Beta-adrenergic receptor (betaAR) stimulation increases cytosolic Ca(2+) to physiologically augment cardiac contraction, whereas excessive betaAR activation causes adverse cardiac remodeling, including myocardial hypertrophy, dilation and dysfunction, in individuals with myocardial infarction. The Ca(2+)-calmodulin-dependent protein kinase II (CaMKII) is a recently identified downstream element of the betaAR-initiated signaling cascade that is linked to pathological myocardial remodeling and to regulation of key proteins involved in cardiac excitation-contraction coupling. We developed a genetic mouse model of cardiac CaMKII inhibition to test the role of CaMKII in betaAR signaling in vivo. Here we show CaMKII inhibition substantially prevented maladaptive remodeling from excessive betaAR stimulation and myocardial infarction, and induced balanced changes in excitation-contraction coupling that preserved baseline and betaAR-stimulated physiological increases in cardiac function. These findings mark CaMKII as a determinant of clinically important heart disease phenotypes, and suggest CaMKII inhibition can be a highly selective approach for targeting adverse myocardial remodeling linked to betaAR signaling.

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The work reported in this article was carried out to determine the role of cardiac enzymes in myocardial infarction. The cardiac enzyme levels of 30 normal subjects and 30 infarcted subjects were determined and compared by statistical analysis. The peak values of the statistical averages of CPK, AST and LDH were compared. The comparison indicated that the peak levels of cardiac enzymes in infarcted subjects were 1.5 to 6.1 times that of the normal subjects. The results also showed that the correlation between the cardiac enzyme concentration levels and the gravity of myocardial infarction was highly significant. From the results, it may be concluded that whenever there is an occurrence of myocardial infarction, higher levels of cardiac enzymes will be present in the blood of the infracted subjects as compared to that in the blood of normal subjects.

Aortopulmonary fistulas are extremely rare and often occur as a result of long-standing aortic aneurysms. They are most frequently due to the erosion of a false aneurysm of the ascending or descending thoracic aorta into the pulmonary artery. Patients generally present with symptoms of acute decompensated heart failure due to a sudden formation of a left-to-right shunt. Here, we present the case of a 63-year-old male who acquired an aortopulmonary fistula four months after undergoing successful bioprosthetic aortic valve replacement.

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