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PubMed2004

[ACE inhibitors in the treatment of ventricular dysfunction caused by cardiotoxic cytostatics].

Morbidity and mortality resulting from cardiotoxic complications of anticancer therapy is still unacceptably high. Despite advances in the understanding of the pathomechanisms of cardiotoxicity, in prevention and detection of these complications, progressive ventricular dysfunction in cancer survivors represents a great therapeutic problem. Ventricular dysfunction is a life-threatening complication particularly in patients treated with anthracycline cytostatics. Anthracycline-induced loss of myocytes leads to an inadequate ventricular hypertrophy, which produces a rise in left ventricular (LV) afterload and deterioration of ventricular contractility culminating in heart failure. Efficacy of angiotensin-converting enzyme (ACE) inhibitors for the treatment of asymptomatic and symptomatic LV dysfunction in various clinical settings has been confirmed in a number of controlled, randomized trials. Until now, there are only few published data supporting the use of ACE inhibitors to treat patients with ventricular dysfunction-induced by anthracyclines. Cardio-protection with ACE inhibitors in children and adolescents treated with anthracyclines in contrast to ACE inhibition in adults after anthracycline therapy is a controversial topic. Evidence from the recent follow up study indicates a progressive deterioration of left ventricular wall thinning in childhood cancer survivors treated with enalapril. The ongoing large controlled, double blind, randomized trials will provide an important information concerning the efficacy of ACE inhibitors to prevent progression of ventricular dysfunction in paediatric oncologic patients.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1997

Ejection fraction and risk of thromboembolic events in patients with systolic dysfunction and sinus rhythm: evidence for gender differences in the studies of left ventricular dysfunction trials.

OBJECTIVES: The aims of this study were to describe the incidence and spectrum of thromboembolic events experienced by patients with moderate to severe left ventricular systolic dysfunction in normal sinus rhythm and to study the association between ejection fraction and thromboembolic risk. BACKGROUND: The annual incidence of thromboembolic events in patients with heart failure is estimated to range from 0.9% to 5.5%. Previous studies demonstrating a relation between worsening left ventricular systolic function and thromboembolic risk are difficult to interpret because of the prevalence of atrial fibrillation, an independent risk factor for thromboembolism, in the patients with a lower ejection fraction. METHODS: This is a retrospective analysis of the Studies of Left Ventricular Dysfunction prevention and treatment trials data base. Patients with atrial fibrillation were excluded, resulting in 6,378 participants in sinus rhythm at the time of randomization. Thromboembolic events include strokes, pulmonary emboli and peripheral emboli. Separate analyses were conducted in each gender because there was evidence of a significant interaction between ejection fraction and gender on the risk of thromboembolic events (p = 0.04). RESULTS: The overall annual incidence of thromboembolic events was 2.4% in women and 1.8% in men. On univariate analysis, a decline in ejection fraction was [corrected] associated with thromboembolic risk in women (relative risk [RR] per 10% decrease in ejection fraction 1.58, 95% confidence interval [CI] 1.10 to 2.26, p = 0.01), but not in men. On multivariate analysis, a decline in ejection fraction remained independently associated with thromboembolic risk in women (RR per 10% decrease 1.53, 95% CI 1.06 to 2.20, p = 0.02), but no relation was demonstrated in men. CONCLUSIONS: In patients with left ventricular systolic dysfunction and sinus rhythm, the annual incidence of thromboembolic events is low. Ejection fraction appears to be independently associated with thromboembolic risk in women, but not in men.

Aged↗

PubMed1999

Differential coronary microvascular function in patients with left ventricular dysfunction of unknown cause--implication for possible mechanism of myocardial ischemia in early stage of cardiomyopathy.

