Showing papers on "Ventricle published in 1983"
TL;DR: The representations of ventricle and arterial system by their Ps-SV relationships are useful in understanding how these two systems determine SV when they are coupled and interact.
Abstract: We developed a framework of analysis to predict the stroke volume (SV) resulting from the complex mechanical interaction between the ventricle and its arterial system. In this analysis, we characterized both the left ventricle and the arterial system by their end systolic pressure (Ps)-SV relationships and predicted SV from the intersection of the two relationship lines. The final output of the analysis was a formula that gives the SV for a given preload as a function of the ventricular properties (Ees, V0, and ejection time) and the arterial impedance properties (modeled in terms of a 3-element Windkessel). To test the validity of this framework for analyzing the ventriculoarterial interaction, we first determined the ventricular properties under a specific set of control arterial impedance conditions. With the ventricular properties thus obtained, we used the analytical formula to predict SVs under various combinations of noncontrol arterial impedance conditions and four preloads. The predicted SVs were compared with those measured while actually imposing the identical set of arterial impedance conditions and preload in eight isolated canine ventricles. The predicted SV was highly correlated (P less than 0.0001) with the measured one in all ventricles. The average correlation coefficient was 0.985 +/- 0.004 (SE), the slope 1.00 +/- 0.04, and the gamma-axis intercept 1.0 +/- 0.2 ml, indicating the accuracy of the prediction. We conclude that the representations of ventricle and arterial system by their Ps-SV relationships are useful in understanding how these two systems determine SV when they are coupled and interact.
741 citations
TL;DR: The proportion of patients with symmetric and distal ventricular hypertrophy was greater than that reported when patients are selected on the basis of M-mode diagnostic criteria and suggests that the recognition and understanding of hypertrophic cardiomyopathy have been biased by patients with asymmetric septalhypertrophy who previously were most readily identified.
291 citations
TL;DR: The left atrial contribution to left ventricular function is increased in patients with remote myocardial infarction, attributed to the Frank- Starling mechanism in the left atrium.
Abstract: Left atrial function was evaluated in patients with and without remote myocardial infarction. The simultaneous left atrial pressure recording and left atrial and left ventricular cineangiograms were obtained with a catheter-tip micromanometer. The pressure-volume curve of the left atrium was composed of an A-loop and a V-loop. The ratio of active atrial emptying to left ventricular stroke volume in patients with myocardial infarction was significantly larger than that in normal subjects (42 +/- 12% vs 29 +/- 10%, p less than 0.05). The left atrial work was also significantly greater in patients with myocardial infarction (1690 +/- 717 mm Hg X ml) than in normal subjects (940 +/- 426 mm Hg X ml, p less than 0.05). The ratio of active atrial emptying to left ventricular stroke volume and left atrial work were significantly related in both normal subjects and patients with myocardial infarction (gamma = 0.72, p less than 0.01). The left ventricular ejection fraction correlated inversely with left atrial work (gamma = -0.5, p less than 0.05). Left atrial work also showed a significant linear correlation with left atrial volume before active atrial emptying (gamma = 0.82, p less than 0.01). We conclude that the left atrial contribution to left ventricular function is increased in patients with remote myocardial infarction. This left atrial contribution to the left ventricle is attributed to the Frank-Starling mechanism in the left atrium.
288 citations
TL;DR: It is suggested that endogenous PGD2 may be involved in the regulation of sleep by acting on the brain structures surrounding the third ventricle in the rhesus monkey.
Abstract: The sleep-inducing effect of prostaglandin D2 (PGD2) was studied in five conscious male rhesus monkeys (Macaca mulatta) maintained in a 12-hr light/dark cycle. PGD2 was infused into the lateral or the third ventricle of the cerebrum slowly and continuously for 6 hr in the light period. Infusion of PGD2 into the lateral ventricle at 15-2250 pmol/min induced natural sleep as identified by electroencephalogram, electromyogram, electrooculogram, body temperature, heart rate, and animal behavior. Although sensitivity to PGD2 was slightly different among individual animals, the amount of total sleep time increased maximally up to 3- to 4-fold over the control level. PGD2 infused into the third ventricle induced effects similar to those observed for the lateral ventricular route, but infusion into the third ventricle was about 1000 times more effective than infusion into the lateral ventricle. In three monkeys, PGD2 increased the amount of sleep in a dose-dependent manner. Bell-shaped dose-response curves were observed for the other two monkeys. Infusion of prostaglandin E2 or F2 alpha into the lateral ventricle caused sedation but slightly reduced the amount of slow-wave sleep and produced increases in heart rate and body temperature. These findings suggest that endogenous PGD2 may be involved in the regulation of sleep by acting on the brain structures surrounding the third ventricle in the rhesus monkey.
215 citations
TL;DR: The majority of patients who have serious ventricular arrhythmias but no apparent structural cardiac abnormalities have abnormal right ventricular biopsy specimens and it is concluded that the arrh rhythmias may be the first manifestation of a variety of primary myocardial abnormalities.
