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PubMed1982

Effect of ventricular hypertrophy on conduction velocity of activation front in the ventricular myocardium.

To study the effect of ventricular hypertrophy on conduction velocity of the activation front noninvasively, transmural conduction indexes were obtained from findings of echocardiography and body surface potential mapping performed in 40 patients with right bundle branch block uncomplicated by the left anterior fascicular block. Because in these patients, left ventricular activation proceeds radially without being modified by right ventricular activation, the index was obtained by dividing ventricular septal thickness measured from the echocardiogram by transmural conduction time, which was taken as the time interval from the onset of the QRS complex to the time when the left ventricular epicardial breakthrough minimum appeared on the potential map. The indexes, ranging from 11 to 45 cm/s, has a good positive linear correlation with the septal thickness (Y = 2.37X - 1.33, correlation coefficient [r] = 0.83) and were abnormally small in some failed hearts. Further, both the mean ventricular activation times in lead V5 and the mean value for total duration of left ventricular activation did not differ significantly in patients with and without left ventricular hypertrophy. These findings suggest that conduction velocity was increased in the hypertrophied ventricle and decreased in the failed hearts. Because there were no significant differences in the mean serum sodium and potassium concentrations in the patients with and without left ventricular hypertrophy, it is concluded that hypertrophy itself most likely caused greater conduction velocity. Enlarged cells and multiple intercalated discs abundant in hypertrophied ventricle would have facilitated intercellular current flow and, hence, conduction velocity and impaired cellular connection in the failed heart would have reduced them. Thus, the transmural conduction index is suggested to be an important aid in interpreting electrocardiograms as well as in estimating the pathologic state of the heart.

Adolescent↗
PubMed1984

Regression of left ventricular hypertrophy from systemic hypertension by enalapril.

Reversal of left ventricular (LV) hypertrophy with medical therapy has been studied increasingly in patients with systemic hypertension. However, serial changes of LV function are not found during reversal of LV hypertrophy in hypertensive patients. Seven patients with LV hypertension were studied to evaluate serial changes of LV mass and function after the initiation of the new converting enzyme inhibitor MK-421. LV mass and function were determined serially at the end of a placebo period and at 5 days, 1 month, 3 months and 7 months after the initiation of MK-421, using both 2-dimensional (2-D) guided M-mode echocardiography and radionuclide techniques. All patients except 1 had LV hypertrophy and all had normal LV function (ejection fraction derived from gated blood pool method greater than 49%). There was an inverse relation between LV fractional shortening (percent FS) and end-systolic stress before medication (r = -0.81, p less than 0.05). LV mass decreased significantly at 3 months and at 7 months (-10%, p less than 0.05, and -12%, p less than 0.01, respectively) accompanied with persistent decrease of mean blood pressure, which occurred as early as 5 days after start of therapy (133 +/- 5 mm Hg at control, to 112 +/- 4 mm Hg at day 5). During reversal of LV hypertrophy, the inverse correlation between FS and end-systolic stress remained significant (r = -0.80 to -0.95, p less than 0.025 for all), with no difference from the placebo period and from this relation in the normal group. Moreover, percent FS, ejection fraction and stroke index remained unchanged. Thus, LV hypertrophy in patients with systemic hypertension can be reversed without deterioration of LV function. Moreover, overall LV function is likely to be determined by afterload even after reversal of LV hypertrophy.

Adult↗
PubMed1986

Performance of primary and derived M-mode echocardiographic measurements for detection of left ventricular hypertrophy in necropsied subjects and in patients with systemic hypertension, mitral regurgitation and dilated cardiomyopathy.

