Observations on the behavior of the right ventricular outflow tract, with reference to its developmental origins

March, Harold W.; Ross, John; Lower, Richard R.

doi:10.1016/0002-9343(62)90030-x

Cited by 49 publications

(13 citation statements)

References 15 publications

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“…1). The observation is consistent with previous reports concerned with regional contraction patterns of the right ventricle (Tobin et al, 1965;Carlsson, 1969;Armour et al, 1970;Raines et al, 1976;Santamore et al, 1979) which suggest that the outflow tract is not only anatomically and embryologically distinct from the rest of the right ventricle (Keith, 1924;Brock, 1955;March et al,1962), but also physiologically distinct, in that its contraction pattern begins later and lasts longer (Raines et al, 1976). It is interesting that this heterogeneity of flow is not as apparent following pharmacological blockade of the autonomic nervous system (Fig.…”

Section: Effects Of Elevated Heart Rate On Transmural Blood Flow and supporting

confidence: 92%

Fractional contributions of the right and left coronary arteries to perfusion of normal and hypertrophied right ventricles of conscious dogs.

Murray¹,

Vatner²

1980

Circulation Research

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SUMMARY The extent to which the blood supply of normal and hypertrophied right ventricles originates from the right and left coronary arteries was investigated in conscious dogs. Right ventricular (RV) hypertrophy, induced by gradual, chronic (4-6 months) stenosis of the main pulmonary artery, was characterized by a 72% increase (P < 0.001) in RV weight to body weight ratio and a 106% increase (P < 0.001) in total RV transmural blood flow per gram (radioactive microsphere technique). In normal dogs, left main coronary artery occlusion (CAO) reduced blood flow only slightly to the central core of the RV free wall, but markedly (P < 0.001) to the peripheral zones. Right main CAO reduced blood flow in both RV central and peripheral zones to similar absolute levels in both normal animals and dogs with RV hypertrophy. Keeping in mind that pre-CAO control levels were greater in the presence of hypertrophy, the magnitude of the reduction in blood flow was significantly greater (P < 0.01) with right CAO in dogs with hypertrophy. Endocardial-epicardial perfusion ratios of both RV central and peripheral zones were significantly reduced (P < 0.02) both at rest and during right CAO in dogs with RV hypertrophy as compared to normal dogs with matched heart rates. These data indicate that the left coronary artery usually supplies a substantial fraction (~37%) of total RV free wall perfusion in normal, conscious dogs. Moreover, it is seen that the marked, selective increases in transmural RV blood flow in RV hypertrophy are provided by the right but not the left coronary artery. Circ Res 47:190-200, 1980NUMEROUS investigations have examined the coronary circulation in normal and hypertrophied left ventricles. Although right ventricular hypertrophy is not encountered in patients as frequently as is left ventricular hypertrophy, it remains an important clinical entity, e.g., in patients with acquired pulmonary hypertension from a variety of etiologies, as well as those with congenital heart disease. We previously have demonstrated in conscious dogs that chronic pressure overload induced by pulmonary artery stenosis is associated with progressive, selective, and marked increases in transmural blood flow per gram of hypertrophied right ventricle (Murray et al., 1979). However, the mechanism for this augmentation in blood flow remains undefined. It is generally known, although largely unquantified, that canine right ventricular blood flow originates normally from both the right and left coronary arteries (Gregg and Fisher, 1963 by an increase in right coronary artery blood flow, but also by enhanced perfusion via either preexisting or newly formed branches of the left coronary artery. If the hypertrophic process stimulates enhanced perfusion of the right ventricle from the left coronary artery, then transmural blood flow per gram of hypertrophied right ventricle should be elevated above normal levels in the presence of acute right coronary artery occlusion. The overall goals of the present study were, first, to quantify the extent t...

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Section: Effects Of Elevated Heart Rate On Transmural Blood Flow and supporting

confidence: 92%

Fractional contributions of the right and left coronary arteries to perfusion of normal and hypertrophied right ventricles of conscious dogs.

Murray¹,

Vatner²

1980

Circulation Research

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“…RV activation has been sparsely studied although RV dysfunction further increases mortality in HF patients6,7. Normally, RV contraction is a complicated peristaltic movement beginning in the inflow region and extending to the outflow tract18. Altered electrical activation with RV pacing may perturb RV hemodynamics1.…”

Section: Discussionmentioning

confidence: 99%

RV Electrical Activation in Heart Failure During Right, Left, and Biventricular Pacing

