Normal myocardial function in severe right ventricular volume overload hypertrophy.

Severe left ventricular volume overloading causes myocardial and cellular contractile dysfunction. Whether this is also true for severe right ventricular volume overloading was unknown. We therefore created severe tricuspid regurgitation percutaneously in seven dogs and then observed them for 3.5-4.0 yr. All five surviving operated dogs had severe tricuspid regurgitation and right heart failure, including massive ascites, but they did not have left heart failure. Right ventricular cardiocytes were isolated from these and from normal dogs, and sarcomere mechanics were assessed via laser diffraction. Right ventricular cardiocytes from the tricuspid regurgitation dogs were 20% longer than control cells, but neither the extent (0.171 +/- 0.005 microm) nor the velocity (2.92 +/- 0.12 microm/s) of sarcomere shortening differed from controls (0.179 +/- 0.005 microm and 3.09 +/- 0.11 microm/s, respectively). Thus, despite massive tricuspid regurgitation causing overt right heart failure, intrinsic right ventricular contractile function was normal. This finding for the severely volume-overloaded right ventricle stands in distinct contrast to our finding for the left ventricle severely volume overloaded by mitral regurgitation, wherein intrinsic contractile function is depressed.

Interaction between transient metabolically mediated dilatation and pressure induced constriction in the canine coronary artery.

This study explored the interaction between metabolically mediated vasodilatation (ventricular extra-activation) and pressure induced vasoconstriction (transient augmentation of aortic diastolic pressure). Eight dogs having formalin-induced heart block were chronically instrumented with aortic and left ventricular catheters and an electromagnetic flow probe on the left circumflex coronary artery. At a heart rate of 60 beats/min a single ventricular extra-activation introduced at 200 ms after the normal paced beat resulted in a 13 +/- 1% decrease in diastolic coronary vascular resistance index (DCVRI) in the first response beat (D1) and a persistent vasodilatation lasting for five beats (D1-D5). An increase in aortic diastolic pressure (32 +/- 3% for 520 +/- 15 ms) resulted in 13 +/- 2% increase in DCVRI in the D1 which was not evident in subsequent beats. Following a combined intervention, DCVRI in D1 was not significantly different from control but DCVRI did decrease to a greater degree in the subsequent response beats (D2-D7). These data indicate that the responses of two opposing vasoactive stimuli, i.e., pressure induced vasoconstriction and metabolic vasodilatation, were negated in the first response beat. The metabolically mediated vasodilatation was unaltered in the subsequent response beats.

Coronary artery restenosis after atherectomy is primarily due to negative remodeling.

The primary cause of restenosis following directional coronary atherectomy (DCA) remains obscure. "Negative remodeling," a decrease in vessel area, is believed to be more causative than is increase in plaque area. The DCA technique used in these patients, designed to facilitate the removal of plaque, should allow a more precise evaluation of the relative roles of these two mechanisms. Twenty-five patients underwent DCA. In 17, complete angiographic and intravascular ultrasound (IVUS) images were obtained before and after DCA and at follow-up (6 to 9 months). Internal elastic lamina (IEL), lumen, and plaque areas were calculated at preatherectomy, postatherectomy, and follow-up. Postatherectomy, the mean IEL area increased by 32% and the mean plaque area decreased by 51%, resulting in a significant mean increase in lumen area, 500%. At follow-up when compared to postatherectomy, the change in IEL area was variable; however, the mean did not change significantly (p = 0.58). Plaque area change, when standardized for initial vessel size, was small (mean increase 2.8 +/- 3.5%). The mean lumen area did not decrease significantly at follow-up (p = 0.43). A highly significant correlation (r = 0.96) was noted between IEL area change and lumen area at follow-up. In contrast, the correlation between plaque area change and lumen area change over the same period was much less significant (r = 0.64). These data indicate that decrease in IEL area primarily is responsible for restenosis.

Transfer of swine major histocompatibility complex class II genes into autologous bone marrow cells of baboons for the induction of tolerance across xenogeneic barriers.

