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PubMed1995

[Remission of left ventricular hypertrophy with ramipril independently of blood pressure changes: the HYCAR study (cardiac hypertrophy and ramipril)].

Most studies of the regression of left ventricular hypertrophy by antihypertensive treatment have methodological weaknesses and have not shown if regression of left ventricular hypertrophy can be obtained independently of blood pressure reduction. In the HYCAR study, after an inclusion phase of 4 to 6 weeks on furosemide (20 mg/day), 115 patients with left ventricular hypertrophy were randomised in a double blind manner to placebo group (N = 40), ramipril, 1.25 mg/day, (N = 38) or 5 mg/day (N = 37) for a period of 6 months. Furosemide was continued during the double blind treatment period. Echocardiography and ambulatory blood pressure monitoring were performed just before the randomisation and at 6 months. At the end of the study, there was no significant difference between the casual and ambulatory blood pressure changes. Expressed in g/m, the left ventricular mass index decreased significantly with respect to placebo in the ramipril 5 mg group (-12.2 +/- 3.9 versus +5.5 +/- 4.3 g/m2, p = 0.003) and in the 1.25 mg group (-7.5 +/- 4.6 g/m2, p = 0.04). The reduction in left ventricular mass index expressed in g/m2 was significant in the 5 mg ramipril (p = 0.008) but not in the 1.25 mg ramipril group (p = 0.06).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1993

Asymmetrical septal hypertrophy in patients with hypertension: a type of hypertensive left ventricular hypertrophy or hypertrophic cardiomyopathy combined with hypertension?

To determine whether asymmetrical septal hypertrophy (ASH) in patients with essential hypertension (HT) is a type of hypertensive left ventricular (LV) hypertrophy or hypertrophic cardiomyopathy (HCM) combined with HT, we investigated a group of 7 hypertensive patients with ASH compared with 12 HCM patients and 10 healthy controls using radionuclide angiography and right ventricular endomyocardial biopsy. The LV time-volume curve and its first and second derivative curves were constructed from cardiac output and time-activity curves constructed by combined forward and reverse-gating from the R wave. The LV wall thickness and ejection fraction were significantly greater in both the HT and HCM groups than in the control group, whereas there were no differences in these indices between the HT and HCM groups. Rapid filling volume index and rapid filling fraction showed significantly lower values in the HCM group than in the control group (p < 0.005). In contrast to the HCM group, these indices in the HT group did not differ from those in the control group. The time to peak filling rate was prolonged in the control, hypertension, and HCM groups in increasing order. Histopathological study revealed a higher incidence of myocardial cell disarray in the HCM than in the HT group. The above results suggest that ASH in hypertensive patients is a type of hypertensive LV hypertrophy.

Analysis of Variance↗

PubMed1985

Rapid ventricular filling in left ventricular hypertrophy: I. Physiologic hypertrophy.

The effects of endurance training on the diastolic properties of the left ventricle were examined by comparing left ventricular filling rates in 11 male distance runners and 12 age-matched nonathletic control subjects selected to have nearly similar heart rates at rest. Maximal oxygen consumption was 69 +/- 11 ml/kg-min for the athletes and 48 +/- 8 ml/kg X min for the control subjects (p less than 0.001). Left ventricular end-diastolic dimension, posterior wall thickness and mass were determined by echocardiography, and average left ventricular filling rate was determined with a nonimaging scintillation probe. Electrocardiographic voltage was significantly greater in the athlete group than in the control group (sums of the voltages of the S wave in lead V1 and the R wave in lead V5 were 40 +/- 10 and 26 +/- 7 mV, respectively) (p less than 0.001), whereas ejection fraction was similar in the two groups. Despite a modest degree of left ventricular hypertrophy in the athlete group compared with the control group (left ventricular mass index 127 +/- 30 and 82 +/- 13 g/m2, respectively) (p less than 0.001), the average left ventricular filling rate was similar in the two groups (2.53 +/- 0.34 versus 2.38 +/- 0.29 end-diastolic counts/s, p = NS). There was no trend for the athletes with a higher left ventricular mass to exhibit a slower filling rate. These findings demonstrate that unlike pathologic hypertrophy associated with chronic hemodynamic over-loading, physiologic left ventricular hypertrophy is not accompanied by slowed left ventricular diastolic filling.

Adaptation, Physiological↗

PubMedDate not supplied

Atrial lipomatous hypertrophy: lipomatous atrial hypertrophy with significant involvement of the right atrial wall.

