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Biomedical subjects

G W Dec

Publications and source records attributed to G W Dec.

At least 55 records · Page 3Linked to original sources
PubMed1996

Left ventricular dysfunction after heart transplantation: incidence and role of enhanced immunosuppression.

BACKGROUND: The purpose of this study was to examine the incidence, natural history, and outcome of left ventricular dysfunction in 102 consecutive heart transplant recipients. Left ventricular dysfunction (defined as a decline in the echocardiographic ejection fraction to < 0.45) occurred in 16 of 102 transplant recipients (16%) at a mean of 9.7 +/- 8.6 (standard deviation) months after transplantation. METHODS: Diagnostic evaluation included right heart catheterization and endomyocardial biopsy in all patients and coronary angiography in 13 patients. RESULTS: Four patients were found to have moderate cellular rejection (International Society for Heart and Lung Transplantation grade 2 or higher) and were treated with enhanced immunosuppression. Two patients had angiographically apparent coronary allograft vasculopathy; both died of electromechanical dissociation within 4 months. The remaining ten patients had no or mild cellular rejection (International Society for Heart and Lung Transplantation grade 0 or 1). Therapy in these ten patients included corticosteroids (n = 8). OKT3 (n = 5), and plasmapheresis (n = 2). Three patients died within 2 months of diagnosis, two from undetected severe coronary allograft vasculopathy and one from unrecognized constrictive pericarditis. The echocardiographic ejection fraction improved in the surviving patients after enhanced immunosuppressive therapy (0.33 to 0.53, p < 0.005). With the benefit of long-term clinical follow-up and autopsy data, the origins of left ventricular dysfunction in the 16 patients included moderate cellular rejection (n = 4), vascular rejection (n = 1), coronary allograft vasculopathy (n = 3), intercurrent cytomegalovirus infection (n = 1), constrictive pericarditis (n = 1), and either mild or no evident rejection (n = 6). Survival of the 16 patients with left ventricular dysfunction was similar to that of the 86 patients without left ventricular dysfunction. CONCLUSIONS: The cause of left ventricular dysfunction after heart transplantation includes cellular rejection, vascular rejection, coronary allograft vasculopathy, cytomegalovirus infection, constrictive pericarditis, and unexplained mechanisms. Given the improvement in left ventricular function observed after empiric therapy with enhanced immunosuppression in patients with left ventricular dysfunction, immune-mediated phenomena may play an important pathogenic role.

Biopsy↗
PubMed1995

Influence of the implantable cardioverter/defibrillator on sudden death and total mortality in patients evaluated for cardiac transplantation.

BACKGROUND: Implantable cardioverter/defibrillators (ICDs) may reduce sudden tachyarrhythmic death in patients with severe left ventricular dysfunction. It is uncertain whether this improves survival, particularly in patients awaiting cardiac transplantation. METHODS AND RESULTS: The effect of treatment for spontaneous ventricular arrhythmias (ICD [n = 59], antiarrhythmic drugs [n = 53], or no antiarrhythmic treatment [n = 179]) on total mortality and mode of cardiac death was analyzed in 291 consecutive patients evaluated for cardiac transplantation between January 1986 and January 1995. There were 109 deaths (37.4%) (63 [21.6%] sudden, 40 [13.7%] nonsudden, and 6 [2.1%] noncardiac) during mean follow-up of 15 months (range, 1 to 118 months). Baseline clinical variables, medical therapies for heart failure, and actuarial rates of transplantation were similar between treatment groups. Kaplan-Meier sudden death rates were lowest in the ICD group, intermediate in the no antiarrhythmic treatment group, and highest in the drug treatment group throughout follow-up (12-month sudden death rates, 9.2%, 16.0%, and 34.7%, respectively; P = .004). Total mortality and nonsudden death rates did not differ. Cox proportional-hazards model revealed that antiarrhythmic drug treatment was associated with sudden death (relative risk, 2.1; 95% CI, 1.04 to 3.39; P = .04) and ICD was associated with nonsudden death (relative risk, 2.26; 95% CI, 1.12 to 4.62; P = .02). CONCLUSIONS: Sudden death rates were lowest in patients treated with ICDs compared with drug treatment or no antiarrhythmic treatment. However, although ICDs reduced sudden death in selected high-risk patients with severe left ventricular dysfunction, the effect on long-term survival was limited, principally by high nonsudden death rates.

