SEARCH · PubMed Health

Results for “Hypertrophy”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 181 records · Page 10Linked to original sources

PubMed1995

Influence of left ventricular hypertrophy on detection of coronary artery disease using exercise echocardiography.

OBJECTIVES: This study examined the influence of left ventricular hypertrophy on the accuracy of exercise electrocardiography and echocardiography for detection of coronary artery disease. BACKGROUND: Electrocardiographic repolarization abnormalities caused by left ventricular hypertrophy compromise the diagnostic accuracy of exercise electrocardiography but not of exercise echocardiography. The relative merits of these investigations are less well defined in patients with hypertrophy but without electrocardiographic (ECG) changes. METHODS: We prospectively evaluated 147 consecutive patients without prior myocardial infarction undergoing both exercise echocardiography and coronary arteriography. Coronary stenoses > 50% diameter were present in 62 patients (42%). Positive test results were defined by a new or worsening wall motion abnormality or > 0.1 mV of ST depression. Echocardiographic left ventricular hypertrophy (mass > 131 g/m2 in men, > 100 g/m2 in women) was identified in 68 patients. A subgroup with clinically suspected hypertrophy was defined according to the presence of ECG evidence of hypertrophy, hypertension or aortic stenosis. RESULTS: The overall sensitivity of exercise echocardiography exceeded that of exercise electrocardiography (71% vs. 54%, p = 0.06). Echocardiographic hypertrophy had no significant effect on the sensitivity of either test. The specificity of exercise echocardiography exceeded that of exercise electrocardiography (91 vs. 74%, p = 0.01). In patients with hypertrophy, the specificity of exercise echocardiography exceeded that of exercise electrocardiography (95% vs. 69%, p < 0.01), whereas among patients without hypertrophy, the specificities (respectively, 87% and 78%) were more comparable. The accuracy of exercise echocardiography exceeded that of the exercise ECG in the overall group (82% vs. 65%, p = 0.002) and in patients with hypertrophy (85% vs. 60%, p = 0.004), but this difference was less prominent in patients without hypertrophy (80% vs. 69%, p = NS). In patients with clinically suspected hypertrophy, exercise echocardiography demonstrated a higher sensitivity, specificity and accuracy than exercise electrocardiography. The cost incurred in the identification of coronary disease was least with a strategy involving use of the exercise echocardiogram instead of routine exercise testing in patients with known or clinically suspected left ventricular hypertrophy. CONCLUSIONS: Exercise echocardiography is more accurate than exercise electrocardiography for the detection of coronary artery disease in patients with known or clinically suspected left ventricular hypertrophy.

Adult↗

PubMed2004

Myocardial blood flow and efficiency in concentric and eccentric left ventricular hypertrophy.

BACKGROUND: It is not clearly understood why concentric left ventricular hypertrophy (increased left ventricular mass and relative wall thickness) is associated with higher cardiovascular risk than eccentric hypertrophy (increased left ventricular mass but normal relative wall thickness). Possible reasons include lower myocardial efficiency or perfusion reserve in concentric than in eccentric hypertrophy. We compared myocardial perfusion reserve and efficiency in normotensive controls and in hypertensive patients with concentric and with eccentric hypertrophy. METHODS: Study subjects comprised 16 patients with hypertension-induced left ventricular hypertrophy and 10 normotensive controls. We measured myocardial perfusion reserve and oxygen consumption by positron emission tomography. We calculated myocardial efficiency by dividing left ventricular minute work by myocardial oxygen consumption. RESULTS: There was no significant difference in myocardial perfusion reserve between patients with concentric (n = 9) as compared to eccentric (n = 7) hypertrophy. However, myocardial perfusion reserve in both patient groups were lower than in controls. Although myocardial efficiency in patients with eccentric hypertrophy and in controls were not different, both values were higher than measurements in patients with concentric hypertrophy (18% +/- 6% v 16% +/- 3% v 13% +/- 4%, eccentric hypertrophy versus controls versus concentric hypertrophy, respectively, P =.04 for both eccentric versus concentric hypertrophy and for controls versus concentric hypertrophy). CONCLUSIONS: Myocardial efficiency but not perfusion reserve is lower in hearts with concentric compared with eccentric left ventricular hypertrophy. This might be an explanation for the higher cardiovascular morbidity and mortality associated with concentric left ventricular hypertrophy.

Adult↗

PubMed2000

Usefulness of left atrial abnormality for predicting left ventricular hypertrophy in the presence of left bundle branch block.

