Quality indicators for the management of heart failure in vulnerable elders.
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Biomedical subjects
Publications and source records attributed to G C Fonarow.
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Despite scientific evidence that secondary prevention medical therapies reduce mortality in patients with established coronary artery disease, these therapies continue to be underutilized in patients receiving conventional care. To address this issue, a Cardiac Hospital Atherosclerosis Management Program (CHAMP) focused on initiation of aspirin, cholesterol-lowering medication (hydroxymethylglutaryl coenzyme A [HMG CoA] reductase inhibitor titrated to achieve low-density lipoprotein [LDL] cholesterol < or =100 mg/dl), beta blocker, and angiotensin-converting enzyme (ACE) inhibitor therapy in conjunction with diet and exercise counseling before hospital discharge in patients with established coronary artery disease. Treatment rates and clinical outcome were compared in patients discharged after myocardial infarction in the 2-year period before (1992 to 1993) and the 2-year period after (1994 to 1995) CHAMP was implemented. In the pre- and post-CHAMP patient groups, aspirin use at discharge improved from 68% to 92% (p <0.01), beta blocker use improved from 12% to 62% (p <0.01), ACE inhibitor use increased from 6% to 58% (p <0.01), and statin use increased from 6% to 86% (p <0.01). This increased use of treatment persisted during subsequent follow-up. There was also a significant increase in patients achieving a LDL cholesterol < or =100 mg/dl (6% vs 58%, p <0.001) and a reduction in recurrent myocardial infarction and 1-year mortality. Compared with conventional guidelines and care, CHAMP was associated with a significant increase in use of medications that have been previously demonstrated to reduce mortality; more patients achieved an LDL cholesterol < or =100 mg/dl, and there were improved clinical outcomes in patients after hospitalization for acute myocardial infarction.
BACKGROUND: The present study aimed to assess use of lipid-lowering medication at discharge in a current national sample of patients hospitalized with acute myocardial infarction and to evaluate factors associated with prescribing patterns. METHODS AND RESULTS: Demographic, procedural, and discharge medication data were collected from 138 001 patients with acute myocardial infarction discharged from 1470 US hospitals participating in the National Registry of Myocardial Infarction 3 from July 1998 to June 1999. Lipid-lowering medications were part of the discharge regimen in 31. 7%. Among patients with prior history of CAD, revascularization, or diabetes, less than one half of the patients were discharged on treatment. In multivariate analysis, factors independently related to lipid-lowering use included history of hypercholesterolemia (odds ratio [OR] 4.93; 95% CI 4.79 to 5.07), cardiac catheterization during hospitalization (OR 1.29; 95% CI 1.24 to 1.34), care provided at a teaching hospital, (OR 1.26; 95% CI 1.22 to 1.32), use of ss-blocker (OR 1.43; 95% CI 1.39 to 1.48), and smoking cessation counseling (OR 1.51; 95% CI 1.44 to 1.59). Lipid-lowering medications were given less often to patients who were older (65 to 74 versus <55 years of age; OR 0.82; 95% CI 0.78 to 0.86), those with a history of hypertension (OR 0.92; 95% CI 0.89 to 0.95), and those undergoing coronary artery bypass graft surgery (OR 0.58; 95% CI 0.55 to 0.60). CONCLUSIONS: Analysis of current practice patterns for the use of lipid-lowering medications in patients hospitalized with acute myocardial infarction reveals that a significant proportion of high-risk patients did not receive treatment at time of discharge.