To evaluate whether or not coronary microvascular dysfunction is associated with exercise-induced myocardial ischemia in left ventricular dysfunction of unknown cause, both the treadmill exercise test (TET) and coronary hemodynamics were studied in 20 patients with impaired left ventricular ejection fraction (<50% by radionuclide ventriculogram), normal cardiac size, normal coronary angiogram and no evidence of clinical heart failure. Ten subjects with atypical chest pain were studied as the control. Coronary hemodynamics were studied both at baseline and after dipyridamole infusion (0.56mg/kg, i.v. for 4'). There was no difference in age, gender, blood pressure, baseline great cardiac venous flow (GCVF) and coronary vascular resistance between ten patients with a positive TET and the other ten with a negative TET. At baseline, coronary sinus oxygen concentration was increased and myocardial oxygen consumption reduced in patients with a positive TET compared with those with negative a TET. After dipyridamole infusion, maximum GCVF (102+/-47 vs. 144+/-31 ml/min, P=0.027) and coronary flow reserve (2.31+/-0.49 vs. 3.00+/-0.61, P=0.012) were significantly reduced and minimum coronary vascular resistance was higher (1.00+/-0.42 vs. 0.63+/-0.12 mmHg/ml/min, P=0.016) in patients with a positive TET than in those with a negative TET. At follow-up, 40% of patients with a positive TET and 10% of those with a negative TET developed clinical heart failure with a dilated left ventricle during a period of 45 months. Thus, coronary microvascular function is heterogeneous in patients with left ventricular dysfunction of unknown cause. In some of them, coronary microvascular dysfunction could be related to the presence of exercise-induced myocardial ischemia, suggesting that similar pathophysiology underlies the early stage of dilated cardiomyopathy and syndrome X.

Adult↗

PubMed1994

Influence of reversible segmental left ventricular dysfunction on heart period variability in patients with one-vessel coronary artery disease.

OBJECTIVES: This study evaluated the relation between reversible segmental left ventricular dysfunction and frequency domain measures of heart period variability in patients with coronary artery disease. BACKGROUND: Heart period variability is frequently reduced in patients with coronary artery disease. However, the mechanisms of this reduction are still unclear. METHODS: Echocardiographic left ventricular wall motion and frequency domain measures of heart period variability were evaluated in 32 patients with one-vessel coronary artery disease before and 16 to 24 days after successful percutaneous transluminal coronary angioplasty. Of these, 12 patients (Group A) had normal and 20 patients (Group B) had abnormal regional wall motion. A control group of 15 healthy subjects (Group C) underwent 24-h Holter recording twice at 2-week intervals to check for spontaneous variations. RESULTS: At baseline, low and high frequency power were lower in Group B than in Groups A and C, whereas no difference was detectable in ultra low and very low frequency and total power. After coronary angioplasty, regional wall motion and frequency domain measures of heart period variability were unchanged in Group A. In Group B the mean (+/- SD) summed segment score improved from 17.1 +/- 3.6 to 12.8 +/- 2.0 (p < 0.01), and mean low and high frequency power (logarithmic units) increased from 6.14 +/- 0.23 to 6.35 +/- 0.34 (p < 0.01) and from 5.43 +/- 0.32 to 5.68 +/- 0.52 (p < 0.01), respectively. Furthermore, low and high frequency power, lower at baseline in Group B than in the other two groups, were comparable in the three groups after coronary angioplasty. CONCLUSIONS: This study demonstrates that segmental left ventricular dysfunction is involved in determining sympathovagal imbalance in patients with one-vessel coronary artery disease; the reversal of left ventricular dysfunction by successful coronary angioplasty improves the heart period power spectrum. Thus, alterations in cardiac geometry influence the discharge of afferent sympathetic mechanoreceptors, contributing to the derangement in autonomic control of heart rate.

Afferent Pathways↗

PubMed1978

Left ventricular dysfunction after intravenous tartar emetic.