The objective of this study was to identify left atrial (LA) abnormality on the electrocardiogram and other related variables as predictors of left ventricular (LV) hypertrophy in the presence of left bundle branch block (LBBB). In the presence of complete LBBB, the diagnosis of electrocardiographic abnormalities is problematic and that of LV hypertrophy remains difficult. The usual electrocardiographic criteria applied for the diagnosis of LV hypertrophy may not be reliable in the presence of LBBB. Therefore, noninvasive criteria will help physicians diagnose LV hypertrophy with electrocardiography. LA abnormality on the electrocardiogram was assessed by 2 independent observers as predictor of LV hypertrophy in the presence of LBBB in 120 patients, and data were compared with those of 100 patients without LA abnormality. LV mass was calculated from echocardiographic data. Besides LA abnormality, the other variables studied for prediction of LV hypertrophy were gender, age, body surface area, body mass index, frontal axis, and QrS duration. Of the 6 criteria analyzed, the P terminal force was found to be the most common and consistent criterion to detect LA abnormality. LV hypertrophy was confirmed by echocardiographic determination of LV mass in both groups. Observers reliably differentiated between the hypertrophied and normal-sized left ventricle in the presence of LBBB by correlating LA abnormality with LV mass determined by echocardiography. Observer 1 detected LA abnormality in 89% and observer 2 in 84% of patients. False-positive results were present in 11% and 16%. The observer's recognition of LA abnormality in the present study was 91%. The 2 observers showed a sensitivity of 81% and 79% and a specificity of 91% and 88%, respectively, when diagnosis of LV hypertrophy was determined. LV mass increased significantly and was diagnostic of LV hypertrophy in 92% of patients with LA abnormality. In the remaining 11 patients (8%), the LA abnormality was of marginal abnormal magnitude. Each 0.01-mV/s increase in LA abnormality gave an increase of 30 g of LV mass. LV mass was increased in 86% of patients when corrected by body surface area. LV hypertrophy in the presence of LBBB on electrocardiography was found in only 13 patients (10%) when the 6 frequently used conventional criteria for diagnosis of LV hypertrophy by electrocardiography were used. Regression analysis revealed LA abnormality to be a strong independent predictor of increased LV mass. Multivariate analysis also revealed age, body mass index, body surface area, frontal axis, and QrS duration to be significant predictors of LV mass. This noninvasive study correlates LA abnormality by electrocardiogram and LV hypertrophy with echocardiography to conclude that LA abnormality was significantly diagnostic of LV hypertrophy in the presence of LBBB. Age, body mass index, body surface area, frontal axis, and QrS duration were also significant predictors of LV mass.

Adolescent↗

PubMed1994

Exercise induces cardiac dysfunction in both moderate, compensated and severe hypertrophy.

BACKGROUND: Ventricular hypertrophy begins as a physiological adaptation to cardiac overload but progresses to a pathological state. We examined whether the extent of hypertrophy influenced the response to exercise in terms of its effects on regional and global ventricular function and transmural myocardial blood flow distribution. METHODS AND RESULTS: Left ventricular (LV) hypertrophy was induced by aortic banding in puppies. The effects of treadmill exercise were compared in sham-operated control dogs (n = 7) and in dogs with moderate LV hypertrophy (47% increase in LV wt/body wt, n = 7) with normal baseline levels of LV systolic and diastolic wall stress and dogs with severe LV hypertrophy (85% increase in LV wt/body wt, n = 18), which exhibited elevated levels of LV systolic wall stress at baseline. The dogs with severe LV hypertrophy were further subdivided into those with either elevated or normal baseline levels of LV end-diastolic pressure and wall stress. The response to exercise in dogs with moderate LV hypertrophy was directionally similar to that of sham-operated control dogs for systemic hemodynamics and global and regional LV function, ie, full and subendocardial wall thickening rose, as did mean and diastolic arterial pressures, shortening fraction, and Vcf. The endocardial/epicardial blood flow ratio did not fall during exercise in these two groups. However, relations comparing either LV shortening, Vcf, or wall thickening with LV systolic wall stress during exercise demonstrated depressed myocardial function in the dogs with moderate LV hypertrophy. In contrast, in dogs with severe LV hypertrophy, exercise reduced LV shortening fraction, Vcf, mean and diastolic arterial pressures, and full and subendocardial wall thickening, and the endocardial/epicardial blood flow ratio fell to 0.73 +/- 0.07. There were no differences observed between the two subgroups with severe LV hypertrophy, but the global and regional wall function responses to exercise were more severely impaired than those in dogs with moderate LV hypertrophy. CONCLUSIONS: Responses of global and regional LV function and transmural myocardial blood flow distribution to exercise were clearly abnormal in dogs with severe LV hypertrophy with elevated baseline levels of LV systolic wall stress whether or not baseline levels of LV end-diastolic wall stress were elevated. Thus, it required more severe LV hypertrophy as well as elevated levels of LV wall stress to elicit qualitatively abnormal regional and global hemodynamic responses to exercise. However, even with moderate LV hypertrophy, which was well compensated under baseline conditions, qualitatively impaired contraction-afterload relations were observed during the stress of exercise.

