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PubMed2000

Ventricular arrhythmias and left ventricular hypertrophy in essential hypertension.

BACKGROUND: Patients with essential hypertension and/or left ventricular hypertrophy and ventricular arrhythmias suffer from an increased mortality rate. In all previous studies on hypertension, the criterion for inclusion was diastolic blood pressure > 95 mmHg. This is a low selective threshold. Our study attempted to evaluate the incidence of ventricular arrhythmia in hypertensive patients not receiving pharmacological treatment and diagnosed by 24-h ambulatory blood pressure monitoring (ABPM), therefore using a more selective criterion than WHO guidelines. METHODS: Hundred-twenty-height consecutive patients with hypertension diagnosed on the basis of WHO guidelines were screened for 24-h ambulatory blood pressure measurement. Eighty-five (66.4%) presented a 24-h mean blood pressure > 135/85 mmHg. All 85 patients were screened for M-mode, B-mode echocardiography, PW Doppler and 24-h ECG Holter recordings. RESULTS: Sixty patients (70.6%) were affected by left ventricular hypertrophy and 25 were free (29.4%). Thirty-six patients (42.4%) had left ventricular diastolic dysfunction, 49 were free (57.6%). According to Lown and Wolf's classification of ventricular arrhythmia, 20 patients (23.5%) presented Grade I arrhythmia, 5 (5.9%) presented Grade II, 4 (4.7%) Grade III, 9 (10.6%) Grade IVA, 20 (23.5%) Grade IVB, 12 (14.1%) Grade V and 15 patients (17.6%) were free from premature ventricular complexes, namely Grade 0 arrhythmia. Left ventricular hypertrophy was found to correlate significantly with the arrhythmia score, r = 0.552 for p < 0.0001. Moreover, left ventricular diastolic dysfunction correlated significantly with the arrhythmia score, r = 0.495 for p < 0.0001. There was also a good correlation between left ventricular hypertrophy and left ventricular diastolic dysfunction, r = 0.616 for p < 0.0001. Among patients affected by left ventricular diastolic dysfunction and left ventricular hypertrophy, the correlation with the arrhythmia score was even closer, r = 0.586 for p < 0.0007. CONCLUSIONS: We conclude that by using a more selective criterion for the diagnosis of hypertension, we can identify patients with a highly significant statistical correlation between left ventricular hypertrophy and ventricular arrhythmia score, and also between diastolic dysfunction and the ventricular arrhythmia score, due to a more severe stage of disease. It is useful to detect those patients affected by ventricular arrhythmias for the primary prevention of major cardiovascular events.

Adult↗
PubMed2002

New insights into the mechanism of the elevation of plasma brain natriuretic polypeptide levels in patients with left ventricular hypertrophy.

BACKGROUND: Messenger RNA of brain natriuretic polypeptide (BNP) is detected in both the atrium and the ventricle in vitro. Clinical usefulness has been shown in assessment of BNP level in patients with left ventricular hypertrophy; however, few studies have reported the role of the atrium and ventricle separately in the secretion of BNP from the hypertrophied heart. OBJECTIVE: To investigate how the atrium and ventricle secrete natriuretic peptides by comparing the regional concentration of atrial natriuretic polypeptide (ANP) or BNP in the hypertrophied heart with clinical parameters. PATIENTS AND METHODS: ANP and BNP were measured in blood samples from the aortic root, the anterior interventricular vein (AIV) and the coronary sinus in 12 control subjects, 10 subjects with hypertensive hypertrophy and eight with non-obstructive hypertrophic cardiomyopathy. The difference in concentration between the aortic root and the AIV and that between the AIV and the coronary sinus was calculated to estimate ventricular and atrial secretion, respectively. RESULTS: Plasma BNP levels correlated significantly with left ventricular mass index, pulmonary artery wedge pressure, stroke volume and left atrial dimension. Stepwise multiple regression analysis identified BNP from the atrium, not the ventricle, as an independent predictor of left ventricular mass. CONCLUSIONS: These data suggest that atrium-derived BNP is a significant predictor of left ventricular mass index in patients with left ventricular hypertrophy. The atrium-derived component contributes significantly to the elevation of plasma BNP level, reflecting atrial pressure and volume loading in left ventricular hypertrophy without systolic dysfunction.

