Ruptured sinus of Valsalva: demonstration by contrast echocardiography during cardiac catheterization.
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Biomedical subjects
Publications and source records attributed to H N Neufeld.
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The incidence of coronary aneurysmatic dilatation without coronary stenosis is rare, and the clinical course of such an entity is unknown. We present five adult patients, four men and one woman, with such an anatomic finding. The age range was 44 to 60 years. In four patients the aneurysmatic dilatations involved multiple coronary sites. The clinical course in all five patients was suggestive of coronary insufficiency. Despite no obstructive disease, two of the patients developed transient ischemic ECG changes accompanied by chest pain, and another two patients demonstrated ischemic exercise nuclear ventriculography response. In time, all five patients developed acute myocardial infarction and recatheterization revealed complete occlusion of a previously nonstenosed aneurysmatic vessel. More information is needed in order to guide therapy. However, prevention of thrombus formation and close follow-up is highly recommended.
Age-adjusted mortality from coronary heart disease (CHD) showed a striking decline in Jews living in Israel between 1974 and 1979. The decline was evident for both males (age-adjusted rate, age 25+, declining from 441 to 347/100,000) and females (declining from 303 to 205/100,000, respectively), and probably for each of the different immigrant groups. A similar decline in Arabs and Druse has not been identified and awaits further analysis. The decline has been associated with the presentation of coronary care units, coronary bypass surgery, improved emergency service and cardiopulmonary resuscitation procedures. The modernization of diagnostic procedures, discharge and rehabilitation, and possibly pharmacologic therapy may also have contributed, but available data do not provide unequivocal proof for the role of secondary prevention. In the realm of primary prevention, evidence for improved screening, treatment and control of hypertension is suggestive but not conclusive. Little, if any, change in serum cholesterol levels and cigarette smoking habits has been observed. A continuous increase of the percent of calories derived from fat has been apparent, while energy derived from carbohydrates, notably starch, has been declining. Thus, changes in CHD mortality were not accompanied by putatively anti-atherogenic trends in eating habits. The reasons behind the striking decline of CHD mortality in Israel are not clear, but so far there is very little in the available data to suggest a meaningful effect of life-style modifications on mortality trends.
Heart studies were carried out in 7 patients with end-stage renal disease (ESRD) who underwent parathyroidectomy for secondary hyperparathyroidism. The studies, which included echocardiography and equilibrium radionuclide angiography (ERNA), were performed prior to parathyroidectomy and 2 weeks, 3 months, and 6 months following it, on a nondialytic day. Heart rate decreased from 89.3 +/- 1.3 to 81.4 +/- 1.5 min-1 (p less than 0.001) following parathyroidectomy and returned to the initial level at 3- and 6-month examination. Cardiac output decreased from 3170 +/- 68 to 2943 +/- 57 ml/min (p less than 0.01) following parathyroidectomy and returned to basal level on 3 and 6-month determinations. End-diastolic dimension (EDD), end-systolic dimension (ESD), septal and posterior wall thickness and shortening fraction (SF) as measured by echocardiography were normal prior to parathyroidectomy and remained unchanged following it. Left ventricular ejection fraction (LVEF), end-diastolic and end-systolic volumes measured by ERNA did not change following parathyroidectomy. This study suggests that hyperparathyroidism has little effect on cardiac performance and, except for a short-lived decrease in heart rate and cardiac output, parathyroidectomy does not affect cardiac performance when performed in patients with preoperatively normal cardiac output.
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Forty-two patients with systolic posterior motion of the mitral valve on M-mode echocardiogram were reevaluated after a mean clinical follow-up of 6.7 years and an echocardiographic follow-up of 5.1 years. A new method for quantitation of mitral valve prolapse (MVP) is presented. A straight line (A) was drawn connecting the site of posterior leaflet motion with the D point of the subsequent diastole. A vertical line (B), termed "the degree of MVP," was drawn from the site of maximal MVP to line A. The degree of MVP was then correlated with various clinical and ECG parameters and with the presence of complications. Measurements could be taken in 21 patients; the mean degree of MVP increased from 5.9 +/- 2.1 to 7.1 +/- 2.9 mm (P less than 0.01), and mean left atrial size increased from 3.0 +/- 0.5 to 3.5 +/- 0.8 cm (P less than 0.01). No correlation was found between the degree of MVP and symptoms, auscultatory findings or the presence of complications. There were no deaths and in none was life-threatening arrhythmia documented. The complications we encountered were endocarditis in five patients, transient ischemic attacks in two and cardiac arrest during surgery in one. We conclude that 1) the degree of MVP can be measured by M-mode echocardiography; 2) there seems to be no correlation between the degree of MVP and the patient's clinical state; 3) complications in MVP are rather frequent; and 4) left atrial size and degree of MVP tend to increase with time, which may indicate a progressive nature of the disease.
