin converting enzyme inhibitors as well as a combined treatment regimen using alpha-receptor blockers together with diuretics and vasodilators can all induce regression of hypertrophy associated with an improvement in left ventricular function. Moreover, an improved coronary reserve may reduce the ischemic risk of the hypertrophied myocardium. However, not all antihypertensive drugs seem equally effective in bringing about coronary regression of left ventricular hypertrophy (LVH). No regression or little regression has been found with diuretic monotherapy despite a satisfactory reduction in blood pressure. On the other hand, a trend towards a regression has been observed in patients in whom treatment with clonidine significantly reduced catecholamines. Recent experimental data in spontaneously hypertensive rats indicate that the impaired coronary reserve can be significantly improved by the long-term administration of blood pressure lowering agents, e.g., by nifedipine or by the combination of metoprolol plus hydralazine.

Cardiomegaly↗
PubMed1995

Ventricular hypertrophy in sleep apnoea.

Ventricular hypertrophy is associated with an increased risk of cardiovascular death and cardiac events. In response to a haemodynamic load, ventricular hypertrophy may either be eccentric (dilation in response to volume overload) or concentric (increase in wall thickness in response to pressure overload). Ventricular hypertrophy increases with age, weight, blood pressure, and the presence of cardiovascular disease. It is greater in men than in women when adjusting for other variables. Echocardiography is the best method for accurate quantification of left ventricular mass and for detecting right ventricular hypertrophy. In obstructive sleep apnoea there are reports of both eccentric and concentric hypertrophy of the left ventricle. However, many of these reports have failed to control for patient weight or age. More recent reports indicate that much of the hypertrophy of the left ventricle reported in obstructive sleep apnoea can be related to patients' age, blood pressure, or size. However, right ventricular hypertrophy appears to be distinctly associated with the presence and severity of obstructive sleep apnoea. Right ventricular hypertrophy secondary to obstructive sleep apnoea may be the substrate for the eventual development of cor pulmonale and right heart failure. Its pathophysiological significance and potential use as a marker of severe OSA requires further investigation. Further investigation into left ventricular hypertrophy and sleep apnoea must control for the potentially confounding variables listed above and will require population-based and/or carefully matched case control studies.

Journal Article↗
PubMed2005

Role of myofibrillogenesis regulator-1 in myocardial hypertrophy.

Myofibrillogenesis regulator-1 (MR-1) is a novel homologous gene, identified from a human skeletal muscle cDNA library, that interacts with contractile proteins and exists in human myocardial myofibrils. The present study investigated MR-1 protein expression in hypertrophied myocardium and MR-1 involvement in cardiac hypertrophy. Cardiac hypertrophy was induced by abdominal aortic stenosis (AAS) in Sprague-Dawley rats. Left ventricular (LV) hypertrophy was assessed by the ratio of LV wet weight to whole heart weight (LV/HW) or LV weight to body weight (LV/BW). Rat MR-1 (rMR-1) expression in the myocardium was detected by immunohistochemical and Western blotting analysis. Hypertrophy was induced by ANG II incubation in cultured neonatal rat cardiomyocytes. The effect of rMR-1 RNA interference on ANG II-induced hypertrophy was studied by transfection of cardiomyocytes with an RNA interference plasmid, pSi-1, which targets rMR-1. Hypertrophy in cardiomyocytes was assessed by [3H]Leu incorporation and myocyte size. rMR-1 protein expression in cardiomyocytes was detected by Western blotting. We found that AAS resulted in a significant increase in LV/HW and LV/BW: 89% and 86%, respectively (P < 0.01). Immunohistochemistry and Western blot analysis demonstrated upregulated rMR-1 protein expression in hypertrophic myocardium. ANG II induced a 24% increase in [3H]Leu incorporation and a 65.8% increase in cell size compared with control cardiomyocytes (P < 0.01), which was prevented by treatment with losartan, an angiotensin (AT1) receptor inhibitor, or transfection with pSi-1. rMR-1 expression increased in ANG II-induced hypertrophied cardiomyocytes, and pSi-1 transfection abolished the upregulation. These findings suggest that MR-1 is associated with cardiac hypertrophy in rats in vivo and in vitro.

Amino Acid Sequence↗
PubMed1989

Sarcolemmal Ca2+ transport activities in cardiac hypertrophy caused by pressure overload.

To examine Ca2+ transport activities in sarcolemmal membrane in cardiac hypertrophy caused by pressure overload, rats were subjected to aortic banding for 28 days. Heart-to-body weight ratio was increased by 46% in aortic-banded animals in comparison with the sham-operated rats. Ouabain-sensitive Na+-K+-ATPase activity in sarcolemma (SL) from hypertrophied hearts was not different from that in the control preparation. The initial rate of Na+-dependent Ca2+ uptake in SL vesicles from the hypertrophied hearts was stimulated by 53% compared with the control vesicles. ATP-dependent Ca2+ uptake and Ca2+-stimulated adenosinetriphosphatase (ATPase) activities in SL from hypertrophied hearts were increased by 35%. The number of Ca2+ channels estimated by [5-methyl-3H]nitrendipine binding was decreased by 33% in SL from hypertrophied hearts. Total and individual phospholipid contents in the hypertrophied heart preparations were not different from those in the control, except that phosphatidylcholine and phosphatidylethanolamine contents were significantly increased. Sarcolemmal preparations from hypertrophied hearts from the 22-wk-old spontaneously hypertensive rats exhibited changes in Na+-Ca2+ exchange and Ca2+-pump activities (similar to those observed in banded hearts), whereas the Na+-K+-ATPase activity decreased, [3H]nitrendipine binding increased, and phospholipid contents were not different. Thus, although differences were defined between two types of hypertrophy, these results suggest alterations in the sarcolemmal Ca2+ transport activities that may serve as an adaptive mechanism for the removal of Ca2+ from the myocardial cells during the development of cardiac hypertrophy.

Animals↗