Adult↗
PubMed2000

[Clinical analysis of 20 cases of adenoidal hypertrophy in adult].

OBJECTIVE: To discuss the diagnosis and properly treatment to the adult adenoidal hypertrophy. METHOD: To do nasal endoscopic and pathologic exam to all the 20 symptomatic patients before conservative or operative treatment. RESULT: The results of exam under endoscope were that 8 patients were hypertrophy I, 8 hypertrophy II, 4 hypertrophy III. Pathologic exam: 7 acute and chronic inflammation, 13 chronic inflammation with hyperplasia. TREATMENT: 10 of them received conservative treatment all have negative result. 6 received traditional operation, 2 of them reoccurred within 1 year. 4 received adenoidectomy and microwave treatment under nasal endoscope, all have good result in the next 1 year. CONCLUSION: Some adults have different sizes of adenoidal hypertrophy. This hypertrophy is different with children's under the pathologic microscope. Operative treatment especially the nasal endoscopic adenoidectomy and microwave treatment is a safe and effective method.

Adenoidectomy↗
PubMed2003

[Differences in clinical and histopathologic features between chronic adenotonsillitis and chronic adenotonsillar hypertrophy].

OBJECTIVES: This study sought to determine the clinical and histopathological differences between chronic adenotonsillitis and chronic adenotonsillar hypertrophy. PATIENTS AND METHODS: This prospective study included 286 patients (147 males, 139 females; mean age 16.6 years; range 3 to 45 years) with chronic adenotonsillitis and 197 patients (98 males, 99 females; mean age 9.5 years; range 2 to 18 years) with adenotonsillar hypertrophy. Clinical and histopathological findings were compared. RESULTS: The mean age was significantly higher (p<0.001) and acute attacks of fever, dysphagia, and sore throat were more frequent in chronic adenotonsillitis. Patients with adenotonsillar hypertrophy more commonly manifested snoring, mouth breathing, and dispnea. Physical examination showed hyperemia of the anterior plica in 93% and 15% in chronic adenotonsillitis and adenotonsillar hypertrophy, respectively. Histopathologically, the former was more commonly associated with severe lymphocyte infiltration to surface epithelium, surface epithelial defects, plasma cells, atrophy, and fibrosis. The sole outweighing difference in favor of chronic adenotonsillar hypertrophy was increased germinal centers. CONCLUSION: Clinical and histopathologic findings suggest that chronic adenotonsillitis and chronic adenotonsillar hypertrophy may be diverse diseases requiring different approaches in treatment.

Adenoids↗
PubMed1992

Effects of enalapril and hydralazine treatment and withdrawal upon cardiovascular hypertrophy in stroke-prone spontaneously hypertensive rats.

OBJECTIVE: To test the hypothesis that effects of angiotensin converting enzyme (ACE) inhibitors upon resistance vessel structure are responsible for their ability to cause long-term reduction in blood pressure. DESIGN: Stroke-prone spontaneously hypertensive (SHRSP) and Wistar-Kyoto (WKY) rats were treated with enalapril or hydralazine from 4 to 15 weeks of age. Effects upon tail-cuff blood pressure, left ventricular hypertrophy and structural indices of the superior mesenteric artery (SMA) and its resistance vessels were assessed at 11 weeks of treatment and up to 11 weeks post-treatment. METHODS: Left ventricular hypertrophy was assessed by left ventricular weight:body weight ratios. Evidence of vascular structural change was obtained from tissue weight:body weight ratios, levels of RNA, DNA and expression of alpha-actin and elastin messenger (m)RNA. RESULTS: The effects of enalapril and hydralazine upon left ventricular hypertrophy in SHRSP were consistent with their respective effects upon blood pressure. Both drugs prevented the development of medial hypertrophy in SMA and resistance vessels. This was accompanied by substantial reductions in RNA:DNA ratios. Alpha-actin mRNA levels were not affected by either drug but elastin mRNA levels were reduced by both drugs. During the first 12 days post-treatment there was evidence of structural change in SMA accompanying the increases in blood pressure but importantly not in the resistance vessels. CONCLUSION: The effects of enalapril upon left ventricular hypertrophy and mesenteric arterial hypertrophy are totally consistent with responses to blood pressure and the persistence of structural changes post-treatment does not underlie the ability of the ACE inhibitors to persistently suppress hypertension.

