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Biomedical subjects

T A Traill

Publications and source records attributed to T A Traill.

At least 37 records · Page 2Linked to original sources

Pulmonary hypertension and interstitial fibrosis in von Recklinghausen neurofibromatosis.

Neurofibromatosis von Recklinghausen (NFvR) has been reported to be associated with diffuse interstitial pulmonary fibrosis. We describe a patient with NFvR presenting in middle age with dyspnea and cyanosis. Chest radiographs showed right ventricular enlargement, dilated proximal pulmonary arteries, and bilaterally increased interstitial markings. Cardiac catheterization showed moderately severe pulmonary hypertension and no evidence of congenital heart defect. The interstitial fibrosis associated with NFvR can result in symptomatic pulmonary hypertension.

Electrocardiography↗

Partial left anomalous pulmonary venous return: a diagnostic dilemma.

Two adults were seen with left partial anomalous pulmonary venous return with intact atrial septum. Both cases had remained undiagnosed despite medical attention since childhood, including previous cardiac catheterization in one patient. Noninvasive tests, indocyanine green dye injections, pulmonary artery angiography, and venous sampling for oximetry high in the superior vena cava above the entry of the innominate vein will help establish the diagnosis of this disorder.

Adult↗

Effect of the addition of propranolol to therapy with nifedipine for unstable angina pectoris: a randomized, double-blind, placebo-controlled trial.

The value of the addition of beta-blockers to coronary vasodilator therapy in the treatment of patients with unstable angina at rest is controversial. We conducted a double-blind, randomized, placebo-controlled 4 week trial of propranolol in 81 patients with unstable angina, 39 of whom were assigned to placebo and 42 of whom received propranolol in a dose of at least 160 mg daily. All patients were also treated with coronary vasodilators, including 80 mg nifedipine daily and long-acting nitrates. The incidences of cardiac death, myocardial infarction, and requirement for bypass surgery or coronary angioplasty did not differ between the two groups (propranolol = 16; placebo = 18). The propranolol group had a lower cumulative probability of experiencing recurrent resting angina than the placebo group (p = .013), and over the first 4 days of the trial the mean number of clinical episodes of angina (propranolol 0.9 +/- 0.2, placebo 1.8 +/- 0.3, p = .036), duration of angina (propranolol 15.1 +/- 4.3 min, placebo 38.1 +/- 8.4, p = .014), and nitroglycerin requirement (propranolol 1.1 +/- 0.3 tablets, placebo 3.5 +/- 0.8, p = .003) were also fewer. Continuous electrocardiographic recording for ischemic ST segment changes revealed fewer daily ischemic episodes in the propranolol group (2.0 +/- 0.5) than in the placebo group (3.8 +/- 0.7, p = .03), and a shorter duration of ischemia (propranolol 43 +/- 10 min, placebo 104 +/- 28 min, p = .039). Thus propranolol, in patients with unstable angina, in the presence of nitrates and nifedipine is not detrimental and reduces the frequency and duration of symptomatic and silent ischemic episodes.

Adult↗

Septal geometry in the unloaded living human heart.

Right ventricular loading leads to diastolic septal flattening in man without necessarily requiring right ventricular pressure to exceed left ventricular pressure. This observation suggested that the unstressed septal configuration is flat and that its normal concave shape is due to the left-to-right transseptal pressure gradient. To examine this hypothesis, we studied septal configuration by two-dimensional echocardiography in nine patients with normal global and regional left ventricular function during surgery for coronary artery disease. The transseptal pressure gradient was obtained from pulmonary capillary wedge pressure minus right atrial pressure. Measurements were obtained at control (open chest, intact pericardium [C]), with the pericardium open (OP), on cardiopulmonary bypass (CPB), and after cardiac arrest (CA). There were no changes in any measurements between C and OP or between CPB and CA. Left ventricular end-diastolic cavity area decreased from 16.5 +/- 2.1 cm2 at C to 11.1 +/- 4.5 cm2 after CPB, and further decreased to 8.9 +/- 3.5 cm2 after CA (p less than .001), yet the septum flattened, as shown by an increase in its radius of curvature from 1.7 +/- 0.5 cm during C to 2.5 +/- 0.7 cm after CPB, and to 2.9 +/- 1.0 cm after CA (p less than .001), or from 0.4 +/- 0.1 to 0.8 +/- 0.4 to 1.1 +/- 0.5 U (p less than .001) when normalized for cavity area. Diastolic transseptal pressure gradient was reduced from 4.1 +/- 2.3 mm Hg during C to 1.1 +/- 1.8 mm Hg after CPB, and to 0.5 +/- 1.4 mm Hg after CA (p less than .01).(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure↗

Organization, development and early results of a heart transplant program. The Johns Hopkins Hospital experience.

