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PubMedDate not supplied

The diffuse hypertrophy of the lower esophagus and the focal hypertrophy of the pyloric musculature in adults.

The diffuse hypertrophy of the lower esophagus is a hypertrophy and hyperplasia of the smooth muscle fibres of the M. propria, together with a distortion of the muscular architecture. The esophagogram reveals an impaired peristalsis and expansile ability of the esophagus lumen. The focal hypertrophy of the pyloric musculature in adults is a locally circumscribed hypertrophy and hyperplasia of the M. propria. The concentric pattern of the M. propria is no longer maintained. Radiologically one recognizes a benign pylorus stenosis with a complete systole and an impaired diastolic dilatation. On the basis of these macroscopical, microscopical and radiological findings both lesions differ from the circular pyloric or esophageal stenosis which occurs at the same anatomical sites. We therefore feel, that both lesions are different entities.

Adult↗

PubMed1976

[Ulcer location in the stomach and pylorantral hypertrophy: problem of correlation of the ulcer location and wall hypertrophy in ulcus ventriculi].

Relationship between gastric ulcer (n = 100) site and antropyloric wall hypertrophy was examined in a prospective study. Irrespective of ulcer multiplicity most ulcers were found to be located at the lesser curvature and at the posterior wall (p less than 0,001); men had significantly more ulcers at the posterior wall than females (p less than 0, 001). Single ulcers and those connected with pyloric stenosis were more distant to the pylorus than multiple ulcers (p less than 0,001). Ulcer location did not relate to hypertrophy of the pyloric channel wall. Observed differences between single and multiple ulcers were limited to wall parts only: the musculature of high located single ulcers was significantly less hypertrophied 2,5 cm orally of the pylorus (p less than 0,02) and that of high multiple ulcers was more hypertrophied at the pylorus (p less than 0,02) than in the other parts. These findings suggest that ulcer variations do not influence the diffuse antropyloric disease in gastric ulcer patients and suggest that the generalized antral changes are prior to gastric ulcer occurance.

Female↗

PubMedDate not supplied

Different fractions in the normal and hypertrophied rat ventricular myocardium: an analysis of two models of hypertrophy.

Long-term hemodynamic overload of the heart leads to an increase in myocardial mass. In most cases it is not known to what degree the single components in the myocardium (water, protein, nonprotein substance) increase. As an answer to the overloading of the myocardium, many authors have established an intensification in the synthesis of myocardial proteins. It is, however, little known which proteins are then more intensively created and accumulated. This study examines the dynamics of the protein and nonprotein content as well as of single protein fractions (sarcoplasmic, myofibrillar, and stromal) in both hypertrophied and normal tissue from rat myocardia. The results revealed that in Goldblatt rats, 4-24 weeks after stenosis of one renal artery, no noteworthy differences in the relationships of protein and nonprotein content were caused by hypertrophy (34-54%) due to left ventricular pressure overload. The same is true of the tissue from moderately hypertrophied myocardia (12-17%) of rats exercised for several weeks by swimming training. Determination of hydroxyproline concentration showed that significant differences in the content of the collagen tissue in relation to control animals of the same age occurred only in Goldblatt rats 24 weels after operation. However, greater alterations in the concentrations of various protein fractions could be registered. The increase in the concentration of myofibrillar proteins in hypertrophied myocardial tissue is of particular significance and is to be considered as an adaption of the muscle to the increased mechanical demands. Certain changes regarding the relation of the single components within the myofibrillar fraction (relation of actomyosin concentration to T-fraction; relation of both components to total fraction), whose cause and significance is as yet unclear, could be observed.

Animals↗

PubMedDate not supplied

Differences between transmitter depletion in human heart hypertrophy and experimental cardiac hypertrophy in Goldblatt rats.

The transmitter depletion of the myocardium in hypertrophy and especially insufficiency has formerly been attributed to a decrease of certain enzymes that are involved in the neurotransmitter synthesis. However, we could show in human auricles recently that one main reason for the catecholamine depletion is the distension of the adrenergic ground plexus in the course of hypertrophy of the myocardial muscle cells. At the same time, electron microscope investigations revealed various changes of the axonal ultrastructure, especially in heart insufficiency. Additional experimental work in renal hypertension of rats should answer the question whether this process occurs also in other parts of the heart and whether it can be followed sequentially during the development of hypertension. In this preliminary report about these studies, attention is drawn to focal transmitter depletion in areas of severe vascular necrosis and inflammation, especially in the right ventricular wall. During the first three months after the beginning of the experiment, the total noradrenaline content decreased only slightly, whereas the concentration of this transmitter is lowered significantly by myocardial growth in both ventricles. It is concluded that there are essential differences between hypertrophy in experimental renal hypertension and human cardiac hypertrophy.