Actuarial Analysis↗
PubMed1995

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.

Disease-Free Survival↗
PubMed1995

Cardiovascular complications following liver transplantation.

BACKGROUND: As the indications for liver transplantation broaden to include older and more critically ill patients, the likelihood of encountering unsuspected cardiovascular disease increases. PURPOSE: This study examined the frequency, type, and subsequent outcome of intra- and postoperative cardiovascular complications that occurred during the first 6 months following liver transplantation. METHODS: The records of 146 consecutive patients who underwent primary liver transplantation were reviewed retrospectively to determine the occurrence of major (myocardial infarction or reversible ischemia, pulmonary edema, cardiogenic shock, symptomatic rhythm disturbances, or pulmonary embolism) and minor (transient hypertension, hypotension, atrial or ventricular premature beats) cardiac events. The relation between such events and actuarial patient survival was evaluated. Stepwise logistic regression analysis was also employed to identify those pre-operative variables that predicted an increased risk of postoperative events or mortality. RESULTS: Cardiac events directly caused or contributed to 4 deaths (2.7%). Ventricular tachycardia/fibrillation was the most frequent intra-operative cardiac complication (3.4%); transient hypotension (post-reperfusion syndrome) was the most common minor event (20%). Thirty-four recipients (23%) developed a major postoperative cardiac complication including pulmonary edema (9%), myocardial ischemia or infarction (5.4%), new dilated cardiomyopathy (3.4%), and ventricular tachycardia (2.7%). Pre-existing cardiac disease and older age (mean age 49 +/- 8 years) at transplantation were the only independent predictors of a major complication. Major cardiac events did not affect 6 month survival but were associated with a lower 5-year survival rate (event: 32% vs event-free: 52%; p = 0.04). The frequency of major intraoperative (21% vs 2%; p = 0.0005) and postoperative (57% vs 17%; p = 0.0001) cardiac complications was significantly higher for recipients with known heart disease (Group A) compared with those without pre-existing heart disease (Group B). Five-year survival in Group A patients was 36% versus 50% for Group B patients; p = 0.45. CONCLUSION: One or more cardiovascular complications occurred in over 70% of liver transplant recipients. Major events were associated with a lower likelihood of long-term survival. Older patients, particularly those with pre-existing but compensated heart disease, are at greatest risk for a major cardiac event and may require more extensive pre-operative risk assessment.

Adolescent↗
PubMed1994

Intraventricular conduction abnormalities in patients with clinically suspected myocarditis are associated with myocardial necrosis.

Twenty-nine patients with suspected myocarditis, either with or without intraventricular conduction abnormalities, were investigated for degree of myocardial necrosis by antimyosin scintigraphy. Among those 29 patients, 16 had intraventricular conduction abnormalities. Antimyosin scans were analyzed for heart/lung ratios and semiquantitative visual uptake scores (0 to 4+ scale). Of the 16 patients with conduction abnormalities, 15 (94%) demonstrated visual antimyosin uptake versus 7 (54%) of 13 cases without conduction abnormalities (p < 0.03). In addition, the heart/lung ratios and uptake scores were significantly higher in the group with conduction abnormalities than in the group without (1.64 +/- 0.31 vs 1.39 +/- 0.20, p < 0.03; and 2.3 +/- 0.7 vs 1.4 +/- 0.7, p < 0.005; respectively). In conclusion, intraventricular conduction abnormalities in patients with suspected myocarditis were more strongly associated with active and more severe myocardial necrosis as judged by antimyosin imaging than patients with normal electrocardiograms.

Adult↗
PubMed1994

Right ventricular dysfunction: an independent predictor of adverse outcome in patients with myocarditis.

