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This study compares remifentanil/propofol (remi/prop) with isoflurane/fentanyl (iso/fen) anesthesia to determine which provides the greater hemodynamic stability, lesser myocardial ischemia, and morbidity with better postoperative outcomes after carotid endarterectomy. Sixty patients undergoing unilateral carotid endarterectomy were randomized to receive either a remi/prop or iso/fen anesthetic. Hemodynamic variables were recorded during the surgical procedure. In addition, transesophageal echocardiography was used to assess evidence of intraoperative regional wall motion abnormalities suggestive of cardiac ischemia. Emergence and extubation times, recovery from anesthesia, hemodynamic instability, nausea, vomiting, and pain in post anesthesia recovery, discharge delays, ICU admittance, hospital discharge, and preoperative and postoperative troponin levels were compared using appropriate statistical methods with P < 0.05 considered significant. The groups were demographically alike. Hemodynamic variables were similar during intubation and throughout surgery. Twenty-two percent of patients receiving iso/fen developed intraoperative regional wall motion abnormalities suggestive of ischemia, whereas no remi/prop patients had changes (P < 0.05). There was no difference in ST-T wave changes after surgery, and no patient had an elevation in troponin I levels. Postoperative variables were similar except that patients who received iso/fen had lower Stewart recovery scores during the first 15 minutes after post anesthesia care unit admission and a higher incidence of nausea and vomiting the day after surgery, whereas patients receiving remi/prop had discharge delays secondary to hypertension. ICU admittance, time to first void, oral intake, and time to hospital discharge were similar between the groups. At 9 times the cost of an iso/fen anesthesia technique, remi/prop offers little advantage over inhalational anesthesia for carotid endarterectomy.

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.

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."

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.

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.

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.

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.

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.

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)

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.

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.

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.

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 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.

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.

Variability of regional myocardial blood flow (RMBF) during reflow after 20 minutes of left anterior descending (LAD) coronary occlusion was measured by the radioactive microsphere technique in nine open-chest dogs. Preocclusion RMBF in the LAD territory was 0.89 +/- 0.27 ml/min/gm. Twenty minutes of LAD occlusion resulted in uniform and severe ischemia (RMBF < or = 0.25 ml/min/gm). After 1 minute of reperfusion, RMBF in the LAD territory rose to 3.48 +/- 1.88 ml/min/gm, and declined to 1.06 +/- 0.29 ml/min/gm after 20 minutes of reperfusion. RMBF variance increased significantly from 0.046 preocclusion to 0.2857 after 1 minute of reperfusion (p < 0.01) and declining to 0.086 after 20 minutes of reperfusion. By contrast, RMBF variance analysis of myocardial segments from the nonischemic left circumflex territory exhibited no significant change throughout the experiment. In any given dog this heterogeneous reperfusion of previously ischemic tissue resulted in a disorganized topography of blood flow rates. Myocardium with relatively high regional flow was intermingled with islands of tissue with relatively low blood flow. In conclusion, despite a relatively uniform and severe myocardial ischemic insult, the subsequent initial hyperemic response during reperfusion exhibits marked spatial heterogeneity. The juxtaposition of myocardial regions exposed to vastly differing rates of oxygen delivery and washout of toxic metabolites may set the stage for nonuniform recovery of myocardial function.

