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Biomedical subjects

J D Carroll

Publications and source records attributed to J D Carroll.

At least 91 records · Page 5Linked to original sources
PubMed1984

Chronic mitral regurgitation: predictive value of preoperative echocardiographic indexes of left ventricular function and wall stress.

The effect of mitral valve replacement on left ventricular volume, mass, function and clinical symptoms was examined in 20 patients with chronic mitral regurgitation. Pre- and postoperative echocardiograms demonstrated that two outcomes could be defined. Left ventricular dimension at end-diastole was reduced to normal postoperatively in the 16 Group I patients, but was unchanged in the 4 Group II patients. The Group I response was associated with a dramatic reduction in left ventricular mass and a decrease in clinical symptoms; all 16 patients reached New York Heart Association functional class I. No change in left ventricular mass was seen in the Group II patients and all four remained symptomatic despite continued medical therapy. Examination of the preoperative echocardiographic measurements indicates that these data have significant prognostic value in predicting surgical outcome. When ventricular dimension at end-systole exceeds 2.6 cm/m2 or fractional shortening is less than 31% or end-systolic wall stress index exceeds 195 mm Hg, all Group II patients are identified and there are no false positive results in Group I. It is concluded that echocardiographic measurements of left ventricular size, function and wall stress can provide important prognostic information in patients with chronic mitral regurgitation. Such data may allow improved patient selection and a better definition of an optimal time for mitral valve replacement.

Aged↗
PubMed1984

Mechanism of tyramine-induced migraine: similarity with dopamine and interactions with disulfiram and propranolol in migraine patients.

In a double-blind crossover study, 8 patients with classical migraine received disulfiram (400 mg/day) for 6 days, alternating with matched placebo tablets at 2 weekly intervals. Intravenous dopamine and tyramine pressor tests were performed on the 3rd and 6th days of each phase, respectively. 50-75% of patients experienced migraine attacks within 24 h of a test. There was no difference in the incidence of attacks between dopamine and tyramine injections. The number of migraine-free days was more during the placebo week than during disulfiram treatment (p less than 0.05). The post-tyramine migraine index correlated directly with the amount of tyramine administered during the dose-response test (r = 0.66), but no such relationship was found with dopamine. In a further study, post-tyramine migraine was observed in only 1 of 5 patients treated with propranolol (80 mg/day) for 4 weeks. Neither disulfiram nor propranolol influenced the tyramine pressor sensitivity. It is concluded that increased adrenergic activity is responsible for more frequent attacks during disulfiram medication. A similar mechanism probably is responsible for post-dopamine/tyramine migraine in susceptible subjects. It is unlikely that tyramine plays any specific role, except via its effect on the adrenergic system, in the pathogenesis of migraine attacks. However, the tyramine challenge test can be useful in the evaluation of a putative antimigranous activity of a new drug.

Adult↗
PubMed1984

[Hemodynamics in ischemia. Systolic phase].

Experimental animal investigations have shown that already after a few seconds of occlusion of a coronary artery a reduction in the systolic myocardial shortening and wall thickening takes place in the corresponding supply area. Following 1-2 minutes of ischemia systolic expansion occurs. Wall-thickness increase and myocardial shortening then take place during the isovolumetric relaxation phase. When at least 25% of the myocardium of the left ventricle becomes acutely ischemic the end-diastolic pressure and end-diastolic volume increase. As a rule an augmentation of myocardial contraction appears in the non-ischemic section of myocardium, which in part takes place through the Frank-Starling mechanism. With a gradual reduction of the coronary inflow, and a decline in the wall thickening of c. 50% of the control value, a significant reduction in blood flow took place only in the innermost quarter of the ventricular wall. With akinesia of the ischemic area, no reduction of the blood flow could be determined in the subepicardial region. Only with the occurrence of dyskinetic wall motion was a transmural reduction of blood flow effected. The ischemic contraction disturbances are fully reversible if coronary occlusion last only a few minutes. With a 15 minute occlusion the recovery time of the myocardial function can require several days (postischemic "stunned myocardium"). The first myocardial necroses occur after 20 minutes of ischemia, and after 3-6 hours of ischemia the infarction is complete.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Output↗
PubMed1983

Systolic function during exercise in patients with coronary artery disease.

