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PubMed1975

Mechanism of left ventricular outlfow obstruction in patients with obstructive asymmetric septal hypertrophy (idiopathic hypertrophic subaortic stenosis).

Left ventricular outflow obstruction in patients with idiopathic hypertrophic subaortic stenosis or obstructive asymmetric septal hypertrophy is due to abnormal forward motion during systole of the anterior mitral leaflet. To determine why some patients with this disease hav left ventricular outflow obstruction whereas others do not, we studied a large number of patiens with assymetric septal hypertrophy using both one- and two-dimensional echocardiography. In 100 patients with asymmetric septal hypertrophy and 22 normal subjects, mitral valve position at the onset of systole was quantitated by measuring the distance from the ventricular septum to the mitral valve and the distance from the mitral valve to the posterior left ventricular wall. None of the normal subjects and only 3 (6 percent) of 51 patients with nonobstructive asymmetric septal hypertrophy had a septal-mitral valve distance of less than 20 mm compared with 23 (66 percent) of 35 patients with obstructive asymmetric septal hypertrophy. Moreover, the mitral valve at the onset of systole was actually positioned forward in the left ventricular activity. Two-dimensional studies in 11 patients with obstructive asymmetric septal hypertrophy revealed that contraction of the malaligned papillary muscles did not cause the abnormal forward mitral valve motion. We propose that the left ventricular outflow obstruction in patients with obstructive asymmetric septal hypertrophy occurs as a result of two factors: (1) narrowing of the left ventricular outflow tract at the onset of systole, and (2) hydrodynamic forces generated by contraction on the left ventricle.

Aortic Stenosis, Subvalvular↗
PubMed1979

Cardiac hypertrophy in early hypertension.

Studies of cardiac hypertrophy in spontaneously hypertensive rats have indicated that left ventricular hypertrophy occurred even in the prehypertensive stage. These findings suggested that other factors besides blood pressure levels, and including possibly a genetic predisposition to myocardial hypertrophy, could play a role in structural cardiovascular alterations in spontaneously hypertensive rats. More recent studies have confirmed these anatomic results; left ventricular hypertrophy was vectorcardiographically detected even in the prehypertensive stage in voth young stroke-prone rats and stroke-resistant spontaneously hypertensive rats. Further, a close relation was found between degree of left ventricular hypertrophy and vascular hypertrophy or hyperplasia; this suggests that early detection of left ventricular hypertrophy may be a useful indicator of the incipient stage of structural vascular changes in genetic hypertension.

Adrenergic beta-Agonists↗
PubMed1988

Effect of mitral regurgitation on diastolic filling with left ventricular hypertrophy.

Earlier studies have suggested that mitral regurgitation (MR) augments early left ventricular (LV) diastolic filling. To determine whether MR affects early diastolic filling in patients with abnormal diastolic filling, transmitral pulsed-wave Doppler recordings were used to study 32 normal subjects, 21 patients with LV hypertrophy, 23 with LV hypertrophy and MR and 15 patients with MR. Patients with MR had increased peak early filling velocities (MR 108 +/- 27 cm/s, normal 80 +/- 16 cm/s, p less than 0.01), peak atrial filling velocities (MR 72 +/- 18 cm/s, normal 55 +/- 12 cm/s, p less than 0.05) and increased deceleration rates (MR 5.0 +/- 1.9 m/s2, normal 3.5 +/- 1.2 m/s2, p less than 0.05). Patients with LV hypertrophy had reduced peak early filling velocities (69 +/- 14 cm/s, p less than 0.05) and increased peak atrial filling velocities (83 +/- 16 cm/s, p less than 0.001). There was also an increase in the atrial filling fraction and reduction in the rapid filling fraction as compared with normal patients. Patients with LV hypertrophy and MR had increased peak early filling velocities (98 +/- 26 cm/s, p less than 0.01 vs normal, p less than 0.001 vs LV hypertrophy patients), increased atrial filling velocities (84 +/- 27 cm/s, p less than 0.001 vs normal), increased deceleration rates (4.4 +/- 2.4 m/s2, p less than 0.05 vs normal) and a normal distribution of diastolic filling. Within the LV hypertrophy and MR group, diastolic filling parameters were similar when patients were subgrouped on the basis of auscultability of MR. MR augments early diastolic filling and may tend to normalize diastolic filling patterns in LV hypertrophy patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiomegaly↗
PubMed1988

