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The changes in left ventricular (LV) structure and geometry that evolve after myocardial injury or overload usually involve chamber dilation and/or hypertrophy. Such architectural remodeling can be classified as eccentric or concentric. Consideration of LV volume, mass, and relative wall thickness (or mass/volume) allows classification of LV remodeling that includes virtually all LV remodeling changes that are seen in health and disease. These various architectural changes generally include the development of LV hypertrophy in a pattern that is closely related to the type of injury or overload, and they are accompanied by differences in cardiac function and hemodynamics. Some patterns of remodeling are associated with adverse outcomes whereas others appear to be adaptive and physiologic without adverse consequences. Considering all patients with LV hypertrophy as a homogenous group is inconsistent with our understanding of the various remodeling patterns that are discussed in this review., (Copyright © 2011 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

To assess the incremental value of velocity of shortening velocity parameters compared with simpler, more widely used, extent of shortening parameters in compensated left ventricular hypertrophy, we studied 52 patients with left ventricular hypertrophy and 63 age-matched controls. Velocity parameters did not provide incremental information beyond that obtained by extent of shortening parameters.

The exercise capacity of patients with congestive heart failure is determined by factors including the interaction of the right and left ventricles and their respective circulations, lung mechanics, skeletal muscle metabolism, and blood flow. Therapeutic efforts should be directed at all of the units in this complex process rather than the response of an individual system. Multiple therapeutic regimens such as nitrates and angiotensin converting enzyme inhibitors in combination with physical training and other therapies that improve pulmonary function produce optimal results. Using this holistic approach to therapy, the physician may have a beneficial impact on the exercise capacity of patients with congestive heart failure.

Background: Left ventricular (LV) midwall geometry has been described conventionally as the sum of the chamber radius and half of the wall thickness; this convention is based on the assumption of uniform transmural thickening during systole. However, theoretical considerations and experimental data indicate that the inner half (inner shell) of the LV wall thickens more than the outer half (outer shell). Thus, an end-diastolic circumferential midwall fiber exhibits a relative migration toward the epicardium during systole. As a result, the conventional method provides an overestimate of the extent of the midwall fiber shortening., Methods and Results: We developed an ellipsoidal model with a concentric two-shell geometry (nonuniform thickening) to assess midwall fiber length transients throughout the cardiac cycle. This modified midwall method was used in the analysis of LV cineangiograms from 15 patients with systemic arterial hypertension and 14 normal subjects. Study groups were classified according to LV mass index (LVMI): 14 normal subjects (group I), eight hypertensive patients with a normal LVMI (group II), and seven hypertensive patients with an increased LVMI (group III). There were no significant differences in LV end-diastolic pressure or volume among the three groups; the ejection fraction was slightly greater in group II (70 +/- 5%) than in groups I (65 +/- 8%) and III (66 +/- 4%), but this trend did not achieve statistical significance. Values for endocardial and conventional midwall fractional shortening (FS) were also similar in the three groups. By contrast, FS by the concentric two-shell geometry (modified midwall method) in group III (16 +/- 2%) was significantly less than that seen in groups I and II (21 +/- 4% and 21 +/- 5%, respectively; both p less than 0.05). This difference achieves greater importance when it is recognized that mean systolic circumferential stress was lower in group III (151 +/- 22 g/cm2) than in groups I and II (244 +/- 37 g/cm2 and 213 +/- 38 g/cm2, respectively; both p less than 0.01). The midwall stress-shortening coordinates in six of the seven group III patients were outside the 95% confidence limits for the normal (group I) subjects. Thus, despite a normal ejection fraction, systolic function is subnormal in hypertensive patients with LV hypertrophy., Conclusions: Chamber dynamics provide an overestimate of myocardial function, especially when LV wall thickness is increased. This is due to a relatively greater contribution of inner shell thickening in pressure-overload hypertrophy.

To determine whether isolated changes in preload (end-diastolic force) can influence myocardial relaxation rate in normal or abnormal (hypoxic or hypertrophic) hearts, isolated LV papillary muscles from normal Wistar-Kyoto (WKY) and spontaneously hypertensive (SHR) rats were studied using physiologically sequenced contractions. While total (systolic) load and late (lengthening) load were held constant, maximum isometric force decline (peak -dT/dt) and maximum isotonic lengthening rate (peak +dL/dt) were measured at seven levels of preload that varied from 115 to 55% of the resting tension at maximum length-tension curves (Lmax). Muscles from normal rats were studied in the oxygenated state (95% O2-5% CO2) and in the hypoxic state (95% N2-5% CO2). Preload did not effect peak -dT/dt or peak +dL/dt in either oxygenated or hypoxic muscles. During hypoxia, peak -dT/dt and peak +dL/dt were 9.5 +/- 1.0 g.mm-2.s-1 and 0.3 +/- 0.1 muscle length/s, respectively, at a preload of 115% compared with 9.0 +/- 1.2 g.mm-2.s-1 and 0.2 +/- 0.1 at a preload of 55%. In separate experiments, the effect of preload on relaxation rate was studied in WKY and SHR rats. In neither group did preload have an independent effect on relaxation rate. In the SHRs, peak -dT/dt and peak +dL/dt were 24.3 +/- 5.3 g.mm-2.s-1 and 0.7 +/- 0.1 muscle length/s, respectively, at a preload of 115% compared with 24.7 +/- 6.6 and 0.8 +/- 0.1 at a preload of 55%. Thus, in hypoxic and hypertrophic myocardium, as in normal muscle, an acute isolated change in preload did not influence the rate of force decline or muscle lengthening.