Abstract: To evaluate possible occult myocardial disease in 18 patients whose only major manifestation of heart disease was spontaneous ventricular tachycardia or fibrillation, right ventricular endomyocardial biopsies were performed None of the patients had symptoms of ischemic or congestive heart disease, and at catheterization none had significant lesions of the coronary arteries or regional wall motion abnormalities of the left ventricle The mean left ventricular ejection fraction (65 +/- 7%), mean right ventricular ejection fraction (55 +/- 9%), mean cardiac index (30 +/- 05 1/min/m2), mean right atrial pressure, mean pulmonary capillary wedge pressure, and mean pulmonary artery systolic pressure were normal However, right ventricular endomyocardial biopsy specimens were abnormal in 16 of 18 (89%) patients: nine (50%) had changes of a significant, although nonspecific, cardiomyopathy with myocellular hypertrophy, interstitial and perivascular fibrosis, and vascular sclerosis; three (17%) had subacute inflammatory myocarditis; two (11%) had diffuse abnormalities of the intramyocardial arteries; and two (11%) had pathologic changes consistent with arrhythmogenic right ventricular dysplasia In the two (11%) patients with normal biopsy specimens, one had Wolff-Parkinson-White syndrome and the other had mitral valve prolapse Although histologic abnormalities were found in 89% of these patients, performance of right ventricular endomyocardial biopsies in this group of patients should be considered a research procedure We conclude that the majority of patients who have serious ventricular arrhythmias but no apparent structural cardiac abnormalities have abnormal right ventricular biopsy specimens and that the arrhythmias may be the first manifestation of a variety of primary myocardial abnormalities
213 citations
TL;DR: End-diastolic and end-systolic volumes (EDV and ESV) were calculated using a disc method with a semiautomatic computer system and the transducer position was found to be anterior and superior to the left ventricular anatomic apex, as evaluated by filming the echo transducers position during cineventriculography.
Abstract: Two-dimensional echocardiography underestimates left ventricular volume compared with cineventriculography. To exclude the influence of difference in heart rate, blood pressure, respiration phases and any effect of the contrast material on left ventricular function, simultaneous studies of two-dimensional echocardiography and cineventriculography-echoventriculography were performed in 46 patients. Apical two-dimensional echocardiograms in the right anterior oblique (RAO) equivalent view were recorded before and during cineventriculography in the 30 degrees RAO projection. End-diastolic and end-systolic volumes (EDV and ESV) were calculated using a disc method with a semiautomatic computer system. The echo transducer position relative to the left ventricular apex and long axis was analyzed. For EDV determined by two-dimensional echocardiography and cineventriculography, the linear regression equation was y = 0.659x + 0.8, SEE = +/- 26.2 ml, r = 0.907. For ESV, the regression equation was y = 0.571x + 17.8, r = 0.938, SEE = +/- 18.6 ml, and for ejection fraction (EF) it was y = 0.606x + 13.0, r = 0.803, SEE = +/- 9.1%. Injection of contrast material resulted in only a small increase of stroke volume, caused by an increase of EDV as analyzed by echoventriculography. In all but two patients, the transducer position was found to be anterior and superior to the left ventricular anatomic apex, as evaluated by filming the echo transducer position during cineventriculography in 46 patients in the 30 degrees RAO projection and in 15 patients consecutively in the 60 degrees left anterior oblique and 30-40 degrees cranial projections. Thus, tangential cuts of the ventricle resulted in underestimation of diameters, long axis and ventricular volumes. These methodologic problems are exacerbated by slice-thickness artifacts. Furthermore, different outlining of left ventricular contour -- outer border of ventricular trabeculae for cine ventriculography and inner border for two-dimensional echocardiography -- seemed to result in underestimation of volume by echocardiography.
208 citations
TL;DR: It is concluded that contraction in the normal left ventricle cannot be assumed to be uniform or symmetrical and should be taken into account when evaluating altered physiologic states and in studying effects of therapeutic interventions.
Abstract: Regional differences in wall motion and wall thickening were quantitated in the normal left ventricle using two-dimensional echocardiography (2-D echo). Using a computer-aided system, the left ventricle was subdivided in a standardized manner into 40 segments of five 2-D echo short-axis cross sections from the mitral valve level to the low left ventricle or apex. Measurements of sectional and segmental cavity areas, muscle areas and endocardial as well as epicardial perimeters, allowed assessment of contractile function using such indexes as endocardial systolic fractional area change (FAC), wall thickening (WTh), and circumferential fiber shortening (shortening). In 50 normal anesthetized, closed-chest dogs (including 10 studies in the conscious state) and in 32 normal humans, left ventricular contractile function increased significantly from base to apex. Thus, in anesthetized dogs, sectional FAC, WTh and shortening increased from left ventricular base to apex as follows: 39.4 +/- 5.1% to 61.6 +/- 7.2%, 20.5 +/- 6.6% to 46.7 +/- 11.5% and 22.7 +/- 3.4% to 35.4 +/- 5.9%, respectively. Similar trends were noted in conscious dogs. In man, sectional FAC, WTh and shortening also increased from the mitral valve to the low left ventricular level: 38.8 +/- 3.3% to 60.7 +/- 4.5%, 23.9 +/- 5.6% to 28.9 +/- 7.6% and 21.4 +/- 5.0% to 30.6 +/- 5.6%, respectively. Detailed segmental analysis in individual cross sections also revealed regional differences in contraction. Generally, contraction was most vigorous in posterior regions of the left ventricle. The septal regions exhibited lowest contraction at the base, but also the greatest increase from base to apex, both in the canine and human. Lateral regions did not show significant changes along the length of the left ventricle. Diastolic wall thickness also varied. We conclude that contraction in the normal left ventricle cannot be assumed to be uniform or symmetrical. These normal regional differences in function should be taken into account when evaluating altered physiologic states and in studying effects of therapeutic interventions.
