Spontaneous regression of cardiomyopathy in a patient with the acquired immunodeficiency syndrome.

Cardiac involvement is common in patients with the acquired immunodeficiency syndrome (AIDS) and, when symptomatic, it portends a poor prognosis. We present a case of marked spontaneous regression of cardiomyopathy in a patient with AIDS. To our knowledge, this is the first reported case of spontaneous recovery of ventricular function in an AIDS patient.

Hemorrhagic compression of the phrenic nerve after streptokinase infusion.

A 72-year-old woman with acute myocardial infarction underwent intravenous streptokinase therapy following an unsuccessful attempt at right subclavian vein catheterization. Three hours after initiation of therapy, chest radiograph revealed a markedly elevated right hemidiaphragm. Subsequent computed tomography and fluoroscopy of the chest revealed paralysis of the phrenic nerve by hematoma. This case demonstrates the hazards of attempted cannulation of noncompressible vessels when fibrinolytic therapy is anticipated.

Methemoglobin levels following intravenous lidocaine administration.

Methemoglobin levels were obtained before and after administration of IV lidocaine in 40 cardiac patients. Patients were given a 1-mg/kg bolus of IV lidocaine hydrochloride, started on a maintenance infusion at 2.0 mg/min, and given a second bolus of lidocaine of 0.5 mg/kg 15 minutes after the initial bolus. The maintenance infusion was adjusted from 1 to 4 mg/min according to clinical needs. Methemoglobin levels were drawn at zero, one, and six hours, and lidocaine levels were drawn at one and six hours after the initial bolus. Elevation of methemoglobin levels after lidocaine administration was statistically significant (P less than .05), but not clinically significant. The highest methemoglobin level obtained was 1.2%. Only one other patient had a level above 1%. No patient developed either signs of lidocaine toxicity or toxic levels of methemoglobin. Routine determination of methemoglobin levels is not clinically indicated following routine lidocaine administration. It may have some as-yet-undetermined value in lidocaine-toxic patients.

Comparative hemodynamic and hormonal response of enoximone and dobutamine in severe congestive heart failure.

The peak hemodynamic effect and hormonal response of the phosphodiesterase inhibitor enoximone (MDL 17,043) were compared with those of dobutamine in 10 patients with severe congestive heart failure. Both agents significantly (p less than 0.05) increased cardiac index, stroke volume index and heart rate. Enoximone tended to decrease mean systemic arterial and pulmonary artery wedge pressures (0.05 less than p less than 0.1), whereas dobutamine did not. Both agents decreased systemic vascular resistance (p less than 0.05). The increase in heart rate was greater with dobutamine than with enoximone (p less than 0.05). Plasma renin activity increased significantly with dobutamine (from 11.3 +/- 13.5 to 17.8 +/- 15.0 ng/ml/hour, p less than 0.01) and with enoximone (from 13.6 +/- 18.3 to 16.6 +/- 18.8 ng/ml/hour, 0.05 less than p less than 0.1). Dobutamine suppressed plasma norepinephrine level (p less than 0.05) and enoximone did not. Neither agent affected the plasma vasopressin level. These data demonstrate a similar acute hemodynamic and hormonal profile for both enoximone and dobutamine. Further, dobutamine, like other beta agonists, provokes renin secretion and may do so to a greater extent than enoximone.

MDL 17,043 therapy in severe congestive heart failure: characterization of the early and late hemodynamic, pharmacokinetic, hormonal and clinical response.

MDL 17,043, an agent with both inotropic and vasodilator properties, was evaluated in the treatment of chronic severe heart failure. The early and late hemodynamic, hormonal, pharmacokinetic and clinical responses to oral MDL 17,043 were studied in 20 patients. MDL 17,043 acutely increased cardiac output from 3.6 +/- 0.9 to 4.6 +/- 1.0 liters/min (+28%, p less than 0.001) and decreased mean pulmonary artery wedge pressure from 24 +/- 8 to 13 +/- 8 mm Hg (-46%, p less than 0.001), mean right atrial pressure from 10 +/- 5 to 4 +/- 4 mm Hg (-60%, p less than 0.001) and mean arterial pressure from 78 +/- 9 to 70 +/- 11 mm Hg (-10%, p less than 0.001). Hemodynamic improvement was sustained for 8 hours. Plasma renin activity tended to increase (0.10 less than p greater than 0.05), plasma norepinephrine tended to decrease (0.10 less than p greater than 0.05) and arginine vasopressin did not show any directional change. Elimination half-life for MDL 17,043 was approximately 20 hours. Hemodynamic responsiveness was maintained in six patients undergoing restudy at 4 weeks. Initial subjective improvement in the 20 patients occurred in 90%, was present at 4 weeks in 50% and continued longer than 3 months in 25%. Side effects occurred in 75% and required cessation of treatment in 10%. Thirteen (93%) of 14 patients on long-term therapy died (median time after start of MDL 17,043 therapy 39 days). Deaths were sudden in 69%. It is concluded that oral MDL 17,043 produces early and late hemodynamic improvement in patients with severe heart failure.(ABSTRACT TRUNCATED AT 250 WORDS)

Plasma vasopressin response to osmotic and hemodynamic stimuli in heart failure.