Animals↗

PubMed1994

Pathophysiological principles of the relation between myocardial hypertrophy of the left ventricle and its regression.

Hypertrophy of the left heart ventricle as a consequence of a haemodynamic overload is a process of ambiguous biological value. Although hypertrophy allows to increase the performance of the ventricle without substantial elevation in wall tension, it represents a risk factor of cardiac morbidity and mortality. The regression of hypertrophy seems to be a rational outcome of this ambivalent situation. Not every reversal of hypertrophied muscle mass, however, can be unambiguously considered therapeutic success. The biological value of hypertrophy regression depends on the type of hypertrophy, on the level of deterioration of the heart by a long-lasting haemodynamic overload, as well as on the way in which the reversal of hypertrophy is achieved. Even in the case when functional characteristics are preserved or even improved compared to the hypertrophied heart, hypertrophy regression need not automatically mean a decrease of the cardiovascular risk induced by ventricular hypertrophy. Regression of hypertrophy may be even disadvantageous in those situations when reduction of hypertrophy and reduction of the haemodynamic overload proceed in a disproportional manner. Spontaneously developing regression of the hypertrophied left ventricle as demonstrated on the model of aortal insufficiency, is an explicitly pathological state, resulting in heart failure. Regression of myocardial hypertrophy should not be considered the primary therapeutic aim but rather a part of the management of haemodynamic overload of the heart. The main aim is to achieve optimal perfusion of the periphery, yet at the same time to provide such conditions which would prevent the working load of the heart to become a limiting factor of survival.

Animals↗

PubMed1983

Prevalence and natural history of electrocardiographic left ventricular hypertrophy.

Left ventricular hypertrophy, particularly on the electrocardiogram, is an ominous, not an incidental accompaniment of hypertension and cardiovascular disease. The prevalence of electrocardiographic left ventricular hypertrophy increases with age with a slight male predominance, and one in 10 persons aged 30 to 62 can expect to have it within 12 years. At any age, cardiac enlargement on roentgenograms is twice as prevalent as electrocardiographic left ventricular hypertrophy, and in only 16 percent of those with x-ray evidence of cardiac enlargement does electrocardiographic left ventricular hypertrophy subsequently develop. Hypertension predisposes and at systolic pressures exceeding 180 mm Hg evidence of electrocardiographic left ventricular hypertrophy develops in 50 percent, with no closer relation to diastolic, than to systolic pressure. In addition to drastic curtailment of life expectancy, electrocardiographic left ventricular hypertrophy is a harbinger of serious cardiovascular disease. Definite electrocardiographic left ventricular hypertrophy is associated with an eightfold increase in cardiovascular mortality and a sixfold increase in coronary mortality. Electrocardiographic left ventricular hypertrophy with repolarization criteria more than doubles the risk of hypertension alone and carries a greater risk of cardiovascular morbidity and mortality than cardiac enlargement. It identifies hypertensive patients with a compromised coronary circulation and myocardial damage. Risk of stroke, cardiac failure, and every clinical manifestation of coronary heart disease is substantially increased. In those with electrocardiographic left ventricular hypertrophy risk of cardiac failure is three times that in those with hypertension alone. Electrocardiographic left ventricular hypertrophy based solely on voltage criteria reflects chiefly the severity and duration of associated hypertension, carrying only half the cardiovascular risk of electrocardiographic left ventricular hypertrophy with repolarization abnormality. The precise pathologic and anatomic meaning of electrocardiographic left ventricular hypertrophy is unclear in view of the modest correlations with anatomic, x-ray, ventriculographic, and electrocardiographic measures of cardiac hypertrophy. The electrocardiographic aberrations are as much a product of myocardial damage as hypertrophy, and their appearance must be regarded as a grave prognostic sign in the course of cardiovascular disease.

Adult↗

PubMed1983

Relation of electrocardiographic abnormalities and patterns of left ventricular hypertrophy identified by 2-dimensional echocardiography in patients with hypertrophic cardiomyopathy.

