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PubMed1994

Left ventricular dysfunction during exercise in patients with angina pectoris and angiographically normal coronary arteries (syndrome X)

Left ventricular function during exercise and recovery was investigated in patients with angina pectoris, ST segment depression during exercise and angiographically normal coronary arteries (syndrome X) using a continuous left ventricular function monitor with cadmium telluride detector (CdTe-VEST). Fourteen patients with syndrome X and 14 patients with atypical chest pain without ST segment depression during exercise and normal coronary arteries (control group) performed supine ergometric exercise after administration of 740-925 MBq of technetium-99m labelled red blood cells, and left ventricular function was monitored every 20 s using CdTe-VEST. Left ventricular ejection fraction (EF) response was impaired (< or = 5% increase from rest to peak exercise) in 11 or 14 patients with syndrome X but in none of the control patients. Resting EF was similar in the two groups (62.1% +/- 6.7% in patients with syndrome X, 61.9% +/- 6.2% in controls); however, EF increase from rest to peak exercise was lower in syndrome X (-3.1 +/- 9.5% vs 14.7% +/- 7.4%, P < 0.001). After cessation of exercise, all patients showed rapid EF increase over baseline and this EF overshoot was lower (19.3% +/- 8.3% vs 26.4% +/- 7.3%, P < 0.001) with the time to EF overshoot longer (114 +/- 43 s vs 74 +/- 43 s, P < 0.05) in patients with syndrome X. Thus, in patients with syndrome X, left ventricular dysfunction was frequently observed during exercise in spite of normal epicardial coronary arteries.

Adult↗
PubMed1995

Importance of a non-dominant right coronary artery occlusion presenting as sudden cardiac death with prolonged right ventricular dysfunction and malignant arrhythmias.

We report a case of a patient who presented with sudden cardiac death secondary to a subtotal occlusion of a small non-dominant right coronary system. Catheterization several weeks following the initial episode revealed persistent severe right ventricular dysfunction with moderate hemodynamic compensation. Continued unstable arrhythmogenic potential at this point led to placement of an AICD device. The case highlights the potential hazard and often complacency involved in dealing with benign appearing lesions as this one.

Arrhythmias, Cardiac↗
PubMed1996

Effects of dobutamine and enoximone on transmitral and pulmonary venous flow characteristics in patients with left ventricular dysfunction after coronary artery bypass grafting.

OBJECTIVES: To assess the effects of dobutamine and enoximone on transmitral (TMF) and pulmonary venous flow (PVF) characteristics. DESIGN: Prospective and randomized. SETTING: A university hospital intensive care unit. PARTICIPANTS: Thirty patients with moderate left ventricular dysfunction after coronary artery bypass grafting (CABG). INTERVENTIONS: Patients received either dobutamine, 10 micrograms/kg/min, or enoximone, 20 micrograms/kg/min, for the treatment of a low cardiac index (CI) (< 2.2 L/min/m2). MEASUREMENTS AND MAIN RESULTS: Both drugs significantly (p < 0.05) increased CI from 1.91 +/- 0.17 (dobutamine) and 1.97 +/- 0.17 (enoximone) at baseline to 2.86 +/- 0.70 and 2.84 +/- 0.39 L/min/m2, respectively. Compared with the enoximone (enox)-treated group, the administration of dobutamine (dob) resulted in significantly (p < 0.05) greater increases in mean arterial pressure (dob: 18 +/- 9% v enox: -2 +/- 7%), heart rate (dob: 24 +/- 13% v enox: 3 +/- 5%) and pulmonary artery pressure (dob: 5 +/- 10% v enox: -4 +/- 9%). In contrast, the increase in stroke volume index was significantly less in the dobutamine-treated group (dob: 22 +/- 27% v enox: 41 +/- 21%). The TMF indices, peak E, and peak A wave increased significantly (p < 0.05) after both dobutamine (baseline: 37.3 +/- 6.7 and 41.1 +/- 9.3; max dose: 42.4 +/- 4.3 and 49.0 +/- 10.2 cm/s) and enoximone (baseline: 36.2 +/- 7.5 and 44.2 +/- 10.9; max dose: 40.5 +/- 5.0 and 49.4 +/- 12.1 cm/s) without significantly altering the E/A ratio. Only dobutamine significantly (p < 0.05) decreased isovolumic relaxation time from 109 +/- 24 to 94 +/- 21 ms. There was no significant change in isovolumic relaxation time between the dobutamine (-12% +/- 17%)- and the enoximone (-4% +/- 21%)- treated group. PVF recordings demonstrated a significant increase in time velocity integrals of the S wave with both dobutamine (12.2 +/- 3.1 v 13.7 +/- 3.2 cm) and enoximone (11.0 +/- 3.0 v 12.2 +/- 3.2 cm). No changes in the systolic fraction of the PVF were noted. CONCLUSIONS: There were no major differences in parameters reflecting diastolic function between the dobutamine- and the enoximone-treated groups.

