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At least 19 recordsLinked to original sources

The relationship of right ventricular hypertrophy, right ventricular failure, and ascites to weight gain in broiler and roaster chickens.

Nine hundred twenty-five male progeny from 50 sire families of a commercial sire line were weighed at 14, 28, and 47 days and scored for right ventricular hypertrophydilation at 48 days. Broilers with marked hypertrophy of the right ventricle at processing (298 of 925) were significantly heavier than their more normal contemporaries at 14 and 28 days of age. These results suggest that rapidly growing broilers are more susceptible to increased pulmonary arterial pressure resulting in right ventricular hypertrophy, right ventricular failure, and ascites than slower-growing broilers. Thirty-five (3.5% of 997) broilers died from right ventricular failure and ascites, and 14 (1.5% of 925) has ascites at processing. Two hundred fifty-nine sibs were kept on full feed to 16 weeks of age. Between 7 and 16 weeks, 68 (26.3%) of these cockerels died from right ventricular failure and ascites and a further 27 (10.4%) had marked right ventricular hypertrophy-dilation when processed at 16 weeks. Thus most of the 298 broilers classified as having marked right ventricular hypertrophy at 7 weeks would likely have died from right ventricular failure and ascites if they had been kept on full feed until 16 weeks.

Animals↗

QRS areas improve the electrocardiographic interpretation of right ventricular hypertrophy.

Right ventricular hypertrophy (RVH) is the most frequent abnormality in children with heart disease. We have developed a computer electrocardiogram (ECG) diagnosis program to evaluate new scalar electrocardiographic criteria for the diagnosis of this condition in children. The overall performance of our program was comparable to that of a pediatric cardiologist. Computer program diagnosis was correct in 93% of 60 individuals using standard criteria and in 97% using our newly developed area criteria. The cardiologist's ECG diagnosis in the same individuals was correct in 99%. The sensitivities of our two new criteria, the R/S area ratio in lead V1 and the R wave area in lead V1, were greater than currently used criteria for the diagnosis of RVH. Computer-derived electrocardiographic measurements, such as areas, can improve the accuracy of the ECG diagnosis of RVH.

Adolescent↗

Usefulness of echocardiographic right ventricular measurements in estimating right ventricular hypertrophy and right ventricular systolic pressure.

Right ventricular wall thickness (T) measurements were made in 111 patients by echocardiography to evaluate their usefulness in diagnossing right ventricular hypertrophy (RVH) and in predicting right ventricular peak systolic pressure (P). Anatomic and echocardiographic findings of RVH were compared in 36 of 111 subjects: diastolic T (dT) and systolic T (sT) had a sensitivity of 90 and 34% and a specificity of 94 and 100%, respectively, in the diagnosis of RVH. Echocardiographic and hemodynamic findings were compared in the remaining 75 of 111 patients undergoing cardiac catheterization: dt was 6.5 +/- 2.7 mm in 46 patients with elevated P (58.2 +/- 30.2 mm Hg) versus 3.8 +/- 0.9 in 29 patients with normal P (26.3 +/- 2.7 mm Hg) (p less than 0.01). The dT and P had a linear correlation (r = 0.92) in 40 patients with right ventricular end-diastolic dimension less than 13 mm/m2. Estimates of P in 22 patients with atrial septal defect and right ventricular end-diastolic dimension greater than 13 mm/m2 were fairly good (r = 0.83). It is concluded that echocardiographic measurements of T are useful in diagnosing RVH and in estimating P.

Adolescent↗

Electrocardiographic differentiation of posterobasal left ventricular hypertrophy from right ventricular hypertrophy.

