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Stress/catecholamine-induced cardiac necrosis. Reduction by beta 1-selective blockade
J M Cruickshank1, G Neil-Dwyer, Y Hayes
1ICI Pharmaceuticals PLC, Macclesfield, England.
Insights
Severe head injury can cause cardiac issues due to high catecholamines. Atenolol, a beta-blocker, significantly reduced cardiac damage and elevated cardiac enzyme levels in patients with severe head injury.
Area of Science:
- Cardiology
- Neurology
- Pharmacology
Background:
- Severe head injury induces a hyperadrenergic state, increasing cardiac morbidity risk.
- Previous studies confirmed cardiac complications in patients with severe head injury.
Purpose of the Study:
- To investigate the relationship between plasma catecholamine levels and cardiac morbidity in severe head injury patients.
- To evaluate the efficacy of atenolol in mitigating catecholamine-induced cardiac damage.
Main Methods:
- 114 hemodynamically stable acute head injury patients were randomized to placebo or atenolol.
- Atenolol was administered intravenously then orally for seven days.
- Plasma catecholamine levels and cardiac-specific isoenzyme CK-MB were monitored.
Main Results:
- A significant positive correlation between norepinephrine and CK-MB was observed in the placebo group (P<0.01).
- Elevated CK-MB levels (compatible with myocardial infarction) occurred in 30% of the placebo group versus 7.4% in the atenolol group (P<0.05).
- Atenolol reduced supraventricular tachycardia, ECG changes, and prevented cardiac necrosis.
Conclusions:
- Beta-1 selective blockade with atenolol significantly inhibits catecholamine-induced cardiac necrosis.
- Atenolol demonstrates potential clinical benefits in managing cardiac complications associated with severe head injury.
Abstract:
Catecholamine-induced cardiac necrosis is a well-described phenomenon. Patients with severe head injury are known to be in a marked hyperadrenergic state and can experience cardiac morbidity; this was confirmed in a pilot study. A further study was then undertaken to examine a possible relationship between plasma catecholamine concentration and cardiac morbidity in patients with severe head injury and to assess the effect of intervention with the beta 1-selective agent atenolol. The study involved 114 hemodynamically stable patients with acute head injury who were randomized, double blind, to either placebo or atenolol given intravenously (10 mg every six hours) for three days and then orally (100 mg once a day) for four days. Both groups were equally stressed in terms of raised arterial norepinephrine levels. In patients receiving placebo, but not in those given atenolol, there was a significant (P less than 0.01) positive correlation between arterial level of norepinephrine and plasma level of cardiac-specific isoenzyme CK-MB. Thirty percent of the placebo group, in contrast to 7.4% of the atenolol group (P less than 0.05), had pathologically elevated CK-MB levels (ie, greater than 3% of total CK, a value compatible with acute myocardial infarction). Atenolol appeared to significantly reduce the likelihood of supraventricular tachycardia and ST-segment and T-wave changes and prevented cardiac necrosis (as determined post mortem). The finding that beta 1-selective blockade significantly inhibits catecholamine-induced necrosis has possible broad clinical implications.