Objectives: The purpose of this study was to estimate the prevalence of potential right to left interatrial shunting and to quantify the morphologic characteristics of the fossa ovalis in adults without a prior history of stroke or systemic embolism., Background: Paradoxic embolization through a patent foramen ovale is an important cardiac mechanism for embolic stroke. Although anatomic and physiologic data obtained by transesophageal echocardiography increase the frequency of demonstration of potential cardiac sources of systemic embolism and occasionally can conclusively demonstrate the mechanism for embolic stroke, the prevalence and prognostic implications of these findings in neurologically healthy persons are still being actively investigated., Methods: Intraoperative transesophageal saline contrast echocardiography was performed on 50 adult patients without prior history of stroke or systemic embolism who were undergoing elective cardiovascular surgery., Results: No patient had a manifest atrial septal defect by right heart oximetric measurements or transesophageal Doppler echocardiographic examination. Eleven of the 50 patients demonstrated right to left atrial passage of saline contrast medium during apnea or after release of 20-cm H2O positive airway pressure, signifying patency of the foramen ovale. These 11 patients with a patent foramen ovale had increased total excursion of the flap valve (septum primum) of the fossa ovalis (1.3 +/- 0.7 cm) compared with findings in the 39 patients without a patent foramen ovale (0.3 +/- 0.5 cm, p < 0.001). All patients with a patent foramen ovale exhibited some mobility of the septum primum and 73% of these patients had > or = 1 cm total excursion of the septum primum. In contrast, 56% of patients without a patent foramen ovale exhibited no motion of the septum primum out of the plane of the atrial septum. The maximal diameter of the fossa ovalis was greater in patients with (1.4 +/- 0.4 cm) than in patients without (1.0 +/- 0.3 cm, p < 0.003) a patent foramen ovale., Conclusions: Hypermobility of the septum primum and enlargement of the fossa ovalis are morphologic findings that occur in the presence of a patent foramen ovale.

Objectives: We postulated that ventricular arrhythmias may arise from the heterogeneous washout of ischemic metabolites. Our objective was to investigate the distribution of extracellular potassium concentration ([K+]o) during myocardial ischemia and reperfusion and to correlate this distribution with regional differences in myocardial blood flow., Background: Our previous study showed that reperfusion after a brief period of ischemia resulted in heterogeneous reflow of the ischemic myocardium., Methods: The changes in regional myocardial blood flow, midmyocardial [K+]o and electrogram duration were quantitated in 14 dogs undergoing 20 min of left anterior descending coronary artery occlusion and 1 min of reperfusion. Regional myocardial blood flow was measured by using 15-microns radioactive microspheres in 1- to 1.5-g full thickness myocardial samples. The [K+]o was measured with intramyocardial K(+)-sensitive electrodes., Results: During coronary occlusion, the ischemic zone exhibited a reduction in regional blood flow to 0.13 +/- 0.06 ml/g per min and increases in [K+]o to 9.3 +/- 2.6 mmol/liter and electrogram duration to 131.8 +/- 38.6% of control. Heterogeneous reduction in regional blood flow at various sites in the ischemic zone had fair correlations with variable increases in [K+]o (r = -0.70) and electrogram duration (r = -0.75). During min 1 of reperfusion, regional blood flow ranged from two to more than seven times baseline, resulting in a disorganized spatial distribution of perfusion with islands of high and low blood flows. Associated with the heterogeneous early reperfusion regional myocardial blood flow, [K+]o and electrogram duration changed at different rates toward normal. Whereas correlation between regional blood flow and [K+]o or standardized electrogram duration was fair during ischemia, this correlation was poor during early reperfusion., Conclusions: Spatial heterogeneity in regional myocardial blood flow during myocardial ischemia and early reperfusion is associated with heterogeneity in [K+]o and electrophysiologic characteristics, which in turn may play an important role in the genesis of arrhythmias arising from the ischemic and reperfused myocardium.

In a sample of 114 patients, 6 patients developed hypertension while taking tricyclic antidepressants. All these patients were diagnosed as having panic disorder, with or without major depression. Half of the 6 patients had a previous diagnosis of hypertension, which had been well controlled by antihypertensive drugs for years. A comparison group of patients with major depression, who had never had panic attacks, had no cases of hypertension induced by these antidepressants. These findings raise the possibility that patients who have panic disorder may experience cardiovascular disregulation that increases their risk for antidepressant-induced hypertension.

