Ventricle In Man Research Articles

The concentration of angiotensins I and II in blood from the pulmonary artery and left ventricle of man.

The concentrations of angiotensin I (AI) and II (AII) were determined by radioimmunoassay in blood from the main pulmonary artery (MPA) and left ventricule (LV) of ten subjects with rheumatic valvular heart disease. The levels of AI were consistently higher in MPA plasma (21.8+/-2.4 pmol/1) than in LV plasma (14.7+/-2.0 pmol/1), paired t, P less than 0.001. The levels of AII were consistently lower in MPA plasma (21.8+/-4.7 pmol/1) than in LV plasma (33.8+/-7.2 pmol/1), paired t, P less than 0.001. The AII antiserum cross-reacted with three metabolites of the hormone, [des-Asp1]angiotensin II, [des-(Asp1, Arg2)angiotensin II [des-(Asp1, Arg2 Val,3]angiotensin II. To characterize the nature of circulating AII immunoreactive material, paper chromatography was used to separate AII from its immunoreactive metabolites. The results showed that 84-100% of the AII immunoreactive material from both MPA and LV plasma chromatographed with the mobility of authentic angiotensin II. The mean pulmonary conversion of endogenous AI was 33+/-4.8% and the net extraction of AII by peripheral tissues was 33+/-4.1%.

Current concepts in cardiology: angiographic evaluation of ventricular function.

Angiographic visualization of the left ventricle makes it possible to determine left-ventricular-chamber dimensions, volume, stroke volume, wall thickness, mass and characteristics of regional wall motion. This information is of value for clinical assessment of the performance characteristics of the left ventricle in man with heart disease.Although the original methods for computing leftventricular-chamber volumes were based on biplane filming, and these methods seem to be the most accurate, methods are now available for computing volumes from large films or from cineangiograms taken in single anteroposterior or right-anterior-oblique projections as well. For computing volumes, the most commonly used methods have used . . .

A geometric basis for calculation of right ventricular volume in man.

AbstractA clinically applicable method for determining right ventricular volume was developed using a new hemielliptical model. The model was derived from a detailed study of right ventricular geometry. Silicone rubber casts were made from 7 adult human right ventricles at autopsy. Cast volumes measured by water displacement ranged from 30 to 144 ml. Serial sections were made of each cast, and the product of the long and short axis of all sections was found to be directly related to the cross‐sectional area and independent of the region or the volume of the ventricle from which the slice originated. Further, using a hemielliptical model, the volume V of each ventricle could be calculated from the equation: V = (π/4) Σ dwh where, d is the depth, w is the width parallel to the septum, and h is the thickness of the cross section. Calculated volume agreed closely with displacement volume throughout (r equals; 0.99, slope equals; 1.05 ± 0.04, intercept equals; −3.6 ± 4., SEE equals; 4.27 ml). Using the same model, calculation of right ventricular surface area was found to agree closely with measured surface area (r equals; 0.99, slope equals; 0.94, intercept equals; −.6, SEE equals; 3.9).This model can be used to calculate right ventricular volumes from biplane radiographs in man using the equation V equals; (π/4)(ARAO·ALAO)/HsbL where ARAO equals; the area of the 30° right anterior oblique image, A, HL equals; the area and height respectively of the 60° left anterior oblique image. For all 7 casts, radiographic volume agreed closely with directly measured volume (slope equals; 0.97, intercept equals; −5.5, r equals; 0.99, SEE equals; 4.7). Evaluation of positional effects showed that radiographic volume was most accurate when the 30° RAO/60° LAO projections were used. This study provides a method of calculating right ventricular volume, based upon right ventricular geometry, that may be applied to evaluating the volume of the right ventricle in man.

