Pitfalls in the diagnosis of periprosthetic valvular regurgitation by pulsed Doppler echocardiography.

Pulsed Doppler echocardiographic diagnosis of periprosthetic valvular insufficiency may be difficult. This report details the pulsed Doppler echocardiographic findings in two patients who developed severe periprosthetic mitral regurgitation after porcine mitral valve replacement. In both patients, mitral regurgitation was difficult to diagnose and left atrial turbulence, when detected, appeared localized, suggesting only mild mitral regurgitation. However, the combination of abnormally high peak transmitral diastolic flow velocity, with a normal pressure half-time, and increased flow velocity in the tricuspid regurgitant jet compatible with severe pulmonary hypertension, in the absence of other apparent left heart disease, suggested the correct diagnosis of severe mitral regurgitation in both cases. Techniques for optimal pulsed Doppler assessment of the mitral anulus region are emphasized, as are the theoretic advantages of continuous wave and color-coded pulsed Doppler echocardiography for detection of periprosthetic regurgitation.

Implications of echocardiographically assisted diagnosis of pericardial tamponade in contemporary medical patients: detection before hemodynamic embarrassment.

Identification of suspected pericardial tamponade and the decision to perform invasive drainage of the pericardial space have historically been based on classic bedside findings. Two-dimensional echocardiography has improved detection of pericardial effusion, but it may be excessively sensitive in evaluation of patients for hemodynamic embarrassment. Therefore, 50 consecutive medical patients were examined who were identified by echocardiography to have probable tamponade (defined as the presence of right heart chamber collapse in the presence of a pericardial effusion) and who underwent combined right-sided cardiac catheterization and percutaneous pericardiocentesis. All patients had elevated pericardial pressure. However, many had minimal evidence of hemodynamic compromise (94% had systolic blood pressure greater than or equal to 100 mm Hg and 58% had a cardiac index greater than or equal to 2.3 liters/min per m2). Pericardiocentesis resulted in hemodynamic improvement, but frequently did not alleviate dyspnea or correct tachycardia. Patients with malignancy as the cause of tamponade had a high mortality rate (the cumulative probability of survival in such patients was only 17% at 1 year). Echocardiographically assisted diagnosis of pericardial tamponade in medical patients results in the identification of a substantial subset of patients with only subtle evidence of hemodynamic compromise. This subset of patients differs sharply from medical patients described in previous reports with classic tamponade. Although the patients can be managed by invasive catheter pericardiocentesis with few complications, the natural history and the optimal management strategy for this group are not resolved.

Doppler echocardiography in cardiac tamponade: exaggerated respiratory variation in transvalvular blood flow velocity integrals.

Pulsed Doppler echocardiography has been used previously to demonstrate marked changes in transvalvular blood flow velocities during cardiac tamponade in laboratory animals and a small number of patients. To further assess the respiratory changes in transvalvular blood flow during tamponade, pulsed Doppler tracings of flow velocity profiles across all four cardiac valves were recorded during inspiration and expiration in 13 patients during cardiac tamponade, in 6 of the 13 patients after relief of tamponade by pericardiocentesis and in 8 normal control subjects. Flow velocity integrals were calculated for each valve during inspiration and expiration. In the setting of cardiac tamponade, inspiration caused an 85 +/- 46% increase in the flow velocity integral across the pulmonary valve, an 81 +/- 34% increase across the tricuspid valve, a 33 +/- 13% decrease across the aortic valve and a 35 +/- 8% decrease across the mitral valve. These phasic respiratory changes were markedly reduced after relief of tamponade (p less than 0.05 compared with tamponade) and were observed to only a minimal extent in the normal individuals (p less than 0.01 compared with tamponade). The exaggerated respiratory variations in transvalvular flow velocity integrals suggest that Doppler evaluation may be a valuable tool in the diagnosis of cardiac tamponade. Transmitral Doppler indexes of left ventricular filling during cardiac tamponade revealed that inspiration caused a shift to increased filling during late diastole, with a greater contribution of atrial systole to total left ventricular filling. These Doppler indexes did not vary significantly with respiration in the group studied after relief of tamponade or in the control group.(ABSTRACT TRUNCATED AT 250 WORDS)

Echocardiographic assessment of aortic valve area in elderly patients with aortic stenosis and of changes in valve area after percutaneous balloon valvuloplasty.

