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Biomedical subjects

S G Shroff

Publications and source records attributed to S G Shroff.

At least 37 records · Page 2Linked to original sources
PubMed1994

Measurement of regional elastic properties of the human aorta. A new application of transesophageal echocardiography with automated border detection and calibrated subclavian pulse tracings.

BACKGROUND: Evaluation of regional aortic elastic properties in humans has been hampered by the need for invasive techniques to access instantaneous aortic pressure, wall thickness, and cross-sectional area or diameter. In this study, a new noninvasive method is presented for quantification of regional aortic elastic properties. METHODS AND RESULTS: Twenty-five patients were studied during transesophageal echocardiographic procedures. Measurements of instantaneous aortic cross-sectional area were obtained with an automated border detection algorithm applied to short-axis transesophageal two-dimensional echocardiographic images of the proximal descending thoracic aorta. Instantaneous aortic wall thickness was derived from combined two-dimensional targeted M-mode end-diastolic wall thickness and instantaneous aortic area measurements. Instantaneous aortic pressures were estimated from calibrated subclavian pulse tracings recorded simultaneously. Data were digitized to generate aortic area-pressure loops. Regional aortic mechanical properties were quantified in terms of compliance per unit length (C is the slope of the area-pressure regression), aortic midwall radius (Rm), and incremental elastic modulus of the aortic wall (Einc). To assess the independent effect of age, Rm and Einc values were compared at a common level of aortic midwall stress (0.666 x 10(6) dynes/cm2). Mean values (+/- SD) for C, Rm, and Einc were 0.01 +/- 0.004 cm2/mm Hg, 1.14 +/- 0.17 cm, and 7.059 +/- 4.091 x 10(6) dynes/cm2, respectively. An inverse linear correlation was found between aortic compliance per unit length and age (r = -.68, P < .0007). Incremental elastic modulus was related to age (r = +.80, P < .00003) in a nonlinear fashion such that it increased sharply after the age of 60 years. Finally, midwall radius was less tightly correlated with age (r = +.45, P < .05). Values for C, Rm, and Einc as well as the age dependency of these properties are similar to those reported previously when invasive techniques were used. CONCLUSIONS: This methodology constitutes a new tool to improve the clinical evaluation of regional aortic elastic properties in multiple disease states.

Adult↗
PubMed1993

Short time-scale LV systolic dynamics: pressure vs. volume clamps and effect of activation.

We recently proposed a new model-based approach to quantifying short time-scale left ventricular (LV) systolic dynamics. In this study we examine the hypothesis that the quantitation of LV dynamics using the proposed approach is independent of external mechanical perturbations and the level of activation. Mechanical perturbation independence was assessed in seven isolated ferret hearts in which controlled changes in pressure (pressure clamp) or volume (volume clamp) were introduced at the time of peak isovolumetric pressure (protocol 1), and responses to these clamps were analyzed over the first 16 ms. The model described both pressure- and volume-clamps responses equally well. Model parameters were not different among various pressure clamps, and parameters estimated from volume clamps could accurately predict responses to pressure clamps [r2 range: 0.993-0.999; normalized root-mean-square error (NRMSE) range: 2.35-5.86%]. To examine activation independence, volume- (4 hearts) and pressure-clamp (4 hearts) responses were obtained and analyzed for baseline and postextrasystolic potentiated beats in a manner similar to protocol 1. The model parameter values estimated from the baseline state accurately predicted responses for the postextrasystolic potentiated state (r2 and NRMSE range for volume-clamp data: 0.989-0.998 and 3.35-6.88%, respectively; r2 and NRMSE range for pressure-clamp data: 0.992-0.996 and 4.26-5.23%, respectively). Thus the proposed approach can dissect the contributions of changes in activation from those due to changes in contractile unit properties on the function of the intact LV.

Animals↗
PubMed1991

Determination of pulse wave velocities with computerized algorithms.