Improved survival and quality of life have resulted in a resurgence in cardiac transplantation and the proliferation of centers contemplating initiation of a transplant program. Organization of such a program requires cooperation among several clinical and non-clinical departments of the hospital. Prior to implementation of such a program, a number of issues need to be addressed, including state authorization, an expeditious method for donor organ retrieval, protocols for recipient selection and evaluation, and perioperative and follow-up care of the transplant recipient. Since July of 1983, 35 patients (27 men and eight women) have undergone orthotopic cardiac transplantation. Transplantation was undertaken for cardiomyopathy (30) or end-stage ischemic heart disease (5). The mean age was 38 years (range, 16 to 57 yrs). Distant organ procurement was used for 83 percent of patients; mean ischemic time was 164 min (range, 75 to 250 min). Current immunosuppressive regimen consists of oral cyclosporine (10 mg/kg) and prednisone. Mean follow-up was 10.3 months (range, two weeks to 27 months). Transient renal dysfunction appeared early in 15 patients. Six deaths have occurred: three from rejection, one from infection, one from metastatic prostate carcinoma, and one from pulmonary hemorrhage. All but three recent patients have been rehabilitated. These initial encouraging results are a result of careful planning, institutional commitment, adequate resources and, most importantly, a dedicated transplant team.

Adolescent↗

Hypertensive hypertrophic cardiomyopathy of the elderly.

Using echocardiography, we identified 21 patients with a syndrome that included severe concentric cardiac hypertrophy, a small left ventricular cavity, and supernormal indexes of systolic function without concurrent medical illness or ischemic heart disease. Thirteen of the patients presented with dyspnea or chest pain. All patients studied had a history of hypertension and were compared with normotensive controls matched for age and sex. The patients were elderly (mean age, 73.3 years), predominantly female (16 patients), and mostly black (15 patients). Their cardiac function was characterized by excessive left ventricular emptying (ejection fraction on two-dimensional echocardiography [patients vs. controls], 79 +/- 4 vs. 59 +/- 5 per cent, P less than 0.001) and abnormal diastolic function as manifested by a prolonged early diastolic filling period (279 +/- 25 vs. 160 +/- 45 msec, P less than 0.001) and reduced peak diastolic dimension increase (11 +/- 4 vs. 16 +/- 5 cm per second, P less than 0.05). In spite of the clinical presentation of heart failure, all of 9 patients receiving either beta-receptor antagonists or calcium-channel blocking agents obtained symptomatic relief, whereas 6 of 12 patients receiving vasodilator medications had severe hypotensive reactions, including one death. We conclude that this unique subset of hypertensive patients has a clinical syndrome that warrants recognition and tailored management.

Adrenergic beta-Antagonists↗

Familial pulmonary valve stenosis, atrial septal defect, and unique electrocardiogram abnormalities.

The familial association of pulmonary stenosis, atrial septal defect, and unique electrocardiographic abnormalities involving a mother and two children is reported. Familial pulmonary stenosis not occurring as part of a named syndrome or without associated multiple congenital abnormalities is rare. The constellation of pulmonary stenosis, atrial septal defect, and the particular electrocardiogram abnormalities present here is to our knowledge previously unreported. The pattern of inheritance is consistent with an autosomal dominant mode of transmission.

Cardiomyopathy, Hypertrophic↗

Heart and heart-lung transplantation: program, development, organization, and initiation.

Since the initiation of cardiac transplantation in 1967, more than 1,000 procedures have been done worldwide. A high percentage of these transplant procedures have been completed in the past few years. In 1983, II centers in the United States performed 173 transplant procedures; by 1984, there were more than 30 heart transplant centers. This sudden increase is due primarily to increasing survival of transplant recipients since the introduction of cyclosporine. However, most transplant surgeons believe that the use of this drug alone will not result in survival results and rehabilitation similar to those obtained in experienced transplant centers. Institutional commitment, adequate resources, attention to detail and most importantly, a dedicated transplant team, are important elements to ensure success. This manuscript will define guidelines for the establishment of a new transplant program and eludicate the organizational details necessary to implement such a program, based on our experience at the Johns Hopkins Hospital over the past two years.

