A model of ischemic mitral regurgitation in pigs with three-dimensional echocardiographic assessment.

BACKGROUND AND AIM OF THE STUDY: Ischemic mitral regurgitation (IMR), the incidence of which is increasing, results from annular and subvalvular remodeling after myocardial infarction (MI). Although a sheep model of IMR has been used extensively over the past two decades, the ventricular, coronary and leaflet anatomy in sheep is significantly different from that in humans. In contrast, pigs are more similar to humans with regard to these parameters, and therefore may serve as a better animal to test emerging new technologies designed to treat IMR. METHODS: Twenty-nine pigs (body weight 30-35 kg) underwent left thoracotomy and ligation of the mid main circumflex and distal right posterior descending coronary arteries to create a posterolateral MI. Of these pigs, 18 were used for acute data acquisition, while 11 surviving animals in the chronic group were assessed at eight weeks after MI. Real-time three-dimensional echocardiography was performed at baseline, and at 30 min and eight weeks after MI, to assess geometric changes in the mitral annulus, mitral leaflets and left ventricle. RESULTS: Compared to baseline, the MR grade was increased significantly at eight weeks (0.7 + 0.5 versus 2.0 +/- 1.2), together with a significant decrease in left ventricular ejection fraction (40.3 +/- 6.6% versus 25.8 +/- 7.7%). Significant increases were also noted at eight weeks in the commissural width (30.1 +/- 3.2 mm versus 35.1 +/- 2.9 mm) and septolateral diameter (25.0 +/- 2.0 mm versus 33.8 +/- 5.9 mm), with a resultant increase in mitral annular area (596 +/- 85 versus 931 +/- 181 mm3) and a decrease in the annular height to commissural width ratio (15.7 +/- 2.6% versus 13.7 +/- 1.9%). The mitral valve tenting volume was also increased significantly (1577 +/- 645 versus 2440 +/- 755 mm3). The distance between the papillary muscle tips at baseline and at eight weeks was increased significantly (23.9 +/- 2.5 versus 30.9 +/- 5.2 mm), as was the distance between the posterior papillary muscle tip and the posterior commissure (20.9 +/- 2.7 versus 24.1 +/- 2.8 mm). CONCLUSION: The surgical model described here reliably replicates the changes seen in humans with IMR. Hence, this model can be used for further studies of the pathophysiology of IMR, and of any novel interventions in this challenging clinical area.

Significance of force transfer in mitral valve-left ventricular interaction: in vivo assessment.

OBJECTIVE: The objective of this study was to assess the combined force transfer from the papillary muscle tips to the mitral valve through the chordae tendineae in vivo, and thereby quantify the force transmitted through the papillary-chordal complex to augment left ventricular ejection. METHODS: In an acute porcine model (n = 8), force transfer between papillary muscles and the mitral valve was recorded on the anterior and posterior papillary muscle tip using dedicated force transducers. Ultrasound sonomicrometry was utilized to record and calculate left ventricular long-axis shortening and mitral annular geometry. The closing force acting on the mitral valve leaflets was calculated as mitral annular area multiplied by the transmitral pressure difference throughout systole. Mitral valve competence was verified before measurements with color Doppler ultrasound. RESULTS: Peak force in the anterior and posterior papillary muscle was 5.9 ± 0.6 N and 5.8 ± 0.7 N (mean ± standard error of the mean), respectively, and peak closing force was 6.8 ± 0.3 N all at a transmitral pressure of 90 mm Hg. Peak rate of left ventricular contraction coincided with peak papillary muscle force. CONCLUSIONS: This study is the first to assess the magnitude and time course of the longitudinal force transmitted through the papillary-chordal complex to the left ventricular wall during ejection. The study also demonstrates a significant force transfer to the closing force acting on the mitral valve leaflets that constitutes an essential component of valvular-ventricular interaction to enhance left ventricular systolic pump performance. The magnitude of the combined papillary muscle force component emphasizes the crucial role of preserving mitral valve-left ventricular continuity in mitral valve surgery.

Tension cost correlates with mechanical and biochemical parameters in different myocardial contractility conditions.