Varma

Jia

Ramanathan

et al. 2010

JACC: Cardiovascular Imaging

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Objective Compare right ventricular (RV) activation during intrinsic conduction to pacing in heart failure (HF) patients. Background Right ventricular (RV) activation during intrinsic conduction or pacing in patients with LV dysfunction (HF) is unclear but may affect prognosis. In cardiac resynchronization therapy (CRT), timed LV pacing (CRT-LV) may be superior to biventricular pacing (CRT-BiV), hypothesized to be due to merging of LV paced and right bundle branch (RBB) mediated wavefronts thus avoiding perturbation of RV electrical activation. We tested this. Methods Epicardial RV activation duration (RVAD: onset to end of free wall activation) was evaluated non-invasively by electrocardiographic imaging (ECGI) in normals (n=7) and compared to HF patients (LVEF 23±10%, n=14). RVAD in HF was contrasted during RV, CRT-BiV, and CRT-LV pacing at optimized AV intervals. Results During intrinsic conduction in HF (n=12), durations of QRS and precordial lead rS complexes were 158±24 and 77±17 ms respectively, indicating delayed total ventricular depolarization but rapid initial myocardial activation. Echocardiography demonstrated no significant RV disease. RV epicardial voltage, activation patterns and RVAD in HF did not differ from normal (RVAD 32±15 vs 28±3 ms respectively, p=0.42). In HF, RV pacing generated variable areas of slow conduction and prolonged RVAD (78±33 ms, p<0.001). RVAD remained delayed during CRT-BiV at optimized atrioventricular intervals (76±32 ms, p=0.87). In contrast, CRT-LV reduced RVAD to 40±26 ms (p<0.016) comparable to intrinsic conduction (P=0.39) but not when atrioventricular conduction was poor or absent. Conclusion In HF patients without RV dysfunction treated with CRT, normal RV free wall activation in intrinsic rhythm indicated normal RBB-mediated depolarization. However, the RV was vulnerable to developing activation delays during RV pacing whether alone or with biventricular CRT. These were avoided by CRT-LV in patients with normal atrioventricular conduction.

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“…Priola et al (13) recorded pressures in the inflow and outflow tracts of the left ventricle and showed that inflow pressure exceeded outflow pressure during diastole and outflow pressure was elevated over inflow pressure during systole. March et al (4) used cine techniques to show that the sinus or inflow region contracts first and forces blood into the infundibulum which first bulges, then contracts in late systole. Such a series of events can lead to inflow-outflow pressure differences during right ventricular contraction similar to those recorded during normal left ventricular contraction.…”

Section: Pace Keefe Armour Randallmentioning

confidence: 99%

Influence of Sympathetic Nerve Stimulation on Right Ventricular Outflow-Tract Pressures in Anesthetized Dogs

Pace

Keefe

Armour

et al. 1969

Circulation Research

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Stellate ganglion stimulation in the anesthetized, open-chest dog consistently resulted in the generation of pressure differences which averaged 20 mm Hg across the infundibular region of the right ventricle. Before stimulation, peak systolic pressures in the sinus and conus were closely matched. Peak sinus pressure showed ah average increase of 184 and 162% during stimulation of the left and right stellate ganglia, respectively. Simultaneously, peak conus pressure showed average increases of 88 and 61% during left and right stellate ganglion stimulation, respectively. In addition, the maximal rate of intrasinus pressure development (dP/dt) was usually elevated above conus dP/dt, and this change contributed to the generation of early systolic pressure differences. Cervical vagosympathetic nerve stimulation following atropine administration also resulted in the generation of infundibular pressure differences, but the latter were less marked than those elicited during stellate ganglion stimulation. Elevations in main pulmonary arterial resistance abolished the induced pressure differences by allowing peak conus pressure to rise to the same extent as peak intrasinus pressure. Simultaneous electromagnetic flow recordings of pulmonary arterial blood flow during stellate ganglion stimulation revealed two-to five-fold increases in maximum flow acceleration with relatively little change in stroke volume. Infundibular pressure gradients which developed in early systole were associated with maximum flow changes in the pulmonary artery.ADDITIONAL KEY WORDS stellate ganglion stimulation pulmonary arterial occlusion pulmonary arterial blood flow sinus and conus regions of the right ventricle vagosympathetic stimulation right ventricular infundibulum • The early anatomical and embryological studies of Sir Arthur Keith (1, 2) demonstrated that the conus arteriosus of the developing embryo was incorporated into the right ventricular myocardium and formed the terminal portion of the infundibulum in the adult heart. The conus homologue on the left side was obliterated during the embryological development of the left ventricle. In lower forms, From the Department of Physiology, Loyola University, Stritch School of Medicine and the Graduate School, 1400 South First Avenue, Hines, Illinois 60141.This work was supported in part by U. S. Public Health Service Grants HE 08682 and CM 999 from the National Institutes of Health.Received October 14, 1968. Accepted for publication, January 24, 1969. such as the tortoise, the conus arteriosus is anatomically distinct from the rest of the right ventricular musculature, and Woodbury and Robertson (3) demonstrated that this region can act as a functional stricture to divert blood through the interventricular foramen to the left ventricle. Studies on the canine heart by March et al. (4) have shown that the inflow or sinus region of the right ventricle is activated before the infundibular region, thus demonstrating physiological inflow-outflow pressure differences. Recently Tobin et al...

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Observations on the behavior of the right ventricular outflow tract, with reference to its developmental origins

Cited by 49 publications

References 15 publications

Fractional contributions of the right and left coronary arteries to perfusion of normal and hypertrophied right ventricles of conscious dogs.

Fractional contributions of the right and left coronary arteries to perfusion of normal and hypertrophied right ventricles of conscious dogs.

RV Electrical Activation in Heart Failure During Right, Left, and Biventricular Pacing

Influence of Sympathetic Nerve Stimulation on Right Ventricular Outflow-Tract Pressures in Anesthetized Dogs

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