The hemodynamic determinants of the time constant of left ventricular (LV) isovolumic pressure (P) decline were studied in 32 anesthetized dogs. The time constant, tau (an index of LV relaxation), was determined from the best exponential fit of the equation P = Poe-t/r, to LVP measured at 5-ms intervals during isovolumic relaxation; Po = LVP at maximum negative dP/dt and t = time. At a constant heart rate of 120 beats/min, tau was determined during steady-state increases in preload (volume expansion), increases in afterload (methoxamine infusion), reductions in afterload (nitroprusside infusion), and in variably afterloaded beats at a constant preload (single-beat interventions). tau was directly related to LV systolic pressure and length during the alterations in LV loading conditions, but tau was not closely related to the extent of fiber shortening. During isoproterenol infusion, relaxation was more rapid (tau), and following the administration of propranolol, relaxation was prolonged (tau). While data from the variably afterloaded contractions indicate the presence of systolic load-dependent LV relaxation velocity, the steady-state studies do not exclude the possibility that altered contractility through reflex or other mechanisms contributes to the observed changes in tau.

During prolonged ischemic cardiac arrest successful myocardial protection depends upon uniform delivery of cardioplegic solutions to all regions of the heart. Accordingly, we studied the regional and transmural distribution of a neutral crystalloid (dextran-saline) solution during normothermic (37 degrees C) ischemia in 18 isolated blood-perfused dog hearts (isovolumic left ventricle). In the baseline state, coronary perfusion pressure was 100 mmHg. At the onset of ischemia and every 15 min throughout ischemia, we infused 100 ml of crystalloid solution (37 degrees C) at a perfusion pressure of 100 mmHg and the distribution of crystalloid solution was assessed (radioactive microsphere technique). The hearts were reperfused after 60 min (n = 9) or 90 mins (n = 9) of ischemia. In the baseline pre-arrest state the left ventricle (LV) received 67 +/- 1.0% of the total coronary blood flow; the LV subendocardial to subepicardial flow ratio was 1.33 +/- 0.18, the LV end diastolic pressure was 7.5 +/- 0.4 mmHg, and mean transmural myocardial adenosine triphosphate (ATP) was 16.4 +/- 1.1 microM/g DW. At the onset and throughout the first 45 mins of ischemia (n = 9), regional and transmural distribution of the crystalloid solution was similar to that of coronary blood flow during the baseline state; there was no change in LV end diastolic pressure, but there was a moderate fall in ATP content (7.26 +/- 1.6 micron/g DW). After 75 mins of ischemia (n = 9), despite the development of ischemic contracture (LV end diastolic pressure exceeded 20 mmHg in all 9 hearts) and marked ATP depletion (2.76 +/- 0.5 microM/g DW), there was an increase in crystalloid solution delivery to the LV as a whole and the subendocardium in particular (the LV received 82 +/- 2.0% and the subendocardial to subepicardial flow ratio was 1.75 +/- 0.1). Even in a subgroup with severe contracture during ischemic arrest (LV end diastolic pressure greater than 60 mmHg, n = 4) there was no reduction in crystalloid solution delivery. Thus, the presence of ischemic contracture does not preclude delivery of crystalloid solution to the LV subendocardium.

The extent to which alterations in the coronary blood flow influence left ventricular (LV) diastolic compliance and wall thickness was studied in isolated, isovolumic (balloon in LV), blood perfused dog hearts. Studies were performed at a ventricular volume which was associated with an LV systolic pressure of 100 mm Hg and changes in LV diastolic pressure (at this constant volume) were taken as changes in LV diastolic complicance. When coronary perfusion pressure was reduced to zero (5 min of global ischemia), LV diastolic wall thickness fell from 9.9 +/- 0.9 mm to 9.2 +/- 0.7 mm (P less than 0.01) and LV diastolic pressure fell only 1.3 mm Hg (from 5.5 +/- 1.0 mm Hg to 4.2 +/- 1.1 mm Hg P less than 0.01). In contrast to these findings in 'near normal' ventricles, global ischemia in severely injured hearts (with unphysiologically high diastolic pressures) resulted in marked reductions in diastolic pressure. Thus, moment to moment changes in coronary blood flow can result in alterations in the diastolic properties of the LV. However, these are extreme interventions, and in the clinical setting, changes in coronary dynamics are unlikely to cause significant changes in LV diastolic pressure.