Adrenergic Fibers↗

PubMed1983

Cardiac hypertrophy in rats after supravalvular aortic constriction. II. Inhibition of cellular autophagy in hypertrophying cardiomyocytes.

Adult male Sprague-Dawley rats were killed by retrograde perfusion fixation 3, 7, 14, 21 and 35 days after supravalvular aortic constriction (n = 33) or sham-operation (n = 25). Subepicardial specimens of the left ventricular myocardium were evaluated by conventional electron microscopic morphometry, and in addition were examined for the occurrence of autophagic vacuoles (AVs) using large test areas (3.9 X 10(4) micron 2 per animal). The quotient of mitochondrial to myofibrillar volume fraction was largely unchanged during hypertrophy but was reduced by 25% compared with controls after termination of growth at 35 days. During the process of hypertrophy which eventually led to an increase in average single cell volume of the cardiomyocytes by 78%, the volume fraction and the numerical density of AVs was significantly lower than in sham-operated rats. The most striking difference was observed 7 days after the operations, the stage at which the growth rate of the cardiomyocytes relative to controls was at its maximum of 4.5% per day. At this point the volume fraction as well as the numerical density of AVs were reduced by about 50% compared with controls. At 14 and 21 days after operation, when the relative growth rate of the hypertrophying cardiomyocytes was still 2% and 1% per day, the AV volume fraction was reduced to a lesser extent (by 47% and 28%, respectively). After termination of adaptive growth at 35 days significant differences in fractional volume and numerical density of AVs were no longer detectable. These results suggest that degradation of cytoplasmic components is inhibited in cardiomyocytes undergoing hypertrophy. Such an anticatabolic reaction seems to play an important role in establishing the positive balance of cellular metabolism generally required for growth processes.

Animals↗

PubMed1981

Electrocardiographic differentiation of posterobasal left ventricular hypertrophy from right ventricular hypertrophy.

Increased terminal rightward forces manifested by S waves greater than the 95th percentile (95%) for age in the left chest leads of the ECG can be produced by right ventricular hypertrophy (RVH) and posterobasal left ventricular hypertrophy (LVH). There are no currently available criteria to differentiate these. The S wave in lead V5 exceeded the 95% for age in 445 of 5,240 patients (8.5%). From these, the ECGs of patients with lesions known to produce "isolated" RVH (46 patients) or LVH (38 patients) were chosen for study. Analysis of these ECGs revealed two patterns in each group: 1. Voltage criteria for ventricular hypertrophy other than SV5 & SV6 were present in 26 patients of the RVH group and 15 of the LVH group; 2. The ECGs of the remaining 20 of the RVH and 23 of the LVH group contained no other voltage criteria to diagnose either RVH or LVH. These 43 ECGs were further analyzed. SV5, SV6 and RV5 were similar in both groups (p greater than 0.01). However, SI, R'V4R, R'V1 and the ratio RV2/SV2 were higher (p less than 0.01) and SV2 was lower (p less than 0.01) in the RVH group. Despite significant differences, there was marked overlap of the data. Therefore, discriminant analysis was performed which suggested RVH if SI greater than 5mm, RV2 greater than 10mm and the ratio RV2/SV2 greater than 0.65, and LVH if SI less than 5 mm, RV2 less than 10mm and the ratio RV2/SV2 less than 0.65. In the frontal plane the mean QRS vector was similar; however, in the horizontal plane, it varied between +60 degrees to +200 degrees in the RVH group and between -10 degrees to -130 degrees in the LVH group. The rotation of the QRS loop in the horizontal plane was clockwise (CW) or figure of eight in RVH group and counterclockwise (CCW) in the LVH group. The orthogonal vector data confirm these results. It is concluded that when SV5 is greater than 95% for age and there are no other clear voltage criteria for ventricular hypertrophy the diagnosis of RVH vs LVH may be made on the basis of the following: RVH: RV2 greater than 10mm, SI greater than 5mm and mean horizontal plane QRS vector between +60 degrees to +200 degrees with a CW or a figure of eight loop and LVH: RV2 less than 10mm, SI less than 5mm and mean horizontal plane QRS vector between -10 degrees to -130 degrees with CCW loop.

