Degree Of Left Ventricular Hypertrophy Research Articles

Relationship between sympathetic activation in hypertension and left ventricular hypertrophy quantified by magnetic resonance imaging

OR-64 Key Words: Cardiac Magnetic Resonance Imaging, Left Ventricular Hypertrophy, Sympathetic Nervous System

Breathlessness in pulmonary hypertension: heart and lung?

As exertional breathlessness is considered the main in these two patients. The pattern of left ventricular outflow exercise limiting problem in heart failure and pulmonary hypertension we assessed two patients with long standing pulmonary hypertension using pharmacological stress echocardiography. We found their exertional breathlessness to be disproportionate to raised pulmonary artery pressure (70 mm Hg) and in one patient exertion was associated with presyncope. The two patients were in sinus rhythm and had some degree of left ventricular hypertrophy due to systemic hypertension but significant mitral regurgitation was absent. A physiological stress echocardiogram confirmed the development of significant left ventricular outflow tract obstruction and both patients developed systolic anterior movement of the mitral valve (SAM) and peak outflow tract gradient of over 100 mm Hg. This was associated with a 30 mm Hg drop in systolic blood pressure and breathlessness but only a modest increase in right sided pressure of 10 mm Hg. The main cause of breathlessness in pulmonary hypertension is low cardiac output and ventilatory inefficiency occurring initially with exertion but later on at rest. The two patients studied had narrowed left ventricular outflow tract, partially contributed to by the reversed septal motion (an echocardiographic feature of pulmonary hypertension) and partially by left ventricular hypertrophy. The combination of a smallish left ventricular cavity and fast heart rate resulted in outflow tract obstruction and hypotension. This did not cause a significant increase in left atrial pressure as shown by the pattern of left ventricular filling, nor significantly raised right ventricular pressure. It appears that the outflow tract obstruction and drop in systolic blood pressure are the main contributing factors for stress induced breathlessness

Abnormal ventricular repolarization in hypertensive patients: role of sympatho-vagal imbalance and left ventricular hypertrophy

Background: An increased risk for life-threatening arrhythmias and sudden death has been observed in hypertensive patients, associated with either left ventricular hypertrophy (LVH) or prolonged QT interval. To investigate the influence of autonomic imbalance and LVH on QT interval in hypertensive patients, we compared two different models of LVH: hypertension and endurance physical training. Methods: Forty-seven untreated subjects affected by essential hypertension and 35 endurance runners, with a similar degree of LVH, were enrolled into the study. All subjects underwent 24-h ambulatory ECG recording and morning blood sampling for catecholamines. Heart rate variability was evaluated by spectral analysis and a computerized algorithm was used to measure the QT interval; QTc was then computed by the Bazett's formula. Left ventricular mass index (LVMI) was assessed by echocardiogram. Results: No difference in LVMI was found between hypertensive patients and athletes. Athletes showed lower heart rate (64±1 vs. 75±1 bpm, p<0.001, mean±S.E.M.) and shorter QTc (401±3 vs. 434±4 ms, p<0.001) than hypertensive patients throughout the 24-h period. Athletes showed a higher vagal drive compared to hypertensive patients as suggested by bradycardia and higher values of vagal indices, which negatively correlated with QTc. Plasma norepinephrine was significantly lower in athletes than in hypertensive patients ( p<0.05) and positively correlated with QTc. Conclusion: Despite similar degrees of LVH, hypertensive patients show QTc lengthening, as compared to athletes. Heart rate variability and plasma norepinephrine levels suggest sympathetic predominance in hypertensive patients, which could contribute to abnormal ventricular repolarization, thus identifying patients with an increased arrhythmic risk.

Polymorphism in gene coding for ACE determines different development of myocardial fibrosis in rats.

