Fasting Plasma Glucose and Glycosylated Hemoglobin
August 1, 1999 2 minutes read
Fasting Plasma Glucose and Glycosylated Hemoglobin
The diagnoses of diabetes mellitus (DM) has important health and social implications. Recent revision of diagnostic criteria for DM suggests that persons with fasting plasma glucose 126 mg/dL or greater be diagnosed as diabetic, whereas previously the diagnostic cutoff had been 140 mg/dL. The current study evaluated whether persons with DM diagnosed by the new criteria manifest abnormal hemoglobin A-1-C levels, the diagnostic marker by which treatment is indicated and monitored.
Davidson and colleagues had data on hand from two large data sets, the National Health and Nutrition Examination Survey (NHANES III) (n = 2284), and the Meta-Analysis Research Group Data Set (MRGDS) (n = 7908), from which they were able to compare impaired fasting plasma glucose levels with hemoglobin A-1-C levels.
Less than 0.2% of persons from NHANES III with fasting plasma glucose over 126 had a hemoglobin A-1-C greater than 7.1%, the generally acknowledged demarcation level indicating necessity for treatment. Similarly, less than 2.5% of MRGDS of subjects had a hemoglobin A-1-C greater than 7.3% when fasting plasma glucose was greater than 126.
Davidson et al suggest that improved accuracy of the diagnosis of diabetes could be achieved by restricting the diagnosis to those with elevated fasting plasma glucose coupled with abnormal hemoglobin A-1-C greater than 7.7, and that individuals with less impairment of hemoglobin A-1-C should be classified as having impaired fasting glucose, treated with diet and exercise alone.
Davidson MB, et al. JAMA 1999;281: 1203-1210.
Clinical Scenario. The ECG shown in the Figure was obtained from a previously healthy 56-year-old man with a history of gradually progressive fatigue. No chest pain. No history of prior infarction. The patient has never smoked. An echocardiogram was diagnostic and distinctly abnormal. Can you guess what the echo might show?
Interpretation. The rhythm is sinus bradycardia at a rate of 50 beats/minute. All intervals are normal. The mean QRS axis is indeterminate (QRS complexes are nearly equiphasic in all six limb leads). There is no ECG evidence of chamber enlargement. In the precordia leads transition occurs early; small q waves are seen in leads I, aVL, and V3 through V6; and there is nonspecific ST segment flattening with shallow T wave inversion in leads V2 to V4.
The overall ECG picture is nonspecific in nature. However, in view of the hints provided in the history (the patient was previously healthy, he does not smoke, and has no history of prior infarction)—the early transition with relatively prominent R waves in anterior precordial leads suggests prominent septal forces. The patient had nonobstructive hypertrophic cardiomyopathy with septal hypertrophy that was disproportionately enlarged compared to left ventricular wall thickness (asymmetric septal hypertrophy or ASH). It is likely that the small narrow q waves in leads V3 through V6 are also the reflection of prominent septal forces. Although the ECG will usually be abnormal in patients with hypertrophic cardiomyopathy, the changes seen are most often nonspecific and nondiagnostic. This would have been the case here had there not been the hints we have given.
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