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PubMed2005

Blockade of MyD88 attenuates cardiac hypertrophy and decreases cardiac myocyte apoptosis in pressure overload-induced cardiac hypertrophy in vivo.

In this study, we evaluated whether blocking myeloid differentiation factor-88 (MyD88) could decrease cardiac myocyte apoptosis following pressure overload. Adenovirus expressing dominant negative MyD88 (Ad5-dnMyD88) or Ad5-green fluorescent protein (GFP) (Ad5-GFP) was transfected into rat hearts (n = 8/group) immediately followed by aortic banding for 3 wk. One group of rats (n = 8) was subjected to aortic banding for 3 wk without transfection. Sham surgical operation (n = 8) served as control. The ratios of heart weight to body weight (HW/BW) and heart weight to tibia length (HW/TL) were calculated. Cardiomyocyte size was examined by FITC-labeled wheat germ agglutinin staining of membranes. Cardiac myocyte apoptosis was determined by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling assay, and myocardial interstitial fibrosis was examined by Masson's Trichrome staining. Aortic banding significantly increased the HW/BW by 41.0% (0.44 +/- 0.013 vs. 0.31 +/- 0.008), HW/TL by 47.2% (42.7 +/- 1.30 vs. 29.0 +/- 0.69), cardiac myocyte size by 49.6%, and cardiac myocyte apoptosis by 11.5%, and myocardial fibrosis and decreased cardiac function compared with sham controls. Transfection of Ad5-dnMyD88 significantly reduced the HW/BW by 18.2% (0.36 +/- 0.006 vs. 0.44 +/- 0.013) and HW/TL by 22.3% (33.2 +/- 0.95 vs. 42.7 +/- 1.30) and decreased cardiomyocyte size by 56.8%, cardiac myocyte apoptosis by 76.2%, as well as fibrosis, and improved cardiac function compared with aortic-banded group. Our results suggest that MyD88 is an important component in the Toll-like receptor-4-mediated nuclear factor-kappaB activation pathway that contributes to the development of cardiac hypertrophy. Blockade of MyD88 significantly reduced cardiac hypertrophy, cardiac myocyte apoptosis, and improved cardiac function in vivo.

Adaptor Proteins, Signal Transducing↗
PubMed2006

Integrin-linked kinase expression is elevated in human cardiac hypertrophy and induces hypertrophy in transgenic mice.

BACKGROUND: Although numerous signaling pathways are known to be activated in experimental cardiac hypertrophy, the molecular basis of the hypertrophic response inherent in human heart diseases remains largely unknown. Integrin-linked kinase (ILK) is a multifunctional protein kinase that physically links beta-integrins with the actin cytoskeleton, suggesting a potential mechanoreceptor role. METHODS AND RESULTS: Here, we show a marked increase in ILK protein levels in hypertrophic ventricles of patients with congenital and acquired outflow tract obstruction. This increase in ILK was associated with activation of the Rho family guanine triphosphatases, Rac1 and Cdc42, and known hypertrophic signaling kinases, including extracellular signal-related kinases (ERK1/2) and p70 S6 kinase. Transgenic mice with cardiac-specific expression of a constitutively active ILK (ILK(S343D)) or wild-type ILK (ILK(WT)) exhibited a compensated ventricular hypertrophic phenotype and displayed an activation profile of guanine triphosphatases and downstream protein kinases concordant with that seen in human hypertrophy. In contrast, transgenic mice with cardiomyocyte-restricted expression of a kinase-inactive ILK (ILK(R211A)) were unable to mount a compensatory hypertrophic response to angiotensin II in vivo. CONCLUSIONS: Taken together, these results identify ILK-regulated signaling as a broadly adaptive hypertrophic response mechanism relevant to a wide range of clinical heart disease.

Alanine↗
PubMed1991

[Lipomatous hypertrophy of the interatrial septum versus lipomatous hypertrophy of the intervenous tubercle].

