The occurrence of ventricular hypertrophy undoubtedly represents an important marker of increased risk for cardiovascular events; therefore, the importance of identifying the patterns of hypertrophy in patients with hypertension is widely justified 1,2 . A recent study by Mensah et al 3 reported that measurement of the left ventricular mass on echocardiography proved to be better for predicting the evolutional process of hypertension as compared with other variables, such as systolic blood pressure, diastolic blood pressure, and hypertension staging 4 . Left ventricular hypertrophy is no longer considered an adaptive process that compensates the pressure imposed on the heart and has been identified as an independent and significant risk factor for sudden death, acute myocardial infarction, and congestive heart failure 4,5 . In cardiac hypertrophy, anomalous collagenous proteins and other types of contractile proteins (myosin with different functional properties) are produced. These myosins show a lower activity of the ATPase enzyme and a lower velocity of power generation. Likewise the formation of anomalous collagenous proteins, changes in contractile proteins also occur. Concomitantly, sarcomeres and fibroblasts proliferate and become hyperplastic. These adaptations aim to maintain the cardiac contractile capacity to compensate the pressure load imposed on the heart 6 . The cardiac adaptive process is not always beneficial for functioning of the heart and causes alteration in myocardial fibers, in the cardiac capacity to respond to adrenergic stimuli, in the left ventricular diastolic function, in the coronary artery flow, and finally in the contractile function 6 . Left ventricular hypertrophy causes important derangements in coronary artery flow. If hypertrophy is mild, the increase in coronary circulation may proportionally accompany the increase in left ventricular mass through vascular neoformation or use of mechanisms of flow reserve. In the cases of significant increase in ventricular mass, generation of new vessels and capillaries is disproportional to the

One thousand women younger than age 50 years suspected of having coronary disease were followed for at least 5 years (average 8.4 years) to determine their course after coronary arteriography. Three patients were lost to follow-up; all had normal arteriograms. The survival rate was 96.9% at 5 years for 761 patients who had less than 50% narrowing of any artery. One patient who had coronary ectasia died within 5 years, and one woman who had minimal lesions suffered sudden death. Seven of 727 women who had normal arteries or less than 30% narrowing of any artery had coronary events (death, myocardial infarction, bypass operation for progressive disease), and six of 34 women who had 30 to almost 50% obstruction of at least one artery had coronary events. Calculations of survival for 236 women who had severe coronary lesions were affected by withdrawal for operation. Five-year survival was 74%.

Both adenosine infusion and adenosine bolus protocols are safe for MCE in humans and can be used for the diagnosis of CAD.

Objective -To test the feasibility, safety and accuracy of the adenosine protocol in the study of myocardial perfusion with microbubbles contrast echocardiography. Methods -

ObjectiveTo compare myocardial contrast echocardiography (MCE) using PESDA and adenosine in bolus (ADN) with myocardial nuclear scintigraphy (NS) ResultsIn 106/125 pts, . . For the LAD territory, concordance was 87.2%; for the RCA, 93.6%; and for the CX, 92.8% (P < 0.001). ConclusionAn excellent concordance exists between MCE and NS in assessing pts for coronary artery disease; therefore, MCE may represent a good alternative for assessing myocardial perfusion.