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PubMed1986

Comparison of M-mode echocardiography and angiography in the evaluation of left ventricular hypertrophy.

The authors analysed in a group of 82 patients with a symmetric left ventricle and a homogeneous ventricular wall thickness the reliability of M-mode echocardiography in recognizing left ventricular hypertrophy. In concentric hypertrophies, a sufficient diagnostic criterion is ventricular wall thickness. Measurement of the interventricular septum offers a better correlation with angiographic values (r = 0.609, p less than 0.001) than measurement of the posterior wall (r = 0.358, p less than 0.01); a correct diagnosis can be determined in 84%. In excentric hypertrophies, the hypertrophy must be assessed on the basis of calculating the left ventricular mass. The most accurate of echocardiographic methods proved to be the calculation according to the authors' own formula (r = 0.760, p less than 0.001), which recognizes left ventricular hypertrophy correctly in 85%. The diagnostic correctness of Teichholz' formula is 80% and of the cubic formula 74%. Fortuin's equations proved to be of no value for documenting ventricular hypertrophy. In a group of 13 patients with hypertrophic cardiomyopathy, the correlation between angiographic and echocardiographic values of the left ventricular mass was very low (r = 0.534, p = 0.05).

Angiography↗
PubMed1987

Recent progress in the electrocardiographic diagnosis of ventricular hypertrophy.

The surface electrocardiogram remains an insensitive method for detection of ventricular hypertrophy. Technical problems related to body size and habitus and distance from the heart cannot be overcome. Coronary arterty disease and amyloidosis, although frequently associated with hypertrophy, tend to obscure the electrocardiographic changes because of the attendant loss of voltage. The progress made in the last 20 years is due primarily to re-evaluation of traditional criteria in terms of careful anatomic correlation. The studies cited have the advantage of using specific clinical diagnoses in a defined population, specific chamber weights, and a 97.5 percentile confidence level for distinguishing normal pathologic and electrocardiographic data from abnormal. They are limited because the results may not apply to females or patients with mitral stenosis and congenital heart disease. In general, the electrocardiogram can be expected to detect left ventricular hypertrophy in six out of ten patients with the disease, and will misdiagnose the problem in about one out of every ten without the disease. Methodology using multiple criteria will achieve the best sensitivity and specificity. Several methods are available and of comparable accuracy. Simplicity of these methods varies widely and will be a factor in the choice of the method selected. The electrocardiogram will perform best in the population of patients with hypertension and aortic stenosis or regurgitation and have its greatest limitation in patients with coronary artery disease and myocardial infarctions. Echocardiography is proven to be more sensitive than the electrocardiogram for detection of left ventricular hypertrophy. Sensitivity is around 90 per cent with 95 per cent specificity. Its major limitations lie in the expense as compared to the electrocardiogram and in inadequate image resolution in a small proportion of patients. In order to achieve the results reported by centers proficient in this technique, careful attention must be paid to precise standardization of measurements and selection of images to be measured. When this is done the echocardiogram certainly offers a distinct advantage over the electrocardiogram in detecting left ventricular hypertrophy. We recommend the use of left atrial abnormality as a criterion to diagnose left ventricular hypertrophy when there is right bundle branch block. When left bundle branch block is present on the electrocardiogram, traditional criteria are probably no more accurate than the bundle branch block itself.(ABSTRACT TRUNCATED AT 400 WORDS)

Bundle-Branch Block↗
PubMed1987

Consequences of reversal of hypertensive cardiac hypertrophy by captopril on left ventricular pumping ability and performance.