191 citations
TL;DR: Two-dimensional echocardiography was prospectively performed on 52 normal volunteers to determine normal left ventricular volume and ejection fraction as a prerequisite to their clinical application, and the Simpson's rule algorithm resulted in smaller values for left Ventricular volume than did any of the area-length algorithms.
190 citations
TL;DR: In this article, ultrasonic dimension transducers were used to measure left ventricular anterior-posterior and septal-free wall minor axis and major axis diameters, and the functional significance of the two types of ventricular interaction was determined.
Abstract: In nine conscious, chronically instrumented dogs, ultrasonic dimension transducers measured left ventricular anterior-posterior and septal-free wall minor axis and major axis diameters. Matched micromanometers measured right and left ventricular transmural and transeptal pressures. Ventricular pressures and volumes were varied by inflation of implanted vena caval and pulmonary artery occluders, and the functional significance of the two types of ventricular interaction, i.e., direct and series, was determined. The left ventricle was represented by a modified ellipsoidal geometry. Left ventricular stroke volume calculated from the dimension data correlated well with that measured directly from ascending aortic electromagnetic flow probes during all interventions (r greater than or equal to 0.96). Partial pulmonary artery occlusion significantly increased right ventricular diastolic and systolic pressures as compared to values obtained during control and venal caval occlusion. During pulmonary artery occlusion, latitudinal septal eccentricity was increased throughout the cardiac cycle compared to control and vena caval occlusion (P less than 0.05), indicating leftward interventricular septal shifting and significant alteration of left ventricular shape. The normalized diastolic pressure-volume curve was shifted to the left with pulmonary artery occlusion compared to control and indicated a decrease in left ventricular chamber compliance. However, when selected cardiac cycles with similar end-diastolic volumes from vena caval and pulmonary artery occlusions were compared, parameters of left ventricular systolic function (stroke volume, percent systolic shortening, peak aortic blood flow, peak left ventricular pressure, and its first derivative) remained relatively constant. These data suggest that mean myocardial fiber length is the major preload determinant of left ventricular systolic function independent of chamber pressure and shape, and that direct ventricular interaction mediated by interventricular septal shifting has minimal effects on systolic myocardial performance in this model. Thus, series ventricular interaction during acute imbalances in biventricular loading, where the output of the right ventricle determines the input of the left, seems to be far more important than direct interaction to the regulation of overall cardiac function.
184 citations
TL;DR: It is concluded that action potential configuration in rat ventricle is heterogeneous, and that this is reflected by the different types of action potentials in isolated myocytes.
Abstract: The objectives of this study were to measure action potential parameters in enzyme-dissociated, adult rat ventricular myocytes stimulated at 1 Hz, to compare these measurements with those obtained from intact ventricular tissue, and to determine myocyte and tissue responses at stimulus frequencies between 0.1 and 5 Hz. Action potentials were characterized in terms of amplitude, overshoot, resting potential, duration at 25% and 75% repolarization (APD25, APD75), and Vmax. Based on statistical differences in APD25 and APD75, myocyte action potentials were classified as type I (3.1 +/- 1.0 and 21.5 +/- 3.6 msec), type II (7.4 +/- 1.1 and 38.2 +/- 6.7 msec), or type III (14.5 +/- 1.9 and 46.0 +/- 4.1 msec). Action potentials corresponding to type I were found in right ventricular endocardium and right papillary muscles, and those corresponding to types II and III in the left ventricular endocardium [apex, middle (II); base (III)] and left papillary muscles (II). Myocytes and papillary muscles responded to increases in driving rate with nearly identical lengthening of APD25 and shortening of APD75. The one exception was at 5 Hz where a lengthening of the APD75 occurred in some myocytes. We conclude that action potential configuration in rat ventricle is heterogeneous, and that this is reflected by the different types of action potentials in isolated myocytes. It is likely that the magnitude of a transient outward current is a determinant of action potential configuration, and that slow reactivation of this current is a significant factor underlying the stimulus frequency response.
183 citations
TL;DR: Whole body nuclear magnetic resonance imaging of the cardiovascular system was carried out in early clinical trials in 244 volunteers and patients using a 3.5 KGauss (0.35 T) unit and preliminary experience indicates the considerable potential of NMR imaging in the evaluation of cardiovascular diseases.
Abstract: Whole body nuclear magnetic resonance (NMR) imaging of the cardiovascular system was carried out in early clinical trials in 244 volunteers and patients using a 3.5 KGauss (0.35 T) unit. The spin echo technique with multiple imaging parameters was used. Blood vessels were clearly discriminated from solid organs and lesions because little or no intraluminal signal is seen with laminar blood flow at normal velocities, whereas a more intense image is generated by solid organs. Characteristic flow signals were observed in normal patients and were accentuated by varying the imaging parameters. Cardiac chambers were well delineated in some patients on nongated images. In one case, internal topography of the ventricles was exquisitely displayed on a gated image. Intraluminal pathology, such as dissection of the aorta, aneurysms of the aorta and left ventricle, and aortic atheroma, was clearly demonstrated. Patency of coronary arterial bypass grafts was shown. Abnormal flow patterns due to slow or turbulent flow ...
TL;DR: It was concluded that, as a result of running exercise, right ventricular growth is analogous to eccentric hypertrophy in which the structural adaptations of the capillary bed can be expected to improve the diffusion and transport of oxygen within the tissue.