In humans, the effect of angiotensin-converting enzyme (ACE) gene polymorphisms in cardiovascular disease is still controversial. In the rat, a microsatellite marker in the ACE gene allows differentiation of the ACE gene polymorphism among strains with different ACE levels. We tested the hypothesis that this ACE gene polymorphism determines the extent of cardiac fibrosis induced by isoproterenol (Iso) in the rat. We used a male F(2) generation (homozygous LL and BB ACE genotypes determined by polymerase chain reaction) derived from two rat strains [Brown-Norway (BB) and Lewis (LL)] that differ with respect to their plasma ACE activities. For induction of left ventricular (LV) hypertrophy (LVH) and cardiac fibrosis, rats were infused with Iso (5 mg x kg(-1) x day(-1)) or saline (control) for 10 days and euthanized at day 1 after the last injection. The interstitial collagen volumetric fraction (ICVF), collagen I, and fibronectin content, but not collagen III content, were significantly higher in the homozygous BB rats than in homozygous LL rats. Differences in metalloprotease (MMP)-9, but not in MMP-2 activities as well as in cardiac cell proliferation, were also detected between LL and BB rats treated with Iso. LV ACE activity was higher in BB rats than LL rats and correlated with ICVF (r = 0.61, P < 0.002). No changes were observed in plasma ACE activities, ANG II plasma or LV levels, plasma renin activity, and ACE and ANG II type 1 receptor (AT1R) mRNA levels in the LV of rats with the two different ACE polymorphisms. Iso induced a similar degree of LVH [assessed by an increase in LV weight 100 per body weight, LV-to-right ventricle (RV) ratio, and LV protein content] in LL and BB rats. We concluded that rats in the F(2) generation with high plasma ACE activity developed more fibrosis but to a similar degree of LVH compared with rats with low plasma ACE activity.

Altered gene expression of adrenomedullin and its receptor system and molecular forms of tissue adrenomedullin in left ventricular hypertrophy induced by malignant hypertension

To investigate the pathophysiological role of adrenomedullin (AM) in left ventricular hypertrophy (LVH) in hypertension, we measured the plasma level, left ventricle (LV) tissue level, and mRNA abundance of AM and the mRNA abundance of the AM receptor system in the LV. We also analyzed the molecular forms of AM in the plasma and LV tissue and investigated the relationships between AM and the degree of LVH. We studied the following three groups: control Wistar Kyoto rats (WKY), control spontaneously hypertensive rats (SHR), and deoxycorticosterone acetate (DOCA)-salt SHR (D-SHR). We measured AM-mature, active form, and AM-total (active form+inactive form) in plasma and the LV by a newly developed immunoradiometric assay. Gene expression of AM was measured by Northern blot analysis and gene expression of AM receptor system components, such as calcitonin receptor-like receptor (CRLR), receptor activity modifying protein 2 (RAMP2), and RAMP3 was measured by the reverse transcription polymerase chain reaction method. After 3 weeks of DOCA treatment, D-SHR was characterized by higher blood pressure, LV weight, and plasma atrial natriuretic peptide levels compared with those in the other two groups. Plasma AM-mature and AM-total levels were significantly higher in D-SHR than in the other two groups, whereas there were no significant differences in the AM-mature/AM-total ratio among the three groups. On the other hand, LV tissue AM-mature and AM-total levels were also significantly higher in D-SHR than in the other two groups, and the AM-mature/AM-total ratio was significantly higher in LV tissues than in plasma. Furthermore, the LV tissue AM-mature/AM-total ratio was significantly higher in D-SHR compared with the other two groups. The LV tissue AM-mature/AM-total ratio was significantly correlated with LV weight/body weight ( r=0.92, p<0.001). The gene expression levels of AM, CRLR, RAMP2, and RAMP3 in the LV were significantly higher in D-SHR than in the other two groups. These results suggest that the AM amidating enzyme activity, ligand, and receptor system are all upregulated in the LV hypertrophy in this malignant hypertensive rat model. Considering that AM serves as a local antihypertrophic autocrine and/or paracrine factor, the induction of AM system observed here may modulate the pathophysiology of LV hypertrophy in certain forms of malignant hypertension.

Alterations in protein kinase C isoenzyme expression and autophosphorylation during the progression of pressure overload-induced left ventricular hypertrophy.