Left ventricular dysfunction had been reported in many patients suffering from schistosomal cor pulmonale. The nocuous agents affecting the left ventricle have not been defined. Antischistosomal therapy is suspected to contribute in the adverse effects on the myocardium, particularly antimonials and niridazole. In this study, the left ventricular performance was studied in 29 patients suffering from schistosomiasis before and 30 min after i.v. therapeutic dose of a tartar emetic. After the injection, the PEPI and PEPI/LVETI were increased, the LVETI was abbreviated, EF. was reduced, the LVEDP was raised, the peak dp/dt and the Vmax were reduced. Toxic effects of the T.E. on the myocardium and diminished contractility of the left ventricle were presumed to be caused by T.E. Other factors adversely affecting the myocardium in patients suffering from schistosomiasis cannot be excluded.

Adolescent↗

PubMedDate not supplied

Cardiopulmonary exercise response in patients with left ventricular dysfunction or heart failure: a noninvasive study by gas exchange and impedance cardiography monitoring.

We investigated the upright bicycle exercise cardiopulmonary response in 20 patients with left ventricular dysfunction (LVD, secondary to previous myocardial infarction, left ventricular ejection fraction range 18-44%). Ten patients (48 +/- 7 years) asymptomatic (I NYHA class) without drug treatment (LVD group). The others (n = 10) (50 +/- 1 years) complained of dyspnea and/or fatigue despite therapy (NYHA II-III). They represented the heart failure (HF) group. Eight sedentary men (40 +/- 10 years) served as controls. Controls and patients performed stress testings under drug treatment, when administered. Anaerobic ventilatory threshold (ATge) was considered as an index of submaximal exercise while peak exercise VO2 (Peak VO2) was considered the maximal volitional exercise capacity. The ratio between minute ventilation (VE) to carbon dioxide release (VCO2) (VE/VCO2) was assessed to evaluate the ventilatory response during exercise. We coupled gas exchange assessment (2001, MGC) with noninvasive monitoring of stroke volume (SV) by impedance cardiography (NCCOM3, BOMED) and total systemic vascular resistances (TSVR; by auscultatory blood pressure measurement). In controls VO2 increase during exercise was related to higher heart rate (HR) and SV both from resting to ATge and from this point to the peak. TSVR declined during both steps. In patients with HF VO2 rose from resting to ATge (by faster HR and unchanged SV). VO2 increased slightly from this point to Peak VO2. This result was related to flat HR increase and unchanged SV as well as TSVR. In patients with LVD VO2 increased similarly to controls from resting to ATge and less above the threshold. In these patients both HR and SV increased during submaximal exercise. From ATge to Peak VO2 only HR increased. TSVR declined significantly similarly to controls. The VE/VCO2 ratio was higher at peak exercise in patients with HF compared to controls. Different determinants were demonstrated in patients with left ventricular dysfunction with mild or symptomatic chronic heart failure (CHF). These findings and the increased ventilatory response in patients with CHF can explain different changes of VO2 in these patients during submaximal and maximal voluntary exercise and contribute to explain exercise-induced exertion in these subjects.

Adult↗

PubMed2007

The impact of Cardiovascular Autonomic Neuropathy in diabetes: is it associated with left ventricular dysfunction?

Cardiovascular Autonomic Neuropathy (CAN) is one of the least understood of all serious complications of diabetes. Besides increasing mortality, CAN may have various clinical sequelae including exercise intolerance, arrhythmias and painless myocardial infarction. But does it also cause left ventricular dysfunction? Patients with diabetes have a greater risk of developing congestive heart failure. Coronary artery disease and hypertension have been notorious in causing left ventricular dysfunction in many of these patients. However, even in their absence, diabetes itself, through several studies, has been proposed to cause the controversial entity, Diabetic Cardiomyopathy (DCM). Various mechanisms have been suggested. CAN through alteration in myocardial blood flow and sympathetic denervation, and through changes in myocardial neurotransmitters, including catecholamines and neurotransmitters of the neuropeptidergic system, has been and is still being studied as one of the main mechanisms to cause left ventricular dysfunction. Earlier detection of CAN and instant initiation of upcoming treatments may be a way to help prevent DCM, and thus improve the morbidity and mortality this causes to patients with diabetes.

