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Effects of acute hyperglycaemia on cardiac function: an echocardiographic study of monozygotic twins
Insights
Acute hyperglycemia in healthy individuals does not replicate the left ventricular diastolic dysfunction seen in type 1 diabetes. This study investigated the impact of hyperglycemia on diastolic function in non-diabetic twins.
Area of Science:
- Cardiology
- Endocrinology
- Diabetology
Background:
- Congestive heart failure, a major complication of type 1 diabetes, is linked to left ventricular diastolic dysfunction.
- The precise mechanisms driving this dysfunction remain unclear and are not explained by blood pressure, microvascular issues, or HbA1c levels.
- Hyperglycemia, a defining characteristic of diabetes, is a potential factor influencing left ventricular diastolic function.
Purpose of the Study:
- To investigate if acute hyperglycemia can induce left ventricular diastolic function changes in healthy subjects comparable to those observed in patients with insulin-dependent diabetes mellitus (IDDM).
Main Methods:
- A cross-sectional study was conducted involving sixteen healthy twins from eight discordant IDDM twin pairs.
- Non-diabetic twins underwent a hyperglycemic clamp to achieve a blood glucose level of 10 mmol/l.
- Doppler echocardiography assessed left ventricular diastolic function, alongside measurements of blood glucose, insulin, and catecholamines.
Main Results:
- Diabetic twins exhibited a significantly lower transmitral Doppler E/A velocity ratio at baseline compared to their non-diabetic counterparts.
- In non-diabetic twins, induced hyperglycemia led to an increased E/A ratio, driven by an increased E velocity and a decreased A velocity.
- No significant alterations in peak E velocity or isovolumic relaxation time were observed in non-diabetic twins during hyperglycemia.
Conclusions:
- The study concludes that acute hyperglycemia and the associated rise in plasma catecholamines do not induce left ventricular diastolic alterations that mimic those seen in IDDM patients.
- This suggests that hyperglycemia alone may not be the primary driver of diastolic dysfunction observed in type 1 diabetes.
Background:
A major cause of morbidity in type I diabetes is congestive heart failure due predominantly to left ventricular diastolic dysfunction. The mechanism of diastolic dysfunction remains unknown and does not relate to blood pressure, microvascular complications and glycated haemoglobin. Hyperglycaemia is the hallmark of diabetes and is a potential determinant of left ventricular diastolic dysfunction.
Objective:
To determine whether acute hyperglycaemia can induce changes in left ventricular diastolic function in normal subjects similar to those observed in insulin-dependent diabetes mellitus (IDDM).
Design:
Cross-sectional study.
Setting:
London teaching hospital.
Subjects:
Sixteen twins from eight identical twin pairs discordant for IDDM (age 18-38 years, five male) were studied; none had a history or evidence of myocardial ischaemia, valvular or primary heart muscle disease, systemic hypertension or nephropathy.
Interventions:
Non-diabetic twins underwent a hyperglycaemic clamp at 10 mmol/l.
Main Outcome Measures:
Doppler echocardiography was performed in basal condition in identical twin pairs discordant for IDDM and repeated in the non-diabetic twins during hyperglycaemia. Blood glucose, insulin and catecholamines were measured at baseline and during hyperglycaemia.
Results:
Transmitral Doppler E/A velocity ratio was significantly lower in diabetic than non-diabetic twins at baseline (1.44 (0.38) vs. 1.51 (0.19), P<0.05). Glucose infusion in the non-diabetic twins resulted in an increase in their E/A ratio (1.51 (0.19) vs. 1.82 (0. 47), P<0.05) due to an increase in E velocity (68 (12) to 64.7 (10. 7), P<0.05) and a decrease in the peak A velocity (42.7 (3.85) to 38. 0 (4.1), P<0.05). No significant changes were observed in peak E velocity or isovolumic relaxation time in the non-diabetic twins between baseline and hyperglycaemia.
Conclusions:
The alterations in left ventricular diastolic function induced by acute hyperglycaemia and consequent increase in plasma catecholamines do not mimic those demonstrated in IDDM patients.