Asymmetry of right ventricular enlargement in response to tricuspid regurgitation.

BACKGROUND: Analysis of right ventricular adaptation to tricuspid regurgitation was studied in 10 heart transplant recipients following inadvertent endomyocardial biopsy disruption of the tricuspid apparatus. METHODS AND RESULTS: Echocardiography demonstrated progressive diastolic right ventricular cavity enlargement (19.5+/-5.0 to 30.3+/-5.4 cm(2), P<0.0002), with disproportionate elongation along the midminor axis (3.5+/-0.6 to 5. 0+/-0.5 cm, P<0.001). As the right ventricle remodeled to more spherical (and less elliptical) proportions, the end-diastolic right ventricular midminor axis/long axis ratio increased significantly from 0.52+/-0.10 to 0.68+/-0.07, P<0.005. CONCLUSIONS: Ventricular enlargement due to right ventricular volume overload results in disproportionate dilation along the free wall to septum minor axis.

"Stunning" of the left atrium after spontaneous conversion of atrial fibrillation to sinus rhythm: demonstration by transesophageal Doppler techniques in a canine model.

OBJECTIVES: This study compared left atrial and left atrial appendage contraction velocities in sinus rhythm before and after a brief period of atrial fibrillation in a canine model. BACKGROUND: In patients, left atrial appendage contraction velocities measured during sinus rhythm after cardioversion from atrial fibrillation are depressed relative to left atrial appendage emptying velocities measured during atrial fibrillation, suggesting that the left atrial appendage is mechanically "stunned." METHODS: This phenomenon was studied in a canine model of acute (60 min) pacing-induced atrial fibrillation followed by spontaneous reversion to sinus rhythm using epicardial and transesophageal pulsed wave Doppler. Unique features of the model include: 1) comparison of left atrial function postconversion to baseline sinus rhythm rather than to measurements during atrial fibrillation, 2) control of the duration of atrial fibrillation and 3) elimination of the extraneous influences of direct current shock and antiarrhythmic agents, which may independently depress left atrial function. RESULTS: Hemodynamic conditions (heart rate, mean arterial pressure, cardiac output, mean pulmonary artery pressure, mean right atrial pressure and mean left atrial pressure) at baseline, during 60 min of atrial fibrillation and after reversion to sinus rhythm were constant throughout the study period. Peak left atrial contraction velocities (measured from the transmitral flow velocity profile) were significantly (p < 0.02) reduced to 64+/-22% of baseline values upon spontaneous conversion of atrial fibrillation to sinus rhythm and recovered to basal values by 20 min after resumption of sinus rhythm. Peak left atrial appendage contraction velocities were significantly (p < 0.001) reduced to 49+/-24% of baseline values upon spontaneous conversion of atrial fibrillation to sinus rhythm and recovered to basal values by 40 min after reversion to sinus rhythm. CONCLUSIONS: Even brief (60 min) periods of atrial fibrillation in normal canine hearts result in marked depression of global left atrial systolic function and regional left atrial (left atrial appendage) systolic function upon resumption of sinus rhythm. This "mechanical stunning" of left atrial systolic function appears to be more profound and of longer duration for the left atrial appendage compared with the left atrium as a whole, which may predispose the appendage to blood stasis and thrombus formation. Chronic models of atrial fibrillation need to be developed to examine the impact of longer periods of atrial fibrillation upon the magnitude and duration of postconversion left atrial "stunning."

Transesophageal echocardiographic assessment of systolic mitral leaflet displacement among patients with mitral valve prolapse.

Though qualitative transthoracic echocardiographic criteria for abnormal systolic leaflet motion are widely accepted as diagnostic characteristics of mitral valve prolapse, transesophageal echocardiographic criteria have not been evaluated against such a standard. Because transesophageal imaging planes are not identical to transthoracic imaging planes, validation of transesophageal echocardiographic criteria for mitral valve prolapse is needed. Eleven patients with mitral valve prolapse (based on physical findings and transthoracic echocardiographic criteria) and 11 healthy persons underwent prospective transesophageal echocardiography in two orthogonal imaging planes. Measurements of maximal leaflet displacement superior to the annular hinge points and mitral prolapse area subtended by the displaced mitral leaflets and the chord connecting the annular hinge points were performed in triplicate and averaged by a blinded observer. Though maximal systolic leaflet displacement was greater among patients with mitral valve prolapse than healthy subjects for both the transesophageal four-chamber (0.66+/-0.39 cm versus 0.05+/-0.11 cm, p < 0.001) and two chamber views (0.57+/-0.44 cm versus 0.20+/-0.25 cm, p < 0.04), no unique value differentiated patients with from those without mitral valve prolapse. Mitral prolapse area was greater for patients with mitral valve prolapse than for healthy subjects in both transesophageal four-chamber (1.23+/-1.18 cm2 versus 0.03+/-0.06 cm2, p < 0.02) and two-chamber views (1.73+/-1.65 cm2 versus 0.21+/-0.31 cm2, p < 0.02). Whereas a mitral prolapse area of 0.20 cm2 uniquely differentiated patients with from those without mitral valve prolapse in the four-chamber view, data overlap prevented determination of a similar diagnostic criterion for the two-chamber view. The difficulty in defining quantitative transesophageal echocardiographic criteria for mitral valve prolapse based on leaflet displacement alone suggested that the simple qualitative observation of leaflet displacement above the annular hinge points should not be used as a defining morphologic criterion for mitral valve prolapse.