Cardiomyocytes express several isoenzymes of protein kinase C (PKC), which as a group have been implicated in the induction of left ventricular hypertrophy (LVH) and its transition to heart failure. Individual PKC isoenzymes also require transphosphorylation and autophosphorylation for enzymatic activity. To determine whether PKC isoenzyme expression and autophosphorylation are altered during LVH progression in vivo, suprarenal abdominal aortic coarctation was performed in Sprague-Dawley rats. Quantitative Western blotting was performed on LV tissue 1, 8 and 24 weeks after aortic banding, using antibodies specific for total PKCalpha, PKCdelta and PKCepsilon, and their C-terminal autophosphorylation sites. Aortic banding produced sustained hypertension and gradually developing LVH that progressed to diastolic heart failure over time. PKCepsilon levels and autophosphorylation were not significantly different from sham-operated controls during any stage of LVH progression. PKCalpha expression levels were also unaffected during the induction of LVH, but increased 3.2 +/- 0.8 fold during the transition to heart failure. In addition, there was a high degree of correlation between PKCalpha levels and the degree of LVH in 24 week banded animals. However, autophosphorylated PKCalpha was not increased at any time point. In contrast, PKCdelta autophosphorylation was increased prior to the development of LVH, and also during the transition to heart failure. The increased PKCdelta autophosphorylation in 1 week banded rats was not accompanied by an increase in total PKCdelta, whereas total PKCdelta levels were markedly increased (6.0 +/- 1.7 fold) in 24 week banded animals. Furthermore, both phosphorylated and total PKCdelta levels were highly correlated with the degree of LVH in 24 week banded rats. In summary, we provide indirect evidence to indicate that PKCdelta may be involved in the induction of pressure overload LVH, whereas both PKCdelta and PKCalpha may be involved in the transition to heart failure.

First-pass MR imaging in the assessment of perfusion impairment in patients with hypertrophic cardiomyopathy and the Asp175Asn mutation of the alpha-tropomyosin gene.

To assess first-pass magnetic resonance (MR) imaging in the evaluation of perfusion impairment in a genetically homogeneous population of patients with hypertrophic cardiomyopathy (HCM) and the Asp175Asn mutation of the alpha-tropomyosin gene and to evaluate the association between hypertrophy and perfusion. Rest-stress first-pass MR imaging with gadopentetate dimeglumine was performed in 17 patients with HCM and the Asp175Asn substitution in the alpha-tropomyosin gene and in five control subjects. Global and segmental first-pass reserve index (FPR) measurements were derived from signal intensity versus time curves. Left ventricular (LV) wall thickness and LV mass index were measured on cine MR images. The Mann-Whitney test was used to evaluate the difference in FPR between the patient group and the control group. The Spearman correlation was used to evaluate the association between LV hypertrophy and FPR. Global FPR was significantly lower in the patients with HCM than in the control subjects (1.12 +/- 0.35 vs 1.80 +/- 0.58, P =.015). In patients with HCM, maximal LV wall thickness and LV mass index correlated negatively with global FPR (r = -0.723, P =.001 and r = -0.598, P =.011, respectively). At the regional level, segmental FPR correlated inversely with LV wall thickness (r = -0.389; P <.001) in patients with HCM. First-pass MR imaging facilitates global and regional evaluation of perfusion impairment in patients with HCM. The severity of perfusion impairment is associated with the degree of LV hypertrophy.

Analysis of Recent Papers in Hypertension

Analysis of Recent Papers in Hypertension

Total peripheral vascular resistance in pediatric renal transplant patients

Abnormal cardiovascular reactivity at rest and during physical exercise may be a risk factor for left ventricular hypertrophy (LVH) in pediatric renal transplanted (Tx) patients. Data on total peripheral vascular resistance (TPR) are not available. Eleven renal Tx patients treated with cyclosporine (7 females and 4 males; mean age 14.6 +/- 3.3 years; mean time since transplantation 43 +/- 35 months) were evaluated for 24-hour blood pressure (BP), TPR and echocardiographic left ventricular mass (LVM). TPR values of patients were compared with data of a group of 11 healthy controls matched for sex and age. Twenty-four-hour ambulatory blood pressure monitoring showed that all but one patient had normal daytime BP values and six patients showed a reduced or inverse nocturnal dip. LVH was found in 72% of the patients. In comparison with healthy controls, patients showed significantly elevated TPR at rest and during exercise suggesting an increased vascular tone. The degree of LVH in these patients is severe and appears disproportionate to the BP values. The high incidence of LVH can reflect an augmented cardiovascular reactivity associated with a disturbed circadian pattern. The increase in TPR and the reduction of the nocturnal fall of BP also might contribute to the development of LVH in young renal Tx patients.