OBJECTIVES: Tension cost, the ratio of myosin ATPase activity to tension, reflects the economy of tension development in the myocardium. To evaluate the mechanical advantage represented by the tension cost, we studied papillary muscle contractility and the activity of myosin ATPase in the left ventricles in normal and pathophysiological conditions. METHODS: Experimental protocols were performed using rat left ventricles from: (1) streptozotocin-induced diabetic and control Wistar rats; (2) N-nitro-L-arginine methyl ester (L-NAME) hypertensive and untreated Wistar rats; (3) deoxycorticosterone acetate (DOCA) salt-treated, nephrectomized and salt- and DOCA-treated rats; (4) spontaneous hypertensive rats (SHR) and Wistar Kyoto (WKY) rats; (5) rats with myocardial infarction and shamoperated rats. The isometric force, tetanic tension, and the activity of myosin ATPase were measured. RESULTS: The results obtained from infarcted, diabetic, and deoxycorticosterone acetate-salt-treated rats showed reductions in twitch and tetanic tension compared to the control and sham-operated groups. Twitch and tetanic tension increased in the N-nitro-L-arginine methyl ester-treated rats compared with the Wistar rats. Myosin ATPase activity was depressed in the infarcted, diabetic, and deoxycorticosterone acetate salt-treated rats compared with control and sham-operated rats and was increased in N-nitro-L-arginine methyl ester-treated rats. These parameters did not differ between SHR and WKY rats. In the studied conditions (e.g., post-myocardial infarction, deoxycorticosterone acetate salt-induced hypertension, chronic N-nitro-L-arginine methyl ester treatment, and streptozotocin-induced diabetes), a positive correlation between force or plateau tetanic tension and myosin ATPase activity was observed. CONCLUSION: Our results suggest that the myocardium adapts to force generation by increasing or reducing the tension cost to maintain myocardial contractility with a better mechanical advantage.

Tension cost correlates with mechanical and biochemical parameters in different myocardial contractility conditions

OBJECTIVES: Tension cost, the ratio of myosin ATPase activity to tension, reflects the economy of tension development in the myocardium. To evaluate the mechanical advantage represented by the tension cost, we studied papillary muscle contractility and the activity of myosin ATPase in the left ventricles in normal and pathophysiological conditions. METHODS: Experimental protocols were performed using rat left ventricles from: (1) streptozotocin-induced diabetic and control Wistar rats; (2) N-nitro-L-arginine methyl ester (L-NAME) hypertensive and untreated Wistar rats; (3) deoxycorticosterone acetate (DOCA) salt-treated, nephrectomized and salt- and DOCA-treated rats; (4) spontaneous hypertensive rats (SHR) and Wistar Kyoto (WKY) rats; (5) rats with myocardial infarction and shamoperated rats. The isometric force, tetanic tension, and the activity of myosin ATPase were measured. RESULTS: The results obtained from infarcted, diabetic, and deoxycorticosterone acetate-salt-treated rats showed reductions in twitch and tetanic tension compared to the control and sham-operated groups. Twitch and tetanic tension increased in the N-nitro-L-arginine methyl ester-treated rats compared with the Wistar rats. Myosin ATPase activity was depressed in the infarcted, diabetic, and deoxycorticosterone acetate salt-treated rats compared with control and sham-operated rats and was increased in N-nitro-L-arginine methyl ester-treated rats. These parameters did not differ between SHR and WKY rats. In the studied conditions (e.g., post-myocardial infarction, deoxycorticosterone acetate salt-induced hypertension, chronic N-nitro-L-arginine methyl ester treatment, and streptozotocin-induced diabetes), a positive correlation between force or plateau tetanic tension and myosin ATPase activity was observed. CONCLUSION: Our results suggest that the myocardium adapts to force generation by increasing or reducing the tension cost to maintain myocardial contractility with a better mechanical advantage.

Left ventricular function assessment using a fast 3D gradient echo pulse sequence: comparison to standard multi-breath hold 2D steady state free precession imaging and accounting for papillary muscles and trabeculations.