Local characteristics of the normal and asynergic left ventricle in man

The significance of ventricular asynergy in determining medical prognosis and surgical risk in patients with coronary artery disease and its delineation by ventriculography have been of increasing interest. To determine the underlying histopathologic and electrographic features of left ventricular asynergy, 39 patients undergoing open heart surgery were studied. Thirty-six histopathologic specimens were obtained in 31 patients (26 as transmural needle biopsies and 10 as aneurysm resections). In four normally contracting areas and 12 hypokinetic areas, neither fibrosis nor early changes of myocardial damage was evident. In contrast, of eight akinetic areas there was more than 50 per cent muscle loss in four and from 30 to 35 per cent muscle loss in three, in only one area was there less than 10 per cent muscle loss. Of 12 dyskinetic zones there was more than 75 per cent muscle loss in 10 zones, 35 per cent in one and no pathologic abnormalities in one. Epicardial electrograms were obtained from 35 areas in 29 patients. Of 10 normally contracting ventricles, in one, pathologic Q waves were demonstrated only over the inferior area. Progressive increases in the severity of asynergy were associated with a progressive increase in frequency of initial abnormal Q waves. In only one of nine hypokinetic areas were epicardial Q waves exhibited, but they were present in six of 10 akinetic and five of six dyskinetic areas. Both histopathologic and electrographic data were available from 20 asynergic areas in 16 patients. Initial epicardial R waves were associated with normal biopsy specimens in seven of eight hypokinetic areas. Of seven akinetic areas, initial R waves were associated with 30 to 35 per cent muscle loss in three; of four areas with initial Q waves, there was a 35 per cent muscle loss in one and more than 50 per cent muscle loss in three. Similarly, of five dyskinetic segments, a QS pattern was associated with more than 75 per cent fibrosis in four. In one dyskinetic area there was an initial R wave in association with a normal appearing biopsy specimen. In summary, a good correlation exists between the severity of asynergy by ventriculography, the degree of muscle loss and the presence of epicardial Q waves. However, a significant amount of histologically and electrographically normal myocardium may be present even in severely asynergic areas.

Effects of isometric exercise on the end-diastolic pressure, volumes, and function of the left ventricle in man.

Changes induced in left ventricular (LV) hemodynamics by isometric exercise were analyzed in 43 patients: 30 with coronary heart disease (CAD), four with noncoronary heart disease, nine normal. Volumes were angiographically determined and correlated with left ventricular end-diastolic pressure (LVEDP) both at rest and during the fifth minute of 30% sustained handgrip (HNG). All normals and eight with CAD improved LV function during HNG. LVEDP decreased or remained constant, end-diastolic volume (EDV) decreased, end-systolic volume (ESV) decreased, as ejection fraction (EF) remained constant. None of these eight CAD cases altered their regional LV contraction pattern during HNG. Twenty-five patients, 21 CAD and four nonCAD, showed diminished LV function during HNG. LVEDP increased, EDV decreased, ESV increased, as EF declined. In these 21 CAD patients, at least one major coronary vessel was narrowed 70% or more and, with but two exceptions, was not supported by adequate collaterals. In 18, new asynergic zones developed in previously normally contracting areas or pre-existing asynergic zones extended during HNG.

Human ventricular refractoriness. Effects of cycle length, pacing site and atropine.

The effective refractory period of the right ventricle (ERP-V) was measured in 27 patients during atrial or ventricular pacing using the ventricular extra stimulus method. Pacing was conducted with impulses of 1.5-2 times diastolic threshold. The ERP-V was directly related to the basic cycle length (BCL) although the ERP-V was always greater for atrial pacing than for ventricular pacing at a given BCL. The ratio ERP-V/BCL was greater at shorter cycle lengths indicating that a larger fraction of the cycle was refractory at faster heart rates. The ratio ERP-V/QT interval did not change over a range of BCLs, but the ratio was larger for atrial pacing (.77 +/- .05 SD) than for ventricular pacing (.60 +/- .05). Atropine (1 mg i.v.) was given to six patients. The drug did not affect the ERP-V in six of eleven determinations, prolonged ERP-V twice and shortened it slightly three times. Measurements were reproducible over an hour but varied at a given BCL when measured on separate days. Asymptomatic repetitive beating occurred in seven of 27 patients when the premature stimulus was within 20 msec of the ERP-V. The effective refractory period of the right ventricle in man can be determined reproducibly and with safety. Changes induced by various perturbations parallel results from in vitro single cell and myocardial studies.

