Valvular heart disease associated with fenfluramine-phentermine.
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Biomedical subjects
Publications and source records attributed to B C Corya.
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Follow-up information was obtained from 148 patients who had normal resting and post-treadmill exercise echocardiograms to determine the prognostic value of a normal exercise echocardiogram in patients evaluated for suspected coronary artery disease. There were 77 men and 71 women with a mean age of 52.5 years and a pretest likelihood of coronary artery disease of 39%. Patients were followed for a mean duration of 28.4 +/- 8.5 months. The exercise ECG was abnormal in 69 patients (47%) including 28 who had ischemic responses. Cardiac events occurred in six patients, three with normal and three with abnormal exercise ECGs. Events occurred only in those patients (6 of 68) who exercised to work loads less than 6 METs or who achieved less than 85% of the age-predicted maximal heart rate. Three patients had coronary artery bypass grafting for angina from 10.5 to 22.5 months after echocardiography. A fourth patient had bypass grafting for mild single-vessel disease at the time of mitral valve replacement. Two patients had myocardial infarctions (0.85% per year) at 7.5 and 41 months after echocardiography. There were no deaths. Coronary revascularization is infrequently required in the 28 months after a normal exercise echocardiogram. A normal exercise echocardiogram in a patient with good exercise capacity was predictive of an excellent prognosis, even in those who had abnormal exercise ECGs. Myocardial infarction and death were rare events, even in patients with decreased exercise capacity.
The purpose of this study was to determine the potential of a clinically adaptable two-dimensional echocardiographic system using computer enhancement and a mathematically defined integrated backscatter ratio for the early detection of ischemic and infarcted myocardium. Fifteen dogs had two-dimensional echocardiograms recorded during either open chest coronary occlusion (n = 5), closed chest occlusion (n = 5), occlusion followed by reperfusion (n = 3) or sham coronary occlusion (n = 2). A serial increase in integrated backscatter ratio, representing differences in returned ultrasound intensities between a reference point and specific myocardial regions, was detected between 7 and 12 minutes of complete occlusion in 9 of 12 animals (p less than 0.05), and at minutes 18, 43 and 67 in the remaining 3 animals. Reperfusion after 20 minutes of occlusion in two studies resulted in normalization of the backscatter ratio. An increase in backscatter ratio was not detected when 5 minute occlusion periods were used or during the 5 hour sham occlusion studies. The computer enhancement techniques utilized in this study provided increased visual detail of intracardiac structures over that provided by routine two-dimensional echocardiograms; myocardial tissue was identifiable in what appeared to be echo-free segments; and boundaries that appeared as noncontiguous horizontal lines on the routine echocardiograms were identifiable as trabeculae. The results indicate that: 1) significant increases in backscatter from nonperfused myocardium are detectable echocardiographically within 12 minutes of coronary occlusion and temporal changes can be assessed in the canine model, and 2) the echocardiographic data acquisition and computer analysis system utilized provide a clinically adaptable approach to identify and map myocardial characteristics in human beings.
Echocardiography directly reflects cardiac anatomy and pathology. A normal two-dimensional and M-mode study rules out a multitude of cardiac pathologies. Echocardiography serves the clinician well in differentiating cardiac from noncardiac symptoms and in providing bedside quantitative assessment of regional and global left ventricular function. It is also invaluable in evaluating valvular disease, pericardial effusion, and intracardiac masses.
During two histoplasmosis outbreaks in Indianapolis 45 patients presented with pericarditis. The pericarditis occurred as a late complication in individual patients and during the outbreak. Risk factors for this complication included young age, immunocompetence, and male sex in persons between 20 and 39 years old. Intrathoracic adenopathy was present in 66% of cases. Since cultures were uniformly negative, including pericardial fluid or tissue from nine patients, serologic studies provided the basis for diagnosis. Although the course was usually benign, nine patients presented with tamponade and another with constrictive pericarditis. Prompt response to antiinflammatory medications and failure to identify H. capsulatum in the pericardial fluid or tissue support a noninfectious, inflammatory mechanism for this complication. Of 20 patients reexamined 1 year later, none had evidence of constriction but three had pericardial thickening by echocardiography. Histoplasmosis should be considered in patients with pericarditis from endemic areas, particularly when associated with intrathoracic adenopathy.
