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PubMed2001

Using 12-lead ECG and synthesized VCG in detection of right ventricular hypertrophy with terminal right conduction delay versus partial right bundle branch block in the pediatric population.

In pediatric electrocardiogram (ECG) analysis, mild right ventricular hypertrophy (RVH) and especially mild RVH with terminal right conduction delay (RVHtcd) are often confused with partial right bundle branch block (PRBBB). This is problematic for computer ECG analysis algorithms and even for most experienced pediatric cardiologists. This study was designed to achieve better classification of mild RVHtcd and PRBBB by combining the 12-lead synthesized vectocardiogram (VCG) transverse plane measurements with scalar ECG measurements. Pediatric ECGs used in the study were recorded with 15 leads and a 500 Hz sampling rate at the Lucile Salter Packard Children's Hospital, Stanford University Medical Center. Out of 4,200 ECGs collected consecutively over a period of 18 months, 447 RVH, 335 RBBB and 589 Normal were interpreted by expert pediatric cardiologists, and were included in the study. Statistical comparison of ECG and VCG measurements were done in stratified ECG sets (412) that have a visually indistinguishable waveform pattern, 117 RVHtcd, 96 PRBBB and 199 normal, showed significant differences in initial and terminal vectors in the transverse plane. The mean angle of the initial vector was anterior (57.2 degrees +/- 41.8) in the normal group, left anterior in the PRBBB group (34.4 degrees +/- 39.5) and in the RVHtcd group (31.9 degrees +/- 41.0) and. The mean angle of the terminal vector was right anterior (158.3 degrees +/- 36.8) in the PRBBB group, rightward (179.7 degrees +/- 29.9) in the RVHtcd group and right posterior (212.6 degrees +/- 37.8) in the normal group. These are clearly applicable features for a classification algorithm. Significantly improved classification results were obtained from a new algorithm using combined ECG and VCG measurements versus an existing algorithm. The limitation of this study stems from the unavailability of a more reliable gold standard. It may be necessary to used body surface potentials obtained with a large number of electrodes to accurately differentiate the study groups.

Adolescent↗
PubMed1981

Scoring technique for diagnosis of ventricular hypertrophy from three orthogonal lead electrocardiogram.

A prospective study for the development of scoring techniques for the diagnosis of ventricular hypertrophy from the three orthogonal lead electrocardiogram was undertaken. A total of 51 hearts was examined at necropsy in a training group on which the scoring techniques were developed and a test group of a further 82 hearts was studied to assess the sensitivity and specificity of the method. The hearts were classified as being normal or having left ventricular hypertrophy, right ventricular hypertrophy, biventricular hypertrophy, or were placed in a borderline category. These classifications were based on the measurement of the weight of the left ventricular free wall, the interventricular septum, and the right ventricular free wall. Classical electrocardiographic variables were selected and assigned a point score on the basis of their diagnostic value. The electrocardiographic diagnosis of left ventricular hypertrophy, right ventricular hypertrophy, and biventricular hypertrophy was then made when the relevant score exceeded four points. After excluding 25 cases which showed conduction defects or were regarded as borderline at necropsy, 57 cases remained in the test group for assessing the technique. The sensitivity and specificity for left ventricular hypertrophy were 65 per cent and 91 per cent, respectively. For right ventricular hypertrophy corresponding results were 53 and 90 per cent. For biventricular hypertrophy the sensitivity was lower at 42 per cent, with a corresponding specificity of 93 per cent. These results represent a considerable improvement over older techniques, with up to a tenfold increase in sensitivity being obtained. The technique can be applied with or without computer assistance.

Adult↗
PubMed1982

Concurrent left and right ventricular hypertrophy in dog models of right ventricular overload.

In two pressure and volume overload models of canine right ventricular hypertrophy, we have demonstrated significant hypertrophy of both the left and the right ventricles. The extent of hypertrophy was correlated positively to the extent of the increase in plasma epinephrine in both volume and pressure overload models. Attenuation or ablation of plasma epinephrine through the administration of propranolol, a beta-adrenergic blocker, or by denervation of the adrenal medulla prevented the hypertrophy process. No hemodynamic parameter was altered consistently in a parallel manner to hypertrophy. This is the first report of concurrent right and left ventricular hypertrophy in response to pressure or volume overload of the right ventricle. These studies further implicate epinephrine as a major trophic hormone of the heart.

Animals↗
PubMed1985

Right ventricular myocardial infarction in patients with chronic lung disease: possible role of right ventricular hypertrophy.