OBJECTIVE: Papillary muscles and trabeculae for ventricular function analysis are known to significantly contribute to accurate volume and mass measurements. Fast imaging techniques such as three-dimensional steady-state free precession (3D SSFP) are increasingly being used to speed up imaging time, but sacrifice spatial resolution. It is unknown whether 3D SSFP, despite its reduced spatial resolution, allows for exact delineation of papillary muscles and trabeculations. We therefore compared 3D SSFP ventricular function measurements to those measured from standard multi-breath hold two-dimensional steady-state free precession cine images (standard 2D SSFP). METHODS AND RESULTS: 14 healthy subjects and 14 patients with impaired left ventricularfunction underwent 1.5 Tesla cine imaging. A stack of short axis images covering the left ventricle was acquired with 2D SSFP and 3D SSFP. Left ventricular volumes, ejection fraction, and mass were determined. Analysis was performed by substracting papillary muscles and trabeculae from left ventricular volumes. In addition, reproducibility was assessed. EDV, ESV, EF, and mass were not significantly different between 2D SSFP and 3D SSFP (mean difference healthy subjects: -0.06 +/- 3.2 ml, 0.54 +/- 2.2 ml, -0.45 +/- 1.8%, and 1.13 +/- 0.8 g, respectively; patients: 1.36 +/- 2.8 ml, -0.15 3.5 ml, 0.86 +/- 2.5%, and 0.91 +/- 0.9 g, respectively; P > or = 0.095). Intra- and interobserver variability was not different for 2D SSFP (P > or = 0.64 and P > or = 0.397) and 3D SSFP (P > or = 0.53 and P > or = 0.47). CONCLUSIONS: Differences in volumes, EF, and mass measurements between 3D SSFP and standard 2D SSFP are very small, and not statistically significant. 3D SSFP may be used for accurate ventricular function assessment when papillary muscles and trabeculations are to be taken into account.

Three-dimensional assessment of papillary muscle displacement in a porcine model of ischemic mitral regurgitation.

OBJECTIVE: Papillary muscle displacement relative to mitral annulus is pivotal in chronic functional ischemic mitral regurgitation. Analysis of 3-dimensional papillary muscle displacement has relied on invasive measurement. In this study, we used noninvasive clinically applicable 3-dimensional morphology cardiac magnetic resonance imaging to define papillary muscle position in a 3-dimensional matrix. METHODS: Fifty pigs (approximately 50 kg) were subjected to posterolateral myocardial infarction and tachycardiac stress. Fourteen animals survived 6 weeks: 10 acquired chronic functional ischemic mitral regurgitation at least grade II and 4 did not. Animals were examined by 3-dimensional morphology cardiac magnetic resonance imaging, and dedicated software enabled assessment of anterior and posterior papillary muscle positions relative to anterior and posterior trigones and posterior mitral annulus. Animals with functional ischemic mitral regurgitation were compared with those without and with 10 healthy controls. RESULTS: Relative to controls, animals with functional ischemic mitral regurgitation at end systole had significantly higher displacements of the posterior papillary muscle from anterior and posterior trigones in lateral and posterior directions, and of anterior papillary muscle from anterior and posterior trigones in apical direction. Relative to animals without functional ischemic mitral regurgitation, there was significantly higher posterior papillary muscle displacement from posterior trigone in lateral direction. Interpapillary muscle distance was the strongest predictor of regurgitant volume (r(2) = 0.85, P < .001). CONCLUSIONS: Three-dimensional morphology cardiac magnetic resonance imaging enabled detailed analysis of local left ventricular remodeling effects causing functional ischemic mitral regurgitation.

Altered tension cost in (TG(mREN-2)27) rats overexpressing the mouse renin gene.