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Single-dimension left ventricular echocardiographic measurements are currently being used in investigational studies as the basis for evaluating cardiac output parameters in normal subjects, even though validity of the method for normal subjects has not been established. We prospectively compared stroke volume derived from M mode left ventricular dimensions (LVID) to Fick stroke volume in 20 patients with no objective evidence of cardiac disease. Based on simultaneous studies, stroke volume by Fick ranged from 39 to 121 ml and cardiac output ranged from 3.9 to 10.4 L/min. Comparing the LVID cubed method with Fick, the correlation coefficient was r = .47 for stroke volume and r = .36 for cardiac output. LVID absolute error in cardiac output ranged -2.11 to +3.21 L/min. Use of other published formulas for calculating stroke volume from LVID did not improve accuracy. These data indicate that stroke volume and cardiac output cannot be accurately measured or reliably estimated from M mode left ventricular internal dimensions.
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Left ventricular (LV) wall motion was evaluated prospectively by M-mode echocardiography for 503 patients, and results were compared with cinearteriographic and ECG findings. M-mode results from 92 of the patients were also compared with two-dimensional echocardiographic (2D) and LV angiographic findings. Abnormal echo motion was found by M-mode in 89 percent of patients with ECG Q waves of infarction and in 61 percent of coronary artery disease (CAD) patients without Q waves. Thirty-four percent of CAD patients had normal wall motion on M-mode examination. More abnormalities were detected when patients were examined using both M-mode and 2D, because M-mode was more sensitive in detecting anterior lesions and 2D was more sensitive in detecting posterior lesions. Both M-mode and 2D showed a low incidence of false-positive diagnosis (less than 2 percent) for patients with normal findings at cardiac catheterization.
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Wall thicknesses were measured and echo densities were evaluated from the left ventricular echograms of 182 patients. The echogram was considered to reflect scar tissue when 1) either the interventricular septum, the posterior left ventricular wall or the anterior left ventricular wall was less than 7 mm thick in mid-diastole and was more echo-producing than its opposing wall or another area of the same wall in a sector scan, or 2) an area of myocardium was 30% less thick than an adjacent area within a sector scan. Myocardial scarring was diagnosed by echocardiography in 52 of the 182 patients. The echocardiographic presence or absence of scarring was confirmed in 95% (173 of 182) of cases, 34 cases by microscopic examination and 139 by surgical appearance. This study shows that M-mode echocardiography is both a sensitive and specfic method for detecting myocardial scar tissue.
A formula was derived for calculating mitral valve stroke volume (MVSV) using the rate of mitral valve (MV) opening (DE slope on the MV echogram), the vertical disease between the mitral leaflet echoes early in diastole (EE), the electrocardiographic PR interval and heart rate. The formula was tested prospectively on 80 consecutive patients from whom 95 simultaneous MV echograms and either thermodilution (45) or Fick (50) cardiac outputs were obtained. Sixteen patients were normal; 54 had coronary artery disease; three had cardiomyopathy; and seven had nonrheumatic mitral regurgitation (MR). Linear regression for stroke volume was r = 0.90, SEE +/- 6, and for cardiac output r = 0.83, SEE +/- 0.5 liter for the 73 patients without MR. The presence or absence of ventricular dyssynergy did not alter statistical findings. MVSV consistently overestimated forward stroke volume for the seven patients with MR. This study shows that the MV echogram provides an accurate, widely applicable method for calculating MVSV.
Echocardiographic findings in patients with ischemic heart disease are described; their correlations with clinical, hemodynamic and angiographic data are presented and discussed. Regional abnormalities of left ventricular wall motion and/or thickening during systole are detected in 84 per cent of patients with acute myocardial infarction and in a high percentage of patients with larger than or equal to 75 per cent narrowing of a major coronary artery. These abnormalities may occur with stress and may be reversible. Left ventricular wall thinning during systole indicates acute ischemia or infarction and thin, dense myocardial echoes indicate scar. Echocardiographic evidence of left ventricular dysfunction is useful in predicting heart failure and mortality in patients with acute myocardial infarction and in predicting surgical mortality for patients undergoing aneurysmectomy and/or coronary artery bypass surgery. Echocardiography has not proved useful in determining graft patency following coronary artery bypass surgery. Technical difficulties and limitations of echocardiography in patients with coronary artery disease are discussed.