To determine the relation between right ventricular hypertrophy and right ventricular myocardial infarction in patients with chronic lung disease, the records of 28 patients with chronic lung disease, inferior myocardial infarction and significant coronary artery disease (group I) and 20 patients with right ventricular hypertrophy, chronic lung disease without inferior myocardial infarction or significant coronary artery disease (group II) were reviewed. Chronic lung disease was diagnosed by clinical criteria, chest radiographs and pulmonary function tests. All patients had postmortem examinations. Patients in group I were classified into two subgroups: group Ia (without right ventricular hypertrophy) and group Ib (with right ventricular hypertrophy). Right ventricular wall thickness was 3.3 mm +/- 0.5 in group Ia, 6.0 mm +/- 1.1 in group Ib and 8.8 mm +/- 2.4 in group II (group Ia versus Ib, p less than 0.001; group Ia versus II, p less than 0.001; group Ib versus II, p less than 0.001). Eleven patients (78.6%) in group Ib (chronic lung disease with both right ventricular hypertrophy and inferior myocardial infarction) had right ventricular myocardial infarction compared with only 3 patients (21.9%) in group Ia (chronic lung disease without right ventricular hypertrophy and with inferior myocardial infarction) (p less than 0.008). Isolated right ventricular myocardial infarction occurred in four patients (20%) in group II (chronic lung disease with right ventricular hypertrophy, but without evidence of infarction of the left ventricle or significant coronary artery disease). There was no significant difference in the extent of anatomic coronary disease in groups Ia and Ib.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2003

Dynamic changes of gene expression in hypoxia-induced right ventricular hypertrophy.

Hypobaric hypoxia induces right ventricular hypertrophy. The relative contribution of pulmonary hypertension, decreased arterial oxygen, and neuroendocrine stimulation to the transcriptional profile of hypoxia-induced right ventricular hypertrophy is unknown. Whereas both ventricles are exposed to hypoxia and neuroendocrine stimulation, only the right ventricle is exposed to increased load. We postulated that right ventricular hypertrophy would reactivate the fetal gene transcriptional profile in response to increased load. We measured the expression of candidate genes in the right ventricle of rats exposed to hypobaric hypoxia (11% O(2)) and compared the results with the left ventricle. Hypoxia induced right ventricular hypertrophy without fibrosis. In the right ventricle only, atrial natriuretic factor transcript levels progressively increased starting at day 7. Metabolic genes were differentially regulated, suggesting a substrate switch from fatty acids to glucose during early hypoxia and a switch back to fatty acids by day 14. There was also a switch in myosin isogene expression and a downregulation of sarcoplasmic/endoplasmic ATPase 2a during early hypoxia, whereas later, both myosin isoforms and SERCA2a were upregulated. When the right and left ventricle were compared, the transcript levels of all genes, except for myosin isoforms and pyruvate dehydrogenase kinase-4, differed dramatically suggesting that all these genes are regulated by load. Our findings demonstrate that hypoxia-induced right ventricular hypertrophy transiently reactivates the fetal gene program. Furthermore, myosin iso-gene and pyruvate dehydrogenase kinase-4 expression is not affected by load, suggesting that either hypoxia itself or neuroendocrine stimulation is the primary regulator of these genes.

Adaptation, Physiological↗
PubMed1987

Right ventricular hypertrophy is an important determinant of right ventricular infarction complicating acute inferior left ventricular infarction.

To explore the role of right ventricular hypertrophy and chronic obstructive pulmonary disease in the pathogenesis of right ventricular infarction, 27 consecutive patients with a first inferior left ventricular infarction were prospectively studied. Right ventricular infarction was diagnosed using established hemodynamic criteria. Right ventricular hypertrophy was defined as right ventricular free wall thickness greater than or equal to 5 mm. Patients were classified into two groups: Group I patients with right ventricular infarction (n = 15), and Group II patients without right ventricular infarction (n = 12). The ratio of forced expiratory volume over forced vital capacity (FEV1/FVC) and forced expiratory flow between 25 and 75% expired volume (FEF) as a percent of predicted values were significantly reduced in Group I versus Group II (90 +/- 5 versus 105 +/- 6% and 63 +/- 13 versus 103 +/- 15%, respectively; p less than 0.05). This was associated with increased right ventricular wall thickness (Group I 5.5 +/- 0.3 mm versus Group II 3.9 +/- 0.2 mm, p less than 0.001). Multiple logistic regression analysis demonstrated that right ventricular wall thickness was the strongest predictor of right ventricular infarction (p less than 0.0005). No significant difference was found in the site of right coronary occlusion, collateral blood supply or extent of coronary artery disease between the two groups. These findings suggest that right ventricular hypertrophy predisposes patients with acute inferior myocardial infarction to right ventricular infarction independent of the site or extent of coronary artery disease.

Adult↗
PubMed1991

Biventricular down-regulation of beta-adrenergic receptors in right ventricular hypertrophy induced by monocrotaline.