Adult↗
PubMed1995

Surgical therapy of chronic heart failure and severe ventricular dysfunction.

Even with multiple medical advancements, heart failure patients still have a dismal prognosis. Technologic improvements in coronary artery bypass graft (CABG) surgery have led to the use of high-risk myocardial revascularization for the treatment of patients with heart failure and severe ventricular dysfunction. This article describes advances in cardiac surgery and their impact on the treatment of heart failure. Postoperative management of the heart failure patient is also discussed. Because patient selection is important in achieving positive surgical outcomes, the role of prospective severity risk score is also addressed.

Heart Failure↗
PubMedDate not supplied

Left ventricular dysfunction and duration of mechanical ventilatory support in the chronically critically ill: a survival analysis.

OBJECTIVE: The purpose of this study was to determine whether there was a greater risk for prolonged duration of mechanical ventilatory support (MVS) for those who demonstrated left ventricular dysfunction (LVD) compared to those without evidence of LVD when controlling for nutritional and general health status and spontaneous breathing pattern. DESIGN: A secondary analysis was used on data obtained in a retrospective survey of patient records. SETTING: Five adult critical care units at an academic medical center in the Midwest. SUBJECTS: Twenty-seven chronically critically ill adults requiring MVS who later successfully weaned from MVS. OUTCOME MEASURE: Duration of MVS. INSTRUMENTATION: LVD was determined with use of a criterion-based checklist. Serum albumin level as determined by the hospital's clinical laboratory served as the indicator of nutritional and general health status. The rapid shallow breathing index was used to describe the spontaneous breathing pattern. RESULTS: Adjusted survival function estimates were obtained on fitting a Cox proportional hazards model. When adjusting for the known covariates, serum albumin level and rapid shallow breathing index, the duration of MVS was significantly longer for those who demonstrated LVD when compared to those without evidence of LVD [X2Wald(1) = 4.72, p < 0.05]. CONCLUSIONS: The findings of this secondary analysis lend support to the fact that when controlling for serum albumin level and rapid shallow breathing index, LVD is related to the duration of MVS in patients who successfully wean.

Aged↗
PubMedDate not supplied

Serial echocardiographic findings early after heart transplantation: evidence for reversible right ventricular dysfunction and myocardial edema.

