Showing papers on "Ventricle published in 1973"
TL;DR: It is concluded that E(t), represented by Emax and Tmax, explicitly reflects the ventricular contractility.
Abstract: As a means of assessing ventricular performance, we analyzed the time-varying ratio of instantaneous pressure, P(t), to instantaneous volume, V(t), in the canine left ventricle. Intraventricular volume was measured by plethysmography, while the right heart was totally bypassed. The cardiac nerves were sectioned, and an epinephrine infusion was used to alter the contractile state. The instantaneous pressure-volume ratio was defined as E(t) = P(t)/[V(t) - Vd], where Vd is an experimentally determined correction factor. We found that (1) all the E(t) curves thus defined were similar in their basic shape and attained their peak near the end of the ejection phase regardless of the mechanical load, the contractile state, or the heart rate, (2) under a constant heart rate and contractile state extensive changes in preload, afterload, or both did not alter the peak value of E(t), Emax, or the time to Emax from the onset of systole, Tmax, and (3) these parameters of E(t) markedly changed with epinephrine infusion ...
1,485 citations
TL;DR: The evolution of premature ventricular contractions in acute myocardial infarction was studied by recording bipolar potentials from the left ventricle before and after coronary artery occlusion in dogs and historical stains of myocardium indicated a relationship between the inhomogeneous distribution of ischemia (stain) and the desynchronization of the electrical activity.
Abstract: The evolution of premature ventricular contractions (PVCs) in acute myocardial infarction was studied by recording bipolar potentials from the left ventricle before and after coronary artery occlusion in dogs. The potentials were recorded from 154 locations in the left ventricular wall as well as at the endocardial and epicardial surfaces. Desynchronization and marked slowing of previously uniform activation was noted and resembled abbreviated, local fibrillation. The dissociation of excitation was either simple, characterized by fragmentation into single delayed spikes, or complex, characterized by numerous spikes. Sustained, desynchronized activity, confined to local myocardial areas, was observed up to 215 msec after the onset of activation. These local areas of sustained excitation functioned as a source of re-entrant activity and were associated with PVCs. Histochemical stains of myocardium indicated a relationship between the inhomogeneous distribution of ischemia (stain) and the desynchronization o...
463 citations
TL;DR: The results indicate that tachycardia may produce incomplete left ventricular relaxation in patients with disorders characterized by ischemia, but not in those with a normal left ventricle, and that an impairment of ventricular Relaxation may be partly responsible for the apparent decrease inleft ventricular diastolic compliance observed during pacing-induced angina pectoris.
Abstract: Rapid atrial pacing was performed in 15 patients at the time of cardiac catheterization. The results indicate that tachycardia may produce incomplete left ventricular relaxation in patients with disorders characterized by ischemia, but not in those with a normal left ventricle. This phenomenon was characterized by (1) a decrease in the peak negative value for first derivative of left ventricular pressure (dP/dt), which was used in the study as an index of left ventricular relaxation rate, (2) an increase in left ventricular diastolic pressure, and (3) a decrease in left ventricular internal diameter. These findings suggest that ventricular relaxation is an important determinant of left ventricular diastolic pressure-volume relations and that an impairment of ventricular relaxation may be partly responsible for the apparent decrease in left ventricular diastolic compliance observed during pacing-induced angina pectoris.
336 citations
TL;DR: The appearance of ventricular arrhythmias during phase 1 of Harris was associated with the appearance in electrograms recorded from within the infarct of continuous electrical activity which extended beyond the T wave of the preceding beat and preceded the onset of the arrhythmia.