Distribution of left ventricular (LV) hypertrophy was assessed by wide-angle, 2-dimensional (2-D) echocardiography in 153 patients with hypertrophic cardiomyopathy and compared with the scalar electrocardiogram in the same patients. The most common electrocardiographic alterations were S-T segment changes and T-wave inversion (61%), LV hypertrophy (47%), abnormal Q waves (25%), and left atrial enlargement (24%). LV hypertrophy on the electrocardiogram was significantly more common in patients with the most extensive distribution of LV hypertrophy on 2-D echocardiogram involving substantial portions of both the ventricular septum and LV free wall (type III; 51 of 69, 74%) than in those with more limited distribution of LV hypertrophy (21 of 84, 25%; p less than 0.001). Most patients with hypertrophic cardiomyopathy and normal electrocardiograms (13 of 23) had localized (type I) hypertrophy, but only 4 had the extensive type III pattern of hypertrophy. Abnormal Q waves were significantly more common in those patients without hypertrophy of the anterior, basal septum (type IV; 15 of 27, 56%) than in those with basal septal hypertrophy (23 of 126, 18%; p less than 0.001); abnormal Q waves were uncommon in extensive type III distribution of hypertrophy (13 of 69, 19%). Thus, although no single electrocardiographic abnormality is characteristic of hypertrophic cardiomyopathy, 2-D echocardiography clarifies the significance of certain electrocardiographic patterns: (1) LV hypertrophy on the electrocardiogram, although present in only about half of the study group, was a relatively sensitive (74%) marker for extensive (type III) LV hypertrophy; (2) abnormal Q waves cannot be explained by ventricular septal hypertrophy alone; and (3) a normal electrocardiogram was most commonly a manifestation of localized LV hypertrophy.

Adolescent↗

PubMed2003

The limited value of plasma B-type natriuretic peptide for screening for left ventricular hypertrophy among hypertensive patients.

BACKGROUND: Several reports have suggested that plasma B-type natriuretic peptide (BNP) levels are elevated in hypertensive patients especially with left ventricular (LV) hypertrophy. However, few data have been available concerning the utility of plasma BNP measurement to identify LV hypertrophy in hypertensive patients in a general population screening context. METHODS: We measured plasma BNP concentrations in 1112 volunteers in a health screening program (mean age, 57 years). All subjects underwent electrocardiography, chest X-ray, and echocardiography. Among the sample, 284 subjects were designated as hypertensive because they were on antihypertensive drugs or showed elevated systemic blood pressure. By echocardiography, 36 of the hypertensive patients showed significant LV hypertrophy. RESULTS: There were no significant differences in age and sex between the LV hypertrophy and non-LV hypertrophy groups. Plasma BNP levels in the LV hypertrophy group were significantly higher than in the non-LV hypertrophy group (19.4 +/- 18.9 v 28.2 +/- 28.2 pg/mL; P <.05). However, the ability of plasma BNP levels to discriminate between LV hypertrophy and non-LV hypertrophy patients was not sufficient as the area under the receiver operating characteristic curve was 0.588 (95% CI: 0.528-0.646) with sensitivity of 50.0% and specificity of 69.0%. Positive and negative predictive values for detecting LV hypertrophy among hypertensive patients were 18.9% and 90.5%, respectively. This ability did not improve significantly when the screening was limited to patients with untreated LV hypertrophy or concentric LV hypertrophy. CONCLUSIONS: Plasma BNP testing in a mass screening setting is of limited use for the identification of LV hypertrophy patients among hypertensive patients with heterogeneous etiology.

Adult↗

PubMed1998

Heparin inhibits mesenteric vascular hypertrophy in angiotensin II-infusion hypertension in rats.

OBJECTIVE: Chronic infusion with angiotensin II increases blood pressure and activates growth mechanisms to produce hypertrophy of the heart and vessels. In order to better understand mechanisms of angiotensin II induced vascular hypertrophy, this study aimed to determine whether heparin, a potent inhibitor of smooth muscle proliferation mechanisms, was able to inhibit vascular hypertrophy. METHODS: Angiotensin II (100, 200 or 300 ng/min/kg s.c.) or a saline vehicle control were infused into rats for 14 days. A separate group of animals were co-infused with heparin (0.3 mg/h/kg i.v.) and angiotensin II (200 ng/min/kg s.c.) to test whether hypertension or hypertrophy were antagonized. Blood pressure was measured by tail cuff method and vessel media cross sectional area was measured by morphometry in aorta and mesenteric arteries. RESULTS: Blood pressure elevation and cardiovascular hypertrophy produced by angiotensin II were strongly dose-dependent. Hypertrophy responses at 14 days of treatment also appeared to be influenced partly by local factors as medial cross sectional area was increased more in mesenteric arteries than in thoracic aorta, and left ventricle weight was least affected. Heparin treatment did not influence the increase of blood pressure in angiotensin II infused animals, but the mesenteric vascular hypertrophy response due to angiotensin II was inhibited by approximately 50%. Inhibition of a modest cardiac hypertrophy and aortic medial hypertrophy did not reach significance. CONCLUSIONS: Angiotensin II infusion produced vascular medial hypertrophy and increased blood pressure, however the inhibitory effect of heparin on hypertrophy in mesenteric arteries was not mediated through angiotensin II induced vasoconstriction or blood pressure elevation. These data suggest that heparin interferes directly with the hypertrophy mechanism in mesenteric arteries, and that heparin-sensitive growth mechanisms are important in mediating angiotensin induced mesenteric vascular hypertrophy.