OBJECTIVES: The study aimed to evaluate the role of obesity in the prognosis of patients with heart failure (HF). BACKGROUND: Previous reports link obesity to the development of HF. However, the impact of obesity in patients with established HF has not been studied. METHODS: We analyzed 1,203 patients with advanced HF followed in a comprehensive HF management program. The patients were subclassified into categories of body mass index (BMI) defined as: underweight BMI <20.7 (n = 164), recommended BMI 20.7 to 27.7 (n = 692), overweight BMI 27.8 to 31 (n = 168) and obese BMI >31 (n = 179). This sample size allows the detection of small effects (0.02), with a power of 0.80 and an alpha level of 0.05 for comparing one-year survival between BMI groups. RESULTS: The four BMI groups had similar profiles in terms of ejection fraction (mean 0.22), sodium, creatinine and smoking. The obese and overweight groups had significantly higher rates of hypertension and diabetes, as well as higher levels of cholesterol, triglycerides and low density lipoprotein cholesterol. The four BMI groups had similar survival rates. Ejection fraction, HF etiology and angiotensin-converting enzyme inhibitor use predicted survival on univariate analysis (p < 0.01), although BMI did not. On multivariate analysis, cardiopulmonary exercise tests, pulmonary capillary wedge pressure and serum sodium were strong predictors of survival (p < 0.05). Higher BMI was not a risk factor for increased mortality, but was associated with a trend toward improved survival. CONCLUSIONS: In a large cohort of patients with advanced HF of multiple etiologies, obesity is not associated with increased mortality and may confer a more favorable prognosis. Further studies need to delineate whether weight loss promotion in medically optimized patients with HF is a worthwhile therapeutic goal.
At the time of initial transplant evaluation, we evaluated the information and counseling needs of 82 outpatients with advanced heart failure and compared them with the needs of 74 of their caregivers. Both groups answered a 23-item questionnaire, which used a 5-point Likert scale to assess needs across 6 sub-scales specific to heart failure and the process of determining transplant eligibility. The 5 most important learning needs of patients and caregivers were similar, and we found significant differences only in the groups' responses to 3 individual questions. We conclude that nurses can meet the needs of patients and their caregivers by providing honest explanations, focusing on enhanced quality of life issues, and giving information for dealing with an emergency.
In heart failure (HF) patients, reflex renal vasoconstriction during exercise is exaggerated. We hypothesized that muscle mechanoreceptor control of renal vasoconstriction is exaggerated in HF. Nineteen HF patients and nineteen controls were enrolled in two exercise protocols: 1) low-level rhythmic handgrip (mechanoreceptors and central command) and 2) involuntary biceps contractions (mechanoreceptors). Renal cortical blood flow was measured by positron emission tomography, and renal cortical vascular resistance (RCVR) was calculated. During rhythmic handgrip, peak RCVR was greater in HF patients compared with controls (37 +/- 1 vs. 27 +/- 1 units; P < 0.01). Change in (Delta) RCVR tended to be greater as well but did not reach statistical significance (10 +/- 1 vs. 7 +/- 0.9 units; P = 0.13). RCVR was returned to baseline at 2-3 min postexercise in controls but remained significantly elevated in HF patients. During involuntary muscle contractions, peak RCVR was greater in HF patients compared with controls (36 +/- 0.7 vs. 24 +/- 0.5 units; P < 0.0001). The Delta RCVR was also significantly greater in HF patients compared with controls (6 +/- 1 vs. 4 +/- 0.6 units; P = 0.05). The data suggest that reflex renal vasoconstriction is exaggerated in both magnitude and duration during dynamic exercise in HF patients. Given that the exaggerated response was elicited in both the presence and absence of central command, it is clear that intact muscle mechanoreceptor sensitivity contributes to this augmented reflex renal vasoconstriction.
Dilated cardiomyopathy is a disease of diverse causes. Untreated, this condition will likely progress to advanced heart failure, sudden death, or both. There have been a number of significant advances in the understanding of the mechanisms involved in the pathogenesis of this disease. Treatments that counteract ventricular remodeling with neurohumoral blockade have substantially improved the outcome for many patients. Although cardiac transplantation is of benefit to patients with advanced disease, the growing donor heart shortage limits this option. New treatments are clearly needed, and many are being actively investigated. As the genetic and cellular derangements that result in dilated cardiomyopathy are better understood, new therapeutic targets will be identified in the quest to restore normal cardiac structure and function.
Acute decompensated heart failure is characterized by hemodynamic abnormalities as well as neuroendocrine activation, which contribute to heart failure symptoms, progressive cardiac dysfunction, and sudden death. The therapeutic goals in patients hospitalized with decompensated heart failure are to reverse acute hemodynamic abnormalities, relieve symptoms, and initiate treatment that will slow disease progression and improve long-term survival. Traditional hemodynamic targets in acute heart failure have been reduction in left and right ventricular filling pressures, reduction in systemic vascular resistance, and increase in cardiac output. Treatments aimed at these targets in patients with acute decompensated heart failure include diuretics, vasodilators, and inotropic agents. In patients hospitalized with acute decompensated heart failure, persistently elevated left ventricular filling pressure has been shown to be highly predictive of an increased risk of fatal decompensation and sudden death. Measures of systemic perfusion, arterial pressure, and vascular resistance have not. Thus, there is a more compelling physiologic rationale for the use of vasodilators than for inotropic agents in these patients. An ideal agent for acute decompensated heart failure would be one that rapidly reduces pulmonary wedge pressure, results in balanced arterial and venous dilation, promotes natriuresis, lacks direct positive inotropic effects, and does not result in reflex neuroendocrine activation.