To assess the predictive value of right ventricular systolic function in patients with active myocarditis, the echocardiograms of 23 patients with biopsy-confirmed myocarditis were reviewed. Right ventricular systolic function was evaluated qualitatively and quantitatively by descent of the right ventricular base. Patients were divided into those with normal right ventricular function, in whom right ventricular descent was 1.9 +/- 0.1 cm, and those with abnormal right ventricular function, in whom right ventricular descent was 0.8 +/- 0.1 cm (p < 0.001). There were no differences between the two groups in age, duration of symptoms, baseline hemodynamics, or histologic assessment. Initial left ventricular ejection fraction was significantly lower in patients with depressed right ventricular function (27.5 +/- 4.9%) compared with that in patients with normal right ventricular function (47.5 +/- 6.3%) (p = 0.01). The likelihood of an adverse outcome, defined as death or need for cardiac transplantation, was greater in patients with abnormal right ventricular function (right ventricular descent < or = 1.7 cm) than in patients with normal right ventricular function (right ventricular descent > 1.7 cm) (p < 0.03). Multivariate analysis revealed that right ventricular dysfunction as quantified by right ventricular descent was the most powerful predictor of adverse outcome.

Female↗
PubMed1994

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.

Acute Disease↗
PubMed1994

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.

Administration, Inhalation↗
PubMed1994

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.

Adult↗
PubMed1993

Transient left ventricular aneurysm in a patient with hypertrophic cardiomyopathy and myocarditis.

Left ventricular wall motion abnormalities, aneurysm formation, and progression to global hypokinesis have been described in patients with myocarditis and in patients with hypertrophic cardiomyopathy. We document a case of reversible aneurysm formation, cardiogenic shock, and complete recovery in a patient with myocarditis and hypertrophic cardiomyopathy. Pathophysiologic mechanisms of myocardial injury and recovery are discussed.

Aged↗
PubMed1993

Long-term outcome of enoximone therapy in patients with refractory heart failure.

Few options are available for patients with severe heart failure that is unresponsive to therapy with digoxin, diuretics, and vasodilators. The clinical responses and predictors of survival were studied in 41 consecutive patients with New York Heart Association (NYHA) class IV heart failure during long-term oral enoximone therapy (mean dose 232 +/- 15 mg/day). The mean age was 60 +/- 1 years, and the initial left ventricular ejection fraction was 0.19 +/- 0.01. The cause of heart failure was either coronary artery disease (n = 23) or dilated cardiomyopathy (n = 18). Symptomatic improvement occurred in the majority (83%) of patients; 24% improved two or more NYHA classes. Although the 12-month mortality rate for the entire group was high (54 +/- 8%), a subgroup of patients with dilated cardiomyopathy achieved a sustained benefit with a decrease in symptoms > 1 NYHA class, fewer hospitalizations, and a survival rate at 24 months of 60%. Multivariate analysis identified the cause of heart failure, left ventricular ejection fraction, and clinical improvement within 60 days of enoximone therapy as predictors of a favorable long-term outcome. The presence of coronary artery disease was most predictive of early mortality (p < 0.0002), with only 5% of patients surviving > 18 months compared to 66% of those with dilated cardiomyopathy. Median survival rates were 132 +/- 31 and 921 +/- 214 days (p < 0.001) for the coronary artery disease and dilated cardiomyopathy populations, respectively. Oral enoximone can provide symptomatic improvement and a palliative option for the majority of patients with refractory heart failure resulting from cardiomyopathy.

Cardiomyopathy, Dilated↗
PubMed1993

Potential impact of pulmonary artery catheter placement on short-term management decisions in the medical intensive care unit.

The purpose of this study was to examine the potential impact of pulmonary artery (PA) catheter placement on short-term management decisions in the medical intensive care unit (ICU). One hundred three patients were examined over an 18-month period. The predominant indications for PA-catheter placement included refractory congestive heart failure, airspace disease, uncertain cardiac filling pressures, or hypotension. In 58 (56%) of the 103 patients, management recommendations changed as a direct result of knowledge gained by PA catheter placement. These changes involved fluid therapy recommendations in 41 patients, vasopressor use in 17 patients, intravenous vasodilator use in 24 patients, and recommendations for the use of inotropic agents in 15 patients. Although 18 patients experienced early or late complications, major events were limited to a single pneumothorax requiring chest tube insertion and four episodes of bacteremia. No deaths were directly attributable to the catheter insertion. In critically ill patients in the medical intensive care unit, PA-catheter placement leads to changes in recommendations for management in a substantial portion of patients with little risk of life-threatening complications in those who receive such invasive monitoring.

Adolescent↗
PubMed1992

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)

Adult↗
PubMed1992

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)

Aged↗
PubMed1992

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.

Cardiac Catheterization↗