Animals↗

PubMed1984

The value of rest and exercise radionuclide ventriculography as compared to echocardiography and angiography in the detection of left ventricular dysfunction in patients with chronic aortic regurgitation.

Symptomatic patients with chronic aortic regurgitation and a left ventricular ejection fraction greater than 0.50, or forward cardiac index greater than 2.5 l/min/m2 at rest, have a much better survival rate than those with a depressed ejection fraction or cardiac index following aortic valve replacement. The annual mortality rate is approximately 2% for those with well preserved ventricular function versus 10% for those with depressed ventricular function at rest. This is in striking contrast to the situation that exists in patients with aortic stenosis, where the long-term survival is similar for those with a normal or depressed left ventricular ejection fraction or cardiac index at rest. Therefore, it would seem to be important to detect incipient left ventricular failure in patients with chronic aortic regurgitation and to intervene surgically before the left ventricular dysfunction becomes irreversible. In patients with a normal left ventricular ejection fraction at rest, maximal supine bicycle exercise testing with radionuclide ventriculography defines a group of patients with truly normal ventricular function (ejection fraction increases by greater than 0.05 ejection fraction units at peak exercise), and a group with incipient left ventricular dysfunction earlier than previously described variables (i.e., left ventricular ejection fraction at rest less than 0.50, left ventricular end-systolic volume index greater than 90 ml/m2, left ventricular end-systolic dimension greater than or equal to 5.5 cm, left ventricular shortening fraction less than or equal to 25%), and generally before the onset of symptoms.

Adolescent↗

PubMed2001

Usefulness of dobutamine stress tests for detection of cardiac abnormalities in dogs with experimentally induced early left ventricular dysfunction.

OBJECTIVE: To determine whether dobutamine stress tests (DST) can be used to detect cardiac dysfunction in dogs with early left ventricular dysfunction (ELVD) induced by rapid right ventricular pacing (RRVP). ANIMALS: 7 adult male Beagles. PROCEDURE: A pacemaker was surgically implanted in each dog at the level of the right ventricular apex. Electrocardiography, Doppler sphygmomanometry, and Doppler echocardiography were performed before and during a DST prior to activation of the pacemaker and every 3 to 4 days during the period of RRVP. Dobutamine stress tests were performed by infusing dobutamine at incremental dosages ranging from 12.5 to 42.5 microg/kg of body weight/min. RESULTS: Clinical signs of congestive heart failure were not observed during the pacing period. However, all dogs developed ELVD associated with significant changes in values for most Doppler echocardiographic variables obtained prior to DST Adverse cardiac effects were not detected during DST. Most Doppler echocardiographic indices of cardiac function were significantly altered in response to dobutamine infusion during the pacing period, compared with prepacing values. However, a dobutamine-induced 2-fold increase in cardiac output was maintained. CONCLUSIONS AND CLINICAL RELEVANCE: Dobutamine stress tests can be safely performed in dogs with experimentally induced ELVD. Dobutamine stress tests may be a sensitive, noninvasive diagnostic method, complementary to standard clinical examinations, for detection of early cardiac dysfunction in dogs asymptomatic for dilated cardiomyopathy.

Animals↗

PubMed1991

Silent left ventricular dysfunction during exercise after coronary artery bypass surgery.