Sensitivity and specificity of electrocardiographic criteria for left and right ventricular hypertrophy in morbid obesity.

To determine the sensitivity and specificity of standard electrocardiographic criteria for left ventricular (LV) and right ventricular (RV) hypertrophy in morbid obesity, resting electrocardiograms and M-mode echocardiograms were obtained in 65 patients whose actual body weight was more than twice their ideal body weight and who were free from hypertension and organic heart disease not directly attributable to obesity. Electrocardiographic criteria for LV hypertrophy were tested using increased LV wall thickness, LV enlargement and increased LV mass (all determined echocardiographically) as diagnostic standards. Electrocardiographic criteria for RV hypertrophy were tested using echocardiographic RV enlargement or RV hypertrophy as a diagnostic standard. Sensitivity values for the electrocardiographic criteria for LV hypertrophy ranged from 0 to 13%, 0 to 20% and 0 to 12% using echocardiographic increased LV wall thickness, LV enlargement and increased LV mass, respectively, as diagnostic standards. Specificity values ranged from 73 to 100%, 87 to 100% and 83 to 100%, respectively, using these diagnostic standards. Sensitivity values for the electrocardiographic criteria for RV hypertrophy ranged from 0 to 16% and specificity values ranged from 95 to 100%. Combining electrocardiographic criteria within groups did not appreciably increase sensitivity and often decreased specificity to unacceptably low levels. The electrocardiogram is very limited in its ability to detect ventricular hypertrophy and chamber enlargement in morbidly obese patients.

Adult↗
PubMed1983

Determinants of left ventricular hypertrophy and function in hypertensive patients. An echocardiographic study.

Hypertensive patients present a wide spectrum of echocardiographic alterations. A review of these changes in 74 patients (37 untreated and 37 treated) revealed left ventricular hypertrophy in 43 (58 percent). There was no significant difference between treated and untreated patients in regard to either the prevalence of left ventricular hypertrophy or of its various subtypes [concentric left ventricular hypertrophy in 15 (20.3 percent), asymmetric septal hypertrophy in 16 (21.6 percent), and combined left ventricular hypertrophy and dilation in 12 (16.2 percent)]. None of the patients who showed asymmetric septal hypertrophy had abnormal motion of the mitral valve. Cardiac performance as judged by left ventricular percent shortening was related inversely to end-systolic stress (p less than 0.001) and positively to the ratio of end-systolic pressure/end-systolic volume (an index of myocardial contractility) (p less than 0.01). Multiple regression analysis showed an increased dependence on afterload (end-systolic stress), when left ventricular hypertrophy developed and especially when it was associated with left ventricular dilation.

Adolescent↗
PubMed1983

Identification of left ventricular hypertrophy: chest roentgenography, echocardiography, and electrocardiography.

The assessment of cardiac anatomy and function in the hypertensive population is an important aspect of the total evaluation of this patient group. The finding of cardiomegaly requires elucidation of its etiology. The finding of left ventricular hypertrophy on electrocardiogram is a harbinger for potential catastrophe, but other studies have indicated that the electrocardiogram may miss a substantial portion of the left ventricular hypertrophy which can be shown by echocardiogram: a normal electrocardiogram does not mean left ventricular hypertrophy is absent. Subtle changes on the electrocardiogram suggestive of left atrial abnormality must be pursued with echocardiography to eliminate the possibility of changes in left ventricular compliance or left ventricular hypertrophy. The prevention of left ventricular hypertrophy (or regression thereof) should be of major consideration to the clinician as he initiates antihypertensive therapy. The finding of left ventricular hypertrophy at the time of diagnosis tells the physician to implement aggressive and effective antihypertensive therapy. The absence of these findings should never imply, however, that therapy be withheld until indices of early or frank left ventricular hypertrophy are apparent.