Animals↗
PubMed1992

Greater incidence of electrocardiographic left ventricular hypertrophy in black men than in white men in Evans County, Georgia.

Population-based studies of black populations in the United States and Puerto Rico have reported higher prevalences of electrocardiographic left ventricular hypertrophy compared to white or lighter-skinned populations residing in the same areas. This study examines the incidence and correlates of electrocardiographic left ventricular hypertrophy in a population-based, biracial cohort of 435 white and 163 black men from the Evans County, Georgia, Heart Study, who were examined at entry in 1960 and reexamined in 1967. Only men over 35 years of age who were free of cardiovascular disease and had normal electrocardiograms at entry were eligible. Black men had a nearly fourfold greater incidence of electrocardiographic left ventricular hypertrophy compared to white men (13.5% vs 3.7%, respectively; incidence ratio 3.7; 95% CI 3.2-4.4). After statistically adjusting for age, systolic blood pressure, weight, and the change in weight and blood pressure, black men had a threefold greater incidence of electrocardiographic left ventricular hypertrophy compared to white men (logistic odds ratio 3.0; 95% CI 1.6-6.1). In summary, black men showed a significantly greater risk of developing electrocardiographic left ventricular hypertrophy at 7-year follow-up in Evans County compared to their white counterparts. This elevated risk could not be explained by the independent or joint effects of risks factors for electrocardiographic left ventricular hypertrophy.

Adult↗
PubMed2004

[Relationship between adenoids hypertrophy and secretory otitis media].

OBJECTIVE: To investigae the cause of secretory otitis media resulting from adenoids hypertrophy and the relationship between adenoids hypertrophy and secretory otitis media. METHOD: According to the grades of adenoids hypertrophy, 140 children were divided into two groups: the group of middle-grade and the group of pathological hypertrophy. The effect about the degree of adenoids hypertrophy resulted in the descendent of middle ear function and the difference of incidence of secretory otitis media were analyzed. RESULT: The incidence of secretory otitis media and the pattern of tympanic press were distinct difference in two groups. CONCLUSION: The results suggested that there was a positive correlation among the grades of adenoids hypertrophy, the descendent degree of middle ear function and the incidence of secretory otitis media.

Adenoids↗
PubMed2004

Diagnostic usefulness of postexercise systolic blood pressure response for detection of coronary artery disease in patients with echocardiographic left ventricular hypertrophy.

BACKGROUND: Although exercise-induced electrocardiographic ST segment changes are used to detect coronary artery disease (CAD), their diagnostic value is markedly decreased in patients with left ventricular (LV) hypertrophy. There have been no reports concerning postexercise systolic blood pressure (SBP) response in patients with ultrasound echocardiographic (UCG) LV hypertrophy and CAD. METHODS: Sixty-six patients with both UCG-LV hypertrophy (LV mass index 134 g/m2 or greater for men or 110 g/m2 or greater for women) and positive ST depression of at least 0.1 mV during treadmill exercise testing were studied. Coronary cineangiograms showed normal coronary arteries in 19 patients (group 1) and significant CAD in 47 patients (group 2). The SBP ratio was calculated by dividing the SBP 3 min after exercise (3 min SBP) by the SBP at peak exercise (peak SBP). RESULTS: There were no significant differences between the two groups in LV mass index, SBP at rest, exercise duration, ST depression (at rest and exercise-induced) or 3 min SBP. However, the SBP ratio was significantly higher in group 2 compared with group 1 (0.87+/-0.11 versus 1.01+/-0.18; P=0.004). Analysis of relative cumulative frequency distributions revealed an SBP ratio of 0.92 as the cutoff point for distinguishing a UCG-LV hypertrophy patient with CAD from one without CAD. The sensitivity, specificity and accuracy with an SBP ratio of 0.92 and an ST segment depression of at least 0.1 mV on treadmill exercise testing for detecting CAD in patients with UCG-LV hypertrophy were 77%, 74% and 76%, respectively. CONCLUSION: These findings suggest that the ratio of early post-exercise SBP to peak exercise SBP may be diagnostically useful in detecting CAD in patients with positive ST depression during an exercise test and UCG-LV hypertrophy.