Global and regional systolic function during exercise were studied at cardiac catheterization with biplane cineangiography and micromanometer pressures in three groups of patients: an ischemia group (n = 22) with exercise-induced asynergy from coronary artery disease, a control group with no or minimal cardiovascular disease (n = 5) and a "scar" group (n = 5) with prior infarction and no new asynergy with exercise. Ventricular emptying curves at rest did not distinguish patients with coronary artery disease from control subjects. During exercise, end-systolic volume increased in all patients in the ischemia group; ejection fraction decreased from 62 to 51% p less than 0.001) despite an increased end-diastolic volume. Stroke volume decreased from 65 to 58 ml/m2 (p less than 0.001) and limited the average increase in cardiac index to 65%. The scar group had no decrease in stroke volume, but end-systolic volume failed to decrease during exercise, as it did in all control subjects (35 to 28 ml/m2, p less than 0.05). An exercise-induced decrease in peak left ventricular pressure in five patients (23%) in the ischemia group was not accompanied by more severe or extensive ischemia as judged by ejection phase indexes. There was a tendency for maximal positive first derivative of left ventricular pressure (dP/dt) to be less (1,912 versus 2,446 mm Hg/s, difference not significant), suggesting an abnormality of pressure generation, not shortening. Global function during exercise in the ischemia group was determined, in part, by the extent of regional dysfunction. Those in whom between three and five regions of eight regions studied had abnormal fractional shortening during exercise had a 6% decrease in ejection fraction, while those with six to eight abnormal regions had a decrease in ejection fraction of 15% (p less than 0.05). In addition, function of nonischemic, noninfarcted myocardium was studied at the base of the left ventricle in those with exercise-induced anteroapical ischemia (n = 4) and those with anteroapical infarction (n = 4). Base fractional shortening and shortening velocity were greater at rest in those with infarction (39% and 1.6 circ/s, respectively) than in control subjects (31% and 1.0 circ/s, respectively, p less than 0.01), indicating a chronic augmentation of shortening. Base shortening velocity during exercise in those developing anteroapical ischemia increased from 1.1 to 1.4 circ/s (p less than 0.005), suggesting an acute augmentation of function balancing the deterioration of anteroapical function. Systolic function in coronary artery disease is determined by acute and chronic alterations in regional function. During exercise, there is an interplay between regional dysfunction from ischemia or infarction and regional hyperfunction of nonischemic myocardium which determines global performance.

Adult↗
PubMed1983

Chronic aortic regurgitation: prognostic value of left ventricular end-systolic dimension and end-diastolic radius/thickness ratio.

The prognostic value of preoperative echocardiographic data was assessed in 32 patients who underwent aortic valve replacement for chronic aortic regurgitation. All patients had preoperative studies and were followed up prospectively for 1 to 6 years after surgery. Postoperatively, 25 patients (Group A) achieved a normal left ventricular end-diastolic dimension and a significant regression of myocardial hypertrophy; 7 patients (Group B) had persistent left ventricular enlargement. During the follow-up period, the patients in Group A had fewer symptoms and used fewer medications than those in Group B. Moreover, survival at 4 years appeared to be better in Group A (96%) than in Group B (71%); two patients in Group B died with congestive heart failure; there were no such deaths in Group A. Preoperatively, a left ventricular dimension at end-diastole (DED) larger than 3.8 cm/m2 body surface area, a dimension at end-systole (DES) greater than 2.6 cm/m2 body surface area, an end-diastolic radius/wall thickness ratio (R/Th) greater than 3.8 or a product of R/Th and left ventricular systolic pressure (P X R/Th) exceeding 600 are predictive of a Group B result. If end-systolic dimension is greater than 2.6 and P X R/Th is greater than 600, all Group B patients can be identified; all but one patient in Group A had an end-systolic dimension less than 2.6 and P X R/Th less than 600. It is concluded that patients with chronic aortic regurgitation who are at risk of persistent postoperative left ventricular enlargement (with associated cardiac symptoms and reduced survival) can be identified by preoperative echocardiography.

Adolescent↗
PubMed1983

Exercise-induced ischemia: the influence of altered relaxation on early diastolic pressures.