To determine which M-mode echocardiographic (echo) measurement best detects left ventricular (LV) hypertrophy, the sensitivity and specificity of upper normal limits of echo LV anatomic measurements (previously shown to have 97% specificity in living normal subjects) were tested in 60 necropsied patients with anatomic hypertrophy and in 28 necropsied patients with normal left ventricles. The prevalence of hypertrophy by each echo criterion was determined in 165 living patients with systemic hypertension, mitral regurgitation or dilated cardiomyopathy. The best separation between patients with normal vs increased necropsy LV mass was obtained using sex-specific echo LV mass index criteria (overall accuracy = 73 of 88 patients, 83%). Lower overall accuracies for separation of patients with and without hypertrophy were observed for echo cross-sectional area (59 of 88 patients, 67%; p less than 0.05 vs LV mass index) and indexes of LV wall thickness (39 to 51%, p less than 0.001). Among 113 living patients with moderate or severe hypertension, mitral regurgitation or dilated cardiomyopathy, LV mass index was increased in 73%, cross-sectional area index in 58% (p less than 0.02 vs LV mass index), and posterior wall thickness, septal thickness and relative wall thickness in only 11 to 32% (all p less than 0.001 vs LV mass index). Thus, an M-mode echo LV mass index of more than 134 g/m2 in men and more than 110 g/m2 in women detects concentric and eccentric LV hypertrophy accurately by comparison with necropsy and clinical reference standards; cross-sectional area is slightly less useful; and other M-mode echo criteria of LV hypertrophy perform too poorly to be clinically applicable.

Adult↗
PubMed1987

Echocardiographic criteria for left ventricular hypertrophy: the Framingham Heart Study.

Of 6,148 original cohort and offspring subjects of the Framingham Heart Study who underwent routine evaluation, a healthy group of 347 men (aged 42 +/- 12 years) and 517 women (aged 43 +/- 12 years) was identified to develop echocardiographic criteria for left ventricular (LV) hypertrophy. Healthy subjects were defined as normotensive, receiving no cardiac or antihypertensive medications, nonobese and free of cardiopulmonary disease. Echocardiographic criteria (in accordance with the American Society of Echocardiography convention) for LV hypertrophy, based on mean plus 2 standard deviations for LV mass, LV mass corrected for body surface area and LV mass corrected for height in this healthy sample are, respectively: 294 g, 150 g/m2 and 163 g/m in men and 198 g, 120 g/m2 and 121 g/m in women. Criteria based on LV mass/height result in higher prevalence rates of LV hypertrophy than LV mass/body surface area while still correcting for body size. The prevalence of LV hypertrophy in the entire study population (using LV mass/height criteria) is 16% in men and 19% in women. Until outcome guided criteria for LV hypertrophy are developed, application of sex-specific criteria based on a healthy population distribution of LV mass offer the best approach to echocardiographic diagnosis of LV hypertrophy.

Adult↗
PubMed1988

Identification of best electrocardiographic leads for diagnosing left ventricular hypertrophy by statistical analysis of body surface potential maps.

In view of the increased risk of cardiovascular mortality associated with left ventricular (LV) hypertrophy, early recognition and quantitation of LV hypertrophy are important clinical goals. The standard 12-lead electrocardiogram is the easiest and most widely used noninvasive method for the diagnosis of LV hypertrophy; unfortunately, the diagnostic accuracy of commonly used electrocardiographic criteria remains unsatisfactory. Body surface potential maps contain diagnostic information not present in conventional lead systems. The present investigation combines the increased information content of surface maps with the power of multivariate statistical techniques in order to identify practical subsets of electrocardiographic leads that would allow improved diagnosis of LV hypertrophy. Discriminant analysis was performed on 120-lead data simultaneously recorded in 250 normal subjects and 214 patients with LV hypertrophy using as features instantaneous voltages on time-normalized P, PR, QRS and ST-T waveforms as well as the duration of these waveforms. Leads and features for optimal separation of 173 normal subjects aged greater than or equal to 30 years from 122 patients with pure LV hypertrophy were selected. A total of 6 features from 5 torso sites accounted for a specificity of 97% and a sensitivity of 94%. The single most potent discriminator was the duration of the P wave; voltages were measured in mid and late P on leads located in the lower left parasternal area, the left precordial region and the upper right back, in mid-QRS on a lead positioned 10 cm below V1 and slightly before the peak of the T wave on a lead in the lower left flank.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Electrocardiographic diagnosis of left ventricular hypertrophy in the presence of complete right bundle branch block.