Antihypertensive Agents↗
PubMed1983

Abnormalities in the coronary circulation that occur as a consequence of cardiac hypertrophy.

Myocardial ischemia is frequently observed in patients with cardiac hypertrophy even when the conduit coronary arteries are normal. Recent studies indicate that impaired coronary reserve in hypertrophied hearts probably occurs because growth of the coronary bed does not keep pace with increases in cardiac mass. The imbalance between vascular proliferation and muscle growth is probably most severe when cardiac hypertrophy is produced by pressure overload. Experimental studies also suggest that abnormalities intrinsic to pressure-hypertrophied heart muscle (decreased capillary density; decreased coronary reserve; electrophysiologic abnormalities) adversely affect the response of the enlarged heart to sudden coronary occlusion. When animals with hypertension and left ventricular hypertrophy are subjected to sudden coronary occlusion, the incidence of sudden cardiac death is increased severalfold and infarct size is substantially augmented. These observations suggest that abnormalities in the coronary microcirculation that accompany cardiac hypertrophy play a significant role in the pathogenesis of the complications associated with cardiac hypertrophy.

Animals↗
PubMed1996

Expression of the cardiac ryanodine receptor in the compensated phase of hypertrophy in rat heart.

OBJECTIVES: Abnormal calcium handling is a general feature of cardiac hypertrophy and alteration in the expression of SR proteins has been suggested to be involved in this alteration. To determine the expression of the cardiac ryanodine receptor (Ry2) gene during compensatory hypertrophy, we studied the mRNA and protein accumulation in left ventricles from rats with 30 to 100% hypertrophy. METHODS: Cardiac hypertrophy was obtained after 1 month of aortic constriction. Ry2 mRNA was analyzed by RNase protection assay, Northern and slot blots, and Ry2 protein by high-affinity [3H]ryanodine binding and Western blot. RESULTS: We demonstrate that: (1) the cardiac Ry2 mRNA concentration is decreased by 50% in severe hypertrophy; (2) both the density of the high-affinity sites and the Ry2 protein level are decreased by 25%; (3) the decrease in the mRNA and protein levels and the number of high-affinity sites are highly correlated to the severity of hypertrophy. CONCLUSION: Our results suggest that, as for SR Ca(2+)-ATPase, there is either a downregulation or a lack of upregulation of the gene coding for the Ry2 in compensatory hypertrophy. The decreased density of Ry2 may alter SR Ca2+ transport and contribute to the impaired Ca2+ handling by slowing the Ca2+ movements.

Animals↗
PubMed1991

Performance of new criteria for right ventricular hypertrophy and myocardial infarction in patients with pulmonary hypertension due to cor pulmonale and mitral stenosis.

Historically, electrocardiographic criteria for right ventricular (RV) hypertrophy has achieved high specificity but low sensitivity. Recently, however, Butler-Leggett et al. have introduced three criteria that attained a 66% sensitivity in a population with RV hypertrophy due to mitral stenosis while maintaining a 95% specificity in an extensive normal control group. Electrocardiographic diagnosis of RV hypertrophy is principally dependent on changes in the QRS complex that may be masked or mimicked by myocardial infarction (MI). This dilemma has been confirmed by documentation of the low specificity of both the Selvester QRS scoring system for MI size estimation (greater than 3 points) and its screening subset (greater than 0 points) in a pure mitral stenosis population. This study introduces the population characterized by RV hypertrophy due to cor pulmonale, which has a mean pulmonary arterial systolic pressure that is higher than the mean for the mitral stenosis population and consequently suggests more severe RV hypertrophy. When compared, the Butler-Leggett criteria for RV hypertrophy are more sensitive in the new population than in the mitral stenosis population (89% versus 60%) and the Selvester QRS scoring system is less specific (12% versus 60%). Three sequential steps are suggested for electrocardiographic analysis: (1) diagnosis of RV hypertrophy using the Butler-Leggett criteria, (2) diagnosis of MI using the Selvester screening criteria in those patients with step 1 negative, and (3) estimation of MI size using the complete Selvester scoring system in patients with step 1 negative and step 2 positive.