Echocardiographic studies, adequate for analysis of aortic valve area using the continuity equation, were obtained in 31 patients aged greater than or equal to 60 years who were undergoing catheterization for assessment of suspected aortic stenosis. Catheterization-determined aortic valve area was 0.74 +/- 0.30 cm2 (mean +/- SD) and Doppler-determined aortic valve areas were 0.68 +/- 0.27 and 0.65 +/- 0.27 cm2, depending on whether peak or mean velocities, respectively, were entered into the continuity equation. There were significant correlations between both of the Doppler-derived and the catheterization-determined aortic valve areas (r = 0.86, p less than 0.001 for both the continuity equation employing peak velocities and the continuity equation employing mean velocities) which were demonstrated to be linear by F test (catheterization area = -0.03 + 1.13 X Doppler area determined using peak velocities, SEE = 0.163 cm2, p less than 0.001; and catheterization area = -0.02 + 1.16 X Doppler area determined using mean velocities, SEE = 0.165 cm2, p less than 0.001). Both sets of correlations had linear regression parameters meeting the conditions for identity. Significant linear correlations were also noted between the non-invasive measurements of aortic valve excursion, ventricular ejection time, time to one-half carotid upstroke, maximal Doppler velocity and maximal Doppler gradient and catheterization aortic valve area, but the correlations were less tight than those between valve areas determined by catheterization and by Doppler continuity equation. Ten of the patients underwent percutaneous balloon aortic valvuloplasty. There were significant linear correlations between aortic valve areas determined by Doppler and catheterization methods both before valvuloplasty (r = 0.77, p = 0.01; p less than 0.001 by F test, SEE = 0.134 cm2) and after valvuloplasty (r = 0.85, p less than 0.01; p = 0.0001 by F test, SEE = 0.161 cm2). Linear regression parameters met the conditions for identity. There was also a significant linear correlation between catheterization and Doppler measurements of absolute change in aortic valve area (r = 0.79, p less than 0.01; p less than 0.001 by F test, SEE = 0.11 cm2). Aortic valve area can be determined reliably by continuity equation in elderly patients. In addition, results of balloon valvuloplasty, measured by changes in catheterization-determined aortic valve area, are accurately reflected by changes in aortic valve area determined using the continuity equation.

Pulsed Doppler echocardiographic evaluation of valvular regurgitation in patients with mitral valve prolapse: comparison with normal subjects.

Pulsed Doppler echocardiography was used to determine prospectively the prevalence of mitral, aortic, tricuspid and pulmonary regurgitation in 80 consecutive patients with mitral valve prolapse and 85 normal subjects with similar age and sex distribution. Mitral valve prolapse was defined by posterior systolic displacement of the mitral valve on M-mode echocardiography of 3 mm or more (40 patients), the presence of one or more mid- or late systolic clicks (61 patients), or both. Mitral regurgitation, detected by pulsed Doppler techniques in 53 patients with prolapse, was holosystolic in 24, early to mid-systolic in 6, late systolic in 15 and both holosystolic and late systolic behind different portions of the valve in 8. Definitive M-mode findings were present in only 27 of the 53 patients, and only 21 had mitral regurgitation audible on physical examination. Tricuspid regurgitation was evident by pulsed Doppler echocardiography in 15 patients (holosystolic in 9, early to mid-systolic in 1, late systolic in 4 and both holosystolic and late systolic in 1); 12 of these 15 patients, including all with an isolated late systolic pattern, had an echocardiographic pattern of tricuspid prolapse, but none had audible tricuspid regurgitation. A Doppler pattern compatible with aortic regurgitation was recorded in seven patients, all without echocardiographic aortic valve prolapse and only two with audible aortic insufficiency. A Doppler shift in the right ventricular outflow tract in diastole, suggestive of pulmonary regurgitation, was recorded in 16 of the 78 patients with an adequate Doppler examination: only 1 of the 16 had audible pulmonary insufficiency. Of the 85 normal subjects without audible regurgitation, pulsed Doppler examination detected mitral regurgitation in 3 subjects (holosystolic in 1 and early to mid-systolic in 2), aortic regurgitation in none, tricuspid regurgitation in 9 (holosystolic alone in 8 and both holosystolic and late systolic in 1) and right ventricular outflow tract turbulence compatible with pulmonary insufficiency in 15. The prevalence of valvular regurgitation, detected by pulsed Doppler echocardiography, is high in patients with mitral valve prolapse. Regurgitation may involve any of the four cardiac valves and is clinically silent in the majority of patients. The prevalence rates of mitral and aortic regurgitation are significantly higher in patients with mitral prolapse than in normal subjects, suggesting that alterations in underlying valve structure in the prolapse syndrome may indeed be responsible for this regurgitation.(ABSTRACT TRUNCATED AT 400 WORDS)

Two-dimensional and Doppler echocardiographic determinants of the natural history of mitral valve narrowing in patients with rheumatic mitral stenosis: implications for follow-up.