The present study aimed to characterize cardiac hypertrophy induced by activation of the renin-angiotensin system in terms of functional alterations on the level of the contractile proteins, employing transgenic rats harboring the mouse renin gene (TGR(mREN2)27). Ca2+-dependent tension and myosin ATPase activity were measured in skinned fiber preparations obtained from TGR(mREN2)27 and from age-matched Sprague-Dawley rats (SPDR). Western blots for troponin I (TnI) and troponin T (TnT) were performed and the phosphorylation status of TnI were evaluated in myocardial preparations. TnT and myosin heavy chain (MHC) isoforms were analyzed by RT-PCR. The pCa/tension relationship was shifted to the right in TGR(mREN2)27 compared to SPDR as indicated by increased Ca2+-concentrations required for half maximal activation of tension (SPDR 5.80, 95% confidence limits 5.77-5.82 vs. TGR(mREN2)27 5.69, 95% confidence limits 5.67-5.72, pCa units), while maximal developed tension was unaltered. Even more pronounced was the shift in the relationship between pCa and myosin-ATPase (SPDR 6.01, 95% confidence limits 5.99-6.03 vs. TGR(mREN2)27 5.77, 95% confidence limits 5.73-5.79, pCa units). The maximal myosin-ATPase activity was reduced in TGR(mREN2)27 compared to SPDR, respectively (211.0 +/- 28.77 micromol ADP/s vs. 271.6 +/- 43.66 micromol ADP/s, P < 0.05). Tension cost (ATPase activity/tension) was significantly reduced in TGR(mREN2)27. The beta-MHC expression was significantly increased in TGR(mREN2)27. There was no isoform shift for TnT (protein and mRNA), as well as TnI, and no alteration of the phosphorylation of TnI in TGR(mREN2)27 compared to SPRD. The present study demonstrates that cardiac hypertrophy, induced by an activation of the renin-angiotensin system, leads to adapting alterations on the level of the contractile filaments, which reduce tension cost.

Assessment of papillary muscle function in patients with inferior wall myocardial infarction using Doppler tissue imaging.

OBJECTIVES: We sought to assess the relationship between infarct status and systolic contractile function of papillary muscle (PM) for patients with inferior wall myocardial infarction (MI). METHODS: Peak systolic velocity (V) of posteromedial PM, systolic strain (epsilon) of posteromedial PM (epsilonPM), V of adjacent inferior wall, and of adjacent inferior wall (epsilonW) were calculated from color Doppler tissue imaging images obtained at apical views in 25 patients with inferior MI and in 13 healthy control subjects. All 25 patients with MI underwent magnetic resonance imaging to assess the infarct status of PM. RESULTS: Compared with the control subjects, patients with MI had significantly lower V of adjacent inferior wall (5.0 +/- 0.8 vs 4.4 +/- 1.1 cm/s, P = .049) and V of posteromedial PM (4.9 +/- 0.8 vs 4.0 +/- 1.2 cm/s, P = .005), and less systolic deformation, as demonstrated by epsilonW (-17 +/- 3 vs -6 +/- 5%, P < .001) and epsilonPM (-24 +/- 5 vs -11 +/- 6%, P < .001). There was a weak positive correlation between epsilonW and epsilonPM (r = 0.393, P = .052) for patients with MI. Magnetic resonance imaging showed total infarct of PM in 14 patients (group A), with the remaining 11 revealing either normal perfusion or partial infarct of PM (group B). Although epsilonW was similar in groups A and B (-5 +/- 5% vs -8 +/- 6%, P = .20), epsilonPM was significantly lower in group B (-7 +/- 4% vs -16 +/- 4%, P = .004). CONCLUSIONS: In patients with inferior wall MI, infarct status of the PM is variable and determines its systolic contractile function, which can be quantified by epsilon measurement using Doppler tissue imaging.

Assessment of papillary muscle function using myocardial velocity gradient derived from tissue Doppler echocardiography.

Papillary muscle (PM) function is vital to mitral valve competence. However, quantitative assessment of the function is difficult due to the complexity of the mitral apparatus. We hypothesized that myocardial velocity gradient (MVG) could be applied to assess PM function. We studied MVG-PM in 123 patients with left ventricular dysfunction (ejection fraction <40%) and 123 normal subjects throughout a systolic phase. MVG-PM in normal subjects was significantly higher than in patients with left ventricular dysfunction (3.6/s vs 1.4/s, p <0.001). MVG-PM reached its peak at early systole and correlated well with PM thickening (r = 0.89). MVG-PM in patients with left ventricular dysfunction correlated with the severity of apical tenting of the mitral valve (y = 0.8x - 0.07, r = 0.72). Patients with lower MVG-PM tended to have less severe mitral regurgitation (y = 0.03x + 0.3, r = 0.83). PM contractility can be quantitatively assessed by calculating the MVG derived from tissue Doppler imaging. PM dysfunction, indicated by lower MVG-PM, decreased mitral leaflet tethering, thus paradoxically decreasing mitral regurgitation severity. MVG is a useful tool in determining the role of PM in functional mitral regurgitation.

