Marie Galvao

Impaired endothelium-mediated vasodilation in the peripheral vasculature of patients with congestive heart failure

Impaired endothelial-dependent vasodilation has been demonstrated in two animal models of congestive heart failure and in the coronary circulation of patients with idiopathic dilated cardiomyopathy. To determine whether this impairment contributes to the abnormal peripheral vasomotor tone in patients with congestive heart failure, the local vascular response to intraarterial infusions of graded concentrations (10(-8) M to 10(-5) M) of acetylcholine (an endothelial-dependent vasodilator) and nitroglycerin (a direct-acting vasodilator) was studied in the superficial femoral artery of 19 patients with congestive heart failure (New York Heart Association classes I to IV) and 6 age-matched normal control subjects. The local vascular response was determined from the arterial blood flow velocity pattern obtained by transcutaneous Doppler ultrasonography. Acetylcholine, 10(-5) M, induced a pattern characteristic of vasodilation in all six normal subjects; mean blood flow velocity for the group significantly increased from 11.9 +/- 2.7 to 44.8 +/- 20.9 cm/s (p less than 0.05). In contrast, the same dose of acetylcholine induced a blood flow velocity pattern characteristic of vasodilation in only 4 of the 19 patients with congestive heart failure. Group mean blood flow velocity did not change significantly. Nitroglycerin, 10(-7) M, induced vasodilation in all 6 normal subjects but in only 1 of 19 patients. Nitroglycerin, 10(-5) M, was administered to 10 patients; all 10 demonstrated a pattern characteristic of vasodilation. Thus, acetylcholine-mediated endothelial-dependent vasodilation appears to be impaired in the peripheral vasculature of patients with congestive heart failure. Both endothelial dysfunction and abnormal vascular smooth muscle responsiveness may contribute to abnormal peripheral vasomotor tone.

Characteristics of peak aerobic capacity in symptomatic and asymptomatic subjects with left ventricular dysfunction

Expired gas analysis was used to determine the aerobic exercise performance of subjects with depressed left ventricular (LV) systolic function and congestive heart failure (CHF). To determine whether subjects with no or minimal CHF have better aerobic exercise performance than do those with overt CHF, oxygen consumption (VO2) at anaerobic threshold (AT) and peak exercise was measured in 184 subjects with LV ejection fraction less than or equal to 0.35 who participated in the Studies of Left Ventricular Dysfunction. Subjects were divided into those with overt CHF needing treatment (treatment trial; n = 20) and those who had neither overt CHF nor treatment for CHF (prevention trial; n = 164). Treatment trial subjects had a lower LV ejection fraction (0.25 +/- 0.07) than did prevention trial ones (0.29 +/- 0.05; p = 0.001), but there were no differences in age, gender, body weight, resting heart rate and blood pressure. Treadmill exercise testing was performed after 2 to 3 weeks of placebo (no angiotensin-converting enzyme inhibitor) treatment. Treatment trial subjects exercised for a shorter time (493 +/- 160 seconds) and attained a lower peak VO2 (13 +/- 4 ml/kg/min) and VO2 at AT (11 +/- 4 ml/kg/min) than did prevention trial ones (842 +/- 277 seconds, and 20 +/- 6 and 16 +/- 5 ml/kg/min, respectively). Analysis of covariance showed that the differences in peak VO2 and VO2 at AT were statistically significant between the 2 trials after adjusting for age, gender, LV ejection fraction and New York Heart Association functional class.(ABSTRACT TRUNCATED AT 250 WORDS)

Reduced peak aerobic capacity in asymptomatic left ventricular systolic dysfunction. A substudy of the studies of left ventricular dysfunction (SOLVD). SOLVD Investigator. Studies of Left Ventricular Dysfunction.

BackgroundPeak oxygen consumption is reduced in patients with symptomatic congestive heart failure, but functional capacity of patients with asymptomatic left ventricular systolic dysfunction has not been assessed by measurement of peak oxygen consumption attained during graded exercise testing. Methods and ResultsPeak oxygen consumption, that is, aerobic capacity (VO2, mL/kg per minute), was determined during graded treadmill exercise using the modified Naughton protocol in 40 patients with left ventricular systolic dysfunction (mean ejection fraction ranging from 14% to 35%; mean, 29%) who, while not receiving any cardiac medications, were totally asymptomatic, and in 41 age-matched normal subjects. Peak exercise duration and VO2 were significantly lower in patients with asymptomatic left ventricular systolic dysfunction than in normal subjects (948 ± 273 versus 1239 ± 372 seconds, P < .001, and 22.1 ± 5.9 versus 29.8 ± 7.7 mL/kg per minute, respectively, P < .001), while asymptomatic patients and normal subjects reached similar respiratory equivalents (1.14 ± 0.11 versus 1.11 ± 0.11 [NS]) and level of perceived exertion, using the modified Borg scale (7.4 ± 2.6 versus 8.1 ± 1.5 [NS]). Heart rate, systemic blood pressure, and oxygen pulse response to peak exercise were significantly lower in asymptomatic patients than in normal subjects. ConclusionsAlthough patients with left ventricular systolic dysfunction can be totally asymptomatic in their daily activities, they have experienced a substantial reduction in peak aerobic capacity when compared with normal subjects of similar age.