To compare the effects of isolated right ventricular pressure and volume overload on left ventricular diastolic geometry and filling, 11 patients with primary pulmonary hypertension, 11 patients with severe tricuspid regurgitation due to tricuspid valve resection and 11 normal subjects were studied with use of Doppler echocardiographic techniques. Right ventricular systolic overload in primary pulmonary hypertension resulted in substantial leftward ventricular septal shift that was most marked at end-systole and early diastole and decreased substantially by end-diastole. Right ventricular diastolic overload after tricuspid valve resection resulted in maximal leftward ventricular septal shift at end-diastole sparing end-systole and early diastole. The early diastolic distortion of left ventricular geometry associated with right ventricular pressure overload resulted in prolongation of isovolumetric relaxation of the left ventricle (129 +/- 39 ms) and a reduction in early diastolic filling compared with values in normal subjects. Late diastolic distortion of left ventricular geometry associated with right ventricular volume overload had no influence on the duration of left ventricular isovolumetric relaxation (52 +/- 32 ms) but caused a reduction in the atrial systolic contribution to late diastolic filling of the left ventricle compared with values in normal subjects. In patients with right ventricular pressure overload, 52 +/- 16% of left ventricular filling occurred in early diastole compared with 78 +/- 11% in patients with right ventricular volume overload (p less than 0.001). The differential effects of systolic and diastolic right ventricular overload on the pattern of left ventricular filling appear to be related to the timing of leftward ventricular septal displacement.

The impact of pericardial constraint on patterns of left ventricular filling was measured by transesophageal pulsed Doppler echocardiography in 30 patients undergoing elective nonvalvular cardiac surgery. Peak early left ventricular filling velocity increased from 0.52 +/- 0.11 to 0.56 +/- 0.15 m/s (p less than 0.05) and early left ventricular filling fraction increased from 60 +/- 9% to 65 +/- 9% (p less than 0.005) after pericardiotomy. The study group was retrospectively subdivided into two groups based on the prepericardiotomy mean right atrial pressure, an index of intrapericardial pressure and hence pericardial constraint. In 13 patients with a mean right atrial pressure less than 6 mm Hg, no significant changes in early left ventricular filling were evident after pericardiotomy. In 17 patients with a mean right atrial pressure greater than or equal to 6 mm Hg indicative of a greater degree of pericardial constraint before pericardiotomy, significant increases in peak early filling velocity (0.52 +/- 0.13 to 0.57 +/- 0.19 m/s, p less than 0.05), peak early filling rate (4.29 +/- 0.67 to 4.66 +/- 0.86 stroke volumes/s, p less than 0.05) and early left ventricular filling fraction (57 +/- 7% to 63 +/- 8%, p less than 0.001) were measured after pericardiotomy. Thus, the pericardium does constrain early left ventricular filling and its effects are more pronounced in patients with an elevated right atrial pressure.

The optimal visualization of the atrial septum and fossa ovalis by transesophageal echocardiography was utilized to demonstrate saline contrast transit across the atrial septum and to relate it to the motion of the flap valve (septum primum) of the fossa ovalis. In three cases, three distinct mechanisms of right to left interatrial shunting in the absence of right ventricular systolic hypertension were identified: 1) transient spontaneous reversal of the left to right atrial pressure differential with each cardiac cycle; 2) sustained elevation of right atrial pressure above left atrial pressure induced by respiratory maneuvers; and 3) aberrant flow redirection across the foramen ovale due to a large right atrial mass. Any of these three mechanisms may be operative during paradoxic embolism in the absence of elevation of right ventricular pressures.

This study reports the intraoperative use of contrast and Doppler echocardiography techniques to diagnose patent foramen ovale (PFO). Fifty patients without known atrial septal defects undergoing elective cardiovascular surgery were studied. A 5-MHz esophageal echocardiographic probe was used to image the fossa ovalis (FO) and 10 ml agitated saline was injected into the right atrium during apnea. Echocardiographic contrast was then injected during end-inspiration at 20-cmH2O airway pressure. When opacification of the right atrium was complete, the airway pressure was released. During these maneuvers, color and pulsed-wave Doppler interrogation of the atrial septum were also performed. Right-to-left passage of saline contrast across the interatrial septum was seen in 11 of 50 patients (22%). Doppler echocardiography demonstrated a PFO in 2 patients without contrast evidence of shunting. Thus, the combination of contrast and Doppler echocardiography identified a 26% (13 of 50) prevalence of PFO, approximating the previously reported autopsy rate of 25%. These contrast and Doppler techniques may be useful in detecting patients at risk for paradoxical emboli and in identifying candidates for closure of the PFO.