BACKGROUND: The present study examined the potential role of gene therapy in the induction of tolerance to anti-porcine major histocompatibility complex (SLA) class II-mediated responses after porcine renal or skin xenografts. METHODS: Baboons were treated with a non-myeloablative or a myeloablative preparative regimen before bone marrow transplantation with autologous bone marrow cells retrovirally transduced to express both SLA class II DR and neomycin phosphotransferase (NeoR) genes, or the NeoR gene alone. Four months or more after bone marrow transplantation, the immunological response to a porcine kidney or skin xenograft was examined. Both the renal and skin xenografts were SLA DR-matched to the transgene, and recipients were conditioned by combinations of complement inhibitors, adsorption of natural antibodies, immunosuppressive therapy, and splenectomy. RESULTS: Although the long-term presence of the SLA transgene was detected in the peripheral blood and/or bone marrow cells of all baboons, the transcription of the transgene was transient. Autopsy tissues were available from one animal and demonstrated expression of the SLA DR transgene in lymphohematopoietic tissues. After kidney and skin transplantation, xenografts were rejected after 8-22 days. Long-term follow-up of control animals demonstrated that high levels of induced IgG antibodies to new non-alphaGal epitopes developed after organ rejection. In contrast, induced non-alphaGal IgG antibody responses were minimal in the SLA DR-transduced baboons. CONCLUSIONS: Transfer and expression of xenogeneic class II DR transgenes can be achieved in baboons. This therapy may prevent late T cell-dependent responses to porcine xenografts, which include induced non-alphaGal IgG antibody responses.

Peripheral tolerance to class I mismatched renal allografts in miniature swine: donor antigen-activated peripheral blood lymphocytes from tolerant swine inhibit antidonor CTL reactivity.

Studies utilizing partially inbred miniature swine have demonstrated that a short course of cyclosporin A leads to indefinite survival of two haplotype class I mismatched renal allografts. In the present study, we have examined peripheral regulatory mechanisms that may be involved in maintenance of tolerance by coculturing PBL from long-term tolerant animals with naive recipient-matched PBL in cell-mediated lympholysis assays. We show that PBL from tolerant animals, primed in vitro with donor Ag, suppress antidonor CTL reactivity by naive recipient-matched PBL. Suppression was not observed when PBL from naive animals, primed with donor-matched PBL, were cocultured with PBL from a second naive animal, nor did PBL from either tolerant or naive recipient-matched control animals, primed with third-party Ag, suppress the generation of anti-third-party CTL by a second naive animal. The suppression was cell dose-dependent, radiation-sensitive, required cell-to-cell contact not reversed by the provision of exogenous IL-2, and associated with lower levels of IL-2R expression on the suppressive effector group (particularly the CD8 single positive cells) when compared with the control effector group. These data indicate an association between the presence of peripheral regulatory cells demonstrable in vitro and the maintenance of tolerance to renal allografts.

Are interatrial band myocytes maximally hypertrophied in normal canine hearts?

In canine right atrial hypertrophy, the cross-sectional area (Axs) of right atrial myocytes increases, whereas the Axs of the broader interatrial band myocytes does not. In the current study, myocyte reconstructions showed that right atrial myocyte length increased in proportion to Axs in right atrial hypertrophy. On the other hand, mean interatrial band myocyte length in both normal and right atrial hypertrophy dogs was roughly inversely proportional to mean Axs, as expected if interatrial band myocyte volume was constant. Plotting mean Axs vs. myocyte length for individual interatrial band myocytes revealed a distribution whose border defined a maximal volume curve; many myocytes were well beneath that curve. Mononuclear myocytes (generally diploid) were limited by a 65,000-micrometer 3 curve, which many binuclear myocytes (generally tetraploid) surpassed; myocyte ploidy thus constrained myocyte volume. However, because many mononuclear and binuclear myocytes had lower volumes, their failure to hypertrophy cannot be attributed to attainment of the maximal volume possible for their ploidy.

Myocardial blood flow in awake dogs with chronic tricuspid regurgitation.

The primary purpose of this study was to define regional blood flow in dogs with chronic tricuspid regurgitation (TR) in order to determine if the marked hypertrophy of the right atria resulted in compromised myocardial perfusion. Myocardial blood flow (ml/min/gm) was measured with radiolabeled microspheres in eight dogs with TR during rest, moderate exercise (5 dogs), and infusion of adenosine (1 mg/kg/min), an index of minimal vascular resistance. Similar measurements were obtained in eight normal dogs. In TR, the ratio of right atrium (RA) and right ventricle (RV) to body weight was greater than in normal dogs, 77% and 30%, respectively. During rest, flow in the RA appendage was less than in nonappendage region in the normal dogs; no differences were noted in TR dogs, indicating an augmented hemodynamic role of the appendage in TR. Both RA and RV blood flow was greater in TR during rest but no other differences in flow were found between the two groups. Minimum vascular resistance in RV but not RA was slightly increased in TR versus normal. During marked myocyte hypertrophy, the vasculature of RA develops sufficiently to provide the same flow capacity as in the normal heart.