Arginine vasopressin (AVP) regulation was studied in 42 patients with severe heart failure (CHF) and 10 patients without CHF during cardiac catheterization. Plasma AVP levels were elevated in CHF compared with non-CHF patients (2.98 +/- 2.48 vs. 1.01 +/- 0.44 pg/ml, P less than 0.01). In non-CHF patients, osmotic loading with angiographic contrast caused increases in plasma osmolality (283 +/- 4 to 290 +/- 5 mosmol/l, P less than 0.05) and AVP (1.01 +/- 0.44 to 1.79 +/- 0.20 pg/ml, P less than 0.001). In 10 CHF patients, similar osmotic loading produced an increase in plasma osmolality (275 +/- 13 to 288 +/- 17 mosmol/l, P less than 0.05) and an exaggerated rise in plasma AVP (3.61 +/- 3.17 to 16.30 +/- 12.17 pg/ml, P less than 0.001). The increase in plasma AVP per unit increase in osmolality was greater (P less than 0.01) in the CHF patients (1.36 +/- 1.25 pg . mosmol-1 . 1(-1)) than in non-CHF patients (0.18 +/- 0.17). To determine whether improved cardiac performance would lower AVP levels, 18 CHF patients received the experimental agent MDL 17,043, with improved cardiac index (1.9 +/- 0.4 to 3.3 +/- 0.7 1 . min-1 . m-2, P less than 0.001). Plasma AVP levels did not change significantly (1.99 +/- 0.74 to 2.81 +/- 2.06 pg/ml), but significant inverse correlations were found between changes in plasma AVP and changes in mean (r = -0.53) and systolic (r = -0.65) arterial pressure after MDL 17,043 infusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute hemodynamic effect of oral MDL 17,043 in severe congestive heart failure.

MDL 17,043, when administered intravenously in humans, produces a significant and salutary hemodynamic response. To determine its acute effect when administered orally (3 mg/kg), 10 patients with severe congestive heart failure were studied by right-sided cardiac catheterization for 8 hours. At 4 hours after drug ingestion, there was significant improvement in several hemodynamic measurements. Cardiac index increased 38% over baseline (from 1.9 +/- 0.4 to 2.6 +/- 0.4 liters/min/m2, p less than 0.01), arteriovenous oxygen difference decreased by 30% (from 8.0 +/- 1.4 to 5.6 +/- 1.2 vol%, p less than 0.01), heart rate increased by 8% (from 85 +/- 16 to 92 +/- 16 beats/min, p less than 0.05), stroke volume index increased by 22% (from 23 +/- 5 to 28 +/- 4 ml/beat/m2, p less than 0.05), left ventricular stroke work increased by 24% (from 18 +/- 5 to 22 +/- 5 g-m/m2, p less than 0.01), mean arterial pressure decreased by 10% (from 79 +/- 6 to 71 +/- 9 mm Hg, p less than 0.01), mean right atrial pressure decreased by 40% (from 10 +/- 5 to 6 +/- 4 mm Hg, p less than 0.01), and mean pulmonary artery wedge pressure decreased by 36% (from 22 +/- 5 to 14 +/- 6 mm Hg, p less than 0.01). Cardiac index, arteriovenous oxygen difference, mean arterial pressure, right atrial pressure, and pulmonary artery wedge pressure remained significantly improved at 8 hours. These findings indicate that MDL 17,043 is active when administered orally and produces beneficial hemodynamic effects for as long as 8 hours.

The acute hemodynamic effects of a new agent, MDL 17,043, in the treatment of congestive heart failure.

MDL 17,043 administered intravenously or orally exerts positive inotropic and vasodilator actions in experimental animal preparations. We studied its acute hemodynamic effects in 15 patients with severe congestive heart failure by right-heart catheterization. Intravenous MDL 17,043 at 10 minutes increased cardiac index (3.4 +/- 0.8 vs 1.9 +/- 0.4 l/min/m2), narrowed arteriovenous oxygen content difference (4.6 +/- 0.8 vs 7.8 +/- 2.0 vol%), increased heart rate (98 +/- 14 vs 89 +/- 18 beats/min), and decreased systemic arterial (67 +/- 10 vs 83 +/- 11 mm Hg), pulmonary capillary wedge (12 +/- 5 vs 24 +/- 5 mm Hg) and right atrial (6 +/- 5 vs 12 +/- 7 mm Hg) mean pressures significantly (p less than 0.001). In 11 patients, hemodynamics were monitored hourly for 6 hours. Compared with baseline, the cardiac index and heart rate were higher and mean systemic arterial pressure was lower for 6 hours; pulmonary capillary and right atrial mean pressures were significantly lower for 5 hours. No serious arrhythmias or side effects occurred. These data suggest that MDL 17,043 may be useful for treating congestive heart failure.