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PubMed1994

Use of the signal-averaged QRS duration for diagnosing left ventricular hypertrophy in hypertensive patients.

We analysed the diagnostic performance of the signal-averaged QRS duration for the detection of left ventricular hypertrophy in 100 consecutive outpatients (62 men and 38 women; mean age, 49.8 +/- 11.8 years) with essential hypertension and compared the results with some of the currently employed electrocardiographic criteria. Forty-eight healthy subjects (24 men and 24 women; mean age, 46.4 +/- 12.1) with normal physical, electrocardiographic and echocardiographic findings served as a control group to derive normal reference values for signal-averaged QRS duration. Twenty-six (26%) hypertensives (22 men and 4 women) had left ventricular hypertrophy echocardiographically defined as a left ventricular mass > or = 261 g in men and > or = 172 g in women or left ventricular mass index > or = 125 g/m2 in men and > or = 112 g/m2 in women. The signal-averaged QRS duration was different in patients with than in those without left ventricular hypertrophy (102.1 +/- 10.8 vs. 95.8 +/- 8.4 ms; P < 0.01). Also, in the group with left ventricular hypertrophy QRS duration was longer, although not significantly different, in men than in women (103.5 +/- 10.7 vs. 94.2 +/- 8.8 ms; P n.s.). The correlation between the signal-averaged QRS duration and left ventricular mass was weak but statistically significant in men (r = 0.34; P < 0.05) in women (r = 0.30; P < 0.05) and in men and women together (r = 0.42; P < 0.01). Partition values of filtered QRS duration > or = 114 ms in men and > or = 107 ms in women were used to diagnose left ventricular hypertrophy as these values were above the upper limits in our control men and women when 95% confidence intervals were calculated. These criteria were insensitive (12%) but highly specific (99%) for left ventricular hypertrophy. The use of a single threshold value of filtered QRS duration > or = 111 ms in both sexes combined improved sensitivity modestly (15%) while maintaining a good specificity (95%). Also, we tested the following standard electrocardiographic criteria: the Sokolow-Lyon index, the Romhilt-Estes point score > or = 4 points and > or = 5 points, the Cornell voltage criteria, the sum of QRS voltages in all 12 leads > 175 mm, and the QRS duration > 90 ms. Sensitivities ranged from 4% to 58% and specificities from 74% to 99%.(ABSTRACT TRUNCATED AT 400 WORDS)

Echocardiography↗
PubMed1992

Electrocardiographic detection of left ventricular hypertrophy by the simple QRS voltage-duration product.

OBJECTIVES: The object of this study was to assess the hypothesis that the product of QRS voltage and duration, as an approximation of the time-voltage integral of the QRS complex, can improve the electrocardiographic (ECG) identification of left ventricular hypertrophy. BACKGROUND: Electrocardiographic identification of left ventricular hypertrophy has been limited by the poor sensitivity of standard voltage criteria. However, increases in left ventricular mass can be more closely related to increases in the time-voltage integral of the summed left ventricular dipole than to changes in voltage or QRS duration alone. METHODS: Antemortem ECGs were compared with left ventricular mass at autopsy in 220 patients. There were 95 patients with left ventricular hypertrophy, defined by left ventricular mass index > 118 g/m2 in men and > 104 g/m2 in women. The voltage-duration product was calculated as the product of QRS duration and Cornell voltage (Cornell product) and the 12-lead sum of QRS voltage (12-lead product). RESULTS: At partitions with a matched specificity of 95%, each voltage-duration product significantly improved sensitivity for the detection of left ventricular hypertrophy when compared with simple voltage criteria alone (Cornell product 51% [48 of 95] vs. Cornell voltage 36% [34 of 95], p < 0.005 and 12-lead product 45% [43 of 95] vs. 12-lead voltage 31% [30 of 95], p < 0.001). Sensitivity of both the Cornell product and 12-lead product was significantly greater than that found for QRS duration alone (28%, 27 of 95, p < 0.005) and the Romhilt-Estes point score (27%, 26 of 95, p < 0.005), and compared favorably with the sensitivity of the complex Cornell multivariate score (44%, 42 of 95, p = NS). Comparison of receiver operating characteristic curves demonstrated that improved performance of the voltage-duration products for the detection of left ventricular hypertrophy was independent of test partition selection. In addition, test performance of the voltage-duration products was not significantly affected by the presence or absence of a bundle branch block. CONCLUSIONS: These data suggest that the simple product of either Cornell or 12-lead voltage and QRS duration can identify left ventricular hypertrophy more accurately than can voltage or QRS duration criteria alone and may approach or exceed the performance of more complex multiple regression analyses.