Effect of the superior vena cava electrode surface area on defibrillation threshold in different lead systems.

Little data is available comparing the efficacy of the Transvene, Endotak C 70 series, and the active CAN configuration on defibrillation success. In addition, the impact of the superior vena cava (SVC) electrode surface area and length on the active CAN system is unknown. Therefore, we compared the defibrillation efficacy of the Transvene and Endotak C 70 series lead systems with and without the active CAN in dogs. Defibrillation threshold (DFT) testing was randomly performed in 20 dogs. In protocol I (10 dogs), DFT energy was compared in three RV/SVC lead systems with an SVC electrode defibrillating surface area of 90 mm2 (Transvene-90), 160 mm2 (Transvene-160), 617 mm2 (Endotak), and an RV/CAN configuration. In protocol II (10 dogs), DFT comparison was performed in the Transvene-90/CAN, Transvene-160/CAN, Endotak/CAN, and RV/CAN configurations. In protocol I, increasing the SVC surface area from 90 to 160 mm2 and from 160 to 617 mm2 significantly lowered DFT energy. The Endotak and the RV/CAN systems provided the lowest DFT energy requirements. In protocol II, the Endotak/CAN system significantly lowered DFT energy compared to the other three lead configurations. In both protocols, the impedance decreased as the SVC surface area increased from 90 to 160 mm2. However, no significant reduction in DFT impedance occurred as the SVC surface area increased from the Transvene-160 to the Endotak lead. Increasing the SVC surface area from 90 to 617 mm2 in a two coil lead system lowered DFT energy to similar levels provided by the RV/CAN configuration. The addition of an SVC electrode with a surface area of 90 or 160 mm2 did not reduce DFT energy compared to the RV/CAN configuration. The Endotak/CAN system, however, provided the lowest DFT requirements.

Myocardial oxygenation in dogs during reactive hyperemia.

The mechanisms of myocardial oxygenation during reactive hyperemia were studied in the beating heart using continuous near infrared (NIR) spectroscopy. In open chest dogs, NIR spectroscopy was used to monitor brief occlusions of the left anterior descending artery. These occlusions produced a precipitous drop in tissue oxygen stores (tHbO2+MbO2), tissue blood volume, and the oxidation level of mitochondrial cytochrome a,a3. Reperfusion produced a rapid increase in the NIR signals to supranormal levels, followed by gradual return to baseline. When the duration of occlusion was increased from 20 to 120 s, an essentially linear increase was produced in the overshoot areas defined by the NIR signals. Near infrared spectroscopy (NIRS) separated reactive hyperemia into two phases according to the tissue level of deoxyhemoglobin and deoxymyoglobin (tHb+Mb): (1) an early phase during which the tHb+Mb level was supranormal, reflecting enhanced O2 extraction; and (2) a late phase during which the tHb+Mb level was below baseline, reflecting decreased O2 extraction and increased tissue O2 availability. During reactive hyperemia, when O2 availability was maximal by NIR spectroscopy, O2 consumption was elevated but submaximal, indicating that MVO2 was not limited by O2 availability. Cytochrome a,a3 oxidation state also was restored fully. Thus, myocardial oxygenation is highly regulated during reactive hyperemia. Cellular O2 supply and mitochondrial oxidation state are restored early during reactive hyperemia by increased O2 delivery, increases in tissue blood volume and enhanced O2 extraction. © 1998 Society of Photo-Optical Instrumentation Engineers.

Impact of defibrillator-can size on defibrillation success with a single-lead unipolar system.

