Socioeconomic status is an important determinant of the use of invasive procedures after acute myocardial infarction in New York State.

BACKGROUND: Patient and hospital characteristics influence the use of invasive cardiac procedures. Whether socioeconomic status (SES) has an influence that is independent of these other determinants is unclear. The purpose of the present study was to examine the influence of household income as a measure of SES on the use of invasive cardiac procedures among a large group of patients with acute myocardial infarction. METHODS AND RESULTS: We analyzed administrative discharge data from 231 nonfederal acute care hospitals in New York State that involved 28 698 black or white inpatients with International Classification of Diseases, Ninth Revision, Clinical Modification code 410.XX in the principal diagnosis position between January 1 and December 31, 1995. Household income was derived from postal ZIP codes and census data. The use of cardiac catheterization, PTCA, CABG, and any revascularization procedure was examined across groups stratified by income. Patients who resided in lower-income neighborhoods were more often female or black, had a higher prevalence of coexistent illness, had a higher use of Medicaid insurance, and were less often admitted to urban hospitals or hospitals that provide on-site CABG and PTCA. Crude and adjusted odds ratios for catheterization, PTCA, CABG, and any revascularization procedure were related to income in a graded fashion. After adjustment, patients in the highest quintile of income were 22% more likely to undergo catheterization, 74% more likely to undergo PTCA, 48% more likely to undergo CABG, and 76% more likely to undergo any revascularization procedure than were patients in the lowest quintile. The difference in cardiac catheterization did not fully account for income-based differences in revascularization, because income remained a significant determinant of revascularization after accounting for whether a catheterization was performed. Even among patients treated in hospitals that provide on-site CABG and PTCA, income was a significant determinant of procedures. CONCLUSIONS: Lower-income patients hospitalized for acute myocardial infarction are more often female or black, have more coexisting illnesses, and are less often admitted to urban hospitals or hospitals that provide CABG and PTCA. Even after adjustment for these and other factors, lower income is a negative predictor of procedure use.

Controlled trial of intravenous immune globulin in recent-onset dilated cardiomyopathy.

BACKGROUND: This prospective placebo-controlled trial was designed to determine whether intravenous immune globulin (IVIG) improves left ventricular ejection fraction (LVEF) in adults with recent onset of idiopathic dilated cardiomyopathy or myocarditis. METHODS AND RESULTS: Sixty-two patients (37 men, 25 women; mean age +/-SD 43.0+/-12.3 years) with recent onset (/=0.10 from study entry, and 20 (36%) of 56 normalized their ejection fraction (>/=0.50). The transplant-free survival rate was 92% at 1 year and 88% at 2 years. CONCLUSIONS: These results suggest that for patients with recent-onset dilated cardiomyopathy, IVIG does not augment the improvement in LVEF. However, in this overall cohort, LVEF improved significantly during follow-up, and the short-term prognosis remains favorable.

Preserved right ventricular ejection fraction predicts exercise capacity and survival in advanced heart failure.

OBJECTIVES: This study was undertaken to determine which exercise and radionuclide ventriculographic variables predict prognosis in advanced heart failure. BACKGROUND: Although cardiopulmonary exercise testing is frequently used to predict prognosis in patients with advanced heart failure, little is known about the prognostic significance of ventriculographic variables. METHODS: The results of maximal symptom-limited cardiopulmonary exercise testing and first-pass radionuclide ventriculography in patients with advanced heart failure referred for evaluation for cardiac transplantation were analyzed. RESULTS: Sixty-seven patients with advanced heart failure (mean [+/- SD]; age 51 +/- 10 years, New York Heart Association functional classes III (58%) and IV (18%); mean left ventricular ejection fraction 0.22 +/- 0.07) underwent simultaneous upright bicycle ergometric cardiopulmonary exercise testing and first-pass rest/exercise radionuclide ventriculography. Mean peak oxygen consumption (VO2) was 11.8 +/- 4.2 ml/kg per min, and mean peak age- and gender-adjusted percent predicted oxygen consumption (%VO2) was 38 +/- 11.9%. Univariate predictors of overall survival included right ventricular ejection fraction > or = 0.35 at rest and > or = 0.35 at exercise and %VO2 > or = 45% (all p < 0.05). In a multivariate proportional hazards survival model, right ventricular ejection fraction > or = 0.35 at exercise (p < 0.01) and %VO2 > or = 45% (p = 0.01) were selected as independent predictors of overall survival. Univariate predictors of event-free survival included right ventricular ejection fraction > or = 0.35 at rest (p = 0.01) and > or = 0.35 at exercise (p < 0.01), functional class II (p < 0.05) and %VO2 > or = 45% (p = 0.05). Right ventricular ejection fraction > or = 0.35 at exercise (p = 0.01) was the only independent predictor of event-free survival in a multivariate proportional hazards model. Cardiac index at rest, VO2, left ventricular ejection fraction at rest, and exercise-related increase or decrease > 0.05 in left or right ventricular ejection fraction were not predictive of overall or event-free survival in any univariate or multivariate analysis. CONCLUSIONS: 1) Right ventricular ejection fraction > or = 0.35 at rest and exercise is a more potent predictor of survival in advanced heart failure than VO2 or %VO2; 2) %VO2 rather than VO2 predicts survival in advanced heart failure; 3) neither %VO2 nor VO2 predicts survival to the combined end point of death or admission for inotropic or mechanical support in patients with advanced heart failure.