Cardiomegaly↗
PubMed1989

31P NMR spectroscopy of hypertrophied rat heart: effect of graded global ischemia.

To investigate the cause for the greater susceptibility of hypertrophied hearts to ischemic injury, we determined the interrelations of total work output, contractile function and energy metabolism in isolated, perfused normal and hypertrophied rat hearts subjected to graded global ischemia. Cardiac hypertrophy was induced by giving rats seven daily injections of either triiodothyronine (0.2 mg/kg) or isoproterenol (5 mg/kg). All hearts were perfused at an aortic pressure of 100 mmHg in the isovolumic mode in an NMR spectrometer (7.05 Tesla). Heart rate, developed pressure, and coronary flow were monitored simultaneously with changes in pH, creatine phosphate, ATP and inorganic phosphate. During pre-ischemic perfusion, the total work output (rate-pressure product) of hyperthyroid hearts was 28% higher than that of control hearts, whereas hearts from isoproterenol-treated animals showed no difference. However, when related to unit muscle mass, work was normal in hyperthyroid hearts and 26% lower after isoproterenol. Contractile function per unit myocardium (developed pressure/g wet weight) was lower in the hypertrophied hearts. ATP content was the same in all groups. Creatine phosphate decreased 41% after triiodothyronine and 25% after isoproterenol. Inorganic phosphate levels and intracellular pH were similar in control and isoproterenol-treated rat hearts, but were higher in the hyperthyroid rat hearts. The phosphorylation potential and the free energy change of ATP hydrolysis were lowered by hypertrophy, the levels correlating with the depressed contractile function. At each ischemic flow rate, both work and contractile function per unit myocardium were the same for all hearts, but the relations between flow and phosphorylation potential were different for each type of heart. Thus, at low flow rates, hypertrophied hearts perform the same amount of work and have the same contractile function as control hearts, but with abnormal changes in energy metabolism, indicating that the relations of energy status to coronary flow, total work output and contractile function are altered during the process of hypertrophy.

Adenosine Triphosphate↗
PubMed1991

Cyclic AMP in myocytes isolated from hypertrophied rat hearts.

Impaired inotropic responsiveness to isoproterenol stimulation has been reported in the hypertrophied hearts of spontaneously hypertensive rats and renal hypertensive rats. This study was carried out in order to investigate the possibility that a defect in cyclic AMP production by cardiac myocytes is responsible for the impaired inotropic responsiveness of these hearts. Basal and isoproterenol stimulated cyclic AMP levels were measured in ventricular myocytes isolated from hypertrophied rat hearts. Cyclic AMP accumulation was also measured in the presence of isobutyl-methyl-xanthine, a phosphodiesterase inhibitor, and the results were compared to the appropriate controls. In the spontaneously hypertensive rat, no changes were detected in the basal or isoproterenol stimulated cyclic AMP formation. This suggests that the biochemical alterations leading to a diminished inotropic response in this model of cardiac hypertrophy involve abnormalities in mechanisms other than cyclic AMP production. In the renal hypertensive rat, basal and isoproterenol stimulated cyclic AMP levels were significantly depressed as compared to controls. This suggests that abnormalities in the signal transduction mechanism and formation of cyclic AMP are, at least in part, responsible for the impaired inotropic responsiveness seen in this model. These results confirm that cardiac hypertrophy is a heterogeneous process. Reduced inotropic responsiveness to isoproterenol stimulation in the hypertrophied hearts of the SHR and the RHR, both models of pressure overload hypertrophy, involve different biochemical alterations. Results of this study suggest that the physiologic response of cardiac hypertrophy may not be as important as the underlying cause of hypertrophic stimuli in determining the pathophysiological consequences.