Serial changes in left ventricular function during exercise were assessed by radionuclide continuous ventricular function monitoring in 80 patients undergoing coronary artery bypass surgery before and after operation. This monitor records serial beat by beat radionuclide and electrocardiographic data and calculates the left ventricular ejection fraction every 20s. The profiles of ejection fractions during graded bicycle exercise were divided into 4 types. In type A, the ejection fraction continued to increase. In type B, the ejection fraction initially increased but decreased in late exercise. In type C, the ejection fraction did not change. In type D, the ejection fraction continued to decrease. Type A is considered to be the normal response to exercise and types B, C and, D are considered to be abnormal responses. Before operation, 8 patients showed type A, 21 type B, 13 type C, and 38 type D. After operation, 53 patients showed type A, 16 type B, 8 type C, and 3 type D. The mean ejection fraction decreased with exercise from 53% +/- 11% to 47% +/- 11% before surgery, but increased with exercise from 55% +/- 10% to 64% +/- 14% after surgery. During postoperative exercise, no patient developed chest pain but 19 patients showed a decrease in the ejection fraction in early or late exercise. A decrease in the ejection fraction is an earlier indicator of myocardial ischaemia than angina or electrocardiographic changes. Silent left ventricular dysfunction during postoperative exercise was considered to reflect myocardial ischaemia resulting from occluded grafts, ungrafted coronary arteries, or inadequate perfusion by arterial grafts. The radionuclide continuous ventricular function monitor can detect silent left ventricular dysfunction after coronary artery bypass surgery.

Adult↗

PubMed2005

[Head to head comparison of dobutamine alone and combined with nitrate stress echocardiography and 99mTc-MIBI/18FDG myocardial SPECT image for diagnosis of viable myocardium in patients with severe left ventricular dysfunction].

OBJECTIVE: This study was sought to compare the sensitivity, specificity and accuracy of (1) dual isotope simultaneous acquisition single-photon emission computed tomography (DISA SPECT) myocardial image with (99m)Tc-sestamibi/(18)F-fluorodeoxyglucose ((99m)Tc-MIBI/(18)FDG); (2) low dose dobutamine alone and combined with Isosorbide Dinitrate (ISDN: Isoket) stress two dimensional echocardiography (2DE) to predict regional movement recovery after revascularization (CRV) in patients with old myocardial infarction (OMI) and severe left ventricular dysfunction. METHODS: Twenty-six patients (mean age 51 +/- 8 years, male 25, female 1) with OMI and severe left ventricular dysfunction (mean left ventricular ejection fraction, LVEF (38.6% +/- 4.9%) underwent low dose dobutamine 10 microg x kg(-1) x min(-1) (Dob10 microg) and ISDN (286 +/- 31 microg/min) combined with Dob5 microg (ISDN-Dob 5 microg) 2DE and DISA SPECT within one week. In echocardiogram and DISA SPECT images: the left ventricle (LV) was divided into 16 segments. The semi-quantitative scoring system was used for both images. Myocardial viability was defined as an improvement of at least >or= 1 grade in at least two contiguous segments at rest 2DE after CRV. The viable segments detecting rate with stress 2DE and DISA SPECT were compared. Compared with the results of post-CRV, the sensitivity, specificity and accuracy of detecting viable segments of two methods were calculated. RESULTS: Among 272 abnormal segments in 26 patients, 156 (57.4%) segments showed contractile improvement after CRV. The viable segments detecting rate with DISA SPECT was 72.4% (134/254), which was significantly higher than the contractile improved rate after CRV (P < 0.001). During Dob10 microg 2DE and ISDN-Dob5 microg 2DE, the detecting rates were 65.5% (163/249) and 65.7% (176/268), respectively, which were both comparable to the improved rate after CRV (both P > 0.05). With DISA SPECT, the sensitivity, specificity and accuracy were 93.7%, 55% and 76.8%, respectively. Compared with DISA SPECT, Dob10 microg 2DE showed similar sensitivity (88.6%), specificity (64.2%) and the accuracy (77.9%). When ISDN combined with Dob5 microg, the sensitivity (91.4%), specificity (68.1%) and accuracy (81.4%)were comparable to those of Dob10 microg 2DE and DISA SPECT (all P > 0.05), while the specificity was even higher than DISA SPECT (P < 0.05). CONCLUSION: In identifying myocardial viability in patients with OMI and severe left ventricular dysfunction, DISA SPECT has higher sensitivity, lower specificity and better accuracy. Dob10 microg and ISDN-Dob5 microg 2DE are both equivalent to DISA SPECT in sensitivities, specificities and accuracies, and even higher in specificity in ISDN-Dob5 microg 2DE.