In isolated heart muscle preparations an abrupt increase in load during the latter portion of contraction (at a time when there is little if any potential to develop additional force) causes a premature and more rapid relaxation; this load-dependent relaxation characterizes relaxation in myocardium with normal sarcoplasmic reticulum. The purpose of our study was to assess whether or not the phenomenon of load-dependent relaxation is present in the intact heart and to describe the left ventricular response to abrupt load increments (volume steps) throughout the cardiac cycle. Using a microcomputer-controlled servo-pump attached to the apex of an intact canine heart, we studied the effects of 6 ml steps on left ventricular pressure transients during relaxation. Each volume step was carried out in a single beat with 20 stabilization beats separating the intervention beats; thus, at a heart rate of 120 beats/min, a sequence of 10 intervention beats could be carried out in less than 2 min. By performing the experiments on a single-beat basis (control vs intervention beat), we were able to minimize reflex and other physiologic feedback mechanisms that might alter the results. Studies were performed in five anesthetized dogs. In ejecting beats, an early step (immediately after aortic valve opening) caused an increase (3%) in the duration of systole (the time from the onset of pressure rise to the instant at which left ventricular pressure had declined to one-half its maximal value); in contrast, a late step (just before aortic value closure) caused a decrease (7%) in the duration of systole.(ABSTRACT TRUNCATED AT 250 WORDS)

Ten normal subjects performed the Valsalva maneuver before and after the administration of propranolol (1 mg/kg). Changes in left ventricular (LV) size and function were assessed with noninvasive techniques (echocardiography and sphygmomanometer). Data were obtained at baseline, at 20 seconds of the strain phase (phase II) and 10 seconds after the release of strain (phase IV). In the control state (before propranolol), blood pressure decreased during phase II and exceeded baseline after the release of strain ("overshoot") in phase IV; after the administration of propranolol, the pressure overshoot characteristic of phase IV was no longer present. End-diastolic dimension decreased during the strain phase, but returned to baseline values during recovery in both control and propranolol states. LV stress-dimension and stress-shortening relations before and after propranolol indicate that an increase in LV contractility beginning during phase II and extending into phase IV was attenuated after propranolol. Although the absence of phase IV blood pressure overshoot may be clinically useful in identifying patients with impaired left ventricular function, beta-adrenergic receptor blocking agents can also produce this hemodynamic response in the presence of normal ventricular function.

The effects of brief periods of graded reductions in perfusion pressure on normally beating and fibrillating hearts were examined. Mechanical and metabolic parameters were studied in the isolated, isovolumic (balloon in left ventricle), blood-perfused dog heart preparation. Experiments were carried out at perfusion pressures of 100, 75, 50, and 25 mm Hg, and comparisons of performance were made at the same ventricular volumes in the beating and fibrillating heart. A fall in perfusion pressure significantly decreased systolic performance in the beating heart. Diastolic pressure-volume relations were not altered by changes in perfusion pressure in the beating heart, but the fibrillating heart became significantly more compliant as perfusion pressure declined. Coronary blood flow and myocardial oxygen consumption were consistently higher during fibrillation than during sinus rhythm, and both parameters declined significantly at decreasing perfusion pressures. The fibrillating heart produced lactate at a perfusion pressure below 65 mm Hg, while the beating heart produced lactate at a perfusion pressure below 35 mm Hg. These studies demonstrate that brief periods of relatively modest decreases in perfusion pressure during ventricular fibrillation alter myocardial energy demand-supply relationships to result in ischemia of the fibrillating heart.

The effects of an acute increase in left ventricular systolic pressure and the effects of an intravenous isoproterenol infusion on myocardial (segment) lengthening rate and chamber (minor axis dimension) filling rate were examined in 12 anesthetized dogs. Measurements of left ventricular systolic pressure (by micromanometer) and of segment length and chamber dimension transients (by ultrasonic crystals) were made in variably afterloaded beats (three-beat descending aortic cross-clamp) before and during an isoproterenol infusion that raised (+)dP/dt by 40%. During the baseline state, we found an inverse relation between the peak rate of increase in minor axis dimension [(+)dD/dt] and systolic pressure over a wide range of systolic pressures (110-160 mm Hg) and end-systolic dimensions (25-40 mm); peak (+)dD/dt and end-systolic dimension were also inversely related. During isoproterenol infusion, end-systolic dimension fell from 29.7 +/- 3.1 to 28.0 +/- 3.1 mm and (+)dD/dt increased from 79.6 +/- 8.0 to 90.1 +/- 8.7 mm/sec; however, the slope and y intercept of the relation between (+)dD/dt and end-systolic dimension were unchanged. Peak (+)dD/dt at a common end-systolic dimension of 31 mm was nearly equal during baseline and isoproterenol states (64.2 +/- 6.3 vs. 65.1 +/- 6.6 mm/sec). Similar results were found using segment length transients. We interpret these data to indicate that (+)dD/dt is strongly influenced by changes in systolic pressure and dimension and that isoproterenol-induced changes in (+)dD/dt are mediated, at least in part, through changes in systolic pressure and dimension.