Fifty patients with rheumatic mitral stenosis were studied with serial two-dimensional and Doppler echocardiography to determine the natural history of changes in mitral valve area and its relation to transmitral gradients and mitral valve morphology. Over the 39-month observation period (range 7 to 74 months) the decline in valve area was 0.09 +/- 0.21 cm2/year. In addition, there were significant increases in total echocardiographic score (p = 0.0001), severity of mitral anulus calcification (p = 0.05) and severity of mitral regurgitation (p = 0.0007). Patients with an echocardiographic score greater than or equal to 8 had a more progressive course. In addition, patients with a more progressive course (decline in valve area greater than or equal to 0.1 cm2/year) had a significantly greater initial mean gradient (p = 0.01), peak gradient (p = 0.007) and total echocardiographic score (p = 0.0008). Initial valve area did not correlate with the rate of stenosis progression. Of 22 patients with an echocardiographic score less than 8 and a peak mitral gradient less than 10 mm Hg, only 1 patient (5%) had a more progressive course, compared with 80% of those with a total echocardiographic score greater than or equal to 8 and a gradient greater than or equal to 10 mm Hg. The rate of mitral valve narrowing in individual patients with rheumatic mitral stenosis is variable. Patients whose valve disease progresses rapidly are those with a greater mitral valve echocardiographic score and higher peak and mean transmitral gradients.(ABSTRACT TRUNCATED AT 250 WORDS)

Pulsed Doppler evaluation of atrial mechanical function after electrical cardioversion of atrial fibrillation.

Full recovery of atrial mechanical activity may not occur immediately after successful electrical cardioversion of atrial fibrillation to sinus rhythm. To examine the time course of recovery of left atrial mechanical function, serial two-dimensional, M-mode and transmitral pulsed Doppler echocardiographic studies were performed in 21 patients after elective direct current cardioversion of atrial fibrillation of 3 weeks' to 24 months' duration (mean 5 months). Over 3 months of follow-up, there were significant increases in both peak A wave velocity (p less than 0.005) and percent atrial contribution to total left ventricular filling (p less than 0.005). Compared with values in a normal control population, peak A wave velocity and percent atrial contribution to total left ventricular filling did not return to normal until 3 weeks after cardioversion in patients who remained in sinus rhythm. Left atrial dimension also decreased over the follow-up period (p less than 0.05) in patients with persistent sinus rhythm. These results may have important implications in guiding the appropriate duration of anticoagulant therapy after cardioversion, and in clinically assessing the hemodynamic benefit of restoring sinus rhythm in an individual patient.

Early reversal of right ventricular dysfunction in patients with acute pulmonary embolism after treatment with intravenous tissue plasminogen activator.

To assess abnormalities of right heart function and their reversal with thrombolysis in pulmonary embolism, serial imaging and Doppler echocardiographic studies were performed before and after a 6 hour intravenous infusion of 80 to 90 mg of recombinant tissue-type plasminogen activator (rt-PA) in seven patients with segmental or lobar acute pulmonary embolism. None of the five men and two women had known prior pulmonary hypertension. Substantial clot lysis and improvement in pulmonary blood flow, as determined by serial pulmonary angiography and perfusion lung scanning, were achieved in all. Coincident with clot lysis, pulmonary artery systolic pressure decreased (from 42 +/- 11 to 26 +/- 7 mm Hg, p less than 0.005), right ventricular diameter decreased (from 3.9 +/- 1.0 to 2.0 +/- 0.5 cm, p less than 0.005) and left ventricular diameter increased (from 3.7 +/- 0.9 to 4.4 +/- 0.6 cm, p less than 0.01). Right ventricular wall movement, initially mildly, moderately or severely hypokinetic in one, two and four patients, respectively, normalized in five and improved to mild hypokinesia in two. Tricuspid regurgitation was present before lytic therapy in six patients. In five, flow velocity in the tricuspid regurgitant jets indicated a peak systolic right ventricular minus right atrial pressure gradient of 25 to 52 mm Hg. Tricuspid regurgitation was detected early after lytic therapy in only two patients. Systolic septal flattening was noted before but not after lysis. These findings confirm that pulmonary emboli may result in appreciable right ventricular dysfunction and dilation, resultant tricuspid regurgitation, abnormal septal position and decreased left ventricular size.(ABSTRACT TRUNCATED AT 250 WORDS)

Two-dimensional and Doppler echocardiographic diagnosis of an aortic to right atrial fistula complicating aortic dissection.