The therapeutic goals for patients hospitalized with acute decompensated heart failure are to reverse acute hemodynamic abnormalities, relieve symptoms, and provide the ability to initiate early treatment, which will decrease disease progression and improve long-term survival. The use of nesiritide on top of standard care, such as diuretic therapy, has been proven to lead to meaningful clinical benefits in a broad range of acutely decompensated heart failure patients. Nesiritide is an attractive therapeutic option because of its more rapid and sustained hemodynamic profile with less adverse effects than alternative heart failure treatments, such as nitroglycerine or dobutamine. The use of nesiritide represents an entirely new treatment approach to reverse acutely decompensated heart failure and to facilitate optimization of the heart failure medical regimen.
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BACKGROUND: On-line physician education is increasing, but its efficacy in comparison with existing self-study methods is unknown. OBJECTIVE: To compare knowledge, learning efficiency, and learner satisfaction produced by self-study of World Wide Web-based and print-based guidelines for care after acute myocardial infarction. DESIGN: Randomized, controlled trial. SETTING: 12 family medicine and internal medicine residency programs at four universities. PARTICIPANTS: 162 residents. INTERVENTIONS: In proctored sessions, participants were randomly assigned to study from printed materials or from SAGE (Self-Study Acceleration with Graphic Evidence), a Web-based tutorial system. Both methods used identical self-assessment questions and answers and guideline text, but SAGE featured hyperlinks to specific guideline passages and graphic evidence animations. MEASUREMENTS: Scores on multiple-choice knowledge tests, score gain per unit of study time, and ratings on a learner satisfaction scale. RESULTS: Immediate post-test scores on a 20-point scale were similar in the SAGE and control groups (median score, 15.0 compared with 14.5; P>0.2), but SAGE users spent less time studying (median, 27.0 compared with 38.5 minutes; P<0.001) and therefore had greater learning efficiency (median score gain, 8.6 compared with 6.7 points per hour; P = 0.04). On a scale of 5 to 20, SAGE users were more satisfied with learning (median rating, 17.0 compared with 15.0; P<0.001). After 4 to 6 months, knowledge had decreased to the same extent in the SAGE and control groups (median score, 12.0 compared with 11.0; P = 0.12). CONCLUSIONS: On-line tutorials may produce greater learning efficiency and satisfaction than print materials do, but one self-study exposure may be insufficient for long-term knowledge retention. Further research is needed to identify instructional features that motivate greater final learning and retention.
The purpose of this study was to assess whether in patients with syncope and heart failure due to nonischemic cardiomyopathy, treatment with an implantable cardioverter-defibrillator (ICD) compared with conventional medical therapy is associated with a reduction in sudden death and total mortality. Patients with advanced heart failure who have syncope have been shown to be at high risk for sudden death. Further risk stratification has been difficult in patients with nonischemic cardiomyopathy in whom inducibility on electrophysiologic study is not predictive of future risk. Of 639 consecutive patients with nonischemic cardiomyopathy referred for heart transplantation, 147 patients with history of syncope and no prior history of sustained ventricular tachycardia or cardiac arrest were identified. Outcomes were compared for the 25 patients managed with an ICD and 122 patients managed with conventional medical therapy. There were no differences in the baseline variables in the 2 groups of patients, including age, ejection fraction, and medical treatments for heart failure, but patients receiving an ICD were more likely to have had nonsustained ventricular tachycardia (56% vs. 15%, p = 0.001). During a mean follow-up of 22 months, there were 31 deaths, 18 sudden, in patients treated with conventional therapy, whereas there were 2 deaths, none sudden, in patients treated with an ICD. An appropriate shock occurred in 40% of the ICD patients. Actuarial survival at 2 years was 84.9% with ICD therapy and 66.9% with conventional therapy (p = 0.04). Thus, in patients with nonischemic cardiomyopathy and syncope, therapy with an ICD is associated with a reduction in sudden death and an improvement in overall survival.