Left ventricular hypertrophy can be reversed by treatment of hypertension with captopril but the consequences of this regression are not yet fully described. We studied the maximal capacity of the hypertrophied and hypertrophy-reversed ventricle to generate pressure during transient total occlusion of the aorta, and also the left ventricular end-diastolic pressure required to meet this maximal effort. Two-kidney, one clip Goldblatt (renal hypertensive rats; RHR) hypertension was induced in 17 Wistar rats, eight of which were treated with captopril (RHR-C: 50 mg/kg given orally) from the fourth to the eighth week. Sham-operated controls (SC) remained untreated, or were treated with similar doses of captopril (SC-C). Significantly lower heart weights were found in RHR-C than in RHR (2.88 +/- 0.15 versus 2.38 +/- 0.04; P less than 0.001). During transient total occlusion of the aorta, the maximal intraventricular pressure developed in RHR-C was not significantly different from that in RHR, but left ventricular end-diastolic pressure was significantly less in RHR-C than in RHR (21.4 +/- 2.2 versus 34.3 +/- 3.8; P less than 0.01). The analysis of pressure-volume characteristics of the hypertrophied left ventricles and those in which hypertrophy was reversed revealed similar compliances between these two groups. Our data suggest that there was a mechanical improvement in the heart function after reversal of left ventricular hypertrophy.

Animals↗
PubMed1988

[Left ventricular hypertrophy in arterial hypertension].

Arterial hypertension is frequently and at an early stage complicated by left ventricular hypertrophy, i.e. an increase in muscular mass due to the proliferation of myofibrillae. This in fact is a physiological mechanism aimed at maintaining systolic function and systemic blood flow rate. Left ventricular hypertrophy may be associated with myocardial alterations, such as increase of collagen, abnormalities of diastolic function, reduced contractility, increased cell excitability and disorders of coronary perfusion. It is responsible for a higher risk of cardiovascular mortality. Antihypertensive treatments, therefore, must not only bring blood pressure down to normal values, but also reduce the myocardial mass. In order to avoid a detrimental effect on coronary reserve, it is highly desirable that arterial hypertension and left ventricular hypertrophy regress simultaneously. Regression of the myocardial hypertrophy associated with arterial hypertension is observed with most antihypertensive drugs, except vasodilators that act directly on the vascular smooth muscle, probably due to stimulation of the sympathetic system. Diuretics also have an inconstant beneficial effect on left ventricular hypertrophy. When a choice has to be made between two drugs that have the same antihypertensive activity, it is the one that also brings about an early and lasting regression of myocardial hypertrophy which must be prescribed.

Cardiomegaly↗
PubMed1988

Subacute effects of propranolol and B 24/76 on isoproterenol-induced rat heart hypertrophy in correlation with blood pressure.

We compared the potential beta-receptor blocker, B 24/76 i.e. 1-(2,4-dichlorophenoxy)-3[2-3,4-dimethoxyphenyl)ethanolamino]-prop an-2-ol, which is characterized by beta 1-adrenoceptor blocking and beta 2-adrenoceptor stimulating properties with propranolol. The studies were performed using an experimental model of isoproterenol-induced heart hypertrophy in rats. A correlation of the blood pressure was neither found in the development nor in the attempt to suppress the development of heart hypertrophy with the two beta-receptor blockers. Both beta-blockers influenced the development of hypertrophy to a different, but not reproducible extent. It was possible to suppress the increased ornithine decarboxylase activity with both beta-blockers in hypertrophied hearts, but there was no effect on the heart mass. Neither propranolol nor B 24/76 could stop the changes in the characteristic myosin isoenzyme pattern of the hypertrophied rat heart. Thus, the investigations did not provide any evidence that the beta-receptor blockers propranolol and B 24/76 have the potency to prevent isoproterenol from producing heart hypertrophy.

Animals↗
PubMed1985

Ultrasound characteristics of myocardial hypertrophy in patients affected by hypertrophic cardiomyopathy.