Abstract: A study was designed to correlate changes in bipolar epicardial electrograms recorded from normal and acutely infarcted myocardium with the onset of ventricular arrhythmias. Electrodes were sewn to selected sites on the left ventricle, and after control electrograms and ECG's were recorded, the left anterior descending coronary artery was doubly ligated close to its origin. Electrograms recorded from within the infarct initially manifested diminished amplitude and increased duration of the deflection which reflected depolarization. The appearance of ventricular arrhythmias during phase 1 of Harris was associated with the appearance in electrograms recorded from within the infarct of continuous electrical activity which extended beyond the T wave of the preceding beat and preceded the onset of the arrhythmia. During the continuous electrical activity, it was not possible to delineate which deflections of the electrogram reflected depolarization or repolarization and it was suggested that the continuous ele...
282 citations
TL;DR: The myocardial component of the syndrome of prolapsed mitral (and/or tricuspid) leaflets is expressed as asynergistic patterns of ventricular motion and usually does not impair over-all cardiac dynamics.
Abstract: Eighty-seven patients with proven mitral leaflet prolapse were studied emphasizing cardiodynamics and left ventricular asynergy. Significant associated features were female preponderance (83%), skeletal anomalies (pectus excavatum, straight back, scoliosis, narrow antero-posterior diameter of the chest), and anomalous coronary arteries (cork-screw patterns, short left main coronary artery, anomalous origin of the coronary arteries). Prolapse of the tricuspid leaflets was found in 15 (54%) who had right ventriculography. Five types of abnormal left ventricular systolic contraction patterns were seen in 82% of the cases and these were categorized as: 1) "ballerina foot" pattern (vigorous posteromedial contraction with anterior convexity), 2) "hour glass" pattern (vigorous ring-like contraction involving the middle portion of the left ventricle), 3) inadequate long axis shortening, 4) posterior akinesis, and 5) cavity obliteration pattern. The over-all left ventricular performance was normal generally, as in...
173 citations
TL;DR: The diameters of large epicardial coronary arteries were measured by quantitative cinearteriography in 99 patients to determine the size of coronary arteries supplying the left ventricle in patients with pure mitral stenosis and in those with the “floppy mitral valve syndrome”.
Abstract: The diameters of large epicardial coronary arteries were measured by quantitative cinearteriography in 99 patients. Average coronary size was larger than normal in patients with lesions associated with left ventricular hypertrophy and∕or dilation. The size of the coronary arteries supplying the left ventricle was normal in patients with pure mitral stenosis and in those with the “floppy mitral valve syndrome” (when mitral regurgitation was slight or absent). The left coronary artery was larger than the right coronary artery in 83% of cases. Measurement of coronary artery size is a simple and useful extension of coronary arteriography.
162 citations
TL;DR: It is suggested that, in myocardium with unrestricted coronary supply, regional distribution of flow is independent of gradients in tissue pressure during the described changes in preload due to an autoregulatory mechanism.
Abstract: The effects of increased ventricular preload on the distribution of regional blood flow in normal and ischemic myocardium were determined in deep and superficial regions of the left ventricle by using labeled microspheres. The ratio of flow in deep regions to flow in superficial regions in nonischemic tissue was 1.06 ± 0.06 and increased to 1.14 ± 0.06 when left ventricular end-diastolie pressure was raised from 4.8 ± 1 mm Hg to 18 ± 2 mm Hg by intravenous infusion of blood. In ischemic areas the ratio of flow in deep regions to flow in superficial regions fell simultaneously from 0.71 ±0.12 to 0.45 ±0.07 (P < 0.001). Control of coronary flow during increased preload was studied in a separate preparation in which coronary flow was decreased in steps by reducing coronary perfusion pressure during periods of constant cardiac performance. The increased preload was associated with loss of autoregulation of coronary flow. It is suggested that, in myocardium with unrestricted coronary supply, regional distribution of flow is independent of gradients in tissue pressure during the described changes in preload due to an autoregulatory mechanism. However, when autoregulation of coronary flow is abolished by coronary artery occlusion, the coronary bed is fully dilated, and distribution of flow is directly dependent on gradients in myocardial tissue pressure. Increased ventricular preload consequently augments the underperfusion of the subendocardial regions of an ischemic area.