Adult↗

PubMed1992

Deep negative T waves associated with reversible left ventricular dysfunction in acute adrenal crisis.

We report two cases of reversible left ventricular dysfunction associated with deep negative T waves during acute adrenal crisis due to isolated deficiency of adrenocorticotrophic hormone. There were no symptoms suggestive of heart disease in either case and left ventricular wall motion abnormalities, present mainly around the left ventricular apex, returned to normal in 1-2 weeks. Deep negative T waves normalized 4 weeks after corticosteroid administration. Acute adrenal crisis should be considered when deep negative T waves are associated with left ventricular dysfunction without cardiac symptoms.

Adrenal Insufficiency↗

PubMed1995

Continuous warm versus intermittent cold blood cardioplegia for coronary bypass surgery in patients with left ventricular dysfunction.

Between October 1991 and March 1994, 108 consecutive patients with moderate to severe left ventricular dysfunction underwent non-emergency isolated coronary artery surgery under the care of one surgeon (A.R.). They were prospectively randomised to receiving either intermittent cold (Group 1-50 patients) or continuous warm (Group 2-58 patients) blood cardioplegia for myocardial protection. There were no significant differences in clinical outcome between the two groups, as judged by operative mortality, rates of perioperative myocardial infarction, the serum CKMB isoenzyme level at 2 and 18 h after operation, need for circulatory support, postoperative neurological deficit, or duration of hospital stay. Group 2 patients required significantly more potassium (68 vs 29 mmol, P < 0.001) to maintain diastolic arrest and also had higher serum potassium levels after removal of the cross-clamp (P < 0.001). However, sinus rhythm returned spontaneously with greater frequency (91.2% vs 45.8%, P < 0.001) in Group 2 patients. In conclusion this report suggests that retrograde continuous warm blood cardioplegia provides comparable myocardial protection to that achieved with retrograde intermittent cold blood cardioplegia in patients with moderate to severe left ventricular dysfunction undergoing isolated coronary artery surgery.

Aged↗

PubMed2003

Use of the peak troponin value to differentiate myocardial infarction from reversible neurogenic left ventricular dysfunction associated with aneurysmal subarachnoid hemorrhage.

OBJECT: Differentiating myocardial infarction (MI) from reversible neurogenic left ventricular dysfunction (stunned myocardium [SM]) associated with aneurysmal subarachnoid hemorrhage (SAH) is critical for early surgical intervention. The authors hypothesized that the cardiac troponin (cTn) trend and/or echocardiogram could be used to differentiate between the two entities. METHODS: A retrospective study was conducted for the period between 1995 and 2000. All patients included in the study met the following criteria: 1) no history of cardiac problems; 2) new onset of abnormal cardiac function (ejection fraction [EF] < 40% on echocardiograms); 3) serial cardiac markers (cTn and creatine kinase MB isoform [CK-MB]); 4) surgical intervention for their aneurysm; and 5) cardiac output monitoring either by repeated echocardiograms or invasive hemodynamic monitoring during the first 4 days post-SAH when the patients were euvolemic. Of the 350 patients with SAH, 10 (2.9%) had severe cardiac dysfunction. Of those 10, six were women and four were men. The patients' mean age was 53.5 years (range 29-75 years) and their SAH was classified as Hunt and Hess Grade III or IV. Aneurysm distribution was as follows: basilar artery tip (four); anterior communicating artery (two); middle cerebral artery (one); posterior communicating artery (two); and posterior inferior cerebellar artery (one). The mean EFonset was 33%. The changes on echocardiograms in these patients did not match the findings on electrocardiograms (EKGs). Within 4.5 days, dramatic improvement was seen in cardiac output (from 4.93 +/- 1.16 L/minute to 7.74 +/- 0.88 L/minute). Compared with historical controls in whom there were similar levels of left ventricular dysfunction after MI, there was no difference in peak CK-MB. A 10-fold difference, however, was noted in cTn values (0.22 +/- 0.25 ng/ml; control 2.8 ng/ml; p < 0.001). CONCLUSIONS: The authors determined the following: 1) that the CK-MB trend does not allow differentiation between SM and MI; 2) that echocardiograms revealing significant inconsistencies with EKGs are indicative of SM; and 3) that cTn values less than 2.8 ng/ml in patients with EFs less than 40% are consistent with SM.