Angiotensin II↗

PubMed1996

Dispersion of the QT interval and autonomic modulation of heart rate in hypertensive men with and without left ventricular hypertrophy.

Left ventricular hypertrophy is an independent risk factor for sudden cardiac death in hypertension, but the mechanisms of electrical instability associated with hypertrophy are not well known. We studied dispersion of the QT interval, an index of inhomogeneity of repolarization, and heart rate variability, a measure of cardiac autonomic modulation, in a randomly selected population of 162 men with systemic hypertension and made comparisons between the patients with echocardiographic evidence of left ventricular hypertrophy (left ventricular mass index > or = 131 g/m2, n = 44) and those without hypertrophy (left ventricular mass index < 131 g/m2, n = 118). The heart rate-corrected QT dispersion (67 +/- 37 versus 53 +/- 21 milliseconds, P < .05) and QT apex dispersion (55 +/- 22 versus 44 +/- 16 milliseconds, P < .01) were significantly longer in the patients with left ventricular hypertrophy than in those without hypertrophy. Thirteen of the 44 patients (30%) with hypertrophy versus 7 of the 118 patients (6%) without hypertrophy had an abnormally long QT apex dispersion ( > 70 milliseconds) (P < .001). The time and frequency domain measures of heart rate variability did not differ significantly between the patient groups with and without left ventricular hypertrophy. The measures of heart rate variability were not related to QT dispersion or left ventricular mass index but had a negative correlation with blood pressure values (eg, r = -.30 between the low-frequency component of heart rate variability and systolic pressure, P < .001). Age, body mass index, antihypertensive medication, and the other demographic variables were similar between the groups, but the patients with left ventricular hypertrophy had higher systolic (P < .01) and diastolic (P < .01) pressures compared with the patients without hypertrophy. Left ventricular hypertrophy in hypertensive men is associated with inhomogeneity of the early phase of ventricular repolarization, favoring susceptibility to reentrant ventricular tachyarrhythmias. Abnormalities in cardiac autonomic function, which may trigger a spontaneous onset of arrhythmias, are related to elevated blood pressure but not specifically to left ventricular hypertrophy.

Adult↗

PubMed1993

The effect of orotic acid treatment on the energy and carbohydrate metabolism of the hypertrophying rat heart.

1. Adenine nucleotide concentrations in normal and one day hypertrophied hearts of untreated, orotic acid (OA), uridine, uracil, dihydroorotate and reserpine pretreated rats were measured. OA treatment increased the ADP concentration 5-fold in one day hypertrophied hearts. Neither uracil, uridine, dihydroorotate nor reserpine treatments changed ADP or total adenylate concentrations at one day of hypertrophy. 2. The adenine nucleotide ratio (ANR) at 0.263 x 10(3) M-1 and the energy charge (0.66) were at their lowest values in OA and in reserpine treated one day hypertrophying hearts. The temporal decline in the indices of energy metabolism corresponded with the OA induced maximum stimulation of contractility and maximum rates of protein, RNA and glycogen synthesis. 3. The phosphorylation state of the adenine nucleotides (PSAN) was both the most sensitive and the best predictive index of the cellular energy status in normal and hypertrophying hearts. The pronounced ability of OA treatment to energize myocyte cytoplasm was shown by the 9- and 6-fold greater values of PSAN over ANR in one and three day hypertrophied hearts. The enhanced PSAN may be the key factor in the mechanism of OA induced enhancement of contractile and synthetic functions of the heart in compensatory hypertrophy. 4. The development of myocardial hypertrophy in untreated rats resulted in a 36% reduction in the cytoplasmic NAD/NADH ratio. In rats treated with OA this redox couple of the hypertrophying heart was more oxidized and was increased by 30% to restore it to the value range of normal heart. 5. The regulatory status of the glycolytic pathway in untreated and OA treated hypertrophying hearts was assessed by comparisons of the mass action ratio (MAR) and equilibrium constants for each of the individual glycolytic reactions. There was an OA induced 2.7-fold increase in glycogen, UDP-glucose and total uridine nucleotides in hypertrophied hearts. The concentrations of seven out of ten glycolytic intermediates, including pyruvate and lactate were increased as a consequence of OA treated hypertrophy. Glycolytic flux was not stalled, rather the pathway was "more open" permitting greater throughput of intermediates with individually increased levels of selected metabolites. OA stimulated hypertrophy did not change the canonical control of glycolysis by the activities and individual MAR values of phosphofructokinase and pyruvic kinase. 6. Elevated levels of Glu 6-P, Fru 6-P and DHAP can force glycolytic intermediate entry into the non-oxidative reaction segment of the pentose pathway (PP), thereby elevating Rib 5-P concentration by reversal of the conventional flux direction of PP.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenosine Diphosphate↗

