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Biomedical subjects

L W Stevenson

Publications and source records attributed to L W Stevenson.

At least 91 records · Page 5Linked to original sources
PubMed1993

Syncope in advanced heart failure: high risk of sudden death regardless of origin of syncope.

OBJECTIVES: The purpose of this study was to assess the importance of syncope as a warning sign for sudden death in advanced heart failure and to determine the relative importance of cardiac syncope and syncope from other causes. BACKGROUND: Despite remarkable advances in the pharmacologic approach to advanced heart failure, 20% to 40% of patients with advanced heart failure will die each year. In such patients, the relation between sudden death and the etiology of syncope has not been evaluated. METHODS: The relation of syncope to sudden death was evaluated in 491 consecutive patients with advanced heart failure (New York Heart Association functional class III or IV), no history of cardiac arrest and a mean left ventricular ejection fraction of 0.20 +/- 0.07. Patients were evaluated for the presence and origin of syncope. The severity of heart failure was assessed from serum sodium levels, ejection fraction, functional class and echocardiographic and hemodynamic variables. RESULTS: Sixty patients (12%) had a history of syncope; the condition had a cardiac origin in 29 (48%) and was due to other causes in 31 (52%). The origin of heart failure was coronary artery disease in 234 patients (48%) and dilated cardiomyopathy in 253 (51%) and its severity was similar in patients with and without syncope. During a mean follow-up interval of 365 +/- 419 days, 69 patients (14%) died suddenly and 66 patients (13%) died of progressive heart failure. The actuarial incidence of sudden death by 1 year was significantly greater in patients with (45%) than in those without (12%, p < 0.00001) syncope. In the Cox proportional hazards model, syncope predicted sudden death independent of atrial fibrillation, serum sodium, cardiac index, angiotensin-converting enzyme inhibition and patient age. The actuarial risk of sudden death by 1 year was similarly high in patients with either cardiac syncope or syncope from other causes (49% vs. 39%, p = NS). CONCLUSIONS: Patients with advanced heart failure are at especially high risk for sudden death regardless of the etiology of syncope.

Adult↗
PubMed1993

Selection and management of patients for cardiac transplantation.

Each month in the United States, approximately 170 patients undergo cardiac transplantation and 300 new candidates are listed. Provision of alternative therapies, identification of the patients who truly have no other option, and management of those candidates until transplantation is performed has created a challenging area of investigation. The results of heart failure trials conducted in populations with milder heart failure may not always extend to advanced heart failure, to which some prognostic and therapeutic principles are unique. Many patients with low ejection fractions and a history of severe heart-failure symptoms can nonetheless enjoy quality of life and survival equivalent to those of patients who have received transplants. Improvements in our ability to design optimal medical therapy and to identify risk factors for early mortality will allow many patients with advanced heart failure to defer or avoid transplantation, and enable the majority of candidates to remain stable until transplantation can be performed.

Contraindications↗
PubMed1993

Managing complications in heart transplant recipients. Improved techniques and medications increase survival rates.

Major problems facing cardiac transplant recipients include rejection, infection, and transplant coronary artery disease. Commonly used antirejection drugs are high-dose corticosteroids and cytolytic agents. Bacterial infections, such as those caused by staphylococci, occur early in the postoperative period, while opportunistic infections, including viral, fungal, and parasitic diseases, occur several weeks after transplant surgery. Coronary angiography is used to detect transplant coronary artery disease, the only definitive treatment for which is retransplantation. A number of promising new immunosuppressive agents and techniques may prevent some complications and further improve the care cardiac transplant recipients receive.

Coronary Disease↗
PubMed1993

Advanced congestive heart failure. Inpatient treatment and selection for cardiac transplantation.