A study of the extent and local distribution of the heart muscle hypertrophy affecting the left ventricle and the septum has been performed in 70 hypertrophic cardiomyopathy patients. According to these signs the patients have been distributed into 5 types. Type I, where the hypertrophy affected only the interventricular septum, appeared in 14.2% of the cases. In type IIa the anterior wall of the ventricle was simultaneously affected (37.1%), in type IIb it was also the lateral wall of the ventricle (30.0%). Type III manifested hypertrophy of the posterior wall (4.3%), type IV affected the apical portion of the left ventricle (8.5% of the patients). Under the heading of type V there figured patients who had a concentric hypertrophy of the whole left ventricle including the septum (5.7%). Among the obstructive forms we revealed especially the types Ia, IIa, IIb. Using the M-mode alone, detection of the hypertrophy was impossible in such patients who had isolated affection of the dorsal part of the septum, the anterolateral or the apical portion of the left ventricle (type Ib, IV and some of the type IIa and IIb patients--a total of 13%). Signs of asymmetrical septal hypertrophy were lacking in 23% of the patients.

Adolescent↗
PubMed1987

[Asymmetric septum hypertrophy in the pressure-overloaded heart].

According to echocardiographic observations, the hypertrophic left ventricle in hypertension and in aortic stenosis is inclined to asymmetric septal hypertrophy. The heart surgeon, after removal of the stenosed aortic valve, is not so rarely forced to resect an additional muscular hump of the basal ventricular septum. These findings contrast with our experiences from autopsy examinations; we see asymmetric septal hypertrophy only in hypertrophic cardiomyopathy (or coronary heart disease). The aim of this study was to demonstrate or refute this impression by measurements of the relevant parameters. In ten hearts with aortic stenosis and in 12 hearts of hypertensive patients there was no evidence of accentuated septal hypertrophy. In some hearts we found a prominent crista supraventricularis, which could explain the echocardiographic feature of a thickened ventricular septum. The muscular hump stenosing the left ventricular outflow tract can easily be explained by concentric hypertrophy. The thickness of the septum corresponded to that of the free wall, but only below the aortic valve did the hypertrophy become functionally relevant. There is no doubt that in certain cases this muscular hump has to be removed. The term asymmetric septal hypertrophy, however, is inadequate.

Aortic Valve Stenosis↗
PubMed1985

[Regional right ventricular hypertrophy in hypertrophic cardiomyopathy and hypertension].

The mode of right ventricular hypertrophy was assessed by two-dimensional echocardiography (2DE) for 24 patients with hypertrophic cardiomyopathy (HCM), and the results were compared with those of 51 patients with hypertension (HT). The patients with HT were categorized in four groups depending on the thickness of the interventricular septum (IVST) and left ventricular posterior wall (PWT): HT-ASH with both left ventricular hypertrophy (LVH) (IVST greater than or equal to 13 mm) and asymmetric septal hypertrophy (ASH) (IVST/PWT greater than or equal to 1.3), severe HT with LVH and without ASH, and mild HT without LVH and ASH. Anterior wall thickness (AWT), posterior wall thickness (PWT), and diaphragmatic wall thickness (DWT) of the right ventricle were obtained from 2DE in the parasternal long-axis view, the short-axis view and subxiphoid view, respectively. These were recorded on video tape, and the measurements were made on the stop frames. Right ventricular hypertrophy (RVH) was estimated by the maximal right ventricular wall thickness (max RVWT), and the ratio of the maximal and minimal thickness (max RVWT/min RVWT) was calculated to evaluate asymmetrical hypertrophy (AH) of the right ventricle (RV). The incidence of RVH (Max RVWT greater than or equal to 5 mm) and asymmetrical hypertrophy (AH) (max RVWT/min RVWT greater than or equal to 1.3) of the RV in HCM, HT-ASH and mild HT were 67% and 41%, 57% and 45%, and 15% and 11%, respectively. The incidence of RVH with AH was more frequent in patients with HCM as well as HT with ASH than in patients with HT without ASH.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Volume↗
PubMed1984

Regression of cardiac hypertrophy with drug treatment in spontaneously hypertensive rats.