Cardiomegaly↗

PubMed1982

Physiologic cardiac hypertrophy corrects contractile protein abnormalities associated with pathologic hypertrophy in rats.

To evaluate the combined effects of cardiac overload imposed by hypertension and by chronic exercise, male and female rats were made hypertensive by unilateral renal artery stenoses and made to exercise in an 8-10-wk swimming program. Sedentary normotensive animals, sedentary hypertensive animals and normotensive animals exposed to the swimming program were also studied. Hypertension was associated with the development of cardiac hypertrophy, and this was exaggerated in hypertensive swimmers. Actomyosin, Ca2+-myosin, and actin-activated Mg2+-myosin ATPase activities were enhanced in normotensive swimmers, depressed in hypertensives and were normal or increased in hypertensive swimmers. Myosin isoenzyme analysis showed a predominant V1 pattern in normals; an increase in percent V1 isoenzyme is swimmers; a predominant V3 pattern in hypertensives; and a return to the predominant V1 pattern in hypertensive swimmers. These findings suggest that the hypertrophy imposed by hypertension and hypertrophy imposed by physical training using a chronic swimming program are distinctly different biological phenomena. Physical training by swimming prevents the changes in cardiac myosin induced by hypertension despite the exaggeration of hypertrophy.

Actomyosin↗

PubMed1990

[Determinants for myocardial hypertrophy in mild essential hypertension. The effect of sodium chloride on left-ventricular hypertrophy].

The impact of clinical parameters on the pathogenesis of myocardial hypertrophy was examined in 75 male patients with mild essential hypertension. Clinical parameters were age, body weight, sodium excretion (as an estimate for dietary salt intake), systolic and diastolic blood pressure at work, casual blood pressure, resting and stress blood pressure during mental stress test and physical exercise. Left ventricular mass as a parameter for the degree of left ventricular hypertrophy was assessed by 2-D guided M-mode echocardiography. Left ventricular mass correlated with body weight (r = 0.47, p less than 0.002), with body mass index (r = 0.48, p less than 0.001), with systolic blood pressure at the worksite (r = 0.28, p less than or equal to 0.05), and systolic blood pressure at rest (r = 0.35, p less than or equal to 0.01), whereas no correlation was found between casual or stress blood pressure readings during physical exercise and mental stress with the degree of left ventricular hypertrophy. Sodium excretion was related to the end-diastolic diameter of the left ventricle (r = 0.33, p less than or equal to 0.01) and to left ventricular mass (r = 0.35, p less than or equal to 0.01). Multiple regression analysis revealed that sodium excretion over 24 hours, systolic blood pressure at the worksite and body mass index were independent determinants of left ventricular mass. Thus, dietary salt intake was found to modulate the degree of left ventricular hypertrophy independently of the pressure load imposed on the myocardium.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1985

[Absence, in the hypertrophied rat heart caused by aortocaval fistula, of several metabolic and electrophysiological changes seen in other models of hypertrophy].

In this work, we compared the electrophysiological and metabolic parameters of a volume overload model of cardiac hypertrophy (aorto-caval fistula) with those of two other models of hypertrophy (aortic stenosis and isoproterenol pretreatment). In these last models, a prolongation of action potential and a decrease of myocardial ATP content are observed. However, these alterations are not shown in the aorto-caval fistulated animals while their heart are well hypertrophied. The amplitude increase of phase 3 AP seemed to be a common factor of these models of cardiac hypertrophy.

Action Potentials↗

PubMed1996

[Differentiation of hypertrophic cardiomyopathy and hypertensive cardiac hypertrophy using the patterns of interventricular septum hypertrophy].