Lipomatous atrial hypertrophy is a generally benign abnormality characterized by the deposition of adipose tissue in the interatrial septum and is usually detected as an incidental echocardiographic finding. We present two cases in which the presence of lipomatous atrial hypertrophy was diagnosed by transthoracic echocardiography, but tangential cuts of a more diffuse lipomatous process suggested the presence of intracavitary right atrial mass lesions. Transesophageal echocardiography provided additional details of significant right atrial wall involvement. In one case computer assisted tomographic scans showed a progression of thickening over a 4-year period. Lipomatous atrial hypertrophy can be a more generalized and progressive abnormality then previously thought and should be considered in the differential diagnosis of echocardiographic intracavitary right atrial masses.

Adipose Tissue↗

PubMed1992

[Hypertrophy or hyperplasia of myocytes in heart hypertrophy?].

One of the most controversial problem 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 there occurs proliferation of the myocyte. This fundamental question of the character of cardiac growth remains unresolved in spite of the wide attention it 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 103 hearts with various forms of cardiac muscle hypertrophy the following parameters were estimated: diameter, length, volume, density and number of myocytes, as well as the density of nuclei of myocytes. The values of all histometric parameters correlated well with the LV weight up to 350 g. In heavier hearts these parameters were approximately at the same magnitude. The number of myocytes was significantly higher in hearts with LV weight above 250 g than in hearts below 250 g: 5.53 x 10(9) vs 4.31 x 10(9), p < 0.001. The influence of coronary artery diameters, degree of atherosclerosis, weight and percent of fibrous tissue and age on LV weight were evaluated as well. From these parameters only coronary artery diameters significantly influenced on LV weight.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiomegaly↗

PubMed1990

[Myocardial structure in various forms of hypertrophy. II. Myocyte hypertrophy or hyperplasia? Results of the study].

In 103 hearts with various forms of cardiac muscle hypertrophy the following parameters were estimated: diameter, length, volume, density and number of myocytes, as well as the density of nuclei of myocytes. The values of all histometric parameters correlated well with the LV weight up to 350 g. In heavier hearts these parameters were approximately at the same magnitude. The number of myocytes was significantly higher in hearts with LV weight above 250 g than in hearts below 250 g: 5.53 x 10(9) vs 4.31 x 10(9), p less than 0.001. The influence of coronary artery diameters, degree of atherosclerosis, weight and percent of fibrous tissue and age on LV weight were evaluated as well. Only coronary artery diameters significantly influenced on LV weight. On the basis of linear discriminant function, three classes of hearts were separated: 1) LV weight 250 g - absence of hyperplasia, only hypertrophy 2) LV weight 251-350 g - hypertrophy + signs of hyperplasia 3) LV weight 350 g - marked signs of hyperplasia Among 18 patients with the LV weight above 350 g (all patients with congestive heart failure), 11 suffered from valvular disease, 3 were postinfarction patients, 2 suffered from primary hypertension and 2 from primary congestive cardiomyopathy. It indicates that, irrespective to the etiologic factor, hyperplasia is a simple result of the cardiac muscle mass increase.

Adult↗

PubMed1988

[Diagnosis of combined myocardial ventricular hypertrophy using precordial mapping. II. Selection of the parameters of the cartogram of diagnostic significance for the differential diagnosis of combined myocardial hypertrophy and its isolated forms].

A new approach to the choice of diagnostic criteria of combined ventricular hypertrophy (CVN) is proposed: after determination of EKG parametres differing from the norm are separately compared to the EKG parametres in isolated left ventricular hypertrophy (LVH) and right ventricular hypertrophy (RVH). The diagnostic parametres were chosen on the basis of computer statistical analysis of EKG-35 data of 136 patients with CVH, 39 with LVH, 57 with RVH and 71 normal subjects. For differentiation from LVH the amplitude/area ratio (S10 + S17 + S24)/(S1 + S8 + S15) and R27/R17 was effectively used, for differentiation from RVH parametres R14/R1 or S25/S27 are recommended. The amplitude parameters provide the sensitivity of the method of 58.8% with the specificity of 94.6%; the use of area ratio of the same waves increases sensitivity up to 72.8% with the specificity of 94.4%. Sensitivity of the method with the use of the Sokolov-Lyon criteria for diagnosis of LVH and RVH in the same groups was 9.6% with the specificity of 94%.

Cardiomegaly↗

PubMedDate not supplied

Studies concerning the role of myocardial hypertrophy and of intramural tension as determinants of the increased voltage in concentric left ventricular hypertrophy.