Serial M-mode and two-dimensional echocardiograms were performed on 10 patients at 1 week, 1 month, and 3 months after heart transplantation to determine early structural and functional changes in the allograft. Standard M-mode echocardiographic measurements of at least five cardiac cycles were averaged. Right ventricular size and function were assessed by mid-ventricular diameter and the right ventricular apex to lateral tricuspid anulus shortening fraction, respectively, on the two-dimensional apical four-chamber view. There were no consistent differences in left ventricular end-diastolic dimension or fractional shortening between study periods. Left ventricular posterior wall thickness decreased from 15 +/- 2 to 11 +/- 1 mm (p = 0.001), and septal thickness decreased from 15 +/- 2 to 12 +/- 2 mm (p = 0.0006) between the 1-week and 3-month studies. Right ventricular cross-sectional dimension increased from 34 +/- 6 to 39 +/- 6 mm (p = 0.047), and right ventricular fractional shortening increased from 13% +/- 3% to 21% +/- 5% (p = 0.0051) between the 1-week and 3-month studies. There were no correlations between any of the above changes and rejection episodes. There was a weak correlation (r = 0.53) between ischemic time and change in posterior wall thickness. Right ventricular dysfunction and increased left ventricular wall thickness presumably caused by interstitial edema appear to be normal findings early after heart transplantation.

Adult↗
PubMed1996

Amniotic fluid embolism causing severe left ventricular dysfunction and death: case report and review of the literature.

Hemodynamic instability in amniotic fluid embolism has previously been demonstrated only by right heart catheterization. We present detailed documentation obtained by echocardiography and cardiac catheterization of a 35-year-old woman who developed amniotic fluid embolism and died from severe left ventricular dysfunction and wide QRS complex tachycardia despite intensive medical therapy (inotropes) and mechanical (intraaortic balloon pump) support.

Abortion, Therapeutic↗
PubMed1997

Alpha 1-adrenoceptor subtypes in rat aorta and mesenteric small arteries are preserved during left ventricular dysfunction post-myocardial infarction.

OBJECTIVE: In heart failure, homologous downregulation of beta-adrenoceptors contributes to impaired adrenergic responsiveness of the myocardium. We evaluated alpha 1-adrenoceptors (alpha 1-AR) in a sparsely innervated and a densely innervated peripheral artery in an experimental model of left ventricular dysfunction post-myocardial infarction. METHODS: [3H]Prazosin binding was determined in arterial segments of Wistar-Kyoto rats (WKY), and of Wistar rats 5 weeks after myocardial infarction (MI) or sham operation (SHAM). RESULTS: In the thoracic aorta (TAO) of WKY, specific prazosin binding was: (i) prevented by the irreversible alpha 1B-AR and relatively selective alpha 1D-AR antagonist, chloroethylclonidine (CEC); (ii) displaced with low affinity (pKi 6.25) by the alpha 1A-AR selective ligand, (+)-niguldipine; and (iii) displaced with both high (pKi 10.4) and low (pKi 7.37) affinity by the alpha 1D-AR antagonist, BMY 7378. In mesenteric small arteries (MSA) of WKY, prazosin binding was: (i) reduced 50% by CEC; (ii) displaced in a biphasic fashion by (+)-niguldipine (pKi 8.60 and pKi 6.22); and (iii) displaced by BMY 7378 with low affinity only (pKi 6.86). Also in TAO of SHAM. prazosin binding was prevented by CEC, but neither 30 nM (+)-niguldipine nor 1 nM BMY 7378 affected it. In MSA of SHAM, prazosin binding was virtually abolished in the presence of 30 nM (+)-niguldipine and was not reduced by 1 nM BMY 7378. In TAO and MSA of MI, compared to SHAM, the density of binding sites tended to be increased rather than decreased and neither the affinity for the ligand nor the effects of alpha 1-AR subtype selective tools were significantly modified. CONCLUSIONS: These findings indicate that: (i) radioligand binding can be applied in intact arterial segments to quantify and characterize alpha 1-AR; (ii) although differences seem to exist between rat strains, alpha 1B-AR and alpha 1D-AR predominate in rat thoracic aorta and alpha 1A-AR and alpha 1B-AR in mesenteric small arteries; and (iii) alpha 1-AR density is not reduced in the poorly innervated aorta and the densely innervated mesenteric small arteries of rats with heart failure due to myocardial infarction.

Adrenergic alpha-Antagonists↗
PubMedDate not supplied

Aerobic capacity and functional classification of patients with severe left-ventricular dysfunction.