Abstract: In our morphometric study of the effects of exercise on the heart, male Wistar-Kyoto rats at 5 weeks of age were subjected daily to a moderate treadmill running program that lasted for 7 weeks. The heart responded to physical conditioning by different magnitudes of tissue growth of the right (22%) and left (7%) ventricular myocardium, the latter change not statistically significant. The increase in right ventricular volume was associated with a 25% enlargement of ventricular area, a 26% average lengthening of the myocytes, and no change in sarcomere length and in ventricular midwall thickness. Exercise produced significant alterations in the quantitative parameters of the microvasculature of the right ventricle, but no appreciable changes in the left ventricle. Right ventricular hypertrophy was characterized by an absolute 44% growth of the endothelial luminal surface brought about through a 16% increase in capillary numerical density, and a 41% augmentation of the total length of the capillary network. Maximum diffusion distance from the capillary wall to the mitochondria of myocytes decreased 10% as a result of capillary proliferation and the lack of lateral expansion of myocyte cross-sectional area. Evaluation of the subcellular constituents of myocytes showed no change in the mitochondria:myofibrils volume ratio, indicating a growth of these components proportional to each other and to the growth of the myocyte population as a whole. It was concluded that, as a result of running exercise, right ventricular growth is analogous to eccentric hypertrophy in which the structural adaptations of the capillary bed can be expected to improve the diffusion and transport of oxygen within the tissue.
TL;DR: This study was designed to develop a two-dimensional echocardiographic method of measuring the mass of the left ventricle that accurately predicted postmortem left ventricular mass and was independent of cardiac cycle phase.
Abstract: This study was designed to develop a two-dimensional echocardiographic method of measuring the mass of the left ventricle. The general formula for an ellipse was used to derive an algorithm that described the shell volume of concentric truncated ellipsoids. In 10 canine left ventricular two-dimensional echocardiograms, this algorithm accurately predicted postmortem left ventricular mass (r = .98, SEE +/- 6 g) and was independent of cardiac cycle phase (systole vs diastole, r = .92).
TL;DR: Methods used to revascularize ischemic myocardium have included arterial reconstruction, coronary artery bypass grafting, providing direct circulation from the intraventricular chamber, and techniques to promote collateral circulation.
Abstract: Methods used to revascularize ischemic myocardium have included arterial reconstruction, coronary artery bypass grafting, providing direct circulation from the intraventricular chamber, and techniques to promote collateral circulation. Ventricular channels from the epicardial surface through the endocardium are readily made with the CO2 laser. Animal experiments suggest that these channels protect the ischemic myocardium and provide circulation to the muscle from the ventricular chamber. Clinical use of the CO2 laser in conjunction with aortocoronary bypass grafting is reported in a patient with three-vessel coronary artery disease and total occlusion of the left anterior descending coronary artery (LAD), and hypokinesis of the anterior wall and apex. Following bypass a series of laser channels were made in the hypokinetic area of the left ventricle. Postoperative myocardial Tc PYP scans were within normal limits, including the previously dyskinetic anterior apical area. Serial EKGs remained unchanged from the preoperative status. Creatinine phosphokinase-myocardial band (CPK-MB) was elevated to 6 on the first and second postop day and was 0 from the third day. The patient was not recatheterized. The technique of myocardial revascularization by laser may be a viable addition to present treatment modalities. Further investigation and long-term follow-up are needed.
TL;DR: Increased myocardial stiffness in addition to a decreased rate of wall thinning and slow active pressure decay contribute to the upward shift in left ventricular pressure-wall thickness and pressure-volume relationships during pacing-induced angina.
Abstract: The left ventricular diastolic pressure-volume relationship shifts upward during angina, but why this happens is not known. To assess regional myocardial stiffness, we studied 12 patients who had coronary artery disease using simultaneous left ventricular micromanometer pressure recording and M-mode echocardiography before and during angina induced by pacing tachycardia. All patients had two- or three-vessel coronary artery disease that involved the posterior left ventricular wall circulation and had positive pacing stress tests, i.e., development of angina and a postpacing rise in left ventricular end-diastolic pressure (15 +/- 3 to 31 +/- 6 mm Hg, p less than 0.001). A marked upward shift in the relationship between the diastolic left ventricular pressure and the posterior wall thickness (h) occurred after pacing tachycardia, but the change in left ventricular posterior wall end-diastolic thickness was minimal (8.9 +/- 2.1 to 9.2 +/- 2.1 mm, NS). After pacing, the peak rate of left ventricular posterior wall thinning decreased (82 +/- 37 to 48 +/- 27 mm/sec, p less than 0.005) and the time constant of relaxation derived from the best exponential fit to the isovolumic left ventricular pressure decay increased (49 +/- 5 to 58 +/- 7 msec, p less than 0.001). Diastolic active left ventricular pressure decay, extrapolated from the exponential fit, was subtracted from the measured left ventricular pressure (which is equal in magnitude but opposite in sign to the radial stress at the endocardium) to calculate residual left ventricular pressure (PR) and hence residual stress (sigma R = -PR). A radial stiffness modulus (ER) was determined by the slope of the PR vs log h plots before and after pacing. Over the same range of residual radial stress (sigma R), ER was always higher during pacing-induced angina, indicating increased residual myocardial stiffness. Increased myocardial stiffness in addition to a decreased rate of wall thinning and slow active pressure decay contribute to the upward shift in left ventricular pressure-wall thickness and pressure-volume relationships during pacing-induced angina.
TL;DR: The contractile state (ejection fraction index-afterload relation) is thus the most sensitive indicator of left ventricular dysfunction in spontaneously hypertensive rats.