In order to study the role of myocardial hypertrophy and of the intramural tension as determinants of the increased voltage in concentric left ventricular hypertrophy, the amplitude of intracellular action potentials in frog and rat myocardium and of monophasic action potentials recorded in dogs by suction electrodes were studied. Increased amplitudes of intracellular action potentials were seen neither in experimental LVH in rats nor during stretch in frog and rat myocardium. The increased intramural tension in dog heart during norepinephrine perfusion or in heart-lung preparation during increased peripheral resistance does not increase the amplitude of monophasic action potentials. The abrupt hypertension induced by norepinephrine is an inadequate model for the study of the effect of increased intramural tension. The increase of the voltage in LVH cannot be accounted for by the increase of action potentials of each hypertrophied fibre. Many factors cooperate in producing increased voltage of LV in LVH.

Animals↗

PubMed1998

Comparison of irbesartan vs felodipine in the regression after 1 year of left ventricular hypertrophy in hypertensive patients (the SILVER trial). Study of Irbesartan in Left VEntricular hypertrophy Regression.

The SILVER (Study of Irbesartan in Left VEntricular hypertrophy Regression) trial is designed to test the hypothesis that the newly developed angiontensin-II receptor antagonist, irbesartan, will produce a greater reduction in left ventricular (LV) mass than felodipine ER, in a population of hypertensive patients defined by seated diastolic blood pressure (SeDBP) in the range 95-115 mmHg or seated systolic blood pressure (SeSBP) in the range 160-200 mm Hg. A population of 360 men and women of non-childbearing potential, >18 years of age, with hypertension, newly diagnosed or after a 3-week washout from previous anti-hypertensive or vasodilator therapies, will be randomised at approximately 80-90 European sites. Add-on therapy with hydrochlorothiazide and atenolol will be allowed for blood pressure control. Patients will be studied by two-dimensional and M-mode echocardiography at baseline (central validation of LV hypertrophy), on randomisation day, and after 6 and 12 months randomised therapy. Blinded analysis of echocardiograms will be performed at a central laboratory, which will provide measurements of the LV mass index (LVMI), determined by M-mode readings according to Devereux formula and using the Penn convention. The primary end-point of the study will be the change in LVMI from baseline to 12 months. The study power is 90% to detect differences between groups from baseline of approximately 8 g/m2.

Adolescent↗

PubMed2005

Estrogen inhibits cardiomyocyte hypertrophy in vitro. Antagonism of calcineurin-related hypertrophy through induction of MCIP1.

Evidence from in vivo studies suggests that some inputs to cardiac hypertrophy are opposed by the actions of estrogen. However, the mechanisms of E2 action in this respect are mainly unknown. An important pathway that is utilized by multiple hypertrophic stimuli involves the activation of the tyrosine phosphatase, calcineurin (PP2B). Here we show that 17beta-estradiol (E2) significantly prevents angiotensin II (AngII)- or endothelin-1 (ET-1)-induced new protein synthesis, skeletal muscle actin expression, and increased surface area in cultured rat cardiomyocytes. ET-1 stimulated calcineurin phosphatase activity, resulting in new protein synthesis, and both were prevented by E2. E2 induced the MCIP1 gene, an inhibitor of calcineurin activity, via phosphatidylinositol 3-kinase, transcriptional, and mRNA stability mechanisms. Small interfering RNA for MCIP1 significantly reversed both the E2 restraint of protein synthesis and the inhibition of AngII-induced calcineurin activity. AngII-induced the translocation of the hypertrophic transcription factor, NF-AT, to the nucleus of the cardiomyocyte and stimulated NF-AT transcriptional activity. Both were prevented by E2. AngII also stimulated the activation of ERK and protein kinase C, contributing to cardiac hypertrophy. E2 inhibited these pathways, related to the stimulation of atrial natriuretic peptide production and secretion. Thus, restraint of calcineurin and kinase signaling to the hypertrophic program underlie these important effects of E2.

Angiotensin II↗

PubMed2002

Comparative effects of candesartan and enalapril on left ventricular hypertrophy in patients with essential hypertension: the candesartan assessment in the treatment of cardiac hypertrophy (CATCH) study.