"Borderline" myocarditis: an indication for repeat endomyocardial biopsy.

Repeat endomyocardial biopsy was performed in 28 patients with dilated cardiomyopathy of less than or equal to 12 months' duration and either symptomatic heart failure or life-threatening ventricular arrhythmias. Myocarditis was strongly suspected clinically in all cases, yet was unconfirmed on initial right ventricular biopsy. Seventeen patients underwent both right and left ventricular biopsy, seven patients had a repeat right ventricular biopsy and four patients underwent repeat left ventricular biopsy alone. The interval between initial and repeat biopsy averaged 31 +/- 6 days. Myocarditis was confirmed on repeat biopsy in 4 of 6 patients whose initial biopsy revealed "borderline" myocarditis (that is, interstitial inflammation but absence of myocyte necrosis) compared with none of the 22 patients whose initial biopsy showed either myocyte hypertrophy or interstitial fibrosis, or both (p = 0.0007). "Borderline" myocarditis on initial biopsy was the only clinical or histologic finding predictive of myocarditis on subsequent biopsy. Repeat endomyocardial biopsy can identify and potentially modify the treatment of an additional group of patients with dilated cardiomyopathy and nondiagnostic initial endomyocardial histologic features. Right ventricular sampling should be repeated in patients whose initial biopsy demonstrates "borderline" myocarditis.

Inotropic effect of nicardipine in patients with heart failure: assessment by left ventricular end-systolic pressure-volume analysis.

Nicardipine, a new dihydropyridine calcium channel blocker, has been investigated for the treatment of coronary artery disease and heart failure. To assess the inotropic effect of nicardipine in humans independent of its vasodilator effect, equihypotensive doses of intravenous nitroprusside (mean infusion rate 65 +/- 13 micrograms/min) and nicardipine (mean dose 5.2 +/- 0.4 mg) were administered to 15 patients with heart failure (New York Heart Association functional classes II to IV, radionuclide left ventricular ejection fraction 0.15 +/- 0.02). Left ventricular micromanometer pressure and simultaneous radionuclide left ventricular volume were obtained at baseline, during nitroprusside infusion, during a second baseline period and during nicardipine infusion. Heart rate did not change significantly with either nitroprusside or nicardipine. Mean systemic arterial pressure decreased by an average of 21 mm Hg with both drugs. A greater decrease in left ventricular end-diastolic pressure occurred with nitroprusside (27 +/- 2 to 14 +/- 2 mm Hg, p less than 0.01) than with nicardipine (27 +/- 2 to 23 +/- 3 mm Hg, p less than 0.05), and pulmonary capillary wedge pressure decreased significantly only with nitroprusside. Cardiac index increased from 1.8 +/- 0.1 to 2.1 +/- 0.1 liters/min per m2 (p less than 0.05) with nitroprusside and to a greater extent from 1.7 +/- 0.1 to 2.4 +/- 0.1 liters/min per m2 (p less than 0.01) with nicardipine. Left ventricular ejection fraction increased with nicardipine (0.15 +/- 0.01 to 0.19 +/- 0.01, p less than 0.01), but not with nitroprusside. Peak positive first derivative of left ventricular pressure (dP/dt) decreased by 9% with both agents.(ABSTRACT TRUNCATED AT 250 WORDS)

Viral myocarditis mimicking acute myocardial infarction.