The lipomatous hypertrophy of the interatrial septum is a clinicopathological entity characterized by an accumulation of fat, not encapsulated but circumscribed in the atrial septum, over the fossa ovalis, and protruding into the right atrium; its thickness exceeding 15 mm. It is clinically associated with atrial electric abnormalities such as disorders of the atrial conduction and supraventricular arrhythmias, difficulty of the venous return and sudden death. In 1669 Lower described at the entrance to the right atrium, between the venae cavae, there is a tubercle formed by an accumulation of fat, covered over with muscular fibres that protrudes into the right atrium, which be called intervenous tubercle. The aim of this work is to find out the normal morphology of the intervenous tubercle and to find out whether or not lipomatous hypertrophy of interatrial septum is related to it in some way, because both coincides anatomically.

Adolescent↗
PubMed1990

[Myocardial structure in various forms of hypertrophy. I. Myocyte hypertrophy or hyperplasia? Pathophysiological aspects and the methods of study].

One of most controversial problems in cardiac muscle pathology is the existence of myocyte hyperplasia. The term hypertrophy indicates an increase in size of the individual muscle cells without changing their total number, whereas in hyperplasia proliferation of the myocyte occurs. This fundamental question of the character of cardiac growth remains unresolved in spite of the wide attention in has received. Contemporary views concerning the cardiac muscle hyperplasia are presented. From clinical point of view the problem is significant for two reasons. The loss of the ability of muscle cells to proliferate is responsible for the irreversible myocardial destruction after injury. From another point of view, if the increase of the heart muscle is maintained, although a complete remission of cardiac hypertrophy becomes impossible. In the light of these controversies we undertook the attempt to solve this complicated problem. Morphometric evaluation of the cardiac myocyte is described in detail.

Anthropometry↗
PubMed1993

[Tissue factors contributing to cardiac hypertrophy in cardiomyopathic hamsters (BIO14.6): involvement of transforming growth factor-beta 1 and tissue renin-angiotensin system in the progression of cardiac hypertrophy].

The present study was performed to determine whether transforming growth factor beta 1 (TGF beta 1) and tissue renin-angiotensin (R-A) system are involved in hypertrophic cardiomyopathy. Cardiomyopathic Syrian hamsters (Bio 14.6) aged 4 and 20 weeks were used as a model of hypertrophic cardiomyopathy and compared with age-matched F1 beta Syrian hamsters. Total RNA was extracted from the left ventricle, and the m-RNA expressions of TGF beta 1 and angiotensinogen (ATN) were examined by Northern blotting or Ribonuclease Protection Assay (RPA). The activity of angiotensin-converting enzyme (ACE) was assayed by the modified method of Tess, using crude membrane fraction prepared from left ventricle. The effect of angiotensin II (A II) on phosphatidylinositol (PI) metabolism was evaluated by the PI -or PIP2 (phosphatidylinositol 4,5-bis phosphate)-specific phospholipase C (PLC), which releases inositol-1,4,5-triphosphate (I P3) and diacylglycerol (DAG) in cardiac myocytes. The m-RNA expressions of TGF beta 1 and ATN were detected in each group of Syrian hamsters (BIO14.6 and F1 beta). TGF beta 1 m-RNA expression was markedly increased in BIO14.6 compared with F1 beta at the age of 4 weeks, and was more intensified at the age of 20 weeks, while no significant difference was demonstrated in the ATN m-RNA expression. ACE activity in the left ventricle was enhanced in 20 week-old BIO14.6 compared with age-matched F1 beta. The activities of PI- and PIP2-specific PLC were enhanced in 20 week-old BIO14.6 in response to A II stimulation. DAG and IP3, which are second messengers and activate protein kinase C. were significantly released from the cardiac myocytes of 20 week-old BIO14.6. These results suggest that the increase in expression of TGF beta 1 gene in the left ventricle may induce cardiac hypertrophy in BIO14.6, and that the exaggerated response of phosphatidylinositol metabolism to A II and the increased activity of ACE in cardiac tissue R-A system may lead to the development of cardiac hypertrophy.