PubMed1995

The effects of modulation of calcium influx through the voltage-sensitive calcium channel on cardiomyocyte hypertrophy.

In human hypertrophic cardiomyopathy and hypertension associated ventricular hypertrophy, chronic use of calcium channel blockers results in a significant regression of hypertrophy. The main objective of this study was to test the hypothesis that modulation of calcium influx through the voltage-sensitive L-type Ca2+ channel directly affects myocardial hypertrophy. Agents that modified calcium influx through the L channel, reduced or enhanced mechanical activity, or uncoupled excitation-contraction coupling were evaluated in cell culture models of myocardial hypertrophy. The calcium channel blocker, verapamil, significantly reduced serum-stimulated cardiomyocyte hypertrophy in a stereoselective manner. The 1,4-dihydropyridine (DHP) calcium channel blocker, nifedipine, also significantly inhibited cardiomyocyte hypertrophy while the DHP calcium channel activator, Bay K 8644, promoted a significant increase in serum-stimulated hypertrophy. Norepinephrine (NE) and, to a lesser degree, isoproterenol (ISO) modulated serum-stimulated hypertrophy. KCl, verapamil, and nifedipine at concentrations that completely arrested beating produced comparable reductions in serum-stimulated hypertrophy. The excitation-contraction uncoupler, 2,3-butanedione monoxime (BDM), KCl and verapamil reduced hypertrophy in high density spontaneously contracting serum-free cardiomyocytes. Addition of NE or serum to BDM treated cells partially offset this reduced hypertrophy. In conclusion, agents that altered calcium influx through the L-type Ca2+ channel or inhibited mechanical activity affected cardiomyocyte hypertrophy. The negative inotropic or chronotropic effects of calcium channel blockers on the heart may contribute to their efficacy in the treatment of myocardial hypertrophy.

Animals↗

PubMed1999

Normal regional distribution of membrane current density in rat left ventricle is altered in catecholamine-induced hypertrophy.

OBJECTIVE: To test the hypothesis that changes in the normal regional distribution of potassium and calcium currents contribute to the different regional changes in action potential duration in isoprenaline-induced hypertrophy in rats. METHODS: Hypertrophy was elicited in rats by seven daily injections of isoprenaline. Left ventricular myocytes were isolated from basal sub-endocardial, basal mid-myocardial and apical sub-epicardial tissue. Membrane currents were measured using the whole-cell patch-clamp technique at 35 +/- 1 degrees C. RESULTS: Cell membrane capacitance was similar in all three groups and was increased by 17% in hypertrophy (P < 0.001, t-test). Changes in the calcium-independent transient outward current (Ito1) density in hypertrophy were different in the three regions (P < 0.05, ANOVA). Ito1 was reduced in sub-epicardial (control, 23.4 +/- 2.0 pA pF-1; hypertrophy, 15.8 +/- 1.5 pA pF-1, P < 0.01 ANOVA) and in mid-myocardial myocytes (control, 24.0 +/- 2.8 pA pF-1; hypertrophy, 13.8 +/- 1.3 pA pF-1, P < 0.01 ANOVA) and was not significantly altered in sub-endocardial myocytes (control, 8.5 +/- 0.7 pA pF-1; hypertrophy, 7.4 +/- 1.8 pA pF-1). Steady-state background current density was reduced in hypertrophy (P < 0.05, ANOVA). The regional difference in steady-state background current in control hearts (P < 0.05, ANOVA) was altered in hypertrophy. Calcium current (ICa) density was similar in the three regions studied in both control and hypertrophied hearts. ICa was reduced in hypertrophy (P < 0.05, ANOVA). CONCLUSION: The normal regional differences in Ito1 are reduced, in steady-state background current are altered and in ICa are unchanged in catecholamine-induced hypertrophy in the rat left ventricle. These data may in part explain the reduction in the normal regional differences in APD observed in hypertrophy.