Patients undergoing valvulectomy for isolated tricuspid valve endocarditis offer the unique opportunity to study the effects of acquired right ventricular volume overload on left ventricular filling in persons free of pulmonary hypertension and preexisting left heart disease. Eleven patients who had undergone total or partial removal of the tricuspid valve were compared with 11 age-matched control subjects; Doppler echocardiographic techniques were used to quantify changes in left ventricular filling and to relate them to changes in left ventricular and left atrial geometry caused by right ventricular and right atrial distension. The late diastolic fractional transmitral flow velocity integral, a measure of the left atrial contribution to left ventricular filling, was significantly decreased in patients undergoing tricuspid valvulectomy compared with control subjects (0.22 +/- 0.11 versus 0.32 +/- 0.09; p less than 0.04). Severe tricuspid regurgitation in these patients resulted in marked right atrial distension, reversal of the normal interatrial septal curvature and compression of the left atrium such that left atrial area was significantly smaller than in control subjects (5.9 +/- 2.2 versus 8.6 +/- 1.2 cm2/m2; p less than 0.005). Acting as a receiving chamber, the left ventricle was maximally compressed by the volume-overloaded right ventricle in late diastole, coincident with the timing of atrial systole, resulting in a significant increase in the left ventricular eccentricity index compared with that in control subjects (1.35 +/- 0.14 versus 1.03 +/- 0.1; p less than 0.001). Thus, right ventricular volume overload due to severe tricuspid regurgitation results in left heart geometric alterations that decrease left atrial preload, impair left ventricular receiving chamber characteristics and reduce the atrial contribution to total left ventricular filling.

Pulsed Doppler mapping of the flow disturbance of mitral insufficiency is commonly employed to estimate the severity of regurgitation. We re-examined the customary pulsed Doppler criterion of relative depth of jet penetration (MR ratio) in 50 patients undergoing left ventriculography and found a modest correlation (r = 0.70) between Doppler and angiographic estimates of regurgitant grade. The MR ratio did not provide statistically significant separation between adjacent angiographic grades 1+ to 3+ (scale 0 to 4+). However, when the data were re-analyzed for the subset of 36 patients with pure mitral regurgitation the correlation between Doppler and angiographic estimates of regurgitant grade improved dramatically (r = 0.88) and MR ratio provided statistically significant separation between all angiographic grades with the sole exception of the distinction between 1+ and 2+ regurgitation. The presence of restriction of the regurgitant orifice in the remaining 14 patients with relative mitral inflow obstruction may result in a nozzle effect on the regurgitant jet which alters the relationship between depth of jet penetration and severity of regurgitation. In this latter group of patients independent pulsed Doppler mapping techniques may provide inaccurate estimates of the angiographic severity of mitral regurgitation.

Since the mechanism by which oxygen reduces infarct size is not yet completely understood, we tested the hypothesis that breathing 100% oxygen may alter regional myocardial blood flow. In 23 anaesthetised open-chest dogs with acute occlusions of the left anterior descending coronary artery or of its apical branch, regional myocardial blood flow was determined by the microsphere technique at 15 and 30 min following coronary artery occlusion. Fifteen treated dogs were ventilated with 100% oxygen beginning 17 min after occlusion (ie, after the first determination of regional myocardial blood flow) and continuing until the end of the experiment, while the other 8 dogs served as controls and were ventilated continuously with room air. In treated dogs, following the administration of 100% oxygen, transmural flow at sites remote from the distribution of the occluded vessel (nonischaemic sites) decreased from 121 +/- 5 before oxygen to 108 +/- 6 cm3 . min-1 . 100g-1 (P less than 0.05). However, in the ischaemic sites it increased from 28 +/- 3 before oxygen to 32 +/- 3 cm3 . min-1 . 100g-1 (P less than 0.05). In the control dogs transmural flow, 15 and 30 min after occlusion, was, in nonischaemic sites, 118 +/- 7 and 125 +/- 10 cm3 . min-1 . 100g-1 NS, and in the ischaemic sites 27 +/- 4 and 25 +/- 3 cm3 . min-1 . 100g-1 NS, respectively. Thus, ventilation with 100% oxygen can augment perfusion of the ischaemic myocardium and this may be, in part, the mechanism by which it reduces infarct size.