Anecdotal reports have shown that myocarditis can mimic acute myocardial infarction with chest pain, electrocardiographic (ECG) abnormalities, serum creatine kinase elevation and hemodynamic instability. Thirty-four patients with clinical signs and symptoms consistent with acute myocardial infarction underwent right ventricular endomyocardial biopsy during a 6.5-year period after angiographic identification of normal coronary anatomy. Myocarditis was found on histologic study in 11 of these 34 patients. Cardiogenic shock requiring intraaortic balloon support developed within 6 h of admission in three (27%) of the patients with myocarditis. The mean age of the group with myocarditis was 42 +/- 5 years. A preceding viral illness had been present in six patients (54%). The ECG abnormalities were varied and included ST segment elevation (n = 6), T wave inversions (n = 3), ST segment depression (n = 2) and pathologic Q waves (n = 2). The ECG abnormalities were typically seen in the anterior precordial leads but were diffusely evident in three patients. Left ventricular function was normal in six patients and globally decreased in the remaining five patients, whose ejection fraction ranged from 14% to 45%. Lymphocytic myocarditis was diagnosed in 10 patients, and giant cell myocarditis was detected in the remaining patient. Four patients with impaired left ventricular function received immunosuppressive therapy with prednisone and either azathioprine (n = 2) or cyclosporine (n = 2). All six patients whose left ventricular function was normal on admission remain alive in functional class I. Of the five patients with impaired systolic function, ejection fraction normalized in three of the four patients who received immunosuppressive therapy within 3 months of treatment and in the one patient who received only supportive therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Positive inotropic and lusitropic effects of intravenous flosequinan in patients with heart failure.

OBJECTIVES: This study was designed to assess the direct effects of flosequinan on myocardial function. BACKGROUND: Flosequinan has been shown to improve symptoms and exercise tolerance in patients with heart failure. Although previous studies have established that flosequinan is a vasodilator, it is not known to what extent direct actions of the drug on myocardial contractility or diastolic properties contribute to its beneficial hemodynamic effects. METHODS: Nitroprusside and intravenous flosequinan were administered sequentially to 18 patients with severe heart failure (New York Heart Association functional class III or IV, left ventricular ejection fraction 0.14 +/- 0.02). Micromanometer left ventricular pressure and radionuclide volume data were combined to construct pressure-volume loops during 1) a baseline period, 2) nitroprusside infusion, 3) a second baseline period, and 4) flosequinan infusion. RESULTS: The peak rate of left ventricular pressure development increased from 899 +/- 84 to 1,070 +/- 94 mm Hg/s (p less than 0.05) with flosequinan. The baseline left ventricular end-systolic pressure-volume relation was constructed in 15 patients from the two baseline pressure-volume loops and from that obtained during afterload manipulation with nitroprusside. During flosequinan administration, the relation between end-systolic pressure and volume was shifted upward and leftward, indicating enhanced contractility, in 14 of 15 patients (p less than 0.001). The maximal rate of decrease in left ventricular pressure during isovolumetric relaxation increased in magnitude with flosequinan from 882 +/- 63 to 1,026 +/- 68 mm Hg/s (p less than 0.05). CONCLUSIONS: These results indicate that intravenous flosequinan has positive inotropic and lusitropic effects in patients with heart failure. Further studies are needed to assess the direct myocardial effects of oral flosequinan.

Hemodynamic effects of inhaled nitric oxide in heart failure.

OBJECTIVES: This study was performed to assess the utility of inhaled nitric oxide as a selective pulmonary vasodilator in patients with severe chronic heart failure and to compare its hemodynamic effects with those of nitroprusside, a nonselective vasodilator. BACKGROUND: Preoperative pulmonary vascular resistance is a predictor of right heart failure after heart transplantation. Non-selective vasodilators administered preoperatively to assess the reversibility of pulmonary vasoconstriction cause systemic hypotension, limiting their utility. METHODS: Systemic and pulmonary hemodynamic measurement were made at baseline, during oxygen inhalation and with the addition of graded doses of inhaled nitric oxide or intravenous nitroprusside in 16 patients with New York Heart Association class III or IV heart failure referred for heart transplantation. RESULTS: Pulmonary vascular resistance decreased to a greater extent with 80 ppm nitric oxide (mean +/- SEM 256 +/- 41 to 139 +/- 14 dynes.s.cm-5) than with the maximally tolerated dose of nitroprusside (264 +/- 49 to 169 +/- 30 dynes.s.cm-5, p < 0.05, nitric oxide vs. nitroprusside). Pulmonary capillary wedge pressure increased with 80 ppm nitric oxide (26 +/- 2 to 32 +/- 2 mm Hg, p < 0.05). Mean arterial pressure did not change with nitric oxide but decreased with nitroprusside. Seven of the 16 patients, including 1 patient who did not have an adequate decrease in pulmonary vascular resistance with nitroprusside but did with nitric oxide, have undergone successful heart transplantation. CONCLUSIONS: Inhaled nitric oxide is a selective pulmonary vasodilator in patients with pulmonary hypertension due to left heart failure and may identify patients with reversible pulmonary vasoconstriction in whom agents such as nitroprusside cause systemic hypotension. Inhaled nitric oxide causes an increase in left ventricular filling pressure by an unknown mechanism.