Bundle-Branch Block↗
PubMed1994

Analysis of transmural trend of myocardial integrated ultrasound backscatter for differentiation of hypertrophic cardiomyopathy and ventricular hypertrophy due to hypertension.

OBJECTIVES: This study was undertaken to differentiate hypertrophic cardiomyopathy from hypertensive hypertrophy using a newly developed M-mode format integrated backscatter imaging system capable of calibrating myocardial integrated backscatter with the power of Doppler signals from the blood. BACKGROUND: Myocardial integrated ultrasound backscatter changes in patients with hypertrophic cardiomyopathy; however, it is unknown whether ultrasound myocardial tissue characterization may be useful in differentiating hypertrophic cardiomyopathy from hypertensive hypertrophy. METHODS: Calibrated myocardial integrated backscatter and its transmural gradient were measured in the septum and posterior wall in 31 normal subjects, 13 patients with hypertensive hypertrophy and 22 patients with hypertrophic cardiomyopathy. The gradient in integrated backscatter was determined as the ratio of calibrated integrated backscatter in the endocardial half to that in the epicardial half of the myocardium. RESULTS: Cyclic variation of integrated backscatter was smaller and calibrated myocardial integrated backscatter higher in patients with hypertrophied hearts than in normal subjects, but there were no significant differences in either integrated backscatter measure between patients with hypertensive hypertrophy and those with hypertrophic cardiomyopathy. Transmural gradient in myocardial integrated backscatter was present only in patients with hypertrophic cardiomyopathy (5.0 +/- 1.8 dB [mean +/- SD] for the septum; 1.2 +/- 1.6 dB for the posterior wall). CONCLUSIONS: Hypertrophic cardiomyopathy and ventricular hypertrophy due to hypertension can be differentiated on the basis of quantitative analysis of the transmural gradient in integrated backscatter.

Acoustics↗
PubMed1996

Effects of chronic hypertension and left ventricular hypertrophy on the extent of infarct expansion in rats.

Left ventricular hypertrophy is an adaptive response to long standing hypertension. However, the influence of left ventricular hypertrophy with hypertension on extent of infarct expansion has not been studied. We compared the effects of left ventricular hypertrophy with hypertension on infarct expansion in spontaneously hypertensive rats (SHR, n = 76), Wistar-Kyoto rats (WKY; n = 46) and spontaneously hypertensive rats treated with delapril, an angiotensin converting enzyme (ACE) inhibitor (SHRD; n = 39). The survival rates at 7 days after myocardial infarction were 41%, 24%, and 46% for WKY, SHR, and SHRD. The survival rate of SHR was significantly lower than those of both SHRD and WKY (P < .05). In the surviving rats (18 SHR, 19 WKY, 18 SHRD), both left ventricular cavity area (LCVA) and the infarct segment length per the noninfarct segment length (FW/IVS), measured as indices of left ventricular dilation, were significantly less in SHR and SHRD than in WKY, and the thickness of the left ventricular free wall (Wth), used as an index of left ventricular thinning, was significantly higher in both SHR and SHRD than in WKY (P < .01). However, there was no significant difference in FW/IVS, LCVA, and Wth between SHR and SHRD. Hemodynamic findings 1 week after coronary occlusion demonstrated that all rats were in heart failure, and there were no significant differences in hemodynamics among the three groups. In conclusion, our findings showed that hypertrophy with hypertension reduced infarct expansion, but that reduction of blood pressure by ACE inhibitor did not reduce infarct expansion more than hypertrophy did. However, this finding suggest that an ACE inhibitor may improve the rate of survival of patients with left ventricular hypertrophy with hypertension.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2006