The patterns of interventricular septal hypertrophy were analyzed on two-dimensional echocardiograms to differentiate hypertrophic cardiomyopathy (HCM) from hypertensive cardiac hypertrophy. The control group comprised 110 patients without cardiovascular disease who were matched for age and gender with the hypertension group. The hypertension group comprised 110 patients with uncomplicated essential hypertension, and the HCM group comprised 32 patients in whom the wall thickness of the interventricular septum was 12 mm or more at the mid-portion and no underlying heart disease responsible for cardiac hypertrophy was detected. The interventricular septal thickness was measured both at the thickest portion within 15 mm distal to the aortoseptal junction (basal portion: B) and at the mid-portion (M) in the end-diastolic image on the left parasternal long-axis tomograms, and the B/M ratio was calculated in each patient. The B/M ratio was 1.07 +/- 0.16 in the control group, 1.19 +/- 0.18 in the hypertension group, and 0.83 +/- 0.12 in the HCM group. Compared with the control group, the B/M ratio was significantly high in the hypertension group (p < 0.05) and significantly low in the HCM group (p < 0.01). These results indicate that hypertrophy of the interventricular septum is dominant at the basal portion in hypertensive patients but at the mid-portion in patients with HCM.

Aged↗

PubMed1997

Left ventricular hypertrophy and arterial hypertrophy.

In the most recent WHO recommendations of 1996 it was reiterated that the classification of HT still remains based on the actual BP figures but also on the importance of target organ lesions. Thus the study of cardiac and vascular function and in particular the presence of hypertrophy or remodeling is of importance. A limited number of studies have examined the prevalence, the association and the correlation between modifications and remodeling in the heart and in the vasculature. It is important to distinguish compliance vessels such as the carotid from resistance vessels such as the radial. For compliance vessels the prevalence of cardiac and vascular hypertrophy are nearly identical being around 5% for normotensive subjects and around 12% for hypertensive subjects. This prevalence of thickening in the intima-media is more evident in subjects with left ventricular hypertrophy (LVH). The left ventricular geometric pattern is also an element to take into account. The presence of concentric remodeling of the left ventricle without LVH has already been associated with an increase in intima-media thickness (IMT). When there is an LVH this IMT is similar in severity to the LVH and in particular concentric. For resistance vessels such as the radial artery the number of studies is limited but a significant correlation between left ventricular mean wall thickness and common carotid artery distensibility and compliance has been found. There is also a significant correlation between the radial median lumen ratio and the relative wall thickness but this correlation disappears when age and systolic BP are taken into account. Thus for this type of vessel it is too early to conclude the elements contributing to structural changes. The determinant factors for these structural changes in the heart and the carotid arteries associated with hypertension are certainly multiple be they haemodynamic, hormonal or genetic. The observation establishing an association between anomalies at cardiac and vascular level may have undoubted diagnostic, prognostic and therapeutic implications which are all intimately related and which require refinement and confirmation.

Antihypertensive Agents↗

PubMed1991

Vasopressin-dependent kidney hypertrophy: role of urinary concentration in protein-induced hypertrophy and in the progression of chronic renal failure.

Recent experiments have shown that the kidney adapts to chronic variations in urine concentration. Glomerular filtration rate (GFR), kidney weight relative to body weight, thickness of inner stripe of the outer medulla, volume of epithelium in early thick ascending limb, and internephron heterogeneity are all decreased by chronic water diuresis and increased by chronic stimulation of urine concentration. It was further shown that the intrarenal pattern of hypertrophy observed after high protein (HP) intake, but not that observed after compensatory hypertrophy or normal growth with age, is exactly similar to that observed after chronic stimulation of urine concentration. Since solute-free water reabsorption (TcH2O) is markedly enhanced by HP diet, this suggests that the increases in GFR and renal mass observed after HP intake are, at least in part, an adaptive response of the kidney to increased urinary concentrating activity. The beneficial effects are induced by protein restriction in chronic renal failure (CRF) could thus be due, in part, to the reduction of this concentrating activity. This hypothesis was confirmed by an experiment performed in rats with experimental chronic renal failure (CRF) in which a chronic increase in water intake, reducing urine osmolality and TcH2O, without any change in food composition or consumption, reduced proteinuria, systemic hypertension, kidney hypertrophy, incidence of glomerulosclerosis, and mortality.

Adaptation, Physiological↗

PubMed2002

Physiologic and pathologic myocardial hypertrophy--physiologic and pathologic regression of hypertrophy?

