Lack of a hypotensive effect with rapid administration of a new aqueous formulation of intravenous amiodarone.

Hypotension is the most frequent adverse event reported with intravenous amiodarone. Hypotension has been attributed to the vasoactive solvents of the standard formulation (Cordarone IV) and is not dose related, but related to the rate of infusion. Drug labeling calls for intravenous amiodarone to be administered over 10 minutes. A new aqueous formulation of amiodarone (Amio-Aqueous) does not contain vasoactive excipients and may be administered safely by rapid administration without hypotension. This hypothesis was tested using combined data of 4 clinical trials; each assessed the development of hypotension prospectively. Hypotension was defined as a 25% decrease in systolic blood pressure (BP), with the development of a systolic BP of <90 mm Hg or a systolic BP that decreased to <80 mm Hg. In all, 358 Amio-Aqueous and 225 lidocaine boluses were administered to 278 patients; 246 had ventricular tachycardia (VT) during drug administration. Hypotension developed in 11% of patients on Amio-Aqueous versus 19% on lidocaine (p = NS), all during VT; most resolved spontaneously with VT termination. With both drugs, hypotension persisted after VT termination in 1% of patients; the incidence of drug-related hypotension occurred in 2% of patients (1% had hypotension requiring treatment). The Amio-Aqueous was discontinued in 1% of patients, and lidocaine was discontinued in 2% of patients because of hypotension. We conclude that Amio-Aqueous is at least as safe as lidocaine in terms of causing hypotension when administered rapidly. This is a significant advantage over the standard amiodarone formulation, because Cordarone cannot be administered by rapid bolus owing to excipient-related hypotension.

Effects of long-term transdermal nitrate treatment on left ventricular function in patients following myocardial infarction.

BACKGROUND: [corrected] Nitrates are widely used for the treatment of myocardial infarction (MI). The large megatrials (GISSI-3 and ISIS-4) did not in fact demonstrate a significant decrease in mortality in the nitrate-treated group. However, examination of the number of postinfarction angina episodes and the occurrence of cardiogenic shock in the GISSI-3 study did reveal significant decreases. HYPOTHESIS: It was hypothesized that chronic nitrate treatment after an MI preserves left ventricular systolic and/or diastolic functions. METHODS: Patients were divided into two groups: those receiving chronic nitrate treatment for 6 months after an MI (n = 30), and those without such treatment (n = 29). Echocardiography was performed 3, 14, 42, and 180 days after the infarction. The changes in early diastolic and atrial contraction-related mitral valve inflow pattern and deceleration time were assayed. Alterations in systolic, diastolic, and atrial reverse flow velocities in the pulmonary vein were measured, as were ejection fraction (EF), the number of registered angina episodes, and the maximal ST-segment depression in response to the stress test. RESULTS: During the 6-month study period, the increase in systolic pulmonary venous flow velocity was significantly larger in the nitrate group than in the controls. The decreases in the velocities of the diastolic and the atrial reverse flow were also more pronounced in the nitrate group than in the controls. The EF was improved only in the nitrate group. Examination of the maximal ST-segment depression in response to the stress test revealed a significant decrease in the nitrate group only. There were no significant differences between the two groups in the number of registered angina episodes or mitral inflow pattern. CONCLUSIONS: The study showed that prolonged nitrate treatment after an MI may help preserve diastolic left ventricular function.

Intravenous lidocaine versus intravenous amiodarone (in a new aqueous formulation) for incessant ventricular tachycardia.

The effectiveness of intravenous amiodarone for the treatment of incessant (shock resistant) ventricular tachycardia (VT) has not been established. This study evaluated the efficacy of a water-soluble amiodarone preparation or lidocaine for the treatment of shock-resistant VT. The trial was a double-blinded parallel design. Patients were randomized to receive up to 2 boluses of either 150 mg intravenous amiodarone or 2 boluses of 100 mg lidocaine followed by a 24-hour infusion. If the first assigned medication failed to terminate VT, the patient was crossed over to the alternative therapy. Twenty-nine patients were randomized to the study (18 received amiodarone and 11 received lidocaine). There were no significant differences between groups with regard to baseline characteristics. Immediate VT termination was achieved in 14 patients (78%) with amiodarone versus 3 patients (27%) on lidocaine (p <0.05). After 1 hour, 12 patients (67%) on amiodarone and 1 patient (9%) on lidocaine were alive and free of VT (p <0.01). Amiodarone had a 33% drug failure rate, whereas there was a 91% drug failure rate for lidocaine. The 24-hour survival was 39% on amiodarone and 9% on lidocaine (p <0.01). Drug-related hypotension with aqueous amiodarone was less frequent than with lidocaine. This study found that amiodarone is more effective than lidocaine in the treatment of shock-resistant VT.

Multiplane Transesophageal Echocardiographic Detection and Differential Diagnosis of Isolated Right Pulmonary Artery Agenesis.

We present a case report of isolated right pulmonary artery agenesis detected by multiplane transesophageal echocardiography (TEE). A special emphasis is placed on its important role in the differential diagnosis and hemodynamic and functional evaluation of patients with unilateral pulmonary oligemia on chest radiograph. We also present a case report of pulmonary embolism with complete obstruction of the right pulmonary artery for better understanding and for comparison of TEE images in patients with pulmonary artery agenesis. (ECHOCARDIOGRAPHY, Volume 13, July 1996)