Morphologie, topographie et nomenclature des muscles papillaires du cœur de l’homme comparés à ceux des mammifères

On the internal or parietal surface of the left ventricle in man and in mammals are two papillary muscles, which are almost identical and well developed. In man, these muscles are known as the m. papillaris parietalis anterior sinister and the m. papillaris parietalis posterior dexter, in mammals, the m. papillaris parietalis cranialis sinister and caudalis dexter, or, in shorter form, mm. papillaris parietalis sinister et dexter. In the right ventricle in man, there are two papillary parietal muscles: the mm. papillares anteriores et posteriores. On the septum of this ventricle there is, as in mammals, a muscle called the m. papillaris septalis medialis seu subarteriosus. Beside it are one or several smaller muscles, varying from one individual to another: the mm. papillares septales accessorii seu parvi. In the right ventricle of the mammalian heart is found, in addition to the m. parietalis septalis subarteriosus, already mentioned, a m. papillaris caudalis, more or less well developed in some species and, in the majority of mammals, the m. papillaris septalis cranials, which is always well developed. In certain mammals, there is, in rare cases, a m. papillaris septomarginalis seu parietalis. It may be said, in conclusion, that, in a large number of mammals, there is, on the internal surface of the external wall of the right ventricle, a reasonably well developed m. papillaris parietalis.

The effect of therapeutic doses of lidocaine hydrochloride on the effective refractory period of the right ventricle in man.

The effect of lidocaine on the effective refractory period of the right ventricle (EVRP) was measured in 10 patients using the extra stimulus technique of progressive introduction of premature stimuli until a response could not be elicited. In four patients lidocaine produced a significant decrease in the EVRP, in a further four patients there was no change, and in the remaining two patients lidocaine produced a significant increase in the EVRP. The effect of the drug on the EVRP could not be correlated with the serum potassium levels. The reasons for the variable effect of lidocaine are attributed to the different action of lidocaine on different components of conduction within the ventricle.

Diastolic compliance of the left ventricle in man

Two coordinates of left ventricular end-diastolic pressure (P) and volume (V) were provided by the Infusion of anglotensin in 22 patients. The slope (k) of the in P-V relation, coupled with knowledge of the operating (end-diastolic) pressure allows determination of end-diastollc volume compliance (dV/VdP). Estimates of end-diastolic compliance from a single coordinate of pressure and volume compared well ( r = 0.90) with the two coordinate method, whereas values for specific compliance (ΔV/V i ΔP) appeared to be misleading in cases of idiopathic hypertrophic subaortic stenosis and congestive cardiomyopathy. Since volume compliance is determined in part by the operating pressure, compliance may be reduced in small, normal or enlarged ventricles. Left ventricular linear compliance was derived from volume compliance and was normalized for left ventricular wall thickness. The product of linear compliance and end-dlastolic stress provides an index of myocardial strain, termed “muscle fiber stretch,” which may be related to systolic performance and thus allow comparison of length-performance relations in ventricles with normal and abnormal compliance.

Restoration of Regional Wall Motion by Nitroglycerin Therapy in Patients with Left Ventricular Asynergy

