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Force-frequency (FFR) and relaxation-frequency relationships (RFR) and post-extrasystolic potentiation (PESP) act as physiologic mirrors reflecting changes in Ca2+ release and uptake by sarooplasmic reticulum (SR). It has been proposed that SR is relatively immature in neonatal animal and FFR and RFR may be impaired in them. We studed certain new aspects of FFR and RFR in 4 neonatal goats (Age: 4 weeks) and 3 adult goats. Left ventricular (LV) dP/dtmax and time constant of relaxation (τ) were calculated from micromanometric LV pressure tracings at increasing heart rates (HR) generated by right ventricular pacing. The phenomenon of PESP was studied by pacing at a constant cycle length(400ms) and by introducing an extrasystole and post-extrasystole at cycle lengths of 250ms and 600 ms, respectively. Both FFR(dP/dtmax vs HR) and RFR (τ vs HR) have biphasic relationships separated by a critical HR at which this transition occurs. Critical HR was nearly identical for both FFR and RFR. Mean critical HR was higher in neonatal vs adult goats (250± 35 vs 180±22 beats/min, p, 0.05). Following ryanodine (a SR Ca2+-release channel blocker), critical HR was shifted to the left in both neonatal and adult goats (170±34 vs 140±28 beats/min). Fig. 1

Recent data suggest that phospholamban (PLB) modulates basal and beta agonist-stimulated myocardial contractility in the isolated heart. To determine the physiological role of PLB in vivo,anesthetized wild type mice (WT, n = 5) and transgenic mice with PLB gene targeted ablation (PLB-KO, n = 4) and overexpression (PLB-DEF, n = 5) were studied with 2D-guided M-mode and Doppler echo using a 9 MHz imaging and 5–7,5 MHz Doppler transducer (Interspec CX 200). Data were acquired in the baseline state (BASE) and after isoproterenol (ISO) injection (1 μg/mg i.p.). Shortening fraction (SF) was calculated from M-mode. The peak early transmitral (Ev) and aortic (Aov) velocities and ejection times were measured using Doppler and the heart ratecorrected velocity of circumferential shortening (Vcfc) was calculated. CON PLB-DEF PLB-OE BASE ISO BASE ISO BASE ISO HR (bpm) 282 ± 49 349 ± 55 * 322 ± 143 424 ± 43 217 ± 34 355 ± 51 * SF (%) 41 ± 3 64 ± 3 * 46 ± 4 62 ± 3 * 41 ± 4 65 ± 4 * Vcfc(circ/s) 10 ± 3 22 ± 3 * 18 ± 7 27 ± 7 7 ± 1 # 20 ± 4 * Ev (cm/s) 40 ± 12 50 ± 3 82 ± l0 † 89 ± 16 † 44 ± 9 # 62 ± 10 *# Aov (cm/s) 65 ± 4 75 ± 17 109 ± 15 † 108 ± 7 † 68 ± 6 # 89 ± 7 * mean ± SD * p l 0.05 vs BASE † p l 0.05 vs CON # vs DEF, ANOVA We conclude: 1) Phospholamban regulates basal left ventricular function in vivoand modulates the sensitivity to βadrenergic stimulation; 2) Assessment of left ventricular function under varying physiological conditions in mice can be performed noninvasively.

An echocardiographic Doppler study in a patient with pulsus paradoxus of respiratory origin demonstrated a large inspiratory increase of tricuspid flow velocity and a corresponding decrease of mitral flow velocity. This “flow paradoxus” is therefore not specific for cardiac tamponade, and provides evidence that decreased left ventricular filling is an important mechanism of pulsus paradoxus observed in severe chronic lung disease.