Exercise capacity and systolic and diastolic ventricular function after recovery from acute dilated cardiomyopathy.

OBJECTIVES: This study was undertaken to determine whether abnormalities in exercise capacity or ventricular function persist after recovery from acute dilated cardiomyopathy. BACKGROUND: Persistent ventricular structural abnormalities could cause abnormalities in exercise capacity or ventricular function. METHODS: The results of rest and exercise first-pass radionuclide ventriculography in 18 patients who were seen within 6 months of the onset of dilated cardiomyopathy and subsequently had a normal rest left ventricular ejection fraction were compared with those of age- and gender-matched control subjects. RESULTS: Patients were studied 144 +/- 34 (mean +/- SEM) days after the onset of left ventricular dysfunction at a time when heart failure symptoms had resolved. Patients with myocyte necrosis, as assessed by endomyocardial biopsy (n = 13) or antimyosin scintigraphy (n = 12), recovered more rapidly than did those without necrosis. Oxygen consumption both at peak exercise (17.7 +/- 1.2 vs. 26.1 +/- 1.5 ml/kg per min, p < 0.05) and at the anaerobic threshold (11.1 +/- 0.5 vs. 17.1 +/- 1.3 ml/kg per min, p < 0.05) was lower in the patients who had recovered from cardiomyopathy than in control subjects. Rest and exercise end-systolic and end-diastolic left ventricular volumes were greater in the patients than in the control subjects, although stroke volumes were similar. Left ventricular filling at rest was lower at diastolic filling intervals of 40% and 90%, and rest and exercise left ventricular early peak filling rate normalized for end-diastolic volume was slower in the patients than in the control subjects. At long-term follow-up of 1,082 +/- 206 days, two patients had a return of heart failure symptoms and a decrease in left ventricular ejection fraction. CONCLUSIONS: Despite the apparent normalization of rest left ventricular ejection fraction, patients who have recovered from dilated cardiomyopathy have abnormalities in aerobic exercise capacity and in left ventricular systolic and diastolic performance.

Antimyosin antibody cardiac imaging: its role in the diagnosis of myocarditis.

Right ventricular endomyocardial biopsy currently remains the procedure of choice for identifying patients with symptomatic heart failure due to myocarditis from the larger population with idiopathic dilated cardiomyopathy. Despite its specificity, the sensitivity of right ventricular biopsy remains uncertain because of the focal or multifocal nature of the disease. Because myocyte necrosis is an obligate component of myocarditis, the use of indium-111 antimyosin imaging was evaluated in 82 patients with suspected myocarditis. Seventy-four patients had dilated cardiomyopathy of less than 1 year's duration (mean left ventricular ejection fraction 0.30 +/- 0.02); eight patients had normal left ventricular function (mean ejection fraction 0.59 +/- 0.03). Symptoms at presentation included congestive heart failure (92%), chest pain mimicking myocardial infarction (6%) and life-threatening ventricular tachyarrhythmias (2%). All patients underwent planar and single photon emission computed tomographic (SPECT) cardiac imaging after injection of indium-111-labeled antimyosin antibody fragments and right ventricular biopsy within 48 h of imaging. Antimyosin images were interpreted as either abnormal or normal and correlated with biopsy results. On the basis of the right ventricular histologic examination, the sensitivity of antimyosin imaging was 83%, specificity 53% and predictive value of a normal scan 92%. Improvement in left ventricular function occurred within 6 months of treatment in 54% of patients with an abnormal antimyosin scan compared with 18% of those with a normal scan (p less than 0.01). Antimyosin cardiac imaging may be useful for the initial evaluation of patients with dilated and nondilated cardiomyopathy and clinically suspected myocarditis.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary endothelial dysfunction in patients with acute-onset idiopathic dilated cardiomyopathy.