153 citations
TL;DR: Results of this correlative study indicate that M-mode echocardiographic scans can detect left ventricular asynergy and may possibly predict regional myocardial involvement in coronary artery disease.
Abstract: The purpose of this study was to determnie if echocardiography could detect left ventricular asynergy. Forty-eight patients underwent selective coronary arteriography and cineventriculography for the evaluation of chest pain. Four patients were studied twice: three before and after myocardial revascularization and one before and after an intervening myocardial infarction. Echocardiographic M-mode scans were registered on a strip chart as the left ventricle was scanned with an ultrasonic beam from the aortic root to the region of the posterior papillary muscle approximately 18 hrs prior to the catheterization studies. Ten of the forty-eight patients had no evidence of coronary artery disease. All ten patients had normal ventriculograms in right anterior oblique projection and their echocardiographic scans showed all areas of the left ventricular posterior wall endocardium to move anteriorly 0.9-1.4 cm (mean 1.2 cm) and all parts of the left side of the interventricular septum to move posteriorly 0.3-0.8 cm...
149 citations
TL;DR: A characteristic abnormality of motion of the interventricular septum was recorded by echocardiography in 17 of 18 patients with left bundle branch block and this abnormality can be explained by asynchronous contraction of the left ventricle with early activation and contraction ofThe sePTum.
Abstract: A characteristic abnormality of motion of the interventricular septum was recorded by echocardiography in 17 of 18 patients with left bundle branch block. Early and abrupt contraction of the septum occurs during the pre-ejection period before the delayed commencement of contraction of the posterior wall of the left ventricle. This abnormality can be explained by asynchronous contraction of the left ventricle with early activation and contraction of the septum but delay in activation and contraction of the left ventricular free wall due to a block in the left bundle branch or its peripheral branches.
141 citations
TL;DR: The findings reemphasize the probable morphogenetic role of blood flow pathways and implicate involvement of the left A-V canal as well as premature closing of foramen ovale and aortic valvular abnormalities in the hypoplastic left heart syndrome.
Abstract: The hypothesis is examined that hemodynamic alterations at the site of the primordial mitral valve may induce malformations that simulate the clinical findings of hypoplastic left heart syndrome. Surgical placement of a nylon device, approximately 90 μ in diameter, into the region of the left atrioventricular (A-V) canal was accomplished in 192 embryos (Hamburger-Hamilton stages 23 to 25). Thirty-nine pairs of experimental and control embryos survived more than 12 days. Twenty-six experimental embryos exhibited various malformations: hypoplastic left atrium and ventricle, mitral valvular atresia, aortic valvular stenosis and tubular hypoplasia of the aorta and brachlocephalic vessels. These findings reemphasize the probable morphogenetic role of blood flow pathways. The findings further implicate involvement of the left A-V canal as well as premature closing of foramen ovale and aortic valvular abnormalities in the hypoplastic left heart syndrome.
136 citations
TL;DR: The observations suggest that the normal physiological response to isometric exertion includes a major increase in left ventricular myocardial contractility, and appears sufficient to account completely for the increased ventricular performance associated with handgrip exercise.