Classes I/II and III of the classification systems of the New York Heart Association (NYHA), Canadian Cardiovascular Society (CCS) and American Medical Association (AMA) were compared with each other and with the Weber classification (O2 uptake, VO2/kg during treadmill walking) in 35 male patients with severe left ventricular dysfunction. Measured end points were ventilatory threshold (VT) and peak exercise. Also investigated was whether the CCS and AMA scales, due to their more stringent differentiation, are more precise than the NYHA system in determining a limited physical capacity and whether there are other differentiating factors useful in classification which may be derived from cardiopulmonary exercise testing. At the VT, the mean VO2/kg did not differ significantly in any classification system between classes I/II and III (12.8 +/- 2.5 vs. 11.1 +/- 2.3 ml/kg/min) and corresponded to Weber class B. At peak exercise, the mean VO2/kg only differed significantly within the NYHA classification; classes I/II (16.3 +/- 3.1 ml/kg/min) corresponded to Weber class B, and class III (13 +/- 3 ml/kg/min) to Weber class C. The individual values displayed a large scatter. Factors differing in classes I/II and III of all three systems at peak exercise were the ventilatory equivalent of O2 and CO2 as well as end-tidal partial pressure for O2 and CO2. At VT these factors showed a separating character only in the AMA classification. It is not possible to determine objective functional impairment by use of the NYHA, CCS and AMA systems because they are not analogous to the Weber system. Nevertheless, these classification systems can be used for clinical assessment and follow-up.

Exercise Test↗
PubMed1992

[The relationship between anomalies in the autonomous nervous system and left ventricular dysfunction in patients with hypertrophic cardiomyopathy].

This study was undertaken to assess autonomic nervous system (ANS) activity and its relation to left ventricular function in 40 patients (mean age: 41 +/- 17 years) with hypertrophic cardiomyopathy (HC), in sinus rhythm, off-drugs. Patients were grouped according to the results of radionuclide angiography: 26 had an ejection fraction > 50% (Group A), whereas 14 had an ejection fraction < or = 50% (Group B). Evaluation of parasympathetic activity showed abnormalities in: heart rate (HR) response during Valsalva (< or = 1.1) in 2 Group A (8%) and 12 Group B (86%) patients (p < 0.001); HR variability during deep breathing (< or = 10 b/min) in 2 Group A (8%) and 14 Group B (100%) patients (p < 0.001); immediate HR response to standing (30:15 < or = 1.0) in 2 Group A (8%) and 6 Group B (43%) patients (p < 0.025). Assessment of sympathetic activity showed abnormalities in: systolic blood pressure fall to standing (> 20 mmHg) in 2 Group B (14%) patients only (NS); diastolic blood pressure response to handgrip (< 10 mmHg) in 4 Group B (29%) patients only (p < 0.025). Thus, in HC: impaired parasympathetic control is common in those patients showing left ventricular dysfunction; concurrent sympathetic abnormality may also occur in this subgroup of patients; ANS dysfunction seems to be merely an epiphenomenon which marks the severity of left ventricular derangement.

Adult↗
PubMed1997

Inhibition of carnitine synthesis protects against left ventricular dysfunction in rats with myocardial ischemia.

During myocardial ischemia, inhibition of the carnitine-mediated transportation of fatty acid may be beneficial because it facilitates glucose utilization and prevents an accumulation of fatty acid metabolites. We orally administered 3-(2,2,2-trimethyl hydrazinium) propionate (MET), an inhibitor of carnitine synthesis, for 20 days to rats. Then we evaluated left ventricular (LV) function during brief ischemia by using a buffer-perfused isovolumic heart model. After 15 min of reoxygenation after the transient ischemia, LV peak systolic pressure (PSP) almost completely returned to the baseline level in rats given MET (96 +/- 4%), whereas it was only partially (77 +/- 16%) recovered in the placebo-treated rats. We induced myocardial infarction in other rats by ligating the left anterior descending coronary artery. Then the animals were given MET for 20 days, and LV function was compared. In the placebo-treated rats (with myocardial infarction, but without drug treatment), LVPSP was lower than that in the sham group [108 +/- 19 (n = 10) vs. 136 +/- 15 mm Hg (n = 13); p < 0.05], and the time constant (T) of LV pressure decay was elongated (36 +/- 4 vs. 30 +/- 7 ms; p < 0.05). In MET-treated groups, however, neither PSP nor T differed from those in the sham group. In conclusion, inhibition of the carnitine-mediated transportation of fatty acid by MET protected against left ventricular dysfunction in acute and chronic myocardial ischemia.