Angiotensin II↗
PubMed1978

Renal hypertrophy in experimental diabetes: a comparison to compensatory hypertrophy.

The kidney growth seen after the induction of experimental diabetes in rats has been compared to the compensatory renal growth after one-sided nephrectomy. After five days the kidney weight had increased from 650 +/- 15 mg in a group of controls to 778 +/- 21 mg in diabetic rats, and 764 +/- 17 mg in unilaterally nephrectomised rats. The increased weight was in both groups reflected in an increased DNA content and increased RNA/DNA and protein/DNA ratios. In a group of rats made diabetic and nephrectomised at the same time, kidney weight increased to 953 +/- 22 mg after five days. When rats were unilaterally nephrectomised after 20 days of untreated diabetes, compensatory growth was much more pronounced than in non-diabetic rats, kidney weight rising from 780 +/- 21 to 1144 +/- 39 mg in five days. Similarly, in rats with established compensatory renal hypertrophy, diabetes induced a very rapid growth of the remaining kidney (1226 +/- 46 mg after five days).

Animals↗
PubMed2005

Electrocardiographic diagnosis of left ventricular hypertrophy: the effect of left ventricular wall thickness, size, and mass on the specific criteria for left ventricular hypertrophy.

BACKGROUND: The purpose of our study was to determine the relative importance and effect of an increased left ventricle wall thickness, left ventricular diastolic diameter, and left ventricular mass (LVM) on the performance of the 4 major electrocardiogram (ECG) criteria of left ventricular hypertrophy (LVH) and to determine how these findings could be incorporated into the routine ECG interpretation of LVH. METHODS: The ECG criteria of LVH that we chose to examine were voltage, repolarization abnormalities, left atrial abnormality, and ventricular conduction time. We analyzed data from 608 consecutive patients with left ventricular wall thickness of >13 mm on the echocardiogram and with a concurrent ECG. We arbitrarily divided patients into 3 groups (groups I-III) according to the calculated LVM. Group I had an LVM of <400 g; group II had an LVM from 400 to 600 g, and group III had an LVM of >600 g. We evaluated the effect of increasing LVM, wall thickness, and ventricular diameter on the performance of the 4 ECG criteria at different severity of thickness, diameter, and mass. RESULTS: An increase in the echocardiogram-derived LVM had significant effect on all 4 ECG criteria. As LVM progressively increased from groups I to III, the frequency of voltage criteria for LVH increased from 52% to 83%; left atrial abnormality rose from 46% to 68%; ST-T wave changes increases from 55% to 95%, and QRS prolongation significantly increased from 42% to 70%. CONCLUSION: Increased wall thickness and ventricular diameter failed to correlate with the overall ECG score or significantly influence the frequency of any of the 4 ECG criteria for LVH in patients when LVM was held relatively constant. We also demonstrated that an increasing number of criteria on the ECG are associated with a greater mean LVM.

Cohort Studies↗
PubMed2006

Tissue velocity echocardiography shows early improvement in diastolic function with irbesartan and atenolol therapy in patients with hypertensive left ventricular hypertrophy. Results form the Swedish Irbesartan Left Ventricular Hypertrophy Investigation vs Atenolol (SILVHIA).