Heart rate variability in patients with cardiac hypertrophy--relation to left ventricular mass and etiology.

BACKGROUND: Decreased heart rate variability (HRV) has been shown to reflect disturbances of the autonomic nervous system that is related to increased cardiovascular mortality. Most studies investigated HRV in patients with systolic left ventricular dysfunction due to remote myocardial infarction or dilated cardiomyopathy. To date, only few data are available on HRV in patients with predominant diastolic dysfunction in the presence of cardiac hypertrophy of different etiologies. METHODS: Time domain analysis of HRV was performed from digital 24-hour Holter electrocardiogram recordings in 86 patients with sinus rhythm and cardiac hypertrophy, which was due to aortic valve stenosis in 33 patients, hypertrophic cardiomyopathy in 29 patients, and hypertensive heart disease in 24 patients. Heart rate variability analysis was compared with 91 healthy controls. RESULTS: The SD of all normal-to-normal R-R intervals (SDNN) was reduced in patients with aortic valve stenosis, hypertrophic cardiomyopathy, and hypertensive heart disease when compared with controls (SDNN 119 +/- 42 vs 154 +/- 36 milliseconds, P < .001). The extent of cardiac hypertrophy indexed by echocardiography based left ventricular mass calculation and increased patient age were independent predictors for depression of SDNN. CONCLUSIONS: Cardiac hypertrophy of various etiologies is related to decreased HRV on 24-hour Holter electrocardiogram. Both the patient age and the extent of left ventricular hypertrophy are independently associated with depression of HRV. These findings are independent of the cause of cardiac hypertrophy. The significance of these findings remains to be determined by future studies.

Aged↗
PubMed2006

Autologous chondrocyte implantation: natural history of postimplantation periosteal hypertrophy and effects of repair-site debridement on outcome.

PURPOSE: Our purposes were to report the clinical outcome of autologous chondrocyte implantation (ACI) patients with graft hypertrophy compared with that of unoperated ACI patients and to longitudinally assess the effects of graft hypertrophy debridement. METHODS: We divided 170 knee ACI patients with a minimum of 2 years' follow-up into groups according to the need for reoperation after ACI and the findings at surgery. Group A (n = 73) comprised patients who did not undergo reoperation, group B (n = 61) comprised patients who underwent reoperation and had findings unrelated to the repair, and group C (n = 36) comprised patients who underwent reoperation and had isolated graft hypertrophy. The International Knee Documentation Committee, modified Cincinnati knee rating, and Short Form 36 physical component scores for the 3 groups were compared. Of the repairs debrided because of graft hypertrophy, 41 were longitudinally assessed with arthroscopy or magnetic resonance imaging. RESULTS: The mean follow-up was 42.2 months. Patch-related problems were seen in 73.7% of cases undergoing reoperation less than 2 years after implantation, whereas cartilage-related problems were the dominant finding more than 2 years after implantation (70.2%). Group A patients fared significantly better than group B or C patients with regard to all 3 parameters measured, with no difference between groups B and C. Longitudinal assessment of 41 hypertrophied repairs revealed 18 with signs of pathology after graft debridement. CONCLUSIONS: This study shows that reoperation is frequent after ACI and is associated with a less satisfying outcome. Furthermore, debridement of a hypertrophied ACI graft appears to be detrimental as shown by longitudinal assessment of repairs. LEVEL OF EVIDENCE: Level IV, therapeutic case series.