Left ventricular hypertrophy is an important complication of essential hypertension. Some antihypertensive drugs have been shown to allow regression of cardiac hypertrophy, both in spontaneously hypertensive rats and in hypertensive patients. Recent results show that the agents which interfere with the functions of the sympathetic nervous system, converting enzyme inhibitors and calcium antagonists are effective in reducing arterial blood pressure and regression of left ventricular hypertrophy. The use of vasodilators and diuretics may under certain circumstances, however, even exacerbate cardiac hypertrophy. Regression of left ventricular hypertrophy in hypertension does not appear to depend solely on reduction of arterial blood pressure. Other factors seem to modulate the myocardial response to antihypertensive treatment. Included among these mechanisms are neural, humoral, haemodynamic and biochemical factors. The available experimental data further suggest that some functional derangements and biochemical changes associated with hypertrophy may be reversed by antihypertensive treatment. There is, however, insufficient experience with human subjects to determine whether a reduction in left ventricular mass is associated with lower incidences of heart failure or mortality than may be achieved by adequate blood pressure control alone.

Adrenergic alpha-Antagonists↗
PubMed1982

Concurrent left and right ventricular hypertrophy in dog models of right ventricular overload.

In two pressure and volume overload models of canine right ventricular hypertrophy, we have demonstrated significant hypertrophy of both the left and the right ventricles. The extent of hypertrophy was correlated positively to the extent of the increase in plasma epinephrine in both volume and pressure overload models. Attenuation or ablation of plasma epinephrine through the administration of propranolol, a beta-adrenergic blocker, or by denervation of the adrenal medulla prevented the hypertrophy process. No hemodynamic parameter was altered consistently in a parallel manner to hypertrophy. This is the first report of concurrent right and left ventricular hypertrophy in response to pressure or volume overload of the right ventricle. These studies further implicate epinephrine as a major trophic hormone of the heart.

Animals↗
PubMed1984

[Relation between asymmetrical hypertrophy of the interventricular septum and plasma levels of catecholamines in normotensive chronic uremic patients undergoing hemodialysis treatment].

Sympathetic-adrenergic activity has been evaluated in 23 chronic uremic, normotensive patients on regular hemodialysis, 7 of which (30.4%) with M-mode and bidimensional echocardiographic finding of asymmetric septal hypertrophy. The sympathetic function has been assessed by measuring arterial plasma norepinephrine and epinephrine levels before and after postural activation, just before and after dialysis. After dialysis, standing caused a significant increase of plasma norepinephrine levels in patients with asymmetric septal hypertrophy in comparison with patients without asymmetric septal hypertrophy and with the control non uremic group. Moreover, a significant decrease in blood pressure and a sharp heart rate increase were noted in the patients without asymmetric septal hypertrophy, whereas mean blood pressure and heart rate were unchanged in the patients with asymmetric septal hypertrophy. These results suggest that increased plasma norepinephrine concentration may have a role in the development of interventricular septal hypertrophy.

Adult↗
PubMed1980

Elastic properties of normal and hypertrophied cardiac muscle.

This brief review addresses itself to the following questions on normal and hypertrophied muscle. 1) What changes, if any, take place in the mechanical properties of cardiac muscle during pressure and volume overload hypertrophy? 2) What parameters may signal preoperatively irreversibility of hypertrophy and chamber enlargement? 3) Are the effects of age and hypertrophy on muscle stiffness similar? 4) What relationships exist between diastolic properties and systolic function? The analyses of the elastic properties of cardiac muscle based on several animal and clinical studies indicate that: a) Muscle stiffness in pressure overload is elevated and is normal in volume overload in the majority of the animal studies. However, the clinical studies support the hypothesis that muscle stiffness remains normal in mild to moderate degrees of valvular disease and is elevated in severe valvular disease. b) Wall stress, volume:mass, and radius:thickness ratios are useful prognostic indicators regarding reversibility of wall hypertrophy and/or chamber enlargement. c) Effects of age and hypertrophy on muscle stiffness are similar for the age range of young adult (6 mo) to old (90 wk) SHR and WKY rats. d) Increased muscle stiffness is invariably accompanied by decreased muscle shortening velocity but rate of force development and peak force may not be impaired.