BACKGROUND: Abnormal diastolic function is common in hypertensive left ventricular hypertrophy (LVH). Early identification and treatment may prevent future cardiovascular events. METHODS: We examined 58 hypertensive patients with LVH, 38 with hypertension but no LVH, and 38 normotensive subjects. The effects of the AT1 receptor blocker irbesartan and the beta1 blocker atenolol on diastolic function during 48 weeks of treatment were evaluated in the LVH group by tissue velocity echocardiography (TVE). We measured basal septal and lateral wall velocities of early (Em) and late (Am) diastolic myocardial wall motion, Em velocity deceleration time (E-decm), and isovolumic relaxation time (IVRTm). For comparison, diastolic function was assessed by conventional mitral pulse wave Doppler echocardiography. RESULTS: Diastolic function was impaired in both hypertensive groups. Irbesartan and atenolol (week 48, septal wall) improved IVRTm (-44%, P<.001, and -19%, P<.001; P<or=.001 between groups), E-decm (+56%, P<.001, and +53%, P<.001), and Em/Am (+11%, P=.396, and +20%, P=.010). Only irbesartan improved E/Em (-4%, P=.052 v +2%, P=.041). For irbesartan, relative changes in IVRTm and in septum thickness were related (P=.017), whereas relative changes in the Em/Am ratio and in heart rate were related for atenolol (P=.027). Alterations in diastolic dysfunction were greater and detected earlier with TVE than with conventional echocardiography. CONCLUSIONS: The TVE is more sensitive than conventional echocardiography in detecting alterations in diastolic function. Both irbesartan and atenolol improve diastolic function, but through different mechanisms. The improvement in IVRTm was greater with irbesartan, and only irbesartan improved E/Em. This may have implications on the treatment of high risk hypertensive patients.

Adrenergic beta-Antagonists↗
PubMed2001

Relation of echocardiographic left ventricular mass and hypertrophy to persistent electrocardiographic left ventricular hypertrophy in hypertensive patients: the LIFE Study.

BACKGROUND: The Losartan Intervention For Endpoint Reduction in Hypertension (LIFE) trial used left ventricular hypertrophy (LVH) on a screening ECG to identify patients at high risk for morbid events. Because of regression to the mean, not all patients who met screening criteria had persistent ECG LVH on the ECG performed at study baseline. METHODS: The relationship of echocardiographic LV mass and LVH to persistence or loss of ECG LVH between screening and baseline evaluation was examined in 906 hypertensive patients in the LIFE study, who had echocardiograms and additional ECG performed at study baseline. Patients were categorized according to the presence or absence of ECG LVH by Cornell voltage-duration product criteria or Sokolow-Lyon voltage criteria; echocardiographic LVH was defined by LV mass index (LVMI) > 104 g/m2 in women and > 116 g/m2 in men. RESULTS: A total of 678 patients (75%) had persistent ECG LVH at baseline evaluation. Compared with the 228 patients without ECG LVH on the second ECG by either criterion, the 106 patients with LVH by both Cornell product and Sokolow-Lyon criteria had significantly higher LVMI (140+/-31 v 114+/-21 g/m2, P < .001) and a higher prevalence of echocardiographic LVH (86% v 55%, P < .001). Patients with ECG LVH on the baseline ECG by either Cornell product criteria (n = 410) or Sokolow-Lyon voltage criteria (n = 162) had intermediate values of LVMI (125+/-25 and 121+/-21 g/m2) and prevalences of echocardiographic LVH (78% and 62%). After controlling for possible effects of age, sex, ethnicity, systolic blood pressure, and body mass index, persistence of ECG LVH on the baseline ECG was associated with an increased risk of echocardiographic LVH: compared with patients with neither ECG criteria for LVH, patients with only Sokolow-Lyon voltage criteria had a 1.2-fold increased risk of echocardiographic LVH, those with only Cornell product criteria had a 2.7-fold increased risk, and patients with both ECG criteria had a 4.1-fold increased risk of echocardiographic LVH (P < .001). CONCLUSIONS: Persistent ECG LVH between screening and LIFE study baseline identified patients with greater LV mass and a higher prevalence of echocardiographic LVH, suggesting that these patients may be at higher risk for subsequent morbid and mortal events.

Aged↗
PubMed2003

Effects of eplerenone, enalapril, and eplerenone/enalapril in patients with essential hypertension and left ventricular hypertrophy: the 4E-left ventricular hypertrophy study.