Establishment of an effective oral medical regimen for a patient with advanced congestive heart failure often requires hospitalization for simultaneous adjustment of volume status and vasodilation. In the hospital, intravenous therapy is begun with nitroprusside sodium (Nipride, Nitropress) and/or nitroglycerin (Nitro-Bid IV, Tridil), combined with intravenous diuretics; it is sometimes necessary to add infusions of dobutamine (Dobutrex) or dopamine hydrochloride (Dopastat, Intropin). After 48 hours of intravenous therapy, most patients can be weaned onto oral vasodilators and eventually discharged. In patients in whom further escalation of therapies is necessary, first intravenous amrinone lactate (Inocor) or milrinone lactate (Primacor) may be added, and then epinephrine or, rarely, norepinephrine (Levophed). Steps beyond that include a trial of intra-aortic balloon counterpulsation, implantation of a mechanical assist device, or use of an external centrifugal pump. Cardiac transplantation is indicated for patients in critical or unstable conditions who have no contraindications to the procedure. The patient's profile for compliance must be carefully evaluated. Reform of the selection process is needed to identify patients who, though not critically ill, will not survive without early transplantation.

Cardiotonic Agents↗
PubMed1992

Effect of direct vasodilation with hydralazine versus angiotensin-converting enzyme inhibition with captopril on mortality in advanced heart failure: the Hy-C trial.

To compare the benefit of angiotensin-converting enzyme inhibition and direct vasodilation on the prognosis of advanced heart failure, 117 patients evaluated for cardiac transplantation who had severe symptoms and abnormal hemodynamic status at rest were randomized to treatment with either captopril or hydralazine plus isosorbide dinitrate (Hy-C Trial). Comparable hemodynamic effects of the two regimens were sought by titrating vasodilator doses to match the hemodynamic status achieved with nitroprusside and diuretic agents, attempting to achieve a pulmonary capillary wedge pressure of 15 mm Hg and a systemic vascular resistance of 1,200 dynes.s.cm-5. Treatment with the alternate vasodilator was started because of poor hemodynamic response or side effects (40% of patients in the captopril group and 22% in the hydralazine group). Adequate hemodynamic response in patients with a serum sodium level less than 135 mg/dl was more likely with hydralazine than with captopril (71% vs. 33%, p = 0.04). Isosorbide dinitrate was prescribed in 88% of the hydralazine-treated patients and 84% of the captopril-treated patients. The hemodynamic improvements from each regimen were equivalent. After 8 +/- 7 months of follow-up, the actuarial 1-year survival rate was 81% in the captopril-treated patients and 51% in the hydralazine-treated patients (p = 0.05). The improved survival with captopril resulted from a lower rate of sudden death, which occurred in only 3 of 44 captopril-treated patients compared with 17 of 60 hydralazine-treated patients (p = 0.01). In the subset of patients who continued treatment with the initial vasodilator, results were similar to those for the entire treatment group.(ABSTRACT TRUNCATED AT 250 WORDS)

Actuarial Analysis↗
PubMed1992

Significance of aborted cardiac arrest and sustained ventricular tachycardia in patients referred for treatment therapy of advanced heart failure.

Cardiac arrest in patients with heart failure may be the result of remediable factors such as pulmonary edema, drug toxicity, or electrolyte abnormalities, or it may be due to primary arrhythmias. The relation of prior aborted cardiac arrest or sustained ventricular tachycardia to subsequent prognosis was assessed in 458 consecutive patients referred for management of advanced heart failure (left ventricular ejection fraction 0.2 +/- 0.07). All patients received tailored vasodilator and diuretic therapy and were then followed as outpatients. Patients were divided into four groups: 388 patients (85%) with no prior cardiac arrest or sustained ventricular tachycardia, 31 patients (7%) with a primary arrhythmia cardiac arrest, 22 patients (5%) with a secondary cardiac arrest, and 17 patients (4%) with sustained ventricular tachycardia without cardiac arrest. Patients with cardiac arrest resulting from a primary arrhythmia were usually treated with antiarrhythmic drugs (25 patients), and five patients received an implantable defibrillator. After hospital discharge actuarial 1-year sudden death risk (17%) and total mortality (24%) rates for the group with primary arrhythmia were similar to corresponding values in patients with no history of cardiac arrest or sustained ventricular tachycardia (17% and 30%, respectively). In patients with a secondary cardiac arrest as a result of exacerbation of heart failure (11 patients), torsade de pointes (10 patients), or hypokalemia (one patient), therapy focused on removal of aggravating factors. Actuarial 1-year sudden death (39%) and total mortality (54%) rates for the group with secondary arrest were higher than for patients without a history of cardiac arrest (p = 0.003 and 0.005, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Actuarial Analysis↗
PubMed1992

Vasodilators. A re-evaluation of their role in heart failure.