Impact of papillary muscles in ventricular volume and ejection fraction assessment by cardiovascular magnetic resonance.

Cardiovascular magnetic resonance (CMR) is an accurate tool for the determination of right and left ventricular volumes and ejection fractions. However, the current standard short-axis technique is time-consuming and thus, often not practicable for routine daily use, because papillary muscles and trabeculations have to be marked and their volumes subtracted from the total ventricular volume. To reduce calculation time we evaluated the volumetric data that included papillary muscle and trabecular volumes and compared the outcome with the results of the standard technique. Thirty patients (17 healthy, 13 with coronary heart disease) were examined by CMR using TrueFISP (Magnetom, Siemens, Erlangen, Germany). Right and left ventricular volumes and ejection fractions were calculated using the standard short-axis technique and then again without subtracting papillary and trabecular volumes. The two methods were compared by determining the differences in results for ventricular volumes and ejection fractions. Statistically significant differences were found between the two methods for right and left ventricular stroke volumes and end-systolic volumes, and left ventricular end-diastolic volumes (EDV) (p < or = 0.011). No significant difference was found for right ventricular end-diastolic volumes (p > or = 0.149) or left or right ventricular ejection fraction (p > or = 0.130). Except in the case of left ventricular EDV, the deviations in the results of method 1 and method 2 did not vary significantly with the presence or absence of heart disease. Measurements were obtained considerably more quickly with the modified method than with the standard short-axis method (25 +/- 4 min vs. 13 +/- 3 min, p = 0.000). Although systematic differences were found when papillary and trabecular volumes were not subtracted, these differences are small and may not be of clinical relevance in healthy subjects or patients with coronary heart disease. Not subtracting the volumes of these structures enables faster determination of right and left ventricular volumes and ejection fractions without loss of the accuracy associated with the standard short-axis technique.

The subvalvular apparatus in rheumatic mitral stenosis: methods of assessment and therapeutic implications.

The assessment of the structure and function of the subvalvular apparatus (SVA) in patients with rheumatic mitral stenosis (MS) is complex, yet is of major importance prior to therapeutic decision making. Currently available methods of assessment are neither sufficiently accurate nor feasible. We review anatomic and functional aspects of the SVA and define SVA involvement in rheumatic MS. The role of various noninvasive and invasive methods for evaluating the integrity and function of SVA in rheumatic MS, as well as clinical implications and pitfalls in assessment of SVA are also discussed.

Assessment of segmental wall motion abnormalities using contrast two-dimensional echocardiography in awake mice.

Murine models of cardiac disease are becoming an important tool for studying pathophysiological processes. Development of methods to accurately assess ventricular function are therefore important. The purpose of this study was to evaluate the feasibility of echocardiographic assessment of segmental wall motion abnormalities in a murine model of myocardial infarction. Two-dimensional contrast (C+) and noncontrast (C-) echocardiography were performed in 76 awake mice 2 days before and 2 days after left coronary ligation. The short-axis images obtained with two-dimensional echocardiography and corresponding postmortem cross-sectional histological samples stained with Evans blue dye were each divided into 16 segments, and all matched segments were examined for correlation between wall motion abnormalities and myocardial hypoperfusion. With the use of contrast enhancement, the number of visualized segments was significantly increased (base: C- 86%, C+ 98%; midpapillary: C- 57%, C+ 89%; apex: C- 30%, C+ 74%). Agreement between echocardiographically assessed regional wall motion abnormalities and pathologically determined hypoperfusion in basal, midpapillary, and apical levels were 90%, 93%, and 93%, respectively. Agreement between echocardiographically normal wall motion and pathologically normal findings in basal, midpapillary, and apical levels were 99%, 88%, and 71%, respectively. Thus echocardiographic assessment of segmental wall motion in awake mice was feasible and the accuracy was improved with the use of a contrast agent.

[Usefulness of helical scanning CT in assessment of left ventricular papillary muscle contractility].