Abstract: Female spontaneously hypertensive and normotensive rats were studied at 6, 12, 18, and 24 months of age to determine which characteristics of myocardial performance herald the onset of left ventricular dysfunction. Peak ejection fraction index was derived from measurements of peak stroke volume (in vivo volume loading) and passive pressure-volume relations. The myocardial stiffness constant (km, slope of the incremental modulus-stress relation, EINC = km sigma), chamber stiffness constant (kc, slope of the chamber stiffness-pressure relation, dP/dV = kcP), and left ventricular cavitary volume-to-wall volume ratio at 10 mm Hg) were calculated from the pressure-volume data and the contractile state was assessed from the ejection fraction index-afterload relations. In the normotensive rats, the myocardial stiffness constant was not affected by age, whereas, in the spontaneously hypertensive rats, the myocardial stiffness constant remained within normal limits until 18 months, at which time a significant increase in this index of myocardial stiffness occurred. Baseline and maximal cardiac indices and ejection fraction index of spontaneously hypertensive rats were normal from 6 to 18 months, but were markedly reduced at 24 months. This reduction in cardiac performance was associated with a decrease in the left ventricular chamber stiffness constant, i.e., kc. This decreased chamber stiffness, which occurred at a time when myocardial stiffness was increased, was due to a greater increase in cavity size than in myocardial stiffness. The left ventricular cavity-to-wall volume ratio of normotensive rats was not affected by age, whereas, in the spontaneously hypertensive rats, this ratio markedly declined by 18 months. The ejection fraction index-afterload relations i.e., a measure of the contractile state, of the 6- and 12-month-old spontaneously hypertensive rats were similar to those of the normotensive rats of all ages. However, a depression in the contractile state of the spontaneously hypertensive rats occurred at 18 months and was further depressed at 24 months. This abnormality of the contractile state was evident before the deterioration of cardiac performance, as reflected in a decrease in baseline and maximal cardiac indices, and dilation of the left ventricle occurred. The contractile state (ejection fraction index-afterload relation) is thus the most sensitive indicator of left ventricular dysfunction in spontaneously hypertensive rats.
TL;DR: To obtain normal values for left atrial function noninvasively, volumes of the left atrium and ventricle were calculated by 2-dimensional echocardiography by using a modified Simpson's rule formula.
Abstract: To obtain normal values for left atrial function noninvasively, volumes of the left atrium and ventricle were calculated in 52 volunteers by 2-dimensional echocardiography. A light pen digitizing and computation system, controlled by a microprocessor, was used to outline the left atrium and ventricle in orthogonal apical views. Then, to calculate end-systolic and end-diastolic atrial and ventricular volumes, a modified Simpson's rule formula was used. End-systolic left atrial volume (mean +/- standard deviation) was 37 +/- 11.7 ml or 21 +/- 6.6 ml/m2. The change in left atrial volume from end-systole to end-diastole was 24 +/- 7.6 ml or 13.5 +/- 4.3 ml/m2, which represented 37 +/- 12.9% of left ventricular stroke volume. The mean fractional emptying of the left atrium was 65 +/- 8.9% and the conduit volume was 41 +/- 14.0 ml or 23 +/- 7.9 ml/m2. These values are similar to those reported in studies in which left atrial function was calculated from contrast angiography.
TL;DR: RVFW disconnection is feasible and applicable to patients with refractory VT originating in the diffusely diseased RVFW, and there was no clinical evidence of hemodynamic impairment.
Abstract: Arrhythmogenic right ventricular dysplasia is a myopathy that affects the right ventricular free wall (RVFW) and gives rise to recurrent reentrant ventricular tachycardia (VT). Because the entire right ventricle is potentially arrhythmogenic, ablating a single site of VT may not eliminate the arrhythmia. We developed an operation to confine any arrhythmic activity arising from the right ventricle to that chamber: total disconnection of the RVFW from the left ventricle. We performed RVFW disconnection in two patients with refractory VT associated with arrhythmogenic right ventricular dysplasia. At least two sites or origin of morphologically distinct VT were identified in the RVFW in each patient. RVFW disconnection was carried out under normothermic cardiopulmonary bypass. An encircling incision was made along the attachment of the RVFW to the aortoventricular unit and the tricuspid annulus; the right coronary artery and its RVFW branches were left intact. Electrical activity of the two chambers became dissociated, and VT arising from the RVFW was confined to that chamber. Postoperatively, there was no clinical evidence of hemodynamic impairment (follow-up 4 months and 3 months). Left ventricular function was unchanged and right ventricular flow was maintained by atrial contraction and motion of the septum toward the RVFW during left ventricular systole. One patient had incessant right ventricular tachycardia confined to the RVFW for 3 weeks. We conclude that RVFW disconnection is feasible and applicable to patients with refractory VT originating in the diffusely diseased RVFW.
TL;DR: It was observed that the progressive increase of ventricular hypertrophy from 4 to 19 months of age did not further increase w/ri in SHR, indicating an increase in overall ventricular size with age and the "Starling mechanism" to maintain a normal stroke volume against the increased afterload for the heart in established hypertension.