Abstract: Left ventricular function during sustained isometric handgrip exercise was studied at the time of cardiac catheterization in 8 normal subjects and 26 patients with heart disease. Both groups showed increases in heart rate, aortic mean blood pressure, and cardiac minute output with no change in systemic vascular resistance. Left ventricular filling pressure and stroke work were measured before and during isometric exercise in I7 cases. In 7 normal subjects, stroke work increased (8i + 8 8 to I04 ± II g m, P< O OI) without a significant change in left ventricularfilling pressure (6-8 + o 8 to 7.5 ± I -2 mmHg, NS) suggesting a shift to a higher ventricularfunction curve. Patients with heart disease, however, showedgreat variability in their stroke work response to isometric exercise (5 with increase, 3 with no change, and 2 with decrease), despite a significant increase in left ventricular filling pressure (9X6 9 mmHg to I5 5±+i6 mmHg, P< o.oi). Myocardial mechanics during isometric exercise were studied in 6 normal subjects and 8 patients with heart disease. Left ventricular pressure-velocity curves were shifted upwards and to the right in all 6 normal subjects and in 7 of the 8 patients with heart disease. Vmax (developed pressure) increased in both normal subjects (74 ±6 to I09± 5 sec -1, + 47%, P< O OI) and to a lesser extent in the patients with heart disease (59 ± 8 to 82+I2 sec + 39%,3 P< o.oi) in response to isometric exercise. Similarly, maximum left ventricular dp/dt increased in both normals (i88i + I63 to 2408+ I29 mmHg/sec, P< o oi) and patients with heart disease (I540 ± I40 to 1976 24I mmHg/sec, P< o oi). These observations suggest that the normal physiological response to isometric exertion includes a major increase in left ventricular myocardial contractility. For the normal heart, this increase appears sufficient to account completely for the increased ventricular performance associated with handgrip exercise. For the diseased heart, increased ventricular performance induced by handgrip appears also to be mediated by increased contractility, but in addition by varying degrees of reliance upon the Frank-Starling mechanism, depending upon the adequacy of inotropic (ccntractility) reserve to meet the stress imposed by isometric exercise.
TL;DR: A method is presented which utilizes two fixed external reference points and the diaphragm as an internal marker to evaluate left ventricular contraction pattern and a better evaluation ofleft ventricular wall motion is obtained.
Abstract: Of two methods utilized to assess ventricular wall motion, one (method A) assumes the left ventricular wall moves symmetrically during contraction toward the approximate geometric center of the left ventricle. The other (method B) assumes the left ventricular wall moves symmetrically toward the base of the heart. Clearly, both methods cannot be correct in all patients. We are presenting a method (R) which utilizes two external markers and the diaphragm as an internal marker to evaluate left ventricular contraction pattern. Of 44 patients studied, the diaphragm moved in four and ventricular wall motion could not be assessed. Fifteen patients had valvular heart disease; six were normal. Findings in method R corresponded to those determined by method B in five of eight patients (63%) with left ventricular hypertrophy and by method A in eight of 13 patients (62%) without left ventricular hypertrophy. This difference was significant ( P
TL;DR: The study provides a simple technique for examining and quantitating localized disorders of wall motion, and the data indicate an association between the sites of major coronary occlusions and characteristic patterns of regional contraction.
Abstract: An angiographic method is introduced that permits detection and quantification of regional disorders of ventricular wall motion in man. The left ventricle is visualized as a muscular cone suspended freely from the atrioventricular ring. This ring, outlined partially by a coronary sinus catheter, serves as a fixed plane of reference for the motion of endocardial segments during systole. Regional motion of the left ventricle is analyzed by plotting the displacement of the apex and 6 hemiaxes during 4 sequential phases of systole. The nonischemic left ventricle (6 patients) revealed synchronous and symmetrical shortening of all segments. The middle and apical hemiaxes of the posterior wall shortened to a greater extent (62 and 70 percent, respectively) than the anterior wall segments (40 to 45 percent), and there was a slight angular displacement (5 °) of the apex toward the anterior wall. Of the ischemic hearts, 6 with predominant right coronary arterial lesions demonstrated posterior akinesis and dyskinesis during early systole and an exaggerated shortening, particularly in the posteroapical segment, during late systole. These findings were associated with a significant apical displacement (23 °) toward the wall opposite the ischemic zone. Six patients with major occlusive disease of the left anterior descending artery showed the same abnormal segmental pattern in an opposite direction. The study provides a simple technique for examining and quantitating localized disorders of wall motion, and the data indicate an association between the sites of major coronary occlusions and characteristic patterns of regional contraction.
TL;DR: A direct relationship existed between the functional properties and the anatomical development of the myocardium and the role of increasing left ventricular mass in this process was not the sole factor that contributed to improved myocardial function with age.
