Safety and cardiac chronotropic responsiveness to the early injection of atropine during dobutamine stress echocardiography in the elderly.

OBJECTIVE: To determine the safety and cardiac chronotropic responsiveness to early atropine dobutamine stress echocardiography (DSE) in the elderly. DESIGN: Retrospective study of 258 patients >or= 70 years who underwent early atropine DSE and 290 patients >or= 70 years who underwent conventional DSE. In the early atropine protocol, atropine was started at 20 microg/kg/min of dobutamine if heart rate was < 100 beats/min, up to 2 mg. The cardiac chronotropic responsiveness in the elderly was compared with a control group of patients < 70 years matched for sex, myocardial infarction, diabetes, and treatment with beta blockers and calcium channel blockers. RESULTS: The dose of dobutamine given to elderly patients was lower during early atropine than during conventional DSE (mean (SD) 29 (7) v 38 (4) microg/kg/min, p = 0.001). Early atropine DSE resulted in diminished incidence of ventricular extrasystoles, non-sustained ventricular tachycardia, bradycardia, and hypotension compared with conventional DSE. In comparison with patients < 70 years, elderly patients required lower doses of dobutamine and atropine and achieved a higher percentage of predicted maximum heart rate (92 (9)% v 88 (10)%, p = 0.0001). Except for more common hypotension (16% v 10%, p = 0.004), no other difference in adverse effects was observed between patients >or= 70 and < 70 years. CONCLUSIONS: Early atropine DSE is a safe strategy in the elderly resulting in lower incidence of minor adverse effects than with the conventional protocol. Elderly patients presented adequate cardiac chronotropic responsiveness to early injections of atropine, requiring lower doses of drugs to reach test end points.

Effects of low doses of inhaled nitric oxide combined with oxygen for the evaluation of pulmonary vascular reactivity in patients with pulmonary hypertension.

The purpose of this study was to evaluate the hemodynamic effects of inhaled nitric oxide in oxygen (NO + O2) in patients with pulmonary hypertension. Eighteen patients (median age 31.5 months) with pulmonary hypertension inhaled through a mask 100% O2 and 20 parts per million NO + inspired O2 fraction (FiO2) at 0.4. Hemodynamic measurements were made at baseline and after O2 and NO + O2 administration. The pulmonary vascular resistance index decreased after inhalation of O2 and NO + O2 (p = 0.0018 and p = 0.0003, respectively), the decrease being significantly greater after NO + O2 (p = 0.0311). Concerning the transpulmonary pressure gradient, a reduction occurred in values after O2 and NO + O2 inhalation when compared with baseline values (p = 0.0014 and p = 0.0008). In patients with congenital heart disease, an increase occurred in pulmonary blood flow after O2 (p = 0.0089) and NO + O2 (p = 0.0019) compared with baseline values, and an increase also occurred in the pulmonary/systemic blood flow ratio after NO + O2 (p = 0.0017). The main side effect related to NO + O2 was pulmonary congestion in 3 patients. Low doses of NO combined with O2 demonstrated a selective pulmonary vasodilator response in patients with pulmonary hypertension. Despite its use for testing pulmonary reactivity, inhalation of NO + O2 should be carefully administered because of the potential risk of pulmonary congestion.

Do cardiologists at a university hospital adopt the guidelines for the treatment of heart failure?

OBJECTIVE: To verify whether the guidelines for the treatment of heart failure have been adopted at a university hospital. The guidelines recommend the following: use of angiotensin-converting enzyme inhibitors for all patients with systolic ventricular dysfunction, use of digitalis and diuretics for symptomatic patients, use of beta-blockers for patients in functional classes II or III, use of spironolactone for patients in functional classes III or IV. METHODS: We analyzed the prescriptions of 199 patients. All these patients had ejection fraction (EF)

Angiotensin-converting enzyme and apolipoprotein B polymorphisms in coronary artery disease.

The association between angiotensin-converting enzyme (ACE) as well as apolipoprotein B polymorphisms and dyslipidemia and coronary artery disease (CAD) is controversial. We assessed the distribution of ACE insertion and/or deletion, apolipoprotein B signal peptide insertion and/or deletion, and apolipoprotein B XbaI restriction fragment length polymorphisms in 388 nondiabetic patients. We studied 112 patients with angiographically defined asymptomatic CAD or with stable functional classes I and II angina and 139 patients with acute myocardial infarction who were age matched to 137 control subjects. Univariate analysis showed higher prevalence of Xba50% reduction of lumen diameter. Overall, multivariable regression disclosed traditional risk factors and elevated levels of apolipoprotein B for men and reduced levels of apolipoprotein AI for women as independent variables for CAD. After adjustment for the most important subset of risk factors (age, hypertension, hypercholesterolemia, and smoking), apolipoprotein B XbaI polymorphism was disclosed as an independent variable for CAD. Apolipoprotein B XbaI was also selected as an independent variable for acute myocardial infarction after adjusting for age, hypertension, hypercholesterolemia, and smoking. Thus, in addition to traditional coronary risk factors, apolipoproteins B and AI, and apolipoprotein B XbaI polymorphism could be considered predictors of CAD.