Animals↗
PubMed1996

[Tolerance of amlodipine in left ventricular dysfunction of ischemic origin].

The aim of this study was to assess the effects of amlodipine on left ventricular function at rest and on effort, at least 30 days after myocardial infarction. The 30 patients included in the study had resting isotopic ejection fractions of 40 to 60%. At inclusion and after 15 days treatment with 10 mg of amlodipine, the patients underwent exercise stress testing with a standard Bruce protocol and resting and exercise isotopic left ventricular ejection fractions were measured. The association of betablockers was allowed but vasodilator therapy was prohibited. During the second exercise stress test, the duration of exercise increased (437 +/- 167 to 518 +/- 154 s; p < 0.002) and the work level rose from 140 +/- 56 to 169 +/- 60 Watts; p < 0.04. The number of electrically positive tests did not change significantly (33 vs 26.7%; NS). The resting ejection fraction did not increase after 15 days treatment with amlodipine (47.4 +/- 6.7 vs 48.3 +/- 8.9%; NS). Similar results were observed with respect to the exercise ejection fraction (51.4 +/- 10.4 vs 52.6 +/- 8.6%; NS). These patients may however be divided into two subgroups. In the first subgroup of 10 patients, the resting ejection fraction rose by more than 5% with amlodipine whereas the exercise ejection fraction remained unchanged (54.4 +/- 7.7% vs 54.5 +/- 7.5% with amlodipine). In the second subgroup of 20 patients, the resting ejection fraction decreased slightly with amlodipine (48 +/- 6.9% vs 45.3 +/- 8%; p = 0.04) but increased significantly on exercise (45.3 +/- 8% vs 51.7 +/- 9.1%; p < 0.0002). Therefore, amlodipine, a new generation calcium antagonist, does not induce any deleterious effect after myocardial infarction with mild left ventricular dysfunction.

Adult↗
PubMed1996

Myocardial defect detected by 123I-BMIPP scintigraphy and left ventricular dysfunction in patients with idiopathic dilated cardiomyopathy.

The present study examined the role of myocardial fatty acid in patients with idiopathic cardiomyopathy (DCM) by means of 123I-beta-methyl-p-iodophenyl pentadecanoic acid (123I-BMIPP) scintigraphy. Thirteen patients underwent 123I-BMIPP imaging, 201Tl imaging and echocardiography. All patients showed defective myocardial uptake of 123I-BMIPP and 201Tl. The left ventricular end-diastolic dimension (64.1 +/- 7.3 mm vs. 55.6 +/- 1.5 mm, p < 0.05) and end-systolic dimension (52.4 +/- 8.0 mm vs. 40.6 +/- 2.1 mm, p < 0.01) were significantly large in the defect group (123I-BMIPP defect score (DS) > 8) than the small defect group (DS < 7). The % fractional shortening (%FS) was also significantly smaller (18.6 +/- 3.8% vs. 27.0 +/- 3.3%, p < 0.01) in the large defect group. The 123I-BMIPP DS correlated statistically with %FS (r = 0.75, p < 0.01), while the 201Tl DS did not (r = 0.41, ns). We conclude that the patients with DCM revealed a 123I-BMIPP uptake defect and the defect reflected the degree of left ventricular dysfunction.