Arthroscopy↗
PubMed2005

cAMP-response element-binding protein mediates prostaglandin F2alpha-induced hypertrophy of vascular smooth muscle cells.

Prostaglandin F(2alpha) (PGF(2alpha)) is a vasoactive factor that causes constriction and hypertrophy of vascular smooth muscle cells (VSMCs). However, the mechanism of PGF(2alpha)-induced hypertrophy is largely unknown. Cyclic AMP-response element (CRE)-binding protein (CREB), the best characterized stimulus-induced transcription factor, activates transcription of target genes with CRE and promotes cell growth. We examined the role of CREB in PGF(2alpha)-induced hypertrophy of VSMCs. PGF(2alpha) induced phosphorylation of CREB at serine 133, which is a critical marker of activation, after 5-10min of stimulation in a dose-dependent manner. Pharmacological inhibition of extracellular signal-regulated protein kinase and p38 mitogen-activated protein kinase (p38-MAPK) suppressed PGF(2alpha)-induced CREB phosphorylation. Inhibition of epidermal growth factor receptor (EGFR) and mitogen- and stress-activated protein kinase-1 also suppressed PGF(2alpha)-induced CREB phosphorylation. Overexpression of dominant-negative form of CREB (AdCREB M1), of which serine 133 was replaced with alanine, inhibited PGF(2alpha)-induced c-fos mRNA expression as well as hypertrophy of VSMCs [hypertrophy index (microg/10(4)cell); control 8.13, PGF(2alpha) 9.85, AdCREB M1 7.91, and AdCREB M1+PGF(2alpha) 8.43]. These results suggest that PGF(2alpha) activated CRE-dependent gene transcription through EGFR transactivation, and the CREB pathway plays a critical role in PGF(2alpha)-induced hypertrophy of VSMCs.

Animals↗
PubMed2004

Enhanced sarcolemmal Ca2+ efflux reduces sarcoplasmic reticulum Ca2+ content and systolic Ca2+ in cardiac hypertrophy.

OBJECTIVE: Recent work has identified reductions in the systolic Ca(2+) transient in cardiac disease states. The aim of the present study was to identify the mechanisms responsible for perturbations of intracellular calcium homeostasis in isolated cardiac myocytes and determine if such changes can quantitatively explain the reduced systolic Ca(2+) transient. METHODS: Left ventricular hypertrophy (LVH) was induced by aortic coarctation in adult ferrets. Changes in intracellular Ca(2+) regulation, sarcolemmal Ca(2+) fluxes and SR function were measured in single left ventricular cardiac myocytes. RESULTS: Cardiac hypertrophy was associated with a 29% increase in action potential duration (APD(90)); a 48% reduction in the amplitude of and 19% slowing in the rate of decay of the systolic Ca(2+) transient; a 20% decrease in SR Ca(2+) content and a 36% increase in inward Na(+)-Ca(2+) exchange current for a given change in [Ca(2+)](i) (all P<0.05). Peak L-type Ca(2+) current density, integrated Ca(2+) influx and SERCA2a protein levels remained unchanged in hypertrophy. By determining the relationship between SR Ca(2+) content and systolic Ca(2+), the reduction in SR Ca(2+) content quantitatively explained the smaller systolic Ca(2+) transient. The reduced SR Ca(2+) content also accounted for a smaller fractional release of Ca(2+) from the SR and lower gain of excitation contraction coupling in cardiac hypertrophy. The increased sarcolemmal-mediated Ca(2+) efflux was sufficient to explain the reduction in SR Ca(2+) content. CONCLUSIONS: The findings indicate that the primary mechanism underlying the smaller systolic Ca(2+) transient amplitude in cardiac hypertrophy is decreased SR Ca(2+) content occurring as a consequence of reduced SR Ca(2+)-ATPase-mediated Ca(2+) uptake and increased sarcolemmal-mediated Ca(2+) efflux from the cell. The increased Na(+)-Ca(2+) exchange-mediated current for a given change in intracellular Ca(2+) concentration provides a mechanism for the development of arrhythmias in the face of a reduced SR Ca(2+) load in cardiac hypertrophy.