A 60 year old woman presented with massive aortic root dilation and sudden cardiovascular collapse 10 years after aortic valve replacement. An aortic to right atrial fistula was diagnosed by echocardiographic imaging and Doppler ultrasound. At operation, the patient was found to have chronic aortic dissection with aneurysm formation. Rupture of the aneurysm into the right atrium was confirmed.

An experimental model of acute and subacute viral myocarditis in the pig.

Twenty-six young pigs were infected with encephalomyocarditis virus, observed clinically, studied at intervals by noninvasive and invasive methods to assess cardiac function and eventually examined pathologically. All infected animals appeared ill, usually manifesting diminished appetite, lethargy and fever. Spontaneous mortality occurred either 1 to 4 or 20 to 21 days after infection. Electrocardiographic abnormalities, seen in the majority of animals, comprised ST-T wave changes, conduction disturbances or ventricular ectopic rhythm. The majority of animals manifested echocardiographic evidence of left ventricular dilation and decreased systolic function, which improved with time in some animals. Hemodynamic studies revealed elevation of biventricular filling pressures in 3 of 10 animals; as a group, infected animals manifested significantly elevated right ventricular filling pressures. In selected animals, the feasibility of gallium scans as well as left ventriculography and coronary angiography was demonstrated. At autopsy, heart weight/body weight ratio was significantly elevated in infected animals. The heart of all but two animals showed active myocarditis associated with fibrosis and focal calcification in the later stages. In general, the cardiovascular manifestations were parallel with those seen in acute and subacute myocarditis in humans. It is concluded that encephalomyocarditis infection in the pig is a large animal model of viral myocarditis suitable for assessing alterations in the structure and function of the cardiovascular system and the effects of interventions.

The pacing stress test: thallium-201 myocardial imaging after atrial pacing. Diagnostic value in detecting coronary artery disease compared with exercise testing.

Many patients suspected of having coronary artery disease are unable to undergo adequate exercise testing. An alternate stress, pacing tachycardia, has been shown to produce electrocardiographic changes that are as sensitive and specific as those observed during exercise testing. To compare thallium-201 imaging after atrial pacing stress with thallium imaging after exercise stress, 22 patients undergoing cardiac catheterization were studied with both standard exercise thallium imaging and pacing thallium imaging. Positive ischemic electrocardiographic changes (greater than 1 mm ST segment depression) were noted in 11 of 16 patients with coronary artery disease during exercise, and in 15 of the 16 patients during atrial pacing. One of six patients with normal or trivial coronary artery disease had a positive electrocardiogram with each test. Exercise thallium imaging was positive in 13 of 16 patients with coronary artery disease compared with 15 of 16 patients during atrial pacing. Three of six patients without coronary artery disease had a positive scan with exercise testing, and two of these same patients developed a positive scan with atrial pacing. Of those patients with coronary artery disease and an abnormal scan, 85% showed redistribution with exercise testing compared with 87% during atrial pacing. Segment by segment comparison of thallium imaging after either atrial pacing or exercise showed that there was a good correlation of the location and severity of the thallium defects (r = 0.83, p = 0.0001, Spearman rank correlation). It is concluded that the location and presence of both fixed and transient thallium defects after atrial pacing are closely correlated with the findings after exercise testing.(ABSTRACT TRUNCATED AT 250 WORDS)

Serial assessment of mitral regurgitation by pulsed Doppler echocardiography in patients undergoing balloon aortic valvuloplasty.