To investigate the changes in beta-adrenergic receptors in the right and left ventricles during the development of cardiac hypertrophy, right ventricular hypertrophy (RVH) was induced in rats by a single injection of monocrotaline (M) (60 mg/kg). The rats demonstrated RVH at 2 weeks and severe RVH with congestive heart failure at 4 weeks after the injection. Changes in the beta-adrenergic receptors in the membrane fractions of both ventricles were examined in the M-treated vs. control rats using 125I-iodocyanopindolol (ICYP). Plasma and tissue catecholamines were measured. Plasma levels of norepinephrine (NE) and epinephrine (EP) showed no change at 2 weeks after the injection. However, at 4 weeks there was a significant increase in NE (p less than 0.01), but not in EP. There was no significant change in NE or EP in either ventricle at 2 weeks vs. the controls. However, at 4 weeks there was a significant increase in both NE and EP in the right ventricle (RV) (p less than 0.05). NE in the left ventricle (LV) tended to increase, but not a significant extent (p less than 0.1). With the development of RVH at 2 weeks, the maximum number of binding sites (Bmax) in both the RV and LV showed a significant decrease (p less than 0.01). There was a 21% decrease of Bmax in the RV and 15% in the LV at 2 weeks vs. the controls. At 4 weeks, the changes in Bmax were more prominent, with a 57% decrease in the RV and 22% in the LV.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Production and reversibility of right ventricular hypertrophy and right heart failure in dogs.

Combined heart-lung transplantation has been used for end-stage primary pulmonary hypertension. Experience with single-lung transplantation for other conditions suggested that associated severe right ventricular dysfunction resulting from increased afterload would recover after placement of a satisfactory lung allograft. Early experience with the application of single-lung transplantation for pulmonary hypertension supports this contention. We devised a reversible canine model of chronic progressive pressure-overloaded right heart failure by pulmonary artery banding to study the echocardiographic, hemodynamic, and pathological reversibility of the failing right heart. Clinical right heart failure was defined as the development of ascites and pleural effusions. Right heart failure developed in 23 dogs 67 to 348 days after banding, and they were divided into two groups to determine its early and long-term effects. Group 1 dogs (n = 11) were either sacrificed immediately after the onset of right heart failure (n = 5) or unbanded (n = 6); group 2 dogs (n = 12) were maintained in right heart failure for 3 months and then either sacrificed (n = 6) or unbanded. Unbanded dogs in both groups were observed for 4 additional months before sacrifice. A control group of 6 normal dogs was sacrificed for pathological comparisons. After unbanding, the right ventricular systolic pressure fell from 97 +/- 17 mm Hg (group 1) and 88 +/- 31 mm Hg (group 2) to 44 +/- 11 mm Hg and 47 +/- 13 mm Hg, respectively. Despite this persistent gradient across the pulmonary artery, echocardiographic and hemodynamic measures of right ventricular function returned to normal, albeit more slowly in the group 2 dogs.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Echocardiographic detection of right ventricular hypertrophy.

M-mode echocardiographic right ventricular wall thickness (RVW) and diastolic right ventricular internal diameter (RVID), when above the accepted normal range (RVW less than or equal to 5 mm, RVID less than or equal to 26 mm), are frequently used clinically to predict the presence of right ventricular hypertrophy. RVID was compared to anatomic right ventricular mass (RVM) in 27 patients and to RVW in 13 patients to determine their accuracy for predicting right ventricular hypertrophy (RVM greater than 65 gm). When increased, both measurements were specific for right ventricular hypertrophy. The specificity for RVW above 5 mm was 100% and for RVID greater than 26 mm was 79%. Neither was a sensitive indicator of hypertrophy. Only 36% of those with anatomic right ventricular hypertrophy had an echocardiographically dilated ventricle, and 67% had a thickened free wall. Neither measurement proved to be an accurate predictor of RVM, with a correlation for RVW of 0.56 and for diastolic RVID of 0.19.

Cardiomegaly↗
PubMed1994

Intraventricular changes in the beta-adrenoceptor-adenylate cyclase system of the rat heart with the progress of monocrotaline-induced right ventricular hypertrophy.

We investigated the changes in the membranous beta-adrenoceptor-adenylate cyclase system in the right ventricle, left ventricle and interventricular septum during the progress of monocrotaline-induced right ventricular hypertrophy and failure. The beta-adrenoceptor density was decreased in hypertrophied right ventricle 2 to 4 weeks after treatment. When the rats showed symptoms of right ventricular failure 4 weeks after treatment, the beta-adrenoceptor density was decreased in the interventricular septum. Both basal and forskolin-stimulated adenylate cyclase activities were decreased in the right ventricle at 3 and 4 weeks, and in the interventricular septum at 4 weeks, after treatment, which indicates that the catalytic activity of adenylate cyclase is reduced. Changes in isoproterenol plus Gpp (NH) p- or sodium fluoride-stimulated adenylate cyclase activity were generally similar to those in basal activity. These data indicate that a chamber-specific decrease in beta-adrenoceptor density begins in the early stages of right ventricular hypertrophy, and that beta-adrenoceptor density and adenylate cyclase activity in the interventricular septum are decreased in the advanced stages of heart failure in monocrotaline-treated rats.

5'-Nucleotidase↗