Hypertrophy of the left ventricle is an adaptive phenomenon of ambiguous biological value. It enables improvement of the heart performance without substantial enhancement of energetic demands. On the other hand, pathologic left ventricular hypertrophy (LVH) is characterized by increased fibrosis, diminished coronary flow reserve and protein remodeling, resulting in increased cardiovascular morbidity and mortality. Achievement of LVH regression is thus considered a principal therapeutic aim. However, the reversal of LVH is a very complex process in which both hemodynamic and non-hemodynamic alterations participate. Reversal of LVH does not mean the re-expression of the original genotype and normalization of myocardial structure and function. It does not guarantee that the heart will be normal in all aspects. Regression of hypertrophy induced by different therapeutic means may exhibit different properties and patterns, with variable biological implications. Physiologic growth stimulators seem to induce LVH without prognostically undesirable alterations. It is a challenge to determine which approach to treatment of hemodynamic overload and concomitant LVH is optimal.

Humans↗

PubMed2002

Nurse-recorded and ambulatory blood pressure predicts treatment-induced reduction of left ventricular hypertrophy equally well in hypertension: results from the Swedish irbesartan left ventricular hypertrophy investigation versus atenolol (SILVHIA) study.

OBJECTIVE: To compare the relationships of treatment-induced reductions of left ventricular hypertrophy to the changes in clinic and ambulatory blood pressure (BP). DESIGN: Double-blind and randomized treatment with irbesartan or atenolol for 48 weeks. PATIENTS: Patients with hypertension and left ventricular hypertrophy (n = 66) with a seated diastolic BP 90-115 mmHg (average of three measurements one minute apart by nurses). MAIN OUTCOME MEASURES: Registrations of echocardiographic left ventricular (LV) mass. Clinic and ambulatory BP. RESULTS: In the total material, nurse-measured BP was reduced by 23 +/- 15/16 +/- 7.7 mmHg and 24-h ambulatory BP fell 20 +/- 15/14 +/- 8.5 mmHg by treatment. The correlation between the change in nurse-measured BP and LV mass index (LVMI) induced by treatment was r = 0.35, P = 0.004 for systolic BP and r = 0.26, P = 0.03 for diastolic BP. Corresponding values for 24-h ambulatory BP were r = 0.29, P = 0.02 and r = 0.35, P = 0.004, respectively, with similar correlations for day- and night-time ambulatory BP. The nurse-recorded BP was slightly higher than ambulatory BP (systolic clinic - systolic 24-h ambulatory BP = 5 mmHg). Using 130/80 mmHg as a cut-off value for normal 24-h ambulatory BP, eight subjects had normal diastolic or systolic ambulatory BP, or both. Interestingly, these patients also experienced LVMI regression following treatment (low/normal ABP, -13 +/- 21 g/m2; remaining patients, -18 +/- 22 g/m2, P > 0.5). CONCLUSIONS: In patients with hypertension and left ventricular hypertrophy, ambulatory BP is not superior to carefully standardized nurse-recorded seated BP in terms of associations with treatment-induced changes in LV mass.

Adult↗

PubMed1974

Work-induced hypertrophy in exercised normal muscles of different ages and the reversibility of hypertrophy after cessation of exercise.

1. Groups of male hamsters of different ages were subjected to a weight-lifting exercise regimen, and the biceps brachii, soleus and extensor digitorum longus (EDL) muscles examined for structural changes occurring in response to the increased workload. In addition, two groups of adult hamsters were left to recover from the exercise stimulus for 5 and 15 weeks respectively.2. All the exercised muscles exhibited muscle fibre hypertrophy, and the extent of the hypertrophy was greater in the younger animals. In all age groups, the biceps brachii and EDL showed more hypertrophy than did the soleus. There was no significant increase in fibre number after exercise.3. In both groups allowed to recover from the exercise stimulus, the fibre dimensions reverted back to those of the control muscles; this appeared to be complete after 15 weeks recovery.4. Electron microscopical studies of fibres from exercised and control biceps brachii revealed no significant changes with exercise in the proportions present of myofibrillar, mitochondrial and tubular components within muscle fibres of the same size.

Age Factors↗

PubMed2002

[Effects of praeruptorin C on cell hypertrophy, intracellular [Ca2+]i, nitric oxide and signal transduction in isolated hypertrophied rat smooth muscle cells induced by angiotensin II].