BACKGROUND: A limited number of studies have evaluated the effect of angiotensin II receptor antagonists (AIIAs) on left ventricular hypertrophy (LVH) in comparison with other antihypertensive drugs, and no large study has compared AIIAs with angiotensin-converting enzyme inhibitors (ACEIs). METHODS AND RESULTS: The CATCH (Candesartan Assessment in the Treatment of Cardiac Hypertrophy) study was a multicenter prospective randomized double-blind trial comparing the effects of candesartan cilexetil (8-16 mg once daily) and enalapril (10-20 mg once daily) with possible addition of hydrochlorothiazide (12.5-25 mg once daily) on echocardiographic left ventricular mass index (LVMI), in 239 hypertensives with LVH (LVMI 120 g/m2 in men and 100 g/m2 in women). Two-dimensionally guided M-mode echocardiograms were carried out at screening (recruiting scan), randomization (baseline scan) and after 24 and 48 weeks of treatment. Baseline and treatment echocardiograms were read at two central labs without knowledge of the scan time sequence. In intention-to-treat (ITT) analyses (196 patients), systolic and diastolic blood pressures (SBP, DBP) were significantly and equally reduced by the two treatments. Candesartan and enalapril reduced LVMI to the same extent, i.e. by 15.0 and 13.1 g/m2 (-10.9 and -8.4%; P<0.001 for both). The proportion of patients achieving normalization of LVMI was non-significantly higher with candesartan (36.3 versus 28.6%). Similar results were obtained in per-protocol (PP) analyses. Cough incidence was lower with candesartan ( P<0.03). CONCLUSIONS: CATCH is the first large study comparing the effects of an AIIA and an ACEI on LVMI. Candesartan cilexetil was found to be equally effective as enalapril in reducing SBP, DBP and LVMI in hypertensives with LVH, according to both ITT and PP analyses.

Adult↗

PubMed2005

Leptin induces vascular smooth muscle cell hypertrophy through angiotensin II- and endothelin-1-dependent mechanisms and mediates stretch-induced hypertrophy.

Various cardiovascular pathologies are associated with vascular smooth muscle cell (VSMC) hypertrophy and elevated plasma leptin levels. We used the rat portal vein (RPV) cultured for three days to investigate the effect of mechanical stretch on autocrine secretion of leptin and the effect of exogenous leptin (3.1 nM) on VSMC. Stretching the RPV significantly up-regulated leptin production by greater than 100-fold and leptin receptor expression by up to 10-fold. In addition, stretch increased tissue weight by 23 +/- 1.3 and 30 +/- 1% (P < 0.05), respectively, in the absence or presence of leptin, although this was significantly attenuated by an antileptin antibody (166 ng/ml). Unstretched RPV weight decreased by 7.5 +/- 1.8% in the absence of leptin, whereas in the presence of leptin, weight increased by 6.5 +/- 1.8% (P < 0.05). VSMC size and [3H]leucine incorporation rates were significantly increased by leptin in stretched and unstretched tissues. Leptin-induced hypertrophy was associated with significant extracellular signal-regulated kinase (ERK1/2) activation as well as increased expression of angiotensinogen, the angiotensin type 1 receptor as well as preproendothelin-1, and the endothelin type A receptor, whereas ERK inhibition or inhibition of either the angiotensin II or endothelin-1 systems at both the synthesis and receptor levels blocked the hypertrophic response. The effects of leptin were also completely blocked by the cholesterol-chelating agent methyl-beta-cyclodextrin. Therefore, our study demonstrates stretch-dependent leptin release and a direct hypertrophic effect of leptin on RPV, the latter likely dependent on intact cholesterol-rich membrane microdomains and locally produced paracrine factors.

Angiotensin II↗

PubMed1995

Quantitative bacteriology of tonsils removed from children with tonsillitis hypertrophy and recurrent tonsillitis with and without hypertrophy.

The aerobic and anaerobic bacterial species and their numbers were studied in tonsillar specimens from children who had undergone elective tonsillectomy: 6 patients with recurrent tonsillitis (RT), 9 with recurrent tonsillitis with hypertrophy (RTH), and 8 with obstructive tonsillar hypertrophy (OTH). Mixed flora were present in all tonsils, yielding an average of 6.7 isolates (5.6 aerobic or facultative and 1.1 anaerobic bacteria). The highest recovery rate of organisms per tonsil was in patients with OTH (7.7 per tonsil), compared to 6.3 per tonsil in RT and 5.9 per tonsil in RTH. The predominant aerobic and facultative organisms were Haemophilus influenzae (22 isolates), Neisseria sp (16), Staphylococcus aureus (14), and Eikenella corrodens (14), and the predominant anaerobic bacteria were Fusobacterium sp (8), Bacteroides sp (7), and Prevotella melaninogenica (5). The number of bacteria per gram of tonsillar tissue varied between 10(4) and 10(8). A higher concentration of S aureus and H influenzae was found in hypertrophic tonsils (RTH and OTH) as compared to RT. These findings suggest the presence of an increased bacterial load and supports an etiologic role for H influenzae and S aureus in hypertrophic tonsils with and without inflammation (RTH and OTH). Further studies to elucidate the effect of selective antimicrobial therapy directed at these organisms may offer an alternative management of hypertrophic tonsils.