The acute effects of hemodialysis on left ventricular (LV) function were studied with the use of externally recorded LV systolic time intervals and echocardiography; 10 patients with normal or near-normal predialysis LV function and no circulatory congestion were studied. Hemodialysis significantly decreased the LV ejection time (LVET) from 270 +/- 9 ms to 237 +/- 10 ms (p less than 0.001); no significant change was noted in the preejection period (PEP). The PEP/LVET ratio increased from 0.41 +/- 0.05 to 0.45 +/- 0.06 (p less than 0.05). The LV end-diastolic dimension decreased from 5.3 +/- 0.3 cm to 4.8 +/- 0.3 cm (p less than 0.001). Fractional shortening and ejection fraction did not change significantly, but hemodialysis slightly increased mean VCF from 1.2 +/- 0.1 s-1 to 1.4 +/- 0.1s-1 (p less than 0.005). Hemodialysis was associated with a 17% decrease (87 +/- 8 ml to 72 +/- 7 ml; p less than 0.001) in LV stroke volume as calculated from echocardiographic data. Small changes in heart rate and blood pressure were insignificant. We conclude that the postdialysis reduction in stroke volume was due primarily to an acute decrease in LV preload; dialysis also appears to be associated with a small increase in the LV contractile state.

Mechanical characteristics of the left ventricle in chronic aortic regurgitation (AR) differ from those in chronic mitral regurgitation (MR). The differences are thought to be responsible, in part, for the changes in left ventricular (LV) function observed after surgical correction of AR or MR. To test this hypothesis, LV stress-dimension-shortening relations were determined before and after valve replacement in patients with compensated and decompensated chronic AR and MR. Echocardiographic data from 32 patients with AR and 20 patients with MR were used; preoperatively, all 52 patients had LV enlargement. Based on postoperative data, 2 subgroups were defined for each lesion: Patients in group A achieved a normal end-diastolic dimension (less than 3.3 cm/m2) and patients in group B had persistent LV enlargement. Preoperatively, the patients in group A with AR had increased peak systolic stress, but end-systolic stress and fractional shortening were normal; the patients in group B with AR had increased peak systolic stress, increased end-systolic stress and depressed shortening. One year after aortic valve replacement the patients in group A had normal systolic wall stresses and normal shortening, whereas those in group B had persistently abnormal wall stresses and a decrease in shortening. Preoperatively, patients in group A with MR had only modest elevations of peak stress, while end-systolic stress and fractional shortening were normal; in patients in group B with MR the peak stress was similar to that seen in group A, but end-systolic stress was increased and shortening was depressed.(ABSTRACT TRUNCATED AT 250 WORDS)

Serial echocardiographic left ventricular (LV) studies were performed in 19 patients before (preop) and after (postop) aortic valve replacement (AVR) for chronic aortic regurgitation (AR); the effect of AVR on LV volume, mass and function was determined from the echocardiographic data. In the 12 patients who were considered to have successful surgical results, the average LV end-diastolic dimension fell from a preop value of 6.9 +/- 0.2 cm to 5.5 +/- 0.2 cm (P less than 0.01) at the time of the early postop study (seven to 10 days). Muscle cross-sectional area (CSA) derived from dimension and wall thickness data was used as an index of LV muscle mass (preop CSA = 26 +/- 1.3 cm2); CSA was unchanged at the early postop study, but subsequently fell to near normal within six months after AVR (20 +/- 1 cm2, P less than 0.01). There was a trend toward improvement in systolic performance by the late postop studies (12+ months). In two out of three patients with postop paravalvular AR, LV dimension increased after an initial fall. Four patients without paravalvular AR failed to show a significant reduction in LV dimension in the postop studies. In this group the preop studies showed a tendency toward a large end-diastolic dimension and decreased fractional shortening, but the single preop parameter which differentiated these four from the successfully treated group was an end-diastolic radius-to-wall thickness (R/Th) ratio greater than or equal to 4. Thus, successful AVR for chronic AR results in the normalization of LV volume and a decrease in LV muscle mass to near normal. The R/Th ratio has important prognostic value which appears to be independent of fractional shortening in some patients with chronic AR.