Adult↗
PubMed1997

Severe right ventricular dysfunction following pericardiocentesis for cardiac tamponade.

The accumulation of fluid in the pericardium in an amount sufficient to cause severe obstruction to blood inflow to the ventricles results in cardiac tamponade. In this condition, relief of intrapericardial pressure by pericardiocentesis usually dramatically improves cardiac output, and can be lifesaving. We report a case of a patient with malignant cardiac tamponade in which cardiogenic shock developed after pericardiocentesis due to severe right ventricular dysfunction.

Adenocarcinoma↗
PubMed1993

Markers of left ventricular dysfunction induced by exercise, dipyridamole or combined stress on ECG-gated myocardial perfusion scans.

An index of left ventricular contraction can be extracted from the cavitary time-activity curve of electrocardiographic (ECG)-gated myocardial perfusion scans. To assess the induction of stress-induced myocardial depression, we compared contraction indexes derived from immediate poststress and delayed 201Tl images with indexes of ventricular dilation and lung uptake in the prediction of severe coronary artery disease (defined as two or more 90% stenoses). Stress procedures were performed in 93 patients with symptom-limited supine bicycle exercise alone, and in 227 with intravenous dipyridamole, combined where possible with exercise. The immediate and delayed contraction indexes reflected left ventricular dysfunction on ventriculography (P < 0.0001), but additionally the immediate index was reduced (P < 0.0001) in severe coronary disease. Stress-induced hypokinesis was seen frequently after each of the test modes. The relationship with angiographic findings was better defined for indexes of contraction than for lung uptake or ventricular dilation (P < 0.01). The prediction of severe coronary disease was optimized by combining the poststress contraction index and lung uptake. These data support the use of ECG-gated myocardial scans in evaluating the functional consequences of stress/imaging procedures.

Biomarkers↗
PubMed1987

Selective right ventricular dysfunction following doxorubicin therapy.

Cardiotoxicity is one of the major side effects of doxorubicin therapy. The side effect presents in an acute and chronic form. It has been observed mainly when the cumulative dosage exceeds 450 mg/m2 of body surface. The cardiotoxicity presents with a low left ventricular ejection fraction. We report three patients who developed selective right ventricular dysfunction, expressed by low right ventricular ejection fraction as measured by radionuclide angiography. This complication was observed with rather low cumulative dosages of the drug (105 to 318 mg/m2). Two of the patients received concurrent mitomycin-C chemotherapy and the third patient underwent prior mediastinal irradiation. The possible mechanism for this selective cardiotoxicity is discussed. Monitoring of right ventricular performance by radionuclide angiography during doxorubicin therapy is recommended so that therapy can be discontinued before the left ventricle is damaged.

Adult↗
PubMed1996

Comparison of rest thallium-201 imaging and rest technetium-99m sestamibi imaging for assessment of myocardial viability in patients with coronary artery disease and severe left ventricular dysfunction.