OBJECTIVES: This study sought to determine whether coronary endothelial dysfunction exists in patients with acute-onset idiopathic dilated cardiomyopathy (DCM) and to explore its relation to recovery of left ventricular systolic function in this patient population. BACKGROUND: Coronary endothelial dysfunction exists in chronic DCM, but its importance in the development and progression of ventricular dysfunction is not known. To address this issue we studied coronary endothelial function in patients with idiopathic DCM <6 months in duration and explored the relation between coronary endothelial function and subsequent changes in left ventricular ejection fraction (LVEF). METHODS: Ten patients with acute-onset idiopathic DCM (duration of heart failure symptoms 2.0 +/- 0.4 months [mean +/- SEM]) and 11 control patients with normal left ventricular function underwent assessment of coronary endothelial function during intracoronary administration of the endothelium-dependent vasodilator acetylcholine and the endothelium-independent vasodilator adenosine. Coronary cross-sectional area (CSA) was determined by quantitative coronary angiography and coronary blood flow (CBF) by the product of coronary CSA and CBF velocity measured by an intracoronary Doppler catheter. Patients with DCM underwent assessment of left ventricular function before and several months after the study. RESULTS: Acetylcholine infusion produced no change in coronary CSA in control patients but significant epicardial constriction in patients with DCM (-36 +/- 11%, p < 0.01). These changes were associated with increases in CBF in control patients (+118 +/- 49%, p < 0.01) but no change in patients with DCM. Infusion of adenosine produced increases in coronary caliber and blood flow in both groups. Follow-up assessment of left ventricular function was obtained in nine patients with DCM 7.0 +/- 1.7 months after initial study, at which time LVEF had improved by > or =0.10 in four patients. Multiple linear regression revealed a positive correlation between both the coronary CSA (r2 = 0.57, p < 0.05) and CBF (r2 = 0.68, p < 0.01) response to acetylcholine and the subsequent improvement in LVEF. CONCLUSIONS: Coronary endothelial dysfunction exists at both the microvascular and the epicardial level in patients with acute-onset idiopathic DCM. The preservation of coronary endothelial function in this population is associated with subsequent improvement in left ventricular function.

Linearity of the left ventricular end-systolic pressure-volume relation in patients with severe heart failure.

The left ventricular end-systolic pressure-volume relation is a relatively load-independent measure of left ventricular contractile function. Linearity of the relation derived from full left ventricular pressure-volume loops has not previously been demonstrated for patients with severe heart failure. Therefore, nine patients with markedly depressed left ventricular systolic function (ejection fraction 0.14 +/- 0.08) were studied with micromanometer left ventricular pressure measurement and simultaneous radionuclide ventriculography. Afterload was reduced with graded infusions of nitroprusside, allowing construction of pressure-volume loops under four afterload conditions in four patients and three afterload conditions in the other five patients. The end-systolic pressure-volume relation derived from the pressure-volume loops was found to be linear for the range of pressures and volumes examined, with correlation coefficients in individual patients ranging from 0.936 to 0.999 (mean 0.981). The mean slope of the relation (or end-systolic elastance) was 0.71 mm Hg/ml (range 0.42 to 1.52), and the extrapolated volume intercept at zero pressure was positive in all patients. An exponential relation between end-systolic elastance and ejection fraction was demonstrated for this group of patients. Approximations of end-systolic elastance obtained from measurements other than the full pressure-volume loops correlated variably with "true" elastance obtained from the pressure-volume loops. The relation between stroke work and end-diastolic volume was nonlinear in most patients. Thus, the end-systolic pressure-volume relation is linear in the "physiologic" range in patients with severe heart failure. This finding should permit construction of the relation from two loading conditions in clinical studies, facilitating its use as an index of contractile function in patients with heart failure.

Effects of atrial natriuretic peptide on myocardial contractile and diastolic function in patients with heart failure.