Action Potentials↗
PubMed2004

Midwall mechanics in physiologic and hypertensive concentric hypertrophy.

OBJECTIVE: We sought to analyze and compare midwall fractional shortening (mFS), and its relations with circumferential end-systolic stress (cESS) and relative wall thickness (RWT), among subjects with physiologic concentric left ventricular (LV) hypertrophy, patients with hypertension and concentric LV hypertrophy, and control subjects. METHODS: A total of 51 normotensive athletes and 56 young patients with hypertension and echocardiographic evidence of concentric LV hypertrophy were enrolled. In addition, 49 age- and sex-matched control subjects were recruited. LV cavity size and wall thicknesses, LV mass, RWT, cESS, and mFS were determined by echocardiography. RESULTS: The 3 groups were similar in age, sex, height, weight, body surface area, LV diameters, and conventional indices of systolic function. LV thicknesses, RWT, LV mass, and LV mass index were similarly increased in the athletes and in the hypertensive group when compared with the control subjects. A similar depression in mFS was observed in both the athletes (22.4 +/- 2.6%) and hypertensive group (22.5 +/- 3.6%) in comparison with the control group (24.5 +/- 2.5%, P =.0003). The depression in mFS was still significant after taking into account the effect of cESS, but was no more evident after indexation of mFS by RWT or LV mass. At regression analysis, the relation between mFS and cESS showed a steeper negative slope in the patients with hypertension than in the other 2 groups. CONCLUSIONS: MFS is similarly depressed in physiologic and hypertensive concentric LV hypertrophy. The depression is abolished by adjustment for RWT or LV mass, suggesting that geometric factors are the major determinants of midwall performance in both types of concentric LV hypertrophy. However, an impaired response to different values of cESS seems to exist only in hypertensive concentric LV hypertrophy, because increasing levels of cESS may be associated with more evident mFS depression in patients with hypertension than in the athletes and control subjects.

Adult↗
PubMed2005

Comparison of cardiac function and valvular damage in children with and without adenotonsillar hypertrophy.

OBJECTIVE: Comparison of cardiac function in children with and without adenotonsillar hypertrophy. METHODS: We examined 28 pediatric patients with adenotonsillar hypertrophy mean aged 7.3+/-2.9 years comprised of 14 females and 14 males (group I). The control group were chosen from 35 healthy sex and age matched children mean aged 7.37+/-2.7 years (group II). Both groups were examined by an otorhinolaryngologist and adenotonsillar hypertrophy was diagnosed with nasal endoscopic method or lateral neck X-ray. All the patients in group I underwent adenotonsillectomy. Cardiologic and echocardiographic examinations were performed in both groups. Echocardiographic examination was done twice in group I (preoperative and postoperative first month) however in group II only once. Preoperative findings of group I compared with the findings of group II. Preoperative and postoperative echocardiographic findings were also compared within group I. The chi-square test and the independent paired-sample t-test were used for statistical analysis. RESULTS: The tricuspid end-diastolic time was the only significant difference in echocardiographic findings between the two groups (104.8+/-28.8 ms versus for 86.4+/-17.32 ms p<0.05). There was no statistical difference between preoperative and postoperative echocardiographic findings in group I. Brady-tachyarrhythmia was detected on electrocardiography - performed with 24h ambulatory electrocardiography - in one patient. To our surprise, in group I five patients had cardiac valve damage: mitral and/or aortic valve insufficiency. These findings were interpreted as silent carditis. CONCLUSION: There was no significant difference in right ventricular function between the children with and without adenotonsillar hypertrophy. Whereas, there was shortening of tricuspid end-diastolic time in group I. However, five patients having adenotonsillar hypertrophy developed a cardiac dysfunction which was not observed in the control group. Therefore, we assumed a correlation between adenotonsillar hypertrophy and possible silent carditis following frequent tonsillitis.

