Biomedical subjects
Publications and source records attributed to Z Sasson.
This article discusses the central role of cardiac ultrasonography-- two dimensional echocardiography, Doppler echocardiography, continuous-wave Doppler, pulsed-wave Doppler--in the clinical assessment and management of patients with hypertrophic cardiomyopathy.
This study was designed to evaluate the relation between severity of obstruction to left ventricular outflow and left ventricular ejection time in hypertrophic obstructive cardiomyopathy. With dual catheters across the left ventricular outflow tract, the pressure gradient and corresponding left ventricular ejection time were measured in 10 patients as the pressure gradient was pharmacologically provoked or abolished, or both. The patients were studied during constant atrial pacing to avoid the potential errors introduced with heart rate correction equations. The pressure gradient was pharmacologically provoked or reduced over a range of greater than or equal to 62 mm Hg per patient. In each patient the left ventricular ejection time varied directly with the pressure gradient (mean r = 0.97, range 0.92 to 1.00). The change in magnitude of the pressure gradient varied directly with the corresponding change in the measured ejection time (mean r = 0.98, range 0.97 to 1.00). When the data from all 10 patients were pooled with use of Weissler's heart rate correction equation, the relation between the corrected left ventricular ejection time and the pressure gradient was still significant and linear (r = 0.86), but less so than in individual patients. This difference was the result of marked interpatient variability in the slope of this linear relation reflecting interpatient differences in other important factors, such as underlying myocardial contractility and stroke volume, that influence left ventricular ejection time. This study demonstrates a clear, direct and highly significant relation between the magnitude of the pressure gradient and the left ventricular ejection time in hypertrophic obstructive cardiomyopathy.(ABSTRACT TRUNCATED AT 250 WORDS)
Surgical ventriculomyectomy and ventriculomyotomy by the aortic approach are safe and effective methods of relieving symptoms and obstruction to left ventricular outflow in patients with hypertrophic obstructive cardiomyopathy. With the addition of Doppler ultrasound to the routine follow-up assessment of these patients an unexpectedly high occurrence of aortic regurgitation was found in the postoperative patients. Because aortic regurgitation has been reported to rarely accompany this condition, 67 patients with hypertrophic obstructive cardiomyopathy were studied clinically and with Doppler echocardiography for the presence and severity of aortic regurgitation. Severity of the regurgitation was quantitated by pulsed or color Doppler echocardiography according to the length and width of the regurgitant jet in at least two views. In 37 patients with hypertrophic obstructive cardiomyopathy who did not undergo surgery, aortic regurgitation was detected in only 1 (3%) by Doppler ultrasound and in none clinically. In 52 patients who did undergo surgery and were studied a mean of 7.8 years postoperatively, aortic regurgitation of trivial to moderate degree was common, being detected in 28 (54%) by Doppler ultrasound and in 6 (12%) clinically. In a subgroup of 22 patients who were studied preoperatively and again early postoperatively (mean 6 weeks), new aortic regurgitation was found in 8 (36%) and was graded as trivial in all. Aortic regurgitation is a common complication related to ventriculomyectomy and ventriculomyotomy in patients with hypertrophic obstructive cardiomyopathy. Although initially trivial, the regurgitation may progress in severity over time. The regurgitation has been well tolerated in all patients studied to date.
The continuous wave Doppler ultrasound signal across the left ventricular outflow tract in hypertrophic cardiomyopathy has a characteristic pattern that is in keeping with the dynamic nature of the pressure gradient in this condition. To determine the accuracy and reliability of the peak Doppler flow velocity signal for measuring the peak pressure gradient in this condition, 340 beats were analyzed from five consecutive patients studied with simultaneous continuous wave Doppler ultrasound and dual catheter pressure recordings across the left ventricular outflow tract. Each patient was studied at steady state and during physiologic and pharmacologic manipulations of the pressure gradient. Peak velocity and calculated peak gradient were determined by two independent observers who did not know the catheter measurements. In addition, 18 beats with well defined flow velocity envelopes were digitized for analysis of the magnitude, timing and contour of the instantaneous Doppler ultrasound and catheter gradients throughout systole. Peak catheter gradient in the 340 beats ranged from 12 to 245 mm Hg. The correlations between the Doppler-derived and catheter peak gradients were close (r = 0.96, SEE = 4 mm Hg for Observer 1 and r = 0.97, SEE = 11 mm Hg for Observer 2). Interobserver variability for measurement of peak flow velocity was small (mean +/- SD 0.16 +/- 0.15 m/s). An interobserver difference greater than 0.3 m/s occurred in 25 of the 340 beats analyzed. By retrospective analysis, this was due to contamination of the outflow tract signal by mitral regurgitation.