Careful determination of pulse wave velocity is important in the study of arterial viscoelastic properties, wave reflections, and ventricular-arterial interactions. In spite of its increasingly widespread use, there is as yet no standardized method for its determination. Most studies have manually identified the transit time of the pressure wave front as it travels over a known distance in the arterial system, but the issues of accuracy and reproducibility have not been addressed. This study was designed to investigate the efficacy of four computerized algorithms in the determination of pulse wave velocities in invasive as well as in noninvasive pressure determinations. The four methods were the identification of: (1) the point of minimum diastolic pressure, (2) the point at which the first derivative of pressure is maximum, (3) the point at which the second derivative of pressure is maximum, and (4) the point yielded by the intersection of a line tangent to the initial systolic upstroke of the pressure tracing and a horizontal line through the minimum point. High-fidelity aortic pressure recordings were obtained in 26 patients with a multi-sensor micromanometer catheter. Noninvasive brachial and radial pressure waveforms were recorded in 11 volunteers with external piezoelectric transducers. The results show that the first derivative method consistently provided results that were different from the other methods for both the invasive and noninvasive methods because of changes in the structure of the upstroke as the arterial pulse propagates distally. Although the minimum method worked well for the invasive determinations, it was erratic with the noninvasive determinations, probably because of the higher amount of noise and reflection in the latter. Among the four algorithms, the second derivative and the intersecting tangents methods worked well with both invasive and noninvasive determinations with mean variation coefficients of less than 7% and correlation coefficients between the methods of greater than 0.90 for all data. In conclusion, computerized algorithms allow accurate determination of pulse wave velocity in invasively and noninvasively measured arterial pressure waveforms.

Adult↗
PubMed1991

Doppler and electromagnetic comparisons of instantaneous aortic flow characteristics in primates.

Assessment of the pulsatile mechanical behavior of the coupled left ventricle and the peripheral arterial circulation requires accurate estimation of instantaneous aortic flow. Before the availability of Doppler technologies, this could only be achieved by invasive techniques. The purpose of this study was to assess the accuracy of Doppler-based measurement of instantaneous aortic blood flow and waveform morphology throughout ventricular ejection when compared with an established invasive method. Accordingly, data from electromagnetic flow and continuous-wave aortic Doppler recordings were simultaneously acquired and compared in five monkeys over a wide range of flows generated by intravenous infusions of the beta-adrenoceptor agonist dobutamine and the alpha-receptor agonist methoxamine. Instantaneous aortic pressure was measured using a high-fidelity micromanometer-tipped catheter placed in the ascending aorta. Excellent correlations were noted for stroke volume, cardiac output, left ventricular ejection time, maximal flow velocity, and maximal rate of change of flow velocity (dQ/dtmax). When compared with electromagnetic flows, continuous-wave aortic Doppler had significantly lower times to maximal flow velocity and dQ/dtmax. Frequency domain analysis indicated that both the magnitude and phase were within +/- 6% up to the third harmonic. Instantaneous comparison disclosed that during early systole (up to 10% of ejection) Doppler was higher than electromagnetic flow rate by 11 +/- 19% (p less than 0.05). At 20-30% of systolic ejection, electromagnetic flow rates were slightly higher than Doppler (5 +/- 4% at 20% of ejection, p less than 0.001 and 2 +/- 3% at 30% of ejection, p less than 0.05). From 40% of ejection to the end of systole, flow rates using both techniques were virtually identical.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Short-time-scale left ventricular systolic dynamics. Evidence for a common mechanism in both left ventricular chamber and heart muscle mechanics.