BACKGROUND: Elevated renin-angiotensin-aldosterone system activity correlates with left ventricular hypertrophy (LVH) and cardiovascular risk, but the relative contributions of angiotensin II and aldosterone remain unclear. This study compared LVH regression during treatment with the selective aldosterone blocker eplerenone, enalapril, and their combination in patients with hypertension. METHODS AND RESULTS: A 9-month, double-blind, randomized study was performed in 202 patients with LVH and hypertension who received eplerenone 200 mg daily, enalapril 40 mg daily, or eplerenone 200 mg and enalapril 10 mg daily. At week 8, hydrochlorothiazide 12.5 to 25 mg and/or amlodipine 10 mg was added if diastolic blood pressure was >90 mm Hg. Change in left ventricular (LV) mass as assessed by MRI was the primary end point. Change in blood pressure, renin-angiotensin-aldosterone system hormones, albuminuria, and safety were also assessed. Eplerenone significantly reduced LV mass from baseline (-14.5+/-3.36 g; n=50) similarly to enalapril (-19.7+/-3.20 g; n=54; P=0.258), but eplerenone/enalapril (-27.2+/-3.39 g; n=49) was more effective than eplerenone alone (P=0.007). All treatments reduced systolic blood pressure and diastolic blood pressure from baseline (eplerenone, -23.8 and -11.9 mm Hg; enalapril, -24.7 and -13.4 mm Hg; and eplerenone/enalapril, -28.7 and -14.4 mm Hg, P=0.048, in systolic blood pressure compared with eplerenone alone). Cough was more common with enalapril than with eplerenone (P=0.033), and elevated potassium was more common with eplerenone. CONCLUSIONS: Eplerenone was as effective as enalapril in LVH regression and blood pressure control. The combination of eplerenone and enalapril was more effective in reducing LV mass and systolic blood pressure than eplerenone alone.

Adult↗
PubMed1999

Impaired force-frequency relations in patients with hypertensive left ventricular hypertrophy. A possible physiological marker of the transition from physiological to pathological hypertrophy.

BACKGROUND: The extent to which force-frequency and relaxation-frequency relations (FFR and RFR, respectively) and exercise-induced adrenergic stimulation affect myocardial inotropic and lusitropic reserves has not been established in patients with left ventricular (LV) hypertrophy (LVH). METHODS AND RESULTS: We calculated the maximum first derivative of LV pressure (LV dP/dtmax) and the LV pressure half-time (T1/2) during pacing, exercise, and isoproterenol infusion in 17 patients with hypertensive LVH and 9 control subjects to investigate the influence of increases in heart rate (HR) and adrenergic stimulation on inotropic and lusitropic reserves. Group A consisted of 10 LVH patients who showed a progressive increase in the HR-LV dP/dtmax relation. Group B consisted of 7 LVH patients in whom the HR-dP/dtmax relation at physiological pacing rates was biphasic. The LV mass index was larger and the LV ejection fraction was smaller in group B than in group A (244+/-72 g/m2 versus 172+/-22 g/m2 and 55+/-18% versus 72+/-6%, respectively; both P<0.05). The increase in LV dP/dtmax was greater during exercise than pacing alone for similar increases in HR in all groups (P<0.05) (group A, 111+/-22% versus 25+/-14%; group B, 105+/-35% versus 14+/-10%; control, 111+/-24% versus 25+/-12%). T1/2 was shorter (P<0.05) during exercise than with pacing alone in all groups (group A, 41+/-6% versus 11+/-3%; group B, 38+/-9% versus 14+/-4%; control, 44+/-6% versus 12+/-5%). Isoproterenol infusion caused similar increases in LV dP/dtmax and similar decreases in T1/2 in all groups. CONCLUSIONS: The FFR was biphasic in patients with severe LVH irrespective of LV function but was preserved in patients with less severe LVH and control subjects. Importantly, the RFR and adrenergic control of both inotropic and lusitropic reserves were well preserved in all LVH patients. A biphasic FFR at physiological pacing rates may be one of the earliest markers of the transition from physiological adaptation to the pathological process in LVH patients.

