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Intracoronary-administered urapidil does not influence myocardial contractility, metabolic activity, or coronary
J G van der Stroom1, H B van Wezel, J J Piek
1Department of Anesthesiology, Academic Medical Center, Amsterdam, The Netherlands.
Insights
Intracoronary urapidil did not affect myocardial contractility or coronary smooth muscle in patients with coronary artery disease (CAD) after percutaneous transluminal coronary angioplasty (PTCA). This study investigated the acute effects of urapidil versus saline.
Area of Science:
- Cardiology
- Pharmacology
- Physiology
Background:
- Coronary artery disease (CAD) affects myocardial function.
- Percutaneous transluminal coronary angioplasty (PTCA) is a common intervention for CAD.
- Understanding the effects of vasoactive drugs on myocardial function is crucial.
Purpose of the Study:
- To compare the acute effects of intracoronary urapidil and saline on myocardial contractility and metabolic activity.
- To evaluate the safety and efficacy of urapidil in patients with CAD undergoing PTCA.
Main Methods:
- Prospective, controlled, open-label study in a university teaching hospital.
- Eight patients with stable CAD undergoing elective PTCA received intracoronary saline followed by 4 mg urapidil.
- Hemodynamic profile, coronary sinus blood flow, left ventricular contractility, and myocardial oxygen consumption were measured.
Main Results:
- Heart rate decreased after saline but increased after urapidil (p = 0.003).
- No significant differences were observed in systemic hemodynamics, left ventricular contractility, coronary dynamics, or myocardial metabolic activity between urapidil and saline.
- An in vitro model established kinetic effects before clinical experiments.
Conclusions:
- Intracoronary bolus administration of 4 mg urapidil showed no detectable effect on myocardial contractility or coronary smooth muscle.
- Urapidil appears safe in awake, nonsurgical CAD patients post-PTCA regarding these parameters.
Objective:
To compare the acute effect of intracoronary administration of urapidil and saline on myocardial contractility and metabolic activity.
Design:
Prospective, controlled, open-label study.
Setting:
University teaching hospital.
Participants And Interventions:
Eight patients with stable coronary artery disease (CAD) undergoing elective percutaneous transluminal coronary angioplasty (PTCA) received normal saline followed by urapidil, 4 mg, injected directly into the left main coronary artery.
Measurements And Main Results:
Because local intracoronary administration is a non-steady-state condition, an in vitro model was used before the clinical experiments to establish the kinetic effects of acute administration of urapidil. The clinical experiments were performed in eight patients with CAD after PTCA. Measurements included a complete hemodynamic profile, coronary sinus blood flow (continuous thermodilution), left ventricular (LV) peak (+) dP/dt, LV peak (-) dP/dt, LV dP/dt/P(D)40, and LV end-diastolic pressures. Arterial and coronary venous blood samples were also obtained for the calculation of myocardial oxygen consumption. Baseline measurements I were first obtained, followed by intracoronary injection of 2 mL of saline. Additional measurements were obtained 1, 5, and 10 minutes after administration of saline. After a resting period (15 minutes), baseline measurements II, and intracoronary injection of urapidil, 4 mg (dissolved in 2 mL saline), additional measurements were obtained 1, 5, and 10 minutes later. Heart rate decreased 2.7+/-3.5 beats/min after injection of saline, whereas heart rate increased 2.0+/-1.8 beats/min after intracoronary urapidil, resulting in a significant difference in treatment effect (p = 0.003). There were no additional differences in treatment effect for any of the other measured or calculated parameters reflecting systemic hemodynamics, LV contractility, coronary dynamics, and myocardial metabolic activity.
Conclusion:
The results suggest that intracoronary bolus administration of preservative-free urapidil, 4 mg, is not associated with any detectable effect on myocardial contractility or coronary smooth muscle in awake nonsurgical patients with CAD, after PTCA.