Two siblings with hypertrophic cardiomyopathy developed spontaneous complete heart block requiring permanent pacemaker implantation at similar ages (29 and 33 years). The clinical, morphological, and haemodynamic expressions of hypertrophic cardiomyopathy differed considerably in these two patients. The sister had severe functional limitation due to dyspnoea, pronounced and diffuse left ventricular hypertrophy (maximum ventricular septal thickness of 41 mm), and left ventricular outflow obstruction (peak subaortic gradient of 75 mm Hg under basal conditions). In contrast the brother was symptom free, had only modest left ventricular hypertrophy which was confined to the anterior ventricular septum (maximal thickness of 16 mm), and had no echocardiographic evidence of subaortic obstruction. These dissimilar findings in siblings with hypertrophic cardiomyopathy suggest that the predisposition to develop complete heart block was probably genetically transmitted, although it was unrelated to the phenotypic and clinical expression of the disease.

Of 965 patients with hypertrophic cardiomyopathy evaluated by echocardiography at the National Institutes of Health during a 7-year period, 23 (2%) had a nonobstructive morphologic form, in which wall thickening occurred predominantly in the apical (distal) portion of the left ventricle. The patients ranged in age from 15 to 69 years (mean, 37) and were predominantly male (14 patients) and white (only 1 was of oriental descent). Fifteen patients had significant functional limitation, which was usually caused by exertional dyspnea and fatigue. Several electrocardiographic patterns were identified in the study group, but only 4 of these patients showed "giant" negative T waves. Only 3 patients had a morphologic expression of apical hypertrophy that closely resembled that described in Japanese patients--that is, hypertrophy that was particularly localized and confined to the true left ventricular apex (2 of these patients had giant negative T waves). Hence, hypertrophy located predominantly in the distal left ventricle was uncommon in our primarily North American patient population with hypertrophic cardiomyopathy. Most of our patients showed morphologic and clinical features that were dissimilar to those found previously in Japanese patients with apical hypertrophy.

Haemolytic anaemia complicating Mycoplasma infection has usually been attributed to IgM cold agglutinins. This report describes a patient with pneumonia due to Mycoplasma pneumoniae in whom severe haemolysis persisted despite declining thermal amplitude and titre of cold agglutinins as the infection resolved. Class-specific anti-globulin (Coombs) testing defined an IgG warm agglutinin coating the patient's erythrocytes that was distinct from the IgM cold agglutinin identified by Sephadex G-200 gel filtration and dithiothreitol inactivation. Monoclonal IgM(gamma) and IgK(k) circulating proteins were identified and immuno-electrophoresis of the cold agglutinin-containing cryoglobulin fraction identified the cold agglutinin as an IgM(gamma). In this patient initially presumed to have cold agglutinin induced haemolysis secondary to Mycoplasma infection, an IgG warm agglutinin was identified as the aetiology for the patient's haemolysis, underscoring the clinical relevance of careful evaluation of the mechanism of haemolysis accompanying Mycoplasma pneumonia.

Fluttering of the anterior mitral leaflet may be absent in patients with moderate to severe aortic regurgitation (AR), suggesting that the volumetric severity of AR alone does not determine the presence or absence of abnormal diastolic mitral valve motion. Fifteen patients with moderate to severe AR and normal mitral valves, 9 of whom demonstrated anterior mitral leaflet fluttering, were studied to elucidate the determinants of abnormal anterior mitral leaflet motion in these patients. Pulsed Doppler mapping of the flow-velocity disturbance of AR demonstrated its presence in the third of the left ventricular outflow tract adjacent to the anterior mitral leaflet in 8 of 9 patients with anterior mitral leaflet fluttering and none of the 6 patients without anterior mitral leaflet fluttering (p less than 0.02). The impact of this regurgitant jet on early diastolic transmitral inflow was examined with pulsed Doppler in these 2 groups of patients with AR and in age-matched control subjects. Deceleration of early diastolic transmitral filling was slower in patients with AR and anterior mitral leaflet fluttering than in age-matched control subjects (283 +/- 107 vs 457 +/- 176 cm/s2, p less than 0.02), whereas it was not significantly different from controls in AR patients without anterior mitral leaflet fluttering. This resulted in significant prolongation of the duration of early diastolic transmitral filling in patients with AR and anterior mitral leaflet fluttering (297 +/- 93 vs 203 +/- 44 ms for age-matched control subjects, p less than 0.02), which was not observed in patients with AR who did not have anterior mitral leaflet fluttering.(ABSTRACT TRUNCATED AT 250 WORDS)