Atrial natriuretic peptide alters left ventricular performance in patients with heart failure. To assess the direct effects of this hormone on myocardial function, its actions were compared with those of the pure vasodilator nitroprusside in 10 patients with heart failure. Simultaneous left ventricular micromanometer pressure and radionuclide volume were obtained during a baseline period, during nitroprusside infusion, during a second baseline period and during atrial natriuretic peptide infusion. The baseline end-systolic pressure-volume relation was generated in nine patients from pressure-volume loops obtained during the two baseline periods and during afterload reduction with nitroprusside. Mean arterial pressure decreased with atrial natriuretic peptide (89 +/- 3 to 80 +/- 2 mm Hg, p less than 0.05) and by a greater amount with nitroprusside (90 +/- 4 to 73 +/- 3 mm Hg, p less than 0.05). Left ventricular end-diastolic pressure also decreased with atrial natriuretic peptide (24 +/- 2 to 16 +/- 3 mm Hg, p less than 0.05) and by a greater amount with nitroprusside (24 +/- 2 to 13 +/- 3 mm Hg, p less than 0.05). Cardiac index increased during infusion of each agent from 2.0 +/- 0.2 to 2.4 +/- 0.2 liters/min per m2 (p less than 0.01). Heart rate increased slightly with nitroprusside but did not change with atrial natriuretic peptide. Peak positive first derivative of left ventricular pressure (dP/dt), ejection fraction and stroke work index were unchanged by either agent. The relation between end-systolic pressure and volume during atrial natriuretic peptide infusion was shifted slightly leftward from the baseline value in four patients, slightly rightward in four and not at all in one patient, indicating no consistent inotropic effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Low-dose enoximone improves exercise capacity in chronic heart failure. Enoximone Study Group.

OBJECTIVES: This study was designed to evaluate the effects of low-dose enoximone on exercise capacity. BACKGROUND: At higher doses the phosphodiesterase inhibitor, enoximone, has been shown to increase exercise capacity and decrease symptoms in heart failure patients but also to increase mortality. The effects of lower doses of enoximone on exercise capacity and adverse events have not been evaluated. METHODS: This is a prospective, double-blind, placebo-controlled, multicenter trial (nine U.S. centers) conducted in 105 patients with New York Heart Association class II to III, ischemic or nonischemic chronic heart failure (CHF). Patients were randomized to placebo or enoximone at 25 or 50 mg orally three times a day. Treadmill maximal exercise testing was done at baseline and after 4, 8 and 12 weeks of treatment, using a modified Naughton protocol. Patients were also evaluated for changes in quality of life and for increased arrhythmias by Holter monitoring. RESULTS: By the protocol-specified method of statistical analysis (the last observation carried-forward method), enoximone at 50 mg three times a day improved exercise capacity by 117 s at 12 weeks (p = 0.003). Enoximone at 25 mg three times a day also improved exercise capacity at 12 weeks by 115 s (p = 0.013). No increases in ventricular arrhythmias were noted. There were four deaths in the placebo group and 2 and 0 deaths in the enoximone 25 mg three times a day and enoximone 50 mg three times a day groups, respectively. Effects on degree of dyspnea and patient and physician assessments of clinical status favored the enoximone groups. CONCLUSIONS: Twelve weeks of treatment with low-dose enoximone improves exercise capacity in patients with CHF, without increasing adverse events.

Ten-year trends in hospital care for congestive heart failure: improved outcomes and increased use of resources.

BACKGROUND: Scarce data are available on long-term trends in hospital mortality, length of stay (LOS), and costs in congestive heart failure (CHF). OBJECTIVE: To assess 10-year trends in the outcomes of patients hospitalized with CHF. METHODS: We studied all 6676 patients with a primary discharge diagnosis of CHF hospitalized from January 1, 1986, through July 31, 1996, at an academic tertiary care center. Hospital mortality, LOS, and costs were adjusted for sociodemographic characteristics, comorbidities, invasive procedures, hospital disposition, and LOS where appropriate. RESULTS: The mean (+/- SD) age of patients was 70+/-13 years; 54.1% were male; 87.0% were white. There was a significant increasing trend in heart failure severity as assessed by a CHF-specific risk-adjustment index. The proportion of patients who underwent invasive procedures (e.g., cardiac catheterization, coronary angioplasty, coronary artery bypass surgery, defibrillator and pacemaker implantation) was significantly higher in the 1994-1996 period. The standardized mortality ratio (observed mortality/predicted mortality) progressively fell during the study period. Compared with patients admitted before 1991, those admitted after 1991 had a 24% lower observed than predicted mortality. Adjusted LOS exhibited a downward trend, ie, 7.7 days in 1986-1987 to 5.6 days in 1994-1996 (P<.001). Unadjusted cost peaked during 1992-1993 and declined thereafter. Adjusted costs in 1994-1996 were not significantly different from those in 1990-1991. CONCLUSIONS: After risk adjustment for sociodemographic characteristics, comorbidities, and disease severity, a significant decrease in in-hospital mortality was observed during the study decade. This decline in hospital mortality occurred in parallel with decreasing LOS and increasing use of cardiac procedures and costs.