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertrophic cardiomyopathy is a diverse clinical and pathophysiologic disorder of unknown cause that principally involves the left ventricle and is manifested as asymmetric or concentric hypertrophy. If asymmetric, the hypertrophy is usually greatest in the ventricular septum, but variations occur in which the hypertrophy may be maximal at the mid-ventricular level, at the apex, or rarely, in the free wall of the left ventricle. Right ventricular involvement is usually less evident. The principal abnormality in systole is the obstruction to left ventricular outflow caused by systolic anterior motion (SAM) of the anterior or posterior mitral leaflet(s) with mitral leaflet-septal contact. SAM occurs as the result of the Venturi forces created by the rapid ejection of blood through an outflow tract that is narrowed by upper septal hypertrophy, drawing the mitral leaflet(s) anteriorly. The time of onset and duration of mitral leaflet-septal contact determine the magnitude of the pressure gradient. Mitral regurgitation invariably accompanies the obstruction to outflow. Ventriculomyectomy surgery, by thinning the septum and widening the outflow tract, abolishes the abnormal mitral leaflet motion and, consequently, the obstruction to outflow and the mitral regurgitation. In symptomatic patients with resting obstruction this form of surgery more dramatically relieves the systolic abnormalities and the accompanying symptoms than any form of medical therapy currently available. The extent of hypertrophy is believed to be the principal determinant of impaired left ventricular relaxation and increased chamber stiffness that characterize diastole in hypertrophic cardiomyopathy. Diastolic dysfunction is common to most such patients irrespective of the presence or absence of outflow obstruction. Calcium entry blockers may improve the left ventricular relaxation process and relieve symptoms in patients with hypertrophic cardiomyopathy, particularly the subgroup with no obstruction to outflow. Atrial and ventricular arrhythmias are responsible for a significant proportion of the morbidity and mortality, and their prevalence appears to depend on the presence of obstruction and the extent of hypertrophy. Thus, the major manifestations of hypertrophic cardiomyopathy in systole and diastole, as well as the disturbances in rhythm, appear to be related to the site and/or extent of the hypertrophic process. We have learned much about hypertrophic cardiomyopathy in the 30 years since its modern description. The vast majority of symptomatic patients can now be improved with specific medical or surgical therapy.(ABSTRACT TRUNCATED AT 400 WORDS)
This study describes the characteristics of a prominent Doppler flow velocity signal representing intraventricular flow during left ventricular isovolumic relaxation. The flow during the isovolumic relaxation period was demonstrated in 60 subjects, including 7 with a normal heart, 26 with hypertrophic cardiomyopathy, 10 with aortic valve disease, 9 with a transplanted heart and 8 others. All had normal to hyperdynamic left ventricular systolic function with some degree of cavity obliteration as seen in the apical two-dimensional echocardiographic views. In contrast, this isovolumic relaxation period flow could not be demonstrated in the absence of cavity obliteration in any of 20 patients with either normal or diminished left ventricular systolic function. Isovolumic relaxation period flow was best recorded from the apical transducer position and was directed toward the apex in all patients. By pulsed wave, and with two-dimensional Doppler ultrasound, the isovolumic relaxation period flow originated within a narrow area in the medial portion of the left ventricle along the middle or basal segments of the interventricular septum, but was recorded over a larger area toward the apex. The peak isovolumic relaxation period flow velocity was recorded just basal to the area of cavity obliteration, usually at the level of the papillary muscles, and ranged from 0.4 to 2.3 m/s (mean of 1.0 m/s). This isovolumic relaxation period flow started with aortic valve closure and, in 50 of the 60 patients, it lasted throughout isovolumic relaxation until mitral valve opening. In the other 10 patients (all with hypertrophic cardiomyopathy), it lasted for only a part (mean 63%) of this period.(ABSTRACT TRUNCATED AT 250 WORDS)
The authors prospectively studied 455 consecutive patients referred to the general medical consultation service for cardiac risk assessment prior to non-cardiac surgery, in order to validate a previously derived multifactorial index in their clinical setting. They also tested a version of the index that they had modified to reflect factors they believed to be important. For patients undergoing major surgery, the original index performed less well in the validation data set than in the original derivation set (p less than 0.05), but still added predictive information to a statistically significant degree (p less than 0.05). The modified index also added predictive information for patients undergoing both major and minor surgery, demonstrating an area under the Receiver Operating Characteristic curve of 0.75 (95% confidence interval of 0.70 to 0.80). A simple nomogram is presented which will enable conversion of pretest probabilities into posttest probabilities using the likelihood ratios associated with each risk score. It is recommended that clinicians estimate local overall complication rates (pretest probabilities) for the clinically relevant populations in their settings before they apply the predictive properties (likelihood ratios) demonstrated in this study in order to calculate cardiac risks for individual patients (posttest probabilities).