Three-dimensional data on the left ventricle at quasi-end-diastole and quasi-end-systole were acquired by helical scanning CT in 12 patients. Short axial images of the left ventricle and long axial images of the papillary muscle were created using multiplanar reconstruction. Left ventricular dimensions and the length of the papillary muscle were measured, and fractional shortening of the papillary muscle was calculated. There was a good correlation between left ventricular dimensions measured by echocardiogram and helical scanning CT (end-diastole: r = 0.94: end-systole: r = 0.86; fractional shortening of left ventricular dimension: r = 0.84). Papillary muscle fractional shortening was 6.3% in the ischemic group and 21.5% in the non-ischemic group (p < 0.005). Helical scanning CT is clinically useful for the assessment of left ventricular papillary muscle function.

Assessment of apical hypertrophic cardiomyopathy using transoesophageal echocardiography.

Two-dimensional echocardiography is the method of choice for imaging and diagnosis in patients with hypertrophic cardiomyopathy. However, ultrasound examination of the left ventricular apex by transthoracic echocardiography is often inadequate so that hypertrophy localised to this region may be missed. The purpose of this study was to evaluate the use of multiplane transoesophageal echocardiography in the diagnosis and assessment of apical hypertrophic cardiomyopathy. Six patients with apical hypertrophic cardiomyopathy underwent transthoracic and multiple transoesophageal echocardiography. Assessment of the proximal left ventricle was possible in all patients by both techniques and normal wall thickness measurements were obtained. Assessment of the distal left ventricle by multiple transesophageal echococardiography revealed hypertrophy of the apex (range 1.7-2.9 cm) and less marked hypertrophy of the distal segments of the left ventricle in all 6 patients (1.4-2.2 cm). Examination of the papillary muscles was also possible and hypertrophy was detected in 2 patients. By transthoracic echocardiography, hypertrophy was detected in the distal left ventricle of 5 patients and values were less than those obtained by multiplane transoesophageal echocardiography. No papillary muscle hypertrophy was seen. The apical segment was imaged in only 4 patients and maximum thicknesses of the apical segment were greater by multiple transoesophageal echocardiographic examination than by transthoracic echocardiography (mean 2.25 +/- 0.4 and 1.97 +/- 0.3 cm, respectively). We conclude that apical hypertrophic cardiomyopathy may be difficult to diagnose using transthoracic echocardiography because of inconsistent imaging of the apical segment. The distribution of hypertrophy may be inappropriately assigned and the severity of wall thickening underestimated. Multiplane transoesophageal echocardiography allows high resolution imaging of all segments of the left ventricle, particularly the apex.

Transesophageal echocardiography and concurrent coronary angiography for the rapid assessment of papillary muscle rupture.

Echocardiography with color flow imaging is valuable for identifying mechanical complications of myocardial infarction. Transesophageal echocardiography is useful for critically ill patients in whom transthoracic imaging is often insufficient. A case of papillary muscle rupture is presented in which transesophageal echocardiography was performed concurrently with coronary angiography. The detailed information obtained from two-dimensional and color flow imaging eliminated the need for diagnostic right heart catheterization and left ventriculography. Transesophageal echocardiography used in this manner can facilitate expeditious surgical management.

Two-dimensional echocardiographic assessment of papillary muscle contractility in patients with prior myocardial infarction.

OBJECTIVES: This study was performed to assess the length and contractile performance of human left ventricular papillary muscles and to determine the relation between papillary muscle dysfunction and mitral regurgitation. BACKGROUND: Assessment of human papillary muscle contractility remains a clinical challenge. METHODS: Two-dimensional echocardiographic examinations were performed in 16 normal subjects and 31 patients with prior myocardial infarction. Apical echocardiograms were used to obtain long-axis views of the anterior and posterior papillary muscles. The end-systolic and end-diastolic lengths of the papillary muscles were measured and fractional shortening was calculated. RESULTS: Fractional shortening in normal subjects was 27 +/- 8% for the anterior papillary muscle and 30 +/- 8% for the posterior papillary muscle. In patients with prior myocardial infarction, a significant decrease in fractional shortening was observed in proportion to the severity of left ventricular wall motion abnormalities at the site of papillary muscle implantation. Moderate or severe mitral regurgitation was significantly more frequent in patients with combined anterior and posterior papillary muscle dysfunction than in those with isolated anterior or posterior dysfunction or with normal function of both papillary muscles (p < 0.05). CONCLUSIONS: Two-dimensional echocardiography is useful for demonstrating abnormal contractility of human left ventricular papillary muscles. Papillary muscle contractility should be analyzed in each case to elucidate the mechanism of mitral regurgitation in patients with papillary muscle dysfunction.