Abstract: Experiments were designed to assess the intrinsic changes in myocardial function with age and to determine the role of increasing left ventricular mass in this process. Isometric ventricular pressure-volume curves and length-tension curves were measured in isolated perfused rat hearts of different ages and masses. Incremental tension, peak active tension, and peak passive tension were less for 10-day-old hearts than they were for older hearts subjected to proportionately equal increases in length. At resting length, peak active tension developed by hearts at least 16 days old was 78% higher than that developed by 10-day-old hearts, and peak passive tension was 133% higher. There was no significant difference between 16-day-old rats and older rats. Thus, by the sixteenth postnatal day, the heart had developed functional maturity. These functional changes appeared to be related to age rather than to left ventricular mass. Histological studies of the left ventricle showed that, at birth, the myofibrils were disoriented with a high ratio of nonmyofibrillar elements to myofibrillar elements. Within 16-20 days after birth, the structural organization and the ratio of nonmyofibrillar elements to myofibrillar elements were similar to the organization and the ratio found in an adult. Thus a direct relationship existed between the functional properties and the anatomical development of the myocardium. Mass per se was not the sole factor that contributed to improved myocardial function with age.
TL;DR: A large increase in taurine concentration, which was confined to the failing right ventricle, may have functional significance since this compound has been linked to cellular calcium ion movement.
TL;DR: It is suggested that hypoxia rapidly produces pulmonary hypertension and its morbid anatomical associations while recovery is equally rapid once the hypoxic stimulus is removed, and appears to be applicable to hypoxic cor pulmonale in man.
Abstract: Three groups of 10 adult male Wistar albino rats were studied. The first was kept for five weeks in a hypobaric chamber exposed to a barometric pressure of 380 mmHg, equivalent to a simulated altitude of 5,500 m above sea level. The second was exposed to the same barometric pressure for five weeks and then allowed to recover in room air for a further period of five weeks. The third group acted as controls and was kept at normal barometric pressure throughout. At necropsy right ventricular weight was expressed as an inverse ratio of left ventricular weight (LV/RV ratio). The thickness of the media of the pulmonary trunk was expressed as a ratio of that of the aorta. The volumes of the carotid bodies were measured by applying Simpson's rule to histological sections. In the first group, exposed to chronic hypoxia without relief, there was hypertrophy of the right ventricle and media of the pulmonary trunk and there was an increase of carotid body volume, as compared with the values obtained in the controls. In the recovery group these three measurements had returned almost to normal. The results appear to be applicable to hypoxic cor pulmonale in man. They suggest that hypoxia rapidly produces pulmonary hypertension and its morbid anatomical associations while recovery is equally rapid once the hypoxic stimulus is removed.
TL;DR: Underperfusion of RV myocardium may be predicted from information derived from RV and aortic pressure tracings, and reducing RV PI initially causes coronary vasodilatation.
TL;DR: The findings suggest that the mechanical lesions of mitral regurgitation and ventricular septal perforation are amenable to surgical intervention if a sufficient amount of residual functional muscle can be preserved in the left ventricle.
TL;DR: High-speed biplane left ventricular cineangiograms were analyzed for changes in volume, shape, and dimensions in 35 patients and differences between the two groups of patients were best expressed by the difference in ejection fraction and globularity of the LV.
Abstract: High-speed biplane left ventricular (LV) cineangiograms were analyzed for changes in volume, shape, and dimensions in 35 patients. Ventriculographic studies in ten normal subjects characterized by an ejection fraction (E.F.) of 67 ± 2% and an end-diastolic volume (EDV) of 90 ± 8 ml/m2 were compared with results from 25 patients with isolated mitral regurgitation of varying severity. Patients with mitral regurgitation (MR) were subdivided according to whether or not the ejection fraction was normal. Those with normal E.F. (70 ± 2%) were termed compensated MR (CMR) and had EDV 192 ± 7 ml/m2. Those with decreased E.F. 34 ± 3% were termed decompensated MR (DMR) and had EDV 277 ± 17 ml/m2. In normal subjects no significant changes in LV dimensions were noted during the isovolumic phase of contraction while in patients with compensated MR the transverse axis shortened an average of 5.2% with no change in the longitudinal axis (L). Changes in geometry prior to ejection were less evident in the group with decompe...