Abstract: The influence of myocardial hypertrophy on left ventricular volume compliance was studied in vitro in isolated hearts of 4 and 19 month old spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY). In both SHR groups diastolic volume compliance was similar to that in the controls, despite the presence of left ventricular hypertrophy. This seems to be mainly due to an altered geometric situation, since with increased wall thickness to internal radius ratio (w/ri), which was at hand, the less are outer myocardial layers stretched at a given increase in ventricular volume. This may imply that these layers will only little interfere with luminal distension (and thereby with diastolic volume compliance) in SHR. It was also observed that the progressive increase of ventricular hypertrophy from 4 to 19 months of age did not further increase w/ri in SHR, indicating an increase in overall ventricular size with age. Left ventricular end diastolic pressure (LVEDP) was also measured in conscious 5 week and 4 month old SHR compared with matched controls. LVEDP increased with the development of hypertension and was significantly elevated in 4 month old SHR. This will increase also the average diastolic pre-stretch of the SHR left ventricle and mobilize the "Starling mechanism" to maintain a normal stroke volume against the increased afterload for the heart in established hypertension. This seems particularly important since the hypertrophic w/ri increase (about 20%) is smaller than the great elevation of mean arterial pressure (40-50%) in SHR.
TL;DR: Biventricular function in patients with the adult respiratory distress syndrome is examined by a combmation of invasively determined pressures and flows and concomitant radionuclide angiography and modilution stroke volume.
TL;DR: During acute RV hypertension, impairment of LV systolic function and rearrangements in LV dynamic geometry are primarily the result of the anatomic contiguity of the two ventricles.
Abstract: Fifteen chronically instrumented, conscious dogs were studied to determine whether, in the intact circulation, mechanical interactions dictated by the anatomic contiguity of the two ventricles significantly alter left ventricular (LV) dynamic geometry and systolic function during acute right ventricular (RV) hypertension. The three-dimensional geometry of the left ventricle was monitored with three pairs of ultrasonic dimension transducers; ventricular pressures were measured with micromanometers. Data collected during pulmonary artery constriction (RV pressure 68 +/- 8/7 +/- 4 mm Hg) were compared with control data collected at matched heart rates (RV pressure 32 +/- 8/4 +/- 4 mm Hg). During pulmonary artery constriction, mean calculated LV end-diastolic volumes decreased from 69.2 +/- 20.0 to 56.2 +/- 21.3 cm3 (p less than or equal to 0.05). Mean systolic stroke volume decreased from 20.6 +/- 5.5 to 14.0 +/- 6.3 cm3 (p less than or equal to 0.05). These changes were entirely accounted for by alterations in the behavior of the LV septal-free wall minor axis and rearrangements in LV equatorial geometry. When the pulmonary artery was constricted, elongation of the septal-free wall axis occurred during isovolumic systole and was accompanied by a reciprocal decrease in anterior-posterior dimension. Most of the decrease in septal-free wall dimension occurred during relaxation and early diastole rather than during ejection. Mean septal-free wall end-diastolic dimension decreased from 5.45 +/- 0.69 to 4.90 +/- 0.75 cm (p less than or equal to 0.05). The mean systolic decrease in septal-free wall dimension fell from 0.36 +/- 0.18 to 0.14 +/- 0.22 cm (p less than or equal to 0.05). The end-diastolic dimensions and systolic shortening of the LV anterior-posterior minor axis and base-apex major axis were not significantly altered by pulmonary artery constriction. These findings suggest that during acute RV hypertension, impairment of LV systolic function and rearrangements in LV dynamic geometry are primarily the result of the anatomic contiguity of the two ventricles.
TL;DR: In the presence of an intact pericardium, atrial systole shifts the stroke volume-enddiastolic pressure relation because it shifts the end-diastolics pressure-diameter relation and it improves left ventricular performance by increasing preload.
Abstract: The influence of atrial systole on the left ventricular function curve (stroke volume vs end-diastolic pressure or end-diastolic diameter) and on the left ventricular end-diastolic pressure diameter relation was studied in nine anesthetized, open-chest dogs whose atrioventricular (AV) node had been completely blocked. Measurements were made during volume loading with the pericardium closed and opened and during alternate AV sequential pacing (to permit atrial contribution to ventricular filling) and AV simultaneous pacing (to prevent atrial contribution). When the pericardium was closed, withdrawal of the atrial contribution shifted the stroke-volume end-diastolic pressure relation downward, but did not shift the stroke volume-end-diastolic diameter relation, i.e., it reduced stroke volume for a given end-diastolic pressure according to a reduction in end-diastolic volume. The downward shift of the stroke volume-end-diastolic pressure relation was caused by an upward shift of the end-diastolic pressure-diameter relation, which, for a given end-diastolic pressure, resulted in a smaller end-diastolic diameter and, thus, in a smaller stroke volume. The reason for the upward shift in the end-diastolic pressure-diameter relation was that the atrium remained full and thus increased pericardial pressure by increasing pericardial volume. Opening the pericardium shifted the end-diastolic pressure-diameter relation downward and to the right, shifted the stroke volume-end-diastolic diameter relation upward and abolished the effect of withdrawal of the atrial contribution on these curves. We conclude that in the presence of an intact pericardium, atrial systole shifts the stroke volume-end-diastolic pressure relation because it shifts the end-diastolic pressure-diameter relation and it improves left ventricular performance by increasing preload.
TL;DR: Right ventricular "pump" function to maintain an adequate left ventricular preload remained unaltered regardless of the presence of pulmonary artery hypertension, and analysis of right ventricular peak-systolic pressure end-Systolic volume ratios implied a concurrent depression inright ventricular contractility at high levels of PAP.
TL;DR: Assessment of right and left ventricular size and function in patients with congenitally corrected transposition of the great arteries found systemic ventricular dysfunction is more common after childhood and may reflect the inability of the anatomic right ventricle to function as the systemic pumping chamber over a normal lifetime.