Relation of twelve-lead electrocardiographic T-wave morphology descriptors to left ventricular mass

Echocardiographically detected left ventricular (LV) hypertrophy is an independent risk factor for sudden cardiac death, and the relative risk increases as LV mass increases. 1 Experimental studies strongly suggest that development of LV hypertrophy creates arrhythmia-generating repolarization abnormalities. 2‐6 The inscription of the T wave on the body surface electrocardiogram (ECG) is generated by repolarization gradients at the myocardial level. 7,8 A change in these gradients has an effect on T-wave morphology. 7‐10 Thus, repolarization gradients, arrhythmic vulnerability, and T-wave morphology are interrelated. 8,11 Recently, novel T-wave morphology descriptors on the 12-lead ECG 12 were shown to carry important prognostic information on arrhythmic susceptibility in patients with coronary artery disease. 13,14 We examined whether T-wave morphology descriptors are associated with echocardiographically determined LV hypertrophy and correlate with the degree of LV hypertrophy. ••• We studied 50 subjects who participated in an ongoing study examining the capability of body surface mapping techniques to detect LV hypertrophy. The LV hypertrophy group (n 35) consisted of 24 patients with hemodynamically significant aortic stenosis and 11 patients with essential arterial hypertension, all of whom had echocardiographic LV hypertrophy by gender-specific criteria (LV mass indexed to body surface area 116 g/m 2 in men; 104 g/m 2 in women). 15 No patient had echocardiographic wall motion abnormalities or pathologic Q waves on the ECG. In addition, no patient with aortic stenosis had 70% stenosis of the luminal diameter in epicardial arteries on routine coronary angiography, and no patient with essential hypertension had a history of effort angina. The control group consisted of 15 healthy middleaged volunteers who had no cardiovascular risk factors or a history or signs of heart disease. In these 15 subjects, a screening echocardiogram showed no evidence of anatomic or valvular abnormalities, and a symptom-limited exercise test without ST-segment

PYK2 expression and phosphorylation increases in pressure overload-induced left ventricular hypertrophy.

Proline-rich tyrosine kinase 2 (PYK2) is a member of the focal adhesion kinase (FAK) family of nonreceptor protein tyrosine kinases. PYK2 has been implicated in linking G protein-coupled receptors to activation of mitogen-activated protein kinase cascades and cellular growth in a variety of cell types. To determine whether PYK2 expression and phosphorylation is altered in left ventricular (LV) myocardium undergoing LV hypertrophy (LVH) and heart failure in vivo, suprarenal abdominal aortic coarctation was performed in 160-g male Sprague-Dawley rats. Immunohistochemistry and Western blotting were performed on LV tissue 1, 8, and 24 wk after aortic banding. Aortic banding produced sustained hypertension and gradually developing LVH. PYK2 levels were increased 1.8 +/- 0.2-, 2.7 +/- 0.6-, and 2.0 +/- 0.2-fold in 1-, 8-, and 24-wk banded animals compared with their respective sham-operated controls. The increase in PYK2 expression was paralleled by an increase in PYK2 phosphorylation, both of which preceded the development of LVH. Immunohistochemistry revealed that enhanced PYK2 expression occurred predominantly in the cardiomyocyte population. Furthermore, there was a high degree of correlation (R = 0.75; P < 0.001) between the level of PYK2 and the degree of LVH in 24-wk sham and banded animals. In contrast, FAK levels and FAK phosphorylation were not increased before the development of LVH. However, there was a high degree of correlation (R = 0.68; P < 0.001) between the level of FAK and the degree of LVH in 24-wk sham and banded rats. There was also a significant increase in the ratio of phosphospecific anti-FAK to FAK at this time point. These data are consistent with a role for PYK2 in the induction of pressure overload-induced cardiomyocyte hypertrophy, and suggest that PYK2 and FAK have distinctly different roles in LVH progression.