There are few data evaluating electrocardiographic diagnosis of left ventricular (LV) hypertrophy in the presence of right bundle branch block (BBB). This study assesses the relative value of multiple electrocardiographic variables for detecting LV hypertrophy in patients with right BBB. LV hypertrophy was defined as LV mass greater than or equal to 215 g calculated from the Penn method using standard M-mode echo measurements. Sixty-two patients were evaluated (ages 41 to 94) and 35 had LV hypertrophy. None of the electrocardiographic criteria was sensitive; the best was mean QRS axis less than or equal to -30 degrees (sensitivity) 52%) and excessive negative P terminal force (sensitivity 28%). Several electrocardiographic variables were specific: Sokolow index greater than or equal to 35 mm (100%), RV5 or RV6 greater than or equal to 25 mm (96.3%), RI + SIII greater than or equal to 25 mm (92.6%) and intrinsicoid deflection greater than or equal to 0.05 seconds (88.5%). Conventional electrocardiographic criteria do not reliably detect LV hypertrophy in the presence of right BBB, but several criteria are relatively specific for LV hypertrophy.

Adult↗
PubMed1989

Diagnostic body surface potential map patterns in left ventricular hypertrophy during PQRST.

Body surface potential maps were recorded from 117 thoracic sites and 3 limb electrodes in 173 normal subjects older than 30 years of age and 122 patients with clinically "pure" left ventricular (LV) hypertrophy. Typical LV hypertrophy map patterns were identified at successive instants during the PQRST waveform by removing from sequential LV hypertrophy maps the corresponding normal variability range at each electrode site. The presence in individual patients of 1 or more patterns typical in time and location of LV hypertrophy allowed retrospective assignment to the LV hypertrophy group. The most consistent discriminant patterns were excessive negative voltages in the anterior torso with reciprocal excess of positive voltages in the upper right chest during the second half of the P wave, excessive negative voltages in the lower right anterior torso at mid-QRS and excessive negative voltages in the left precordium with reciprocal excess of positive voltages in the upper right chest throughout ST-T. Best classification results were achieved with ST-T features, followed by features from the P wave, the QRS waveform and the PR segment. Cumulative use of ST-T and P features yielded a specificity of 94% with a sensitivity of 88%. Little improvement was obtained by the addition of QRS and PR information. The discriminant map criteria were applied to body surface potential maps from 169 new subjects (77 normal subjects ages 20 to 30 years and 92 patients with complicated LV hypertrophy). Little modification in specificity (93%) and sensitivity (90%) was observed. The performance of commonly used standard lead criteria was also tested.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1991

Abnormal left ventricular diastolic filling in eccentric left ventricular hypertrophy of obesity.

Left ventricular (LV) diastolic filling pattern of obese subjects with eccentric LV hypertrophy was studied. Findings were compared with those of normal control subjects and hypertensive patients with concentric LV hypertrophy. M-mode, 2-dimensional and Doppler echocardiograms were recorded in 11 obese (body mass index greater than 30 kg/m2) normotensive patients with eccentric LV hypertrophy, 10 normal control subjects, and 18 nonobese, hypertensive patients with concentric LV hypertrophy whose antihypertensive medications were discontinued 2 weeks before study. LV hypertrophy was defined as LV mass/height greater than 143 g/m. Hypertrophy in the obese patients was eccentric: Their LV internal dimension (61 +/- 3 mm) was greater than that of hypertensive patients (55 +/- 5 mm, p less than 0.001) and normal control subjects (55 +/- 2 mm, p less than 0.01); their septal (10.7 +/- 0.7 mm) and posterior (10.9 +/- 0.6 mm) wall thicknesses were smaller than those of the hypertensive patients (12.2 +/- 1.7 mm, p less than 0.05 and 11.7 +/- 1.2 mm, respectively, difference not significant). Pulsed-wave Doppler echocardiographic filling indexes were used to evaluate LV diastolic filling. Obese patients had a higher peak velocity of atrial filling (69 +/- 14 vs 54 +/- 15 cm/s, p less than 0.05), lower early/atrial filling velocity ratio (1.0 +/- 0.26 vs 1.32 +/- 0.21, p less than 0.05), prolonged deceleration half-time (108 +/- 9 vs 86 +/- 15 ms, p less than 0.01) and lower peak filling rate corrected to stroke volume (4.08 +/- 0.68 vs 4.96 +/- 0.88 stroke volume/s, p less than 0.05) than normal control subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Morphologic, hemodynamic and coronary perfusion characteristics in severe left ventricular hypertrophy secondary to systemic hypertension and evidence for nonatherosclerotic myocardial ischemia.