Left ventricular pressure (LVP) decay and early diastolic pressures were studied at rest and during exercise in three groups of patients. Patients in the ischemia group (n = 15) had coronary artery disease and developed new regional wall motion abnormalities documented by biplane LV cineangiography during exercise. Patients in the control group (n = 4) had a normal exercise response. Patients in the scar group (n = 5) had prior infarction, akinetic scars and no ischemia with exercise. Isovolumic pressure data were used to compute the time constant (T) of LVP decay (from the linear relation of LVP and negative dP/dt) and an extrapolated baseline pressure (PB) at dP/dt = 0. During exercise in the ischemia group, minimal LV diastolic pressure (PL) increased from 9 +/- 3 to 21 +/- 5 mm Hg (p less than 0.001), end-systolic volume increased from 38 +/- 7 to 55 +/- 8 ml/m2 (p less than 0.001) and PB rose from -10 +/- 7 to 11 +/- 8 mm Hg (p less than 0.001); T decreased (from 55 +/- 9 to 37 +/- 8 msec, p less than 0.001), although inadequately, compared with the decrease in the control group (from 49 +/- 15 to 22 +/- 2 msec, p less than 0.01). Relaxation at PL during exercise was incomplete in the ischemia group (2.2 +/- 0.4 T) and complete in the control group (3.8 +/- 0.7 T, p less than 0.05). The time course of LVP fall was extrapolated from the isovolumic period into the passive LV filling phase. The extrapolated pressure at the time PL occurred (PE) rose from 0 +/- 4 to 20 +/- 7 mm Hg with ischemia (p less than 0.001). Thus, the characteristics of LVP decay can account for the elevated early diastolic pressures during ischemia. In contrast, the scar group maintained a low PL during exercise (11 +/- 3 to 8 +/- 3 mm Hg), even though T decreased inadequately (from 66 +/- 10 to 36 +/- 5 msec, p less than 0.01), because PB did not shift upward. Ischemia-related pressure elevations involve both delayed relaxation and a pressure baseline shift. During exercise, LVP decay is normally adjusted to maintain low diastolic pressures; with exercise-induced ischemia, LVP decay is abnormal and early diastolic pressures are severely elevated.

Adult↗
PubMed1983

Dynamics of left ventricular filling at rest and during exercise.

Left ventricular filling dynamics were examined at rest and during supine bicycle exercise in 33 patients at cardiac catheterization; 23 had coronary artery disease (ischemia group), five with prior infarction had an akinetic area at rest (scar group), and five had minimal cardiovascular disease (control). Peak filling rate and mean filling rate during the first half and second half of diastole were assessed by biplane angiography. Simultaneous micromanometer pressures were used to compute the time constant of isovolumic pressure decay (T). Peak filling rate and mean filling rate during the first half of diastole increased with exercise in all groups (from 615 to 1050 and 358 to 681 ml/sec in controls and comparably in the scar group and from 697 to 1035 and 347 to 768 ml/sec in the ischemia group). However, T was greater (reduced rate of pressure decay) with exercise in the ischemia group (38 vs 26 msec in controls; p less than .05). Changes in the atrial driving pressure for filling appeared to counterbalance the difference in T. Mean filling rate during the second half of diastole increased with exercise in controls and in the scar group but only modestly in the ischemia group (from 202 to 349 ml/sec). The reduction in late diastolic filling during exercise-induced ischemia was associated with increased filling in early diastole, with a middiastolic volume increase from 160 to 186 ml and an upward shift in the diastolic pressure-volume relation. Thus left ventricular filling is not impaired at rest in patients with coronary artery disease who have normal ejection fractions. Furthermore, the augmentation of early filling induced by exercise is not blunted but is maintained during ischemia, apparently at the expense of elevated left atrial pressure. However, late filling is restricted with ischemia by an increase in impedance.

Cardiac Catheterization↗
PubMed1982

Amyloid cardiomyopathy: characterization by a distinctive voltage/mass relation.

Fourteen patients with biopsy-proved systemic amyloidosis underwent noninvasive cardiac testing to assess the presence and severity of cardiac amyloidosis. There was a clear tendency for electrocardiographic voltage to be low (sum of S wave in lead V1 plus R wave in lead V5 or V6 [SV1 + RV5 or V6] = 14.6 +/- 4.8 mm; normal range 15 to 35) and echocardiographic muscle cross-sectional area to be increased (11.4 +/- 2.7 cm2/m2; normal range 6 to 10). When the electrocardiographic or the echocardiographic data were examined individually, and especially when they were compared and contrasted with similar measurements from patients with pericardial disease (n = 8) or aortic valve disease (n = 24), it was apparent that the electrocardiogram and the echocardiogram had limited specificity in the diagnosis of amyloidosis. However, when the analysis combined these two techniques, a distinctive pattern emerged. There was an inverse correlation between voltage and muscle cross-sectional area (r = -0.79) in patients with amyloidosis; moreover, marked derangement of the voltage/cross-sectional area relation was associated with clinical symptoms and mortality. In addition, patients with amyloidosis and cardiac symptoms had abnormal left ventricular chamber radius to wall thickness ratios, consistent with infiltration of the myocardium as the primary abnormality in cardiac amyloidosis.

