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Objectives: We sought to examine the relationship between coronary flow reserve (CFR) and myocardial capillary density (MCD) in patients with idiopathic dilated cardiomyopathy, heart failure, and normal coronary arteries., Background: Coronary flow reserve is depressed in patients with idiopathic dilated cardiomyopathy, particularly in those with end-stage congestive heart failure., Methods: We studied 18 patients, 48 +/- 10 years of age, who had a mean New York Heart Association functional class of 2.9 +/- 1.3, mean left ventricular ejection fraction of 22 +/- 8%, and mean pulmonary capillary wedge pressure of 23 +/- 10 mm Hg. CFR measurements were made with a 0.014-inch pressure-temperature sensor-tipped guide wire placed in the distal left anterior descending coronary artery. Thermodilution curves were constructed in triplicate at baseline and during maximum hyperemia induced by intravenous adenosine. CFR was calculated from the ratio of mean transit times. Right heart endomyocardial biopsies were performed during the same procedure. Autopsied specimens from nonfailing hearts were used as controls. The tissue was histochemically stained with CD-34 for morphometric measurements of MCD., Results: We observed a close linear relationship between CFR and MCD (r = 0.756, p = 0.0001). The MCD in 7 patients with a CFR >or=2.5 (73.2 +/- 16) was similar to that measured in normal control patients, (85 +/- 11, p = NS). In contrast, the MCD in 11 patients with a CFR <2.5 was 33.2 +/- 14, which was significantly lower than in patients with heart failure and normal CFR (73.2 +/- 16, p = 0.001) or in controls (85 +/- 11, p < 0.0001)., Conclusions: A marked decrease in MCD was found in patients presenting with congestive heart failure as the result of idiopathic dilated cardiomyopathy and a depressed CFR.

Objectives: We prospectively investigated the causes of anemia in patients with advanced congestive heart failure (CHF)., Background: Anemia is common in patients with advanced CHF, and its etiology is generally considered to be multifactorial. However, despite its importance, precise information is lacking regarding the prevalence of putative etiologic factors., Methods: Patients who were hospitalized for decompensated advanced CHF and who were stabilized after their initial treatment underwent evaluation of "clinically significant" anemia, defined as a hemoglobin content <12 g/dl for men and <11.5 g/dl for women. Patients with a serum creatinine concentration >3 mg/dl or patients with concurrent diseases that are known to cause anemia were not included. The initial evaluation included measurements of vitamin B(12), folic acid, thyroid-stimulating hormone, erythropoietin, lactate dehydrogenase, Coombs test, multiple fecal occult tests, and bone marrow aspiration. Patients without diagnosis by these methods underwent red cell mass measurement with (51)Cr assay., Results: The mean age of the 37 patients was 57.9 +/- 10.9 years and mean left ventricular ejection fraction 22.5 +/- 5.9%. Iron deficiency anemia was confirmed by bone marrow aspiration in 27 patients (73%), 2 patients (5.4%) had dilutional anemia, and 1 patient (2.7%) had drug-induced anemia. No specific cause was identified in 7 patients (18.9%) who were considered to have "anemia of chronic disease." Serum ferritin for the iron-deficient patients was not a reliable marker of iron deficiency in this population., Conclusions: In this group of patients, iron deficiency was the most common cause of anemia. The iron status of patients with end-stage chronic CHF should be thoroughly evaluated and corrected before considering other therapeutic interventions.

Objectives: We sought to prospectively and randomly compare survival with clinical and hemodynamic variables in patients with congestive heart failure (CHF) treated with standard versus high doses of enalapril., Background: Angiotensin-converting enzyme (ACE) inhibitors produce hemodynamic and symptomatic benefits in patients with CHF, but there is still controversy about the optimal dose in this clinical setting., Methods: Two hundred and forty-eight patients with advanced CHF (age 56.3+/-12 years) were randomized to receive a maximal tolerated dose of enalapril, up to 20 mg/day in group 1 (mean dose achieved 17.9+/-4.3 mg/day, n = 122) and 60 mg/day in group 2 (mean dose achieved 42+/-19.3 mg/day, n = 126)., Results: At enrollment, patients in group 1 were in New York Heart Association (NYHA) functional class 2.6+/-0.7 and had a mean systolic blood pressure (SBP) of 117+/-18 mm Hg, a mean heart rate (HR) of 85+/-16 beats/min and a left ventricular ejection fraction (LVEF) of 20.0+/-9.8%. In group 2, patients were in NYHA class 2.6+/-0.7; their SBP was 118+/-17 mm Hg, HR 83+/-15 beats/min and LVEF 18.8+/-8.1%. There were no significant differences in these characteristics between the two groups of patients at enrollment. After 12 months of follow-up, 22 (18%) of 122 patients in group 1 and 23 (18%) of 126 patients in group 2 had died (p = 0.995, with 80% power of the study to detect a delta difference of 13%). The NYHA class was the same (1.9+/-0.7) in both groups; SBP was 111+/-16 and 111+/-17 mm Hg, HR 77+/-12 and 79+/-13 beats/min and LVEF 31+/-19% and 30+/-12% in groups 1 and 2, respectively. These differences were not statistically significant. The study had a power of 80% to detect (p = 0.05) the following changes: 13% in death rate, 0.25 units in NYHA class, 6 mm Hg in SBP, 5 beats/min in HR and 6% in LVEF., Conclusions: No significant differences were found in survival and clinical and hemodynamic variables between patients receiving standard and those receiving high doses of enalapril.