Consumer Behavior↗

Operative intervention for postinfarction angina.

Thirty-four patients (26 men and 8 women) underwent myocardial revascularization following myocardial infarction (MI) at the Johns Hopkins Hospital during 1980 through 1982. Average age was 59 years. Of the 33 patients with unstable angina, 61% had ischemia in the infarct zone and 39% had "ischemia at a distance." Mean time from MI to operation was 16 days. The MIs were equally divided between a transmural and a subendocardial location. Eleven patients had a history of congestive heart failure. Intraaortic balloon pumping was used preoperatively for anginal stabilization in 14 patients. Mean ejection fraction for the group was 52%. There were 3 operative deaths, all 3 due to myocardial failure. Late follow-up (mean, 13.7 months; range, 6 to 35 months) is complete for 28 patients. There was 1 late death, secondary to cardiac failure. There were no late MIs. Angina had recurred in 5 patients, but only 2 were taking antianginal medication. At the time of follow-up, 52% of patients were in New York Heart Association Functional Class I. This experience suggests that operative intervention for postinfarction angina can be accomplished with an acceptable mortality and thereby increase survival, reduce the later occurrence of MI, and relieve angina in this high-risk group.

Aged↗

Acute nifedipine withdrawal: consequences of preoperative and late cessation of therapy in patients with prior unstable angina.

Reports of acute ischemic events after withdrawal of calcium antagonist therapy in outpatients and during bypass surgery in patients with prior angina at rest prompted the examination of the effect of nifedipine withdrawal in 81 patients who had completed a prospective, double-blind randomized trial of nifedipine versus placebo for rest angina. Thirty-nine patients underwent bypass surgery for uncontrolled angina or left main coronary artery disease. No significant difference between patients withdrawn from nifedipine or placebo was seen in the incidence of perioperative myocardial infarction, hypotension requiring intraaortic balloon counterpulsation, vasopressor or vasodilator requirements or incidence of significant arrhythmias. An additional 42 patients had completed 2 years on a protocol consisting of nitrates and propranolol in addition to nifedipine or placebo. During a mean of 66 hours of continuous monitoring after withdrawal of nifedipine or placebo, heart rate and blood pressure were unchanged. A worsening of previously present angina at rest occurred in five patients who had continued to experience rest angina before drug withdrawal, four of whom were withdrawn from nifedipine. No patient with class I to III angina experienced new onset of rest angina during drug withdrawal. No patient experienced myocardial infarction. There was no significant difference between patients withdrawn from nifedipine or placebo in the duration or frequency of ischemic ST changes on continuous electrocardiographic monitoring, or in duration or positive results of serial exercise treadmill testing. Thus, no early adverse effects of acute nifedipine withdrawal were found in patients with prior rest angina at the time of bypass surgery or in stable patients receiving long-term medical therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Angina Pectoris↗

Effect of nitroprusside on hydraulic vascular loads on the right and left ventricle of patients with heart failure.

We studied the effect of nitroprusside on the hydraulic vascular load of the right and left ventricle in seven patients with severe left ventricular failure. At doses of 0.25-0.75 micrograms/kg/min, stroke volume increased progressively from 40.1 to 48.6 ml and left ventricular end-diastolic pressure decreased from 24.5 to 11.2 mm Hg. Accompanying this improvement in left ventricular performance were dose-related decreases in mean ventricular pressures, pulmonic and systemic resistances and the lower-frequency components of input impedance moduli. Characteristic impedance and both total and oscillatory external power were decreased in the pulmonic, but not the aortic, vasculature. In this class of patients, right ventricular unloading is a striking and direct effect of nitroprusside and may account, in part, for improved left ventricular performance through ventricular interdependence.

Adult↗

Incomplete filling and incoordinate contraction as mechanisms of hypotension during ventricular tachycardia in man.