Abstract: Twenty-four quantitative cineangiographic studies were performed in 19 patients with congenitally corrected transposition of the great arteries to assess right and left ventricular size and function. Ages ranged from 7 days to 44 years and associated lesions included ventricular septal defect (13 of 19), pulmonary stenosis (9 of 19), and systemic (tricuspid) valvular insufficiency (7 of 19). Systemic (anatomically right) ventricular end-diastolic volume was within normal limits in most patients and averaged 119% of predicted normal. Pulmonary (anatomically left) ventricular end-diastolic volume also was normal in most patients, averaged 112% of predicted, and was not different from systemic (right) ventricular end-diastolic volume. Systemic ventricular ejection fraction (RVEF) averaged 0.61 ± 0.02 and was not different from pulmonary ventricular ejection fraction (LVEF) (0.65 ± 0.02), but important differences were apparent when age was considered. With exclusion of 2 patients with hypoplastic systemic ventricles and 2 studies performed 17 years had a definitely low RVEF and 1 of 5 had a value at the lower limit of normal. In children, systemic and pulmonary ventricular pump function is usually normal in congenitally corrected transposition of the great arteries and any deviation from normal should suggest ventricular hypoplasia or an increase in afterload. After childhood, systemic ventricular dysfunction is more common and may reflect the inability of the anatomic right ventricle to function as the systemic pumping chamber over a normal lifetime in most patients with congenitally corrected transposition of the great arteries.
TL;DR: In patients with hypertrophic cardiomyopathy, systolic anterior motion of the posterior mitral leaflet is not uncommon, constitutes a previously undescribed mechanism for dynamic subaortic obstruction, and is due to a malformation of the anterior mitral Leaflet.
Abstract: Dynamic obstruction to left ventricular outflow in patients with hypertrophic cardiomyopathy usually occurs when the anterior mitral leaflet moves forward in systole and approaches or contacts the ventricular septum. However, we have recently identified, by M mode and two-dimensional echocardiography, 21 patients with hypertrophic cardiomyopathy who had a unique pattern of mitral valve motion characterized by abnormal mitral valve coaptation and systolic anterior motion of the posterior mitral leaflet. This abnormality of mitral valve motion was most reliably identified with two-dimensional echocardiography in views of the left ventricle obtained from the apex. At end-diastole the anterior and posterior mitral leaflets did not appear to coapt at their distal free margins. Rather, at mitral valve closure, the anterior mitral leaflet contacted the basal portion of posterior mitral leaflet. Subsequently, during systole the "residual" distal portion of posterior mitral leaflet approached or contacted the ventricular septum. Morphologic observations in nine other patients with hypertrophic cardiomyopathy suggested that systolic anterior motion of the posterior mitral leaflet is due to elongation of the middle scallop of the posterior leaflet, which probably comes into apposition with the ventricular septum during systole by passing through the space created by the normal pattern of chordal attachments onto the anterior mitral leaflet. Of the 16 patients who underwent cardiac catheterization, nine had basal subaortic gradients of 20 to 85 mm Hg, which were apparently due to moderate or marked systolic anterior motion of the posterior mitral leaflet. Ventricular septal myotomy-myectomies were performed in two patients and resulted in markedly diminished systolic anterior motion of the posterior mitral leaflet in each and abolition of subaortic gradient in the one patient who underwent postoperative cardiac catheterization. Hence, in patients with hypertrophic cardiomyopathy, systolic anterior motion of the posterior mitral leaflet (1) is not uncommon (identifiable in about 10% of a consecutively studied series of patients), (2) constitutes a previously undescribed mechanism for dynamic subaortic obstruction, and (3) is due to a malformation of the posterior mitral leaflet.
TL;DR: There was a significant inverse relationship between the RVEF and pulmonary artery pressure and the sensitivity of RVEf greater than .45 in diagnosing pulmonary hypertension was .76 and other significant determinants of right ventricular function, including right coronary disease, left ventricularfunction and tricuspid regurgitation were considered.
TL;DR: It is demonstrated that ventricular tachycardia, not ventricular fibrillation, was the predominant rhythm induced during programmed ventricular stimulation in these survivors of cardiac arrest and that the IACD effectively responded to a wide range of ventricularTachy Cardiac Arrest rates as well as ventricular Fibrillation.
Abstract: An R-wave synchronous implantable automatic cardioverter-defibrillator (IACD) was evaluated in 12 patients with repeated episodes of cardiac arrest who remained refractory to medical and surgical therapy. Seven men and 5 women, average age 61 years, surgically received a complete IACD system. Coronary artery disease was found in 11 and the prolonged Q-T syndrome in 1. The average ejection fraction was 34%, and 6 patients had severe congestive heart failure (New York Heart Association class III or IV). The IACD is a completely implantable unit consisting of 2 bipolar lead systems. One system uses a lead in the superior vena cava and on the left ventricular apex through which the cardioverting pulse is delivered. The second system employs a close bipolar lead implanted in the ventricle for sensing rate. After the onset of ventricular tachycardia or fibrillation, the IACD automatically delivers approximately 25 J. Postoperative electrophysiologic study in 10 and spontaneous ventricular tachycardia in 1 patient demonstrated appropriate IACD function and successful conversion in all with an average of 18 ± 4 seconds. The induced arrhythmias were ventricular tachycardia (160 to 300 beats/min) in 9 and ventricular fibrillation in 1. These data demonstrate that ventricular tachycardia, not ventricular fibrillation, was the predominant rhythm induced during programmed ventricular stimulation in these survivors of cardiac arrest and that the IACD effectively responded to a wide range of ventricular tachycardia rates as well as ventricular fibrillation. Use of the IACD offers an effective means of therapy for some patients who otherwise may not have survived.