Patients with the clinical diagnosis of ischemic heart disease who were found to be free of significant coronary artery atherosclerotic disease (n = 150) underwent coronary vasodilator reserve testing, 2-dimensional echocardiography, and dipyridamole limited-stress thallium testing. After exclusions (predominantly for technically poor coronary artery Doppler signals or suboptimal echocardiography), 100 patients formed the study population. The purpose was to characterize typical cardiac and coronary artery findings in hypertensive patients with severe left ventricular (LV) hypertrophy (n = 15) and to investigate the evidence for myocardial ischemia unrelated to coronary atherosclerosis in early and advanced hypertensive heart disease. Normotensive and hypertensive control groups without LV hypertrophy (n = 12 and 34, respectively) were used for comparison. Severe LV hypertrophy was defined as LV mass index greater than or equal to 50% above established gender specific norms using 2-dimensional-directed M-mode echocardiography and the cube equation corrected to agree with necropsy estimates of mass. Clinical characteristics more often associated with severe LV hypertrophy were black race (67%), diabetes mellitus (33%), proteinuria (47%) and elevated creatinine (1.5 +/- 0.9 mg/dl). Baseline electrocardiograms and dipyridamole limited-stress thallium scans were highly likely to be abnormal (94 and 73%, respectively). Both eccentric and concentric cardiac hypertrophies were found in the severe group. Ejection fraction was significantly lower (0.51 vs 0.68, p = 0.002) and basal coronary flow velocity higher (12.0 vs 5.0 cm/s, p = 0.0004) among these patients when compared with normotensive control patients. Coronary flow reserve did not differ between control groups but was significantly depressed in patients with severe LV hypertrophy (2.5 vs 3.9, p = 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Pressure-induced cardiac hypertrophy: changes in Na+,K+-ATPase and glycoside actions in cats.

Effects of myocardial hypertrophy caused by pressure overload on sarcolemmal Na+,K+-ATPase and positive inotropic action of strophanthidin were examined in cats. Partial ligation of the main pulmonary artery for four weeks resulted in right ventricular hypertrophy with no significant changes in left ventricular muscle. Hypertrophy was associated with a reduction in the number of active Na+,K+-ATPase units. Affinity of the remaining enzyme for [3H]ouabain was unchanged. No apparent right or left shift in dose-response curve for the positive inotropic effect of strophanthidin was observed and toxic concentrations of strophanthidin were unchanged; however, the degree of the positive inotropic effect produced by high concentrations of strophanthidin was significantly smaller in hypertrophied muscle. Moreover, decreases in developed tension rather than tachyarrhythmias was the predominant form of toxicity observed in hypertrophied muscle. These results indicate that myocardial hypertrophy reduces the number of active Na+,K+-ATPase units per milligram protein, decreases maximal positive inotropic effect of strophanthidin, and alters the prevailing form of strophanthidin toxicity.

Animals↗
PubMed1992

Catecholamine-induced cardiac hypertrophy uncouples beta-adrenoceptors from slow calcium channels.