Adenoids↗
PubMed2005

Oxidants and antioxidants in tonsillar and adenoidal tissue in chronic adenotonsillitis and adenotonsillar hypertrophy in children.

OBJECTIVE: The aim of the study is to determine the possible role of oxidants and antioxidants in the pathogenesis of chronic adenotonsillitis and adenotonsillar hypertrophy in children. PATIENTS AND METHODS: The children were divided into infection and hypertrophy groups, which were comparable according to age and gender distribution. The infection group was consisted of 20 children with the diagnosis of chronic adenotonsillitis and the hypertrophy group was made up of 19 children with adenotonsillar hypertrophy to whom adenotonsillectomy was performed. Preoperative blood levels of erythrocyte MDA, serum MDA, erythrocyte catalase and serum catalase, and adenoidal and tonsillar tissue levels of MDA and catalase were studied. RESULTS: There were significant increase in tonsil MDA, adenoid MDA, tonsil catalase and adenoid catalase levels in infection group (p<0.05). CONCLUSION: Oxidants and antioxidants are found to have an important role in the pathogenesis of adenotonsillar hypertrophy and chronic adenotonsillitis. These findings strengthen the hypothesis that indicates adenotonsillar hypertrophy and chronic adenotonsillitis are different diseases of the same tissues.

Adenoids↗
PubMed2005

Neurocognitive abilities in children with adenotonsillar hypertrophy.

OBJECTIVE: Sleep apnea is one of the most deleterious disorders in children with adenotonsillar hypertrophy because it can induce hypoxemia of brain. Sleep apnea may lead to failure to thrive or to physical and mental delay in development, including cognitive disturbances. The aim of this study was to analyze the influence of adenotonsillar hypertrophy, causing obstructive sleep apnea on neurocognitive abnormalities. We were interested in sensorimotor coordination, perception, memory, learning ability, concentration, focused attention and language reception. MATERIALS AND METHODS: We examined 221 children. One-hundred and seventeen children had sleep apnea caused by adenotonsillar hypertrophy: 87 children aged 6-9 years and 34 children aged 10-13 years. The control group, without adenotonsillar hypertrophy, consisted of 104 healthy children. Both groups of children with and without apnea were examined psychologically to determine abilities and minor neurocognitive deficit. The token test (TT), diagnosis test of brain dysfunction (DCS-test), Luria auditory verbal learning test (LAVLT) and Rey complex figure test (RCFT) were applied to both groups. The tests: TT, DCS-test, RCFT were used to investigate the level of sensorimotor integration and perception processes. Memory and learning abilities were measured using LAVLT. The TT assessed language dysfunction in children. RESULTS: This study shows that adenotonsillar hypertrophy in children aged 6-9 years is associated with neurocognitive abnormalities such as: memory problems, concentration of attention deficits, learning disability, language dysfunction, lower sensorimotor integration and perception. The older children (aged 10-13 years) with adenotonsillar hypertrophy had memory problems and learning disabilities. They are likely to be caused by of concentration of attention deficits. The older children were found to have more severe language dysfunction. CONCLUSIONS: Our study shows that sleep apnea may lead to neurocognitive deficits. The results may be helpful in the process of making decision for or against surgery in doubtful cases. It is important to know the problems connected with apnea in order to recognize them and help the child develop by providing adequate treatment and cognitive stimulation.

Adenoids↗
PubMed2004

Detection of cervical nerve root hypertrophy by ultrasonography in chronic inflammatory demyelinating polyradiculoneuropathy.