Colour flow Doppler maps the extent of the flow velocity disturbance of aortic regurgitation onto the two dimensional echocardiographic image of the left ventricular cavity. The spatial extent of this flow velocity disturbance expressed as a percentage of end diastolic left ventricular cavity area (CD%) was compared to regurgitant fraction (RF), measured volumetrically, in nine open chest dogs with varying degrees of surgically created aortic regurgitation (RF 0-85%). Right heart bypass controlled venous return to the left atrium and hence net left ventricular output, while total left ventricular output was measured with an aortic electromagnetic flow probe under various loading conditions, achieving mean diastolic transvalvular pressure gradients of 23-114 mm Hg, net left ventricular outputs of 750-3000 ml.min-1 and diastolic filling periods of 162-320 ms. A linear correlation between CD% and RF (r = 0.89) was demonstrated over this wide range of loading conditions. At a given transvalvular diastolic pressure gradient [68(SD9) mm Hg] CD% was linearly proportional to regurgitant aortic orifice area (r = 0.87). Thus CD% is proportional to the volumetric severity of aortic regurgitation under a wide range of haemodynamic conditions and varies appropriately with regurgitant aortic orifice area when diastolic transvalvular pressure gradient is held constant. The application of these principles to the non-invasive quantitation of valvular regurgitation by colour Doppler appears feasible.

Osmotic diuresis resulting from the administration of angiographic contrast poses the potential threat of marked volume losses obligated by the renal excretion of non-reabsorbable solute. We prospectively assessed urinary excretion of solute and water following cardiac angiography in 14 euvolemic subjects without preexisting renal disease, by a protocol that allowed each patient to serve as his own control. During the initial 6 h after the beginning of angiography, contrast administration resulted in increased total osmolar excretion from a control rate of 0.79 +/- 0.09 to 1.09 +/- 0.09 mOsm/min (P less than .05) with a return to control values thereafter. Surprisingly, sodium, potassium, and chloride excretion rates did not differ significantly from control values. After subtraction of the molar contribution of electrolytes, urea, and creatinine from the total osmolar excretion rate, it was apparent that the "residual osmolar excretion rate" of 0.48 +/- 0.05 mOsm/min was markedly elevated over the control value of 0.11 +/- 0.05 mOsm/min (P less than .01), reflecting the excretion of contrast agent. Despite the marked osmotic diuresis, urine output during this period (3.9 +/- 0.2 cc/min) did not differ significantly from the control value of 4.0 +/- 0.3 cc/min. We conclude that marked volume losses are not a necessary concomitant of contrast-induced osmotic diuresis in the euvolemic cardiac patient without renal disease.