Bacterial Infections↗

PubMed1996

[Effects of Peucedanum praeruptorum extractum on blood pressure, left ventricular hypertrophy and hemodynamic changes in left ventricular hypertrophied hypertensive rats].

After intragastric administration of Peucedanum praeruptorum (PPE) 0.6 g/100 g body weight, the blood pressure was decreased significantly in both the normal and the left ventricular hypertrophied hypertensive (LVH) rats. The PPE could still prevent the formation of the left ventricular hypertrophy in renovascular hypertensive rats, the ratio of weight of left ventricular over the weight of body was reduced markedly than that of the LVH group, and was nearly the same of the sham-operated group. The PPE could improve both the systolic and diastolic function than that of the LVH group in the isolated heart, especially, the flow of the coronary artery was increased significantly.

Animals↗

PubMed1986

Difference in the response to isoproterenol between asymmetric septal hypertrophy and symmetric hypertrophy in patients with hypertrophic cardiomyopathy.

The response to isoproterenol was studied in 9 patients with hypertrophic cardiomyopathy (HCM) and asymmetric septal hypertrophy (ASH), 9 patients with HCM and symmetric hypertrophy (SH), and 9 normal controls (NC), using digitized M-mode echocardiography. There was no significant difference in fractional shortening (FS) between ASH and SH, nor between SH and NC before isoproterenol infusion. During isoproterenol infusion, however, FS was significantly greater in ASH (60 +/- 6%) than in SH (53 +/- 7%) and NC (49 +/- 5%) (p less than 0.05, p less than 0.01, respectively), and normalized peak rate of change of left ventricular dimension during systole (pVs) was greater in ASH (7.7 +/- 1.5/s) than in SH (5.2 +/- 0.8/s) and in NC (4.9 +/- 0.8/s) (p less than 0.001, p less than 0.001, respectively). This study shows that the response to isoproterenol of ASH differs from those of SH and of NC and suggests hypersensitivity of the beta-adrenergic receptor system in ASH and the possibility that ASH is a different clinical entity than SH.

Cardiomyopathy, Hypertrophic↗

PubMed1989

Calcium sensitivity and unloaded shortening velocity of hypertrophied and non-hypertrophied skinned human atrial fibres.

The mechanical properties of myocardium of different animals are modified by a chronic increase in haemodynamic load. In this study differences in calcium sensitivity and maximum unloaded shortening velocity of hypertrophic and non-hypertrophic chemically skinned human atrial fibres are characterized. Investigating right atria of 34 patients, possible correlations are studied between preoperative atrial pressure, degree of hypertrophy (estimated from the muscle fibre diameter), calcium responsiveness (pCa50 eliciting half-maximum contraction) and Vmax (unloaded shortening velocity). Hypertrophic fibres from atrial appendages of patients having an increased right atrial pressure (RAP 8.5 +/- 1.6 mm Hg) and suffering from mitral valve disease (stenosis and insufficiency combined) had a fibre diameter of 18.0 +/- 0.9 microns. They also had a higher calcium sensitivity (pCa50 5.65 +/- 0.08) and a lower unloaded shortening velocity (1.7 +/- 0.1 muscle lengths/s) than non-hypertrophic fibres from the appendages of patients with normal right atrial pressure (RAP 3.2 +/- 0.5 mm Hg) and coronary heart disease (CHD: pCa50 5.45 +/- 0.04; Vmax = 3.4 +/- 0.2 muscle lengths/s; fibre diameter 12.8 +/- 0.4 microns). Thus non-hypertrophic fibres from control CHD patients differed significantly (p less than 0.01) from hypertrophied atrial fibres of patients with mitral valve disease and with combined valve disease (MAV, pCa50 = 5.58 +/- 0.05, Vmax 2.0 +/- 0.3 muscle lengths/s, fibre diameter 14.6 +/- 0.9 microns) or aortic valve disease (stenosis combined with insufficiency, fibre diameter 14.8 +/- 1.4 microns, pCa50 5.56 +/- 0.03, Vmax 2.0 +/- 0.24 muscle length/s; RAP 11.0 +/- 2.6 mm Hg).(ABSTRACT TRUNCATED AT 250 WORDS)

Calcium↗

PubMed1996

Altered signal transduction system in hypertrophied myocardium: angiotensin II stimulates collagen synthesis in hypertrophied hearts.