Over the past 25 years, the concept of circulation in heart failure has evolved from that of a simple circuit with a weak pump and high pressures to a complex integrated system of cellular modification, cardiac compensation and systemic neurohumoral responses. The original model of cardiac afterload as the systemic vascular resistance has been refined to reflect the interdependence of preload and afterload and the central role of atrioventricular valve regurgitation. It is becoming increasingly apparent that the impact of vasodilator therapy far exceeds the direct haemodynamic effects on preload and afterload, and depends on the mechanism by which vasodilation is achieved, with increasing emphasis on those agents which oppose neurohumoral activation. The potential goals of therapy have broadened to include not only haemodynamic stabilisation through tailored therapy for patients referred with advanced heart failure, but also the prevention of disease progression for patients with asymptomatic ventricular dilation. As the different profiles of heart failure have come to be recognised, the purpose and design of vasodilator treatment must now be considered individually for each patient.

Cardiac Output, Low↗
PubMed1992

Modeling distribution of donor hearts to maximize early candidate survival.

BACKGROUND: Priority for cardiac transplantation should reflect the relative waiting list mortality and operative mortality of outpatient candidates and critical candidates. METHODS AND RESULTS: To determine how to distribute donor hearts for maximal overall survival, a Markov model of eight states was constructed from current statistics for outpatient sudden death, deterioration to critical status, operative mortality for outpatients, and operative mortality for critical candidates. Because the fraction of hearts offered to critical candidates varied, expected survival at 1 year was calculated. To determine the factors most critical in determining priority policy, current conditions were then varied over a fourfold range. Priority for critical candidates maximized overall candidate survival (with and without transplantation), increasing 1-year survival to 78% compared with 66% if hearts were offered only to outpatients. The benefit of giving priority to critical patients persisted when current group mortality rates were individually halved or doubled because these rates were still small compared with the 100% expected mortality of critical patients without transplantation. If the outpatient sudden death rate and the operative mortality for critical patients were doubled simultaneously, however, there was a slight negative impact on survival if critical candidates received priority. Regardless of changes in subgroup outcomes, the distribution of donor hearts had a relatively modest impact on survival because of the large excess of candidates. CONCLUSIONS: Critical candidates for transplantation should continue to receive priority even if their operative mortality increases above current levels. However, postoperative outcomes must be assessed in relation to changing pretransplantation risks. Distribution of donor hearts will be most beneficial when it is possible to identify the waiting patients at greatest risk for sudden death and deterioration without transplantation.

Death, Sudden, Cardiac↗
PubMed1991

Sustained reduction in valvular regurgitation and atrial volumes with tailored vasodilator therapy in advanced congestive heart failure secondary to dilated (ischemic or idiopathic) cardiomyopathy.