Mitral regurgitation was serially assessed by pulsed Doppler echocardiography in 144 patients undergoing balloon aortic valvuloplasty for symptomatic aortic stenosis. Regurgitant scores of 0, 1, 2 and 3 were assigned to pulsed Doppler patterns corresponding to no, mild, moderate and severe mitral regurgitation, respectively. Before balloon aortic valvuloplasty, mitral regurgitant score correlated significantly (p less than 0.005) but weakly with aortic valve area (r = -0.24), left ventricular ejection fraction (r = -0.34) and left ventricular systolic pressure (r = 0.23). There was no significant correlation between mitral regurgitation and either mean catheterization or mean Doppler aortic valve gradient. Balloon aortic valvuloplasty produced significant decreases in both catheterization and Doppler mean transvalvular aortic valve gradients (56 +/- 19 to 31 +/- 12 and 60 +/- 19 to 48 +/- 16 mm Hg, respectively; both p less than 0.0001) and a significant increase (p less than 0.0001) in aortic valve area assessed by catheterization (0.6 +/- 0.2 to 0.9 +/- 0.3 cm2). Left ventricular ejection fraction did not change, but cardiac output increased (p less than 0.001) and pulmonary capillary wedge pressure decreased (p less than 0.0001). Pulsed Doppler findings of mitral regurgitation were present in 102 of the 144 patients. Eighty-eight patients had a score compatible with mild or more severe degrees of mitral regurgitation, and 49 had a score indicative of moderate or severe valvular insufficiency. In the entire group of 144 patients, mitral regurgitant score decreased significantly from 1.1 +/- 1.0 to 1.0 +/- 1.0 (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Impaired left atrial mechanical function after cardioversion: relation to the duration of atrial fibrillation.

OBJECTIVES: We hypothesized that the time course of the recovery of atrial systolic function may be related to the duration of atrial fibrillation before cardioversion and sought to study noninvasively the recovery of left atrial mechanical function utilizing serial transthoracic Doppler studies. BACKGROUND: Recovery of atrial mechanical function may be delayed for several weeks after successful cardioversion of atrial fibrillation to sinus rhythm. METHODS: After successful cardioversion, 60 patients with atrial fibrillation of brief (< or = 2 weeks, 17 patients), moderate (> 2 to 6 weeks, 22 patients) or prolonged (> 6 weeks, 21 patients) duration were followed up with serial transmitral pulsed Doppler echocardiography immediately (60 patients) and at 24 h (45 patients), 1 week (41 patients), 1 month (31 patients) and > 3 months (30 patients) after cardioversion. RESULTS: Atrial mechanical function is greater immediately and at 24 h and 1 week after cardioversion in patients with "brief" compared with "prolonged" atrial fibrillation. In all groups, atrial mechanical function increases over time, ultimately achieving similar levels. Full recovery of atrial mechanical function, however, is achieved within 24 h in patients with brief atrial fibrillation, within 1 week in patients with moderate-duration atrial fibrillation and within 1 month in patients with prolonged atrial fibrillation. CONCLUSIONS: Recovery of left atrial mechanical function is related to the duration of atrial fibrillation before cardioversion. These findings have important implications for assessing the early hemodynamic benefit of successful cardioversion.

The pacing stress test reexamined: correlation of pacing-induced hemodynamic changes with the amount of myocardium at risk.

To assess the relation between extent of ischemia and the magnitude of hemodynamic changes, 25 patients (5 with normal coronary arteries and 20 with significant coronary obstructive disease) were studied with rapid atrial pacing and thallium scintigraphy at the time of cardiac catheterization. Hemodynamic variables were measured before, during and after maximal pacing. Thallium was injected intravenously during maximal pacing and scans in three standard views were obtained immediately in the catheterization laboratory, with delayed scans obtained 4 hours after the cessation of pacing. The three thallium scans were each subdivided into five segments, and a thallium score was obtained on the basis of the total number of segments that were hypoperfused. Each patient was assigned a total thallium score corresponding to thallium defects at maximal pacing, as well as a redistributed thallium score corresponding to the difference between thallium score at maximal pacing and that 4 hours later. With pacing, patients with normal coronary arteries demonstrated no significant change in baseline hemodynamic variables, whereas patients with coronary artery disease exhibited a decrease in cardiac index, an increase in systemic vascular resistance, a widening of arteriovenous oxygen difference, an increase in pulmonary capillary wedge pressure and mean pulmonary artery pressure during maximal pacing and an increase in left ventricular end-diastolic pressure immediately after pacing. There was a significant correlation (Spearman rank r = 0.64, p less than 0.01) between redistributed thallium score and an increase in left ventricular end-diastolic pressure in the postpacing period. Moreover, there was an even higher correlation (Spearman rank r = 0.90, p less than 0.001) between total thallium score and the postpacing increase in end-diastolic pressure. It is concluded that in patients with coronary artery disease the magnitude of pacing-induced hemodynamic changes reflects both the amount of myocardial tissue at ischemic jeopardy and the total mass of hypoperfused myocardium during maximal pacing stress.