Objectives: The aim of this study was to evaluate the efficacy of a single dose of intravenous amiodarone in facilitating defibrillation of ventricular fibrillation refractory to lidocaine and epinephrine plus direct current countershocks in experimental acute myocardial infarction., Background: Amiodarone has been hailed as the most effective single antiarrhythmic drug for the treatment of ventricular arrhythmias. However, intravenous amiodarone has only sporadically been used in the defibrillation of ventricular fibrillation in acute myocardial infarction., Methods: Acute myocardial infarction was induced in 60 dogs by ligation of the proximal left anterior descending coronary artery for 2 h. Animals that developed spontaneous ventricular fibrillation were treated with lidocaine and epinephrine plus five direct-current countershocks. Dogs with ventricular fibrillation refractory to this regimen were randomized to further treatment with additional intravenous administration of epinephrine and bolus lidocaine plus < or = 15 direct-current countershocks (group I) or administration of amiodarone, 10 mg/kg body weight intravenously, followed by defibrillation with direct-current counter-shock (group II)., Results: Sixteen (27%) of the 60 dogs in which the protocol was attempted developed spontaneous ventricular fibrillation 21 min after ligation and were included in the study. Lidocaine and epinephrine plus five direct-current countershocks succeeded in converting ventricular fibrillation in one dog (6%). The other 15 dogs were randomized to group I (8 dogs) or group II (7 dogs). Defibrillation was achieved in one of the eight dogs in group I and in six of the seven dogs in group II (p < 0.005)., Conclusions: In an experimental model of acute ischemia, intravenous amiodarone (10 mg/kg) influences positively the response to defibrillation of ventricular fibrillation refractory to lidocaine and epinephrine plus direct current countershocks.

The abdominal aortic counterpulsation device is a round pumping chamber with a valveless opening which is implanted retroperitoneally on the abdominal aorta. The Utah driver is connected to the device through an air conduit and is synchronized on the electrocardiographic signal to provide diastolic aortic augmentation. For comparison an intraaortic balloon was also driven by the Utah driver system. The abdominal aortic counterpulsation device (stroke volume = 30, 40 and 60 ml) and the intraaortic balloon pump (balloon volume = 20 ml) were tested in dogs with acute left ventricular failure. The abdominal aortic counterpulsation device was also tested in normal animals. In acute left ventricular failure the abdominal aortic counterpulsation device at a stroke volume of 30, 40 or 60 ml decreased left ventricular end-diastolic pressure by an average of 28.56 (p less than 0.001), 39.56 (p less than 0.001) and 44.14% (p less than 0.005), respectively; aortic end-diastolic pressure by 24.11 (p less than 0.001), 26.67 (p less than 0.001) and 19.57% (p less than 0.01); and aortic systolic pressure by 18.56 (p less than 0.002), 26.0 (p less than 0.001) and 22.43% (p less than 0.005). It increased cardiac index by 27.58 (p less than 0.02), 35.59 (p less than 0.005) and 43.42% (p less than 0.001) and it provided peak aortic diastolic augmentation of 64.5 (p less than 0.001), 69.78 (p less than 0.001) and 74.43% (p less than 0.001), respectively, above the control aortic end-diastolic pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

The antiarrhythmic efficacy and safety of intravenous recainam, a newly synthesized compound displaying potent class I antiarrhythmic activity, were tested in 10 hospitalized patients with frequent (greater than 30/h) complex ventricular ectopic beats. There were seven men and three women of average age 57 years (range 21 to 74); five had ischemic heart disease, three had cardiomyopathy and two had valvular heart disease. Recainam was given as a 3.0 mg/kg per 40 min loading infusion followed by a 0.9 mg/kg per h maintenance infusion over a 24 hour observation period. Arrhythmia response was assessed both in the short term (comparing 2 hours before and 1 hour after drug loading) and in the long term (comparing 48 hours before drug loading and 23 hours of maintenance infusion). The median frequency of total premature ventricular complexes decreased in the short term by 99.6% (from 392.5 to 1.5/h, p less than 0.005) and in the long term by 99.7% (from 435 to 1.3/h, p less than 0.01). Repetitive beats were suppressed by a median of 100% both in the short term (p less than 0.006) and during 24 hour infusion (from 80.9 to 0/h, p less than 0.003). More than 90% suppression of repetitive beats occurred in all 10 patients (100%) and more than 90% suppression of total arrhythmias occurred in 9 patients (90%) during the maintenance period. Electrocardiographic PR and QRS intervals increased by 19% (p less than 0.001) and 24% (p less than 0.003), respectively, during therapy, but the JTc interval decreased (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)