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Increased cardiac output and lowered peripheral resistance during metoprolol treatment
Insights
Metoprolol treatment lowered blood pressure in hypertensive patients. Initially, cardiac output decreased, but after 24 months, total peripheral resistance dropped, normalizing cardiac output and blood pressure.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Hypertension is a significant risk factor for cardiovascular disease.
- Metoprolol is a commonly prescribed beta-blocker for managing hypertension.
Purpose of the Study:
- To investigate the effects of metoprolol on blood pressure, cardiac output, and left ventricular (LV) wall thickness in hypertensive patients.
- To elucidate the mechanisms underlying blood pressure reduction during metoprolol therapy.
Main Methods:
- Echocardiography was used to assess cardiac parameters every six months.
- Blood pressure, cardiac output (CO), and total peripheral resistance (TPR) were monitored during the study.
Main Results:
- After six months, metoprolol reduced blood pressure (177/110 to 147/88 mm Hg) and significantly decreased CO (6.1 to 5.0 l/min) with unchanged LV wall thickness.
- By 24 months, LV wall thickness decreased (p<0.02), TPR reduced (23.4 to 17.3 mm Hg/l/min, p<0.02), and CO increased to pretreatment levels (6.7 l/min).
Conclusions:
- Metoprolol effectively lowers blood pressure in hypertensive individuals.
- The initial blood pressure reduction is associated with decreased cardiac output, while sustained reduction involves decreased total peripheral resistance, potentially linked to arterial vessel wall remodeling.
Abstract:
Echocardiography was performed at every six months in hypertensives well controlled on metoprolol, 100 mg twice a day. After six months' treatment blood pressure was reduced from 177/110 mm Hg to 147/88 (p less than 0.02). LV wall thickness (septum + posterior wall) was unchanged 2.10 cm (2.14), and a significant drop in cardiac output (CO) to 5.0 l/min (6.1, p less than 0.02) was recorded (pretreatment values in brackets). After 24 months' treatment LV wall thickness was reduced to 1.94 cm (p less than 0.02), total peripheral resistance (TPR) to 17.3 mm Hg/l/min (23.4, p less than 0.02) and CO increased to 6.7 l/min (6.1, n.s.). After six months' treatment, there was thus a drop in BP with a significant drop in CO and unchanged TPR. After 24 months' treatment, however, CO was back to the pretreatment level and the drop in BP was entirely caused by a drop in TPR which was probably secondary to a reduction in the wall thickness of the arterial resistance vessels as judged by the relationship between the reduction in wall thickness in the LV and the reduction in TPR during the treatment.