To determine whether Doppler color flow mapping could be used to quantify changing levels of regurgitant flow and define the technical variables that influence the size of color flow images of regurgitant jets, nine stable hemodynamic states of mitral insufficiency were studied in four open chest sheep with regurgitant orifices of known size. The magnitude of mitral regurgitation was altered by phenylephrine infusion. Several technical variables, including the type of color flow instrument (Irex Aloka 880 versus Toshiba SSH65A), transducer frequency, pulse repetition frequency and gain level, were studied. Significant increases in the color flow area, but not in color jet width measurements, were seen after phenylephrine infusion for each regurgitant orifice. For matched levels of mitral regurgitation, an increase in gain resulted in a 125% increase in color flow area. An increase in the pulse repetition and transducer frequencies resulted in a 36% reduction and a 28% increase in color flow area, respectively. Jet area for matched regurgitant volumes was larger on the Toshiba compared with the Aloka instrument (5.2 +/- 3.1 versus 3.2 +/- 1.2 cm2, p less than 0.05). Color flow imaging of mitral regurgitant jets is dependent on various technical factors and the magnitude of regurgitation. Once these are standardized for a given patient, the measurement of color flow jet area may provide a means of making serial estimates of the severity of mitral insufficiency.

To simplify transmitral volume flow determination by Doppler echocardiography, a formula for calculating mean mitral valve orifice area using M-mode echocardiography without any 2-dimensional measurements was developed and evaluated in this study. The maximal mitral orifice area was assumed to be circular and its diameter was calculated from the maximal M-mode mitral leaflet separation. The maximal area was multiplied by the mean to maximal anterior mitral leaflet excursion ratio to correct for phasic changes in flow orifice area during ventricular filling. This measurement had a high correlation (r = 0.97, standard error of the estimate + 0.26 cm2) with mean mitral valve orifice area calculated from frame-by-frame analysis of short-axis 2-dimensional echoes in a select group of 10 normal volunteers and 10 patients with cardiomyopathy who had very high quality images of the mitral valve leaflet tips. Cardiac output calculated using the new method for orifice area estimation combined with apex view mitral valve Doppler velocities was then validated in 48 consecutive patients undergoing thermodilution cardiac output determinations with a close correlation between Doppler and thermodilution cardiac output (2.3 to 6.1 liter/min, r = 0.93, standard error of the estimate = 362 ml). The correlation improved when 12 patients with mild mitral insufficiency were excluded (r = 0.95). The M-mode echocardiogram-derived mitral valve orifice method combined with Doppler mitral valve velocities is accurate, easy to perform, has a high success rate and should increase the applicability of Doppler echocardiography for estimation of cardiac output.

We studied eight open-chest dogs to determine whether there is regional variation in pericardial contact pressure (PCP). Flat, air-filled balloons were used to measure PCP simultaneously over the lateral walls of the right and left ventricles while cardiac volume was varied by dextran infusion. End-diastolic and mean PCP were significantly higher over the left than right ventricle at high (20.3 +/- 1.0 mmHg) and middle levels (13.7 +/- 0.9 mmHg) of left atrial pressure. At high left atrial pressures, the end-diastolic PCP over the lateral left ventricle was 9.1 +/- 2.4 mmHg compared with 4.3 +/- 2.3 mmHg over the lateral right ventricle (P less than 0.05). At middle levels of left atrial pressures, end-diastolic PCP was 6.2 +/- 3.5 mmHg over the left ventricle and 1.5 +/- 2.4 mmHg over the right ventricle (P less than 0.05). These variations in PCP persisted after severing the pericardial diaphragmatic attachments and after turning the dogs such that one or the other balloon was dependent. Regional distribution of PCP was studied by positioning a single balloon sequentially at multiple ventricular sites. PCP was consistently higher over the lateral wall of the left ventricle than either the anterior or posterior walls of the right or left ventricle. After aortic occlusion, end-diastolic PCP increased more over the left than right ventricle. In contrast, with pulmonary artery occlusion, end-diastolic PCP increased more over the right than left ventricle. Pericardial pressure varies regionally, and a single pericardial pressure may be an oversimplification when used to describe pericardial restraint on the cardiac volume.