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Radionuclide ventriculographic studies were performed at rest and during exercise on 30 consecutive men, aged 21 to 35 years with diabetes mellitus without evidence of coronary artery or any other cardiovascular disease, and in 20 normal age-matched subjects. Sixteen (53%) were treated with insulin and 14 (47%) were treated with either diet (6 patients) or oral antidiabetic therapy (8 patients). All patients from both groups had normal left ventricular (LV) ejection fraction (EF) at rest. In 5 of the 30 diabetic patients (17%), LVEF decreased after exercise, in 8 (27%) it remained unchanged and in 17 it increased normally. Mean LVEF at rest and after exercise in this group was 66 +/- 7% and 72 +/- 7% (+/- standard deviation), respectively. In all normal subjects, LVEF increased after exercise. Mean LVEF at rest and after exercise in the normal group was 66 +/- 7% and 76 +/- 9%, respectively. No patient had evidence of regional dysfunction at rest or after exercise. LV function was not related to serum glucose levels during the test, modality of treatment, insulin dependency or duration of the disease. Three of 4 patients with diabetic microvascular complications showed LV dysfunction. In 4 of 5 patients in whom LVEF decreased after exercise, thallium studies showed normal perfusion. Thus, diabetes mellitus may cause exercise-induced global LV dysfunction in young men with no evidence of cardiovascular disease. This phenomenon apparently does not seem to follow the known course of diabetic microvascular complications.
Thirty-seven patients with discrete subaortic stenosis (DSS) underwent 2-dimensional echocardiography (2-D echo) and cardiac catheterization. The peak systolic pressure gradients ranged from 0 to 150 mm Hg. Thirty-two patients had membranous DSS and 5 had fibromuscular DSS. Of 37 patients with DSS, 2-D echo diagnosed the presence and type in 35; in 2, a membrane was demonstrated by angiography. Of the 35 patients accurately diagnosed by 2-D echo, angiography corroborated the diagnosis in 33, but failed to show the membrane in 2. Subsequent cardiac surgery confirmed the accuracy of the echocardiographic diagnosis in these 2 patients. In all patients with membranous DSS, the anterior insertion of the membrane was demonstrated. In 9 of them the posterior insertion was demonstrated by tilt of the transducer but the anterior insertion disappeared. In 4 patients both insertions were demonstrated simultaneously and in 3 patients the membrane was demonstrated as a continuous line. In 4 of the 5 patients with fibromuscular DSS, both insertions of the lesion were demonstrated simultaneously. However, 2-D echo was unsuccessful in assessing the severity of obstruction. In only 1 patient did demonstration of the whole subaortic membrane as a continuous line below the aortic valve correlate with severe obstruction. Thus, the presence and type of DSS, but not the degree and severity, can be accurately and reliably diagnosed by means of 2-D echo.
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In order to determine whether pulmonic regurgitation (PR) can be reliably diagnosed using contrast echocardiography, we studied 24 subjects using echocardiography during intravenous injections of 5% dextrose solution. Twelve were without PR, and twelve had PR (10 after intracardiac repair of tetralogy of Fallot, one after a Brock procedure for pulmonic stenosis, and one after insertion of a right ventricle-pulmonary artery conduit for pseudo truncus arteriosus). Two blinded independent observers correctly diagnosed PR in all patients when it was present, and correctly excluded it in 11 of 12 of the patients without PR. They disagreed in one patient who had an unusual contrast pattern during diastole. Four postoperative patients had PR by contrast echocardiography despite the absence of a cardiac murmur at the time of their study. We conclude that contrast echocardiography is a safe, simple, sensitive, and specific method for diagnosing PR. Some methodologic suggestions and limitations of the method are discussed.
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Carbon dioxide laser energy was used for the dissolution of atheromatous plaques. Flexible, nontoxic infrared optical fibers were used for the transmission of the carbon dioxide laser beam intraarterially. Dissolution of plaques and recanalization of obstructed arteries were achieved both in vitro and in vivo with controllable damage to the vessel walls.
Sinus nodal dysfunction (SND) and complete heart block (CHB) in congenital heart disease (CHD) are commonly associated with congestive heart failure, syncopal attacks, and sudden death. Permanent cardiac pacing (PCP) is required to avoid these manifestations which are frequently associated with a high rate of complications, particularly in the younger age group. Twenty patients with CHD aged 4 months to 46 years underwent pacemaker implantation. Twelve (60%) were less than 20 years of age. CHB was present in 15 patients: in 10 it developed 1 week to 11 years following surgery, in two it was congenital, and in three patients it developed spontaneously with previous conduction disturbances. SND was present in 5 patients: it was congenital in two patients and developed post-operatively in three. Seventeen patients are alive and no syncopal attacks or bradyarrhythmias were recorded 2.5 to 12.5 years following the initiation of PCP. Improvement in the cardiac output was noted in most patients with heart failure. The three patients who died had adequately functioning pacemakers. Only nine re-implantations were needed, seven of them in adult patients after closure of an atrial septal defect. Our experience indicates a favourable outcome for patients with CHD needing PCP.