To characterize the contour and duration of aortic flow-velocity waveforms in the normal human, the ascending aorta of 23 persons without evidence of cardiovascular disease was examined systematically with pulsed Doppler echocardiography. In 16 of the 23 subjects, measurements throughout the ascending aorta showed flow-velocity waveforms of similar contour and duration, characterized by flow-velocity peaking in early to midsystole, with most flow velocity (60 +/- 4%) occurring in the first half of the available systolic ejection period, and then gradually decreasing to 0 baseline coincident with aortic valve closure. In the other 7 subjects, aortic flow-velocity waveforms recorded at most of the sampling sites also revealed a normal flow-velocity pattern; however, in each of these subjects, 1 to 3 sites that displayed a distinct alteration from the normal pattern were also identified. The waveforms recorded from these latter sites were characterized by flow-velocity peaking earlier in systole and decelerating to 0 baseline approximately 100 ms before aortic valve closure; consequently, a particularly large fraction of flow velocity (88 +/- 9%) occurred in the first half of the systolic ejection period. These apparently shortened waveforms were always detected at sites near the medial aortic wall and often at or near the junction of the ascending and transverse aorta. Hence, aortic flow-velocity waveforms with altered contour and duration (resembling those recorded in patients with obstructive hypertrophic cardiomyopathy) were infrequently identified by pulsed Doppler echocardiography in subjects with normal hearts and were not characteristic of the overall aortic flow-velocity pattern in any of these subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Clinical and morphologic features of 34 patients with hypertrophic cardiomyopathy and particularly marked left ventricular hypertrophy were analyzed. Only patients with a ventricular septal thickness of at least 35 mm (range to 52 mm) were selected for the study; 31 (90%) had a diffuse pattern of hypertrophy also involving substantial portions of the left ventricular free wall. Despite similar left ventricular morphology, these patients exhibited a broad spectrum of clinical findings and natural history. Ten patients (29%) had hemodynamic or echocardiographic evidence of basal subaortic obstruction (average gradient, 63 mm Hg); however, the majority (24 [71%]) had no evidence of obstruction at rest, despite substantial hypertrophy of the basal anterior portions of septum and free wall. Although the electrocardiograms of most patients (76%) showed patterns of left ventricular hypertrophy, the magnitude of precordial QRS complexes was not markedly increased (S wave in lead V1 or V2, 27 +/- 15 mm; R wave in lead V5 or V6, 21 +/- 9 mm). The clinical course was variable in 30 patients who were followed up for at least 1 year (mean 6 years). Although no patient died, nine (30%) have exhibited clinical deterioration, including two who spontaneously developed complete heart block and one who collapsed with ventricular fibrillation but survived. However, the clinical condition of the majority of patients (21 [70%]) remained unchanged or improved. At the most recent evaluation, 20 (67%) of the 30 patients were asymptomatic or only mildly symptomatic, including 7 who remained without symptoms throughout the period of follow-up.(ABSTRACT TRUNCATED AT 250 WORDS)

In patients with primary pulmonary hypertension, competition between the right and left ventricles for the limited pericardial space results in distortion of left ventricular geometry reflected in displacement of the ventricular septum toward the left ventricular cavity. Left ventricular shape is most dramatically deranged at end-systole and early diastole, suggesting the possibility that the distribution of left ventricular diastolic filling might be altered. To investigate this hypothesis, nine patients with primary pulmonary hypertension and nine normal individuals were studied with echocardiographic techniques. Left ventricular isovolumic relaxation time was significantly prolonged in patients with primary pulmonary hypertension by comparison with normal individuals (129 +/- 36 versus 53 +/- 9 ms, p less than 0.005) and the fraction of the transmitral flow velocity integral occurring in the first half of diastole was significantly less than in normal individuals (38 +/- 14% versus 70 +/- 9%, p less than 0.005). Measurement of fractional changes in short-axis left ventricular cavity area similarly demonstrated that in patients with primary pulmonary hypertension fractional early diastolic cavity expansion (32 +/- 11%) was significantly less than in normal individuals (78 +/- 9%, p less than 0.005). In patients with primary pulmonary hypertension, the ventricular septum was abnormally flattened toward the left ventricular cavity at end-systole (normalized septal curvature 0.04 +/- 0.19) and remained that way throughout early diastolic filling but returned toward normal at end-diastole (normalized septal curvature 0.68 +/- 0.19, p less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

In order to measure the protective effect of interventions following coronary artery occlusions in dogs, the creatine kinase activity of myocardial tissue was assayed after 24 h and related to the myocardial blood flow of that tissue measured with 85Sr labelled microspheres injected 15 min after occlusion. This assay showed normal levels when flow exceeded 50 cm3.min-1.100 g-1. In myocardium with flow reduced to 0 to 15 cm3. min-1.100g-1, creatine kinase activity was 7.6 +/- 0.6 IU.mg-1 protein in control dogs and 13.1 +/- 1.8 IU.mg-1 protein (P less than 0.01) in dogs given 500 NF units.kg-1 of hyaluronidase 20 min after occlusion. Where myocardial blood flow was reduced to 16 to 50 cm3. min-1. 100g-1, creatine kinase activity was increased from 14.1 +/- 1.1 to 20.5 +/- 1.4 IU.mg-1 protein by hyaluronidase. This method therefore assesses ischaemic damage independent of electrophysiological measurements and confirms myocardial preservation by hyaluronidase.