Prognostic differences between patients with anterior or inferior myocardial infarction are often related to such variables as previous infarction or the size of the myocardial infarct. We examined the determinants of mortality in 997 hospital survivors of acute Q wave infarction (anterior in 449, inferior in 548) who, although not preselected, were well matched with respect to age, sex and prior infarction or congestive heart failure. Additionally, there was no significant difference in peak serum creatine kinase (CK) between the groups with anterior and inferior infarction (1,459 ± 1,004 versus 1,357 ± 1,036).Among the patients with anterior infarction who died during the 1 year follow-up period, 56% died in the first 60 days after hospital discharge compared with 18% of those without inferior infarction (p < 0.01). Survival curves then became nearly identical at 3 months, and remained so until 1 year when the total mortality rate was 10% for the anterior and 7% for the inferior infarction group (p = NS). Variables associated with heart failure during the hospital phase were more prevalent in anterior infarction, but rales above the scapulae during the hospital stay (p < 0.0001) and ventricular gallop at the time of discharge (p < 0.0001) were the top two predictors of 1 year mortality by both univariate and multivariate analysis in inferior infarction. Age (p < 0.0001) and peripheral edema (p < 0.0001) were the strongest predictors of mortality in anterior infarction. Previous infarction, although just as common in the group with anterior infarction, was present at 1 year in 48% of nonsurvivors of the group with inferior infarction compared with only 19% of survivors (p < 0.0001).Thus, in matched patients with anterior or inferior infarction who survive hospitalization, there is a significantly higher mortality rate up to 60 days after discharge in those with anterior infarction, with a tendency toward higher late mortality in those with inferior infarction. In the latter, signs of heart failure in the hospital, particularly in patients with prior infarction, identified those at higher risk of mortality.

Echocardiographic and hemodynamic data were measured in nine closed chest dogs during graded cardiac tamponade (pericardial pressure 5, 10, 15 mm Hg) before and after production of diffuse acute ischemic right ventricular dysfunction. Right ventricular dysfunction was produced by intracoronary injection of nonradioactive microspheres (mean diameter +/- SD 54 +/- 4 microns) and caused a significant increase in right atrial pressure (7.6 +/- 1.4 vs. 1.6 +/- 1 mm Hg, p less than 0.001) and cross-sectional areas of both the right atrium (8.3 +/- 0.3 vs. 5.6 +/- 0.2 cm2, p less than 0.001) and right ventricle (8.8 +/- 0.4 vs. 5.7 +/- 0.4 cm2, p less than 0.001). Right atrial and ventricular collapse required a significantly larger pericardial effusion and pericardial pressure after right ventricular infarction than before. Mean aortic pressure had fallen 1.9 +/- 2% and 6.5 +/- 6.9% at the time of right atrial collapse (p = NS before vs. after right ventricular dysfunction) and 3 +/- 4.1% and 20.1 +/- 20.8% at the time of right ventricular collapse (p less than 0.03) before and after right ventricular dysfunction, respectively. In the presence of ischemic right ventricular dysfunction, echocardiographic signs of cardiac tamponade are less sensitive and occur later in the hemodynamic progression of cardiac tamponade. Pulsus paradoxus with cardiac tamponade was not prevented by coexisting ischemic right ventricular dysfunction.

Atrial fibrillation (AF) is a common arrhythmia, affecting approximately 5% of the population older than 65 years; the arrhythmia is associated with significant morbidity and mortality, and it is challenging and often frustrating to treat [(1,2)][1]. There is a tendency for AF to become chronic and

cardiac explanation and autotransplantan12:171. Orringer MB, Sisson JC, Glazier G, et al. Surgical treatment of cardiac pheochromocytoma. J Thorac Cardiovasc Surg 198%89:753. Wilson AC, Bennet RC, Niall JF, Clarebrough JK, Doyle AE, Laus W. An unusual case of intra-thoracic pheochromocytoma. Aust NZ J Surg 1974;44z27. Besterman E, Bromley LL, Peart WS. An intrapericardial pheochromocytoma. Br Heart J 1984;3&318. Geisler F, Barath G, Jaeck D, et al. Un cas de pheochromocytome a loclisation cardiaque. Presse Med 198$1&1024. Sawyer WJ, Moser M, Mattingly TW. Pheochromocytoma and the abnormal electrocardiogram. AM HEART J 1954; 48~42.