A ortocoronary bypass operation has a variable effect on the function of the left ventricle. 1 Bourassa MG L’Esperance J Campeau L et al. Fate of left ventricular contraction following aorto-coronary venous grafts. Early and late post-operative modifications. Circulation. 1972; 46: 724-730 Google Scholar , 2 Chatterjee K Swan HJC Parmley WW et al. Influence of direct myocardial revascularisation on left ventricular asynergy and function in patients with coronary heart disease.. Circulation. 1973; 47: 276-286 Crossref PubMed Scopus (216) Google Scholar , 3 Rees G Bristow JD Kremkau EL et al. Influence of aorto-coronary bypass surgery on left ventricular performance.. N Engl J Med. 1971; 284: 1116-1121 Crossref PubMed Scopus (141) Google Scholar This may be due, in part, to inability to predict the behavior of regional wall abnormalities following revascularization. Areas of asynergy may have pronounced influence on left ventricular function, 4 Herman MV Heinle RA Klein MD et al. Localized disorders in myocardial contraction: Asynergy and its role in congestive heart failure.. N Engl J Med. 1967; 277: 222-232 Crossref PubMed Scopus (404) Google Scholar , 5 Baxley WA Jones WD Doslye HT Left ventricular anatomical and functional abnormalities in chronic postinfarction heart failure.. Ann Intern Med. 1971; 74: 499-508 Crossref PubMed Scopus (27) Google Scholar and yet traditional hemodynamic techniques measure the integrated response of the left ventricle as though all segments made a uniform contribution to total function. Previous investigations show that abnormal wall motion occurs in zones supplied by those arteries with critical stenosis. 6 Sniderman AD Marpole D Fallen EL Regional contraction patterns in the normal and ischemic left ventricle in man.. Am J Cardiol. 1973; 31: 484-489 Abstract Full Text PDF PubMed Scopus (72) Google Scholar , 7 Gorlin R Klein MD Sullivan JM Prospective correlative study of ventricular aneurysm with special reference to mechanistic concept and clinical recognition.. Am J Med. 1967; 42: 512-531 Abstract Full Text PDF PubMed Scopus (198) Google Scholar

Predominant right ventricular dysfunction after right ventricular destruction in the dog

Right and left ventricular function was assessed by observing the response to rapid blood volume expansion before and after extensive cauterization of the right ventricle in open chest dogs. In the control period, left ventricular end-diastolic pressure surpassed right ventricular end-diastolic pressure by an average of 11.5 mm Hg after volume expansion whereas, after destruction of the right ventricle, pressure in this chamber surpassed pressure in the left ventricle by an average of 4 mm Hg. In contrast, after left ventricular damage, left ventricular end-diastolic pressure averaged 25 mm Hg more than right ventricular end-diastolic pressure. Despite extensive damage to the right ventricular free wall, the right ventricle continued to generate a near normal pressure and aortic flow could be increased above control levels by volume expansion. We conclude that, in contrast to previous evidence, damage to the right ventricle produces a syndrome of predominant right ventricular dysfunction. However, cauterization of the entire free wall of the right ventricle does not reproduce the more profound right ventricular dysfunction noted in infarction of the right ventricle in man.

Contraction of the hypertrophied left ventricle in man studied by cineradiography of epicardial markers

The shape of the hypertrophied left ventricle during contraction and the shortening of epicardial dimensions were studied by postoperative cineradiographic studies of opaque markers placed at the time of aortic valve replacement in 10 patients with severe isolated aortic valve disease. The control group comprised 8 patients with a nonhypertrophied left ventricle who were treated successfully for pure mitral stenosis by closed mitral valvotomy. The extent of shortening during systole of epicardial chords across the left ventricular base and longitudinally from base to apex anteriorly and inferiorly were, respectively, 15.8, 14.3 and 16.1 percent (mean 15.4 percent) in the control group and 10.3, 7.1 and 5.4 percent (mean 7.6 percent) in patients with left ventricular hypertrophy. Thus, myocardial shortening was reduced generally in the patients with hypertrophy, but base to apex lengths were more affected and individual chords showed the most abnormal patterns of shortening during systole. In 2 patients with aortic regurgitation of recent onset, these abnormalities were less severe. Furthermore, the patterns of abnormal contraction remained unchanged in 4 patients studied serially over periods of 6 months to 2 years postoperatively despite electrocardiographic evidence of some resolution of left ventricular hypertrophy. It was therefore concluded that impaired myocardial function and an abnormal pattern of left ventricular contraction accompany severe left ventricular hypertrophy in aortic valve disease and improvement develops slowly or not at all after removal of the abnormal load.

Maximum rate of pressure decline in the normal, hypertrophied and dilated left ventricle in man

Maximum rate of pressure decline in the normal, hypertrophied and dilated left ventricle in man

A cineangiocardiographic study of the regional contraction sequence of the normal and diseased left ventricle in man.