Effects of atrial natriuretic peptide on left ventricular function in hypertension.

Atrial natriuretic peptide (ANP) has natriuretic and vasodilator actions that lower arterial pressure and may be beneficial to hypertensive patients. To assess the effects of ANP on left ventricular function in patients with hypertension, we compared it with the pure vasodilator nitroprusside. Simultaneous left ventricular micromanometer pressure and radionuclide volume were obtained at baseline, during nitroprusside infusion, during a second baseline period, and during ANP infusion in 10 patients with hypertension. Mean arterial pressure fell during ANP and nitroprusside. Heart rate and plasma norepinephrine levels increased by similar amounts during the two agents, whereas cardiac index and stroke volume index were unchanged during both. Peak positive left ventricular dP/dt fell similarly during ANP and nitroprusside, but left ventricular dP/dt at a developed pressure of 40 mm Hg, a less load-dependent index of contractility, was unchanged during both. The relation between end-systolic pressure and volume during ANP infusion was not shifted leftward or rightward from that during nitroprusside infusion, indicating no inotropic effect. Both ANP and nitroprusside shortened at time constant of isovolumic relaxation calculated by the logarithmic method but did not change the time constant calculated by the derivative method. Peak filling rate was unchanged from baseline during both agents. ANP did not shift the end-diastolic pressure-volume point away from the relation constructed from baseline and nitroprusside points. We conclude that ANP has no direct effect on myocardial contractile or diastolic function in patients with hypertension.

Outcomes in recipients of combined heart-kidney transplantation: multiorgan, same-donor transplant study of the International Society of Heart and Lung Transplantation/United Network for Organ Sharing Scientific Registry.

In patients awaiting heart transplantation, end-stage disease of a second organ may occasionally require consideration of simultaneous multiorgan transplantation. Outcome statistics in multiorgan transplant recipients are needed to define optimal utilization of scarce donor resources. Incidence of cardiac allograft rejection, actuarial recipient survival, and cardiac allograft rejection-free survival were evaluated in 82 recipients of 84 simultaneous heart and kidney transplants. Twenty-three of the 82 dual-organ recipients have died with 1, 6, 12, and 24-month actuarial survival rates of 92%, 79%, 76%, and 67%, respectively. The actuarial survival rates in the heart-kidney recipients were similar to those observed in 14,340 isolated heart recipients (United Network for Organ Sharing Scientific Registry) during the same period (92%, 86%, 83%, and 79%, respectively; P=0.20). Clinical data on all episodes of treated rejection in either organ and on immunosuppressive regimens were available on 56 patients; 48% of these patients have had no rejection in either organ, 27% experienced heart rejection alone, 14% experienced kidney rejection alone, and 11% had both heart and kidney allograft rejection. Heart allograft rejection was less common in heart-kidney recipients, as compared with isolated heart transplant recipients; 0, 1, and > or = 2 treated cardiac allograft rejection episodes occurred in 63%, 20%, and 18% of heart-kidney recipients compared with 46%, 27%, and 28% of 911 isolated heart recipients reported by Transplant Cardiologists' Research Database (P=0.02). The rejection-free survival rates at 1, 3, and 6 months were 88%, 74%, and 71% in the double-organ recipients, as compared with 66%, 44%, and 39%, respectively, in the single-organ recipients. Compared with isolated heart transplantation, combined heart-kidney transplantation does not adversely affect intermediate survival and results in a lower incidence of treated cardiac allograft rejection. The findings suggest that combined heart-kidney transplantation may be an acceptable option in a small subset of potential heart transplant recipients with severe renal dysfunction.

Complement activation products in plasma after heart transplantation in humans.