Adult↗
PubMed2005

[Assessment of coronary reserve in patients with hypertensive disease and without hypertrophy left ventricular].

AIM: To study relationship between coronary reserve and left ventricular geometry. METHOD AND MATERIAL: Transesophageal cardiac pacing was carried out in 53 patients with hypertensive disease. Thirty five patients (66%) had left ventricular hypertrophy which was eccentric in 16 and concentric in 19. RESULTS: Myocardial ischemia was induced during pacing in 79.2% of patients; it was painful in 45.2 and painless -- in 54.8% of patients. Test with esophageal pacing was positive in 91.4 and 55.6% of patients with and without left ventricular hypertrophy, respectively. In patients with concentric hypertrophy frequency of positive tests was higher and level of coronary reserve lower than in patients with eccentric left ventricular hypertrophy. There was negative correlation between pacing rate at myocardial ischemia induction and left ventricular myocardial mass index. Painless ischemia was more frequent among patients with left ventricular hypertrophy. Twelve of 42 patients (28.3%) with positive result of pacing had no clinical signs of ischemic heart disease. CONCLUSION: Left ventricular hypertrophy limits coronary reserve, increases prevalence of painless myocardial ischemia. Transesophageal pacing enables detection of preclinical signs of lowered coronary reserve.

Adult↗
PubMed2005

Reversal of left ventricular hypertrophy by propranolol in hypertensive rats.

BACKGROUND: Hypertension contributes significantly to the development of left ventricular hypertrophy. Left ventricular hypertrophy is associated with increased incidence of sudden cardiac death. Recognition and management of hypertension is, therefore, imperative. OBJECTIVE: To establish whether propranolol can reverse left ventricular hypertrophy in hypertensive rats. METHODS: Hypertension was induced in male albino rats by giving them 1% NaCl solution as their only drink for four weeks. Propranolol was then administered orally to one of the four groups of rats used in this study. Systolic blood pressure of each rat was measured twice a week using a modified tail-cuff method. Each rat was then sacrificed, its heart excised from the chest cavity and geometric studies carried on the left ventricle. RESULTS: Excessive intake of sodium salt by the rats caused an increase in their systolic blood pressure which was accompanied by left ventricular hypertrophy. The elevated blood pressure (139.4 +/- 0.5 mm Hg) was, however, brought back to normal (108.4 +/- 0.2 mm Hg) by propranolol. Data on weight, thickness, and volume of the left ventricle strongly indicated that propranolol can reverse ventricular hypertrophy. CONCLUSION: Propranolol reverses left ventricular hypertrophy besides lowering elevated systolic blood pressure in rats.

Adrenergic beta-Antagonists↗
PubMed2005

[Relationship between the inhibitory effects of PNS on cardiac hypertrophy and its action on neurohormonal factor].