Balloon dilation of mitral stenosis in adult patients: postmortem and percutaneous mitral valvuloplasty studies.

Preliminary reports have documented the utility of percutaneous balloon valvuloplasty of the mitral valve in adult patients with mitral stenosis, but the mechanism of successful valve dilation and the effect of mitral valvuloplasty on cardiac performance have not been studied in detail. Accordingly, mitral valvuloplasty was performed in five postmortem specimens and in 18 adult patients with rheumatic mitral stenosis, using either one (25 mm) or two (18 and 20 mm) dilation balloons. Postmortem balloon dilation resulted in increased valve orifice area in all five postmortem specimens, secondary to separation of fused commissures and fracture of nodular calcium within the mitral leaflets. In no case did balloon dilation result in tearing of valve leaflets, disruption of the mitral ring or liberation of potentially embolic debris. Percutaneous mitral valvuloplasty in 18 patients with severe mitral stenosis (including 9 with a heavily calcified valve) resulted in an increase in cardiac output (4.3 +/- 1.1 to 5.1 +/- 1.5 liters/min, p less than 0.01) and mitral valve area (0.9 +/- 0.2 to 1.6 +/- 0.4 cm2, p less than 0.0001), and a decrease in mean mitral pressure gradient (15 +/- 5 to 9 +/- 4 mm Hg, p less than 0.0001), pulmonary capillary wedge pressure (23 +/- 7 to 18 +/- 7 mm Hg, p less than 0.0001) and mean pulmonary artery pressure (36 +/- 12 to 33 +/- 12 mm Hg, p less than 0.01). Left ventriculography before and after valvuloplasty in 14 of the 18 patients showed a mild (less than or equal to 1+) increase in mitral regurgitation in five patients and no change in the remainder.(ABSTRACT TRUNCATED AT 250 WORDS)

Production of abnormal systolic sounds by vibration of torn leaflet of porcine xenograft.

A 72-year-old woman was initially seen with increasing dyspnea and a new murmur occurring six years after mitral valve replacement with a glutaraldehyde-stabilized porcine xenograft. Prominent systolic sounds, superimposed on a softer holosystolic murmur, were audible, with a frequency of 22 to 40 Hz documented by phonocardiography. The mitral valve echo showed a prominent systolic flutter with frequency characteristics identical to those of the discrete systolic sounds, indicating that fluttering of the mitral valve was responsible for the generation of the unusual auscultatory findings. A torn porcine cusp was found at operation.

Echocardiographic recognition of pulmonary arterial disease and determination of its cause.

Echocardiography provided the initial diagnosis of significant pulmonary hypertension, unrelated to left heart pathologic conditions, in 10 patients: four with acute pulmonary embolism; five with chronic pulmonary hypertension, primary in three patients and secondary to tumor emboli in the other two patients; and one with Eisenmenger's syndrome due to previously unsuspected atrial septal defects. Referral diagnoses were pericardial disease in five patients (including three with suspected tamponade), and right ventricular infarction versus pericarditis, atrial septal defect, dyspnea, inferoposterior infarction (by electrocardiography), and Ebstein's malformation in one patient each. The echocardiographic diagnoses were confirmed by lung scan (ventilation/perfusion mismatches were interpreted as high probability for pulmonary emboli in all four patients considered to have acute pulmonary emboli by echocardiographic study), pulmonary angiography (one patient), cardiac catheterization (four patients), and autopsy (three patients). No patient had evident aortic or mitral valvular, myocardial, or other left heart pathologic condition. In acute pulmonary embolism, mean right ventricular diameter was increased at 4.2 cm (range 3.2 to 6 cm) and right ventricular wall thickness was normal (mean 4.5 mm, range 3 to 5 mm). Moderate or marked right ventricular hypokinesis was noted in two patients each. Doppler examination, performed in three patients, revealed tricuspid regurgitation in all, with an increased flow velocity suggestive of mild to moderate systolic pulmonary hypertension (right ventricular minus right atrial pressures of 28 to 36 mm Hg). Patients with chronic pulmonary hypertension also had right ventricular dilatation (mean 4.4 cm diameter, range 3 to 5.4 cm) and hypokinesis (marked in four and moderate in one patient), but wall thickness was increased in all (mean of 9 mm, range 6 to 14 mm) and the flow velocities in the tricuspid regurgitant jets, detected by Doppler in all patients, suggested higher right ventricular minus right atrial pressures of 44 to 104 mm Hg (mean 64 mm Hg). The single patient with Eisenmenger's syndrome had right ventricular dilatation (3.2 cm), hypertrophy (10 mm), and hypokinesis (mild). Only the patient with Eisenmenger's syndrome had Doppler or contrast echocardiographic evidence for an intracardiac or extracardiac shunt. In the absence of left heart pathologic conditions, right ventricular dilatation and hypokinesis strongly suggest pulmonary arterial or primary right ventricular disease.(ABSTRACT TRUNCATED AT 400 WORDS)