Changes in the parameters of Ca(2+)-dependent slow action potentials (APs) and in their sensitivity to noradrenaline, forskolin, dibutyryl-cAMP and extracellular Ca2+ concentration were studied and compared in left ventricular trabeculae from normal control rats and rats with cardiac hypertrophy. Cytochemical studies were also carried out to determine changes in the activity of membrane-bound adenylate cyclase. Hypertrophy was induced by administration of 5 mg/kg isoproterenol once daily for 7 days. In hypertrophied cardiac muscle, the overshoot of the slow APs was increased by 75%, the maximum rate of rise (Vmax) increased by 76% and the AP duration at 50% repolarization (APD50) prolonged by 56%. The Vmax, an indicator of the slow inward Ca2+ current, increased, in a dose-dependent manner, in response to the beta-adrenoceptor agonist noradrenaline, the adenylate cyclase activator forskolin, the protein kinase activator cAMP and elevated Ca2+ concentration in normal control preparations, whereas in hypertrophied myocardium, the beta-agonist noradrenaline and the adenylate cyclase activator forskolin had no effect. In cytochemical studies with ATP as substrate, adenylate cyclase activity was localized in the sarcolemma, and significantly fewer reaction products appeared on the outer side of the cell membrane in hypertrophied myocytes than in control myocytes. The results suggest that catecholamine-induced cardiac hypertrophy damages the catalytic subunit of membrane-bound adenylate cyclase, thus uncoupling beta-adrenoceptors from slow Ca2+ channels in the transmembrane signalling process.

Action Potentials↗
PubMed1990

Alterations in dietary sodium affect isoproterenol-induced cardiac hypertrophy.

To assess the role of dietary sodium in the regional development and pathogenesis of isoproterenol (ISO)-induced cardiac hypertrophy, male Fischer rats (150-175g n = 65) were divided into control (C) and ISO-treated (I) and three dietary sodium subgroups; low (8.7-13 mEq/kg) (LS), normal (173.9 mEq/kg) (NS) and high (1378 mEq/kg) (HS). Diets began 2 weeks prior to a 7 day continuous infusion of ISO (Alzet miniosmotic pump; 3 mg/kg/day). Mean total heart weight of all I rat groups was larger than in C rats (p less than 0.05). However, low sodium diet ameliorated the percent increase, compared to respective controls, in total heart weight (LSI, 20 +/- 3%; NSI, 26 +/- 6; HSI, 24 +/- 2 (p less than 0.05). Regionally, dietary sodium level did not alter the degree of hypertrophy in the left ventricle plus septum (LVS), but sodium restriction sharply reduced the severe right ventricular (RV) and atrial hypertrophy present in the NSI and HSI rats (LVS: LSI, 18 +/- 2%; NSI, 20 +/- 2; HSI, 15 +/- 2; RV: LSI, 21 +/- 7%; NSI, 45 +/- 9, HSI, 40 +/- 2; atria: LSI, 46 +/- 17; NSI, 73 +/- 23; HSI, 78 +/- 9). Isoproterenol produced diffuse and focal myocardial fibrosis in the subepimyocardium of the LVS with occasional foci of fibrosis in the RV and the subepimyocardium of the LVS. Quantitative analysis demonstrated an increased volume percent of connective tissue limited to the LVS subendomyocardium in all three ISO-treated groups compared to controls (p less than 0.05). These data shows that isoproterenol produces greater hypertrophy of the RV and the atria than the LVS and that dietary sodium restriction selectively decreases the degree of hypertrophy of the RV and the atria produced by ISO. The findings also indicate that the myocardial hypertrophy due to ISO is independent of myocardial injury and is thus, not merely a compensatory response to myocyte loss but rather a direct result of beta-adrenergic stimulation.

Aldosterone↗
PubMed1991

Altered responsiveness of hypertrophied rat hearts to alpha- and beta-adrenergic stimulation.

Inotropic responsiveness to alpha- and beta-adrenergic agents was examined in pressure-overload hypertrophied rat hearts. Pressure overload was induced in rats by abdominal aortic constriction. Three weeks post-constriction, hearts were isolated and perfused with buffer containing various concentrations of (1) calcium (2) isoproterenol (3) forskolin, or (4) phenylephrine. The change in rate of left ventricular pressure development (delta + dP/dt) with increasing perfusate calcium concentrations was comparable in hypertrophied hearts of aortic-constricted rats (AC) and hearts of sham-operated rats (SO). However, with isoproterenol or forskolin stimulation, inotropic responsiveness (delta + dP/dt) was 50% lower in hypertrophied hearts of AC. This was associated with significantly lower tissue cAMP levels. Beta-adrenoceptor number and affinity were unchanged in the hypertrophied myocardium. Maximum inotropic responsiveness to phenylephrine was also lower in hypertrophied hearts and was associated with reduced alpha-adrenoceptor numbers. The data suggest that altered inotropic responsiveness to alpha-adrenergic stimulation may, in part, be due to reduced cardiac alpha-adrenoceptor density. However, post-receptor mechanisms including alterations in cAMP metabolism may contribute to the reduced responsiveness to beta-adrenergic stimulation in hypertrophied hearts of AC.