Transesophageal echocardiographic assessment of the contribution of intrinsic tissue thickness to the appearance of a thick mitral valve in patients with mitral valve prolapse.

OBJECTIVES: This prospective, blinded transesophageal echocardiographic study was performed to determine the relative contributions of leaflet redundancy and overlap versus intrinsic tissue thickening as mechanisms for the apparent increase in diastolic thickness of the mitral valve. BACKGROUND: Increased diastolic thickness of the mitral valve has been identified as an echocardiographic feature that predicts subsequent adverse sequelae in patients with mitral valve prolapse (MVP). METHODS: Eleven patients with clinical and transthoracic echocardiographic evidence of MVP and 11 age-matched control subjects underwent protocol transesophageal echocardiography to image the mitral valve in two orthogonal planes and to measure its thickness in systole and diastole. RESULTS: Maximal diastolic width of the slack, unloaded anterior leaflet was significantly greater in patients with MVP than in control subjects (mean +/- SD: 0.64 +/- 0.20 cm vs. 0.30 +/- 0.04 cm, p < 0.001). Similarly, diastolic posterior leaflet width was greater in patients with MVP (0.67 +/- 0.39 cm vs. 0.31 +/- 0.06 cm, p < 0.01). In contrast, minimal systolic width of the distended pressure-loaded mitral valve was not significantly different between patients with MVP and control subjects for either the anterior (0.22 +/- 0.05 cm vs. 0.20 +/- 0.04 cm, p = NS) or the posterior (0.25 +/- 0.07 cm vs. 0.24 +/- 0.05 cm, p = NS) leaflets. The percent change in leaflet width from diastole to systole (% delta W), an index of the contribution of dynamic factors (e.g., leaflet redundancy and overlap) to the apparent increase in diastolic leaflet thickness, was significantly greater in patients with MVP than in control subjects for both the anterior (% delta W 62 +/- 13% vs. 34 +/- 16%, p < 0.001) and the posterior (% delta W 54 +/- 19% vs. 22 +/- 21%, p < 0.005) leaflets. CONCLUSIONS: The apparent increase in diastolic mitral leaflet thickness in patients with MVP versus control subjects is largely attributable to dynamic factors such as leaflet redundancy, overlap and deformation. During diastole, when the mitral leaflets are slack and unstressed, the leaflets appear markedly thickened in patients with MVP. In contrast, during systole, when developed intraventricular pressure distends the leaflets, causing them to stretch and balloon into the left atrium, the intrinsic tissue thickness is much less than that measured in diastole. These findings have important implications for the morphologic criteria used to diagnose MVP and the potential pathophysiologic mechanisms for adverse sequelae in this syndrome.

Pressure and volume loading of the right ventricle have opposite effects on left ventricular ejection fraction.

