Influence of atenolol on coronary artery spasm after acute myocardial infarction in a Japanese population.

BACKGROUND: Japanese patients with acute myocardial infarction (MI) have a greater incidence of coronary artery spasm than Caucasians. Some beta-blockers have been reported to aggravate coronary spasm. This study sought to assess the effects of beta-adrenoceptor blockade on coronary vasospasm in Japanese patients with acute MI who had been treated with primary angioplasty. METHODS: In 69 patients we analyzed the effect of atenolol 50 mg/day initiated the day after emergency primary angioplasty on the results of intracoronary ergonovine provocation test performed 4 weeks after onset. RESULTS: Among 35 patients in the atenolol group, the drug was discontinued in 9 (26%) due to hemodynamic compromise. The remaining 26 in the atenolol group and 34 in the control group underwent the spasm provocation test. Atenolol did not significantly increase the incidence of coronary vasospasm (31% vs. 15% in the atenolol and control groups, respectively, p= 0.135). Multivariate analysis revealed that only the pre-provocation diameter of the distal segment of the infarct-related artery predicted coronary spasm whereas atenolol did not. CONCLUSIONS: This study showed that atenolol 50 mg/day did not increase coronary spasm in Japanese acute MI patients. It is suggested that beta-blockers can be safely used soon after coronary intervention for acute MI without the risk of increasing coronary spasm; however, attention should be paid to hemodynamic change in the acute phase.

Subclinical Becker's muscular dystrophy presenting with severe heart failure.

We describe a rare case of Becker's muscular dystrophy (BMD) in a 28-year-old man complicated by rapidly progressing heart failure without apparent clinical signs of neuromuscular disease. He showed rhabdomyolysis, which repeatedly occurred causing acute renal failure as heart failure worsened. His serum creatine kinase (CK) level was generally below 300 IU/l. However, it exceeded more than 10,000 IU/l at the time of myoglobinuria. This suggests that the worsening of heart failure could induce rhabdomyolysis in a BMD patient. Gene analysis for BMD should be considered when the elevation of serum CK is noted in heart failure.

Oxygen radicals mediate ultrastructural and metabolic protection of preconditioning in vivo in pig hearts.

Ischemic preconditioning (PC) preserves myocardial high-energy phosphate metabolites and intracellular pH during subsequent sustained ischemia. Generation of reactive oxygen species may be required to mediate PC, as seen in vitro. In the present study, the effects of inhibiting reactive oxygen species generation during a PC protocol in vivo using an open-chest porcine model were examined. Myocyte ultrastructural changes assessed by electron microscopy were correlated with phosphorus nuclear magnetic resonance spectroscopy data. Open-chest pigs underwent 60 min of left anterior descending coronary artery occlusion. PC was elicited by a single episode of 5 min occlusion and 5 min reperfusion. The cell-diffusible hydroxyl radical and superoxide radical scavenger, N-2-mercapto-propionyl glycine (MPG, 20 mg/kg), or placebo saline were infused for 40 min, starting 30 min before PC (PC plus MPG group, n=10; and PC group, n=9). After PC, ATP and intracellular pH were significantly preserved through 25 min of ischemia (control versus PC, 46+/-3% versus 55+/-5% of baseline [P<0.05]; and control versus PC, 6.18+/-0.08 versus 6.42+/-0.03 [P<0.05], respectively). Phosphocreatine was significantly preserved through 20 min of ischemia (control versus PC, 0+/-0% versus 7+/-2% of baseline [P<0.05]). The preservation of high-energy phosphate metabolites and intracellular pH was abolished by inhibiting the generation of reactive oxygen species with MPG. Preservation of high-energy phosphate metabolites with PC was associated with reduced ultrastructural damage, as seen by electron microscopy, including less myocyte swelling, myofibrillar disruption and nuclear chromatin margination. The present study demonstrates the importance of reactive oxygen species generation in mediating PC preservation of myocyte ultrastructure and high-energy phosphate metabolites during prolonged ischemia in vivo.