The regional contraction sequence of the left ventricle (LV) was analyzed by 16mm. cineangiocardiograms (in LAO, 40 frames per sec.) of 5 control subjects, 4 patients with mitral insufficiency, 2 with idiopathic hypertrophic subaortic stenosis (IHSS), 2 with idiopathic myocardial hypertrophy and 3 of myocardial disease with LV dilatation.The LV cavity was divided into basal, middle and apical portion, and internal width (diameter) for each portion was measured on a line drawn perpendicular to the long axis at 3 equally spaced points. The time course of the length of the diameters in percentage of the initial length was compared, and circumferential shortening velocity (Vcs) and total extent of circumferential shortening were calculated for each diameter. Regional contraction sequence was also analyzed by superimpositon of serial LV silhouettes during systole.In control subjects, a synchronized contraction sequence was suggested, and regional circumferential shortening velocity was inversely related to the initial length of corresponding diameter. In hypertrophied and dilated hearts of mitral insufficiency or in IHSS, an earlier onset and/or more rapid contraction of the basal portion were noted. The possible relationship between asynchronism of the contraction sequence and alterations of ventricular geometry and of myocardial architecture of the LV were discussed. In myocardial disease with dilated LV, both shortening velocity and extent of shortening were markedly reduced.The method described here allows direct observation of the pattern of regional contraction sequence and also gives clinical indices of contractile state of the myocardium in normal and diseased LV in man.

Contractile state of the left ventricle in man: instantaneous tension-velocity-length relations in patients with and without disease of the left ventricular myocardium.

The contractile state of the left ventricle in man was analyzed by correlating left ventricular (LV) dimensional changes during contraction determined from cineangiograms, with simultaneous measurements of LV pressure. The mechanical characteristics of ventricular contraction were expressed quantitatively by deriving the extent and velocity of circumferential fiber shortening at the midwall and the time course of LV wall tension (stress); the instantaneous relations between tension, velocity, and length were then examined. In 6 patients without LV disease, wall tension became maximal soon after the onset of ejection, then declined rapidly; in 9 patients with LV disease, tension fell only slightly with continued ejection. The extent of shortening of the minor LV circumference was consistently less in patients with LV disease than in those without such disease. Velocity of circumferential fiber shortening throughout contraction ranged from 0.22 to 1.11 circumferences/sec in patients with LV disease and from 1.66 to 2.71 circumferences/sec in patients without LV disease, at comparable levels of wall tension (137 to 467 g/cm 2 , and 175 to 409 g/cm 2 , respectively). The initial rate of change of velocity of the circumferential fibers at the onset of ejection also was less than in the group without LV disease. The velocity of shortening of the contractile elements at maximum wall tension was 0.11 to 0.87 circumferences/sec in patients with LV disease and 1.46 to 2.04 circumferences/sec in patients without LV disease.

Clinical and physiologic sequelae of large ventricular septal defects

The clinical and hemodynamic data in twenty-nine patients with large ventricular septal defects are analyzed. Evidence of heart failure is uncommon in those with pulmonary vascular disease and/or pulmonic stenosis alone, in contrast to those in whom certain other additional congenital lesions are present. These data are analyzed in terms of a physiologically single ventricle which exists when a large ventricular septal defect is present. Obligatory beat to beat synchronicity of the right ventricular and systemic arterial systolic pressure is discussed and its use in the diagnosis of the physiologically single ventricle in man outlined. Evidence is presented that in the face of a physiologically single ventricle, ventricular failure is most likely to occur when a volume or flow load is present in addition to right ventricular hypertension. The evolution and hemodynamic recognition of ventricular failure in the face of a physiologically single ventricle is discussed.

The relationship between the timing of atrial systole and the useful work of the left ventricle in man

Beat-to-beat variations of as much as 100 per cent in the external left ventricular stroke work have been found in 3 patients with acquired, chronic, complete heart block studied during idioventricular pacing. These changes in work output reflect the presence or absence of a preceding atrial contraction, its placement in time, and the cardiac rate.