In a study of 11 dogs, we assessed whether the defibrillation energy requirements of a single transvenous right ventricular electrode/defibrillator can system depended on the can size. We compared the defibrillation threshold obtained with 65% fixed-tilt biphasic shocks with 20, 40, and 80 ml surface area defibrillator cans. The energy was delivered between a right ventricular coil inserted through the jugular vein and the can placed in the subcutaneous tissue of the left superior chest wall. The testing order of each can size was randomly determined. Triplicate defibrillation thresholds were obtained with each can. Despite a higher impedance (20 ml 85 +/- 22 ohms vs 80 ml 71 +/- 16 ohms, p < 0.01), the 20 ml can resulted in a similar defibrillation threshold compared with the 80 ml (20 ml 7.6 +/- 2.8 J vs 80 ml 7.5 +/- 3.4 J) and the 40 ml cans (20 ml 7.6 +/- 2.8 J vs 7.5 +/- 3.4 J). In conclusion, with the unipolar lead system the can size does not appear to be a factor limiting defibrillation success. Even a can the size of a pacemaker does not appear to significantly affect the defibrillation efficacy of this lead system.

Regional vascular reserve in canine atria and ventricles during rest and exercise.

Vascular reserve, which defines the capacity for further vasodilation in a given physiological or pathological condition, has not been measured in the canine atria. This study defines, in normal dogs, the regional vascular reserve simultaneously measured in the atria (appendage, nonappendage regions) and in the ventricles during rest and two levels of exercise. Blood flow was determined using 11.4 +/- 0.1 microns radiolabeled microspheres. Vascular reserve (percent for each region) is the ratio of vascular conductance during each condition to maximum vascular conductance. Maximum vascular conductance was estimated by infusing adenosine intravenously. For a given physiological condition regional vascular conductance varied two- to threefold. The vascular reserve of each of the regions decreased progressively from rest to mild exercise to moderate exercise. Regional vascular reserve for both atria, the right ventricle, and the epicardial layer of the left ventricle was essentially uniform for a given condition: rest 93 +/- 0.4%, mild exercise 81 +/- 1.2%, and moderate exercise 69 +/- 1.5%. This similarity in vascular reserve implies that for a given physiological condition a common mechanism precisely regulates myocardial perfusion in these cardiac regions as a function of the total vasodilator capacity.

Regional changes in myocyte structure in model of canine right atrial hypertrophy.

To investigate regional variation of myocyte response to atrial hypertrophy, control dogs were compared with dogs with right atrial hypertrophy created by induction of tricuspid regurgitation; after 1 yr, right atrial-to-body weight ratio increased 122% over controls. One section from the interatrial band, appendage and nonappendage roofs, and nonappendage side of each atrium of each dog was stained to reveal myocyte outlines and transverse tubules; myocyte cross-sectional areas were measured and transverse tubule prevalence was estimated. In control dogs, interatrial band myocytes were significantly larger and had more transverse tubules than other atrial myocytes. With atrial hypertrophy, right interatrial band myocytes did not increase significantly in size, whereas other right atrial myocytes nearly doubled in size, approaching the size of interatrial band myocytes without approaching the content of transverse tubules. Left atrial myocytes did not increase in size. Thus hypertrophic response of atrial myocytes to hemodynamic stress depends on the region in which the myocytes are found, and atrial hypertrophy does not demand transverse tubule proliferation.

Myocardial oxygenation in dogs during partial and complete coronary artery occlusion.

Regional myocardial oxygenation was assessed during partial and complete coronary artery occlusion using near infrared spectroscopy. In eight open-chest dogs, partial occlusions resulting in an approximately 42% decrease in left anterior descending coronary artery (LAD) blood flow produced an approximately 21% decrease in tissue O2 stores (tissue oxyhemoglobin plus oxymyoglobin) and no change in the oxidation level of mitochondrial cytochrome aa3. An approximately 81% reduction in LAD blood flow produced nadir levels of tissue oxyhemoglobin plus oxymyoglobin, maximal levels of deoxyhemoglobin plus deoxymyoglobin, a decline in tissue blood volume, and an approximately 39% decrease in cytochrome aa3 oxidation level. These changes were associated with an approximately 52% decrease from the preischemic baseline in mean transmural myocardial blood flow, measured by radiolabeled microspheres, and an approximately 41% decrease in myocardial O2 consumption. Complete occlusion resulted in further decreases in myocardial blood flow, O2 consumption, tissue blood volume, and cytochrome aa3 oxidation state but also produced increases in tissue O2 stores to above the nadir levels noted during partial occlusion. These results indicate that decreases in O2 delivery during partial coronary occlusion increase O2 extraction to sustain mitochondrial O2 availability, but as little as a 52% reduction in myocardial blood flow produces maximal O2 extraction and depletion of tissue O2 stores. Mitochondrial O2 availability is restricted further during complete occlusion because of limited O2 delivery and, possibly, decreases in tissue blood volume and O2 extraction.