Control of arteriolar resistance in heart failure. Partial attenuation of specific phosphodiesterase inhibitor-mediated vasodilation by digitalis glycosides.

BackgroundThe vasodilatory response to local specific type III phosphodiesterase inhibition with amrinone was evaluated before and immediately after local administration of digoxin in 14 patients with severe congestive heart failure (CHF). Methods and ResultsA 3F polyethylene catheter was inserted into the common femoral artery for drug administration and pressure monitoring. Mean blood flow velocity (MBFV) was continuously determined in the superficial femoral artery by transcutaneous Doppler ultrasonography. After intra-arterial administration of 10 mg amrinone, group MBFV increased from 7.7±1.4 to 16.0±2.1 cm/sec (p < 0.05, n = 10). Local administration of 20 μg digoxin, which was infused over 20 minutes, did not alter group MBFV (i.e., 8.2±1.6 versus 7.6±1.5 cm/sec;p = NS, n =10). The second administration of 10 mg amrinone, which immediately followed completion of local digoxin infulsion, increased group MBFV but to a lesser extent than that produced by the first amrinone administration (i.e., 11.9±1.9 versus 16.0±2.1 cm/sec; p < 0.05, n = 10). When placebo was administered instead of digoxin, group MBFV was similar after the first and second administrations of amrinone (i.e., 15.3±3.3 versus 15.6±3.8 cm/sec; p = NS, n = 4) ConclusionsAlthough local administration of digoxin did not significantly alter baseline vascular tone in patients with CHF, it substantially decreased the direct vasodilatory effect induced by specific type III phosphodiesterase with amrinone.

HFSA and AAHFN Joint Position Statement: Advocating for a Full Scope of Nursing Practice and Leadership in Heart Failure

The Heart Failure Society of America (HFSA) and theAmerican Association of Heart Failure Nurses (AAHFN)share a common core mission to improve outcomes ofpatients with heart failure. A recent report underscoredthe importance of increasing advocacy efforts to enablenurses to practice to the full extent of their education andtraining and engage in full partnership with physiciansand other health professionals in redesigning health care.

Perceived barriers and facilitators to patients receiving 60 minutes of heart failure education: A survey of AAHFN members

Since its inception, the American Association of Heart Failure Nurses (AAHFN) has assisted heart failure nurses providing appropriate education for their patients. In the most recent strategic plan the Board of Directors specifically targeted ways to enhance and expand patient education resources that our members can use in their clinical practice. This is particularly important as the recognition of 60 min, of inpatient education has been set as a goal by programs that measure outcomes and recognize quality.1,2 The goal of 60 min was supported by research that found a reduction in early readmission in those patients with a total of at least 1 h of inpatient education.3 To provide a baseline assessment as part of our quality improvement efforts, AAHFN devised a survey for membership that would: 1. Assess heart failure (HF) patient provision of 60 min of patient education (60MPE) and preparation for self-care, 2. Identify the barriers to patient education, 3. Assess the difficulty of teaching various topics, and 4. Examine institutional and nurse variables that promote 60MPE. A brief report of the results of the first question was published in a recent AAHFN publication.4 This paper provides a more detailed report of the survey.

HFSA and AAHFN joint position statement: Advocating for a full scope of nursing practice and leadership in heart failure

CHRISTOPHER S. LEE, RN, PhD, BARRY H. GREENBERG, MD, ANN S. LARAMEE, APRN, MS, SUSAN E. AMMON, RN, MS, FNP, MARILYN PRASUN, PhD, CCNS-BC, MARIE GALVAO, MSN, ANP-BC, CHFN, LYNN V. DOERING, DNSC, M. EUGENE SHERMAN, MD, LYNNE WARNER STEVENSON, MD, DOUGLAS D. GREGORY, PHD, PAUL A. HEIDENREICH, MD, MS, NAVIN K. KAPUR, MD, JOHN B. O’CONNELL, MD, ANNE L. TAYLOR, MD, JOSEPH A. HILL, MD, PhD, LINDA BAAS, RN, PhD, ACNP, CHFN, ASHLEY GIBBS, RN, MSN, ANP/GNP-BC, CHFN, KISMET RASMUSSON, FNP-BC, CHFN, CONNIE LEWIS, MSN, ACNP-BC, NP-C, CCRN, CHFN, PEGGY KIRKWOOD, RN, MSN, ACNPC, AACC, CHFN, JUANITA REIGLE, RN, MSN, ACNP-BC, CHFN, LISA RATHMAN, MSN, CRNP, CHFN, AND CYNTHIA BITHER, RN, MSN, APN-C, ACNP-C