Recovery of coronary function and morphology during regression of left ventricular hypertrophy.

To investigate changes in coronary morphology and haemodynamic function during regression of established left ventricular hypertrophy (LVH) following surgical unloading. LVH was induced in guinea-pigs by aortic banding and sham operated animals served as controls. We examined the degree of LVH, coronary haemodynamic function and contemporaneous vessel morphology 42 days post-operation. Identically treated animals were debanded and the same parameters measured after 1, 3 and 6 weeks to assess haemodynamic and morphological changes as hypertrophy regressed. Banding resulted in an aortic pressure gradient of 41+/-9 mmHg and increases in heart/body weight ratio (46%), myocyte size (26%) and a doubling of arteriolar wall thickness, all P<0.01. These changes were accompanied by a reduction in coronary reserve (38%) and significantly (P<0.01) decreased maximal response to acetylcholine (70%), sodium nitroprusside (87%), adenosine (70%) and reactive hyperaemia (52%). Surgical debanding normalised the systemic haemodynamics and removed the aortic gradient after 7 days. There was some limited improvement in coronary structure and, to a lesser extent, function despite the continued presence of significant LVH. This had completely regressed to normal levels 23 days after debanding and was accompanied by normalisation of coronary structure and function, although systolic impedance to flow remained significantly increased. After 44 days, debanding resulted in complete cardiac morphological and functional recovery. Left ventricular haemodynamic unloading can result in complete normalisation of LVH, coronary morphology and haemodynamic function. Although morphological and functional recovery were closely correlated, recovery of coronary morphology and function slightly preceded that of the myocardium in this aortic banded/debanded model.

Coronary microcirculation in essential hypertension: a quantitative myocardial contrast echocardiographic approach.

The aims of the present study were: (a) to demonstrate whether quantitative myocardial contrast echocardiography can detect the increase in coronary flow induced by dipyridamole infusion vasodilation through the myocardial opacification due to the transit of microbubbles, both at rest and after dipyridamole induced vasodilation; (b) to explore the coronary microcirculatory function before and after dipyridamole in two different models: asymptomatic and relatively young hypertensive patients with a mild degree of left ventricular hypertrophy, and healthy controls. Two groups of strictly age-matched males were studied (case-control study): 10, relatively young and asymptomatic essential hypertensive patients with a mild degree of left ventricular hypertrophy with a normal left ventricular function, and 10 healthy controls. The main findings were: the microbubbles' appearance area was significantly lower in hypertensive patients than in controls (P<0.05) because of a significantly lower time to peak. The peak intensity at rest was higher in hypertensives than in controls (P<0.05); but the per cent increase after vasodilatory stimulus was significantly higher in controls (+71% in controls vs +31% in hypertensives; P<0.05). The microbubbles' disappearance area was comparable in both groups at rest; the per cent increase of this parameter after dipyridamole was significantly higher in controls (+124%) than in hypertensives (+90%) (P<0.05). The results achieved in this study documented that the coronary microcirculation in hypertensive patients presenting a mild degree of left ventricular hypertrophy, explored with quantitative myocardial contrast echocardiography, showed a different behaviour in comparison with controls, in the vasodilatory response to dipyridamole. The coronary microcirculation in hypertensives showed a reduced vasodilation capacity of the resistance arterioles under dipyridamole induced vasodilatation, and a possible impairment of the endothelium dependent vasodilation. This happened despite an increase in the left ventricular mass, where the relation between capillary bed distribution and hypertrophied myocardium (rarefaction phenomenon) is not completely respected.

Modifications of the cardiovascular system with aging.