Based on the premise that short-time-scale, small-amplitude pressure/volume/outflow behavior of the left ventricular chamber was dominated by dynamic processes originating in cardiac myofilaments, a prototype model was built to predict pressure responses to volume perturbations. In the model, chamber pressure was taken to be the product of the number of generators in a pressure-bearing state and their average volumetric distortion, as in the muscle theory of A.F. Huxley, in which force was equal to the number of attached crossbridges and their average lineal distortion. Further, as in the muscle theory, pressure generators were assumed to cycle between two states, the pressure-bearing state and the non-pressure-bearing state. Experiments were performed in the isolated ferret heart, where variable volume decrements (0.01-0.12 ml) were removed at two commanded flow rates (flow clamps, -7 and -14 ml/sec). Pressure responses to volume removals were analyzed. Although the prototype model accounted for most features of the pressure responses, subtle but systematic discrepancies were observed. The presence or absence of flow and the magnitude of flow affected estimates of model parameters. However, estimates of parameters did not differ when the model was fitted to flow clamps with similar magnitudes of flows but different volume changes. Thus, prototype model inadequacies were attributed to misrepresentations of flow-related effects but not of volume-related effects. Based on these discrepancies, an improved model was built that added to the simple two-state cycling scheme, a pathway to a third state. This path was followed only in response to volume change. The improved model eliminated the deficiencies of the prototype model and was adequate in accounting for all observations. Since the template for the improved model was taken from the cycling crossbridge theory of muscle contraction, it was concluded that, in spite of the complexities of geometry, architecture, and regional heterogeneity of function and structure, crossbridge mechanisms dominated the short-time-scale dynamics of left ventricular chamber behavior.

Animals↗
PubMed1991

Left ventricular function depends on previous beat ejection but not previous beat pressure load.

Previous beat contraction history, in which the performance of the left ventricle on any one beat is influenced by the mechanical events of the previous beat, may be important in the beat-to-beat regulation of left ventricular performance in the intact cardiovascular system. Prior studies of this phenomenon have established that mechanical events of the previous beat influence the function of the current beat, but it is not known whether the important mechanical influence is exerted by previous beat ejection or previous beat pressure. In addition, the magnitude of the effect of previous beat contraction history on left ventricular performance is unknown. To make these determinations, we performed experiments in six isolated rabbit left ventricle preparations buffer perfused at 30 degrees C. Left ventricular pressure and volume were controlled precisely with a servo-controlled linear motor system. After steady-state ejecting conditions were established by clamping left ventricular ejection pressure at 60% of peak isovolumic pressure, single test beats, which were pressure clamped at 40%, 60%, 80%, and 100% of peak isovolumic pressure, were introduced and followed by an isovolumic reference beat. As the level of pressure clamp decreased from 100% to 40%, developed pressure on the isovolumic beat following the single test beats increased from 139 +/- 15 (mean +/- SD) to 151 +/- 13 mm Hg. Similarly, peak positive left ventricular dP/dt increased from 1,718 +/- 209 to 1,864 +/- 181 mm Hg.sec-1 (both p less than 0.01). Multiple regression analysis showed that this increase in left ventricular function was related to previous beat ejection but not to previous beat pressure load or relaxation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Relation between mixed venous oxygen saturation and cardiac index. Nonlinearity and normalization for oxygen uptake and hemoglobin.

The ability of mixed venous oxygen saturation (SvO2) monitoring to reflect changes in cardiac index (CI) with therapy in critically ill patients is unclear. To this end, SvO2 and CI were measured before and during an infusion of enoximone and/or dobutamine in 30 patients with advanced heart failure. A nonlinear relationship was observed between SvO2 and CI with the nonlinear correlation coefficient being 0.52. On normalizing for individual differences in hemoglobin and oxygen consumption, this correlation coefficient became 0.90. Further analysis of individual data was performed using linear regression, and the slopes and correlation coefficients were found to span a wide range slope: -10.0 to 30.9 min-m2/L, r: -0.27 to 0.99). However, the mean slope and correlation coefficient for patients with baseline CI and SvO2 less than 21/min/m2 and less than 55 percent were 18.3 min-m2/L and 0.87, respectively, while those for the remainder of patients were only 3.1 min-m2/L and 0.42, respectively. Thus, the nonlinear correlation coefficient of the SvO2-CI relationship in a group of patients is dependent on the homogeneity of their oxygen consumption and hemoglobin concentration. Furthermore, the ability of SvO2 to serve as a therapeutic indicator in any given patient is dependent on baseline SvO2 and CI.