Aging↗
PubMed1984

[Hypertrophic cardiomyopathy with ventricular septal hypertrophy localized to the apical region of the left ventricle (apical ASH)].

Clinical and morphologic features are described in a subgroup of 22 patients with hypertrophic cardiomyopathy, who showed ventricular septal hypertrophy localized to the apical region (apical asymmetric septal hypertrophy: apical ASH). All patients had ventricular septal thickness of 17 mm or less with an average of 13 +/- 3 mm in the M-mode echocardiograms. In contrast, the two-dimensional echocardiograms demonstrated septal hypertrophy localized to the apical region, with an average septal thickness of 20 +/- 3 mm at the mitral valve and papillary muscle levels. On the left ventriculogram, 82% of patients with apical ASH showed inward concavity of the right-inferior wall of the left ventricle, indicating hypertrophy of the ventricular septum. However, no patient showed spade-like appearance of the left ventricle and only two showed giant T wave inversion exceeding 10 mm. Echocardiographic examination performed in eight affected relatives revealed typical asymmetric septal hypertrophy (ASH) in four relatives, one of them showing a resting pressure gradient of 30 mmHg in the left ventricle. The remaining four relatives showed similar apical ASH. When compared with patients of typical ASH, patients with apical ASH demonstrated significantly greater cardiac size, left ventricular end-diastolic pressure, left atrial and left ventricular diameters and significantly lower percent fractional shortening. Atrial fibrillation, B bump of the mitral echogram and heart failure were more frequent in this subgroup of patients. Thus, apical ASH appeared to be a part of the morphologic spectrum of hypertrophic cardiomyopathy with ASH and to be a separate disease entity from apical hypertrophy previously described in Japan. Severely impaired diastolic performances associated with mild to moderately depressed systolic function of the left ventricle were the characteristic clinical features of the subgroup of patients with apical ASH.

Adolescent↗
PubMed1984

[Evaluation of septal hypertrophy and wall dynamics by biventricular cineangiography and endomyocardial biopsy].

To clarify clinically the pathogenesis of septal hypertrophy in terms of its morphology and wall dynamics, simultaneous biventricular cineangiography (BVG) and endomyocardial biopsy of the left ventricle were performed for patients with left ventricular hypertrophy. The patients were categorized in four groups according to their clinical and BVG findings; 1) 24 normal control subjects (C), 2) 39 patients with hypertension and symmetrical septal hypertrophy (SH-HT), 3) 17 patients with hypertension and asymmetrical septal hypertrophy characterized by the ratio (IVS/PW) greater than or equal to 1.3 by BVG, and 4) 25 patients with hypertrophic cardiomyopathy (HCM). The BVG's configuration of the septum in SH-HT showed a normal form of septal hypertrophy (NH form) essentially similar to that of the control subjects (N form), except for septal thickness increases of more than 10 mm. In HCM, a triangle or shell (TS) form or spindle (S) form of the septum was demonstrated by BVG. The TS form was characterized by straight or convex thickening of the septum from its center to its base toward the left ventricle. The S form was characterized by convex thickening localized to the central part and a relatively thin base. However, the configuration in ASH-HT was either the NH form (7 cases) or the TS or S form (10 cases). The configuration in ASH-HT with the NH form was not distinguishable from that of SH-HT, nor was the configuration in ASH-HT with the TS or S form distinguishable from that of HCM. Systolic thickening (%) of the septum and systolic shortening (%) of the septal length decreased significantly in this order: C, SH-HT, ASH-HT with the NH form, and ASH-HT with the TS or S form. Those of HCM were similar to those of ASH-HT with the TS or S form. In the cases of the N or NH form, there was a negative correlation between systolic thickening (%) and thickness of the septum in diastole. In cases with the TS or S form, systolic thickening (%) was not affected by the thickness of the septum in diastole, and a lower value was observed in all cases. Histological studies of endomyocardial biopsies revealed a positive correlation between the transverse diameters of the myocytes and the total systemic peripheral resistance (TSPR) in 25 patients with SH-HT. In 12 patients with HCM, there was no correlation, and severe hypertrophy of the myocytes was observed despite a lower TSPR.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1983

[Pulsed Doppler echocardiographic assessment of diastolic left ventricular hemodynamics in hypertrophic cardiomyopathy: relationship between the mode of left ventricular filling and the distribution of left ventricular hypertrophy].