Action Potentials↗

PubMed2005

Targeting calcineurin and associated pathways in cardiac hypertrophy and failure.

Cardiac hypertrophy occurs in response to long-term increases in haemodynamic load related to a variety of physiological and pathological conditions. Cardiac hypertrophy developing in pathological conditions with increased load often progresses to a decompensated stage with cardiac contractile dysfunction, clinical signs of heart failure and premature death. Cardiac hypertrophy associated with adverse outcomes is said to be maladaptive. Conversely, there are settings where cardiac hypertrophy appears to be purely adaptive (e.g., hypertrophy in response to regular physical exercise). In these circumstances, hypertrophy is associated with preserved contractile performance and a favourable prognosis. Cardiac myocyte hypertrophy is controlled by growth factor receptors and mechanical stress sensors which activate a complex network of signalling pathways. These pathways promote a multitude of qualitative and quantitative changes in gene expression levels in cardiomyocytes. Reprogramming of gene expression, much more than cardiac (myocyte) hypertrophy per se, ultimately determines if cardiac hypertrophy will be adaptive or maladaptive. Pharmacological modification of gene expression in the hypertrophied heart may, therefore, be an attractive approach to prevent or even treat maladaptive hypertrophy and heart failure. Calcineurin is a serine-threonine phosphatase that is activated by sustained increases in [Ca2+]i in cardiomyocytes. Although it has been firmly established that calcineurin plays a critical role in the development of cardiac hypertrophy, the question of whether calcineurin activation serves an adaptive or maladaptive role is still unresolved. An answer to this question is crucial if calcineurin is to be developed as a drug target. The authors propose that calcineurin acts as a double-edged sword; excessive activation of calcineurin is maladaptive, its activation at endogenous levels and at specific subcellular microdomains, however, promotes adaptation. Calcineurin itself may, therefore, not be a convenient target for drug development. However, because maladaptive hypertrophy is ultimately a transcriptional disorder, definition of the transcriptional programme activated by distinct calcineurin activation levels may permit identification of novel, attractive drug targets.

Calcineurin↗

PubMed1988

[Morphological problems in cardiac hypertrophy].

Ventricular hypertrophy is categorized as (1) volume hypertrophy (eccentric hypertrophy or hypertrophy with dilatation), and (2) pressure hypertrophy (concentric hypertrophy or hypertrophy without dilatation). Hypertrophy per se is considered as a reaction to hemodynamic overload, both in occasions of excessive volume and of elevated pressure except in (idiopathic) cardiomyopathies. In patients with volume hypertrophy, some alteration of myocardial architecture is inevitable if the volume load exceeds a critical degree. Such alteration is characterized by deterioration of the median circular muscular layer of the ventricle resulting from over-stretching of the horizontally-coursing myocyte bundles. Hypertrophy of the inner oblique muscular layer of the left ventricle in cases with mitral regurgitation, and of the outer oblique muscular layer in cases with aortic regurgitation develops according to the changing configuration of the left ventricle; globular in the former, and elongated in the latter. In patients with pressure hypertrophy, there is some increase of the myocyte mass, with a disarrangement at the anterior triangle of the interventricular septum. The latter is physiologically situated at the anterior margin of the septum between the outer and median layers of both the ventricles. This seems to be a prelude to thickening of the septum and tends to hypertrophy of the free wall. A reduction in the deranged myocyte mass due to fibrosis or adiposis corresponds to arrest of the active hypertrophic process, and it may be the beginning of decompensation of cardiac function. Peculiar modes of dilatation and hypertrophy in cardiomyopathies have common denominators with those of known etiologies.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiomegaly↗

PubMed1985

[Apical hypertrophy and its genetic and acquired factors].