Adult↗
PubMed1990

Relation between left ventricular systolic resistance and contractile rate processes.

To test the hypothesis that left ventricular (LV) systolic resistance is determined by the intrinsic rate processes of the contractile system, we studied 40 spontaneously hypertensive male rats (SHR). Thyroid hormone manipulation was used to alter isomyosin composition and consequently the rate processes of the contractile system. Seven groups of rats were studied: control (SHRC, n = 9); propylthiouracil (PTU) treated for 10 days (SHRP-10, n = 5), 20 days (SHRP-20, n = 5), and 30 days (SHRP-30, n = 6); and thyroxine treated for 5 days (SHRT-05, n = 5), 10 days (SHRT-10, n = 5), and 15 days (SHRT-15, n = 5). In situ (n = 40) and isolated (n = 14; 5 SHRP-30, 5 SHRC, and 4 SHRT-15) heart experiments were performed. In comparison to SHRC, we observed the following: 1) LV pump performance was not different in any of the thyroxine-treated groups, whereas with PTU, pump performance was significantly depressed in rats with greater than 80% slow myosin. 2) Normalized LV peak elastance (Emaxn) was significantly increased in the SHRP-30, whereas it was not altered after thyroxine. These observations were further confirmed in the isolated heart on the basis of peak isovolumetric stress-strain relations. 3) Thyroxine increased and PTU decreased theoretical maximum flow (Qmax; a measure of LV resistance); thus an inverse relation between Qmax and percent slow myosin was observed (r2 = 0.86). 4) The time to peak isovolumetric pressure was increased in SHRP-30 and decreased in SHRT-15. The relaxation process was significantly slower for SHRP-30 group and was unchanged for SHRT-15 group. These observations support our hypothesis that LV systolic resistance quantifies an intrinsic rate-dependent property of the myocardium and that isomyosin composition is one of its determinants. In addition, with changes in isomyosin composition toward predominantly slow myosin, the responses in Emaxn and Qmax are discordant, which may be responsible for the preservation of pump performance. This underscores the importance of quantifying both LV systolic resistance and elastance in the assessment of the functional status of the LV as a mechanical pump.

Animals↗
PubMed1989

Myocardial collagen and mechanics after preventing hypertrophy in hypertensive rats.

To determine if a remodeling of the collagen matrix would occur in the absence of hypertrophy and cell necrosis and if such a remodeling could alter active and passive stiffness of the intact myocardium, five rats with genetic hypertension (SHR) were treated (SHRT) with hydralazine for 32 weeks, beginning at four weeks of age, and compared to six age- and sex-matched SHR and seven Wistar-Kyoto genetic control rats (WKY). Left ventricular (LV) weight of SHRT was 17% lower (P less than .001) than that of SHR and 19% higher (P less than .01) than that of WKY. Collagen volume fraction of SHR (13.7 +/- 3.2%) and SHRT (9.9 +/- 1.8%) were greater (P less than .01) than WKY (5.0 +/- 1.9%). Diastolic and systolic stress-strain relations were determined in the isolated heart. A comparison of these relations revealed: 1) a 24% increase in passive stiffness for SHR and SHRT; and 2) a reduced zero-strain intercept (41% to 54%) and slope (36% to 48%) of the developed stress-strain relation for the SHRT. Thus, in SHR, collagen remodeling occurred in the absence of hypertrophy which suggests that the muscular and collagenous compartments of the myocardium are under separate controls. The excess accumulation of collagen in SHR and SHRT leads to abnormal passive stiffness, and the prevention of hypertrophy with hydralazine reduces active stiffness.

Animals↗
PubMed1989

Left ventricular systolic resistance in rats with hypertension and hypertrophy.