Echocardiographic septal and posterior wall thicknesses and the percent change with systole were measured in 146 patients with the following diagnoses: acute myocardial infarction (40), chronic coronary artery disease (49), congestive cardiomyopathy (8), atrial septal defect (20), and no cardiac disease (29). Mean diastolic thicknesses for the groups of patients with coronary artery disease and congestive cardiomyopathy were not significantly different from normal although there were abnormal values for individual patients within each group. Mean diastolic thickness of the septum was greater than normal for the group with atrial septal defect (P less than 0.02). Wall thinning with systole was associated with acute infarction or ischemia (P less than 0.0001); decreased thickening (less than normal) commonly occurred in patients with acute myocardial infarction, chronic coronary artery disease, and congestive cardiomyopathy. Patients with atrial septal defect had normal thickening with abnormal motion. Results of this study show that 1) systolic thinning is indicative of an acute event; 2) abnormal changes in systolic wall thickening occur commonly in patients with coronary artery disease or congestive cardiomyopathy; and 3) abnormal wall motion may occur without abnormal wall thickening, as the echoes of patients with atrial septal defect indicate.
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Impaired left ventricular performance, one of the hallmarks of coronary artery disease, can be detected by echocardiography in various ways. One of these approaches is the recording of abnormal wall motion. Because of the way in which the left ventricle can be examined echocardiographically, this technique has the capability of detecting regional wall abnormalities. In fact echocardiography is probably the most sensitive technique available, including even contrast ventriculography, for the detection of akinetic, hypokinetic or dyskinetic wall segments. With increasing experience it is apparent that more areas of the left ventricle can be examined echocardiographically than had previously been thought possible. Newer techniques include directing the ultrasonic beam not only through the body of the left ventricle but also toward the apical portion of the ventricle near the vicinity of the papillary muscles. In addition the true anterior left ventricular wall can be examined by moving the transducer laterally away from the left sternal border. Yet another approach utilizes a subxiphoid position for the transducer while the ultrasonic beam is directed through the medial portion of the septum and posterolateral wall of the left ventricle. M-mode scanning techniques together with recently developed cross-sectional echocardiographic instruments give great promise of improved detection of abnormalities of ventricular shape, especially the presence of aneurysms. The cross-sectional approach makes it possible to examine the left ventricular apex, an area virtually impossible to record with M-mode echocardiography. Recording of left ventricular dimensions and abnormal mitral valve motion may help in assessing overall left ventricular performance. A dilated left ventricular dimension in the vicinity of the mitral valve seems to be an ominous finding both in patients with acute myocardial infarction and in patients with chronic coronary disease being considered for possible surgery. Another echocardiographic sign of abnormal ventricular performance is altered closure of the mitral valve, which reflects a significantly elevated left ventricular diastolic pressure. These echocardiographic techniques are still in the investigational stages and are more technically difficult than the usual echocardiographic applications. However, the preliminary data are encouraging and make us hopeful that echocardiography will prove to be an important tool in the overall evaluation of the left ventricle in patients with coronary artery disease.
Myocardial lesions are frequently seen at necropsy after fatal carbon monoxide poisoning. Clinically, while there have been numerous reports of chest pain and electrocardiographic changes associated with acute carbon monoxide poisoning, other evidence for left ventricular abnormality has not been reported. The echocardiographic findings in five cases of non-fatal poisoning are presented here. Abnormal left ventricular wall motion was shown by echocardiography in 3 cases. Motion returned to normal in 2 of the 3 in follow-up tracings. Echocardiograms on 3 of the 5 patients showed mitral valve prolapse. Though the mitral valve prolapse may have been present before the poisoning, the reported high incidence of papillary muscle lesions in fatal cases suggests a possible relation of the prolapse to the effects of the carbon monoxide poisoning.