OBJECTIVES: We prospectively compared myocardial uptake of thallium-201 (201Tl) at rest with rest technetium-99m (99mTc) sestamibi uptake in the same patients, using quantitative singlephoton emission computed tomography (SPECT). BACKGROUND: Because of only slightly delayed redistribution, 99mTc-sestamibi uptake at rest may be less than 201Tl uptake, thereby underestimating the extent of viability. METHODS: Twenty patients (2.25 stenoses per patient) with a mean left ventricular ejection fraction of 33 +/- 2% underwent early and 3-h delayed rest 201Tl SPECT, rest 99mTc-sestamibi SPECT and two-dimensional echocardiography. RESULTS: The 280 scan segments were classified as either a normal, mild reduction in viability, defined as delayed 201Tl uptake < or = 75% and > or = 5%, or a severe reduction in viability, defined as delayed 201Tl uptake < 50%. Mild and severe defects were further classified as fixed or having rest 201Tl redistribution. Comparisons by patients were made using repeated measures analysis of variance and Dunnett's multiple comparisons test to compare 99mTc-sestamibi with initial rest 201Tl and delayed 201Tl uptake. Twenty patients had at least one mild fixed defect (95 total segments). The average percent uptake in these defects for initial 201Tl, delayed 201Tl and 99mTc-sestamibi was 62.5 +/- 2.7%, 63.1 +/- 7.1% and 67.3 +/- 9.7%, respectively (p = NS). Twelve patients (27 segments) had mild redistribution defects on serial rest 201Tl imaging. The average percent uptake was 61.6 +/- 5.2% for initial 201Tl, 67.0 +/- 9.1% for delayed 201Tl and 67.7 +/- 12.4% for 99mTc-sestamibi defects. Technetium-99m sestamibi uptake was not significantly different than that for delayed 201Tl but was significantly greater than initial 201Tl uptake. Seventeen patients (52 segments) had severe fixed 201Tl defects. The average percent uptake was 38.9 +/- 7.3% for initial 201Tl, 38.3 +/- 12.2% for delayed 201Tl and 42.7 +/- 14.2% for 99mTc-sestamibi defects in these patients (p = NS). Ten patients (19 segments) had severe redistribution defects on rest 201Tl imaging. The average percent uptake was 37.0 +/- 8.5% for initial 201Tl, 42.9 +/- 8.6% for delayed 201Tl and 44.5 +/- 11.3% for 99mTc-sestamibi defects. As was seen for mild 201Tl redistribution defects, 99mTc-sestamibi uptake was significantly higher than initial 201Tl uptake, but not significantly different than delayed 201Tl uptake in these severe defects. CONCLUSIONS: Technetium-99m sestamibi uptake after injection at rest is comparable to 201Tl uptake after injection at rest in patients with severe coronary artery disease and left ventricular dysfunction, suggesting comparable worth for viability assessment.

Cell Survival↗
PubMed1996

Baseline quality of life as a predictor of mortality and hospitalization in 5,025 patients with congestive heart failure. SOLVD Investigations. Studies of Left Ventricular Dysfunction Investigators.

This study examined the independent relation of health-related quality of life (HRQL) to mortality and congestive heart failure (CHF)-related hospitalizations in patients with an ejection fraction of < 0.35 followed for a mean of 36.5 months. A brief HRQL questionnaire was administered at baseline to patients randomized to placebo or enalapril in the Studies of Left Ventricular Dysfunction (SOLVD) trial. Participants had an ejection fraction of < 0.35 and either symptomatic CHF (treatment trial, n = 2,465) or asymptomatic CHF (prevention trial, n = 2,560). Baseline assessment of HRQL predicted mortality and CHF-related hospitalizations in symptomatic and asymptomatic patients randomized to enalapril and placebo treatment. Domains that were the stronger univariate predictors of mortality and CHF-related hospitalizations were activities of daily living (relative risk [RR] for mortality: 1.163, p < 0.000; for hospitalization: 1.215, p < 0.000), general health (RR for mortality: 1.205, p < 0.000; for hospitalization: 1.188, p < 0.000), and social functioning (RR for mortality 1.098, p < 0.000; for hospitalization: RR 1.156, p < 0.000). In the multivariate model, activities of daily living (RR for mortality 1.41, p < 0.000; for hospitalization: RR 1.43, p < 0.002), general health (RR for mortality 1.21, p < 0.000; for hospitalization RR 1.16, p < 0.013) and heart failure symptoms (RR for mortality 1.02, p < 0.025; for hospitalization RR 1.03, p < 0.004) were found to be independent risk factors. HRQL independently predicted mortality and CHF-related hospitalizations after adjustment for ejection fraction, age, treatment, and New York Heart Association classification in patients with an ejection fraction of < 0.35, randomized to enalapril and placebo treatment. HRQL provides additional clinical information regarding disease course and outcome that is not captured by traditional indexes of clinical status.

Activities of Daily Living↗