Traditional indexes of ventricular performance often fail to identify differences between the normal and hypertrophied ventricle. This may not be the case for load-independent mechanical properties, elastance, and resistance. Accordingly, we derived these properties of the intact left ventricle (LV) in 25-wk-old male spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto controls (WKY) using in-situ and isolated hearts. We found that 1) pump performance was similar in SHR and WKY, both at base line and after dextran; 2) the peak systolic elastance (Emax) was higher and theoretical maximum flow (Qmax, inverse of ventricular resistance) was lower in SHR; (3) slopes of peak isovolumetric pressure-volume and stress-strain relations were significantly higher in SHR; and 4) although end-diastolic pressure-volume relation for SHR was shifted to the right, there was no difference in end-diastolic stress-strain relations. Thus elastance in hypertrophied LV is augmented due to both an increase in muscle mass and the force-generating capacity of the myocardium. Furthermore, we propose that the decrease in Qmax seen in SHR reflects a change in certain velocity-dependent properties of the myocardium, whereas the preservation of pump performance is a result of the opposing effects of increased Emax and decreased Qmax. These observations underscore the importance of quantifying systolic resistance, together with elastance, for a better assessment of the LV as a mechanical pump.

Animals↗
PubMed1989

Fibrillar collagen and myocardial stiffness in the intact hypertrophied rat left ventricle.

This study tested the hypothesis that with hypertrophy, the proportion, distribution, and structural alignment of fibrillar collagen are important determinants of myocardial stiffness. Toward this end, the collagen volume fraction (morphometry), the transmural or subendocardial distribution of collagen, and the structural arrangement of fibrillar collagens (picrosirius red) were examined in the hypertrophied ventricle secondary to pressure overload (abdominal aorta banding or perinephritis), isoproterenol, and pressure overload plus isoproterenol. In the same hearts, the slopes of the systolic and diastolic stress-strain relations of the left ventricle, representing its active and passive stiffness, respectively, were obtained. In comparison with controls, we found 1) for a moderate rise in transmural collagen, active and passive stiffness increased with pressure-overload hypertrophy; 2) following isoproterenol alone there was a marked increase in subendocardial collagen, and active and passive stiffness increased; 3) in pressure-overload hypertrophy plus isoproterenol, active stiffness declined. Passive stiffness was increased except when fibrosis and thinning of the interventricular septum occurred, in which case it decreased; and 4) fibrillar collagens involved in remodeling included the formation of either collagen strands and fibers in a greater number of previously collagen-free intermuscular spaces in pressure-overload hypertrophy, or a dense crisscrossing latticework of fibers that encircled muscle fibers after isoproterenol. Thus, an increase in fibrillar collagen in pressure-overload hypertrophy is partially adaptive in that it enhances the tensile strength and three-dimensional delivery of force by the myocardium, but at the expense of reducing distensibility. The appearance of a dense collagen meshwork within the subendocardium after isoproterenol can be considered pathological in that it entraps muscle fibers causing active stiffness to fall while impairing distensibility. Finally, fibrosis may paradoxically reduce passive stiffness if it leads to a thinning of the interventricular septum.

Animals↗
PubMed1989

Pathophysiology of the failing heart.

Cardiac (or myocardial) failure of acute onset or of chronic duration is the result of a structural and/or biochemical remodeling of the myocardium. This, in turn, compromises the contractile performance of the myocardium. The hypertrophic growth of myocytes and the architectural transformation of ventricular chamber size and shape--while initially useful compensatory responses--do not prevent the inevitable appearance of pump failure where oxygen delivery to the metabolizing tissues becomes inadequate. Indeed, the severity of cardiac failure can be judged from the level of oxygen consumption that elicits this state of impaired oxygen supply and demand. A better understanding of the mechanical behavior of the ventricular chamber, including its elastic and resistive properties, together with recent advances in our ability to measure instantaneous ventricular pressure and volume, may prove useful in identifying pathologic features of hypertrophy and dilatation in individual patients. In grading the severity of failure and comparing groups of patients, a normalization of the mechanical parameters by differences in chamber size, shape, and mass is necessary. Symptomatic cardiac failure, based invariably on inadequate oxygen delivery and/or pulmonary congestion, is more commonly the result of ventricular systolic dysfunction. Abnormalities in diastolic function, including ventricular relaxation and filling, while less common and often associated with preserved systolic pump function, do occur. Finally, it must be recognized that the failing ventricle carries an additional hydraulic load that arises from the arterial circulation to which it is coupled.(ABSTRACT TRUNCATED AT 250 WORDS)

Forced Expiratory Flow Rates↗
PubMed1988

Collagen remodeling of the pressure-overloaded, hypertrophied nonhuman primate myocardium.