Animals↗
PubMed1991

Cardiac hypertrophy due to pressure and volume overload: distinctly different biological phenomena?

Myocardial hypertrophy is a morphological adaptive response to chronic work overload imposed on the heart. It has been categorized into two distinct basic types: concentric hypertrophy, occurring in response to a sustained pressure overload in which wall thickness increases without chamber enlargement, and eccentric hypertrophy, in response to a chronic volume overload in which chamber volume enlarges without a relative increase in its wall thickness. It should be emphasized, in this context, that these adjectives are somewhat confusing, since the hypertrophy observed is not eccentric in the fashion often seen in the left ventricle of patients with hypertrophic cardiomyopathy. In fact, the hypertrophy is concentric in both instances, but is associated with an increase in chamber volume when described as eccentric, yet occurring with a maintained volume when said to be concentric. In rats made anemic by iron deficiency, the volume overloaded heart achieves an adaptive increase in mass characterized as hypertrophy occurring in the setting of dilated ventricle. This so-called eccentric hypertrophy depends on catecholamines as possible signals for myocardial growth, and progresses with preserved ultrastructure and contractile performance of the cardiac muscle. A gradually imposed volume overload results in a harmonious growth of the heart (it retains a relative normal shape, becoming a magnified normal heart), probably mediated by release of catecholamines into the myocardium. This process resembles the normal cardiac growth in response to the obligatory volume load imposed by an increasing cardiac output (greater metabolic demands) and blood volume.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Can changes in sarcolemmal membranes account for the altered inotropic responsiveness in hypertrophied heart?

Hypertrophy is an adaptive mechanism of the heart subjected to pressure overload. Ultrastructural, electrophysiological and mechanical changes occur during this adaptation. A decrease in the inotropic responsiveness of the hypertrophied heart has often been observed as compared to the normal heart. Four sarcolemmal mechanisms that could account for this modification have been described. The mechanism of action of each system (calcium channel, alpha-and beta-adrenergic systems, (Na+,K+)-ATPase) of the hypertrophied heart has been compared to that of the normal heart. In spite of the paucity of results available relating to the calcium channel, the lengthening of the action potential in every case of compensatory hypertrophy could be explained by an altered functioning of the calcium channel. alpha- and beta-adrenergic systems in the hypertrophied heart could be modified at the receptor level itself, or at another level in the cascade of events under their control. For example, two different models of hypertrophy showed a decreased inotropic responsiveness correlated to a defect in the GS regulatory protein. The modification of the ouabain-receptor (Na+,K+)-ATPase mediates a decrease and a prolongation of the inotropic response. According to the modifications of each system, a direct relationship does not seem to exist between the stimulated membrane system and the inotropic responsiveness of the hypertrophied heart.

Cardiomegaly↗
PubMed1995

Dissociation of cardiac hypertrophy, myosin heavy chain isoform expression, and natriuretic peptide production in DOCA-salt rats.