Adrenergic alpha-Agonists↗
PubMed1985

Decreased sodium-potassium pump activity in isolated hypertrophied feline ventricular myocytes.

The activity of the Na-K pump was assessed in normal and hypertrophied isolated feline myocytes by measuring ouabain-sensitive 42-K uptake. Right ventricular hypertrophy was produced in feline myocardium by placing a constricting band around the pulmonary artery of adult cats. High yields of calcium tolerant myocytes were isolated from the right and left ventricle of banded and sham operated animals. Intracellular sodium (Na) and potassium (K) concentrations (mM) were not significantly different (P greater than 0.5) in normal (Na: 13.2; K: 133.4) and hypertrophied (Na: 12.3; K: 127.5) myocytes. Morphometric analysis demonstrated a 26% increase in width and a 42% increase in volume of hypertrophied myocytes, however, the sarcomere length (1.9 mu) was not different in both cell types. The rate constant (k, min-1) describing 42-K uptake and the calculated total K influx (I, pmol/cm2/sec) were not significantly different (P greater than 0.5) in normal (k = 0.059; I = 15.9) and hypertrophied (k = 0.062; I = 15.3) cells. Ouabain-sensitive (active) K influx, a measure of Na-K pump activity, was maximally inhibited at 10(-4)M ouabain in both cell types. At this concentration, ouabain-sensitive K uptake was decreased 23.5% in hypertrophied myocytes compared to control. The decrease in active K influx may be due to a decrease in the activity of the Na-K ATPase and/or to a reduction in the passive movement of sodium and potassium down their electrochemical gradients.

Animals↗
PubMedDate not supplied

Hypertrophic cardiomyopathy. The importance of the site and the extent of hypertrophy. A review.

Hypertrophic cardiomyopathy is a diverse clinical and pathophysiologic entity that involves principally the left ventricle and is caused by asymmetric or concentric hypertrophy of unknown cause. If asymmetric, the hypertrophy is usually greatest in the ventricular septum, but variations occur in which the hypertrophy may be maximal at the apex, at the midventricular level, or, rarely, in the free wall of the left ventricle. Right ventricular involvement is usually less evident. The principal abnormality in systole is the obstruction to left ventricular outflow caused by upper septal hypertrophy narrowing the outflow tract and setting the stage for Venturi forces to cause systolic anterior motion of the anterior or posterior mitral leaflets. The time of onset and duration of mitral leaflet-septal contact determine the magnitude of the pressure gradient. Mitral regurgitation invariably accompanies the obstruction to outflow. Ventriculomyotomy-myectomy surgery, by thinning the septum and widening the outflow tract, abolishes the abnormal mitral leaflet motion and, consequently, the obstruction to outflow and the mitral regurgitation. This form of surgery more dramatically relieves the systolic abnormalities and the accompanying symptoms than any form of medical therapy available today. The extent of hypertrophy is believed to be the principal determinant of the impaired left ventricular relaxation and increased chambers stiffness (decreased compliance) that characterize diastole in hypertrophic cardiomyopathy. Relaxation is impaired by the contraction load (the obstruction), by a decrease in the principal relaxation loads, by a pathologic degree of nonuniformity of contraction and relaxation, and in all likelihood, by impaired inactivation of the biochemical processes responsible for contraction (? due to primary or ischemia-induced calcium overload). Calcium channel-blocking agents may dramatically improve left ventricular relaxation by speeding up the inactivation process, by decreasing the degree of nonuniformity, or by altering the contraction and relaxation loads in a favorable manner. Atrial and ventricular arrhythmias are responsible for a significant proportion of the morbidity and mortality, and their occurrence also appears to depend on the extent of hypertrophy. Thus, the major manifestations of hypertrophic cardiomyopathy in systole and diastole as well as the disturbances of rhythm appear to be related to the site and/or extent of the hypertrophic process.(ABSTRACT TRUNCATED AT 400 WORDS)

Angiography↗
PubMed1992

The hypertrophied myocardium and coronary disease. Structural changes in patients submitted to aortocoronary bypass surgery.