Several studies have demonstrated abnormal MRI findings in chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), especially hypertrophy and abnormal enhancement of spinal nerve roots, but there have been few reports on ultrasonographic findings of spinal nerve roots in CIDP. To determine whether ultrasonography (US) enables detection of hypertrophy of the cervical nerve roots, how frequently hypertrophy occurs in CIDP, and whether US findings correlate with any clinical and laboratory features, US of cervical nerve roots was performed using a 7.5-MHz linear-array transducer in 13 CIDP patients and 35 control subjects. A coronal oblique plane with a transducer placed on the lateral side of the neck was used to visualize the cervical nerve roots just after their point of exit from the cervical foramina, and their diameters were measured. US demonstrated hypertrophy of the cervical nerve roots in 9 (69%) of the 13 CIDP patients as compared with findings in control subjects. The degree of hypertrophy was significantly associated with the level of CSF protein (chi2=5.8, p<0.05, logistic simple regression analysis) but not with other clinical features. US is considered to be a useful method for evaluating cervical nerve root hypertrophy, which is frequently seen in patients with CIDP, particularly in patients with elevated level of CSF protein.

Adult↗
PubMed1995

Left ventricular hypertrophy is more prevalent in patients with systemic hypertension with extracranial carotid arterial disease than in patients with systemic hypertension without extracranial carotid arterial disease.

The mechanism of the association between LV hypertrophy and ECAD is unknown and needs to be investigated. Whether LV hypertrophy in patients with systemic hypertension is a marker for ECAD or contributes to ECAD needs to be investigated. The association between LV hypertrophy and significant ECAD was independent of the level of blood pressure in our patients. Coronary atherosclerosis in our patients with signifciant ECAD may have contributed to the increased prevalence of LV hypertrophy. The association between LV hypertrophy and significant ECAD may contribute to the high incidence of stroke in patients with LV hypertrophy. This is currently under investigation by our group.

Aged↗
PubMed1995

Evidence favoring the hypothesis that ventricular arrhythmias have prognostic significance in left ventricular hypertrophy secondary to systemic hypertension.

In the present review 6 lines of evidence will be discussed that suggest a prognostic significance for ventricular arrhythmias in patients with systemic hypertension and left ventricular hypertrophy: (1) in patients with systemic hypertension there is a statistical relation between asymptomatic ventricular arrhythmias and left ventricular hypertrophy; (2) in nonhypertensive left ventricular hypertrophy the prognostic value of ventricular arrhythmias is well known; (3) left ventricular hypertrophy is related to sudden death in patients with systemic hypertension; (4) it is generally acknowledged that ventricular arrhythmias are a frequent cause of sudden death; (5) there is experimental evidence to support the arrhythmic risk of left ventricular hypertrophy; and (6) it has been recently demonstrated that ventricular arrhythmias influence mortality in patients with left ventricular hypertrophy secondary to systemic hypertension. However, whether asymptomatic ventricular arrhythmias are specific markers for more severe sustained arrhythmias, or just markers for a more severe stage of the disease, remains to be determined.

Arrhythmias, Cardiac↗
PubMed1995

Which definition for echocardiographic left ventricular hypertrophy?

Left ventricular (LV) hypertrophy is diagnosed on the basis of LV mass measurement at echocardiography. However, various thresholds for defining LV hypertrophy have been published, ranging from 111 to 134 g/m2 and from 100 to 125 g/m2 in men and women, respectively. The aim of our study was to evaluate variations in the prevalence of LV hypertrophy induced by the application of different threshold values among hypertensive subjects. LV mass was calculated in 349 hypertensive patients from an M-mode LV tracing obtained by left parasternal view in 83% and by subcostal view in 17% of patients. The prevalence of LV hypertrophy ranged from 17% to 39%, according to the threshold value applied (from 10% to 47%, and from 19% to 39% in women and men, respectively). As expected, the prevalence of LV hypertrophy in obese patients of both sexes was higher when applying the usual height-indexed threshold (143 and 102 g/m for men and women, respectively) than when applying the usual body surface area-indexed threshold (134 and 110 g/m2 for men and women, respectively). The use of normalized thresholds when comparing different indexation methods (in this case, 145 g/m for men, 120 g/m for women) will minimize these variations in part due to the threshold choice. Considering the clinical and therapeutic implications associated with the presence of LV hypertrophy, better standardization of definitions is needed; this could be based either on better-designed cooperative normality studies or meta-analysis of risk stratification.