Increased terminal rightward forces manifested by S waves greater than the 95th percentile (95%) for age in the left chest leads of the ECG can be produced by right ventricular hypertrophy (RVH) and posterobasal left ventricular hypertrophy (LVH). There are no currently available criteria to differentiate these. The S wave in lead V5 exceeded the 95% for age in 445 of 5,240 patients (8.5%). From these, the ECGs of patients with lesions known to produce "isolated" RVH (46 patients) or LVH (38 patients) were chosen for study. Analysis of these ECGs revealed two patterns in each group: 1. Voltage criteria for ventricular hypertrophy other than SV5 & SV6 were present in 26 patients of the RVH group and 15 of the LVH group; 2. The ECGs of the remaining 20 of the RVH and 23 of the LVH group contained no other voltage criteria to diagnose either RVH or LVH. These 43 ECGs were further analyzed. SV5, SV6 and RV5 were similar in both groups (p greater than 0.01). However, SI, R'V4R, R'V1 and the ratio RV2/SV2 were higher (p less than 0.01) and SV2 was lower (p less than 0.01) in the RVH group. Despite significant differences, there was marked overlap of the data. Therefore, discriminant analysis was performed which suggested RVH if SI greater than 5mm, RV2 greater than 10mm and the ratio RV2/SV2 greater than 0.65, and LVH if SI less than 5 mm, RV2 less than 10mm and the ratio RV2/SV2 less than 0.65. In the frontal plane the mean QRS vector was similar; however, in the horizontal plane, it varied between +60 degrees to +200 degrees in the RVH group and between -10 degrees to -130 degrees in the LVH group. The rotation of the QRS loop in the horizontal plane was clockwise (CW) or figure of eight in RVH group and counterclockwise (CCW) in the LVH group. The orthogonal vector data confirm these results. It is concluded that when SV5 is greater than 95% for age and there are no other clear voltage criteria for ventricular hypertrophy the diagnosis of RVH vs LVH may be made on the basis of the following: RVH: RV2 greater than 10mm, SI greater than 5mm and mean horizontal plane QRS vector between +60 degrees to +200 degrees with a CW or a figure of eight loop and LVH: RV2 less than 10mm, SI less than 5mm and mean horizontal plane QRS vector between -10 degrees to -130 degrees with CCW loop.

Cardiomegaly↗

Reduction of maximal coronary vasodilator capacity in conscious dogs with severe right ventricular hypertrophy.

Right coronary reactive hyperemia and the maximal coronary vasodilator response to adenosine were examined in conscious, normal dogs and dogs with right ventricular (RV) hypertrophy. RV hypertrophy was induced by chronic (5-7 months) pulmonary artery stenosis. With RV hypertrophy, RV weight to body weight ratio rose by 70% (P < 0.001), right coronary artery blood flow (Doppler ultrasonic technique) rose from 17 +/- 1 to 51 +/- 5 ml/min, and RV transmural blood flow (radioactive microsphere technique) increased from 0.78 +/- 0.06 to 1.62 +/- 0.10 ml/min per g, while the RV endocardial:epicardial perfusion ratio decreased from 1.36 +/- 0.04 to 1.0 +/- 0.02. Excess blood flow debt repayment following release of a 15-second right main coronary artery occlusion was attenuated markedly (P < 0.001) to 107 +/- 22% from the normal value of 325 +/- 41%. Maximal coronary vasodilator capacity (to iv adenosine) was reduced in the hypertrophied right ventricle, as reflected by a lower (P < 0.05) level of maximal transmural blood flow and a higher (P < 0.02) level of minimum coronary vascular resistance per gram of hypertrophied right ventricle compared to normal. During maximal coronary vasodilation, the endocardial:epicardial perfusion ratio decreased (P < 0.001) below unity in the hypertrophied right ventricle to a level (0.83 +/- 0.06) significantly lower (P < 0.001) than normal (1.16 +/- 0.03). Thus, the development of severe RV hypertrophy is characterized by an attenuated coronary response to acute ischemia and by a reduction in maximal coronary vasodilator capacity. We conclude that the increase in cardiac mass which results from chronic pulmonary artery stenosis is not accompanied by a proportionate increase in cross-sectional area of coronary vessels supplying the hypertrophied ventricle.

Adenosine↗

Reduction of I(Ca,L) and I(to1) density in hypertrophied right ventricular cells by simulated high altitude in adult rats.

The present paper describes the effect of a simulated hypobaric condition (at the altitude of 4500 m) on morphological characteristics and on some ionic currents in ventricular cells of adult rats. According to current data, chronic high-altitude exposure led to mild right ventricular hypertrophy. Increase in right ventricular weight appeared to be due wholly or partly to an enlargement of myocytes. The whole-cell patch-clamp technique was used and this confirmed, by cell capacitance measurement, that chronic high-altitude exposure induced an increase in the size of the right ventricular cells. Hypertrophied cells showed prolongation of action potential (AP). Four ionic currents, playing a role along with many others in the precise balance of inward and outward currents that control the duration of cardiac AP, were investigated. We report a significant decrease in the transient outward (I(to1)) and in the L-type calcium current (I(Ca,L)) densities while there was no significant difference in the delayed rectifier current (I(K)) or in the inward rectifier current (I(K1)) densities in hypertrophied right ventricular cells compared to control cells. At a given potential the decrease in I(to 1) density was relatively more important than the decrease in I(Ca,L) density. In both cell types, all the currents displayed the same voltage dependence. The inactivation kinetics of I(to 1) and I(Ca,L) or the steady-state activation and inactivation relationships were not significantly modified by chronic high-altitude exposure. We conclude that chronic high-altitude exposure induced true right ventricular myocyte hypertrophy and that the decrease in I(to 1) density might account for the lengthened action potential, or have a partial effect.