OBJECTIVE: To study the effects of total saponins of Panax notoginseng (PNS) on the overall model and vitro model of cardiac hypertrophy, and investigate the mechanism of its action. METHOD: Cardiac hypertrophy of rats due to pressure overload was induced by constricting of abdominal aorta. The rats were given ip PNS for three weeks after operation. Three weeks later, the systolic blood pressure (SBP), heart weight (HW), left ventricular weight (LVW), the ratio of HW/BW, LVW/BW (LVI) and the myofibril diameters (MD) in left ventricles were measured. Cardiac hypertrophy was induced by norepinephrine (NE) in cultured neonatal rat myocardial cells. PNS were given to the cultured myocardial cells, 72 hours later, the cell surface area and protein content (used as the index of cardiac hypertrophy) were determined. RESULT: PNS inhibited the markers of cardiac hypertrophy in rats (HW/BW, LVI, MD) in a dose dependent manner, but SBP of rats wasn't obviously influenced; 0.1-0.5 g x L(-1) PNS significantly inhibited the NE induced increase of surface area and protein content in the cultured myocardial cells, P < 0.01. CONCLUSION: PNS can prevent the overall model and vitro model of cardiac hypertrophy in rats, and this action may be related to its inhibitory action on neurohormonal factor NE, but not on pressure overload.

Animals↗
PubMed2006

Effect of eicosapentaenoic acid on the different endothelin system components in endothelin-1-induced hypertrophied cardiomyocytes.

The cardiovascular benefit of fish oil, including eicosapentaenoic acid (EPA), in humans and experimental animals has been reported. The role of endothelin-1 (ET-1) in cardiac hypertrophy is well known. Endothelin-1 stimulates prepro-ET-1 mRNA expression in cardiomyocytes, and the autocrine/paracrine system of ET-1 is important for cardiomyocyte hypertrophy. Although many studies link EPA to cardiac protection, the effect of EPA on cardiac hypertrophy has yet to be clarified. Recently, we demonstrated that ET-1-induced cardiomyocytic change could be prevented by pretreatment with EPA. The present study investigated the changes of different components of the ET system at the mRNA level in ET-1-administered cardiomyocytes, and examined the effect of EPA pretreatment. Ventricular cardiomyocytes were isolated from 2-day-old Sprague-Dawley rats, cultured in Dulbecco's modified Eagle's medium and Ham F12 supplemented with 0.1% fatty acid-free bovine serum albumin for 3 days. At Day 4 of culture, the cardiomyocytes were divided into 3 groups: control group, ET-1-treated (0.1 nM) group, and ET-1-treated group pretreated with EPA (10 microM). Twenty-four hours after treatment, the gene expressions of different components of the endothelin system in three experimental groups were evaluated by real-time polymerase chain reaction. Prepro-ET-1 mRNA expression was 53% upregulated in ET-1-induced hypertrophied cardiomyocytes and suppressed in the EPA-pretreated group. Endothelin-converting enzyme-1 (ECE-1) was also increased in ET-1-administered cardiomyocytes by 42% compared with the control group and was reversed in the EPA-pretreated group. The two receptors of ET system, ET(A) and ET(B), tended to be increased in the ET-1-treated group, but no statistical significance was seen among study groups. Endothelin-1 increased prepro-ET-1 and ECE-1 mRNA expression in hypertrophied-neonatal cardiomyocytes, and this was reversed with EPA pretreatment. Thus, EPA may play a crucial role in the regression of ET-1-induced cardiomyocyte hypertrophy, partly through the suppression of ET-1 and ECE-1 expression.

Animals↗
PubMedDate not supplied

The prevalence of microalbuminuria and ECG left ventricular hypertrophy in hypertensive patients in private practices in South Africa.

