Key result
Alinidine lowers heart rate by ~14 bpm and decreases cardiac output without altering stroke volume.
Why the study?
The haemodynamic effects of alinidine, a specific sinus node inhibitor without beta adrenergic receptor interaction, were not well characterized in patients with unstable angina or myocardial infarction.
Does alinidine alter haemodynamic parameters in patients with unstable angina, myocardial infarction, or heart failure?
Does alinidine alter haemodynamic parameters in patients with unstable angina, myocardial infarction, or heart failure?
Alinidine effectively reduces heart rate without affecting stroke volume, though it decreases cardiac output and may precipitate signs of heart failure in a small subset of patients.
Alinidine is a new sinus node inhibitor which does not interact with the beta adrenergic receptors. Its haemodynamic effects were studied in 57 patients; 24 with unstable angina, 9 with myocardial infarction and heart rate greater than 100 bpm but without heart failure. 10 with myocardial infarction treated with vasodilators and 14 with severe heart failure or shock. After dosages up to 40 mg alinidine, heart rate decreased by 14 +/- 7 bpm, mean arterial pressure was reduced by 3 +/- 6 mmHg, stroke volume remained unchanged while cardiac output decreased 0.5 +/- 0.61 min-1 and systemic vascular resistance increased. Signs of heart failure developed in 3 patients, although overall left ventricular filling pressure remained unchanged. The haemodynamic response to alinidine warrants further studies of its efficacy in patients with angina or sinus tachycardia.
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Simoons et al. (1984) studied Unstable angina or myocardial infarction (n=57). Alinidine was evaluated on Haemodynamic effects (heart rate, mean arterial pressure, stroke volume, cardiac output). Alinidine at dosages up to 40 mg decreased heart rate by 14 +/- 7 bpm and mean arterial pressure by 3 +/- 6 mmHg, while stroke volume remained unchanged and cardiac output decreased.
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