We examined the relationship between cardiac hypertrophy, myosin heavy chain (MHC) isoform expression, and production of atrial natriuretic factor (ANF) and brain natriuretic peptide (BNP) before and after the development of DOCA-salt hypertension. DOCA-salt rats exhibited significant left ventricular hypertrophy at the prehypertensive stage (1 week of treatment), without MHC isoform switch or change in natriuretic peptide gene expression. In the hypertensive stage (5 weeks of treatment), pronounced left ventricular hypertrophy was observed, and this was characterized by an increase in beta-MHC protein, resulting in a switch from 90% alpha-MHC to 51% alpha-MHC and 49% beta-MHC. ANF and BNP mRNA levels and peptide content were significantly increased at this stage. Unexpectedly, the MHC isoform switch was evident in the non-hypertrophied right ventricle to the same degree as in the left ventricle. Natriuretic peptide production was also increased in the right ventricle at 5 weeks of treatment, but to a lesser degree than in the left ventricle. In contrast, in the hypertrophied left atrium there was no MHC isoform switch, while ANF and BNP mRNA levels were augmented. Plasma ANF was significantly increased in the prehypertensive stage; this was accompanied by a partial depletion of atrial ANF stores. Plasma BNP was increased only in the hypertensive stage, reflecting an increase in ventricular BNP synthesis and secretion. These results suggest that 1) cardiac hypertrophy, MHC isoform expression, and stimulation of natriuretic peptide production are processes that may be dissociated from each other; 2) increases in plasma ANF without a concomitant increase in plasma BNP reflect atrial hemodynamic overload, while increases in both ANF and BNP in plasma are associated with ventricular hypertrophy; and 3) there exist differences in the storage, secretion, and processing patterns of ANF and BNP in the atria.

Animals↗
PubMed1993

Cardiac beta-adrenoceptors, G-proteins and adenylate cyclase regulation during myocardial hypertrophy.

The role of the beta-adrenoceptor-G-protein-adenylate cyclase system in the pathogenesis of cardiac hypertrophy was studied. We have used a minipig model of pressure-overload cardiac hypertrophy secondary to aortic banding. Four groups of five animals were used: minipigs made hypertrophic were evaluated 2 months (CH2 group) and 9 months (CH9 group) later and compared to controls (C2 and C9 groups, respectively). A decrease in beta-adrenergic receptor density and an increase in antagonist affinity were shown in left ventricular membranes of hypertrophied animals compared with controls. In both groups, CH2 and CH9, an increase in EC50 for isoproterenol-stimulated adenylate cyclase activity, an increase in forskolin-stimulated adenylate cyclase activity and a diminished inhibition by carbachol of isoproterenol-stimulated adenylate cyclase were observed. In contrast, fluoride-stimulated adenylate cyclase activity was markedly increased only in the end stage of hypertrophy. alpha s-cholera toxin-catalysed ADP-ribosylation is increased in early hypertrophy and then decreases with late hypertrophy and a similar pattern is observed with alpha o pertussis toxin-catalysed ADP-ribosylation, whereas alpha i-ADP-ribosylation remains unchanged. Tissue content of Gs-, Gi- and Go-proteins, as assessed by specific antibodies, was found unchanged in CH9 and CH2 groups when compared with that in C9 and C2 control groups, respectively. Modifications in Gs functional activity in later hypertrophic stages, expressed as alterations in cholera toxin ADP-ribosylation and adenylate cyclase fluoride responsiveness, may be important in the pathogenesis of decompensation from compensated hypertrophy to cardiac failure.

Adenylate Cyclase Toxin↗
PubMed2005

Impaired insulin-signaling in hypertrophied hearts contributes to ischemic injury.

Despite increased glucose utilization by hypertrophied myocardium, these hearts exhibit a slower rate of glucose uptake (GU). We hypothesized that, in hypertrophied myocardium, a defect of the insulin-responsive glucose transporter is responsible for impaired GU and metabolism during ischemia, contributing to post-ischemic myocardial dysfunction. In a rabbit model of pressure-overload hypertrophy, GU ((31)P NMR spectroscopy) and total/phosphorylated insulin-signaling intermediates were assayed: insulin-receptor, insulin-receptor-substrate-1 (IRS-1), phosphatidylinositol-3-kinase (PI3-k), GLUT-4 translocation and contractile function in an isolated heart ischemia/reperfusion model. Total protein was not different between hypertrophied and control hearts. Phosphorylation of IRS-1 and PI3-k activity was significantly lower in hypertrophy during ischemia. GU was impaired pre-ischemia in hypertrophy, remained lower during early reperfusion, and was associated with impaired recovery of contractile function. In conclusion, a defect in IRS-1 phosphorylation and PI3-k activation in hypertrophied hearts restricts insulin-mediated GLUT-4 translocation and ischemia, a known stimulus of GLUT-4 translocation, does not compensate for this defect.