Adult↗
PubMed1982

Regression of myocardial hypertrophy: electrocardiographic-echocardiographic correlations after aortic valve replacement in patients with chronic aortic regurgitation.

Serial electrocardiographic and echocardiographic left ventricular (LV) studies were performed in 21 patients before and after aortic valve replacement (AVR) for chronic aortic regurgitation. Changes in voltage (SV1 + RV5-6) after AVR were assessed and evaluated relative to changes in LV mass. Muscle cross-sectional area (CSA) derived from echocardiographic dimension and wall thickness data was used as an index of LV muscle mass (LV hypertrophy greater than 10 cm2/m2). In 15 patients, voltage was reduced after AVR: Seven had normal voltage (48 +/- 17 mm to 25 +/- 6 mm, p less than 0.005) and eight still had increased voltage (61 +/- 17 mm to 40 +/- 4 mm, p less than 0.01). Patients with normal voltage had complete regression of hypertrophy by echocardiography (CSA decreased from 13 +/- 3 cm2/m2 to 9 +/- 1 cm2/m2, p less than 0.025), while those who had persistently increased voltage had incomplete regression (15 +/- 2 cm2/m2, p less than 0.001). Reduction in voltage generally occurred in the first 6 months after AVR. Three patients with unchanged voltage had evidence of paraprosthetic regurgitation and minimal change in CSA. Three other patients with voltage had evidence of paraprosthetic regurgitation and minimal change in CSA. Three other patients with persistent LV enlargement without paraprosthetic regurgitation had a severe intraventricular conduction delay. Data from 59 electrocardiographic-echocardiographic studies before and after AVR revealed a strong correlation (r = 0.81) between voltage and muscle CSA. After surgical correction of chronic aortic regurgitation, regression of LV hypertrophy can be assessed by serial electrocardiographic studies. These ECG data identify patients with complete, incomplete or no regression of LV hypertrophy.

Aortic Valve↗
PubMed1981

Appropriate death: college students' preferences vs. actuarial projections.

Appropriate death was defined as the kind of death a person might choose for himself/herself, if given a choice. Ss were 382 college students who stated their preferences for (a) age at time of death; (b) cause of death; (c) site of death; and (d) means of disposal of remains. Preferences were compared with national actuarial projections. The preferred average life expectancy for women was lower than the national average life expectancy (p less than .001). Natural causes and accidents were oversubscribed, while cardiovascular ailments and cancer were undersubscribed as causes of death. A non-institutional site for death was preferred by 91.3% of the Ss; 39% of all deaths now occur outside an institution. Traditional burial underground was the choice of just more than half the sample, but a slight trend toward less traditional means of disposal of remains was noted over the five semesters of the study.

Adult↗
PubMed1981

Three measures of death anxiety: birth order effects and concurrent validity.

Investigated the concurrent validity of three measures of death anxiety and the effect of birth order on death anxiety as measured by each of the scales. Ss were 100 undergraduate students at a large, private, midwestern university. Results showed significant intercorrelations (p less than .001) among the three scales; only one scale (Templer) differentiated first-born and only children from later-born children. The former had higher death anxiety scores (p less than .05).

Adult↗
PubMed1981

Cerebrospinal fluid concentrations of propranolol, pindolol and atenolol in man: evidence for central actions of beta-adrenoceptor antagonists.

1 Single and multiple oral dose studies of the penetration into CSF of three beta-adrenoceptor antagonists were performed in groups of patients needing lumbar puncture as part of their neurological investigation. Propranolol, pindolol and atenolol were chosen because of their differing physico-chemical properties. 2 The CSF concentration of propranolol (lipid-soluble) and pindolol (moderately lipid-soluble) was proportional to the free plasma concentration and was similar to, although generally lower than, that theoretically predicted. 3 The CSF concentrations of the poorly lipid-soluble atenolol were similar in different patients and were independent of plasma concentration. This may be due to the slow rate of diffusion of atenolol into CSF preventing the predicted concentrations being achieved.

Adrenergic beta-Antagonists↗