BACKGROUND: Complement activation has recently been implicated as a contributing factor to early and late allograft dysfunction in cardiac transplantation. The current study was designed to determine whether measurement of plasma complement fragments C4d and SC5b-9 would be useful in detecting acute rejection or accelerated graft atherosclerosis (AGA) in cardiac allograft recipients. METHODS: We measured complement activation products, C4d (classical pathway) and SC5b-9 (terminal pathway), at the time of routine endomyocardial biopsy in heart transplant recipients. Ten patients in the immediate posttransplantation period (0-100 days) and 19 patients more than 6 months after transplantation were studied. RESULTS: No correlation was found between plasma levels of complement activation fragments and the presence of biopsy-proven acute allograft rejection or AGA (assessed by coronary angiography). However, plasma C4d and SC5b-9 were significantly elevated in 9 of 10 and 7 of 10 patients, respectively, in the immediate posttransplantation period. This was followed by progressive decrease in the levels of C4d and SC5b-9 fragments during the first 4-6 weeks after transplantation. CONCLUSION: We conclude that measuring plasma levels of fragments C4d and SC5b-9 is not a useful noninvasive method for detecting acute rejection or AGA after heart transplantation. However, this study provides further evidence that early complement activation after heart transplantation may play a pathogenic role in allograft injury.

Left ventricular diastolic function in patients with left ventricular systolic dysfunction due to coronary artery disease and effect of nicardipine.

To assess the effect of nicardipine on left ventricular (LV) diastolic function independent of concurrent effects on loading conditions in patients with LV systolic dysfunction due to coronary artery disease, equihypotensive doses of intravenous nitroprusside and nicardipine were administered to 12 patients with congestive heart failure due to previous myocardial infarction (LV ejection fraction less than 0.40). LV micromanometer pressure and simultaneous radionuclide volume were obtained during a baseline period, during nitroprusside infusion, during a second baseline period and during nicardipine infusion. Mean systemic arterial pressure decreased an average of 21 mm Hg with nitroprusside and 19 mm Hg with nicardipine. A greater decrease in LV end-diastolic pressure was observed with nitroprusside (29 +/- 2 to 15 +/- 2 mm Hg, p less than 0.01) than with nicardipine (29 +/- 2 to 25 +/- 3 mm Hg, p less than 0.05). There was a decrease in the time constant of relaxation during nitroprusside but not during nicardipine infusion. There was enough overlap in LV volumes in the baseline and nitroprusside periods to compare diastolic pressure-volume relations over a common range of volumes in 4 patients, and enough overlap in the baseline and nicardipine periods in 11 patients. The relation was shifted downward in 3 of 4 patients taking nitroprusside and in 6 of 11 patients taking nicardipine. The relation between end-diastolic pressure and volume was not shifted with nicardipine.(ABSTRACT TRUNCATED AT 250 WORDS)

Socioeconomic status as an independent risk factor for hospital readmission for heart failure.

The management of heart failure is characterized by high rates of hospital admission as well as rehospitalization after inpatient treatment of this disorder, whereas skillful medical care may reduce the risk of hospital admission. The purpose of this study was to examine the relation between income (as a measure of socioeconomic status) and the frequency of hospital readmission among a large and diverse group of persons treated for heart failure. We analyzed administrative discharge data from 236 nonfederal acute-care hospitals in New York State, involving 41,776 African-American or Caucasian hospital survivors with International Classification of Diseases, Ninth Revision, Clinical Modification codes for heart failure in the principal diagnosis position between January 1 and December 31, 1995. Household income was derived from postal ZIP codes and census data. We found that patients residing in lower income neighborhoods were more often women or African-Americans, had more comorbid illness, had higher use of Medicaid insurance, and were more often admitted to rural hospitals. There was a stepwise decrease in the crude frequency of readmission from the lowest quartile of income (23.2%) to the highest (20.0%) (p <0.0001 for Mantel-Haenszel chi-square test for trend across all quartiles; p <0.0001 for comparison between quartiles 1 and 4). After adjustment for baseline differences and process of care, income remained a significant predictor, with an increase in the risk of readmission noted in association with lower levels of income (adjusted odds ratio for quartile 1:4 comparison, 1.18; 95% confidence interval, 1.10 to 1.26, p <0.0001). We conclude that lower income patients hospitalized for treatment of heart failure in New York differ from higher income patients in important clinical and demographic comparisons. Even after adjustment for these fundamental differences and other potential confounding factors, lower income is a positive predictor of readmission risk.