BACKGROUND: During static exercise in normal healthy humans, reflex renal cortical vasoconstriction occurs. Muscle metaboreceptors contribute importantly to this reflex renal vasoconstriction. In patients with heart failure, in whom renal vascular tone is already increased at rest, it is unknown whether there is further reflex renal vasoconstriction during exercise. METHODS AND RESULTS: Thirty-nine heart failure patients (NYHA functional class III and IV) and 38 age-matched control subjects (controls) were studied. Renal blood flow was measured by dynamic positron emission tomography. Graded handgrip exercise and post-handgrip ischemic arrest were used to clarify the reflex mechanisms involved. During sustained handgrip (30% maximum voluntary contraction), peak renal vasoconstriction was significantly increased in heart failure patients compared with controls (70+/-13 versus 42+/-1 U, P=0.02). Renal vasoconstriction returned to baseline in normal humans by 2 to 5 minutes but remained significantly increased in heart failure patients at 2 to 5 minutes and had returned to baseline at 20 minutes. In contrast, during post-handgrip circulatory arrest, which isolates muscle metaboreceptors, peak renal vasoconstriction was not greater in heart failure patients than in normal controls. In fact, the increase in renal vasoconstriction was blunted in heart failure patients compared with controls (20+/-5 versus 30+/-2 U, P=0.05). CONCLUSIONS: During sustained handgrip exercise in heart failure, both the magnitude and duration of reflex renal vasoconstriction are exaggerated in heart failure patients compared with normal healthy humans. The contribution of the muscle metaboreceptors to reflex renal vasoconstriction is blunted in heart failure patients compared with normal controls.
Despite clear and consistent clinical-trial evidence that secondary-prevention medical therapies reduce mortality in patients with established coronary artery disease, these therapies are underutilized in patients receiving conventional care. To address this issue, a Cardiac Hospitalization Atherosclerosis Management Program (CHAMP) focused on initiation of aspirin, cholesterol-lowering medication (3-hydroxy-3-methylglutaryl-coenzyme A [HMG-CoA] reductase inhibitor titrated to achieve low-density lipoprotein [LDL] cholesterol < 100 mg/dL), beta-blocker, and angiotensin-converting enzyme (ACE)-inhibitor therapy in conjunction with diet and exercise counseling before hospital discharge in patients with established coronary artery disease was designed and implemented at the University of California Los Angeles (UCLA) Medical Center starting in 1994. This treatment program was based on the hypothesis that initiation of therapy in the hospital setting would result in higher utilization rates both at the time of discharge and during longer-term follow-up. Implementation of this program involved the use of a focused treatment guideline, standardized admission orders, educational lectures by local thought leaders, and tracking/reporting of treatment rates. To assess the impact of the program, treatment rates and clinical outcome were compared in patients discharged in the 2-year periods before and after CHAMP was implemented. Hospital-based treatment protocols such as CHAMP have the potential to significantly increase treatment utilization of therapies previously demonstrated to improve survival and thus substantially improve the outcome of the 2 million patients diagnosed and hospitalized each year with coronary artery disease.
BACKGROUND: The BVS 5000i external pulsatile assist device is used to support patients with reversible cardiogenic shock. Its low cost and potential for insertion without cardiopulmonary bypass make it an attractive option. METHODS: Nineteen status I patients failing inotropic support were treated with the BVS 5000i with the intention of short-term bridge to transplant. Fourteen patients received left ventricular support whereas 5 received biventricular support. Cardiopulmonary bypass was used in less than 50% of patients. RESULTS: Median support time was 7 days. The 2 myocarditis patients were weaned from support. Twelve patients were transplanted and there were 5 deaths on support. Overall 14 of 19 were transplanted or weaned. One-year survival was 79%. Median hospital stay was 31 days. CONCLUSIONS: The BVS 5000i can be used for short-term mechanical assist toward transplantation in selected patients for whom a donor can be expected soon. The device may provide a cost-effective, short-term strategy to optimize end-organ function before orthotopic heart transplant, particularly for patients who are predictably not ideal to be discharged with implantable left ventricular assist device treatment.