Animals↗
PubMed2007

Roles of cyclooxygenase-2 and phosphorylated Akt (Thr308) in cardiac hypertrophy regression mediated by left-ventricular unloading.

OBJECTIVES: Cyclooxygenase-2 is associated with cardiac hypertrophy during chronic heart failure and is regulated through the PI3K/Akt pathway. Cyclooxygenase-2-induced cell growth through Akt phosphorylation was demonstrated in vitro. In chronic heart failure, left ventricular assist devices lead to hypertrophy regression and molecular changes. Therefore, the expression of cyclooxygenase-2, phosphorylated Akt (p-Akt), and p-Erk 1/2, as well as cardiac hypertrophy before and after left ventricular assist device insertion, was investigated. METHODS: In myocardial tissue before and after left ventricular assist device insertion, the expression of cyclooxygenase-2, p-Akt (Thr308), p-Akt (Ser473), and p-Erk 1/2 was demonstrated by immunohistochemistry and quantified by morphometry. Colocalization of cyclooxygenase-2 and p-Akt (Thr308) was investigated by immuno-doublestaining. RESULTS: A significant decrease of cyclooxygenase-2, p-Akt (Thr308), p-Akt (Ser473), and p-Erk 1/2 protein expression and hypertrophy regression was observed after left ventricular assist device insertion. A significant correlation between cyclooxygenase-2 and p-Akt (Thr308) expression, as well as between cyclooxygenase-2 expression and cardiomyocyte diameter, was observed before, but not after, left ventricular assist device insertion. Only cyclooxygenase-2-positive cardiomyocytes showed significant hypertrophy regression on unloading. Sarcoplasmic colocalization of cyclooxygenase-2 and p-Akt (Thr308) is present before left ventricular assist device insertion and is decreased after unloading, whereas the normal myocardium is completely devoid of it. CONCLUSIONS: Left ventricular assist device treatment is associated with a significant decrease of cyclooxygenase-2, p-Akt (Thr308), p-Akt (Ser473), and p-Erk 1/2, and cardiac hypertrophy regression of cyclooxygenase-2-positive cardiomyocytes. The significant correlation and colocalization in cardiomyocytes of cyclooxygenase-2 and p-Akt (Thr308) before left ventricular assist device insertion suggests a cross-talk between the 2 molecules in the progression of cardiac hypertrophy, which is reversibly regulated by the left ventricular assist device.

Adolescent↗
PubMed2006

Potassium channel remodeling in cardiac hypertrophy.

Cardiac hypertrophy is an adaptive process against increased work loads; however, hypertrophy also presents substrates for lethal ventricular arrhythmias, resulting in sudden arrhythmic deaths that account for about one third of deaths in cardiac hypertrophy. To maintain physiological cardiac function in the face of increased work loads, hypertrophied cardiomyocytes undergo K(+) channel remodeling that provides a prolongation in action potential duration and an increase in Ca(2+) entry. Increased Ca(2+) entry, in turn, activates signaling mechanisms including a calcineruin/NFAT pathway to permit remodeling of the K(+) channels. This results in a positive feedback loop between the K(+) channel remodeling and altered Ca(2+) handling; this loop may represent a potential therapeutic target against sudden arrhythmic deaths in cardiac hypertrophy. The purposes of this review are to: (1) discuss types of K(+) channels and their mRNA that undergo remodeling in cardiac hypertrophy; (2) report on recent research on molecular mechanisms of K(+) channel remodeling; and (3) address physiological events underlying new therapeutic modalities to ameliorate arrhythmias and sudden death in cardiac hypertrophy.

Action Potentials↗