[An assessment of myocardial contractility in experimental atherosclerosis]. / Otsenka sokratimosti miokarda pri éksperimental'nom ateroskleroze.

Experimental atherosclerosis reduced the parameters of the myocardium contractility in rats: the time of reaching the maximum of isometric contractions and the relative time of relaxation were shortened, and the velocity of the muscle shortening was decelerated. These changes seem to be due to a developing hypertrophy of the right ventricle's papillary muscles. The specific feature of the myocardium in rats with atherosclerosis involves a phenomenon of mechanochemical dissociation (inactivation) due, probably, to the effect of dyslipoproteinemia on the contractile processes.

Radioisotopic assessment of peripheral and cardiac muscle involvement and dysfunction in polymyositis/dermatomyositis.

99mTc-pyrophosphate musculoskeletal imaging and 99mTc-red blood cell gated blood pool imaging were performed on 10 patients with documented polymyositis/dermatomyositis. Abnormal 99mTc-pyrophosphate uptake by peripheral muscles was found in 8 patients (6 mild, 2 marked). Cardiac uptake occurred in 5 patients and was 3+ in 2 with cardiovascular symptoms. These 2 patients also had abnormal EF on gated blood pool imaging. Patients without myocardial 99mTc-pyrophosphate uptake had normal EF. Patients with myocardial 99mTc-pyrophosphate uptake had abnormal wall motion, in proportion to the degree of uptake. Response to therapy and outcome were poorer in patients with marked scintigraphic changes. These findings suggest that the magnitude of 99mTc-pyrophosphate myocardial uptake may have prognostic implications in these patients.

Clinical assessment of the right ventricle anterior papillary muscle extrasystoles with Holter recordings.

To assess the short-term behavior of the right ventricle anterior papillary muscle extrasystoles (APME) based on Holter recording and exercise data, 20 subjects (age 31.5 +/- 13.7 years) with otherwise normal electrocardiogram were studied. APME was diagnosed when it resembled LBBB morphology, with downward oriented AQRS in the frontal plane, slurred r wave in lead V1, and an R/S ratio less than 1 in this same lead. Except for palpitations in ten patients, there were no other symptoms related to the arrhythmia. Two Holter recordings, 30 to 330 days apart, were performed and their results compared. In the first Holter recording, the average rate of VPB/minute was 9.9 +/- 2.5 (xg +/- SD). Half of the patients had couplets and five had ventricular tachycardia. In the second Holter recording, the average rate of VPB/minute was 8.7 +/- 3. In eight cases, couplets were recorded, in half of which one or more episodes of ventricular tachycardia were also noted. Six patients showed another VPB morphology distinct from APME. Stress test suppressed VPB in 10/13 patients, couplets in 2/3 and ventricular tachycardia in the only one with this arrhythmia at the start of the test. Repetitive forms vs APME frequency and vs heart rate exhibited an inverse relationship. We conclude that APME is a clinical condition with both high and stable VPB levels, which can be found in subjects with otherwise normal hearts and in the short-term has a spontaneous uncomplicated outcome.

Assessment of myocardial function by calculation of two energetic parameters from pressure-volume relations and wall thickness in human ventricles.

For defining myocardial performance in chronic cardiac diseases and during acute pharmacological interventions we created a new index of performance based on myocardial mechanical and energetic counterparts. From angiocardiographic pressure-volume data the pressure-volume integral is analyzed and divided by left ventricular muscle mass, yielding work done by a unit of myocardium (E1). From pressure-volume data the stress-time integral integral of sigma.t is evaluated by using an ellipsoidal calculation model. In order to compare E1 with the integral of sigma.t the integral of sigma.t is transformed into energetic units on the basis of new physiologic myothermal findings (E2). Then, the sum of E1 and E2 (i.e.,the maximum of mechanical performance), the ratio of E1 to the sum of E1 and E2 can be defined (i.e., the myocardial work related to the energy consumed during a contraction). By calculating E1 and E2, we are able to analyze the myocardial efficiency of work production. These parameters are proposed for judging the myocardial performance and efficiency in congestive heart failure and the effects of positive inotropic substances and vasodilators.