TL;DR: It is proposed that the shift in blood flow away from the left ventricular inner layer is exaggerated in patients with coronary artery disease, resulting in subendocardial ischemia and hypoxia during tachycardia.
Abstract: We investigated the hypothesis that tachycardia augments the time of systolic compression of coronary blood vessels and shifts coronary blood flow from the subendocardial (inner) to the subepicardial (outer) layer of the left ventricle. Coronary blood flow distribution was determined in tranquilized dogs by the radioactive microsphere technique, with injection of approximately 200,000 spheres, 15 , into the left ventricular chamber. During the control period (mean heart rate 73 beats/min), there were consistent differences in the sphere concentrations (blood flow) in different regions of the heart, and the inner layer of the left ventricle always received more spheres than its outer layer. The mean inner/outer sphere ratios were 1.26 for the free wall and 1.39 for the septal wall. Tachycardia (heart rates of 151 and 193 beats/min) induced by atrial pacing or administration of atropine increased total coronary blood flow but systematically altered its distribution: The increase in blood flow to the atria was much greater than that to the ventricles, and the inner/outer sphere ratio of the left ventricle decreased in proportion to the increase in heart rate. Although the redistribution of coronary blood flow was not accompanied by chemical signs of myocardial hypoxia in these normal dogs, we propose that the shift in blood flow away from the left ventricular inner layer is exaggerated in patients with coronary artery disease, resulting in subendocardial ischemia and hypoxia during tachycardia.
TL;DR: It is suggested that one appropriate way to evaluate chronic changes in cardiac compliance is to assess the diastolic pressure-volume relation or the pressure-circumference relation over a range of pressures up to end-diastolics pressure, or over the range of volume accompanying the stroke volume.
Abstract: There is evidence that most alterations in inotropic state occurring under normal circumstances do not substantially influence diastolic compliance, except perhaps in the rapid phases of cardiac filling. Nevertheless, recent studies have clearly shown that left ventricular compliance can be markedly altered in chronic disease states, acute myocardial infarction, chronic ventricular hypertrophy and failure and chronic dilatation influencing diastolic compliance in an important manner. The large shift to the right of the pressure-volume relation observed in the chronically dilated left ventricle allows the ventricle to operate from a large radius and to deliver a normal or increased stroke volume without a great increase in end-diastolic pressure. On the other hand, the decrease in compliance without a shift to the right that appears to occur in acute myocardial infarction may increase filling pressure without this mechanical advantage and be detrimental. The question of when and by what mechanism changes in heart size and compliance appear to become irreversible seems to be amenable to experimental study and could have important clinical implications. It is suggested that one appropriate way to evaluate chronic changes in cardiac compliance is to assess the diastolic pressure-volume relation or the pressure-circumference relation over a range of pressures up to end-diastolic pressure, or over the range of volume accompanying the stroke volume. This approach, encompassing a normal cardiac filling cycle, and defined as “functional compliance,” should offer useful clinical information on the filling characteristics of the ventricle relative to pressures transmitted in retrograde manner to the lungs or the systemic venous circulation. The assessment of the passive stress-strain relation of the myocardium itself in the whole heart remains a difficult and challenging problem.
TL;DR: The data suggest that the difference in dilator responses in the two beds results from greater withdrawal of adrenergic constrictor tone to skeletal muscle than to skin, and low pressure baroreceptors in atria or pulmonary vessels did not contribute to vasodilator responses to left ventricular outflow obstruction.