Seventeen patients with coronary disease submitted to myocardial revascularization were studied. Ten patients had a hypertrophied ventricle, and 7 had normal ventricular mass. Myocardial biopsies were obtained before ischemia and at the time of reperfusion and were assessed for: volume fraction of fibrous tissue, myocyte diameter, morphometric mitochondrial studies and ultrastructural changes. The volume fraction of fibrous tissue in patients with hypertrophied ventricle was 1.9 +/- 0.04, and in patients with normal ventricular mass was 0.9 +/- 0.01 (p less than 0.05). The diameter of the myocyte was 23 +/- 0.3 microns and 18 +/- 1.2 microns for patients with hypertrophied and normal ventricular mass, respectively (p less than 0.01). The value of volumetric density for pre-ischemia samples in patients with a hypertrophied ventricle was 23 +/- 2.2 and in patients with normal ventricular mass was 35 +/- 2.7 (p less than 0.02). Grades 3 and 4 of damaged mitochondria were significantly increased in reperfusion samples from patients with a hypertrophied ventricle compared to pre-ischemia samples. Collagen growth was increased in hypertrophied hearts which were also more sensitive to the ischemia/reperfusion mechanism.

Biopsy↗
PubMed1993

Acetylcholine levels, choline acetyltransferase and acetylcholinesterase molecular forms during thyroxine-induced cardiac hypertrophy.

The effects of left ventricular hypertrophy induced by hyperthyroidism on three biochemical markers of parasympathetic innervation were investigated. In response to subcutaneous injections of thyroxine (400 micrograms/kg; T4) for 6 days, the left ventricle, but not the right, developed significant hypertrophy (20%). In the enlarged left ventricle, acetylcholine (ACh) content and choline acetyltransferase (ChAT) activity per chamber were elevated approx. 25-30%, although no change in these two markers was evident when the data were expressed per unit wet weight. Immunoblot analysis showed that the relative abundance of ChAT protein increased in the hypertrophied left ventricle in correlation with the increased ChAT activity. No changes in ACh content, ChAT activity and ChAT relative abundance were evident in the right ventricle of T4-treated animals. Although hyperthyroidism did not alter AChE specific activity (per unit wet weight) in the left ventricle, the percent activities of the individual AChE globular forms were affected in this chamber. Specifically, T4-treatment reduced the percent activity of globular (G)4 AChE by 20% and increased that of the combined G1 and G2 AChE pool by 15%. Interestingly, in the hypertrophied left ventricle total AChE activity in its extracellular or functionally-relevant pool was reduced due to a loss of G4 AChE activity. These results show that a compensatory increase in parasympathetic innervation can occur during hyperthyroid-induced left ventricular hypertrophy. However, the reduced activity of the functionally-relevant AChE pool suggests that the clearance of ACh after release may be slowed in the hypertrophied left ventricle.

Acetylcholine↗
PubMed1995

Infraspinatus muscle hypertrophy and wasting of axillary folds as the important signs in Duchenne muscular dystrophy.

Eighty-four patients with Duchenne muscular dystrophy (DMD) were examined clinically for hypertrophy and wasting in different muscles, parts of the muscles or muscle groups. Some muscles were examined under mild contraction to bring out any subclinical pseudohypertrophy. Findings revealed infraspinatus muscle hypertrophy to be significantly frequent (88%) and closely second to well known calf hypertrophy (94%). Infraspinatus hypertrophy was noted in 5 such DMD patients in whom calf hypertrophy was unremarkable. The wasting was consistently observed in the muscles forming anterior and posterior axillary folds. In conclusion, infraspinatus muscle hypertrophy and wasting of axillary folds are the important supportive clinical evidences during the examination of DMD patients.

Adolescent↗