The influence of being overweight or obese on hospital and late (1 year) mortality and reinfarction was studied in 1760 patients with acute myocardial infarction. Body mass index (BMI) was used to categorize patients as normal weight (BMI 30). Clinical features and prognosis were compared in 658 normal weight patients, 884 overweight patients, and 218 obese patients. Complications during hospitalization and 1-year reinfarction rates following discharge were similar among the weight subsets. Hospital mortality was 13% in obese patients, similar to the 14% hospital mortality in normal weight patients, but significantly more than that in overweight patients (9%, p < 0.05). When stratified according to age, 30% of obese patients ≥65 years died in the hospital, compared to 13% of overweight patients (p < 0.001), and 17% of normal weight patients (p < 0.01). In patients less than 65 years, the obese group had a 6% mortality compared to a hospital mortality of 5% in overweight and 8% in normal weight groups (NS). In a multivariate analysis, obesity was an independent predictor of hospital death in the older, but not in the younger patient subset. One-year mortality for patients discharged from the hospital was significantly less in obese than in normal weight patients (7% vs 13%, p < 0.05), but not different from the 11% mortality rate in overweight patients. Differences in mortality disappeared when patients were age stratified. Excessive early mortality following myocardial infarction is strongly influenced by obesity in older patients, but obesity appears to have no significant influence on 1-year outcome or on early prognosis in patients younger than age 65.

We compared the consequences of acute anterior and posterior wall ischemia on regional left ventricular function in seven open-chest dogs. Circumferentially oriented sonomicrometers were implanted in the midwall of the anterior and posterior left ventricle. The left anterior descending (LAD) and left circumflex (LCX) coronary arteries were each occluded for 3 min, with 45 min of reperfusion between the two occlusions. The ischemic areas at risk, as assessed by postmortem perfusion techniques, were similar for anterior (34.5 +/- 12.5 g) and posterior (32.3 +/- 9.4 g) wall ischemia. Both occlusions produced a similar increase in end-diastolic pressure. After LAD occlusion, total segment shortening (end diastole to aortic valve closure) in the nonischemic posterior wall increased from 8.0 +/- 3.9 to 10.8 +/- 4.4%, solely caused by increased isovolumic shortening. In contrast, with LCX occlusion, total segment shortening in the nonischemic anterior wall increased significantly more, from 10.5 +/- 3.8 to 14.6 +/- 4.2% caused by nearly equal increases in isovolumic and ejection phase shortening. Thus, with both LAD and LCX occlusions, there was increased shortening in nonischemic areas during isovolumic systole, which was “wasted” in paradoxically stretching the ischemic zone. However, a compensatory increase in nonischemic area ejection phase shortening occurred only with LCX occlusions. These findings may explain the greater functional impairment that occurs with LAD than LCX occlusions.

It is not known whether Doppler echocardiography can accurately follow changes in right-sided cardiac hemodynamics after a therapeutic intervention in patients with pulmonary artery (PA) hypertension. Therefore, Doppler measurements of the maximal velocity of the tricuspid regurgitant jet and the acceleration time of the PA velocity profile were obtained in 28 patients before and after pulmonary thromboendarterectomy for chronic thromboembolic PA hypertension. Doppler values were compared with hemodynamic variables obtained at cardiac catheterization. Postoperatively, decreases in mean PA pressure (50 +/- 14 to 28 +/- 8 mm Hg), transtricuspid systolic pressure difference (69 +/- 21 to 36 +/- 14 mm Hg) and Doppler measurement of the maximal velocity of the tricuspid regurgitant jet (4.1 +/- 0.7 to 2.7 +/- 0.5 m/s) were noted, while acceleration time increased (57 +/- 16 to 94 +/- 18 ms, all p less than 0.001) compared with preoperative values. For the population as a whole, the calculated systolic transtricuspid pressure difference determined from the maximal velocity of tricuspid regurgitation correlated well with the catheterization systolic transtricuspid pressure difference (r = 0.93, p less than 0.001) and the acceleration time correlated with mean PA pressure (r = -0.81, p less than 0.001). More importantly, the change in the maximal velocity of tricuspid regurgitation for postoperative patients was found to correlate with the change in catheterization systolic transtricuspid pressure difference (r = 0.82, p less than 0.001), while the change in acceleration time correlated weakly with the change in mean PA pressure (r = -0.41, p = 0.053).(ABSTRACT TRUNCATED AT 250 WORDS)