Adrenergic beta-Agonists↗
PubMed1990

Tsk mice with genetic emphysema. Right ventricular hypertrophy occurs without hypertrophy of muscular pulmonary arteries or muscularization of arterioles.

The causes for the development of right ventricular hypertrophy (RVH) in emphysema are not fully understood. In the 1960s, studies of RVH in association with emphysema found no correlation between the extent of tissue damage in the lung and the RV weight. This was thought to disprove the theory that the RVH was due to an increase in pulmonary vascular resistance secondary to capillary destruction. In the present study, the development of RVH was investigated in tight-skin (tsk) mice with genetic emphysema. RVH started to develop in mature to senescent animals between 8 and 16 months of age and progressed thereafter. At 24 months of age, RV weight and the ratios RV/body weight and RV/LV + S weight were, respectively, 52, 96, and 60% greater than in control (pa) mice. At this time blood gas analysis revealed hypoxemia in tsk but not in pa mice. The mean linear intercept of tsk mice was 83% larger and the surface area of the walls of distal air spaces per unit lung volume was 40% smaller than in pa mice. There was a strong correlation between the severity of emphysema, assessed by both techniques, and the RV/LV + S ratio (p less than 0.001 for both). No muscularized arterioles were seen in the tsk mice, and the medial thickness of muscular arteries was almost identical in the two groups. This demonstrates that in emphysema, RVH can develop in the absence of pulmonary vascular changes and is probably due to tissue (and thus capillary) destruction.

Animals↗
PubMed2000

Experimental studies on myocardial stretch and ventricular arrhythmia in hypertrophied and non-hypertrophied hearts.

Hypertension affects about 5% of western populations and in the majority of cases it is of unknown aetiology. It exposes the heart to greater levels of myocardial stretch as a result of increased systolic pressure and peripheral resistance. Under certain circumstances myocardial stretch may trigger arrhythmias but the mechanisms and clinical importance of this phenomenon are unclear. This article outlines the risks of sudden cardiac death conferred by hypertension and left ventricular hypertrophy, presents the results of experiments using an animal model of myocardial stretch and discusses some possible mechanisms underlying stretch-induced arrhythmias which may be important in hypertensive patients.

Animals↗
PubMed1993

Improved ECG models for estimation of left ventricular hypertrophy progression and regression incidence by redefinition of the criteria for a significant change in left ventricular hypertrophy status. The MRFIT Research Group. Multiple Risk Factor Intervention Trial.

Three sets of left ventricular hypertrophy (LVH) criteria were evaluated in terms of their utility for LVH progression and regression incidence estimation. Incidence comparisons were performed with and without taking short-term variability into consideration using electrocardiographic records taken at the baseline and the first annual follow-up examination of 11,969 men, aged 37 to 55 years, at the baseline of the Multiple Risk Factor Intervention Trial. Short-term total technical and biologic variability (95% range) was determined from the records of 104 men invited for a repeat electrocardiographic recording at 2-week or shorter intervals from the first recording. The results indicated that after elimination of the false fraction due to normal variability, the residual incidence estimates are so low that their utility and statistical power in monitoring changes in LVH status is very limited. It is concluded that a redefinition of LVH progression and regression criteria is needed to enhance their utility in clinical trials.

Adult↗
PubMed1985

Rapid ventricular filling in left ventricular hypertrophy: II. Pathologic hypertrophy.