Cardiac muscle is tethered within a fibrillar collagen matrix that serves to maximize force generation. In the human pressure-overloaded, hypertrophied left ventricle, collagen concentration is known to be increased; however, the structural and biochemical remodeling of collagen and its relation to cell necrosis and myocardial mechanics is less clear. Accordingly, this study was undertaken in a nonhuman primate model of left ventricular hypertrophy caused by gradual onset experimental hypertension. The amount of collagen, its light microscopic features, and proportions of collagen types I, III, and V were determined together with diastolic and systolic mechanics of the intact ventricle during the evolutionary, early, and late phases of established left ventricular hypertrophy (4, 35, and 88 weeks, respectively). In comparison to controls, we found 1) increased collagen at 4 weeks, as well as a greater proportion of type III, in the absence of myocyte necrosis; 2) collagen septae were thick and dense at 35 weeks, while the proportion of types I and III had converted to control; 3) necrosis was evident at 88 weeks, and the structural remodeling and proportion of collagen types I and III reflected the extent of scar formation; and 4) unlike diastolic myocardial stiffness, which was unchanged at 4, 35, or 88 weeks, the systolic stress-strain relation of the myocardium was altered in either a beneficial or detrimental manner in accordance with structural remodeling of collagen and scar formation. Thus, early in left ventricular hypertrophy, reactive fibrosis and collagen remodeling occur in the absence of necrosis while, later on, reparative fibrosis is present.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Physiologic response to the inotropic and vasodilator properties of enoximone.

In patients with chronic cardiac failure, improvement in ventricular function is observed after the administration of enoximone, a phosphodiesterase inhibitor with inotropic and vasodilator properties. The relative contributions of positive inotropy and vasodilation to the improvement in pump performance, however, remain uncertain. Therefore, findings from a series of dog experiments designed to resolve this issue are reviewed. Also, our current understanding of the physiologic response to enoximone in patients with cardiac failure, including the responses of myocardial oxygen consumption and efficiency, are considered. It is concluded that, enoximone produces a substantial (66 +/- 2% in dogs) increase in contractility, a relatively minor increase in heart rate (0 to 12%) and a decrease in systemic vascular resistance (-28 to -49%). These are the ranges of average responses based on review of published findings. These physiologic responses lead to an improvement in the pumping function of the failing heart; cardiac output (23 to 83%) and stroke work index (17 to 88%) are increased, and pulmonary capillary wedge pressure (-19 to -59%) and right atrial pressure (-29 to -60%) are decreased. The influence of enoximone on myocardial oxygen consumption is less consistent (-18 to +33%). Nevertheless, enoximone improves the efficiency of the failing heart.

Animals↗
PubMed1987

Physiologic versus pathologic hypertrophy and the pressure-overloaded myocardium.