In order to clarify left ventricular relaxation and filling in different types of hypertrophic cardiomyopathy (HCM), velocity patterns of blood flow at the inflow tract of the left ventricle (LV) were recorded by pulsed Doppler echocardiography and compared with those of normal subjects (26 cases). Forty-one patients with HCM were classified into the following 4 groups according to the distribution of LV hypertrophy and the evidence of cavity obstruction of the LV; with asymmetric septal hypertrophy (ASH: 15 patients), apical hypertrophy (APH: 10), diffuse hypertrophy ( DIH : five) and obstruction of the LV cavity (HOCM: 11). The HOCM group consisted of five cases of ASH type and six of APH or DIH type. Acceleration time (AT), deceleration time (DT) and the A/D ratio were measured on the pulsed Doppler echocardiogram. The M-mode echogram of the LV was recorded and subsequently digitized to obtain peak LV filling rate. The results were as follows: AT was significantly prolonged in 4 groups of HCM compared with that of the normal subjects. But there was no significant difference in AT among various HCM groups. DT was markedly prolonged in 4 groups of HCM compared with that of the normal subjects, but DT was significantly shortened in the ASH group compared with that of the APH or HOCM group. DT of the HOCM group was divided into the following 2 types according to the duration; normal or slightly prolonged DT (three cases) and markedly prolonged DT (eight). The former group belonged to the ASH type of LV hypertrophy in all cases, and two of them showed a third heart sound. An apical diastolic murmur was recorded in four patients of the ASH group, and six of the HOCM (five cases with ASH type and one with APH type). The A/D ratio was significantly increased in 4 groups of HCM compared with that of the normal subjects. But there was no significant difference among HCM groups. Diastolic descent rate (DDR) of the mitral valve echogram was significantly reduced in 4 groups of HCM compared with that of the normal subjects, particularly in the ASH and HOCM groups. DDR was roughly correlated with DT in the HCM group (r = -0.40, p less than 0.02). Peak LV filling rate was markedly decreased in the ASH, APH and HOCM groups compared with that of the normal subjects. There was a significant negative correlation between peak LV filling rate and DT (r = -0.49, p less than 0.01). In conclusion, the mode of LV filling in HCM showed various patterns according to the location of ventricular hypertrophy and the presence of cavity obstruction of the LV.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1994

Regression of hypertensive myocardial hypertrophy does not affect ultrasonic myocardial reflectivity: a tissue characterization study.

OBJECTIVE: Ultrasonic backscatter from the myocardial walls is directly related to the morphometrically or biochemically evaluated collagen content in man, and shows a normal pattern of quantitatively assessed ultrasonic backscatter in hypertensive patients, even in the presence of left ventricular hypertrophy. Whether the pharmacologically induced regression of left ventricular hypertrophy in hypertensive patients is accompanied by a disproportionate increase in relative connective tissue content is not yet known. The objective of the present study was to assess the effects of regression of left ventricular hypertrophy on the quantitatively evaluated myocardial reflectivity in essential hypertensives. DESIGN: We evaluated 19 mild-to-moderate essential hypertensives with echocardiographically assessed left ventricular hypertrophy, before and after 8 months' effective antihypertensive therapy with 20-40 mg enalapril once a day, associated with diuretics or calcium antagonists, or both, in six patients to achieve optimal blood pressure control. Using a modified echo machine developed in the Institute of Clinical Physiology, Pisa, an on-line radio-frequency analysis was performed to obtain quantitative operator-independent measurements of the integrated backscatter signal of the ventricular septum and the posterior wall. The integrated values of the radio-frequency signal from the myocardial walls were normalized for those from the pericardial interface and were expressed as percentages (integrated backscatter index). RESULTS: In comparison with baseline, the treated hypertensives showed significant decreases in mean blood pressure, left ventricular mass index, and septal and posterior wall thickness. However, integrated backscatter index values were similar at baseline and after therapy for both the septum and the posterior wall. CONCLUSION: Antihypertensive therapy with enalapril does not increase myocardial reflectivity, although it does induce regression of left ventricular hypertrophy. This suggests that, in accord with experimental data, regression of hypertrophy is achieved by enalapril through a proportionate regression of the myocyte and connective tissue components of the myocardium.