Action Potentials↗

Reliability of echocardiography in the diagnosis of right ventricular hypertrophy.

The right ventricular (RV) wall thickness and dimension were measured by the technique of echocardiography in 62 patients. Thirty-six of these patients died, and the RV wall thickness was measured at necropsy for comparison with the echocardiographic measurements. The necropsy RV wall thickness measured 3.3 ± 0.6 mm in patients without right ventricular hypertrophy (RVH) and 5.9 ± 0.9 mm in patients with RVH (P<.01). The echocardiographic measurements of the diastolic RV wall thickness correlated well with the necropsy measurements of the RV wall thickness (r=.83). The sensitivity and specificity of the echocardiographic criteria in detecting RVH was superior to the electrocardiographic (ECG) criteria. Furthermore, the echocardiographic technique was useful in evaluating RVH in 18 patients with an abnormal ECG due to right or left bundle branch block or myocardial infarction. We conclude that echocardiography is reliable in diagnosing RVH.

Adolescent↗

Cardiac performance and myocardial blood flow in pigs with compensated right ventricular hypertrophy.

Compensated right ventricular hypertrophy (RVH), defined by a greater than 100% RV weight increase compared to 17 normal animals, was created in 17 young pigs by pulmonary arterial banding. RVH was associated with significant elevations (p less than 0.001) in RV peak dP/dt, RV stroke work, RV minute work and RV rate-pressure product compared to normal animals matched by body weight. RV peak dP/dt showed a positive correlation (p less than 0.001) with RV peak systolic pressure in normals; however, this relationship was lost in banded animals since progressively higher RV pressures were not associated with concomitant increases in RV peak dP/dt, thus, suggesting an intrinsic difference between right and left ventricles when working at systemic arterial pressures. Time to RV peak dP/dt became progressively longer (p less than 0.05) as RV weight increased in the RVH animals. When indices of cardiac work were normalized for RV weight, the RVH group could not be distinguished from normals suggesting that the performance per unit weight of RV muscle in RVH was unchanged. Total RV blood flow, measured by radioactive microspheres, closely followed (p less than 0.001) increases in RV mass in banded animals. Blood flow . g-1 muscle in RV and septal right side were unaltered in RVH; however, regional perfusion of the left ventricle (p less than 0.001) and septal right side were unaltered in RVH; however, regional perfusion of the left ventricle (p less than 0.001) and septal left side (p less than 0.02) increased significantly. There were regional variations in RV perfusion which were maintained in compensated RVH; stress (isoprenaline infusion) caused significant increases in blood flow to all regions of the heart in normal and RVH animals (p less than 0.001), but relative regional distribution was maintained. Our observations suggest a relationship between myocardial work and blood flow in RVH such that RV perfusion . g-1 is elevated to meet haemodynamic requirements once RV regional work . g-1 become greater than normal.

Animals↗

Impaired left ventricular postischemic function and metabolism in chronic right ventricular hypertrophy.

Chronic right ventricular hypertrophy (RVH) has been shown to produce changes in left ventricular diastolic properties but minimal effects on left ventricular systolic function. We studied the effects of chronic pressure overload RVH on left ventricular systolic function before and after reversible hypothermic global ischemia. RVH was induced by pulmonary artery banding (PAB) in newborn piglets (5 to 7 days). At 2 months of age the PAB group (n = 6) and a control group (n = 8) were subjected to cardiac arrest on cardiopulmonary bypass with cold crystalloid cardioplegia (10 degrees C) for 2 hr and were reperfused for 1 hr. Left ventricular function was assessed by a conductance catheter in the left ventricle measuring the end-systolic pressure-volume relationship (Emax). Preischemic and postischemic Emax were the same in the control group (4.1 +/- 0.4 mm Hg/ml before vs 4.1 +/- 0.4 mm Hg/ml after ischemia), but significantly different in the PAB group (4.7 +/- 0.5 mm Hg/ml before vs 2.97 +/- 0.7 mm Hg/ml after ischemia, p less than .05). There also was a marked drop in ATP and phosphocreatine (CP) content in the PAB group during ischemia (ATP, 20 +/- 2 mmol/kg dry wt before vs 10 +/- 2 mmol/kg dry wt after ischemia, p less than .05; PC, 26 +/- 3 mmol/kg dry wt before vs 11 +/- 1 mmol/kg dry wt after ischemia, p less than .05). In the control group there was no change in ATP content and, although CP did drop by end-ischemia, there was complete recovery by 1 hr of reperfusion but minimal CP recovery in the PAB group.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