BACKGROUND: Left ventricular ejection fraction has been reported to be depressed in patients with right ventricular volume overload (RVVO) due to Ebstein's anomaly and uncomplicated atrial septal defect, whereas it is usually preserved in right ventricular pressure overload (RVPO) due to congenital pulmonic stenosis. In the present study, we examined the hypothesis that the differential timing of active displacement of the ventricular septum into the left ventricle in RVPO (end systole) and RVVO (end diastole) results in opposite effects of RVPO and RVVO on left ventricular ejection fraction. METHODS AND RESULTS: Ten patients with severe tricuspid regurgitation after tricuspid valve resection for endocarditis and 10 patients with primary pulmonary hypertension were studied as models of isolated RVVO and RVPO, respectively. Left ventricular ejection fraction, end-diastolic volume, and regional systolic shortening were measured with the use of echocardiographic techniques in these 20 patients and 10 healthy control subjects. In RVPO, despite marked underfilling of the left ventricle relative to the healthy control subjects (end-diastolic volume, 48 +/- 26 versus 77 +/- 20 mL; P < .02), left ventricular ejection fraction was similar to that of the control subjects (56 +/- 5% versus 60 +/- 4%; P = .07) and only 1 of 10 RVPO patients had an ejection fraction of less than 50%. In contrast, in RVVO the left ventricle was volume replete (end-diastolic volume, 84 +/- 26 versus 77 +/- 20 mL; P = NS), but left ventricular ejection fraction was significantly depressed (51 +/- 4% versus 60 +/- 4%, P < .001) compared with the control subjects, and 4 of 10 RVVO patients had an ejection fraction of less than 50%. Analysis of systolic fractional shortening along two perpendicular short-axis diameters and the mutually orthogonal long axis demonstrated isolated augmentation of fractional shortening in the ventricular septal-to-posterolateral free wall dimension in RVPO (47.4 +/- 13.7% versus 34.2 +/- 13.1%, P < .05) and isolated depression of fractional shortening along that same dimension in RVVO (13.7 +/- 11.8% versus 34.2 +/- 13.1%, P < .001) compared with the control subjects. CONCLUSIONS: End-systolic leftward ventricular septal shift in RVPO results in isolated augmentation of systolic shortening in the septal-to-free wall dimension, whereas end-diastolic leftward ventricular septal shift in RVVO results in isolated reduction in systolic shortening in the septal-to-free wall dimension. As a result, despite relative underfilling of the left ventricle in RVPO, resting left ventricular ejection fraction is preserved, whereas ejection fraction is depressed for the volume-replete left ventricle of patients with RVVO.

Effects of contrast media on coronary hemodynamics and myocardial metabolism.

RATIONALE AND OBJECTIVES: This study was designed to compare the effects of ionic contrast medium (CM), Renografin-76 (R76), and nonionic CM, Omnipaque-350 (OM350), on coronary hemodynamics and myocardial metabolism. METHODS: In 10 open-chest, atrial-paced dogs, 4 mL of R76 and OM350 were injected into the left anterior descending coronary artery. Coronary blood flow (CBF), myocardial oxygen consumption (MVO2), lactate extraction (LE), left ventricular (LV) dp/dt, and aortic systolic pressure (AOP) were measured. RESULTS: The maximal CBF changes caused by OM350 and R76 were 23.7 +/- 3.3 mL/minute and 18.3 +/- 3.3 mL/minute (NS), respectively. OM350 produced an increase in LV dp/dt by 378 +/- 85 mm Hg/second, which was different from -244 +/- 65 mm Hg/second by R76 (P < .05). The changes in MVO2 and LE after OM350 injection were 2.6 +/- 0.6 mL/minute and 10.2 +/- 5 microM/minute, respectively; those were different from -0.1 +/- 0.4 mL/minute, and -7.7 +/- 5.1 microM/minute after R76 injection (P < .05). CONCLUSION: Although both agents increased CBF, they appeared to act by different mechanisms. That a direct coronary vasodilator effect is the main action of R76 on coronary vascular response is suggested by decreasing myocardial contractility and oxygen consumption. However, OM350, by enhancing both parameters, may augment CBF at least in part by autoregulation.

Effect of acute pericardial tamponade on the relative contributions of systolic and diastolic pulmonary venous return: a transesophageal pulsed Doppler study.

The effect of acute pericardial tamponade on pulmonary venous return was assessed by transesophageal pulsed Doppler echocardiography. In 14 open-chest anesthetized dogs peak pulmonary venous flow velocities in systole (VJ) and in diastole (VK) were measured during apnea and atrial pacing while acute tamponade was induced by intrapericardial instillation of 0.9% sodium chloride solution. Before intravascular volume expansion, induction of acute tamponade resulted in a significant decline in VK (43 +/- 17 to 19 +/- 8 cm/sec; p < 0.05) but no change in VJ or the ratio VJ/VK. After intravascular volume expansion, induction of acute tamponade resulted in significant reductions in VJ (43 +/- 9 to 29 +/- 10 cm/sec; p < 0.001) and VK (37 +/- 19 to 15 +/- 11 cm/sec; p < 0.001). The effect was disproportionately greater on VK, however, resulting in a significant increase in VJ/VK (1.51 +/- 0.84 to 2.58 +/- 1.41; p < 0.001). The disproportionate effect of acute tamponade on VK suggests that increased pericardial pressure directly constrains diastolic filling of the left atrium as a conduit to the left ventricle and that it does not decrease the systolic and diastolic phases of pulmonary venous return uniformly. Intravascular volume expansion increases cardiac output before acute tamponade, but during acute tamponade it amplifies the disproportionate impact of increased pericardial pressure on left ventricular diastolic filling as the left ventricle is constrained within the fluid-filled pericardial sac.

