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Reduction of stress/catecholamine-induced cardiac necrosis by beta 1-selective blockade
Insights
Atenolol administration in head injury patients reduced cardiac damage markers and arrhythmias. This beta-blocker therapy protected against myocardial injury and infarction, as evidenced by lower creatine kinase-myocardial band levels.
Area of Science:
- Cardiology
- Neurology
- Pharmacology
Background:
- Patients with acute head injury often experience physiological stress.
- This stress can lead to elevated cardiac markers and arrhythmias.
- The role of beta-blockers in mitigating cardiac complications in head injury is not fully understood.
Purpose of the Study:
- To investigate the effect of atenolol on cardiac injury markers in hemodynamically stable patients with acute head injury.
- To assess the incidence of myocardial damage and infarction in patients receiving atenolol versus placebo.
- To evaluate the impact of atenolol on cardiac arrhythmias and electrocardiographic changes.
Main Methods:
- A randomized, double-blind study involving 114 hemodynamically stable patients with acute head injury.
- Patients received either intravenous/oral atenolol or placebo for 7 days.
- Arterial noradrenaline, creatine kinase-myocardial band (CKMB), and electrocardiographic changes were monitored.
Main Results:
- A significant positive correlation between arterial noradrenaline and CKMB was observed in the placebo group (p<0.01), but not in the atenolol group.
- Myocardial damage (CKMB >3%) occurred in 30% of placebo patients versus 7.4% of atenolol patients (p<0.05).
- Atenolol significantly reduced supraventricular tachycardia, ST-T wave changes, and prevented cardiac necrosis.
Conclusions:
- Atenolol administration appears to protect against myocardial injury and infarction in patients with acute head injury.
- Beta-blocker therapy may mitigate stress-induced cardiac complications following head trauma.
- Further research is warranted to confirm these findings and establish clinical guidelines.
Abstract:
114 haemodynamically stable patients with acute head injury were randomised, double-blind, to either placebo or atenolol given intravenously (10 mg every 6 h) for 3 days then orally (100 mg daily) for a further 4 days. Both groups were equally stressed as shown by raised arterial noradrenaline levels. In patients receiving placebo, but not in those receiving atenolol, there was a significant (p less than 0.01) positive correlation between arterial noradrenaline and levels of the myocardial isoenzyme of creatine kinase (CKMB). 30% of the placebo group compared with 7.4% of the atenolol group (p less than 0.05) showed CKMB levels greater than 3% of total creatine kinase (compatible with myocardial damage). CKMB levels greater than 6% of total creatine kinase (compatible with acute myocardial infarction) were present in 16.7% of patients receiving placebo but in no patients receiving atenolol (p = 0.053). Atenolol appeared to reduce significantly the likelihood of supraventricular tachycardia and ST-segment and T-wave changes and prevented cardiac necrosis seen at necropsy.