Abstract: Reflex vascular responses to acute left ventricular outflow obstruction were studied in anesthetized dogs. The studies were done to compare the effects of activation of ventricular baroreceptors on vascular resistance in skeletal muscle (gracilis muscle) and skin (hindpaw); to identify afferent and efferent pathways which mediate the reflex vasodilatation; and to assess the relative contribution of ventricular baroreceptors and baroreceptors in left atrium and pulmonary vessels in responses to left ventricular outflow obstruction. The gracilis artery and the cranial tibial artery to the paw were perfused separately at constant flow. Changes in perfusion pressure to each bed reflected changes in vascular resistance. Outflow obstruction was produced by inflating a balloon in the left ventricular outflow tract for 15 s while pressures in the left ventricle and aortic arch were measured.
Inflation of the balloon increased left ventricular pressure and decreased pressure in the aortic arch. Low and high levels of obstruction produced dilator responses averaging -5±3 (SE) and -42±11 mm Hg in muscle and -1±1 and -3±2 mm Hg in paw. Denervation, phentolamine, and glyceryltrinitrate caused greater dilatation in paw than did left ventricular outflow obstruction. This indicates that dilator responses in the paw were not limited by a low level of resting neurogenic constrictor tone or by a negligible dilator capacity of these vessels.
Obstruction to left ventricular inflow increased left atrial pressure, but did not cause reflex vasodilatation. This suggests that low pressure baroreceptors in atria or pulmonary vessels did not contribute to vasodilator responses to left ventricular outflow obstruction.
Vasodilator responses to outflow obstruction were blocked by bilateral vagotomy, sectioning the sciatic and obturator nerves, and administration of phentolamine, but were not decreased by atropine or tripelennamine.
The results indicate that activation of left ventricular baroreceptors produces striking vasodilatation in skeletal muscle, but only slight vasodilatation in skin. The data suggest that the difference in dilator responses in the two beds results from greater withdrawal of adrenergic constrictor tone to skeletal muscle than to skin. Activation of sympathetic cholinergic or histaminergic dilator pathways does not contribute to the dilatation.
TL;DR: It is felt that preoperative evaluation of children with VSD and PAB should include evaluation of the left ventricular outflow tract to be certain that no obstruction is present, and the development of subaortic stenosis was not suspected prior to the second catheterization.
Abstract: Palliation of children with large ventricular septal defects (VSD) by pulmonary artery banding (PAB) is associated with a variety of unfavorable sequelae. We document another possible complication of PAB, the development of subaortic stenosis, which occurred in 4 of 40 infants with large VSD and PAB. Prior to surgery all had congestive heart failure, cardiomegaly, pulmonary plethora, and biventricular or right ventricular hypertrophy on electrocardiogram. At cardiac catheterization all had large VSD with pulmonary artery hypertension. No gradient between left ventricle and systemic artery was demonstrated. PAB was followed by improvement in all four children. Repeat catheterization at 4 to 11 years of age revealed that they had developed a significant (30 to 100 mm Hg) gradient across the left ventricular outflow tract. Although the etiology of the subaortic stenosis is not known, it is felt that the hypertrophied and possibly leftward deviated conal septum was impinging on the left ventricular outflow tract in three of the four. Since the subaortic stenosis was not suspected prior to the second catheterization, we feel that preoperative evaluation of children with VSD and PAB should include evaluation of the left ventricular outflow tract to be certain that no obstruction is present.
TL;DR: A striking finding in the immediate postnatal period was a doubling of the left ventricular output shortly after birth with an associated increase in cardiac dimensions.
TL;DR: Neither the cardiac output nor the left ventricular end-diastolic pressure correlated closely with size of the noncontractile area, but the ejection fraction was a more sensitive indicator and correlated well with the extent of regional contraction abnormality.