To define the extent of left ventricular ejection and filling abnormalities in patients with mild hypertension, a non-imaging nuclear probe was used to generate high resolution time-activity curves in 25 patients with an average systolic blood pressure of 154 +/- 20 mm Hg and diastolic pressure of 98 +/- 8 mm Hg. The hypertensive patients did not meet electrocardiographic criteria for left ventricular hypertrophy, and none had evidence of ischemic or other cardiac disease. Compared with 25 age-matched normal subjects who had average systolic and diastolic pressures of 123 +/- 10 and 79 +/- 8 mm Hg, respectively, the hypertensive patients had a significantly lower ejection rate (2.00 +/- 0.20 versus 2.34 +/- 0.36 end-diastolic counts/s for the control group, p less than 0.05) and ejection fraction (58 +/- 4.9 versus 62 +/- 4.4) (p less than 0.05). The hypertensive patients had a markedly lower average rapid left ventricular filling rate (1.87 +/- 0.32 versus 2.69 +/- 0.41 counts/s for the control group, p less than 0.001). Although there was a modest inverse relation between echocardiographic left ventricular mass index and filling rate in the hypertensive patients (r = -0.59, p less than 0.01), 4 of 12 hypertensive patients with normal left ventricular mass index had a depressed filling rate. All of the hypertensive patients with increased left ventricular mass index had an abnormal left ventricular filling rate (less than 1.89 end-diastolic counts/s).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1996

Quantification and distribution of alpha 1-adrenoceptor subtype mRNAs in human prostate: comparison of benign hypertrophied tissue and non-hypertrophied tissue.

1. There are at least three alpha 1-adrenoceptor subtypes, alpha 1a, alpha 1b and alpha 1d, in human tissues. Using an RNase protection assay, we have now determined the amount of each subtype mRNA in human prostatic tissue, for both benign prostatic hypertrophy (BPH) and non-BPH. In all tissue samples examined, the predominant subtype mRNA was alpha 1a. The total abundance of alpha 1-adrenoceptor mRNA in BPH samples was over six times that in non-BPH samples. This increase was mostly accounted for by alpha 1a, which was almost nine times as abundant in BPH samples as in non-BPH samples. The abundance of alpha 1b was almost the same between BPH and non-BPH samples, and the abundance of alpha 1d in BPH samples was about three times that in non-BPH samples. The ratio of the numbers of the subtype mRNAs, alpha 1a: alpha 1b: alpha 1d, was 85:1:14 in BPH samples and 63:6:31 in non-BPH samples. 2. In situ hybridization studies showed no significant differences in the tissue localization of alpha 1-adrenoceptor subtype mRNAs between BPH and non-BPH samples. alpha 1a and alpha 1d were clearly detected in the interstitium of the prostate, where alpha 1a was stained more intensely than alpha 1d, and the positive sites were primarily smooth muscle cells. In contrast, alpha 1b staining was very faint. 3. This increase in mRNA abundance may be directly related to the contraction of prostatic tissue that leads to obstruction of the urinary tract in BPH patients. Specifically, our data suggest that increased expression of the alpha 1a subtype may be primarily responsible for the contraction of the prostate.

Aged↗
PubMed1987

[Diagnosis of combined myocardial ventricular hypertrophy using precordial mapping. I. Selection of the most informative cartogram leads in the diagnosis of combined myocardial hypertrophy].

On the basis of verified material (136 patients with combined myocardial hypertrophy--CMH, 39 with left ventricular hyperthrophy, 57 with right ventricular hyperthrophy and 71 normal subjects) a principally new approach to computerized quantitative analysis of the EKG data has been worked out. Results of study of the informative value of 35 praecordial EKG in the diagnosis of CMH are presented. The authors propose to use the amplitude and area of S and R waves as well as their sum calculated with the use of non-traditional leads. This method makes it possible, when CMH differs from the norm, to increase the sensitivity of the electrocardiography up to 86.8% and its specificity up to 91.5%, which is more effective than the traditional Sokolov-Lyon criteria (sensitivity of 64% and specificity of 87.3%). Nevertheless, these characteristics are ineffective in differential diagnosis because increase in these values can be observed also by isolated hyperthrophy.

Cardiomegaly↗