Although apical hypertrophy is characterized by a spade-like configuration of the left ventricle and giant negative T waves on electrocardiograms, the identity of apical hypertrophy in the disease spectrum of hypertrophic cardiomyopathy (HCM) is not fully established. The present study compared the demography, familial occurrence, and acquired factors of 43 patients who had apical hypertrophy with those of 104 patients who had asymmetric septal hypertrophy (ASH). Demographically, apical hypertrophy occurred predominantly in middle-aged males (86%). Family surveys showed that 13% of siblings of apical hypertrophy were affected, significantly less than in obstructive (31%) or non-obstructive (29%) HCM with ASH. Thirty-eight percent of siblings of ASH patients less than 35 years of age were affected, with a male/female ratio of 4/5, suggesting an autosomal dominant inheritance. The acquired factors associated with apical hypertrophy were assessed in a case-control study. Relative risk (odds ratio) of the condition was 3.46 (p less than 0.05) in those with histories of hypertension, and increased further to 8.09 (p less than 0.001) in those who were often hypertensive according to their physician's evaluations. Thus a strong association of hypertension with apical hypertrophy was suggested. However, hypertension in this condition was usually mild and labile, the blood pressure reverted to the normal range within several days of hospital admission, implying that transient hypertension during daily activity is associated with apical hypertrophy. Therefore, blood pressure response during exercise stress tests of 25 patients with apical hypertrophy was compared with that of age- and sex-matched controls. Slopes of linear regression between systolic blood pressure and heart rate and oxygen consumption during exercise, were used as indices of blood pressure response. They were significantly greater in apical hypertrophy than in the controls (1.2 +/- 0.4 vs 0.9 +/- 0.3, p less than 0.01 and 4.3 +/- 1.7 vs 2.8 +/- 0.8, p less than 0.001). This trend was observed even in patients without histories of hypertension. These findings suggested that apical hypertrophy has an inheritance pattern different from that of ASH, and has a possible association with acquired factors such as hypertension. Therefore, apical hypertrophy seemed to be a disease entity distinct from HCM with ASH, though it might be included in the disease spectrum of HCM.

Adult↗

PubMed1996

Left ventricular hypertrophy regression as a process with variable biological implications.

OBJECTIVE: To determine whether myocardial hypertrophy regression, similarly to hypertrophy itself, is a process of variable nature with different biological implications. DATA SOURCES: Current Contents and MEDLINE searches under myocardial hypertrophy and regression of hypertrophy-related headings were conducted. DATA EXTRACTION: The search covered the period from 1969 to 1994, and 89 articles dealing with both human and animal studies were used. DATA SYNTHESIS: The positive adaptive effect of left ventricular myocardial hypertrophy may be counterbalanced by increased incidence of heart failure, myocardial infarction or sudden death. The risk of undesirable cardiovascular events varies according to the character of hypertrophic growth. Reduction of cardiac mass to that of a normal heart need not always mean that the ventricle is normal in all aspects. Several forms of left ventricular hypertrophy regression may be distinguished. The hypertrophy regression of the athletic heart is of a physiological nature. The spontaneous regression of left ventricular hypertrophy as seen in the rabbit model of aortic insufficiency has a pathological aspect resulting in heart failure. The nature of therapeutically induced regression of hypertrophy may vary according to fibrotic tissue concentration, energetical state and the function of the regressed heart. CONCLUSION: The biological implication of hypertrophy regression varies especially with respect to the nature of hypertrophy and the mode of achievement of hypertrophied mass reversal. Only long term prospective studies can clarify the question as to which types of hypertrophy regression result in decreased cardiovascular risk.

Animals↗

PubMed1993

Effect of hypertrophy induced by pressure overload or volume overload on reperfusion induced arrhythmias in anaesthetised rats.

OBJECTIVE: The aim was to determine the effect of myocardial hypertrophy on the incidence and severity of arrhythmias following reperfusion after experimental coronary artery occlusion, and to establish if the effect differed between pressure overload hypertrophy and volume overload hypertrophy. METHODS: The experiments were performed in rats. Pressure overload hypertrophy was induced by aortic banding, and volume overload hypertrophy by perforation of the aortic valve. Four weeks after surgery, coronary artery occlusion and reperfusion experiments were performed. RESULTS: Both pressure and volume overloaded hearts exhibited a similar degree of left ventricular hypertrophy of about 45% weight gain compared to control animals. The total number of ventricular premature beats during reperfusion was not significantly increased in either model of hypertrophy. In contrast to volume overload, the incidence of reperfusion induced ventricular fibrillation was significantly increased in pressure overloaded hearts. Furthermore, there was a significant correlation between number of ventricular premature beats and degree of left ventricular hypertrophy, as well as between duration of ventricular tachycardia and degree of hypertrophy in the pressure overloaded group. Such correlations were not observed in hypertrophy due to volume overload. Neither volume nor pressure overload hypertrophy significantly increased mortality from ventricular fibrillation. CONCLUSIONS: An increase in cardiac mass per se does not necessarily aggravate reperfusion arrhythmias. The susceptibility to arrhythmias in this model seems to be critically dependent on the nature of the stimulus triggering left ventricular hypertrophy.

Animals↗