Regional blood flow in canine atria during exercise.

Global and regional atrial blood flow was measured with radioisotope-labeled microspheres in eight dogs during rest and two levels of exercise. Both mean right and left atrial blood flow increased significantly (P < 0.05) to a similar degree with each level of exercise (right atria: 0.27 +/- 0.04, 0.89 +/- 0.11, and 1.57 +/- 0.21 ml.min-1 x g-1; left atria: 0.35 +/- 0.04, 0.90 +/- 0.09, and 1.61 +/- 0.17 ml.min-1 x g-1). Atrial blood flow during exercise is greater than anticipated if increased heart rate was the sole cause. In both right and left atria the ratio of appendage to nonappendage flow was significantly (P < 0.005) less than one during resting conditions (0.42 +/- 0.04 and 0.81 +/- 0.05, respectively), not different from unity during mild exercise, and significantly (P < 0.02) greater than one during moderate exercise (1.10 +/- 0.03 and 1.16 +/- 0.05, respectively). This disparity in the blood flow to the appendage and nonappendage regions suggests that the appendage plays an augmented hemodynamic role during exercise, thus requiring a larger proportion of the nutrient flow.

Dynamic mechanisms of cardiac oxygenation during brief ischemia and reperfusion.

Myocardial oxygenation may be altered markedly by changes in tissue blood flow. During brief ischemia and reperfusion produced by transient occlusion of the left anterior descending artery in 10 open-chest dogs, changes in the oxygenation of tissue hemoglobin (Hb) plus myoglobin (Mb) and the oxidation-reduction (redox) state of mitochondrial cytochrome aa3 were monitored continuously using near-infrared spectroscopy. The nondestructive optical technique indicated that coronary occlusion produced an abrupt drop in tissue oxygen stores (tHb02 + Mb02), tissue blood volume (tBV), and the oxidation level of cytochrome aa3. Changes in the cytochrome oxidation state were related inversely to transmural collateral blood flow within the ischemic region (r = 0.77) measured with radiolabeled microspheres. Furthermore, there was a direct relationship (r = 0.91) between collateral blood flow and the tissue level of desaturated Hb and Mb (tHb + Mb). Reperfusion after 2 min of ischemia led to a synchronous overshoot of baseline in coronary flow and tBV followed by supranormal increases in tHb + Mb02 and the oxidation level of cytochrome aa3. The tHb + Mb level increased transiently during reperfusion. This response correlated inversely with collateral flow during ischemia (r = 0.91). Accordingly, the time required to reach peak tHb + Mb levels was shortest in dogs with high collateral flows (r = 0.75). Thus collateral blood flow partially sustains myocardial oxygenation during coronary artery occlusion and influences tissue reoxygenation early during reperfusion.

Compliance of left atrium with and without left atrium appendage.

Compliance of the left atrial chamber was estimated with and without the appendage intact in six isolated canine left atria. Pressure-volume determinations were measured over a range of 5-30 mmHg for the whole left atrium and were repeated with the appendage excluded. The slope of the pressure vs. normalized volume data for the left atrium without the appendage (10.45 +/- 0.87) was significantly greater (P less than 0.01) than with the appendage intact (4.10 +/- 0.72). These data suggest that the left atrial appendage is more compliant than the remaining left atrium. Assuming that this relationship remains in vivo, the left atrial appendage may play an augmented role in maintaining hemodynamic function when filling pressures are elevated.

Regional atrial blood flow in dogs. Effect of hypertrophy on coronary flow reserve.

Little is known regarding regional atrial blood flow responses during varying hemodynamic states in both the normal and hypertrophied atria. This study was undertaken to develop a canine model of chronic atrial hypertrophy and to define in both this group and in normal dogs the regional blood flow response to acute atrial fibrillation and to measure coronary flow reserve. In the 12 dogs with atrial but not ventricular hypertrophy the mean left and right atrial weights were 75 and 47% respectively greater than in the normal group. Blood flow in the normal dogs was less in the appendage than in the non-appendage region for both atria and increased significantly during atrial fibrillation. Similar findings were noted in the hypertrophy group except that during control conditions the left atrial appendage flow was similar to the nonappendage flow. Minimal vascular resistance for the hypertrophy group, 39 +/- 3 was significantly (P less than 0.05) greater when compared to the normal group 28 +/- 2 mmHg/cm3 per min per g. Thus, significant regional blood flow differences occur in both the normal and hypertrophied atria. In addition, atrial hypertrophy does not alter the autoregulatory capacity to the hemodynamic stress of atrial fibrillation but does reduce coronary flow reserve.