Impairment of myocardial vascular responsiveness after transient myocardial ischemia and reperfusion.

Coronary vascular responses after brief periods of myocardial ischemia are impaired. Whereas some studies suggest that the ischemic insult selectively depresses endothelium-dependent vasodilator mechanisms, other studies indicate that even responses to direct vascular smooth-muscle relaxants such as adenosine may be decreased. This study was undertaken to measure regional myocardial blood flow (RMBF) responses to adenosine (a direct coronary vasodilator) and serotonin (an indirect, endothelium-dependent vasodilator) in myocardium subjected to regional ischemia followed by reperfusion. Temporary regional ischemia was achieved by 20 minutes of occlusion of the left anterior descending coronary artery (LAD) followed by 20 minutes of reflow in 10 open-chest anesthetized dogs. In the left circumflex coronary artery (LCX) territory, which served as a nonischemic control, RMBF (measured with radioactive microspheres) increased significantly in response to left atrial infusions of adenosine (1.29 +/- 0.27 to 3.89 +/- 3.89 +/- 2.15 ml/min/gm; p < 0.001) and serotonin (1.29 +/- 0.27 to 3.29 +/- 1.49 ml/min/gm; p < 0.001) and the percent reduction in coronary vascular resistance (% delta CVR) was comparable for these two pharmacologic probes (65% +/- 26% vs 62% +/- 19%; difference not significant [NS]). In contrast, in the myocardium supplied by the LAD, which was subjected to ischemia followed by reperfusion, the augmentation of RMBF by adenosine (1.07 +/- 0.29 to 1.82 +/- 1.35 ml/min/gm; p < 0.001) and serotonin (1.07 +/- 0.29 to 2.37 +/- 1.21 ml/min/gm; p < 0.001) was blunted.(ABSTRACT TRUNCATED AT 250 WORDS)

Right ventricular volume overload results in depression of left ventricular ejection fraction. Implications for the surgical management of tricuspid valve disease.

BACKGROUND: Right ventricular volume overload (RVVO) occurring in conditions such as Ebstein's anomaly may result in depression of left ventricular ejection fraction (LVEF). This study tests this hypothesis by measuring LVEF in 10 patients with RVVO due to tricuspid valve resection for isolated tricuspid valve endocarditis and in 10 age-matched healthy persons. METHODS AND RESULTS: When the modified Simpson's rule was applied to echocardiographic images, LVEF for patients with RVVO measured significantly lower than for age-matched healthy subjects (51 +/- 4% versus 60 +/- 4%, P < .0001). Depression of LVEF does not result simply from reduced venous return to the left ventricle, since left ventricular end-diastolic volume was not significantly different between patients with RVVO and age-matched healthy persons (84 +/- 26 versus 77 +/- 20 mL, NS). Possible explanations for the depression in LVEF may relate to the decreased relative contribution of left atrial systole to left ventricular filling (demonstrated by transmitral pulsed Doppler) or to the mechanical effects of ventricular septal paradox (demonstrated by the abnormal leftward ventricular septal flattening and increase in short-axis cavity eccentricity at end diastole, which returns to normal at end systole) in patients with RVVO. CONCLUSIONS: These findings suggest that surgical excision of the tricuspid valve results in isolated RVVO, which creates not only diastolic overload of the right heart but also depression of LVEF.

Alterations in transmitral flow dynamics in patients with early mitral valve closure and aortic regurgitation.