Adult↗
PubMed2002

Involvement of cyclin D activity in left ventricle hypertrophy in vivo and in vitro.

OBJECTIVE: Cardiac hypertrophy is induced by a number of stimuli and can lead to cardiomyopathy and heart failure. Present knowledge suggests that cell-cycle regulatory proteins take part in hypertrophy. We have investigated if the D-type cyclins are involved in cardiac hypertrophy. METHODS: The expression and activity of the D-type cyclins and associated kinases in cardiomyocytes were studied during angiotensin II- and pressure overload-induced hypertrophy in rats (Rattus norvegicus) and in isolated, neonatal cardiomyocytes. Expression of the D-type cyclins was manipulated pharmacologically and genetically in neonatal myocytes. RESULTS: In the left ventricle, there was a low, constitutive expression of the D-type cyclins, which may have a biological role in normal, adult myocytes. The protein level and the associated kinase activity of the D-type cyclins were up-regulated during hypertrophic growth. The increase in cyclin D expression could be mimicked in vitro in neonatal cardiac myocytes. Interestingly, the cyclin Ds were up-regulated by hypertrophic elicitors that stimulate different signalling pathways, suggesting that cyclin D expression is an inherent part of cardiac hypertrophy. Treatment of myocytes with the compound differentiation inducing factor 1 inhibited expression of the D-type cyclins and impaired hypertrophic growth induced by angiotensin II, phenylephrine and serum. The response to hypertrophic elicitors could be restored in differentiation inducing factor 1-treated myocytes by expressing cyclin D2 from a heterologous promoter. CONCLUSION: Our results point to the D-type cyclins as important regulators of cardiac hypertrophy. This supports the notion that cell-cycle regulatory proteins regulate hypertrophic growth.

Angiotensin II↗
PubMed2003

Asynchronous development of electrical remodeling and cardiac hypertrophy in the complete AV block dog.

OBJECTIVE: Left ventricular hypertrophy has been associated with the prolongation of QT-time, and an increased risk of ventricular arrhythmias. The renin angiotensin system has been implicated in the development of ventricular hypertrophy. At 5 weeks complete AV block (CAVB) in the dog, there is: (1) biventricular hypertrophy associated with a transient activation of components of the renin angiotensin system, (2) increased APD, more pronounced in the left than in the right ventricle leading to spatial dispersion of repolarization, and (3) enhanced susceptibility to drug-induced torsade de pointes arrhythmias. To investigate whether these remodeling processes develop in parallel, time dependency was assessed in absence or presence of the AT1 receptor-blocker Irbesartan. METHODS AND RESULTS: Dogs in sinus rhythm, 2 and 5 weeks CAVB were compared to dogs chronically treated with Irbesartan (30 mg/kg BID). Endocardial monophasic APD of left and right ventricle was measured and susceptibility to torsade de pointes was tested by infusing Dofetilide (0.025 mg/kg/5'). Hypertrophy was determined by relating heart-to-body weight at sacrifice. Left ventricular APD had increased more than right ventricular APD at 2 and 5 weeks CAVB, leading to an increase in spatial dispersion. At that time torsade de pointes were evocable in the majority of the dogs. Hypertrophy had only developed completely at 5 weeks CAVB. Irbesartan had no effect on electrical and structural parameters or on arrhythmogenicity. CONCLUSIONS: In the CAVB dog ventricular hypertrophy is not a prerequisite for electrical remodeling or drug-induced torsade de pointes, and the AT1-receptor has no dominant role in the completion of these remodeling processes.

Angiotensin II↗