Aging is accompanied by significant cardiovascular modifications, both structural and functional. A slight degree of left ventricular hypertrophy develops, while the resting heart rate and early filling rate are somewhat decreased. In contrast, end-diastolic and end-systolic dimensions, stroke volume, and ejection fraction are largely unchanged. The effort tachycardic and inotropic responses are clearly attenuated, whereas the concomitant increase in end-diastolic diameter is enhanced. Large arterial conduits become less distensible and somewhat hypertrophic. Total blood volume is reduced, whereas total peripheral resistance is moderately increased. Neurohumoral systems relevant to cardiovascular regulation are nonuniformly affected by aging: the sympathetic nervous system is overactive and the circulating levels of vasopressin and atrial natriuretic factor are enhanced, while the activity of the renin-angiotensin system is blunted. Elderly individuals have altered cardiovascular homeostasis, with a typical propensity to postural and postprandial hypotension. "Spontaneous" blood pressure variability is increased, whereas heart rate variability is diminished. Vagally mediated chronotropic responses, including those dependent on baroreflex modulation, are attenuated, although end-organ (cardiac) parasympathetic responsiveness is exaggerated. Arterial baroreceptor control of blood pressure is largely preserved in advanced age, whereas cardiopulmonary-mediated reflex responses are definitely impaired.

Reduced anisotropy of action potential conduction in left ventricular hypertrophy.

The aim of this study was to determine if anisotropic action potential conduction was altered during development of left ventricular hypertrophy (LVH). Isolated guinea pig left ventricular preparations from hearts that had developed LVH were used to measure conduction velocity in longitudinal and transverse orientations to the fiber direction. A variable degree of LVH was induced by placing a ring around the ascending aorta for 50 to 250 days. Results were compared with an age-matched control group that underwent a similar operation but with no ring placement. LVH was measured as the heart-to-body-weight ratio (HBR), which correlated with an increase of mean myocyte cross-sectional area. Longitudinal conduction velocity (LCV) declined progressively as HBR increased (mean +/- SD: sham vs LVH: HBR 3.74 +/- 0.30 g/kg vs 4.53 +/- 0.52 g/kg; LCV 72.8 +/- 15.5 vs 63.6 +/- 11.1 cm/sec). Mean transverse conduction velocity (TCV) was greater in LVH compared with control (20.5 +/- 4.7 cm/sec vs 25.4 +/- 8.1 cm/sec), but there was no significance in the trend as a function of HBR. The anisotropic ratio (LCV/TCV) significantly declined as HBR increased. The time constant of the foot of the action potential was smaller in the transverse compared with the longitudinal dimension. There was no influence of hypertrophy. The decrease of LCV and reduction of the anisotropic conduction ratio suggest remodeling of the tissue in LVH. The consequences for the generation of arrhythmias are discussed.

Prevalence of cardiovascular damage in early renal disease.

There is a large burden of cardiovascular disease in early renal disease due to multiple risk factors. Although left ventricular hypertrophy (LVH) is prevalent early in the process of progressive renal decline, it is associated with a number of modifiable risk factors (e.g. anaemia and systolic blood pressure (BP)). More importantly, treatment of modifiable risk factors in renal disease can delay progression. It is important to define anaemia physiologically and to remember that it is also associated with a number of cardiovascular risk factors that may/may not be independent of each other. In a recent prospective, multicentre Canadian study of early renal disease patients prior to dialysis (n=446), the baseline prevalence of LVH increased both with decreasing renal function and decreasing haemoglobin (Hb) levels. Notably, Hb levels within current guideline target levels were still associated with a very high degree of LVH. Over a 12-month period, only a decrease in Hb and an increase in systolic BP, and baseline left ventricular mass index (LVMI) predicted left ventricular growth. Patients whose cardiac symptoms progressed over 12 months were those who experienced a significant fall in BP and a significant increase in LVMI during that time. In the future, steps are needed to ensure early identification of both renal disease and specific risk factors. Recognizing modifiable risk factors and addressing them early in the course of renal disease will facilitate the improvement of patient outcomes.