Adult↗

PubMed1993

Prediction of mortality and morbidity with a 6-minute walk test in patients with left ventricular dysfunction. SOLVD Investigators.

OBJECTIVE: To study the potential usefulness of the 6-minute walk test, a self-paced submaximal exercise test, as a prognostic indicator in patients with left ventricular dysfunction. DESIGN: Data were collected during a prospective cohort study, the Studies of Left Ventricular Dysfunction (SOLVD) Registry Substudy. SETTING: Twenty tertiary care hospitals in the United States, Canada, and Belgium. PARTICIPANTS: A stratified random sample of 898 patients from the SOLVD Registry who had either radiological evidence of congestive heart failure and/or an ejection fraction of 0.45 or less were enrolled in the substudy and underwent a detailed clinical evaluation including a 6-minute walk test. Patients were followed up for a mean of 242 days. OUTCOME MEASURES: Mortality and hospitalization. RESULTS: During follow-up, 52 walk-test participants (6.2%) died and 252 (30.3%) were hospitalized. Hospitalization for congestive heart failure occurred in 78 participants (9.4%), and the combined endpoint of death or hospitalization for congestive heart failure occurred in 114 walk-test participants (13.7%). Compared with the highest performance level, patients in the lowest performance level had a significantly greater chance of dying (10.23% vs 2.99%; P = .01), of being hospitalized (40.91% vs 19.90%; P = .002), and of being hospitalized for heart failure (22.16% vs 1.99%; P < .0001). In a logistic regression model, ejection fraction and distance walked were equally strong and independent predictors of mortality and heart failure hospitalization rates during follow-up. CONCLUSION: The 6-minute walk test is a safe and simple clinical tool that strongly and independently predicts morbidity and mortality in patients with left ventricular dysfunction.

Aged↗

PubMed1999

Racial differences in the outcome of left ventricular dysfunction.

BACKGROUND: Population-based studies have found that black patients with congestive heart failure have a higher mortality rate than whites with the same condition. This finding has been attributed to differences in the severity, causes, and management of heart failure, the prevalence of coexisting conditions, and socioeconomic factors. Although these factors probably account for some of the higher mortality due to congestive heart failure among blacks, we hypothesized that racial differences in the natural history of left ventricular dysfunction might also have a role. METHODS: Using data from the Studies of Left Ventricular Dysfunction (SOLVD) prevention and treatment trials, in which all patients received standardized therapy and follow-up, we conducted a retrospective analysis of the outcomes of asymptomatic and symptomatic left ventricular systolic dysfunction among black and white participants. The mean (+/-SD) follow-up was 34.2+/-14.0 months in the prevention trial and 32.3+/-14.8 months in the treatment trial among the black and white participants. RESULTS: The overall mortality rates in the prevention trial were 8.1 per 100 person-years for blacks and 5.1 per 100 person years for whites. In the treatment trial, the rates were 16.7 per 100 person-years and 13.4 per 100 person-years, respectively. After adjustment for age, coexisting conditions, severity and causes of heart failure, and use of medications, blacks had a higher risk of death from all causes in both the SOLVD prevention trial (relative risk, 1.36; 95 percent confidence interval, 1.06 to 1.74; P=0.02) and the treatment trial (relative risk, 1.25; 95 percent confidence interval, 1.04 to 1.50; P=0.02). In both trials blacks were also at higher risk for death due to pump failure and for the combined end point of death from any cause or hospitalization for heart failure, our two predefined indicators of the progression of left ventricular systolic dysfunction. CONCLUSIONS: Blacks with mild-to-moderate left ventricular systolic dysfunction appear to be at higher risk for progression of heart failure and death from any cause than similarly treated whites. These results suggest that there may be racial differences in the outcome of asymptomatic and symptomatic left ventricular systolic dysfunction.