Afterload reduction therapy can acutely improve hemodynamic function in patients with advanced heart failure; however, it is unknown if initial reductions in mitral and tricuspid regurgitation and atrial volumes can be sustained with oral therapy. Atrial volumes and atrioventricular valve regurgitation were measured using 2-dimensional and Doppler echocardiography with color-flow imaging in 14 patients with dilated heart failure (ejection fraction 17 +/- 4%) before and after 3 +/- 1 days of intensive vasodilator and diuretic therapy tailored to hemodynamic goals. Echocardiography was repeated again after 6 +/- 2 months on oral vasodilators and a flexible diuretic regimen. Acute therapy reduced systemic vascular resistance from 1,760 +/- 460 to 1,010 +/- 310 dynes.s.cm-5, pulmonary artery wedge pressure from 30 +/- 5 to 17 +/- 4 mm Hg, and right atrial pressure from 13 +/- 5 to 7 +/- 3 mm Hg, and led to a 61% increase in stroke volume (from 36 +/- 10 to 58 +/- 14 ml) (p less than 0.01). Mitral and tricuspid regurgitation, determined by color-flow fraction, initially decreased from 0.34 +/- 0.17 to 0.20 +/- 0.20 and from 0.33 +/- 0.15 to 0.13 +/- 0.13, respectively (p less than 0.001). This reduction was sustained at 6 months. Significant decreases occurred with acute therapy, with further reductions at 6 months in both mean left atrial volume (from 100 +/- 25 to 80 +/- 19 to 65 +/- 15 cm3) and right atrial volume (from 85 +/- 23 to 64 +/- 23 to 52 +/- 14 cm3) (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1991

Late potentials are unaltered by ventricular filling pressure reduction in heart failure.

Exacerbation of heart failure may increase susceptibility to arrhythmias. Therefore tests to assess the risk of arrhythmia, performed after hemodynamic improvement, may be of limited value. To determine whether hemodynamic improvement alters ventricular late potentials detected by signal-averaged ECG, we studied 27 consecutive patients with dilated heart failure (left ventricular ejection fraction 0.20 +/- 0.06, 15 with coronary artery disease) before and 3 +/- 2 days after tailored vasodilator and diuretic therapy reduced ventricular filling pressures. QRS duration, terminal QRS amplitude (root mean square [RMS]), and low-amplitude (less than 40 microV) signal (LAS) duration were determined by an automated algorithm from the vector magnitude of the QRS high-pass filtered at 25 Hz and at 40 Hz. Despite marked decreases in pulmonary capillary wedge (27 +/- 7 to 16 +/- 5 mm Hg, p less than 0.001) and right atrial (13 +/- 7 to 7 +/- 4 mm Hg, p less than 0.001) pressures and a 20% increase in cardiac output, there was not a significant change in QRS duration, RMS, or LAS. Before and after therapy late potentials, defined as abnormal QRS duration RMS, or LAS, were present in 14 (52%) patients with filtering at 25 Hz and in 22 (81%) patients with filtering at 40 Hz. The signal-averaged ECG after hemodynamic improvement predicted the results during exacerbation of heart failure in all patients. Thus in patients with advanced heart failure the signal-averaged ECG obtained after hemodynamic improvement reflects the findings during exacerbation of heart failure.

Arrhythmias, Cardiac↗
PubMed1991

Quantification of absolute myocardial perfusion at rest and during exercise with positron emission tomography after human cardiac transplantation.

The maximal exercise capacity of cardiac transplant recipients is reduced compared with that of normal subjects. To determine if this reduced exercise capacity is related to inadequate myocardial perfusion during exercise, myocardial perfusion was measured noninvasively with use of positron emission tomography and nitrogen (N)-13 ammonia. Twelve transplant recipients with no angiographic evidence of accelerated coronary atherosclerosis were studied. Serial N-13 ammonia imaging was performed at rest and during supine bicycle exercise. The results were compared with those from 10 normal volunteers with a low probability of having cardiac disease. A two-compartment kinetic model for estimating myocardial perfusion was applied to the data. Transplant recipients achieved a significant lower exercise work load than did the volunteers (42 +/- 16 vs. 128 +/- 22 W), but a higher venous lactate concentration (31.3 +/- 14.9 vs. 13.7 +/- 4.1 mg/100 ml). Despite the difference in exercise work load, there was no significant difference in the cardiac work achieved by transplant recipients and normal subjects as evidenced by similar rate-pressure products of 24,000 +/- 3,400 versus 21,300 +/- 2,800 betas/min per mm Hg, respectively. In addition, myocardial blood flow during exercise was not significantly different between the two groups (1.70 +/- 0.60 vs. 1.56 +/- 0.71 ml/min per g, respectively). This study demonstrates that the myocardial flow response to the physiologic stress of exercise is appropriate in transplant recipients and does not appear to explain the decreased exercise capacity in these patients.