Lack of association among five genetic polymorphisms of the renin-angiotensin system and cardiac hypertrophy in patients with aortic stenosis

Background Patients with aortic stenosis (AS) have left ventricular hypertrophy (LVH). It is thought that LVH in these patients is a consequence of chronic left ventricular pressure overload. However, there is only a poor correlation between the degree of AS and the degree of LVH. Genetic polymorphisms of the renin-angiotensin-aldosterone system (RAAS) have been considered to trigger the response of the left ventricle to chronic pressure overload and determine the degree of LVH in patients with AS. Methods One hundred five consecutive patients with symptomatic AS were examined by echocardiography and left heart catheterization to determine the severity of AS and LVH. Five genetic polymorphisms of the RAAS (ACE, AGTR1, AGT, CMA, CYP11B2) were analyzed in all patients and the results of genetic analysis were correlated to severity of AS and LVH to determine the importance of the polymorphisms for LVH. Results All tested genotypes were in Hardy-Weinberg equilibrium and allele frequencies were similar to other study populations. There was no correlation between the severity of AS and the severity of LVH. There was no association between the five tested genotypes of the RAAS and the severity of AS (mean gradient and area of the aortic valve) or LVH (LV muscle mass). Conclusion We conclude that LVH in patients with AS is not determined by the tested genetic polymorphisms of the RAAS. (Am Heart J 2001;141:671-6.)

A simple method for assessing the regression or progression of ventricular hypertrophy in the growing child and adult: the value of left ventricular wall-to-cavity ratios.

To establish the normal range of diastolic and systolic left ventricular wall-to-cavity ratios. Two hundred and sixty-two normal subjects (age 0-40 years), 15 children with valvar aortic stenosis and 11 childhood athletes were studied with M-mode echocardiography. Values of diastolic septum-to-cavity ratio and diastolic left ventricular wall-to-cavity ratio were not influenced by sex nor, in adults, by height, weight or body surface area. There were slight age variations from 0-15 years of age, but not in adults from 15-40 years of age. Values of diastolic left ventricular wall-to-cavity ratio in neonates were 0.18 (95% confidence limits 0.17-0.19); in 3-5 year olds 0.16 (0.15-0.16); and in adults 0.18 (0.17-0.19). In valvar aortic stenosis there is a positive correlation between the Doppler-estimated pressure gradient and the degree of left ventricular hypertrophy, as expressed by both diastolic and systolic left ventricular wall-to-cavity ratio (r = 0.90;P < 0.00001 and r = 0.85;P = 0.00006 respectively). Diastolic septum and left ventricular wall-to-cavity ratios accurately differentiate physiological from pathological left ventricular hypertrophy in the growing child. Because these ratios are independent of sex and body size, they may also be more sensitive than absolute wall thickness in the detection of abnormal left ventricular hypertrophy in adults.

An Athlete's Heart in the Context of Evaluation of the Degree of Left Ventricular Hypertrophy

An Athlete's Heart in the Context of Evaluation of the Degree of Left Ventricular Hypertrophy

Myocardial cell damage in human hypertension

OBJECTIVESThe goal of this study was to investigate the presence of myocardial cell damage in patients with systemic hypertension and its relationship with left ventricular hypertrophy (LVH).BACKGROUNDAlthough initially compensatory, LVH adversely affects myocellular integrity and contributes to congestive heart failure in hypertensive patients. Noninvasive detection of myocardial damage can be of value.METHODSWe performed imaging studies with 111In-labeled monoclonal antimyosin antibodies to identify myocardial damage in 39 patients with systemic hypertension and variable degrees of LVH. Three groups were considered: 16 asymptomatic patients with normal echocardiographic left ventricular mass (LVM) (group I); 14 asymptomatic patients with LVH (group II) and 9 patients with symptomatic hypertensive heart disease and advanced LVH (group III). The severity of myocardial damage was represented as heart-to-lung (target-to-background) antibody uptake ratio (normal: <1.55).RESULTSMean LVM index was 105 ± 14 g/m2 in group I, 124 ± 24 in group II and 174 ± 29 in group III. Heart-to-lung ratios of antimyosin uptake were: 1.45 ± 0.14 in group I, 4 of the 16 (25%) patients showing an abnormal scan; 1.50 ± 0.07 in group II with abnormal scans in 2 of the 14 (16%) patients and 1.77 ± 0.16 (p < 0.001) in group III, all 9 patients presenting with abnormal antimyosin scans. On multivariate regression analysis LVM index was the main variable that independently correlated with the degree of myocardial uptake of antimyosin (r = 0.815; p = 0.001).CONCLUSIONSThis study provides the first in vivo evidence of myocyte damage in patients with hypertension. The severity of myocardial damage can be related to the magnitude of LVH.