Hypertensive cardiac hypertrophy is associated with the accumulation of collagen in the myocardial interstitium. Previous studies have demonstrated that this myocardial fibrosis accounts for impaired myocardial stiffness and ventricular dysfunction. Although cardiac fibroblasts are responsible for the synthesis of fibrillar collagen, the factors that regulate collagen synthesis in cardiac fibroblasts are not fully understood. We investigated the effects of angiotensin II on cardiac collagen synthesis in cardiac fibroblasts of 10-week-old spontaneously hypertensive rats and age-matched WKY rats. Basal collagen synthesis in cardiac fibroblasts from spontaneously hypertensive rats was 1.6-fold greater than that in the cell of WKY rats. Angiotensin II stimulated collagen synthesis in cardiac fibroblasts in a dose-dependent manner. The responsiveness of collagen production to angiotensin II was significantly enhanced in cardiac fibroblasts from spontaneously hypertensive rats (100 nM angiotensin II resulted in 185 +/- 18% increase above basal levels, 185 +/- 18 vs 128 +/- 19% in WKY rats, P < .01). This effect was receptor-specific, because it was blocked by the competitive inhibitors saralasin and MK 954. These results indicate that collagen production is enhanced in cardiac fibroblasts from spontaneously hypertensive rats, that angiotensin II has a stimulatory effect on collagen synthesis in cardiac fibroblasts, and that cardiac fibroblasts from spontaneously hypertensive rats are hyper-responsive to stimulation by angiotensin II. In the hearts of spontaneously hypertensive rats, mRNA of the renin-angiotensin system (renin, angiotensinogen, angiotensin converting enzyme) was expressed. Levels of angiotensinogen and renin mRNA expressed in ventricles, and angiotensinogen mRNA expressed in fibroblasts from SHR were higher than those from WKY. ACE mRNA was also more strongly expressed in the ventricles and fibroblasts from SHR compared with those of WKY. These findings suggest that the cardiac reninangiotensin system may play an important role in collagen accumulation in hypertensive cardiac hypertrophy (fig.4).

Angiotensin II↗

PubMed2001

Evaluation of septal hypertrophy and systolic function in diseases that cause left ventricular hypertrophy: a 3-dimensional echocardiography study.

OBJECTIVES: The goals of this study were to determine regional systolic function of the septum and to relate it to regional wall thickness and wall stress. BACKGROUND: Wall thickening, a parameter of systolic function, is determined by wall thickness and wall stress. In patients with hypertrophic obstructive cardiomyopathy (HOCM), hypertrophic nonobstructive cardiomyopathy (HNCM), and hypertensive heart disease (HHD), regional systolic function of normal and hypertrophic septal regions has been incompletely characterized by 2-dimensional echocardiography. Thus, multiplane transesophageal echocardiography with 3-dimensional reconstruction of the septum was used. METHODS AND RESULTS: In 49 patients (15 controls, 11 with HOCM, 8 with HNCM, and 15 with HHD) 4 parallel (2 basal and 2 apical) equidistant short-axis cross sections from base to apex were obtained from the reconstructed septum. In each short-axis cross section, 6 wall-thickness measurements were made in 15 degrees intervals at end diastole and end systole, for a total of 48 measurements in each patient. Fractional thickening was calculated as wall thickening divided by end-diastolic wall thickness. Wall thickness of the basal cross sections was significantly thicker (P < .001) in HOCM and HNCM than in HHD. However, circumferential wall thickness was more evenly distributed in HNCM and HHD when compared with HOCM. In the basal cross sections, fractional thickening was similarly reduced in all hearts, though basal wall stress was significantly different in all groups (P < .001). In the apical cross sections, wall thickness was similar in all diseased hearts, but fractional thickening was better (P < .001) and wall stress lower (P < .001) in HNCM than in HOCM and HHD. CONCLUSIONS: In septal regions without or with only mild hypertrophy, regional systolic function is preserved and appears to be determined by hemodynamic factors such as wall stress. However, in regions with moderate to severe hypertrophy, systolic function is markedly and uniformly impaired in all groups, which seems not to be caused by differences in wall thickness and wall stress but by the degree of the myocardial disease process.

Cardiomyopathy, Hypertrophic↗