INTRODUCTION: In South Africa a cluster of cardiovascular diseases accounts for 17% of all deaths. It is also predicted that South Africa will face an epidemic of chronic kidney disease due to obesity, type 2 diabetes and hypertension. It is important to estimate the burden of underlying cardiovascular and renal disease in South Africa. OBJECTIVES: The primary objective of the study was to establish the prevalence of left ventricular hypertrophy by ECG criteria, and micro- and macroalbuminuria in mild, moderate and severe hypertensive groups. The secondary objective was to establish the prevalence of left ventricular hypertrophy and micro- and macroalbuminuria in hypertensive patients with underlying type 2 diabetes. METHODS: Patients > or = 35 years with essential hypertension with or without type 2 diabetes were recruited from 100 general practices throughout South Africa. BP, weight, height, waist circumference and urinary albumin/creatinine ratio were measured, and an ECG was performed. The Sokolow-Lyon and Cornell criteria were used for estimation of left ventricular hypertrophy. An overall prevalence rate was determined using weights from the severity category distribution inside the study population. RESULTS: One thousand and ninety-one patients were available for analysis. There were 530 (48.5%) males and 561 (51.5%) females, 691 (63.3%) whites, 162 (14.8%) blacks, 150 (13.7%) Asians and 88 (8.1%) Coloureds. Of the patients, 10.9% had newly diagnosed hypertension, 20% had type 2 diabetes, and 38.1% mild, 32.1% moderate and 30.6% severe hypertension. The prevalence of left ventricular hypertrophy in the sample weighted to the hypertensive population over the age of 35 years with access to medical aids was 18.9%. Relative to white ethnicity, black ethnicity (OR 2, p = 0.03), and relative to mild hypertension, moderate (OR 2.2, p = 0.05) and severe hypertension (OR 4.9, p < 0.0001) were independent predictors of left ventricular hypertrophy. The overall prevalence of micro- and macroalbuminuria in the weighted sample was 21.3 and 4.1%, respectively. In the diabetics the prevalence of microalbuminuria was 32.3% and macroalbuminuria 10.4%, respectively. The independent predictors of microalbuminuria or worse were severe hypertension (OR 2.9, p < 0.0001), type 2 diabetes (OR 2.5, p < 0.002), and Asian ethnic group (OR 2, p = 0.02). CONCLUSIONS: The study, based on a convenience sample of hypertensives from private practices in South Africa showed that the prevalence of left ventricular hypertrophy and microalbuminuria or worse was 18.9 and 25.4%, respectively.

Adult↗
PubMed1990

Renal hypertrophy, growth factors, and nephropathy in diabetes mellitus.

In early type 1 diabetes mellitus, hypertrophy of the kidney is a consistent finding. It is easily diagnosed using current noninvasive methods, especially ultrasonography. Renal functional changes occur in association with hypertrophy, most notably glomerular hyperfiltration. The structural counterpart of this functional change is an early increase in capillary filtration surface area. In most forms of nondiabetic renal hypertrophy, kidney size is closely linked to GFR, but in diabetes, hypertrophy persists after the clinical onset of overt kidney disease (microalbuminuria, hypertension, decreased GFR, etc). The fact that growth factors produced by the kidney can act in both an autocrine and paracrine fashion raises the possibility that the local effects of such substances may act as local mediators of kidney growth, but no such factor has been identified as the initiating or sustaining factor in diabetic hypertrophy. Failure of renal hypertrophy to reverse following strict glycemic control for a few months may turn out to be an important prognostic indicator of future progression of the renal disease, but this remains to be studied in a large group of patients.

Animals↗
PubMed1990

[An assessment of the relative contribution of the processes of cellular proliferation, polyploidization and hypertrophy to the increase in liver mass at various stages in the postnatal development of rats].

Changes in isolated hepatocyte dry mass, its ploidy and liver mass at different stages of the rat postnatal ontogeny were investigated. The determination of these processes and special calculation made it possible to estimate quantitatively a relative contribution of cell proliferation, polyploidization and hypertrophy, not associated with DNA synthesis to the increase in the liver mass at different stages of the rat development. During the first week after the rat's birth, its liver growth is provided by 61 and 39% with hepatocyte proliferation and hypertrophy, respectively. Between the 14th and the 21st days of development, when considerable functional changes occur in the rat liver, the contributions of proliferative and polyploidization processes, and of cell hypertrophy into the liver mass increasing are roughly identical. Later on, the contribution of cell hypertrophy into the liver growth is noticeably reducing to reach within 1-2 months only 1%. On this developmental stage the liver mass increment by 2/3 is provided due to cell proliferation and by 1/3--to its polyploidization. As a whole, the accelerated growth of the rat liver from the birth to sex puberty is described as follows: the contribution of processes of proliferation and polyploidization, and of cell hypertrophy correspond to 28, 30 and 42%, respectively; afterwards, the liver growth being retarded. Within the period from 2 to 6 months, the liver mass increase is provided mainly (up to 76%) by cell proliferation, the shares of polyploidization and cell hypertrophy being 8 and 16%, respectively.