TL;DR: The view that elasticity-or the end-systolic pressure-volume relationship- serves in a given heart to quantify contractility is supported.
Abstract: To characterize the mechanical properties of the contracting left ventricle, we studied the changes in left ventricular systolic pressure following step-like perturbations (+/- 3 ml) in ventricular volume, using an isovolumically beating, isolated canine heart preparation. Three mechanical properties (elasticity, resistance, and a deactivation effect) were identified. The elastic property differs from the traditional parallel and series elastic elements; it is a time-varying elasticity that includes active and passive effects of volume changes. Furthermore, it could not be represented by a simple time-varying elasticity, but required a second factor to express the dependence of end-systolic elasticity on the timing of the volume step. This effect was represented by a "volume influence factor," which may arise from length-dependent activation. The resistive property appeared to be related to force-velocity behavior of the myocardium. Each mechanical property reacted characteristically to steady state changes in ventricular filling volume or contractile state produced by dobutamine (2-13 micrograms/min). Our findings indicate that elasticity was the property most sensitive to changes in contractile state; these changes increased peak isovolumetric pressure 54% on average, and raised elastic stiffness 40% above control (which was 5.1 mm Hg/ml). Changes in ventricular filling volume only prolonged, but did not alter, the level of elastic stiffness attained at peak pressure. These results support the view that elasticity--or the end-systolic pressure-volume relationship--serves in a given heart to quantify contractility. The "volume influence factor" was not affected by either filling volume or contractile state. Resistance increased in direct proportion with ventricular pressure, but this linear relation was not altered greatly by changes in contractile state or in ventricular filling volume. At 100 mm Hg, ventricular resistance averaged 0.11 mm Hg/ml per sec. Finally, deactivation was greater the later in systole a volume step was imposed, and this pattern was independent of changes in ventricular filling volume and in contractile state.
TL;DR: Vernal function curves plotted from data obtained under conditions of altered cardiac filling volume before and after the three dialysis maneuvers demonstrate that ultrafiltration produced a pure Frank-Starling effect, while hemodialysis with or without volume loss produced a shift in the ventricular function curves, which demonstrated an increase in the contractile state of the left ventricle.
Abstract: Prior studies of the effect of hemodialysis on left ventricular function have not distinguished between the removal of uremic toxins and the change in cardiac filling volume To separate these effects, left ventricular function was examined by serial echocardiography in five stable hemodialysis patients before and after three different dialysis procedures: (a) hemodialysis with volume Loss, (b) ultrafiltration (volume loss only), and (c) hemodialysis without volume loss The patients were similarly studied under control conditions and after increased (5 degrees of head-down tilt for 90 min) and decreased (lower body negative pressure) cardiac filling volume After hemodialysis with volume loss, end-diastolic volume (EDV) decreased from 167 to 128 ml (P less than 0001) and end-systolic volume (ESV) decreased from 97 to 51 ml (P less than 0001) without a change in stroke volume (SV) Ejection fraction increased from 42 to 52% (P less than 0001) and mean velocity of circumferential fiber shortening (VCF) increased from 061 to 104 circumferences (circ)/s (P less than 0001) After ultrafiltration, EDV decreased from 167 ml to 124 ml (P less than 0001) and SV from 73 ml to 39 ml (P less than 0001), without significant changes in ESV or VCF In contrast to the maneuvers in which volume loss occurred, after hemodialysis without volume loss ESV decreased from 95 to 66 ml (P less than 0001) and SV increased from 74 ml to 97 ml (P less than 0001) without changes in EDV EF increased from 44 to 59% (P less than 0001) and VCF increased from 064 to 126 circ/s (P less than 0001) Ventricular function curves plotted from data obtained under conditions of altered cardiac filling volume before and after the three dialysis maneuvers demonstrate that ultrafiltration produced a pure Frank-Starling effect, while hemodialysis with or without volume loss produced a shift in the ventricular function curves, which demonstrated an increase in the contractile state of the left ventricle The changes in left ventricular function produced by regular hemodialysis are the combined effects of a decrease in EDV and an increase in the contractile state of the left ventricle
TL;DR: The right ventricle (RV) is an integral component of the body's gas transport system and its contribution to sustaining circulatory homeostasis is without question.
Abstract: The right ventricle (RV) is responsible for accepting venous blood and propelling it to the lungs where it is oxygenated and its CO2 eliminated. Under normal conditions, at rest and during exercise, the pressure required by the RV to maintain the cardiac output (CO) is modest. The functional significance of the RV in sustaining circulatory homeostasis, therefore, appears to be minimal. However, whenever pulmonary vascular resistance (PVR) is elevated (e.g., left heart failure or pulmonary vascular disease) or whenever venous return is reduced (e.g., hypovolemia, increased pleural pressure), the necessity of this pulsatile pump is without question. As a muscular pump, the thin-walled RV is not unlike the left ventricle (LV) except that during diastole it is twice as distensible as the LV and during systole its stroke volume is twice as sensitive to the level of ejection pressure. However, under conditions of chronic pressure overload, the RV will hypertrophy and become capable of generating systemic levels of pressure. This is particularly necessary during physical activity in patients with pulmonary vascular disease. Thus, the RV is an integral component of the body's gas transport system and its contribution to sustaining circulatory homeostasis is without question.