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Ehud Grossman, MD; Judith Carroll, MD; Talma Rosenthal, MD
Tel Hashomer, Israel

Arch Intern Med. 1993;153(1):126.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

We welcome the comments by Leibowitz and Bursztyn raising an additional possible explanation for the accelerated development of left ventricular hypertrophy in non—insulin-dependent diabetes mellitus. We agree with these authors that ambulatory blood pressure monitoring is more closely related to left ventricular mass than are casual blood pressure measurements.¹ However, even ambulatory blood pressure monitoring has been only weakly related to echocardiographic left ventricular mass,¹ indicating other nonhemodynamic causes for the development of left ventricular hypertrophy. In a substantial number of our patients with 24-hour blood pressure monitoring, there was no significant difference in the nocturnal decline of blood pressure level between the diabetic and the nondiabetic patients. Thus, lack of nocturnal decline in the blood pressure level is difficult to integrate with the accelerated development of left ventricular hypertrophy in diabetic patients. Moreover, Barbagallo et al² recently have suggested that ambient blood glucose level, independent of . . . [Full Text PDF of this Article]

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