The myocardium consists of myocytes and capillaries embedded in a connective tissue matrix. Myocardial mass, which is predominantly a function of myocyte size, is determined by systolic tension; when systolic pressure is gradually elevated above the normal range, mass will increase. The hypertrophic process is a continuum consisting of subtle transitions that take place within the muscular, collagenous, and vascular compartments; these transitions, however, need not be temporarily concordant. We would identify three phases to the hypertrophic process. First, there is an evolutionary phase, whereby the structural and biochemical remodeling of the various compartments of the myocardium is in transition, with each compartment having its own rate of adjustment. During this evolutionary phase, myocardial contractility, as reflected by stress-length and stress-velocity relations, may or may not be normal, but ventricular pump function and O2 delivery are preserved. Second, there is a physiologic phase during which the structural and biochemical remodeling of the compartments reaches a coordinated balance. The myocardial stress-length relation and ventricular function are each normal, but rate-dependent indices of contractility may be abnormal. During the physiologic phase of hypertrophy, the remodeled myocardium will revert to normal when the abnormal loading condition is removed. Finally, there is a pathologic phase. In this phase, compartment remodeling is no longer balanced (e.g., the ratio of structural versus maintenance proteins), and length and rate-dependent indices of myocardial contractility are depressed. Ventricular pump function is also abnormal in the pathologic phase; consequently. O2 delivery to the tissues is impaired. This imbalance in O2 demand and supply may be apparent at rest in more advanced expressions of disease or may appear during the physiologic stress of exercise in less severe disease. In the latter case, the patient's aerobic capacity is reduced to the extent that it can be used to grade the severity of heart failure and to predict the cardiac reserve. During the pathologic phase of hypertrophy, the structural and biochemical remodeling of the myocardium may be irreversible, although this may not be the case for each compartment. Finally, it is important to distinguish cardiac (or myocardial) failure from the clinical syndrome of congestive heart failure. The latter arises from congested organs and hypoperfused tissues; its clinical manifestations are dependent on the activation of the adrenergic nervous and renin-angiotensin-aldosterone systems and the presence of a salt-avid kidney. Congestive heart failure is a late clinical feature of chronic pressure overload and pathologic hypertrophy.

Animals↗
PubMed1987

Collagen in the hypertrophied, pressure-overloaded myocardium.

The extracellular structural protein, collagen, is responsible for the functional integrity of the myocardium permitting reversible interdigitation and transmission of force between contracting myocytes. In the pressure-overloaded, hypertrophied myocardium, clinical and experimental evidence indicates that the proportion of collagen relative to muscle is increased. Factors that appear to influence collagen growth during the hypertrophic process include age, species, the rapidity with which the overload occurs, the nature of the lesion leading to the pressure-overload, and the severity and duration of the overload. Morphologically, the heart's collagen matrix consists of a complex weave with tendinous insertions that surrounds myocytes grouping them into myofibers, strands of collagen that connect adjoining myofibers, and collagenous struts that join myocytes to other myocytes and capillaries. In a primate preparation of perinephritis with systemic hypertension, it was observed that the tendinous elements of the weave and the strands of collagen lying between myofibers were increased in number and physical dimension. The functional consequences of a remodeling of the collagen matrix that accompanied myocardial hypertrophy remain to be elucidated. A better understanding of the dynamic behavior of the collagen matrix may offer new insights into the pathogenesis of ventricular dysfunction that accompanies the chronic pressure-overloaded state.

Animals↗
PubMed1985

Evidence and quantitation of left ventricular systolic resistance.

Instantaneous left ventricular pressure is a function of both volume (elastic behavior) and flow (resistive behavior). However, a quantitative description of ventricular resistance and its effects on ventricular performance remains to be elucidated. Accordingly, ventricular resistive behavior was studied in six isolated canine hearts. Our experimental findings indicate 1) for a specified time (ts), volume (Vs), and contractile state (CS), the ventricular pressure-flow relation was linear (r = 0.96-0.99) within the range of flows examined (0-250 ml/s); 2) ventricular resistance increased with increments in ts, Vs, and CS, whereas the zero-pressure flow intercept was invariant; 3) resistance could be uniquely quantified as a linear function of isovolumetric pressure. In six experiments, the slope of this relationship ranged from 1.1 to 2.1 X 10(-3) s/ml while the intercept did not differ from zero; and 4) end-systolic elastance, estimated from end-systolic pressure-volume data, was in substantial error under the conditions of finite (greater than 35 ml/s) end-systolic flows. Finally, the results from a computer simulation of the coupled ventricular-arterial system indicated that ventricular resistance primarily affects the pulsatile nature of aortic flow. The unique isovolumetric pressure-resistance relation suggests that the rate-limiting properties of the contractile process may be causally related to the observed ventricular resistive behavior.

Animals↗