Cardiomegaly↗
PubMed2004

Regulation of protein kinase C isozymes in volume overload cardiac hypertrophy.

Protein kinase C (PKC) is a family of at least 11 isozymes and known to play a crucial role in myocardial growth. The present study was performed to investigate whether PKC-isozymes are differentially regulated during the development of volume-overload cardiac hypertrophy. After 2, 7 and 30 days of sham or aortocaval shunt operation in male Wistar rats, PKC-activity and the expression of cardiac PKC-isozymes (PKC-alpha, delta and epsilon) were determined at the protein and at the mRNA-level in the left and the right ventricle separately. Myocardial hypertrophy after 2, 7 and 30 days of aortocaval shunt was more pronounced in the right than in the left ventricle. Right ventricular hypertrophy was associated with an increased PKC-enzyme activity, a selectively enhanced protein expression of cytosolic PKC-delta (day 7: +83 +/- 12%, day 30: +94 +/- 14%) and PKC-alpha (day 7: +48 +/- 11%, day 30: +62 +/- 16%) and a transcriptional upregulation of the absolute mRNA-levels of these PKC-isozymes in the aortocaval shunt group as compared to controls. In contrast, the expression of PKC-epsilon was unchanged. A significant upregulation of PKC-delta both on the protein and on the mRNA-level was also noted in volume-overload induced left ventricular hypertrophy, whereas the expression of PKC-alpha and PKC-epsilon were not altered. Furthermore, the expression of calcineurin in both ventricles was not significantly changed in response to volume-overload. This study characterizes in the left and right ventricle a differential regulation of the dominant PKC-isozymes in volume-overload cardiac hypertrophy both at the protein and at the mRNA-level.

Animals↗
PubMed2005

Microarray analysis reveals pivotal divergent mRNA expression profiles early in the development of either compensated ventricular hypertrophy or heart failure.

Myocardial right ventricular (RV) hypertrophy due to pulmonary hypertension is aimed at normalizing ventricular wall stress. Depending on the degree of pressure overload, RV hypertrophy may progress to a state of impaired contractile function and heart failure, but this cannot be discerned during the early stages of ventricular remodeling. We tested whether critical differences in gene expression profiles exist between ventricles before the ultimate development of either a compensated or decompensated hypertrophic phenotype. Both phenotypes were selectively induced in Wistar rats by a single subcutaneous injection of either a low or a high dose of the pyrrolizidine alkaloid monocrotaline (MCT). Spotted oligonucleotide microarrays were used to investigate pressure-dependent cardiac gene expression profiles at 2 wk after the MCT injections, between control rats and rats that would ultimately develop either compensated or decompensated hypertrophy. Clustering of significantly regulated genes revealed specific expression profiles for each group, although the degree of hypertrophy was still similar in both. The ventricles destined to progress to failure showed activation of pro-apoptotic pathways, particularly related to mitochondria, whereas the group developing compensated hypertrophy showed blocked pro-death effector signaling via p38-MAPK, through upregulation of MAPK phosphatase-1. In summary, we show that, already at an early time point, pivotal differences in gene expression exist between ventricles that will ultimately develop either a compensated or a decompensated phenotype, depending on the degree of pressure overload. These data reveal genes that may provide markers for the early prediction of clinical outcome as well as potential targets for early intervention.

Animals↗