Simplified Method for Calculating Left Ventricular Volume from Angiocardiograms

Measurement of volume and volume change of the left ventricle in man extends our understanding of the response of the heart to stress (1, 2) and may provide information of diagnostic importance. In particular, measurement of left heart volumes during the cardiac cycle permits quantitation of valvular insufficiency (3, 4) with the possibility of yielding information about myocardial function. At the present time, angiographic (5) and indicator dilution (6) technics are the only ones available for measuring the volume of a single heart chamber in man. Although the validity of quantitation by angiography has been established (7, 8), such methods have been regarded as too time-consuming for routine clinical use. The present communication describes a clinically applicable procedure for measuring left ventricular volume, based on the method of Arvidsson (5), which requires measurement of only four pairs of angiocardiograms. Methods Sixty-six subjects were studied during diagnostic cardiac catheterization. Selective angiocardiography was performed while the patient was in the supine position and under light anesthesia. Simultaneous recording of arterial pressure, electrocardiogram, and time of x-ray exposure permitted correlation of the radiographic appearances with the events of the cardiac cycle (Fig. 1). Angiocardiograms, measured to the nearest 1 mm as indicated in Figure 2, were used in this study only if they showed adequate opacification of left heart chambers during sinus rhythm. Patients with atrial fibrillation were excluded unless a reasonably regular ventricular contraction was shown during the period of filming. The volume of the left atrium (VLA) was calculated for each pair of angiocardiographic exposures by: where a, b, and c are atrial semiaxes in centimeters and j1 and f2 are the anteroposterior and lateral magnification factors, respectively, measured for each subject. The volume of the left ventricle (VLV) was calculated for each pair of angiocardiographic exposures by: where L, the true long axis of the ventricular ellipsoid is given by: in which β is the angle between the horizontal and the measured long axis, D, of the ventricular ellipsoid in the lateral projection, and A, B, and C are ventricular axes in centimeters. Composite left atrial and ventricular volume curves were constructed by plotting the volumes calculated from an angiographic pair against the time, expressed in fractions of a second, after the R wave of the electrocardiogram at which the exposures were made (4). Values for end-diastolic volume (VED) and end-systolic volume (VES) were determined from these composite volume curves. The records of arterial pressure, time of x-ray exposures, and electrocardiography were then submitted to an independent observer (R.G.G.) who picked two film pairs to represent the end-diastolic volume and two to represent end-systolic volume. For measurement of end-diastolic volume, exposures made just before the Q wave of the electrocardiogram were selected because previous experience indicated that ventricular volumes are maximal at this time. The larger of these was chosen as the end-diastolic volume.

Validation of a method for measuring the output of the right ventricle in man by inscription of dye-dilution curves from the pulmonary artery.

Indicator dilution curves have been inscribed through a cardiac catheter from the pulmonary artery in nine normal subjects. The suitability of these curves for measuring the right ventricular output has been investigated by comparing the calculated values of flow with those obtained from brachial arterial curves and from application of the direct Fick. The results indicate that both the pulmonary and brachial arterial flows agree with the Fick within ±15%. The advantages of using the pulmonary artery as a sampling site are stressed. These include a) the absence of a capillary bed between the injection and sampling points, and b) a considerable reduction in the contamination of the primary curve by recirculating indicator. The theoretical possibility of individually measuring the outputs of the right and left ventricles is also discussed. Submitted on August 2, 1957

Catheterization of the left ventricle in man; study of right bundle branch block by simultaneous intracardiac electrocardiography of both ventricles.

Simultaneous catheterization of the left and right ventricles was performed in a case of right bundle branch block. It was thought that in right bundle branch block the polarity of the initial deflection of the potentials obtained in the left ventricular cavity could be studied without interference of those contributed by the right ventricular cavity. A description of the technic employed is given. The results confirm those obtained in dogs. There is initial negativity of the potentials obtained within the left ventricular cavity.