Effect of nitroglycerin on myocardial collateral conductance in awake dogs.

Conductance of the coronary collateral circulation during the course of two abrupt circumflex coronary occlusions (pre- and posttreatment with nitroglycerin) was measured in awake dogs approximately 2 wk after collateral vessels were stimulated to develop. The pressure gradient from the central aorta to the distal circumflex coronary artery was measured, and myocardial blood flow was determined by 9-microns radioactive microspheres at 30 s and 4 min after coronary occlusions. Collateral conductance was calculated as mean collateral blood flow divided by the mean aorta-coronary pressure gradient. Before nitroglycerin, collateral conductance increased in all eight dogs from 30 s to 4 min by a mean value of 0.006 +/- 0.003 ml.min-1.g-1.mmHg-1. After nitroglycerin administration, the conductance at 30 s increased from the prenitroglycerin control value of 0.009 +/- 0.008 to 0.014 +/- 0.012 ml.min-1.g-1.mmHg-1, P less than 0.03. The mean change in conductance from 30 s to 4 min postnitroglycerin 0.003 +/- 0.003 ml.min-1.g-1.mmHg-1 was significantly less than during prenitroglycerin (P = 0.01). These data indicate that an increase in conductance during coronary occlusion occurs even in the immature collateral circulation. This effect presumably takes place in the arterial smooth muscle at the origin of the collateral vasculature.

Effect of atrial natriuretic factor on transmural myocardial blood flow distribution in the dog.

These studies were designed to define the effect of atrial natriuretic peptide (ANP) on coronary flow. ANP was infused as a bolus directly into the left circumflex coronary artery in doses ranging from 0.05 to 5 micrograms in nine open-chest, anesthetized dogs. Coronary flow was measured with an electromagnetic flowmeter. Regional transmural myocardial blood flow and distribution were measured with 11.3 +/- 0.25 micron radionuclide-labeled microspheres. No significant change was noted in systemic hemodynamics (heart rate, arterial pressure, left atrial pressure, or cardiac output) during the course of the studies. ANP produced a transient vasodilatation of coronary resistance vessels and increased flow by 41% after both the 2.5 and 5 micrograms doses. The vasodilatation occurred uniformly throughout the ventricular wall so that the endocardial/epicardial flow ratio remained constant. There was no evidence of coronary vasoconstriction. The peak vasodilatation response occurred 28 +/- 7 sec after the beginning of the infusion of ANP and lasted approximately 3 min. These data support the hypothesis that ANP administration is associated with a vasodilator response in the coronary resistance vessels that may be modulated through either the release of another vasodilator substance or another mechanism.

Validation of in vivo two-dimensional echocardiographic dimension measurements using myocardial mass estimates in dogs.

The accuracy of in vivo measurements of left ventricular wall thickness and chamber size by means of two-dimensional echocardiography was investigated by comparing left ventricular mass estimates obtained at end diastole in 15 closed-chest dogs with a wide range of left ventricular weights. The systolic and diastolic echocardiographic mass estimates were compared with the actual weights of the freshly excised, stripped left ventricles immediately following death. The mean +/- SD of the weighed mass of the excised ventricles was 104 +/- 25 gm. The mean predicted left ventricular mass with the use of the cylinder-ellipse geometric model and gross anatomic sections corresponding to the echocardiographic imaging planes was 106 +/- 26 gm (r = 0.97 compared to the actual weight). The mean echocardiographic estimate of left ventricular mass at end diastolic was 107 +/- 24 gm (r = 0.98 compared to the weight) and 105 +/- 26 gm at end systole (r = 0.95 compared to the weight). The correlation between the echocardiographic mass estimate at end diastole and the echo mass estimate at end systole was 0.95. Regression analysis failed to demonstrate a significant over- or underestimation of the actual weight by the calculated mass with the use of either the gross anatomic or the in vivo echocardiographic dimension measurements.