Abstract: Thirty-one patients with coronary artery disease, 25 of whom had a chronic localized noncontractile area in the anteroapical region of the left ventricle, were studied at rest by means of left heart catheterization, left cineventriculography and selective coronary arteriography. The left ventricular volume, stroke volume, ejection fraction, left ventricular end-diastolic pressure, cardiac output and the surface area of the noncontractile area were measured. The patients with a noncontractile area were classified in 4 groups according to the size of the noncontractile area relative to the end-diastolic left ventricular surface area. The relative size of the non-contractile area ranged from 5 to 47 percent. Six patients with uncomplicated coronary artery disease comprised the control group. The critical size of the noncontractile area beyond which significant functional derangement occurred appeared to be 20 to 30 percent of the left ventricular internal surface area. The end-diastolic volume increased significantly and the ejection fraction was reduced to less than half of normal when the regional noncontractile area was larger than the critical size. Neither the cardiac output nor the left ventricular end-diastolic pressure correlated closely with size of the noncontractile area. In contrast, the ejection fraction was a more sensitive indicator and correlated well with the extent of regional contraction abnormality. In this study, double vessel disease was most common, followed by single vessel disease. Obstruction of the left anterior descending coronary artery was significant in the formation of anteroapical noncontractile regions.
TL;DR: Measurements based on angiographic left ventricular volumes should be valid and correspond closely to the control state for the period ofleft ventricular opacification, and demonstrate no significant change.
Abstract: Changes in human circulatory physiology occurring in the minutes after intracardiac injection of angiographic contrast material have been well documented, but little information is available for the period of left ventricular opacification. The immediate and instantaneous effect on left ventricular function of the rapid intracardiac injection of 1 ml/kg body weight of 75 percent sodium-meglumine diatrizoate (Hypaque M®) into the pulmonary artery, left atrium or left ventricle in 43 adult patients was studied by measurement during angiography of (1) peak aortic root blood velocity in 28 patients, (2) instantaneous stroke volume (computed from the velocity tracing) in 28 patients, (3) heart rate in 41 patients, (4) left ventricular end-diastolic pressure in 17 patients, and (5) left ventricular end-diastolic and end-systolic volumes (calculated from the single-plane cineangiogram) in 14 patients. During left ventricular opacification, variables 1 through 4 differed only slightly from control values; the only statistically significant changes were in peak velocity after pulmonary arterial injection (114 percent of control, control = 100 percent), heart rate after left atrial injection (93 percent of control) and left ventricular end-diastolic pressure after left ventricular injection (110 percent of control). Sequential left ventricular end-diastolic and end-systolic volumes measured over 3 to 5 cardiac cycles demonstrated no significant change. We conclude that measurements based on angiographic left ventricular volumes should be valid and correspond closely to the control state. The major hemodynamic changes secondary to contrast injection occur later, beginning 15 to 30 seconds after injection.
TL;DR: The roentgenographic relationship of the left ventricle and inferior vena cava correlated poorly with left ventricular size, and subgrouping of patients according to specificleft ventricular hemodynamic alterations did not improve correlations.
Abstract: In order to assess the accuracy of radiographic parameters of left heart enlargement, quantitative biplane angiographic data was compared to chest X-ray data in 254 adults with various heart diseases. Cardiac silhouette volume measured from PA and lateral chest roentgenograms compared most favorably to the sum of the left ventricular mass, end-diastolic volume, and left atrial maximal volume (r = 0.78, P < 0.01; 79% accuracy). The cardiothoracic ratio gave 70% accuracy (r = 0.64, P < 0.01). Subgrouping of patients according to specific left ventricular hemodynamic alterations did not improve correlations. The roentgenographic relationship of the left ventricle and inferior vena cava correlated poorly with left ventricular size. Of 99 patients with increased left atrial maximal volumes, 81 had visible posterior displacement of the barium-outlined esophagus by the left atrium.
TL;DR: A rare congenital heart in which there was a canal between the aorta and right ventricle in an infant boy who died approximately six hours after birth is examined, and this aortico-right ventricular tunnel is considered to be analogous to aortICO-left ventricular Tunnel, previously described.
TL;DR: The short interval elapsing between inscription of RVA and RVOT electrograms suggested that propagation from apex to outflow tract did not occur in a linear fashion, as when these sites were stimulated directly.