Analysis of Variance↗

PubMed2001

Lesser response to angiotensin-converting-enzyme inhibitor therapy in black as compared with white patients with left ventricular dysfunction.

BACKGROUND: Black patients with heart failure have a poorer prognosis than white patients, a difference that has not been adequately explained. Whether racial differences in the response to drug treatment contribute to differences in outcome is unclear. To address this issue, we pooled and analyzed data from the Studies of Left Ventricular Dysfunction (SOLVD) prevention and treatment trials, two large, randomized trials comparing enalapril with placebo in patients with left ventricular dysfunction. METHODS: We used a matched-cohort design in which up to four white patients were matched with each black patient according to trial, treatment assignment, sex, left ventricular ejection fraction, and age. A total of 1196 white patients (580 from the prevention trial and 616 from the treatment trial) were matched with 800 black patients (404 from the prevention trial and 396 from the treatment trial). The average duration of follow-up was 35 months in the prevention trial and 33 months in the treatment trial. RESULTS: The black patients and the matched white patients had similar demographic and clinical characteristics, but the black patients had higher rates of death from any cause (12.2 vs. 9.7 per 100 person-years) and of hospitalization for heart failure (13.2 vs. 7.7 per 100 person-years). Despite similar doses of drug in the two groups, enalapril therapy, as compared with placebo, was associated with a 44 percent reduction (95 percent confidence interval, 27 to 57 percent) in the risk of hospitalization for heart failure among the white patients (P<0.001) but with no significant reduction among black patients (P=0.74). At one year, enalapril therapy was associated with significant reductions from base line in systolic blood pressure (by a mean [+/-SD] of 5.0+/-17.1 mm Hg) and diastolic blood pressure (3.6+/-10.6 mm Hg) among the white patients, but not among the black patients. No significant change in the risk of death was observed in association with enalapril therapy in either group. CONCLUSIONS: Enalapril therapy is associated with a significant reduction in the risk of hospitalization for heart failure among white patients with left ventricular dysfunction, but not among similar black patients. This finding underscores the need for additional research on the efficacy of therapies for heart failure in black patients.

Adult↗

PubMed1999

[1998 prognosis of left ventricular dysfunction in a maximum care non-university hospital. Analysis of the Ludwigshafen LVD Registry].

BACKGROUND: Prognostic data on heart failure rely on epidemiological studies or large clinical trials. These data are not to transfer easily on everyday practice. OBJECTIVE: To assess the prognosis of left ventricular dysfunction under the therapeutic conditions of the 1990s. SETTING: Nonuniversity tertiary care hospital. PATIENTS AND METHODS: Since January 1995 consecutive and complete registry of all inpatients presenting with a left ventricular dysfunction (EF < 45%). No exclusion criteria. RESULTS: n = 512, mean age 64 years, 77% male, mean NYHA class 2.5, left ventricular EF 31%. ETIOLOGY: 58% coronary heart disease, 28% dilated cardiomyopathy. Medical treatment consisting of 91% ACE inhibitors, ACE inhibitor dosage 52% of the recommended dose, 42% beta-blockers, 70% diuretics, and 63% digitalis. Follow-up completeness 95.5%. One-year mortality 64/489 patients (13.9%). Determinants of mortality: NYHA III/IV, EF < 30%, malignant disease, age > 75 years. CONCLUSION: In spite of the aforementioned medical treatment and a proportion of 14.8% implanted defibrillators in 1998, the one-year mortality of ventricular dysfunction is as high as 13.9%. In everyday practice the prognostic effect of ACE inhibition and beta-blockade is not completely utilized.

Adrenergic beta-Antagonists↗