Ammonia↗
PubMed1991

Decreasing survival benefit from cardiac transplantation for outpatients as the waiting list lengthens.

Many patients are accepted for cardiac transplantation during a period of clinical instability associated with a high risk of death, even though most can be discharged home to await transplantation. As the waiting lists lengthen, priority is awarded solely on the basis of the waiting time of outpatients, who now usually undergo transplantation after they have already survived a major period of jeopardy. To determine the impact of the current waiting times and priority system on the previously expected benefit offered by transplantation, 1-year actuarial survival without transplantation was recalculated after each month without transplantation for 214 potential candidates with an ejection fraction of 0.17 +/- 0.05 discharged on tailored medical therapy after evaluation. These data were compared with the 1-year survival data of 88 outpatients who underwent transplantation. Actuarial survival after 1 year was 67% on tailored therapy compared with 88% after transplantation (p = 0.009). Death without transplantation was sudden in 43 of 51 patients, resulting from hemodynamic decompensation in 8. For outpatients already surviving 6 months without transplantation, actuarial survival over the next 12 months was 83% without transplantation. Thus, the expected improvement in survival after transplantation would be only 5% over the subsequent year for patients waiting 6 months, which is the waiting time for many outpatients. Such patients should be reevaluated to determine whether transplantation remains indicated during the next year.

Actuarial Analysis↗
PubMed1991

Differentiating cardiomyopathy of coronary artery disease from nonischemic dilated cardiomyopathy utilizing positron emission tomography.

To determine if imaging of blood flow (using N-13 ammonia) and glucose metabolism (using F-18 2-deoxyglucose) with positron emission tomography can distinguish cardiomyopathy of coronary artery disease from nonischemic dilated cardiomyopathy, 21 patients with severe left ventricular dysfunction who were evaluated for cardiac transplantation were studied. The origin of left ventricular dysfunction had been previously determined by coronary angiography to be ischemic (11 patients) or nonischemic (10 patients). Images were visually analyzed by three observers on a graded scale in seven left ventricular segments and revealed fewer defects in dilated cardiomyopathy compared with ischemic cardiomyopathy for N-13 ammonia (2.7 +/- 1.6 versus 5 +/- 0.6; p less than 0.03) and F-18 deoxyglucose (2.8 +/- 2.1 versus 4.6 +/- 1.1; p less than 0.03). An index incorporating extent and severity of defects revealed more homogeneity with fewer and less severe defects in subjects with nonischemic than in those with ischemic cardiomyopathy as assessed by imaging of flow (2.8 +/- 1.8 versus 9.2 +/- 3; p less than 0.001) and metabolism (3.8 +/- 3.3 versus 8.5 +/- 3.6; p less than 0.005). Diagnostic accuracy for distinguishing the two subgroups by visual image analysis was 85%. Using previously published circumferential count profile criteria, patients with dilated cardiomyopathy had fewer ischemic segments (0.4 +/- 0.8 versus 2.5 +/- 2 per patient; p less than 0.01) and infarcted segments (0.1 +/- 0.3 versus 2.4 +/- 1.4 per patient; p less than 0.001) than did patients with cardiomyopathy of coronary artery disease. The sensitivity for differentiating the two clinical subgroups using circumferential profile analysis was 100% and the specificity 80%. An index incorporating both number and severity of defects derived from circumferential profile analysis was significantly lower in subjects with dilated cardiomyopathy than in ischemic cardiomyopathy (0.3 +/- 0.8 versus 2.7 +/- 2.4; p less than 0.005). Thus, noninvasive positron emission tomographic imaging with N-13 ammonia and F-18 deoxyglucose is helpful in distinguishing patients with severe left ventricular dysfunction secondary to coronary artery disease from those with nonischemic cardiomyopathy, and a semiquantitative index such as circumferential profile analysis is superior to that of visual analysis alone.

Adult↗