Prediction of severity of aortic stenosis: accuracy of multiple noninvasive parameters.

PURPOSE: As newer non-medical techniques are developed to treat older patients with severe aortic stenosis, reliable noninvasive diagnosis of the condition will become increasingly important. For this reason, the accuracy of multiple noninvasive indexes for quantitation of the severity of aortic stenosis was evaluated, relative to catheterization-determined aortic valve area. PATIENTS AND METHODS: To evaluate the accuracy of multiple noninvasive parameters in assessing the presence and extent of aortic valve narrowing, noninvasive and catheterization correlations of the severity of aortic stenosis were obtained on 121 occasions in 81 patients (mean age, 76 +/- 11 years). Forty patients had studies performed before and after valvuloplasty. Noninvasive studies included the time to one-half carotid upstroke and carotid ejection time, corrected for heart rate, measured from a carotid pulse tracing; M-mode echocardiographic aortic valve excursion; mean pressure gradient across the aortic valve assessed by Doppler technique; the ratio of the peak to mean pressure gradient by Doppler; and Doppler aortic valve area assessed using the following continuity equation: aortic valve area = A X V/V1, where A = left ventricular outflow tract area, V = peak left ventricular outflow tract velocity, and V1 = peak velocity in the aortic stenotic jet. Mean aortic valve gradients and area (calculated using the Gorlin formula) were also assessed at cardiac catheterization. RESULTS: The correlations between the catheterization measurement of aortic valve area and the various noninvasive measurements were as follows: time to one-half carotid upstroke (r = -0.32, p less than 0.001); corrected left ventricular ejection time (r = -0.24, p less than 0.05); aortic valve excursion (r = 0.51, p less than 0.001); mean gradient by Doppler study (r = -0.44, p less than 0.001); mean gradient by catheterization analysis (r = -0.55, p less than 0.001); peak to mean gradient ratio measured by continuous wave Doppler (r = 0.38, p less than 0.001); and aortic valve area assessed using the Doppler continuity equation (r = 0.85, p less than 0.001). CONCLUSION: Noninvasive determination of aortic valve area using the continuity equation is an accurate means of assessing the severity of aortic stenosis. Although multiple other noninvasive parameters also correlate with aortic valve area measured at catheterization, there is too much scatter of data points to permit accurate prediction of catheterization aortic valve area in any given patient.

Absence of pulsus paradoxus in a patient with cardiac tamponade and coexisting pulmonary artery obstruction.

Pulsus paradoxus is a key physical finding in patients with cardiac tamponade. This report describes a 38-year-old woman with metastatic adenocarcinoma who had cardiac tamponade confirmed by cardiac catheterization. Pulsus paradoxus was notably absent. No evidence could be found for an atrial septal defect, significant aortic regurgitation, elevated left ventricular diastolic pressure, or localized tamponade, previously described disorders in which pulsus paradoxus may not be seen when tamponade occurs. The lack of pulsus paradoxus in this case was attributed to right ventricular pressure overload due to mechanical obstruction of the pulmonary artery.

Inheritance of the mitral valve prolapse syndrome. Discussion of a three-dimensional penetrance model.

The families of 12 probands with classic mitral valve prolapse were studied for evidence of mitral valve prolapse. Seventy parents, sibs, and progeny were included in the analysis. Forty-seven percent (16 of 34) of progeny were affected compared with 30 percent (3 of 10) of parents. Thirty-eight percent (10 of 26) of sibs were affected. A three-compartmental penetrance model was devised to account for the variation in expression with age. This includes a latent stage (time before onset of signs), an affected stage, and a stage in which the subjects are withdrawn (because of treatment, regression, or death). The implications of this model are discussed.