We sought to determine mechanisms for decrease of cardiac output and for hypotension during ventricular tachycardia (VT) in man. Two-dimensional and M mode echocardiograms and left ventricular pressure from micromanometer-tipped catheters were obtained in 20 patients before, during, and at the end of induced hypotensive VT. Patients were divided into two groups according to left ventricular function in sinus rhythm as assessed by angiographic ejection fraction (EF) before electrophysiologic study. Group 1 (n = 8) had angiographic EF greater than or equal to 50% in normal sinus rhythm, and group 2 (n = 12) had EF less than or equal to 40%. During VT, left ventricular cavity volume (as indexed by short- and long-axis two-dimensional end-diastolic cavity areas) was markedly reduced in group 1, from 19.7 +/- 2 to 8.6 +/- 2 cm2 (p less than .001) and from 32.0 +/- 8 to 22.5 +/- 7 cm2 (p less than .001), respectively, but was only slightly reduced in group 2, from 34.1 +/- 6 to 31.5 +/- 7 cm2 (p = .044) and from 45.0 +/- 8 to 49.4 +/- 7 cm2 (p = NS), respectively. Conversely, left ventricular systolic function during VT (as indexed by fractional reduction in two-dimensional short- and long-axis areas) was markedly depressed in group 2, from 25.6 +/- 6% to 4.2 +/- 4% (p = .005) and from 13.7 +/- 3% to 1.8 +/- 0.8% (p less than .001), respectively, but remained at control levels in group 1. Left ventricular end-diastolic pressures increased in group 1, from 11.8 +/- 2 to 27.7 +/- 8 mm Hg (p = .005) and did not change in group 2 during VT. Pressure-dimension loops from left ventricular pressure and M mode echocardiographically determined cavity dimensions generated from the end of the VT episodes showed that diastolic pressure-dimension relationships returned to control levels with the first prolonged diastolic interval in group 1 patients, indicating that incomplete relaxation was the mechanism responsible for reduction of cardiac output during VT in these patients. Coordination of contraction and relaxation (indicated by the percent ratio of the pressure-dimension loop area to the area of the rectangle just enclosing the loop) decreased from 37 +/- 11% to 16 +/- 13% in group 2 patients during VT (p = .013) but remained at control levels in group 1 patients. Thus, during VT patients with impaired left ventricular function in sinus rhythm (group 2) developed severe discoordination, and patients with normal or near-normal function (group 1) developed incomplete relaxation to account for stroke volume deterioration and hypotension.

Adolescent↗

Presystolic mitral closure sound in aortic regurgitation with left ventricular hypertrophy and first degree heart block.

We report a patient who developed aortic regurgitation and first degree atrioventricular block caused by infective endocarditis complicating aortic valve stenosis. There was premature closure of the mitral valve and, in the absence of an Austin Flint murmur, a simultaneous high frequency sound was audible which we regard as a presystolic first heart sound. That such a sound may be associated with valve closure, even though this precedes electrical and mechanical ventricular systole, provides further support for the valvular origin of the first heart sound.

Aged↗

Wall thickness changes considered as regional myocardial function in ischemic heart disease.

Dynamic changes in left ventricular wall thickness represent a function of the myocardium which can be described, in normal subjects or in disease, without reference to behavior of other parts of the wall. Abnormalities of amplitude, rate and timing of wall thickness change interact in influencing overall ventricular performance, so that even this local function cannot be expressed as a single "index". Infarcted and acutely ischemic myocardium display reduced amplitude of thickness change. The degree to which they also show delayed wall dynamics in man is uncertain. Cross-sectional echocardiography has not been used to examine this aspect of regional thickness change, mainly because of the difficulties of processing "real-time" images. In the stable state of ischemic heart disease, such as exists in patients with angina, abnormalities of timing are common, even in the absence of significant reduction in overall thickness change, and lead to impaired energy transfer from the myocardium to the circulation. The degree of organization involved in normal myocardial function is better appreciated when one considers the complex phenomena which result from its disruption. In particular, rapid wall thinning in early diastole, normally associated with rapid filling, is revealed as an inherent property of the wall when it becomes dissociated from filling because relaxation is incoordinate. This demonstration of the active processes involved in ventricular relaxation provides an example of how the study of ischemic heart disease, in its differing local effects, may provide insight into the normal physiology of the myocardium.

Coronary Disease↗