Hypertrophic cardiomyopathy is a diverse clinical and pathophysiologic entity that involves principally the left ventricle and is caused by asymmetric or concentric hypertrophy of unknown cause. If asymmetric, the hypertrophy is usually greatest in the ventricular septum, but variations occur in which the hypertrophy may be maximal at the apex, at the midventricular level, or, rarely, in the free wall of the left ventricle. Right ventricular involvement is usually less evident. The principal abnormality in systole is the obstruction to left ventricular outflow caused by upper septal hypertrophy narrowing the outflow tract and setting the stage for Venturi forces to cause systolic anterior motion of the anterior or posterior mitral leaflets. The time of onset and duration of mitral leaflet-septal contact determine the magnitude of the pressure gradient. Mitral regurgitation invariably accompanies the obstruction to outflow. Ventriculomyotomy-myectomy surgery, by thinning the septum and widening the outflow tract, abolishes the abnormal mitral leaflet motion and, consequently, the obstruction to outflow and the mitral regurgitation. This form of surgery more dramatically relieves the systolic abnormalities and the accompanying symptoms than any form of medical therapy available today. The extent of hypertrophy is believed to be the principal determinant of the impaired left ventricular relaxation and increased chambers stiffness (decreased compliance) that characterize diastole in hypertrophic cardiomyopathy. Relaxation is impaired by the contraction load (the obstruction), by a decrease in the principal relaxation loads, by a pathologic degree of nonuniformity of contraction and relaxation, and in all likelihood, by impaired inactivation of the biochemical processes responsible for contraction (? due to primary or ischemia-induced calcium overload). Calcium channel-blocking agents may dramatically improve left ventricular relaxation by speeding up the inactivation process, by decreasing the degree of nonuniformity, or by altering the contraction and relaxation loads in a favorable manner. Atrial and ventricular arrhythmias are responsible for a significant proportion of the morbidity and mortality, and their occurrence also appears to depend on the extent of hypertrophy. Thus, the major manifestations of hypertrophic cardiomyopathy in systole and diastole as well as the disturbances of rhythm appear to be related to the site and/or extent of the hypertrophic process.(ABSTRACT TRUNCATED AT 400 WORDS)
Echocardiographic and Doppler studies are invaluable in the detection and management of patients with hypertrophic cardiomyopathy, since virtually all aspects of the disorder can be evaluated. Echocardiography is the primary method of diagnosis, and hemodynamic studies are required usually only when surgery is contemplated. All patients should if possible undergo complete M-mode, two-dimensional, Doppler, and color flow studies to define the extent of hypertrophy, the hemodynamic subgroup, quantitation of left ventricular outflow obstruction, mitral regurgitation when present, and an assessment of diastolic function. Patients undergoing medical or surgical therapy for this disorder should have repeat studies performed to assess the effects of therapy on the degree of obstruction and diastolic dysfunction.
The risk of cardioembolic events and the role of anti-coagulation therapy in the management of patients with lone atrial flutter is not well defined in the medical literature. We report the case of an otherwise healthy 42-year-old man with chronic established atrial flutter, unassociated with any other heart disease or systemic illness, with transesophageal echocardiographic findings of a mobile left atrial appendage thrombus. The literature to date, potential mechanisms, and recommendations are discussed. The role of transesophageal electrocardiography and anticoagulation in atrial flutter may need to be considered more seriously, especially if atrial flutter has been present for a prolonged period of time.
Abnormalities of diastolic filling are increasingly recognized as a cause of symptoms and predictors of outcome in patients with most forms of heart disease. Noninvasive assessment of diastolic filling is possible in almost all patients, but accurate evaluation must relate echocardiographic Doppler measurements to the complex physiologic and hemodynamic factors responsible for normal and abnormal filling. This evaluation has been facilitated by recent correlation of Doppler measurement of mitral and pulmonary venous inflow with hemodynamic studies. These studies have confirmed that when a careful, integrated approach is taken, Doppler flow patterns can document a progressive pattern of abnormality in many conditions. Impaired left ventricular (LV) relaxation is seen early and is recognized by a decrease in early transmitral LV filling and an increased proportion of filling during atrial contraction. As abnormalities progress, increasing LV chamber stiffness and elevated left atrial pressure lead to a "pseudonormal" filling pattern that previously has caused considerable confusion. This can be unmasked by careful evaluation of pulmonary venous inflow and the use of the Valsalva maneuver. When marked diastolic abnormalities are present, LV filling has restrictive features characterized by rapid early filling, a very stiff left ventricle with high filling pressures, and a poor prognosis. Routine measurement of indexes of diastolic filling have been hampered by uncertainty as to what should be measured, what techniques should be used, definition of normal values, and a clear method of reporting findings. This report represents the efforts of a Canadian consensus group to define a national standard for the performance and reporting of echocardiographic Doppler studies of diastolic filling.