Aging↗
PubMed1989

[A case of sciatica with hypertrophy of the calf].

Hypertrophy of the calf associated with sciatica is rare. In the present case there was hypertrophy, predominantly of type I fibers, which showed a high percentage to the detriment of type II fibers. In the previously reported cases, the type of hypertrophied fibers was variable and pseudomyotonic discharges were inconstantly recorded. The mechanism underlying the hypertrophy is unknown. Inequality of size of muscle fibers could result from proximity of atrophic fibers and those with compensatory hypertrophy. The increased proportion of type I fibers could be the consequence of compensatory hypertrophy induced by lesions of synergic muscles and/or muscle compartments.

Female↗
PubMed1983

Dissociation of effects of hypertrophy from hypertension on cardiac beta-receptors in renovascular hypertensive rats.

Reduction in density of beta-adrenoceptors has been demonstrated in the hypertrophied left ventricle (LV) of renovascular hypertensive rats (RHR). In order to investigate the relative role of cardiac hypertrophy as distinct from hypertension, LV beta-receptors were determined in RHR four days after nephrectomy of the clipped kidney (RHR-Nx) when blood pressure was reduced but hypertrophy still evident; the results were compared with those obtained in age-matched untreated RHR and sham operated rats (SHAM). As expected, blood pressure (BP) was reduced four days after nephrectomy (150 +/- 3 versus 212 +/- 11 mmHg untreated RHR, P less than 0.001) but LV hypertrophy had not regressed (3.07 +/- 0.16 versus 3.58 +/- 0.24 mg/g, NS). Ventricular beta-receptor density was reduced in both RHR (1.601 +/- 0.078 pmol/g) and RHR-Nx (1.667 +/- 0.124 pmol/g) compared with SHAM (2.033 +/- 0.06 pmol/g, P less than 0.05 for both). The dissociation constant (Kd) was not different among the three groups. Thus, the reduction of beta-adrenergic receptors in the hypertrophied LV of RHR persisted even when BP was lowered by nephrectomy, suggesting that hypertrophy per se rather than hypertension accounted for that reduction in cardiac beta-receptors.

Animals↗
PubMed1995

[Is reversal of left ventricular hypertrophy a priority in patients with hypertension?].

Left ventricular hypertrophy is frequent in hypertension although there is no close correlation between the level of blood pressure and the cardiac mass. The HYCAR study has shown a dissociation in the reversibility of left ventricular hypertrophy: ramipril at doses of 1.25 or 5 mg per day reduces left ventricular mass independently of its effects on the blood pressure. Nevertheless, it remains to be shown by a prospective study that the reduction of the blood pressure and the cardiac mass have additional benefits in the prevention of coronary artery disease in hypertensive subjects. In the meantime, two points resume the objectives of treatment of hypertension with respect to left ventricular hypertrophy and coronary risk. Firstly, prevention of left ventricular hypertrophy is better than its cure. Early prevention is based on accurate measurement and interpretation of the blood pressure according to international recommendations. Prevention necessitates good control of the blood pressure and it would appear to be particularly effective in patients who respond well to angiotensin converting enzyme inhibitors. Secondly, when left ventricular hypertrophy is present, it is possible to reduce the left ventricular mass: however, it remains to be seen whether this is accompanied by a normalisation of structure and function. This requires control of the blood pressure using either an angiotensin converting enzyme inhibitor in good responders to this family of drugs or another type of antihypertensive agent. In the latter case, the association of a low dose of ramipril may be envisaged when left ventricular hypertrophy persists despite good control of the blood pressure. This hypothesis requires testing with an appropriate prospective therapeutic trial.

Animals↗