Ten patients with severe aortic regurgitation (AR) and early diastolic mitral closure demonstrated by M-mode echocardiography (group I) were compared to 10 age-matched patients with severe AR and normal timing of mitral closure to quantify the accompanying alterations in transmitral flow dynamics assessed by pulsed Doppler echocardiography. Transmitral filling period expressed as a fraction of the time available for diastolic filling was significantly shortened in group I patients relative to group II patients (0.50 +/- 0.10 vs 1.04 +/- 0.09, p < 0.001) because early mitral closure truncated transmitral filling and obliterated the atrial contribution to left ventricular filling. The rapid diastolic filling period normalized for the time available for diastolic filling was also shortened for group I patients relative to group II patients (0.49 +/- 0.11 vs 0.64 +/- 0.19; p < 0.05). Early mitral closure in group I patients was functionally incomplete because 9 of the 10 patients had diastolic mitral regurgitation, which was not detected in any patients in group II (p < 0.001). Thus the group I patients with early mitral closure and severe aortic regurgitation had truncated transmitral inflow and diastolic mitral regurgitation. These patients had higher pulmonary capillary wedge pressures (32 +/- 6 vs 11 +/- 9 mm Hg; p < 0.001) and more severe functional limitation (p < 0.001) than group II patients.

Dose-response study of intravenous torsemide in congestive heart failure.

In a double-blind dose-response study, 49 patients with New York Heart Association functional class III or IV heart failure were randomized to receive a single intravenous dose of 5, 10, or 20 mg torsemide or 40 mg furosemide. Torsemide produced dose-related decreases in body weight and increases in sodium and chloride excretion and urine volume. With the 20 mg dose of torsemide and the 40 mg dose of furosemide, body weight decreased significantly relative to baseline, and total and fractional 24-hour urinary excretion of sodium, chloride, and potassium and urine volume increased significantly. The 10 mg torsemide dose also produced a significant increase in urine volume. The results indicate that intravenous torsemide is effective for the acute treatment of sodium and fluid retention resulting from moderate to severe congestive heart failure.

The effects of loading changes on intraoperative Doppler assessment of mitral regurgitation.

Anesthetic agents may significantly alter the patient's blood pressure, and thus affect the intraoperative assessment of mitral regurgitation. This study examined the impact of an increase in afterload on a variety of parameters thought to reflect the severity of mitral regurgitation, and related them to changes in hemodynamic parameters. Twenty-four patients with mitral regurgitation undergoing cardiac surgery were studied. Following the induction of anesthesia, color-flow mapping of the entire left atrium was performed, and pulmonary vein flow was then measured. Phenylephrine was administered to increase the patients' blood pressures to their preoperative values, and the assessment was repeated. Regurgitant jet area increased 56% (482 +/- 405 v 750 +/- 440 mm2 P < 0.001), and there were significant reductions in systolic pulmonary venous velocity (0.33 +/- 0.17 v 0.18 +/- .31 m/s P < .01) with increases in diastolic flow (0.43 +/- 12 v 0.58 +/- 0.18 m/s P < .001). These changes in pulmonary venous flow were not related to the changes in the driving force across the incompetent mitral valve. Also, an additional six patients developed systolic flow reversal after phenylephrine administration. Intraoperative hemodynamic variations can significantly alter the apparent severity of mitral regurgitation, and this factor must be considered during decision making.

Echocardiographic diagnosis of paradoxical embolism and the potential for right to left shunting.

Echocardiographic techniques are useful in establishing the presumptive clinical diagnosis of paradoxical embolism. Once a clinical diagnosis of systemic embolism has been established and a potential systemic venous source for embolic material has been diagnosed, echocardiographic (and particularly transesophageal echocardiographic techniques) can readily establish the presence or absence of an intracardiac communication and can help define the potential for right to left shunting across that communication (using saline contrast techniques). Except for the rare circumstance where echocardiography has been used to actually image paradoxical embolization in progress (such as may occur during intraoperative monitoring), the technique can only show the potential for such a mechanism for systemic embolization. Because patency of the foramen ovale is a common anatomic variant (occurring in approximately 25% of subjects) and transesophageal contrast echocardiography will show at least transient right to left shunting in most patients with patent foramen ovale, a mechanistic relationship between such findings and the occurrence of a systemic embolic event cannot be immediately inferred. Clinical assessment of alternative mechanisms for systemic embolization is required to judge the likelihood that the potential for paradoxical embolization is, in fact, the cause for systemic embolism in a given patient.

Transthoracic and transesophageal echocardiography for the evaluation of cardiac tumors, thrombi, and valvular vegetations.

Echocardiography is commonly used for the detection, assessment, and diagnosis of intracardiac masses. Since the introduction of M-Mode ultrasound in 1954, the subsequent development of two-dimensional Doppler, and transesophageal echocardiographic techniques have shown clinical efficacy in the evaluation of intracardiac pathology. The various presentations of cardiac tumors, thrombi, and valvular vegetations can pose a diagnostic challenge. In addition, once a diagnosis is established, data regarding risk stratification and prognosis are often required for further management. Echocardiography can serve these clinical needs.