We studied the value of two-dimensional Doppler echocardiographic color flow mapping for identifying normal transvalve flow profiles and valve malfunction in 20 patients with Bjork-Shiley prosthetic valves. Seven patients had Bjork-Shiley prosthetic valves in the aortic position alone, seven in the mitral position, and six had prosthetic valves in both the aortic and mitral positions. In 10 patients with normally functioning mitral valves, the ratios of the maximal major and minor Doppler-imaged orifice flow diameters to the valve ring diameters were 25 +/- 3% (mean +/- SD) and 24 +/- 3%, respectively, similar to values reported in in vitro studies. No mitral regurgitation was found in these patients by two-dimensional Doppler echocardiographic flow mapping or by spectral Doppler. Of the 10 clinically normal aortic Bjork-Shiley valves, no valvular regurgitation was found by color flow mapping, whereas mild aortic regurgitation was found in two patients with the use of spectral Doppler. Malfunction of six valves was documented in five patients and was confirmed by cardiac catheterization and/or surgery. These included one case of focal fibrous ingrowth involving primarily the minor orifice of a mitral prosthetic valve, one case of mitral valve prosthetic thrombosis with decreased major and minor orifice flow diameters and valvular regurgitation, and four cases of paravalvular regurgitation involving prosthetic valves in the aortic position (three patients) and the mitral position (one patient). Two-dimensional Doppler echocardiographic flow mapping provides new observations that may aid in identifying Bjork-Shiley prosthetic valve malfunction. By localizing precisely the site of prosthetic stenosis or regurgitation, it may also assist in defining the cause of valve malfunction.

To help clarify the mechanism of outflow tract obstruction and systolic anterior motion of the anterior leaflet of the mitral valve and their relation to the geometry of the left ventricle, we studies left ventricular outflow tract flow in 20 patients with hypertrophic cardiomyopathy (HCM) using two-dimensional Doppler flow mapping. We compared our results with outflow tract flow in 10 patients with isolated valvular aortic stenosis, (AS) and with those in 10 healthy volunteers. In HCM, a 94- to 145-degree angle (mean 111.4 ± 11.9 degrees) developed between the direction of left ventricular outflow tract flow acceleration and aortic valve outflow, resulting in posterolaterally directed left ventricular outflow jets. The angle of the outflow jet and the peak velocity of the jet measured with continuous wave Doppler (as an indicator of the severity of obstruction) correlated well (r = −0.81, SEE = 7.8 degrees). Jet narrowing during ejection measured just proximal to the point of systolic anterior motion was 42 ± 11% in HCM and was outflow occurred proximal to systolic anterior motion of the mitral valve, and color M-mode demonstrated temporal and spatial flow acceleration proximal to systolic anterior motion, providing evidence for obstruction at that site. In AS, left ventricular outflow tract jets were more parallel to the axis of aortic outflow (129 to 153 degree, 138.4 ± 8.1 degrees). Jet narrowing was only 8 ± 5% compared to HCM (both p < 0.05), and flow acceleration occurred proximal to the stenotic valve. In normal subjects, turbulent jets were not observed and the angle between left ventricular outflow tract flow and aortic flow was 149.6 ± 2.5 degrees. Our results are consistent with a venturi effect proximal to the mitral valve contributing to the development of systolic anterior motion and outflow tract obstruction, and highlight the importance of ventricular geometry as a determinant of obstruction in HCM.

To improve the accuracy of Doppler echocardiographic indices of left ventricular filling, we derived two indices of instantaneous transmitral flow with the use of Doppler velocities and M-mode echocardiography. These indices were calculated from the product of pulsed Doppler mitral velocities and either the excursion of the anterior mitral leaflet or the separation of both mitral leaflets as measures of the changing mitral orifice area. The derived flow indices and the mitral velocities alone were compared to left ventricular filling as determined by radionuclide ventriculography in 24 patients. When compared as areas under the matched decile divisions of the derived filling sequences by linear regression analysis, the relationship for combined Doppler and M-mode versus radionuclide left ventricular filling was closer to the line of identity (slope = 0.98 and 0.94 using the anterior mitral leaflet and both mitral leaflets, respectively, both p = NS versus the line of identity) than was the relationship for mitral velocities alone versus radionuclide left ventricular filling (slope = 0.74, p less than 0.05 versus the line of identity). The instantaneous mitral volume flow indices more closely resemble the time course and shape of radionuclide left ventricular filling curves than do mitral velocities alone, and the application of these indices should assist the quantitative description by Doppler echocardiography of left ventricular filling.