AIM: To investigate the effects of praeruptorin C (Pra-C) on smooth muscle cell (SMC) hypertrophy, intracellular calcium ([Ca2+]i), nitric oxide (NO) content and influence on cellular signal transduction in isolated cultured rat smooth muscle cell (SMC). METHODS: Hypertrophied smooth muscle cells (HSMCs) were induced by angiotensin II (Ang II), cell area was measured under inverted microscope. Nitric oxide (NO) concentration was measured using Griess method. [Ca2+]i was measured using Fura-2/AM. The responses to [Ca2+]i elevation stimulated by KCl (60 mmol.L-1 or norepinephrine (10 mumol.L-1) were observed by incubation with phorbol 12-myristate 13-acetate (PMA), staurosporine (ST), the agonist and inhibitor of protein kinase C (PKC), and pertussis toxin (PTX), the sensitive toxin of Gi. RESULTS: The cell area of SMCs were decreased by 39.01% (P < 0.001) and NO content of SMCs were significantly increased in Pra-C + Ang II group. In presence of 60 mmol.L-1 KCl or 10 mumol.L-1 NE, [Ca2+]i of SMCs in Pra-C + Ang II group was significantly decreased than that of Ang II group (P < 0.001) and closed to the normal group. Incubation of SMCs with PMA, ST and PTX, [Ca2+]i of SMCs in Ang II group was increased by PMA and decreased by ST and PTX, but that of Pra-C + Ang II group was similar to the normal group. CONCLUSION: These findings suggest that Pra-C can reduce vascular hypertrophy in isolated rat HSMCs, and this is associated with improvement of SMCs [Ca2+]i level, NO content and cellular signal transdution of PKC and Gi.

Angiotensin II↗

PubMed1992

Myocyte cellular hypertrophy and hyperplasia contribute to ventricular wall remodeling in anemia-induced cardiac hypertrophy in rats.

To determine the effects of chronic anemia on the functional and structural characteristics of the heart, 1-month-old male rats were fed a diet deficient in iron and copper, which led to a hemoglobin concentration of 4.63 g/dl, for 8 weeks. At sacrifice, under fentanyl citrate and droperidol anesthesia, systolic, diastolic, and mean arterial blood pressures were decreased, whereas differential pressure was increased. Left ventricular systolic pressure and the ventricular rate of pressure rise (mmHg/s) were reduced by 9% and 14%, respectively. Moreover, developed peak systolic ventricular pressure and maximal dP/dt diminished 14% and 12%. After perfusion fixation of the coronary vasculature and the myocardium, at a left ventricular intracavitary pressure equal to the in vivo measured end diastolic pressure, a 10% thickening of the left ventricular wall was measured in association with a 13% increase in the equatorial cavitary diameter and a 44% augmentation in ventricular mass. The 52% hypertrophy of the right ventricle was characterized by an 11% thicker wall and a 37% larger ventricular area. The 33% expansion in the aggregate myocyte volume of the left ventricle was found to be due to a 14% myocyte cellular hypertrophy and a 17% myocyte cellular hyperplasia. These cellular parameters were calculated from the estimation of the number of myocyte nuclei per unit volume of myocardium in situ and the evaluation of the distribution of nuclei per cell in enzymatically dissociated myocytes. Myocyte cellular hyperplasia provoked a 9% increase in the absolute number of cells across the left ventricular wall. In contrast, myocyte cellular hypertrophy (42%) was responsible for the increase in myocyte volume of the right ventricle. The proliferative response of left ventricular myocytes was not capable of restoring diastolic cell stress, which was enhanced by the changes in ventricular anatomy with anemia. In conclusion, chronic anemia induced an unbalanced load on the left ventricle, which evoked a hyperplastic reaction of preexisting myocytes, in an attempt to normalize diastolic wall and myocyte stress.

Anemia↗

PubMed2004

[Left Ventricular Hypertrophy in Hypertension. Part III. Reversibility of Left Ventricular Hypertrophy During Treatment With Antihypertensive Drugs].

Results of prospective trials of effects of various antihypertensive drugs on left ventricular hypertrophy in patients with hypertensive disease are reviewed. According to 2 meta-analyses angiotensin converting enzyme inhibitors are most effective inducers of regression of left ventricular hypertrophy. However in comparative randomized trials in patients with hypertension ability of diuretics, lipophilic beta-adrenoblockers, long-acting calcium antagonists, and angiotensin receptor blockers to cause regression of left ventricular hypertrophy was not inferior to that of angiotensin converting enzyme inhibitors.

Angiotensin-Converting Enzyme Inhibitors↗